Week 1: Non-systems domain
Modalities:
Modality Indications
Ultrasound(conversion) Acute & post acute
conditions (non
thermal) calcium
deposits, chronic
inflammation,
delayed soft tissue
healing, dermal
ulcers, joint
contracture, muscle
spasm, trigger
points, pain, scar
tissue
Phonphoresis Pain modulation,
decrease
inflammation in
subacute and chronic
ms conditions.
Contraindications
Parameters
Desired Outcomes
Possible Side Effects
Acute & post acute
conditions (thermal),
areas of active
bleeding, areas of
decreased
temperature
sensation, areas of
decreased
circulation, DVT,
infection,
malignancy, over
cement or plastic,
over a pacemaker,
vascular insufficiency
Generous amount of
coupling agent.
Transducer size-most
common is 5cm.
Intensity: 1 w/cm2
and 3 w/cm2. Lower
intensities for acute
conditions or thin
tissue. Frequency
(depth) 3MHz used
for 1-2cm and 1 MHz
used for 5cm. Duty
cycle-100% =thermal
effects. Duty cycle
=on time/on time +
off time x 100.
Mode: pulsed 20%,
Treatment intensity:
1-3 w/cm2. Time: 510 minutes.
Medications used:
anti-inflammatory
and analgesics.
Modulate pain,
increase connective
tissue extensibility,
reduce or eliminate
soft tissue
inflammation,
accelerate rate of
tissue healing,
wound healing,
reduce muscle
spasm
Hot spot, pain, dull
ache.
Pain modulation,
decrease
inflammation in
subacute and chronic
ms conditions.
Not likely to burn
Acute & post acute
conditions (thermal),
areas of active
bleeding, areas of
decreased
temperature
sensation, areas of
decreased
circulation, DVT,
infection,
malignancy, over
cement or plastic,
Moist Heat Modulate pain,
increase connective
tissue extensibility,
reduce
inflammation,
increase tissue and
wound healing,
reduce muscle
spasm.
over a pacemaker,
vascular insufficiency
Impaired circulation,
Impaired cognitive
function, Impaired
sensation, Malignant
tumors, over blood
clot, over
pacemaker, over
plastic components.
Paraffin Modulate pain,
increase connective
tissue extensibility,
reduce
inflammation,
increase tissue and
wound healing,
reduce muscle
spasm.
Impaired circulation,
Impaired cognitive
function, Impaired
sensation, Malignant
tumors, over blood
clot, over
pacemaker, over
plastic components.
Fluidotherapy Modulate pain,
increase connective
tissue extensibility,
reduce
inflammation,
increase tissue and
wound healing,
reduce muscle
spasm.
Impaired circulation,
Impaired cognitive
function, Impaired
sensation, Malignant
tumors, over blood
clot, over
pacemaker, over
plastic components.
Decrease muscle
spasm, decrease
tone, increase blood
flow to treatment
area, increase
capillary
permeability,
increased collagen
extensibility,
increased nerve
conduction velocity
Decrease muscle
spasm, decrease
tone, increase blood
flow to treatment
area, increase
capillary
permeablity,
increased collagen
extensibility,
increased nerve
conduction velocity
Decrease muscle
spasm, decrease
tone, increase blood
flow to treatment
area, increase
capillary
permeability,
increased collagen
extensibility,
increased nerve
Burns, rashes, skin
irritation
Reaction to paraffin,
spread of bacteria,
burns,
Spread of bacteria,
burns,
conduction velocity
Diathermy Modulate pain,
increase connective
tissue extensibility,
reduce
inflammation,
increase tissue and
wound healing,
reduce muscle
spasm.
Impaired circulation,
Impaired cognitive
function, Impaired
sensation, Malignant
tumors, over blood
clot, over
pacemaker, over
plastic components.
Ice Massage Inflammation, pain
control, abnormal
tone, acute or
chronic pain, bursitis,
muscle spasm, MS
trauma, trigger
points, tendonitis
Cold intolerance,
cold urticaria
(hypersensitivity),
infection, over an
area of compromised
circulation, over
regenerating
peripheral nerves,
PVD, Raynaud’s, skin
anesthesia
Cold intolerance,
cold urticaria
(hypersensitivity),
infection, over an
area of compromised
circulation, over
regenerating
peripheral nerves,
PVD, Raynaud’s, skin
anesthesia
Cold intolerance,
cold urticaria
Ice Pack(conduction) Inflammation, pain
control, abnormal
tone, acute or
chronic pain, bursitis,
muscle spasm, MS
trauma, trigger
points, tendonitis
Ice bath Commonly use for
the immersion of the
Decrease muscle
spasm, decrease
tone, increase blood
flow to treatment
area, increase
capillary
permeability,
increased collagen
extensibility,
increased nerve
conduction velocity
Decrease blood flow
to area, decrease
spasticity, decreased
edema, decreased
metabolic rate,
decreased nerve
conduction velocity,
increase pain
threshold
Hot spots, dull ache,
periosteal pain
Applied every 1-2 hrs
for 10-20 minutes.
Maintained at 010°F.
Decrease blood flow
to area, decrease
spasticity, decreased
edema, decreased
metabolic rate,
decreased nerve
conduction velocity,
increase pain
threshold
Red or dark pink.
Abnormal: Erythema
of the skin with
wheal formation,
associated c severe
itching, decreased
BP, increased HR
Temperature ranging
from 55-64° F. Body
Decrease blood flow
to area, decrease
Inappropriate due to
dependent position
Apply the ice
massage to an area
no larger than 4x6
inches in slow
overlapping circles.
Treat 5-10 minutes
or until analgesia
occurs.
Cold, burning,
aching, and
numbness
distal extremities
Cryocuff To combine cold and
compression, most
often used on the
knee and post
operatively to
decrease pain
Vapocoolant Reduce muscle
Spray(evaporation) spasms, trigger
points, myofascial
referred pain
TENS Acute or chronic pain
modulation.
(hypersensitivity),
infection, over an
area of compromised
circulation, over
regenerating
peripheral nerves,
PVD, Raynaud’s, skin
anesthesia
Cold intolerance,
cold urticaria
(hypersensitivity),
infection, over an
area of compromised
circulation, over
regenerating
peripheral nerves,
PVD, Raynaud’s, skin
anesthesia
Cold intolerance,
cold urticaria
(hypersensitivity),
infection, over an
area of compromised
circulation, over
regenerating
peripheral nerves,
PVD, Raynaud’s, skin
anesthesia
Patient with demand
type pacemaker,
TENS is not applied
over neck, eyes,
head, or following a
CVA or seizures
part should be
immersed for 15-20
minutes.
spasticity, decreased
edema, decreased
metabolic rate,
decreased nerve
conduction velocity,
increase pain
threshold
Can provide hours of
mild cooling
Decrease blood flow
to area, decrease
spasticity, decreased
edema, decreased
metabolic rate,
decreased nerve
conduction velocity,
increase pain
threshold
Red or dark pink.
Abnormal: Erythema
of the skin with
wheal formation,
associated c severe
itching, decreased
BP, increased HR
Hold 18-24 inches
away from
treatment area,
spray at 30° angle
and sweep spray.
Muscle should be
passively stretched
before and during.
10-15 minutes
treatment time.
See therapy ED book
for all the different
parameters and
conditions.
Increase ROM,
reduce spasm/pain
Frosting of the skin
Acute or chronic pain
modulation.
Burns from exposed
wires, Pain with
treatment, to strong
of current, improper
electrode placement
NMES Disuse atrophy,
impaired ROM,
muscle spasm,
muscle reeducation,
spasticity
management
Premod Modulate pain,
increase muscle
strength, increase
ROM, decrease
edema
Iontophoresis Analgesia, calcium
deposits, Dermal
ulcers, edema
reduction, fungal
infections,
hyperhydrosis,
muscle spasm
FES Disuse atrophy,
impaired ROM,
muscle spasm,
muscle reeducation,
spasticity
management
IFC Modulate pain,
increase muscle
strength, increase
ROM, decrease
edema
If the patient has a
pacemaker, unstable
arrhythmias, seizure
disorders, over
carotid sinus, active
bleeding, metal
implants,
If the patient has a
pacemaker, unstable
arrhythmias, seizure
disorders, over
carotid sinus, active
bleeding, metal
implants,
Impaired skin
sensation, allergy to
agent, cuts, bruises
or broken skin, over
metal
Amplitude- titanic
muscle contraction,
Pulse rate- 50-70
PPS, pulse duration
150-200 usec
Disuse atrophy,
impaired ROM,
muscle spasm,
muscle reeducation,
spasticity
management
Burns from exposed
wires, Pain with
treatment, to strong
of current, improper
electrode placement
Amplitude- strong
but comfortable,
pulse rate- 1-5 PPS,
pulse duration- 150300 usec, mode
continuous,
Modulate pain,
increase muscle
strength, increase
ROM, decrease
edema
Burns from exposed
wires, Pain with
treatment, to strong
of current, improper
electrode placement
Direct current, max
intensity 4-5 mA.
Negative electrode
should be twice as
large as positive
electrode.
Skin irritation, pain,
rash, allergic
reaction to agent,
burns,
If the patient has a
pacemaker, unstable
arrhythmias, seizure
disorders, over
carotid sinus, active
bleeding, metal
implants,
If the patient has a
pacemaker, unstable
arrhythmias, seizure
disorders, over
carotid sinus, active
Tetanic muscle
contraction, pulse
rate 30-85 pps,
duration 15-30 min,
Decrease In
Analgesia, calcium
deposits, Dermal
ulcers, edema
reduction, fungal
infections,
hyperhydrosis,
muscle spasm
Disuse atrophy,
impaired ROM,
muscle spasm,
muscle reeducation,
spasticity
management
Modulate pain,
increase muscle
strength, increase
ROM, decrease
edema
Burns from exposed
wires, Pain with
treatment, to strong
of current, improper
electrode placement.
Amplitude- strong
but comfortable,
pulse rate- 1-5 PPS,
pulse duration- 150300 usec, mode
Burns from exposed
wires, Pain with
treatment, to strong
of current, improper
electrode placement
bleeding, metal
implants,
continuous,
Lumbar Traction Disk Herniation, Joint
hypomobility, muscle guarding,
nerve root impingement, muscle
spasm, subacute pain,
osteophyte formation.
Bone disease, fractures,
dislocation, pregnancy,
osteoprosis, acute
sprains/strains, aortic aneurysm,
hiatal hernia
Cervical Traction Disk Herniation, Joint
hypomobility, muscle guarding,
nerve root impingement, muscle
spasm, subacute pain,
osteophyte formation
Biofeedback Bowel incontinence, CP,
hemiplegia, impaired motor
control,muscle spasms, spinal
cord injuries, urinary
incontinence
Bone disease, fractures,
dislocation, pregnancy,
osteoprosis, acute
sprains/strains,
Conditions where muscle
contraction is detrimental, skin
irritation at the electrod site.
Force of 25% of total body weight
will allow stretching soft tissue
and treat muscle spasms and disk
protusions, force of 50% is used
to actually separate the
vertebrae. Time: 10-30min.
Force on initial treatment should
be 7-10% of patients body
weight, 11-15 pounds. 20-30
pounds will be necessary for joint
distraction.
Two active electrodes should be
place parallel to the muscle
fibers, The reference electrode
can be placed anywhere on the
body, isometric contraction hold
for 6-10 sec. duration 5-10 min
for muscle re-education
Descriptor
Temperature
Cool
67.0-80.0F (19.0-27.0C)
Cold
55.0-67.0F(13.0-19.0C)
Very Cold
32.0-55.0F(0.0-13.0C)
a. Intermittent Compression Pump
Definition
Pneumatic unit designed to apply external
pressure to an edematous body part by a
two layered nylon or plastic appliances
shape to fit either the upper or lower
extremity used to help reduce edema.
Treatment should be a minimum of 2 hours
for every 24 hours and should provide
pressure less than 50mmHg for upper
extremities. and 60 mmHg for lower
extremities to be safe and effective. The
pressure is applied for 45-90 seconds and
then released for 15-30 minutes. The
frequency is between 304 weeks
Indication
Contraindications
Postmastectomy lymphedema. Open
the lymphatic channels using manual
lymphatic massage prior to using the
pup
Patients with arterial insufficiency have
increased peripheral resistance, and
compression increases it further
Traumatic edema
Infections at the site of treatment may
be spread by introducing bacteria into
the lymphatic or venous drainage
Dependent edema of pregnancy
Any thrombi present may become
mobile
Venous insufficiency
Edema in patients with congestive heart
failure should not be treated, because
the increased peripheral resistance
increases the work of the heart.
Definition
Condition
Indication
Ion (Polarity)
Contraindications
Amputations
Edema in patients with kidney
dysfunction should not be treated,
because the kidney may not be able to
excrete teh additional fluid
Prevention of thrombophlebitis
postsurgically
Obstructed lymphatic channels do not
allow drainage. Treatment is ineffective,
and the patient may experience
increased pain
Stasis ulcers
Displaced fractures. Treatment may
displace them further
Mode of Action
Concentration of
Solution
Dosage
Athletes Foot
Copper (+)
Fungicidal
1% copper sulfate
sodium
10mA for 15 minutes,
2x/week
Slow Healing Wound
Zinc (+)
Bactericidal
1.0 M zinc oxide gel
(8.138 g zinc oxide
powder, 10g glycerol,
10g bentonite, 71.862 g
water)
3-6mA for 20 minutes,
increased to25-30
minutes at end of each
of first 2 weeks; 5 days
a week for 3 weeks.
Definition
Indication
Contraindications
Posttraumatic Edema
Hyaluronidase (+)
Breaks down hyaluronic
acid
150 units of
hyaluronidase in 250
mL of a buffer solution
that consists of (1)
sodium acetate 3H2O:
11.42 g (2) Glacial
acetic acid: 0.923 mL
(3) distilled H2O,
quantum satis (qs):
1000 mL
20mA for 20 0minutes
3x/week
Plantar Warts
Salicylate (-)
Removal and relief of
pain
2% sodium salicylate in
aqueous solution
10mA times min; once
per week for 2-3
treatments
Trigger Points
Procaine or Lidocaine
(+)
Local anesthesia (use
with caution)
1% solution in 60-80%
alcohol with 1:20,000
adrenalin
20-30 mA for 20-30
minutes 1-3 times per
week
Acute RA
Citrate (-)
Prevents local
autoimmune response
1% potassium citrate in
distilled water
7.5-10 mA for 20
minutes; daily 3x/week
Peripheral Circulatory
Deficit
Histamine (+)
Vasodilator
1:10,000 histamine
diphosphate
3-12 mA for 5-20 minute
(approximately 60 mA
times minute); 2-3
x/week
Gout
Lithium (+)
Competes with sodium
in formation of urate
lithium urate is soluble
2% lithium chloride
5mA for 20 minutes;
one time per week for 4
weeks
Definition
Myositis Ossificans
Indication
Acetate (-)
Absorption of calcium
Contraindications
3mL of 2% acetic acid in 4 mA for 20 minutes;
distilled water
followed by ultrasound
for 8 minutes at 1.5
W/cm2 at 50% duty
cycle
Choosing an Assistive Device
2.
Amount of Weight Bearing
Unilateral LE WB
Restriction
Bilateral LE WB Restriction
PWB almost full WB
1 Standard Cane
2 Standard Canes
Dec PWB
1 Crutch
Lofstrand Crutches
Dec, Dec PWB
2 Canes
2 Crutches or Walker
Dec, Dec, Dec PWB
2 Crutches
2 Crutches or Walker
TT
2 Crutches or walker
Unable to walk
NWB
2 Crutches or walker
Unable to walk
Amount of Strength
Unilateral LE Weakness
Bilateral LE Weakness
Minimal Weakness
1 Standard Cane
2 Standard Canes
Decreased Strength
1 Quad Cane
2 Quad Canes
Dec, Dec Strength
1 Crutch
Lofsrtand Crutches
Significant Weakness
2 Crutches or Walker
2 Crutches or Walker
Balance Impairment
Ambulatory Assistive
Device
Minimally Impaired
1 Cane
Min-Mod Impaired
1 Lofstrand crutch
Moderately Impaired
2 Crutches or Walker
Significantly Impaired
2 Crutches or walker and
guarding.
Precautions Definition
Standard Precautions Universal precautions and are
designed for the care of all
patients in hospitals regardless of
infection or diagnosis.
Droplet Precautions Reduce the risk of droplet
transmission of infectious agents
through the mouth, nose,
coughing, sneezing, talking, or
suctioning. Travel 3 ft or less.
Contact Precautions Reduce the risk of transmission
of infectious agents through
direct or indirect contact.
Airborne Precautions Reduce the risk of airborne
transmission of infectious agents
through evaporated droplets in
Indications
Procedure: Hand washing, wear
gloves and change between
tasks, wear mask or gown if risk
of spalashing body fluids.
Private room, may share room if
pt has same microorganism,
maintain at least 3 ft between pt
and staff. Room door may remain
open, wear a mask when working
within 3 feet. Limit pts transport
outside of room, pt should wear
mask during transport.
Private room, may share. Use of
gloves when entering room,
change of gloves, wear a gown if
necessary, limit pts transport, do
not share equipment
Private room with monitored air
pressure, 6-12 air changes within
the room per hour, room door
Common Situations
Every hospital patient.
Bacterial: meningitis, pneumonia,
sepsis, pertussis, strep
Viral: adenovirus, influenza,
mumps, paroviarus, rubells
GI, respiratory, skin or wound
infections, multi-drug resistant
bacteria, e-coli, diphtheria,
herpes, impetigo, scabies, zoster
Measles, varicella, tuberculosis
air or dust particles
should remain closed with pt
remaining in room, respiratory
protection worn when entering
the room, limit pts transport
outside the room, pt should wear
mask during transport.
Research Terminology Definition
Sensitivity When referring to a medical test, sensitivity refers to the percentage
of people who test positive for a specific disease among a group of
people who have the disease. A true positive. SnNout: a negative
test rules it out.
Specificity When referring to a medical test, specificity refers to the percentage
of people who test negative for a specific disease among a group of
people who do not have the disease. A true negative. SpPin: a
positive test rules it in.
Independent Variable The variable that is presumed to have caused or influenced the
dependent variable. In research, the IV is what is controlled or
manipulated by the researcher.
Dependent Variable The response or outcome assumed to be caused by the effect of the
IV.
Control Group A group against which the treatment group is compared. Should be
statistically identical to the treatment group, except for the variable
of interest that is being evaluated in the experiment. Used to help
isolate the effect of the IV and eliminate the unintended influence of
extraneous factors that can confound the results.
Research Design The overall strategy that you use to integrate the different
components of the study in a coherent and logical way
Positive Likelihood Ratio Probability of an individual with the condition having a positive test.
Negative Likelihood Ratio Probability of an individual with the condition having a negative test.
Randomization A means of assigning subjects to groups in a experiment so that each
subject has an equal chance of being assigned to each group. The
most robust method of random assignment is accomplished by
computer-generated random numbers or random number tables.
P Value The probability that a particular statistical result could have
happened by chance. When the p-value is smaller than the stated
value of alpha, or level of significance, the null hypothesis is rejected.
When the p-value is larger than the stated value of alpha, or level of
significance, the null hypothesis is not rejected.
Blinding Conditions that are imposed to keep groups of individuals from
knowing which subjects have or have not received an intervention.
Used to reduce bias and the placebo effect.
Intrarater reliability The consistency or equivalent of repeated measurements made by
the same person over time.
Interrater reliability The consistency or equivilance of measurements made by more than
one person. Interrater reliability indicates the agreement of
measurements taken by different examiners.
Nominal Classification scale. Qualitative rather than quantitative. Ex. Blood
type, type of breath sound, and type of arthritis.
Ordinal Ranking scale. Intervals between ranks may not be equal. Ex. MMT
grades, levels of assist, pain, and joint laxity grades.
Interval Intervals between adjacent values are equal, but no true zero point.
Ex. Temperature.
Ratio Intervals between adjacent values are equal and there is a true zero
point. Ex. ROM, distance walked, time to complete activity (seconds),
nerve conduction velocity.
Mean The average; sum of all the values divided by the number of values
Median Middle value, 50%
Mode The value that occurs most.
t-test An inferential statistical procedure for estimating a population mean
or comparing two means when the population is normally
Chi-square test
Reliability
Validity
Levels of Evidence
distributed and the population variance is not known.
A nonparametric statistical procedure for nominal data. The test
evaluates the difference between observed and expected
frequencies to examine the association or independence between
categorical variables.
Is the reproducibility or repeatability of measurements.
Is the degree to which a useful or meaningful interpretation can be
inferred from a measurement.
Systematic Review, Meta-analysis, Randomized Controlled Trial,
Cohort study, Case control, Cross-sectional study, case or report or
case series.
Equipment & Devices:
Assistive and Adaptive Devices:
*Pressure relief push-ups are required, typically ever 15-20 minutes.
*Folding frames make wheelchair transport and storage easier. Rigid frames are typically lighter and sturdier.
Standard adult w/c dimensions for environmental access:
360° turning space = 60 inches X 60 inches (5ft x 5ft)
90° turning space= minimum of 36 inches
Minimum for doorways and halls=32 in; ideal is 36 inches
Countertops= no higher than 31 inches
Ramps=recommended ratio of slope to rise is 1:12 (for every inch of vertical rise, 12 inches of ramp is required) 8.3% grade; minimum of 36
inches wide, with nonslip surface; handrail waist high for ambulators (34-38 inches) and should extend 12 inches beyond the top and bottom of
runs; ramp should have level landing at top and bottom.
Wheelchair measurements:
Measurement
Seat height
Instructions
Measure from the user’s heel to the popliteal
fold and ADD 2 inches to allow clearance of
Average adult size
19.5-20.5 inches
Seat depth
Seat width
Back height
Armrest height
footrest
Measure from users posterior buttock, along
the lateral thigh to the popliteal fold and
SUBTRACT 2 inches.
Measure the widest aspect of the user’s
buttocks, hips or thighs and ADD ~2 inches.
Measure from the seat of the chair to the
floor of axilla with the user’s shoulder flexed
to 90° and then SUBTRACT ~4 inches. This will
allow the final back height to be below the
inferior angles of the scapulae. *Consider seat
cushion
Measure from the seat of the chair to the
olecranon process with the user’s elbow
flexed to 90° and then add ~ 1 inch. *Consider
seat cushion
16 inches
18 inches
16-16.5 inches
9 inches above the chair seat
Device
Walker: Can be used with all levels of weight
bearing. Should allow 20-25° of elbow flexion.
Ascending stairs
The pt should place the walker on the
opposite side of the handrail and turn the
walker sideways. The pt should then grasp the
handrail with one hand and the top of the
walker’s handpiece with the other hand. Using
the handrail and walker for stability, the pt
takes a step up with in uninvolved extremity.
The involved extremity is then advanced to
the same step and the walker follows.
Descending stairs
The walker is positioned in a similar manner as
described previously. The pt uses the handrail
and top of the walker for stability while
lowering the involved lower extremity. The
uninvolved LE is then lowered and the walker
follows.
Axillary crutches: Can be used with all levels
of weight bearing, however require higher
level of coordination for use. Crutch height
should be adjusted no greater than 3 finger
widths from the axilla. Handgrip should be
The pt should use the handrail and turn the
crutch sideways. This will result in pt grasping
the handrail and crutch with the same hand.
Pt will advance with uninvolved extremity
followed by involved.
Pt lowers involved LE and the crutch to the
next step followed by the uninvolved
extremity.
adjusted to the ulnar styloid process and allow
for 20-25° elbow flexion.
Cane: Provides minimal stability and support
for pts during ambulation. A straight cane
should not be utilized for pts that are partial
weight bearing. Small base & large base quad
canes proved a larger BOS & can better assist
w limiting weight bearing. Cane is typically
used on opposite side of an involved LE.
The pt should use the handrail and turn the
cane sideways. This will result in the pt
grasping the handrail and the cane with the
same hand. The pt should use the handrail
and advance the uninvolved LE to the next
step. The pt will then advance the involved LE.
Pt lowers involved LE to next step followed by
uninvolved LE.
Orthotics:
1. Foot orthosis (FO)-may be attached to the interior of the shoe (inserted pad) or the exterior (Thomas heel). Soft inserts reduce areas of
high loading, restrict forces, and protect painful or sensitive areas.
Ex: Metatarsal pad-located posterior to MT heads; moves pressure from the heads to the shafts; allows more push-off in weak or
inflexible feet.
Ex. Cushion heel-cushions and absorbs forces at heel contact; used to relieve strain on plantar fascia in plantar fasciitis.
Ex. Heel-spur pad.
Longitudinal arch supports: prevent depression of the subtalar joint and correct for pes planus; flat foot can be flexible or rigid.
Ex. Scaphoid pad-used to support the longitudinal arch.
Ex. Thomas heel-a heel wedge with an extended anterior medial border used to support the longitudinal arch and correct for flexible pes
valgus (pronated foot)
Posting:
Rearfoot posting-alters the position of the subtalar joint, or rearfoot, from heel strike to footflat. Must be dynamic, control but not
eliminate joint motion.
Ex. Varus post (medial wedge)-limits or controls eversion of the calcaneus and internal rotation of the tibia after heel strike. Reduces
calcaneal eversion during running.
Ex. Valgus post (lateral wedge)- controls the calcaneus and subtalar joint that are excessively inverted and supinated at heel strike.
Forefoot posting: supports the forefoot
Ex. Medial wedge prescribed for forefoot varus.
Ex. Lateral wedge prescribed for forefoot valgus.
Rocker bar-located proximal to MT heads; improves weight shift onto metatarsals.
Rocker bottom-builds up the sole over the metatarsal heads and improves push-off in weak or inflexible feet, May also be used with
insensitive feet.
2. Ankle-foot orthosis (AFO): consists of a shoe attachment, ankle control, uprights, and a proximal leg band.
Ankle controls:
1. Free motion-provides mediiolateral stability that allows free motion in DF and PF.
2. Solid ankle-allows no movement; indicated with severe pain or instability.
3. Limited motion: allows motion to be restricted in one or both directions
-Bichannel adjustable ankle lock (BiCALL)-an ankle joint with the anterior and posterior channels that can be fit with pins to reduce
motion or springs to assist motion
-Anterior stop (dorsiflexion stop)-determines the limits of ankle DF. If set to allow too much DF knee buckling could result.
-Posterior stop (plantar flexion stop) determines the limits of ankle PF. If set for too much PF, knee recurvatum could result.
-Solid AFO-limits all foot and ankle motion.
*Molded AFO’s are contraindicated for individuals with changing leg volume.
3. Knee-ankle foot orthosis (KAFO)-consists of a shoe attachment, ankle control, uprights, knee control, and bands or shells for the calf and
thigh.
Craig-Scott knee-ankle-foot Orthosis-designed specifically for persons with paraplegia, This design allows a person to stand with a posterior lean
of the trunk.
4.Hip-knee-ankle-foot orthosis( HKAFO)-indicated for pts with hip, foot, knee, and ankle weakness. It consist of bilateral knee-ankle-foot
orthoses with an extension to the hip joints and a pelvic band, The orthosis can control rotation at the hip and abd/add. The orthosis is heavy
and restricts pts to a swing-to or swing-through gait pattern.
5.Reciprocating gait orthosis (RGO)-is a derivative of the HKAFO and incorporates a cable system to assist with advancement of the Les during
gait. When the pt shifts weight onto a selected LE, the cable system advances the opposite LE. The orthoses are used primarily for pts with
paraplegia.
Lower Limb Prosthetics
Transtibial (below knee) prosthesis:
Foot ankle assembly: Functions to- absorb shock at heel strike, plantarflex in early stance, permits metatarsophalangeal hyperextension in late
stance, cosmetic replacement of foot.
1.Solid ankle cushion heel (SACH) foot-the most commonly prescribed foot; non-articulated; contains an energy-absorbing cushion heel and
internal wooden keel that limits sagittal plane motion, primarily plantarflexion. Permits a very small amount of mediolateral and transverse
plane motion. Assists in hyperextension of knee during stance.
2.Solid ankle flexible endoskeleton (SAFE) foot-nonarticulted foot, similar to SACH foot, prescribed for more active individuals.
3.Flex-foot-a leaf-spring shank (not a foot) used with an endoskeletal prosthesis, the long band of carbon fiber originates directly from the
shank;
Stores energy in early stance for later use during push-off; prescribed for more active individuals.
4.Single axis foot-an articulated foot with the lower shank; motion is controlled by anterior and posterior rubber bumpers that limited DF and
PF; more stable (permits only sagittal plane motion); may be prescribed for individuals with bilateral transfemoral amputations.
Sockets:
1.PTB (patellar tendon-bearing) socket- a total contact socket that allow for moderate loading area of the patellar tendon.
Pressure-sensitive areas of the transtibial residual limb include: anterior tibia, anterior tibial crest, fibular head and neck, fibular nerve.
Pressure-tolerant areas of the transtibial residual limb include: patellar tendon, medial tibial plateau, tibial and fibular shafts, distal end (rarely,
may be sensitive)
Transfemoral (above knee) prosthesis:
1.Single axis-permits knee motions to occur around a fixed axis, knee flexion is needed during late stance and swing, sitting, and kneeling.
Pressure-sensitive areas of the typical transfemoral residual limb: distolateral end of the femur, pubic symphysis, perineal area.
Pressure –tolerant areas of the typical transfemoral residual limb: ischial tuberosity, gluteals, lateral sides of residual limb, distal end (rarely, may
be sensitive)
Transfemoral gait deviations:
1.Circumduction-prostheis swings out to side in arc. Possible causes: a long prosthesis, locked knee, small or loose socket, inadequate
suspension, foot plantar flexed, abduction contracture, poor knee control
2.Abducted gait-prosthesis is laterally displaced to the side. Possible causes: crotch or medial wall discomfort, long prosthesis, low lateral wall or
malignment, tight hip abductors
3.Vaulting-pt rises up on the sound limb to swing the prosthesis through. Possible causes: prosthesis too long, inadequate suspension, socket too
small, prosthetic foot set in too much plantarflexion, too little knee flexion
4.Lateral trunk bending during stance-trunk bends toward the prosthetic side. Possible causes: low lateral wall, short prosthesis, high medial
wall, weak abductors, abductor contracture, hip pain, short amputation limb
5.Forward flexion during stance-trunk bends forward. Possible causes: unstable knee unit, short ambulatory aids, hip flexion contracture
6.Lumbar lordosis during stance-exaggeration of the lumbar curve. Possible causes: insufficient support from anterior or posterior walls, painful
ischial weight bearing, hip flexion contracture, weak hip extensors or abdominals.
7.High heel rise-during early swing, the heel rises excessively. Possible causes: inadequate knee friction, too little tension in the extension aid
8.Terminal swing impact-the prosthesis comes to a sudden stop as the knee extends during lat swing. Possible causes: insufficient knee friction
or too much tension in the extension aid; pt fears that the knee will buckle, forceful hip flexion.
9.Swing phase whips: at toe-off, the heel moves either medially or laterally. Possible causes; socket it rotated, knee bolt is rotated, foot is
malaligned. *Whip termed by direction of heel.
10.Foot rotation at heel strike-as the heel contacts the ground, the foot rotates laterally, sometimes with vibratory motion. Possible causes: foot
is malaligned, stiff heel cushion, or plantar flexion bumper.
11.Foot slap-excessive PF at heel strike. Possible causes: heel cushion or PF bumper is too soft.
12.Uneven step length-pt favors sound limb and limits weight-bearing time on the prosthetic limb. Possible causes: socket discomfort or poor
alignment; hip flexion contracture or hip instability.
Transtibial amputation:
1. Excessive knee flexion during stance. Possible causes: socket may be aligned too far forward or tilted anteriorly; plantar flexion bumper
is too hard and limits plantar flexion; high heel shoes; knee flexion contracture or weak quads.
2. Inadequate knee flexion during stance. Possible causes: socket may be aligned too far back or tilited posteriorly; plantar flexion bumper
or heel cushion too soft, how heel shoes; anterodistal discomfort, weak quads.
3. Lateral thrust at midstance. Possible causes: foot is inset too much
4. Medial thrust at midstance. Possible causes: foot is outset too much.
5. Drop off or premature knee flexion in late stance. Possible causes: socket is set too far forward or excessively flexed; dorsiflexion
bumper is too soft, resulting in excess dorsiflexion of the foot; prosthetic foot keel too short; knee flexion contracture.
6. Delayed knee flexion during late stance: pt feels as though walking “uphill.” Possible causes: socket is set too far back or lacks sufficnet
flexion; dorsiflexion bumper is too stiff causing excess plantar flexion; prosthetic foot keel too long.
Safety and protection
•Ergonomics
-
A therapist must consistently use proper body mechanics when treating patients and avoid unnecessary stress and starin by
maintaining proper alignment within the musculo system.
- Principles of proper body mechanics
o Use the shortest lever arm possible
o Stay close to the patient when possible
o Use large muscles to perform heavy work
o Maintain a wide base of support
o Avoid any rotary movement when lifting
o Attempt to maintain your center of gravity
•Posture Awareness
-
Use plumb line as a tool to determine verticality. Although desirable, rarely will a given patient demonstrate ideal posture with all
the anatomical landmarks.
•Medical Equipment
-
Feeding devices
o Nasogastric tube (NG tube)- short term liquid feeding and medication administration.
o Gastric tube (G tube)- Inserted into a small incision in the abdomen, long term feeding.
o Jejunostomy tube (J tube)- inserted into the jejunum, used for long term feeding.
- Monitoring devices
o Arterial line- used to measure blood pressure or to obtain blood samples.
o Central Venous pressure Catheter- Measuring pressures in RA or superior vena cava
o Indwelling right atrial catheter (hickman)- used for long-term administration of substance into the venous system.
o Intracranial pressure monitor- measures the pressure exerted against the skull. Normal pressure: 90-180 mm H20
o Oximeter- used to determine the oxygen saturation of the blood
o Pulmonary artery catheter (swan-ganz catheter)- used to provide continues pulmonary artery pressure.
- Sterile Techniques
o All items on the sterile field must be and remain sterile
o Sterile gowns are only considered sterile in the front from the waist level upwards, including sleves.
o Only the top surface of the table or sterile drape is considered sterile, outtter 1 inch is not.
o Do not talk sneeze or cough.
o Any item that positions or falls below waist level is considered contaminated.
o Sterile filds should never be left alone
•Emergency Preparedness
-
CPR
o Compression comes first, then focus on airway and breathing.
o No more look, listen, and feeling. Call 911 immediately
o Push chest at least 2 inches down on adults
o 100 compressions/min
o Don’t stop pushing, no interruptions
- First Aid
o Use gloves when touching all body fluids
o Change gloves between tasks
o Wear mask/eye protection
•Abuse Recognition
-
PT’s are mandated reporters of neglect and/or abuse of children, elders, and the disabled in all 50 states
o Signs and symptoms of abuse/neglect






Unexplained physical injuries
Withdrawal
Increased agitation
Increased depression
Malnutrition
Substandard care of personal hygiene
Professional Responsibilities
Documentation:
Legal requirements: Must comply with applicable jurisdictional requirements, all handwritten entries should be in ink, charting errors should be
corrected by drawing a single line through the error and initialing and dating the chart, should include the referral method (direct access, seflreferral), should include indication of no shows and cancellations.
Defensible documentation: Limit use of abbreviations, date and sign all entries, document legibly, report progress towards goals regularly,
document at the time of the visit when possible, clearly identify note types (daily, progress), include all related communications, include missed
or cancelled visits, demonstrate skilled care, demonstrate discharge planning through the episode of care.
Patient Rights:
HIPPA-Pt confidentiality is maintained in all oral, written, and electronic forms, physical identifabilitiy of pts must be reduced, charts and other
documentation must be stored out of public view and secured, faxes must be sent with cover sheets, cover sheets should be used on clip boards
t hat contain pts paperwork. An individual can access all of their medical records. Providers have 30-60 days to respond.
a. Ethical Issues:
i. Autonomy- requires the wishes of competent individuals must be honored. Autonomy is often referred to as self-determination
ii. Beneficence- A moral obligation of heath care professionals to act for the benefit of others
iii. Confidentiality- the holding of professional secrets or discussions keeping client information within appropriate limits
iv. Duty- the obligation that individuals have to society
v. Fidelity - Related to confidentiality and is defined as the moral duty to keep commitments that have been promised
vi. Justice- The quality of being just of fair; righteousness
vii. Nonmaleficience- the obligation of health care providers to above all else, do no harm.
viii. Paternalism- A term used when someone fails to recognize another individuals rights to autonomy
ix. Rights- The ability to take advantage of a moral entitlement to do something or not to do something
x. Veracity- Obligation of heath care providers to tell the truth.
b. Legal
Term
Definition
Abandonment
unacceptable one-sided termination of services by a health care professional without patient
consent or agreement
Administrative law
administrative agencies at the federal and state level develop rules and regulations to supplement
statutes and executive orders
Common Law
Refers to court decisions in the absence of statutory law often creates legal precedent in areas
where statues have not been enacted.
Constitutional law
Involves law that is derived form the federal constitution. The US Supreme Court is responsible for
ultimately interpreting and enforcing the Constitution
Informed Consent-
The patient is required to sign a document and given permission to the health care professional to
render treatment. This should be obtained from the patient in accordance with the standards of
practice prior to initiation of treatment. The patient has the right to full disclosure of treatment
procedures, risks, expected outcomes, and goals.
Malpractice
The failure to exercise the skills that would normally be exercised by other members of the
profession with similar skills and training. this can include areas of professional negligence, breach
of contract issues, and intentional conduct by a health care professional
Term
Definition
Negligence
The failure to do what a reasonable and prudent person would ordinarily have done under the
same or similar circumstances for a given situation. In order to prove negligence the plaintiff must
prove all of the following:
1. THere was a duty owed to the plaintiff by the defendant
2. There was a breach of that duty under conditions that constituted negligence and
the negligence was the proximate cause of the breach
3. there was damage to the plaintiff’s person or property
Risk management
The identification analysis and evaluation of risks and the selection of the most advantageous
method for treating them
Statutory law
Congress and state legislatures are responsible for enacting status. Examples of federal statutes
affecting health care include the Americans with Disabilities Act and the Family and Medical Leave
Act
Tort-
A private or civil wrong or injury, involving omission and/or commission.
Role of PTA:
PTA is a technically educated health care provider who assists the PT in the provision of PT. The PT is directly responsible for the PTA s actions
related to pt/client management. In general, the PT is not required to be on-site for direction and supervision but must be available at least by
telecommunications. The PTA makes modifications to selected interventions either to progress the pt as directed by the PT or to ensure pt safety
and comfort.
Reimbursement Practices:
Private health insurance companies: fee for service basis. Stock, mutual, and non-profit insurance companies.
Government Health Insurance-uses private contractors to manage the payment process of each health plan.
Medicare Part A: provides benefits for care provided in hospitals, outpatient diagnostic services, extended care facilities, hospice, and short term
care at home required by an illness for which the pt is hospitalized. Enrollment is automatic and funding is through payroll taxes.
Medicare Part B: provides benefits for outpatient care, physician services, and services ordered by physicians such as diagnostic tests, medical
equipment, and supplies. Enrollment is voluntary and funding is through premiums paid by beneficiaries and general federal tax revenues.
Medicaid provides basic medical services to the economically indigent population who qualify by reason of low income or who qualify for
welfare or public assistance benefits in the state of their residence.
IFC model-International Classification of Functioning, Disability and Health Model=Is a classification of health and health-related domains.
PT Examination—Cardiopulmonary
Great vessels of the heart:
1. Aorta-the body’s largest artery and the central conduit of blood from the heart to the body. The aorta begins at the upper
part of the left ventricle, and after ascending for a short distance arches backward and to the left (arch of the aorta). It
then descends within the thorax and passes into the abdominal cavity (abdominal aorta).
2. Superior vena cava-the vein that returns venous blood from the head, neck, and arms to the right atrium.
3. Inferior vena cava-the vein that returns venous blood from the lower body and viscera to the right atrium.
4. Pulmonary arteries-the arteries that carry deoxygenated blood from the right ventricle to the left and right lungs.
5. Pulmonary veins-the veins that carry oxygenated blood from the right and left lungs to the left atrium.
Heart chambers and valves:
•Superior chambers of the heart (right atrium and left atrium). The wall between the atria is the atrial septum.
•The two inferior chambers of the heart are the right ventricle and left ventricle. The wall between the ventricles is the ventricular
septum.
•The right chambers collect blood from the body and pump it to the lungs. The left chambers collect blood from the lungs and pump
it to the rest of the body.
•The heart has 4 valves that function to maintain unidirectional blood flow. The atrioventricular valves (AV) are between the atria
and ventricles and are named by the number of leaflets or cusps. The right AV valve or triscupid valve, has 3. It controls blood flow
between the RA and RV. The left AV valve, or mitral valve has 2. It controls blood flow between the LV and aorta; the pulmonary
valve is between the RV and pulmonary artery.
•Venous blood from the superior and inferior vena cava enters the RA and is pumped through the triscuspid valve into the RV. The
tricuspid valve closes while the RV contacts to pump blood through the pulmonary valve into the pulmonary trunk, which divides the
right and left pulmonary arteries serving the right and left lungs, respectively. After picking up oxygen and releasing carbon dioxide
in the pulmonary capillaries, oxygenated blood returns via the pulmonary veins to the LA. Contraction of the LA forces blood through
the mitral valve into the LV. The mitral valve closes when the LV contracts to pump blood through the aortic valve into the aorta
where it is distributed into the coronary circulation and systemic circulation.
Cardiac Cycle:
Atrial systole-the contraction of the right & left atria pushing blood into the ventricles.
Atrial diastole-the period between atrial contactions when the atria are repolarizing.
Ventricular systole-contraction of the right and left ventricles pushing blood into the pulmonary arteries and aorta.
Ventricular diastole-the period between contractions when the ventricles are repolarizing.
Stroke volume-the amount of blood ejected with each myocardial contraction; normal range is 55-100 ml/beat. Its influenced by:
Left Ventricular end diastolic volume: the amount of blood left in the ventricle at the end of diastole, also known as preload. The
greater the preload, the greater the quantity of blood pumped.
Afterload-the force the LV must generate during systole to overcome aortic pressure to open the aortic valve.
Cardiac Output-the amount of blood discharged from the left or right ventricle per minute. Normal range is 4-5L. Determined by
measuring HR x SV.
Ejection fraction-percentage of blood empties from the ventricle during systole; a clinically useful measure of LV function. Normal
averages >55%.
*Diastolic filling time decreases with increased HR and with heart disease.
Heart Sounds:
S1 sound (“lub”)-normal closure of mitral and triscupid valves; marks beginning of systole. High frequency sound with lower pitch
and longer duration than S2. Decreased in 1st degree heart block.
S2 sound (“dub”)-normal closure of aortic and pulmonary valves, marks end of systole. High frequency sound with higher pitch and
shorter duration than S1. Decreased in aortic stenosis.
Extra sounds: Murmurs
1. Systolic-falls between S1 and S2. May indicated valvular disease or may be normal.
2. Diastolic-falls between S2 and S1. Usually indicates valvular disease.
3. Thrill-an abnormal tremor accompanying a vascular or cardiac murmur, felt on palpation.
Bruit-adventitous sound or murmur (blowing sound) of arterial or venous origin, common in carotid or femoral arteries; indicative of
atherosclerosis.
Gallop rhythm-an abnormal heart rhythm with three sounds in each cycle; resembles the gallop of a horse.
1. S3; vibrations of the distended ventricle walls due to passive flow of blood from the atria during the rapid filling phase of
diastole. Normal in healthy young children, abnormal in adults, may be associated with heart failure. “ventricular gallop”
2. S4; pathological sound of vibration of the ventricular wall with ventricular filling and atrial contraction. May be associated
with HTN, stenosis, MI. “atrial gallop”
Auscultation of heart sounds
Procedure:
The bell or diaphragm of the stethoscope is held directly on the pts bare skin with enough pressure to provide a skin seal while the pt breathes
quietly through the nose.
Listen over four designated auscultatory areas:
Aortic area-2nd intercostal space at the right sternal border
Pulmonic area-2nd intercostal spaceat the left sternal border
Mitral valve-5th intercostal space, medial to the left midclaviciular line
Triscupid area-4th intercostal space at the left sternal border
Picture on page 264 of scorebuilders.
Examine heart rhythm:
A 12 lead EKG provides 12 views of the heart. It is used to assess cardiac rhythm, to diagnose the location, extent, and acuteness of myocardial
ischemia and infarction, and to evaluate changes with activity.
Waveforms and Intervals:
1.
2.
3.
4.
P wave-atrial depolarization
PR interval-time for atrial depolarization and conduction from the SA node to the AV node. Normal duration is 0.12 to .20 seconds.
QRS complex-Ventricular depolarization and atrial repolarization. Normal duration is 0.06 to 0.10 seconds.
QT interval-Time for both ventricular depolarization and repolarization. Normally ranges from .20 to 0.40 seconds, depending on heart
rate.
5. ST segment-isoelectric period following QRS when the ventricles are depolarized.
6. T wave-ventricular repolarization
Sinus Node Rhythms:
1. Normal sinus rhythm-atrial depolarization begins in the SA node and spreads normally throughout the electrical conduction system with
a HR between 60-100 bpm.
2. Sinus bradycardia-sinus rhythm with a HR less than 60 bpm (in adults)
3. Sinus tachycardia-sinus rhythm with a HR more than 100 bpm.
4. Sinus arrhythmia-a sinus rhythm, but with quickening and slowing of impulse formation in the SA node resulting in a slight beat-to-beat
variation of the rate.
5. Sinus arrest-a sinus rhythm, except with intermittent failure of the either the SA node impulse formation or AV node conduction that
results in the occasional complete absence of P or QRS waves.
Atrial dysrhythmias:
Condition:
Premature atrial contractions (PAC)- occur
when an ectopic focus in the atrium
initiates an impulse before the SA node.
Clinical significance:
PACs are very common and generally
benign, but may progress to atrial flutter,
tachycardia or fibrillation. May occur with
a normal HR (from caffeine, stress,
smoking, alcohol) and any type of heart
disease
EKG reading
The p wave is premature with abnormal
configuration.
Atrial flutter-An ectopic, very rapid atrial
tachycardia. Atrial rate of 250-350 bpm;
ventricular rate dependent upon AV node
conduction.
Occurs with valvular disease (especially
mitral), ischemic heart disease,
cardiomyopathy, hypertension, acute
myocardial infarction, chronic obstructive
lung disease, and pulmonary emboli. Signs
and symptoms include palpitations,
lightheadedness, and angina due to a
rapid rate. Stagnation of blood may
predispose to thrombi in the atria
Occurs in healthy hearts and in pts with
coronary artery disease, hypertension,
and valvular disease. Symptoms may
include palpitations, fatigue, dyspnea,
lightheadedness, syncope, and chest pain.
Stagnation of blood may predispose to
thrombi in the atria.
Saw-tooth shaped P waves (also known as
flutter waves) are characteristic.
Atrial fibrillation-a common arrhythmia
where the atria are depolarized between
350 and 600 times a min.
EKG shows characteristically
irregular undulations of EKG baseline
without discrete P waves.
Ventricular arrhythmias:
Condition:
Premature ventricular complex (PVC)premature depolarization arising the in
ventricles due to an ectopic focus. Unifocal
Clinical significance:
A common arrhythmia that occurs in healthy
and diseased hearts. Pt may be asymptomatic
or have palpitations. Common causes include
EKG reading:
On EKG, the P wave is usually absent and the
QRS complex has a wide and aberrant shape.
PVCs arise from the same ectopic focus and
have the same configuration. Multifocal PVCs
arise from different ectopic foci and have
different configurations.
Bigeminy-normal sinus impulse is followed by
a PVC.
Trigeminey-PVC occurs after every two normal
sinus impulses.
anxiety, caffeine, stress, smoking, and all
forms of heart disease.
Ventricular tachycardia (v-tach)-3 or more
consecutive PVCs at a ventricular rate of >150
bpm.
V-tach longer than 30 seconds is a life
threatening arrhythmia and requires
immediate medical intervention. Pts are not
able to maintain an adequate blood pressure
and eventually become hypotensive. V-tach
may degenerate into ventricular fibrillation
causing cardiac arrest. Common causes
include MI, cardiomyopathy, and valvular
disease.
P waves are absent and QRS complexes are
wide and aberrant in appearance.
Ventricular fibrillation (v-fib)-Ventricles do not
beat in a coordinated fashion, but fibrillate or
quiver asynchronously and ineffectively. No
cardiac output; pt becomes unconscious.
A lethal tachyarrhythmia requires immediate
defibrillation. Additional measures include
medications to support the circulation and
intravenous antiarrythmic agents. Common
causes include heart disease of any type, MI,
and cocaine use.
EKG shows characteristic fibrillatory waves
with an irregular pattern that is either coarse
or fine.
Ventricular asystole-Ventricular standstill with
no rhythm.
Requires immediate defibrillation and/or
medications to stimulate cardiac activity.
Common causes include acute MI, ventricular
rupture, cocaine use, lightning strikes, and
electrical shock.
EKG records a straight-line pattern.
AV Conduction Blocks:
1st degree AV block: PR interval is longer than 0.2 seconds, but relatively constant from beat to beat.
•Clinical significance: No symptoms or significant change in cardiac function. PR interval may become prolonged for many reasons include
medications that suppress AV conduction.
2nd degree AV block: AV conduction disturbance in which impulses between the atria and ventricles fail intermittently. Two major types: Mobitz
type 1 block (also called Wenckebach block) and Mobitz type 2 block
•Clinical significance: Mobitz I-progressive prolongation of PR interval until one impulse is not conducted (generally benign)
Mobitz II-consecutive PR intervals are the same and normal followed by nonconduction of one or more impulses (a more serious condition). If
heart rate is slow, cardiac output will decrease with the blocked impulse. Also, 2nd degree AV block may progress to 3rd degree AV block
3rd Degree AV block (complete heart block)-All impulses are blocked at the AV node and none are transmitted to the ventricles. The atria and
ventricles are paced independently; atrial rate > ventricular rate.
•Clinical significance: Considered a medical emergency requiring a pacemaker. If the ventricular rate is too slow, the cardiac output drops and
the pt may faint. Common causes include degenerative changes of the conduction systems, digitalis, heart surgery, and acute MI.
Signs and Symptoms
Right Sided Heart
Failure
Nausea
anorexia
weight gain
ascites
right upper quadrant pain.
Increase in RAP, CVP,
Jugular venous distention
Positive heptojugular reflex
right ventricular eave
Murmur of tricuspid insufficiency
Hepatomegaly
Peripheral edema
Signs and Symptoms
Left Sided Heart
Failure
Fatigue
cough
shortness of breath
DOE
Orthopnea
PND
Diaphoresis
Tachycardia
S3 Gallop
Crackles
Increased PAP, PAWP, SVR
Laterally displaced PIM
Left ventricular heave
Pulsus alternans
confussion
decreased urine output
Cheyne Stokes respiration (advanced failure)
Murmur of mitral insufficiency
Tests of peripheral arterial circulation:
Ankle brachial index (ABI)-the ratio of lower extremity pressure divided by upper extremity pressure.
-Performed in UE at brachial artery, LE at posterior tibial and dorsalis pedis arteries.
ABI assists in risk stratification for cardiovascular disease:
<0.90 is associated with 2-4 fold increased risk for cardiovascular events and death.
ABI < 0.50: increased risk of progression to severe or critical limb ischemia in 1 year.
>1.40
Indicates non-compliant arteries
1.00-1.40
Normal
0.91-0.99
Borderline
< or equal to 0.90
<or equal to 0.50
Abnormal
Severe arterial diease, risk for critical limb ischemia, may have pain at
rest
Exercise Stress/Tolerance Testing:
-Serves as a basis for exercise prescription, used as a screening measure for CAD in asymptomatic individuals.
-A pharmacological stress test is used when a patient is unable to perform a regular ETT.
Testing modes: Treadmill and cycle ergometry (leg or arm tests), step test.
Maximal ETT: defined by target endpoint HR. Should only be completed in settings with advanced cardiac life support.
-Age predicted maximum heart rate: 220-age
-Heart rate range (Karvonenen’s): 60%-80% (HR max-resting HR) + resting HR=target HR
Submaximal ETT: Symptom limited or terminated at 85% of age predicted HR max; safe in all settings
Continuous ETT: workload is steadily progressed; step test allowing pt reach steady state, ramp test-pt is not permitted to reach steady state.
Absolute indications for terminating an exercise test:
1.
2.
3.
4.
5.
6.
Drop in SBP>10 mm Hg from baseline despite increase in workload with other evidence of ischemia
Moderately sever angina (three on a scale of four)
Increasing nervous system symptoms (ataxia, dizziness)
Signs of poor perfusion (cynaosis, pallor)
Sustained ventricular tachycardia
1.0 mm ST elevation in leads without diagnostic Q waves
Pulmonary Anatomy:
Muscles of inspiration: diaphragm (primary), external intercostals, and internal intercostals and considered principal muscles of inspiration.
Accessory muscles of inspiration: sternocleidomastoid, scalenes, pec major & minor, and serratus anterior.
Muscles of exhalation: results from passive recoil of the lungs and rib cage. During forceful breathing the rectus abdominus, external oblique,
internal oblique, and transverse abdominus depress the lower ribs and compress the abdominal contents, thus pushing up the diaphragm and
assisting with active exhalation.
Alveolar-capillary units-The bronchi branch many times before terminating in the acinus or respiratory unit of the lung. Oxygen diffuses across
the alveolar-capillary septum into the red blood cells in the lung capillaries where it combines with hemoglobin to be transported back to the
heart. Carbon dioxide diffuses in the opposite direction.
Pleurae-a membranous serous sac called visceral pleura covers each lung. The pleura covering the surface of the lungs is called the visceral
pleura. The pleural tissue covering the inner surfaces of the chest wall, ribs, vertebrae, diaphragm, and mediastinum is called parietal pleura.
Normally, the two pleurae remain in contact throughout the respiratory cycle, separated only by serous fluid. Under abnormal circumstances,
the pleural space may contain air (pneumothorax) blood (hemothorax), pus or increased amounts of serous fluid, which compress the lung and
cause respiratory distress.
Pulmonary circulation- the portion of the circulatory system that carries deoxygenated blood from the heart to the lungs via the pulmonary
arterial trunk, right and left pulmonary arteries, lobar arteries, arterioles, and capillaries. The pulmonary circulation returns oxygenated blood
from the lungs to the left atrium via the pulmonary veins.
Bronchial circulation-the portion of the circulatory system that supplies oxygenated blood to the bronchi and connective tissue of the lungs via
the bronchial arteries, which drain directly into the bronchial veins.
Lung Volumes & Capacities:
Anatomic dead space volume (VD)
Expiratory reserve volume (ERV)
Forced expiratory volume (FEV)
Forced vital capacity (FVC)
Functional residual capacity (FRC)
Inspiratory capacity (IC)
Inspiratory reserve volume (IRV)
The volume of air that occupies the non-respiratory conducing airways
The maximal volume of air that be exhaled after a normal tidal
exhalation. ERV is approximately 15% of total lung volume.
The maximal volume of air exhaled in a specified period of time:
usually the 1st, 2nd and 3rd second of a forced vital capacity maneuver.
The volume of air expired during a forced maximal expiration after a
forced maximal inspiration.
The volume of air in the lungs after normal exhalation. FRC=ERV + RV.
FRC is approximately 40% of total lung volume.
The maximal volume of air that can be inspired after a normal tidal
exhalation. IC=TV + IRV. IC is approximately 60% of total lung volume.
The maximal volume of air that can be inspired after normal tidal
Minute volume ventilation (VE)
Peak expiratory flow (PEF)
Residual volume (RV)
Tidal volume (TV)
Total lung capacity (TLC)
Vital capacity (VC)
volume inspiration. IRV is approximately 50% of total lung volume.
The volume of air expired in one minute. VE=TV x respiratory rate.
The maximum flow of air during the beginning of a forced expiratory
maneuver.
The volume of gas remaining in the lungs at the end of a maximal
expiration. RV is approximately 25% of total lung volume.
Total volume inspired and expired with each breath during quiet
breathing. TV is approximately 10% of total lung volume. (500ml)
The volume of air in the lungs after a maximal inspiration; the sum of
all lung volumes. TLC=RV + VC or TLC= FRC + IC
The volume change that occurs between maximal inspiration and
maximal expiration. VC= TV + IRV + ERV. VC is ~75% of total lung
volume.
Normal breath sounds:
Tracheal & bronchial sounds-Loud, tubular sounds normally heard over the trachea. Inspiratory phase is shorter than the expiratory phase and
there is a slight pause between them.
Vesicular breath sounds-High pitched, breezy sounds normally heard over the distal airways in healthy lung tissue. Inspiratory phase is longer
than expiratory phase and there is no pause between them.
Adventitous breath sounds:
Crackles (also termed rales, crepitations): a crackling sound heard usually during inspiration that indicates pathology) atelectasis, fibrosis,
pulmonary edema)
Wheezes: a musically pitched sound, usually heard during expiration, caused by airway obstruction (asthma, COPD, foreign body aspiration)
Lung Lobe Location & Postural Drainage Position
Lobe
Position
Right or Left Anterior Upper Lobe/Segment
Supine in a reclined seated position with knees supported
Right or Left Posterior Apical Segment
Seated and slumped over a pillow with lower extremities supported in a
comfortable position
Right and Left Anterior Segments
Supine with knees supported with a pillow
Right Posterior Segment
Prone slightly on the left side
Left Posterior segment
Prone with left side of torso propped up on pillows. Torso is at a 45
degree angle.
Right Middle Lobe
Supine with right side propped up on pillows and lower extremities
elevated 12 inches
Left Ingular
Supine with left side propped up on pillows and lower extremities
elevated 12 inches
Anterior Segments (Lower Lobes)
Supine with knees supported with pillows and lower extremities elevated
18 inches
Right Lateral Segment
Left sidelying with lower extremities elevated 18 inches
Left Lateral Segments
Right sidelying with lower extremities elevated 18 inches
Posterior segments
Prone in comfortable position/neutral spine with pillows under abdomen
and comfortable feet position with pillows under lower legs with lower
extremities elevated 18 inches
Superior Segments
Prone in comfortable position/neutral spine with pillows under abdomen
and comfortable feet position with pillows under lower legs.
Arterial blood gases:
pH
7.4 (7.35-7.45)
PaCO2 (amount of carbon dioxide within arterial blood)
40 mm Hg at sea level breathing ambient air (35-45mm Hg)
PaO2
97 mm Hg at sea level breathing ambient air (80-100 mm Hg)
HCO3- (amount of bicarbonate ions within arterial blood)
24 mEq/L (22-26)
SaO2
95-98%
*By convention, ABG results are written or spoken in the following
order: pHPaCO2PaO2HCO3- (e.g. 7.4/40/97/24)
Acidemia
Elevated acidity of blood (pH < 7.35)
Alkalemia
Decreased acidity of blood (pH > 7.45)
Eucapnia
Normal level of CO2 in arterial blood (35-45 mm Hg)
Hypercapnia
Elevated level of CO2 in arterial blood( > 45 mm Hg)
Hyopcapnia
Low level of CO2 in arterial blood (<35 mm Hg)
Hypoxemia
Low level of O2 in arterial blood (PaO2 < 80 mm Hg)
Mild hypoxemia
PaO2 60-79 mmHg
Moderate hypoxemia
PaO2 40-59 mmHg
Severe hypoxemia
PaO2 < 40 mmHg
Hypoxia
Low level of O2 in the tissue despite adequate perfusion of the tissue
*An increase in the PaCO2 decreases the body’s pH. A decrease in the PaCO2 raises the body’s pH.
*Supplemental oxygen is usually prescribed when the PaO2 falls below 55 mmHg.
Other values:
White Blood Cells (WBCs)
Red Blood Cells (RBCs)
Erethrosedimentation Rate (ESR)
Hematocrit
Platelet
4300-10,800
Male: 4.6-6.2 Female: 4.2-5.9
Male: <15 mm/hr Female: <20
Male: 45%-52% Female: 37%-48%
150,000-450,000
Sodium
Calcium
Potassium
Magnesium
Total cholesterol
LDL
HDL
Triglyceride
135-146
8.4-10.4
3.5-5.5
1.8-2.4
<200
<100
<40
<150
Acid-Base balance
Type
Respiratory alkalosis
pH
PaCO2
HCO3-
Causes
Alveolar
hyperventilation
↑
↓
WML
Respiratory acidosis
↓
↑
WNL
Alveolar
hypoventilation
Metabolic alkalosis
↑
WNL
↑
Metabolic acidosis
↓
WNL
↓
Bicarbonate
ingestion, vomiting,
diuretics, steroids,
adrenal disease
Diabetic, lactic, or
uremic acidosis,
prolonged diarrhea
Signs & Symptoms
Dizziness, syncope,
tingling, numbness,
early tetany
Early: anxiety,
restlessness,
dyspnea, headache
Late: confusion,
somnolence, coma
Vague symptoms:
weakness, mental
dullness, possibly
early tetany
Secondary
hyperventilation
(Kussmaul breathing),
nausea, lethargy,
coma
Common Disorders/Pathology of the Cardiopulmonary System:
Pathology
Aneurysm
What is it
A localized abnormal
dilation of a blood vessel,
usually an artery. Common
sites include the thoracic
& abdominal aorta and
vessels within the brain.
Etiology
Congenital defect;
weakness in the wall of
vessel often due to chronic
HTN, connective tissue
disease (Marfan
Syndrome), trauma,
infection
Angina pectoris
A transient precordial
sensation of pressure or
discomfit resulting from
myocardial ischemia.
Common types of angina
pectoris are : Stable
(occurs at predictable level
of exertion, responds to
rest or nitroglycerin)
Unstable (usually is more
intense, lasts longer, is
precipitated by less
exertion, occurs
spontaneously at rest, is
progressive) Prinzmetal or
Inadequate blood flow &
oxygenation of the heart
muscle mostly due to
coronary artery disease.
Signs & Symptoms
Variable based on the site.
Aortic aneurysms are
usually asymptomatic, but
may include generalized
abdominal or LBP.
Abdominal aortic
aneurysms may cause
pulsations near the navel.
A cerebral aneurysm can
cause a sudden and severe
headache, nausea &
vomiting, stiff neck,
seizure, loss of
consciousness, & double
vision.
Usually described as
pressure, heaviness,
fullness, squeezing,
burning or aching behind
the sternum, but may also
be felt in the neck and
back, jaw, shoulders, and
arms. The sensation may
be associated with
difficulty breathing,
nausea or vomiting,
sweating, anxiety, or fear.
It is typically triggered by
exertion or strong emotion
and subsides with rest.
Treatment
Antihypertensive
medications may be
recommended for HTN.
Surgery is recommended
to repair large aortic
aneurysms and consists of
replacing the aneurysm
with a synthetic fabric
graft. Two surgical options
for ruptured brain
aneurysms are surgical
clipping & endovascular
coiling.
Tx for acute angina include
supplemental oxygen,
nitroglycerin, and rest.
Chronic or recurring
angina pectoris is treated
with long-acting nitrates,
beta blockers, and calcium
channel blockers.
Angioplasty with stenting
of the coronary arteries or
coronary artery bypass
surgery (CABG) may be
performed when
medications are not
effective.
Atherosclerosis
variant angina (occurs due
to coronary artery spasm
most often associated
with coronary artery
disease)
A slow progressive
accumulation of fatty
plaques on the inner walls
of arteries. Over time the
plaque can restrict blood
flow, causing a blood clot.
Although the exact cause
is unknown, the process
may begin with damage or
injury to the inner wall of
the artery from HTN, high
cholesterorl, smoking or
diabetes. Over time, fatty
plaques made of
cholesterorl and other
cellular waste products
build up at the site of the
injury & harden,
narrowing the artery and
impacting blood flow.
Chronic venous
insufficiency (CVI)
A condition in which the
veins and valves in the LE
are damaged and cannot
keep blood flowing toward
the heart. This causes
veins to remain filled with
blood.
Weak or damaged valves
inside the veins. Risk
factors include age, female
gender, obesity,
pregnancy, and prolonged
sitting or standing.
Atrial septal defect (ASD)
A hole in the wall of heart
separating the right & left
atria. In fetal circulation,
there is normally an
opening between the two
Congenital heart defects
arise from errors early in
the heart’s development.
Genetics & environmental
factors may play a role.
Varies based on the
severity of disease & the
artery affected. When the
coronary arteries are
affected, angina pectoris
may result. When cerebral
arteries are affected,
numbness or weakness of
the arms or legs, difficulty
speaking or slurred
speech, or drooping face
muscles may result. When
peripheral arteries are
affected, intermittent
claudication may result.
Leg swelling, varicose
veins, aching, heaviness or
cramping, itching, redness
or skin ulcers of the legs
and ankles.
Small to moderate sized
defects may produce no
symptoms or symptoms
that appear after 30 years
of age. Large or long
Lifestyle changes,
medications, & surgery.
Changes include cessation
of smoking, regular
exercise, healthy diet,
stress management.
Medications may include
antihypertensive,
antiplatelet, and
antilipidemic agents.
Surgical procedures may
include angioplasty,
endarterectomy, and
bypass surgery.
Compression stockings
and elevation of the legs
help decrease chronic
swelling. Varicose vein
stripping may be
performed for cases with
persistent leg pain or skin
ulcers due to poor
circulation.
Surgical closure is
recommended if the
defect is large, the heart is
swollen or symptoms
occur. A non-surgical
Cor Pulmonale
Coronary Artery Disease
(CAD)
atria to allow blood to
bypass the lungs. This
opening is termed
foramen ovale and usually
closes at birth. If the ASD
persists, blood continues
to flow from left to the
right atria and is called a
shunt. In severe cases,
blood may flow from the
right to the left atria.
Also known as pulmonary
heart disease, refers to
hypertrophy of the right
ventricle cased by altered
structure or function of
the lungs.
Is the narrowing or
blockage of the coronary
arteries due to
atheromatous plaques
resulting in diminished
blood flow.
Pulmonary hypertension
from chronically increased
resistance in the
pulmonary circulation
CAD is thought to begin
with damage or injury to
the inner layer of a
coronary artery.
Cholesterol then tends to
accumulate at the site. If a
plaque ruptures, platelets
will clump at the site to try
to repair the artery. This
clump can block the
artery, leading to a heart
attack.
standing atrial septal
defects may cause: heart
murmur, SOB, fatigue,
swelling of the legs, heart
palpitations, frequent lung
infections, stroke, cyanosis
of the skin.
procedure involves placing
a device into the heart and
across the ASD using a
catheter.
The cardinal symptom is
progressive shortness of
breath, especially with
exertion. Other signs &
symptoms are fatigue,
palpitations, atypical chest
pain, swelling of the Legs,
dizziness, & syncope.
The degree of stenosis
required to produce signs
& symptoms varies with
the oxygen demand. The
diminished blood flow
may cause angina,
shortness of breath or
other symptoms, which
may not be felt until >70%
of the lumen is occluded.
A complete blockage can
cause a heart attack.
Supplemental oxygen
sufficient to maintain SaO2
>90% and or PaO2 >60 mm
Hg. General measures
include diuretics &
anticoagulation.
Aggressive modification of
atherosclerosis risk factors
to slow progression and
induce regression of
existing plaques and
restore or improve
coronary blood flow. This
includes smoking
cessation; weight loss; a
heart healthy diet low in
saturated fat, cholesterol
and sodium; regular
exercise. Drug therapy
includes antiplatelet
agents (aspirin,
Deep Vein thrombosis
(DVT)
A condition in which a
blood clot forms in one or
more of the deep veins,
usually in the lower
extremities. DVT is a
serious condition because
the clot can break loose
and travel to the lungs,
resulting in a pulmonary
embolism.
Any condition that impairs
normal circulation or
normal blood clotting.
Many factors increase the
risk of a DVT including
prolonged sitting or bed
rest, inherited blood
clotting disorders, injury or
surgery of the veins,
pregnancy, cancer, birth
control or hormone
replacement therapy,
being overweight, obesity,
and smoking.
About 50% of DVT cases
are asymptomatic. When
signs & symptoms occur
they can include swelling,
pain, redness, and warmth
in the affected leg.
Endocarditis
Is inflammation of the
endothelium that lines the
heart and cardiac valves. If
left untreated,
endocarditis can damage
and destroy heart valves
and become life
threatening.
May develop slowly,
depending on the cause of
the infection and if the
heart is affected, but can
include fever, chills, heart
murmur, fatigue,
shortness of breath,
weight loss, blood in urine,
and skin petechiae.
Heart Failure “congestive
heart failure”
Is a progressive condition
in which the heart cannot
maintain a normal cardiac
Caused by bacteria that
may enter the blood from
catheters or needles,
dental procedures, gum
disease, sexually
transmitted disease or
inflammatory bowel
disease. Individuals with a
damaged heart valve, and
artificial heart valve or
other heart defects are at
the greatest risk.
CAD, HTN, DM, MI,
abnormal heart valves,
and cardiomyopathy.
SOB, fatigue and
weakness, swelling in the
legs, feet and abdomen,
Clopidogel), ACE
inhibitors, angiotensin II
receptor blockers and
statins.
The goal of tx is to prevent
the blood clot from getting
bigger and to prevent it
form breaking loose and
causing a pulmonary
embolism. Medications
include anticoagulant and
thrombolytic agents.
“Filters” may be surgically
inserted into the vena
cave to prevent clots from
reaching the lungs.
Compression stockings
may be recommended to
reduce blood pooling.
Antibiotics are the first
line of treatment. Surgery
may be needed to treat
persistent infections or
replace a damaged heart
valve.
Sometimes treating the
underlying cause can
correct heart failure
Heart murmur
output to meet the body’s
demands for blood and
oxygen. Heart failure often
develops after other
conditions have damanged
or weakened the heart.
The ventricles weaken and
dilate to the point that the
heart can’t pump
efficiently. It can affect the
right side, left side, or both
sides of the heart, but
typically begins with the
left ventricle. The term
“congestive heart failure”
comes from blood backing
up into the liver,
abdomen, legs, and lungs.
The condition can be acute
or chronic.
An abnormal swishing or
whooshing sound heard by
auscultation sometime
during the cardiac cycle.
Innocent heart murmurs
occur when blood flows
rapidly through the heart
due to activity, pregnancy,
fever, and anemia.
Abnormal heart murmurs
may be caused by
turbulent blood flow
through a damaged or
narrowed heart valve or a
hole in one of the heart’s
walls. Other causes
include rheumatic fever,
endocarditis, calcified
rapid or irregular
heartbeat with S3 or S4
heart sound, persistent
cough or wheezing and
weight gain from fluid
retention.
(repairing a damaged
heart valve or controlling
an abnormal heart
rhythm). In most cases, tx
is a balance of
medications, devices, and
lifestyle changes to help
the heart contract
normally. Medications
include anticoagulants,
antihypertensives, and
digitalis to increase the
strength of contraction. In
severe cases, surgery and
medical devices may be
needed to correct the
underlying cause of the
heart failure.
Innocent murmurs are not
usually associated with
other signs or symptoms.
Abnormal murmurs may
be associated with
cyanosis, limb edema,
shortness of breath,
enlarged neck veins,
weight gain, chest pain,
dizziness, and fainting.
Innocent murmurs usually
do not require treatment.
Treatment for abnormal
heart murmurs depends
on the underlying cause
and can include
medications or surgery.
Common medications are:
digoxin, anticoagulants,
diuretics, and other
antihyperstensive agents.
Surgical procedures
include valve replacement
or patching atrial or
valves, and mitral valve
prolapsed.
Primary or essential
hypertension has no
known cause. HTN with an
identified cause (usually
renal disease) is called
secondary HTN.
ventricular septal defects.
Hypertension
Arterial hypertension in
adults is a sustained
elevation of systolic
pressure >140 mm Hg or
diastolic pressure >90 mm
Hg.
HTN is often
asymptomatic until
complications develop in
the organs. An S4 heart
sound is an early sign.
Severe HTN (diastolic
>120) can cause significant
CNS symptoms (confusion,
cortical blindness,
hemiapresis, seizures)
cardiovascular symptoms
(chest pain, dyspena) and
renal involvement.
Lymphedema
Edema, or swelling, due to
an accumulation of lymph
in the extremities
Primary lymphedema is a
rare, inherited condition
caused by problems with
the development of lymph
vessels. Causes of
secondary lymphedema
include any condition or
procedure that damages
or obstructs lymph nodes
or vessels
Swelling with the
restricted motion of the
upper or lower extremity,
arching and heaviness or a
felling of fullness, brawny,
fibrous, non pitting edema
in one or more limbs.
Myocardial Infarction
AKA heart attack, a MI
occurs when the blood
Most occur when a
ruptured atherosclerotic
Chest discomfort with
pressure, squeezing or
Recommendations include
lifestyle modifications (30
min/day exercise, weight
loss to a BMI of 18.5-24,
smoking cessation,
reduced intake of sodium
and alcohol, increased
consumption of fruits,
vegetables, low fat dairy
and medications. Classes
of medications for HTN
include diuretics, beta
blockers, calcium channel
blockers, ACE inhibitors.
There is no cure, but
treatments focused on
reducing swelling and
controlling pain may
lessen symptoms and slow
or halt progression.
Treatments include: gentle
active exercise, pressure
gradient bandages,
massage, pneumatic
compression, and
compression garments.
Surgery to remove excess
tissue in the affected
extremity may be
considered.
Treatment of MI varies
from medication to
Peripheral arterial disease
flow through one or more
of the coronary arteries is
severely reduced or cut off
completely. This causes
irreversible necrosis to the
portion of myocardium
supplied by the blocked
artery.
plaque or blood clot blocks
the flow of blood through
a coronary artery. An
uncommon cause is a
spasm of a coronary artery
pain, shortness of breath,
discomfort in the upper
body including the arms,
shoulder, neck or back,
nausea, vomiting,
dizziness, sweating, and
palpitations.
Stenotic, occlusive, and
aneurismal diseases of the
aorta and peripheral
arteries.
Caused primarily by
atherosclerosis and
thromboemboic processes
that alter the structure
and function of the aorta
and its branches
Fatigue, aching,
numbness, or pain
primarily in the buttock,
thigh, calf, or foot at rest
or when walking, poorly
healing wounds of the legs
or feet, distal hair loss,
trophic skin changes, and
hypertrophic nails.
surgery or both,
depending on the severity
and the amount of heart
damage. Medications used
to treat the acute MI
include anticoagulants and
thrombolytic agents, pain
relievers,
antihypertensives and
cholesterol lowering
medications. Surgical
procedures may include
coronary angioplasty with
stenting or bypass surgery.
Recommended lifestyle
changes.
For pts with asymptomatic
disease, tx consist of
smoking cessation, lipid
lowering medications, and
control of diabetes and
HTN (with beta blockers).
For pts with disabling
intermittent claudication,
treatment consists of
revascularization
procedures (stent, lasers)
and surgery (bypass) may
be recommended.
Supervised exercise
training should be
performed for a minimum
of 30-45 minutes, at least
3x a week, for a minimum
of 12 weeks.
Rheumatic Fever
Acute respiratory distress
syndrome (ARDS)
Atelectasis
An inflammatory disease
that can develop as a
complication of untreated
or poorly treated strep
throat from group A
streptococcus bacteria.
Rheumatic fever can
damage the heart valves
and cause heart failure.
Is a sudden respiratory
failure due to fluid
accumulation in the
alveoli. ARDS usually
occurs in people who are
already critically ill or who
have significant injuries.
Severe shortness of breath
develops within a few
hours to a few days after
the original disease or
trauma. ARDS is fatal in
25-40% of the people who
develop it.
Streptococus pyogenes or
group A strep that cause
strep throat or scarlet
fever.
A condition in which one
or more areas of the lungs
collapse or do not inflate
properly
Conditions and factors
that prevent deep
breathing and coughing
can cause it. These include
Mechanical cause is from
fluid leaking from the
smallest blood vessels in
the lungs into the alveoli.
Injuries include: severe
viral or bacterial
pneumonia, heart failure,
serious head or chest
injury, fxs, smoke
inhalation, near drowning,
prolonged use of large
volumes of supplemental
oxygen, drug overdose,
shock.
Result from the
inflammation of the heart,
joints, skin or central
nervous system that may
include red, swollen, fever,
and painful joints, heart
palpitations, chest pain,
shortness of breath, and
skin rash.
Varies based on the cause.
Usually include SOB,
labored and unusually
rapid breathing,
hypotension, confusion,
extreme fatigue, cough,
and fever.
If a small area of the lung
is affected, there may be
no signs or symptoms. If a
large area is affected,
The goals of treatment are
to destroy group A strep
bacteria, relieve
symptoms, and control
inflammation. Medications
include antibiotics and
anti-inflammatory agents.
It is important to identify
the cause of ARDS bc it can
determine treatment and
predict the chances for
survival. The first goal of
treatment is to get oxygen
to the lungs and organs.
Most people will be
treated with supplemental
oxygen and mechanical
ventilation. Treating the
underlying condition then
becomes equally
important. Medications
are given to prevent and
treat infection, relieve
pain, provide sedation,
and prevent blood clot
formation.
Deep breathing, changing
positions, and airway
clearance techniques
assist to fully expand the
Lung cancer (bronchial
carcinoma)
Bronchiectasis
Refers to any epithelias
carcinoma occurring in the
bronchopulmonary tree.
Cancers are broadly
divided into two main
groups: small cell lung
carcinomas and non-small
cell lung carcinomas,
including squamous cell
carcinoma,
adenocarcinoma, and
large cell carcinoma
A progressive obstructive
lung disease that produces
abnormal dilation of a
bronchus. This is an
irreversible condition
usually associated with
chronic infections,
aspiration, cystic fibrosis
or immune system
impairment. The bronchial
walls weaken over time
due to infection and allow
for permanent dilation of
bronchi and bronchioles.
post operataive pain,
pleural effusion, tumor,
ARDS, asthma, COPD, and
cystic fibrosis.
there may be cyanosis,
shortness of breath,
increased breathing rate,
and increased HR.
Smoking is the primary
cause of the majority of
lung cancers, but it can
occur in people who have
never smoked or had
prolonged exposure to
secondhand smoke. In
these cases, the exact
etiology may be unknown.
A new cough or changes in
a chronic cough, coughing
up blood, shortness of
breath, wheezing, weight
loss, and bone pain.
Typically, signs &
symptoms are not present
until the disease is
advanced.
Injury to the airways or
lung infection (pneumonia,
whooping cough, measles,
tuberculosis, fungal
infections).
Consistent productive
cough, hemoptysis, weight
loss, anemia, crackles,
wheezes, and loud breath
sounds.
lungs. Supplemental
oxygen, nebulized
bronchodilators, and
mucolytic agents.
Bronchoscopy may be
used to remove foreign
objects or mucous plugs
blocking the airways.
Surgery (wedge resection,
segmental resection,
lobectomy,
pneumonectomy,
chemotherapy, and
radiation therapy.
Medications include
antibiotics,
bronchodilators,
expectorants, and
mucolytics.
Chronic Obstructive
Pulmonary Disease
Cystic fibrosis
Emphysema
Refers to a group of lung
diseases that block airflow
due to narrowing of the
bronchial tree.
Emphysema and chronic
bronchitis are the two
main conditions that make
up COPD. Pts have an
increased total lung
capacity with a significant
increase in residual
volume.
Is an autosomal recessive
genetic disease of the
exocrine glands that
primarily affects the lungs,
pancrease, liver,
intestines, sinusues, and
sex organs. People who
have CF inherit two faulty
CF genes, one from each
parent.
The alveolar walls are
gradually destroyed and
the alveoli are turned into
large, irregular pockets
with gaping holes in the
walls. In addition, the
elastic fibers that hold
open the bronchioles are
Caused by long term
smoking
Excessive mucus
production, chronic
productive cough,
wheezing, shortness of
breath, fatigue, and
reduced exercise capacity.
Medications, surgery,
maintaining good
nutrition, and airway
clearnance, breathing
exercises.
The causative factor is a
mutation of the cystic
fibrosis transmembrane
conductance regulator or
chromosome 7. A
defective gene and its
protein product cause the
body to produce unusually
thick, sticky mucus that
leads to life threatening
lung infections, obstructs
the pancreas, and inhibits
normal digestion and
absorption of food.
Smoking is the leading
cause.
Vary with progression and
may include salty tasting
skin, persistent and
productive coughing,
frequent lung infections,
wheezing, shortness of
breath, poor
growth/weight gain in
spite of a good appetite,
and frequent greasy, bulky
stools.
Antibiotics, nutritional
supplements, pancreatic
enzyme replacements,
mucolytics, and
bronchodilators. PT
includes airway clearance,
breathing techniques,
assisted cough, and
ventilatory muscle
training. General exercise
is indicated to improve
overall strength and
endurance, except with
severe lung disease.
Medications,
supplemental oxygen,
antibiotics (if bacterial
infection is present).
Surgery, maintaining good
nutrition. Etc.
Shortness of breath,
wheezing, chronic
coughing, orthopnea,
barrel chest, increase use
of accessory muscles,
increased respiration rate,
fatigue, and reduced
exercise capacity.
Pleural effusion
destroyed, so that they
collapse during exhalation,
not letting air escape from
the lungs. The alveoli are
permanently overinflated
and dead space increase
within the lungs.
Is a buildup of fluid in the
pleural space between the
lungs and chest cavity. The
excess fluid can push the
pleura against the lung
making it hard to breath,
and in some cases, causing
atelectasis. If the fluid gets
infected and turns into an
abscess, the condition is
called empyema.
Pleuritis, or inflammation
of the visceral and parietal
pleura. Pleuritis can be
caused by a viral infection,
pneumonia, and RA.
Shortness of breath. If the
fluid becomes infected,
dry cough, fever, and chills
may appear.
Fever, cough, SOB,
sweating, shaking chills,
chest pain that fluctuates
with breathing, headache,
muscle pain, and fatigue.
Extreme shortness of
breath, a feeling of
suffocating or drowning,
gasping for breath,
anxiety, restlessness, a
sense of apprehension,
coughing, frothy blood
tinged sputum, chest pain,
irregular pulse.
Pneumonia
Refers to inflammation of
the lungs
Usually caused by
bacterial, viral, fungal, or
parasitic infection
Pulmonary edema
Occurs when fluid collects
in the alveoli within the
lungs, making it difficult to
breathe. *Acute
pulmonary edema is a
medical emergency.
Occurs when the left
ventricle is unable to
pump blood adequately
(left sided heart failure).
Pressure increases inside
the left atrium and then in
the pulmonary veins and
capillaries, causing fluid to
be pushed through the
capillary walls into the
If the pleuritis is caused by
a bacterial pneumonia, an
antibiotic will be used.
Most viral infections run
their course without
requiring treatment.
NSAIDS may help relieve
some of the signs and
symptoms. If the fluid
buildup is large, a chest
tube may be inserted to
drain the fluid.
Antibiotics, antiviral
agents, antifungal agents.
Lifestyle remedies include
rest and drinking plenty of
fluids.
Supplemental oxygen and
medications. Call 911 for
acute pulmonary edema.
Pulmonary embolism
Pulmonary Fibrosis
alveoli. Non cardiac
pulmonary edema, fluid
leaks from the capillaries
within the alveoli since the
capillaries themselves
become more permeable.
PE is a condition where
Caused by blood clots
one or more arteries in the from LEs.
lungs become blocked. PE
can be life threatening but
prompt treatment with
anti-clotting medications
can greatly reduce the risk
of death.
A condition in which
microscopic damage to the
alveoli causes irreversible
scarring of the interstitial
tissue. Normally, the tissue
is highly elastic, expanding
and contracting with each
breath. Scarring makes the
interstitial tissue stiff and
thick and the alveoli less
flexible, making breath
more difficult.
Cause is unknown. Chronic
exposure to silica dust,
asbestosis, grain dust,
sugar cane, and bird and
animal droppings can
cause pulmonary fibrosis.
Radiation for lung or
breast cancer, chemo
drugs, certain
antiarrhythmic
medications, and some
antibiotics and can also
cause fibrosis.
Sudden onset of SOB,
chest pain that becomes
worse with deep
breathing, coughing
sputum. Extremity
swelling, fainting.
SOB, especially during or
after physical activit, and a
dry cough which usually
does not appear until the
disease is advanced and
irreversible lung damage
has already occurred.
Fatigue, unexplained
weight loss, and aching
muscles and joints.
Prompt treatment of
anticoagulants and
thrombolytic agents
greatly reduces the risk of
death. Surgery may be
done to remove the clot.
Prevention includes
compression stockings,
pneumatic compression,
physical activity, and
drinking fluids.
Lung scarring is
irreversible and no current
treatment has proven
effective in stopping the
progression of the disease,
some tx may improve
symptoms temporarily &
improve quality of life.
Corticosteriods and
immunosuppressive
agents are often
prescribed initially. Lung
transplantation may be
used in cases of advanced
disease. Supplemental
oxygen and pulmonary
rehab.
Restrictive Lung
Dysfunction (RLD)
RLD is an abnormal
reduction in lung
expansion and pulmonary
ventilation
Caused by abnormal lung
parenchyma (atelectasis,
pneumonia, pulmonary
fibrosis, pulmonary
edema, ARDS, abnormal
pleura (pleural effusion,
fibrosis, pneumothorax,
hemothroax, and
disorders affecting
ventilatory pump function.
Dyspnea on exertion, a
persistent non productive
cough, increased
respiratory rate,
hypoxemia, decreased
vital capacity, abnormal
breath sounds.
Antibiotics for pneumonia,
treatment of edema,
reversal of CNS
depression. Mechanical
ventilation, supplemental
oxygen, nutrition support,
muscle training.
Common Diagnostic Procedures:
1. Holter monitoring-EKG electrodes record 24-48 hours or longer to evaluate cardiac rhythm.
2. Angiography-inject a contrast medium into the blood vessels. Can show the location of plaques in the arteries and the extent of
occlusion.
3. Bronchoscopy-Direct visualization of the bronchial tree via fiberoptic instrument that transmits image to screen.
4. Cardiac catheterization-thin, inserted into an artery in the leg or arm where a contract dye is injected.
5. Carotid ultrasound-uses sound waves to examine and visualize the structure and function of the carotid arteries.
6. Chest radiograph-used to visualize the location, size, and shape of the heart, lungs, blood vessels, ribs, and bones of the spine. Can also
reveal fluid in the lungs or pleural space, pneumonia, emphysema, cancer or other conditions.
7. Computed tomography (CT)-uses an x-ray machine that rotates around a pt lying on a table. The pictures are slices of the body called
tomograms and each picture is called a computed tomograph.
8. Echocardiography-uses high frequency sound waves non invasively to evaluate the functioning of the heart via real time images. Can
provide information on the size and function of the ventricles, thickness of the septums, and function of the walls, valves, and chambers.
9. Fluroscopy-A continuous x-ray procedure that shows the heart and lungs. Involves a high dose of radiation, it has largely been replaced
by echocardiography.
10. Magnetic Resonance Imaging (MRI)-uses a magnetic field and radio waves to create 3D images of the heart and blocked vessels to assess
the size and function, thickness, and damage or heart disease. Limited for imaging the lungs.
11. Positron Emission Tomography (PET)-imaging test in which a small amount of radioactive material is injected, inhaled, or swallowed,.
Radioactive material tends to accumulate in areas with high levels of chemical activity corresponding to areas of disease. PET is useful in
evaluating heart disease and cancer.
Cardiovascular/pulmonary Systems:
Innervation of the Heart:
12. The sympathetic influence is achieved by release of epinephrine & norepinephrine. Sympathetic nerves stimulate the chambers to beat
faster (chronotrophic effect) and with greater force of contraction (inotroophic effect). Sympathetic activation leads to ↑ cardiac
contractility, ↑HR, venoconstriction, and arterial vasoconstriction, ultimately leading to ↑BP.
13. The parasympathetic influence is achieved via acetylcholine release from the vagus nerve. Parasympathetic nerves slow the heart rate
(chronotrophic effect) primarily through their influence on the SA node. Parasympathetic leads to a ↓HR and a small decrease in
contractility, resulting in a ↓ in BP.
14. Valsalva Maneuver: Forced expiration against a closed glottis produces ↑ intrathoracic pressure, ↑central venous pressure and ↓
venous return. The resultant decrease in cardiac output and BP is sensed by baroreceptors, which reflexively increase HR and myocardial
contractility.
15.
Pathology
Cerebrovascular
Accident (CVA)
Diagnosis
Occurs when there is an
interruption of cerebral
circulation that results
in cerebral insufficiency,
destruction of
surrounding brain
tissue, and subsequent
neurological deficit.
Laboratory/Imaging
CT can confirm an area
of infarct in the brain
and its vascular origin,
however it can present
as negative for up to a
few days after the
event. MRI allows for
the diagnosis of
ischemia within the
brain almost
immediately after
onset. PET can provide
info regarding cerebral
perfusion and cell
function.
Ultrasonography
identifies areas of
diminished blood flow
in vessels and
angiography may
Management/Prognosis
Medical management
will initially include
medically stabilizing the
pt through medication
and surgical
intervention. PT in acute
phase focuses on
positioning, pressure
relief, sensory
awareness re-education,
balance, ROM, weightbearing, facilitation,
postural control. Rehab
can include Bobath’s
NDT, Brunnstrom’s
Movement therapy,
Rood, Kabat, Knott, PNF.
The outcome depends
on pts overall health,
level of cognition, motor
identify a clot and
determine if surgical
intervention is
necessary.
Congestive Heart
Failure (CHF)
Left sided heart failure:
generally associated
with signs of pulmonary
venous congestion.
Right sided heart
failure: associated with
signs of systemic
venous congestion.
Occurs when the heart
can no longer meet the
metabolic demands of
the body. The heart’s
inability to pump a
sufficient amount of
blood occurs when
there in insufficient or
defective cardiac filling
and/or impaired
contraction & emptying
of the heart. The
impairment in cardiac
output causes the body
to compensate for this
deficit and this results
in an increase in blood
volume, cardiac filling
pressure, HR, and
cardiac muscle mass. A
pt with CHF will initially
Urinalysis and a CBC
count that includes
electrolyte, thyroid
stimulating hormone,
blood urea nitrogen
(BUN), and serum
creatinine levels should
be performed. A chest
x-ray,
electrocardiogram, and
echocardiogram are
also recommended. A
Doppler
echocardiogram can
determine systolic &
diastolic performance,
the cardiac output
(ejection fraction), and
pulmonary artery and
ventricular filling
pressures.
recovery, and family
support. The first 3
months of recovery
typically reveals the
most measureable
neurologic recovery and
is usually a good
indicator of the longterm outcome.
Research shows a pt can
continue to improve for
an average of 2-3 years
post CVA.
CHF is a common
disorder. A pt can live
with CHF and should
benefit from PT in order
to improve endurance
and strength after a
decline in function from
hospitalization or bed
rest. After diagnosis
there is mean of 3.2
years of survival for men
and 5.4 years for
females.
Cystic Fibrosis (CF)
show signs of
tachycardia. Other signs
include venous
congestion, high
catecholamine levels, &
impaired cardiac
output, sudden weight
gain, SOB, S3 gallop.
Is an inherited disease
that affects the ion
transport of the
exocrine glands
resulting in impairment
of the hepatic,
digestive, respiratory,
and reproductive
systems. The disease
causes the exocrine
glands to overproduce
thick mucus,
overproduce normal
secretions or
overproduce sodium &
chloride. Mostly affects
children, African
American followed by
Caucasians.
Neonates meconium
can be tested as a
screening tool for
increased albumin. The
quantitative pilocarpine
iontophoresis sweat
test is the sole
diagnostic tool in
determining the
presence of CF. Sodium
& chloride amounts
greater than 60 mEq/l
(standard value is 40
mEq/l) is a positive
diagnosis for CF. The
sweat test should be
performed twice to
ensure accuracy.
Chest PT should be
performed several times
a day and includes
bronchial drainage,
percussion, vibration,
breathing and assistive
cough techniques &
ventilatory muscle
training. A pt with CF
will require intermittent
PT thought their life.
The goals are to
maximize secretion
clearance from the
lungs, optimize
pulmonary function,
and maximize the pts
quality of life. CF is a
terminal disease,
however, the median
age of death as
increased to 35 years of
age due to early
detection and
comprehensive
management. The most
Emphysema
Refers to a pathologic
accumulation of air in
the lungs found with
COPD. COPD is the
second leading cause of
disability in individuals
under 65 years of age
worldwide. Emphysema
results from a nonreversible injury and
destruction of elastic
protein within the
alveolar walls.
X-ray is utilized to
visually evaluate the
shape and spacing of
the lungs. Other
imaging studies include
a planogram to detect
bullae and a
bronchogram to
evaluate mucus ducts
and detect possible
enlargement of the
bronchi. Arterial blood
gases may indicated a
↓ PaO2. Impaired
FEV1,vital capacity and
forced vital capacity.
Total lung capacity,
residual volume, and
functional residual
volume will be ↑.
Lymphedema PostMastectomy
Lymphedema following
a mastectomy is termed
secondary lymphedema
and is the result of
Lymphedema classified
into 3 stages. Stage I:
pitting edema that
reduces with elevation
common cause of death
is respiratory failure.
Males generally have a
better prognosis than
females.
Pharmacological
intervention, oxygen
therapy, PT. PT
intervention consist of
generalized exercise,
endurance training,
pursed-lip breathing,
ventilatory muscle
strengthening, chest
wall exercises, and pt
education on posture,
airway secretion
clearance. Emphysema
is a chronic progressive
disease process. Pts
require ongoing medical
care and intermittent
physical therapy
intervention. Life
expectancy decreases to
less than 5 years with
severe expiratory
slowing measured at a
rate of <1 L of air during
FEV1.
Pharmacological
intervention or natural
substances that increase
proteolysis and
damage to the
lymphatic nodes and
vessels during surgery.
Excessive accumulation
of lymph fluid within
the soft tissues is
caused by an excess
load of lymph fluid or
inadequate transport
capacity within the
lymphatic system
secondary to the loss of
homeostasis.
Myocardial Infarction
(MI)
Occurs when there is
poor coronary artery
perfusion, ischemia,
and subsequent
necrosis of the cardiac
overnight and does not
exhibit any fibrotic
changes. Stage II:
identified by some
fibrotic changes that
being to occur &
increase in non-pitting
edema that does not
reduce with elevation.
Stage III: is
characterized by skin
changes, frequent
infections, and severe
edema that is nonpitting and fibrotic.
Diagnosis is confirmed
through history,
observation, and
several diagnostic tools
to rule out other
disorders. A Doppler is
used to rule out DVT. CT
or MRI to rule out
malignancy. A
lymphoscintigram is a
nuclear medicine
procudre that tests the
function of the
lymphatic system.
Primary tool to detect
MI is a 12 lead EKG. An
inverted T wave
indicates myocardial
ischemia, elevated ST
macrophage activity. No
cure. Surgery is used in
the treatment of severe
cases.PT follows a
treatment approach
termed combined
decongestive
physiotherapy (CDP).
Lymphedema is
progressive if left
untreated, but can be
managed through
intervention and
education. Pts must
comply with a home
program and must
remain aware of all
activities that place the
pt at an increased risk
for lymphedema.
Stabilize the pt and
initiate pharmacological
intervention to hinder
the evolution of the MI.
Cardiac rehab is
Restrictive Lung
Disease (RLD)
tissue usually due to
thrombus, arterial
blockage or
atherosclerosis. The
location and severity of
the infarct will
determine symptoms
and overall clinical
picture.
segment indicates acute
infarction, and a
depressed ST segment
indicates a pending
subendocardial or
transmural infarction. A
blood serum analysis
can be utilized to
determine the level of
selected cardiac
enzymes. CPK, AST, and
lactic dehydrogenase
can be dramatically
altered during and after
a MI.
Is a classification of
disorders caused by a
pulmonary or
extrapulmonary
restriction that
produces impairment in
lung expansion and an
abnormal reduction in
pulmonary ventilation.
There are multiple
conditions that can
cause restrictive lung
disease. Pulmonary
restriction can be
caused by tumor,
A chest radiography is
utilized to evaluate lung
structure and evidence
of fibrosis, infiltrates,
tumor, and deformity.
Arterial blood gas
analysis may indicated a
decrease in PaO2. VC,
FVC, and TLC will be
impaired. Normal
residual volume, and
expiration flow rates.
ERV and FRC are often
decreased.
recommended status
post MI. The pt should
start in the coronary
care unit (CCU) and
progress through each
of the phases of cardiac
rehab. P that that has
experienced an MI may
be able to return to all
previous activities after
successful completion of
a cardiac rehab
program. A pt must
continue to reduce the
modifiable risk factors
and maintain an
appropriate level of
exercise in order limit
another MI.
PT includes body
mechanics, posture
training, diaphragm and
ventilatory muscle
strengthening,
relaxation and energy
conservation. Outcome
is based on the etiology
of the restrictive lung
disease and pt response
to PT intervention.
Some disorders require
surgical intervention
that alleviates the
condition while other
interstitial pulmonary
fibrosis, scarring within
the lungs, and
pneumonia.
Extrapulmonary
restrictions include
pleural effusion, chest
wall stiffness, structural
abnormality, postural
deformity, muscle
weakness, and central
nervous system injury.
RLD includes a ↓ in
lung & chest wall
compliance, ↓in lung
volumes and an ↑ in
the work of breathing.
A pt with restrictive
lung disease is
characterized by a
reduction of lung
volumes, ↓ chest
mobility, ↓breath
sounds, SOB,
hypoxemia, rapid and
shallow respiratory
pattern, ineffective
cough.
are progressive and
irreversible. Some pts
with end-stage disease
may be candidates for
lung transplantation,
however most
eventually progress to
ventilatory failure.
16.
17. Description of Blood Gases:
Arterial Blood Gas (ABG)
Are collected to evaluate acid-base status (pH), ventilation (PaCO2), and
oxygenation of arterial blood (PaO2). The partial pressure of oxygen in
arterial blood PaO2 and the percent oxygen saturation of hemoglobin
Cardiac Biomarkers
Cholesterol Test
Complete Blood Count
(CBC)
(SaO2) provide information about how well the lungs are functioning to
oxygenate the blood. The partial pressure of carbon dioxide in arterial
blood (PaCO2) provides info on how well the lungs are able to remove
carbon dioxide. Changes in PaCO2 directly affect the balance of pH in the
body. Blood pH is tightly regulated, as an imbalance in either direction can
affect the nervous system and can cause convulsions or coma. Bicarbonate
(HCO3-) is an important component of the chemical buffering system that
keeps the blood from becoming too acidic or basic and is often part of an
ABG test.
Certain enzymes leak out of the heart cells and into the blood after a
myocardial infarction. Cardiac enzyme studies measure the levels of
creatine phosphokinase (CK) and the protein troponin in the blood. CK-MB
is a relatively specific test for myocardial infarction. It appears in blood
approximately 4 hours after infarction, peaks at 12-24 hours, and declines
over 48-72 hours. Cardiac troponin-I is also a specific marker for infarction,
and unlike CK-MB levels, it remains elevated for 5-7 days.
Also called a lipid panel or lipid profile, a cholesterol test measures the
amount of cholesterol and triglycerides in the blood in order to determine
the risk of atherosclerosis. Cholesterol is carried in the circulation in
association with lipoproteins. A complete lipid profile includes the
measurement of 4 types of lipids in the blood: total cholesterol, highdensity lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL)
cholesterol, and triglycerdies. HDL cholesterol is referred to as the “good”
cholesterol because it helps carry away LDL cholesterol and is protective
against atherogenesis. LDL is referred to as the “bad” cholesterol since it is
associated with the buildup of fatty plaques within the arteries which
reduce blood flow. The body converts any calories it does not need to use
right away into triglycerides, which are stored in adipose tissue. High levels
of triglycerides are seen in overweight people, in those consuming too
many sweets or too much alcohol, and in people with diabetes who have
elevated blood sugar levels.
Measures red blood cell count, white blood cell count, white blood cell
differential, platelets, hemoglobin, and hematocrit. A CBC is performed to
assess health, to diagnose and monitor a medical condition, and to
Hematocrit (Hct)
Partial Thromboplastin
Time (PTT) and
Prothrombin Time (PT)
monitor the effects of medical treatment.
Is the percentage of red blood cells in total blood volume. A low
hematocirt may indicate anemia, blood loss, and vitamin or mineral
deficiencies. A high hematocrit may indicate dehydration or polycythemia
vera, a condition that causes an overproduction of red blood cells.
PTT and PT tests measure how quickly the blood clots. The tests are
commonly used to monitor oral anticoagulant therapy or to screen for
selected bleeding disorders. The tests examine all of the clotting factors of
the intrinsic pathway with the exception of platelets. Partial
thromboplastin time is more sensitive than prothrombin time in detecting
minor deficiencies.
18.
19. Arterial blood gases:
pH
PaCO2 (amount of carbon dioxide within
arterial blood)
PaO2
HCO3- (amount of bicarbonate ions within
arterial blood)
SaO2
*By convention, ABG results are written or
spoken in the following order:
pHPaCO2PaO2HCO3- (e.g.
7.4/40/97/24)
Partial Thromboplastin Time (PTT)
Acidemia
Alkalemia
Eucapnia
Hypercapnia
Hyopcapnia
Hypoxemia
Mild hypoxemia
7.4 (7.35-7.45)
40 mm Hg at sea level breathing ambient air (35-45mm
Hg)
97 mm Hg at sea level breathing ambient air (80-100
mm Hg)
24 mEq/L (22-26)
95-98%
26-39 seconds
Elevated acidity of blood (pH < 7.35)
Decreased acidity of blood (pH > 7.45)
Normal level of CO2 in arterial blood (35-45 mm Hg)
Elevated level of CO2 in arterial blood( > 45 mm Hg)
Low level of CO2 in arterial blood (<35 mm Hg)
Low level of O2 in arterial blood (PaO2 < 80 mm Hg)
PaO2 60-79 mmHg
Moderate hypoxemia
Severe hypoxemia
Hypoxia
PaO2 40-59 mmHg
PaO2 < 40 mmHg
Low level of O2 in the tissue despite adequate perfusion
of the tissue
20. *An increase in the PaCO2 decreases the body’s pH. A decrease in the PaCO2 raises the body’s pH.
21. *Supplemental oxygen is usually prescribed when the PaO2 falls below 55 mmHg.
22.
23. Other values:
White Blood Cells (WBCs) (Leukocytes) 4300-10,800
Red Blood Cells (RBCs) (Erythrocytes)
Male: 4.6-6.2 Female: 4.2-5.9
Erethrosedimentation Rate (ESR)
Male: <15 mm/hr Female: <20
Hematocrit
Male: 45%-52% Female: 37%-48%
Platelet
150,000-450,000
Sodium
135-146
Calcium
8.4-10.4
Potassium
3.5-5.5
Magnesium
1.8-2.4
Total cholesterol
<200
LDL
<100
HDL
<40
Triglyceride
<150
24.
25. Pharmacological Management of Heart and Vascular Diseases:
Drug
Alpha
Adrenergic
Antagonist
Agents
Action
Indications
Reduce
peripheral
vascular tone
by blocking
alpha-1
adrenergic
receptors. This
Hypertension,
benign prostatic
hyperplasia
Side Effects
Dizziness,
palpitations,
orthostatic
hypotension,
drowsiness
Implications
for PT
Use caution
when rising
from a
sitting or
lying
position due
to the risk of
Examples
Cardura
(doxazosin,
Minipress
(prazosin),
Hytrin
(terazosin)
action causes
dilation of
arterioles &
veins and ↓
BP.
AngiotensinConverting
Enzyme (ACE)
inhibitor Agents
Decrease blood
pressure and
afterload by
suppressing the
enzyme that
converts
angiotensin I to
angiotensin II.
HTN, congestive
heart failgure
Hypotension,
dizziness, dry
cough,
hyperkalemia,
hyponatremia
Angiotensin II
receptor
antagonist
angents
Block
angiotensin II
receptors
which limit
vasoconstrictio
n & stimulation
of vascular
tissue
Divided into 4
classes. Class I
HTN, congestive
heart failure
Dizziness, back
and leg pain,
angina
pectoris
Cardiac
arrhythmias
Unique to the
specific
Antiarrhythmic
Agents
dizziness
and/or
orthostatic
hypotension
. Closely
monitor pt
during
exercise.
Avoid
sudden
changes in
posture due
to the risk of
dizziness &
fainting
from
hypotension
. Pts w heart
failure
should avoid
rapid
increases in
physical
activity.
Minimal
implications
for PT
Encourage
pts to
Capoten
(captorpril),
Vasotec
(enalapril),
Prinivil
(lisinopril),
Altace
(ramipril)
Cozaar
(losartan),
Atacand
(candesartan),
Diovan
(valsartan)
Sodium
channel
(sodium
channel
blockers)contorl cardiac
excitation &
conduction.
Class II (beta
blockers)inhibit
sympathetic
activity by
blocking Badrenergic
receptors. Class
III-prolong
repolarization
by inhibiting
both potassium
& sodium
channels & are
often
considered the
most effective
antiarrhytmic
agent. Class IV(calcium
channel
blockers)depress
depolarization
& slow
conduction
through the AV
node.
antiarrhythmic
agent;
exacerbation
of cardiac
arrhythmias,
dizziness,
hypotension
adhere to
the
prescribed
dosing
schedule
and
immediately
report any
adverse
reactions to
a healthcare
professional
.
blockers:
quinidine
(generic),
Xylocaine
(lidocaine)
Beta blockers:
Tenormin
(atenolol)
Prolonged
repolarization
: Cordarone
(amiodarone
Calcium
channel
blockers:
Cardizem
(diltiazem)
Anticoagulant
Agents
Inhibit platelet
aggregation &
thrombus
formation
Antihyperlipide
mia Agents
There are 5
categories of
lipid-modifying
agents. The
most
commonly used
drugs, the
statins, inhibit
enzyme action
in cholesterol
synthesis,
break down
LDL, ↓
triglyceride
levels, and ↑
HDL levels. The
Post
percutaneous
transluminal
coronary
angioplasty &
coronary artery
bypass graft
surgery,
prevention of
venous
thromboemboli
m&
cardioembolic
events in pts
with atrial
fibrillation &
prosthetic heart
valves
Hyperlipidemia,
atherosclerosis,
prevent
coronary events
in pts with
existing coronary
disease, diabetes
or PVD
Hemorrhage,
↑ risk of
bleeding,
gastrointestina
l distress with
oral
medication
A therapist
must be
careful to
avoid injury
secondary
to the risk of
excessive
bleeding or
bruising. Pt
education
regarding
common
side effects
is also
indicated to
protect the
pts.
Heparin,
Coumadin
(warfarin),
Lovenox
(enoxaparin)
Headache, GI
distress,
myalgia, rash
Aerobic
exercise can
increase
high density
lipoproteins
and
maximize
the effects
of drug
therapy
Lipitor
(atorvastatin),
Zocor
(simvastatin),
Tricor
(fenobibrate)
Antithrombotic
(antiplatelet)
agents
Beta Blocker
Agents (BetaAdrenergic
Blocking Agents)
other
categories are
bile acid
sequestrants,
nicotinic acid,
cholesterol
absorption
inhibitors, &
fibric acid
derivatieves
Antithrombotic
agents inhibit
platelet
aggregation
and clot
formation
Decrease the
myocardial
oxygen demand
by decreasing
heart rate and
contractility by
blocking Badrenergic
receptors
Post-myocardial
infarction, a-fib,
prevent arterial
thrombus
formation
HTN, agina,
arrhythmias,
heart failure,
migraines,
essential tremor
Hemorrhage,
thrombocytop
enia, potential
liver toxicity
with the use of
aspirin, GI
distress
Bradycardia,
cardiac
arrhythmias,
fatigue,
depression,
dizziness,
weakness,
blurred vision
Must be
careful to
avoid injury
secondary
to the risk of
bleeding.
HR & BP
response to
exercise will
be
diminished.
Rate of
perceived
exertion
may be used
to monitor
exercise
intensity.
Closely
monitor pts
during
positional
changes due
Bayer
(aspirin),
Plavix
(clopidogrel),
Persantine
(dipyridamole
)
Tenormin
(atenolol),
Lopressor
(metoprolol),
Inderal
(propanolol)
Calcium Channel
Blocker Agents
Decrease the
entry of
calcium into
vascular
smooth muscle
cells resulting
in diminished
myocardial
contraction,
vasodilation,
and ↓ oxygen
demand of the
heart
HTN, angina
pectoris,
arrhythmias,
congestive heart
failure
Dizziness,
headache,
hypotension,
peripheral
edema
to an ↑ risk
for
orthostatic
hypotension
.
HR & BP
response to
exercise will
be
diminished.
Monitor pt
closely
when
moving to
an upright
position
secondary
to dizziness
and/or
orthostatic
hypotension
. Observe
the Pt for
signs &
symptoms
of
congestive
heart failure
such as
worsening
peripheral
edema,
dyspnea or
weight gain.
Norvasc
(amlodidine),
Procardia
(nifedipine),
Calan
(verapamil)
Cardizem
(dilitazem)
Diuretic Agents
↑ the
excretion of
sodium & urine.
This causes a
reduction in
plasma volume
which ↓ blood
pressure.
Classifications
include
thiazide, loop,
and potassium
sparing agents.
HTN, edema
associated with
heart failure,
pulmonary
edema,
glaucoma
Dehydration,
hypotension,
electrolyte
imbalance,
polyuria,
↑LDL,
arrhythmias
Nitrate Agents
↓ ischemia
through
smooth muscle
relaxation and
dilation of
peripheral
vessels
Angina pectoris
Headache,
dizziness,
orthostatic
hypotension,
reflex
tachycardia,
nausea,
vomiting.
Positioning
changes can
increase the
risk of
dizziness
and falls due
to ↓ BP.
Monitor pts
closely for
signs &
symptoms
of
electrolyte
imbalance
and muscle
weakness or
cramping.
Pts must be
educated to
come to a
standing
position
slowly.
Sublingual
administrati
on of
nitroglycerin
is the
preferred
method to
treat an
acute
angina
attack.
Thiazide:
Diuril
(chlorothiazid
e)
Loop: Lasix
(furosemide)
Potassium
sparing:
Dyrenium
(triamterene)
Nitrostat
(nitroglycerin)
, Isordil
(isosorbide
dinitrate),
Amyl nitrite
solution for
inhalation.
Positive
Inotrophic
Agents
↑the force and
velocity of
myocardial
contraction,
slow the HR,
↓conduction
velocity
through the AV
node, & ↓ the
degree of
activation of
the
sympathetic
nervous
system.
Heart failure,
atrial fibrillation
Cardiac
arrthytmias, GI
distress,
dizziness,
blurred vision
Thrombolytic
Agents
Facilitate clot
dissolution
through
conversion of
plasminogen to
plasmin.
Plasmin breaks
down clots &
allows occluded
vessels to
reopen to
maintain blood
flow.
Acute
myocardial
infarction,
pulmonary
embolism,
ischemic stroke,
arterial or
venous
thrombosis
Hemorrhage
(specifically
intracranial in
certain
populations),
allergic
reaction,
cardiac
arrhythmia
Therapists
should
monitor HR
during
activity,
teach the pt
and fam to
take the pts
pulse, and
seek health
care
providers
advice for
rates less
than 60
bpm or
more than
100 bpm.
Therapist
must be
careful to
avoid
situations
that may
cause
trauma due
to altered
clotting
activity.
Lanoxin
(digoxin)
Linlytic
(urokinase),
Activase
(alteplase)
Pharmacological Management of Airway and Lung Diseases:
Drug
Action
Indications
Side Effects
Arrhythmia
s, postural
hypotensio
n, GI
distress,
dizziness,
drowsiness,
headache,
blurred
vision,
fatigue,
nausea,
thickening
of
bronchial
secretions
Corticoster
oid:
systemic
side affects
are
decreased
with the
inhaled
form, but
may
include
damage of
supporting
tissues, skin
breakdown,
Antihistamine
Agents
Block the effects
of histamine
resulting in a ↓
in nasal
congestion,
mucosal
irritation, &
symptoms of the
common cold,
sinusitis,
conjunctivitis, &
allergies
Respiratory
seasonal
allergies,
rhinitis &
sneezing from
the common
cold, allergic
conjunctivitis,
motion
sickness, and
Parkinson’s
disease
AntiInflammatory
Agents
Inhaled
corticosteroids,
leukotriene
modifiers, &
mastcell
stabilizers help
prevent
inflammatory
mediated
bronchoconstrcit
on by inhibiting
production of
inflammatory
cells, suppressing
release of
Bronchospasm,
asthma
Implications
for PT
Increase
guarding
when rising
from a sitting
or lying
position due
to the risk of
orthostatic
hypotension.
Closely
monitor pt
during
exercise.
Instuct the
pt in the use
of correct
use the
inhaler and
to rinse their
mouth with
water after
use to avoid
irritation of
local
mucosa.
Advise the
pts that
these agents
Examples
Benadryl
(diphenhydramin
e), Allegra,
Zyrtec, Claritin
Corticosteroid:
Qvar, Pulmicort,
AeroBid
Leukotriene
modifier: Zyflo
Mast cell
stabilizer:
Nasalcrom
inflammatory
mediators
(cytokines,
prostaglandins,
leukotrienes),
and reversing
capillary
permeability, in
turn reducing
airway edema.
Bronchodilator
Agents
Relieve
bronchospasm by
stimulating the
receptors that
cause bronchial
Bronchospasm,
wheezing, and
SOB in asthma
& COPD
osteoporosi
s, ↓bone
density,
glaucoma,
and
delayed
growth.
Local
effects
include
nasal
irritation
and
dryness,
sneezing
and bloody
mucus;
Leukotrien
e modifier:
liver
dysfunction
; Mast cell
stabilizer:
bronchospa
sm, throat
and nasal
irritation,
cough, GI
distress
Paradoxical
bronchospa
sm, dry
mouth, GI
distress,
are not
bronchodilat
ors and
should not
be used to
treat acute
episodes of
asthma.
Should
advice pts to
take their
bronchodilat
or
Anticholinergic:
Atrovent, sprivia.
Sympathomimeti
cs: Ventolin,
Primatene mist,
smooth muscle
relexation or by
blocking the
receptors that
trigger
bronchoconstricti
on. Primary
classifications
include
anticholinergic,
sympathomimeti
cs, & xanthine
derivatives.
Expectorant
Agents
Increase
respiratory
secretions which
help to loosen
mucus. Reducing
the viscosity of
secretions and
increasing
sputum volume
improves the
efficiency of the
cough reflex and
of ciliary action in
removing
accumulated
secretions.
chest pain,
palpitations
, tremor,
nervousnes
s. Long
acting
sympathom
imetics,
including
salmeterol,
increase
the risk of
asthma
related
death.
Cough
associated with
respiratory
tract infections
and related
conditions such
as sinusitis,
pharyngitis,
bronchitis, and
asthma, when
complicated by
tenacious
mucus or
mucus plugs
and congestion
GI distress,
drowsiness
medication
as prescribed
before
therapy and
to bring their
short acting
meds with
them.
Cardiac or
vision
abnormalitie
s may
indicate
toxicity, and
physician
should be
notified
immediatley.
Therapists
can exploit
the effects of
expectoratnt
agents by
performing
airway
clearance
interventions
within one
hour after
drug
administratio
n. Encourage
pts to take
meds with a
Serevent.
Xanthine
derivative: TheoDur,
Aminophylline
Mucinex
(guaifenesin),
terpin hydrate
Mucolytic
Agents
↓ the viscosity
of mucus
secretions by
altering their
composition and
consistency,
making them
easier to
expectorate.
They are
administered by
a nebulizer.
Vicous mucus
secretions due
to pneumonia,
emphysema,
chronic
bronchitis, and
cystic fibrosis
Pharyngitis,
oral
mucosa
inflammati
on, rhinitis,
chest pain
glass of
water.
Exploit the
effects by
performing
airway
clearance
interventions
Pulmozyme,
Mucosil or
Mycomyst
Cardiovascular/pulmonary/lymphatic Interventions:
Aerobic Exercise Prescription:
Aerobic exercise, or cardiorespiratory endurance exercise, refers to submaximal, rhythmic repetitive exercise of large muscle groups during
which adenosine triphosphate is synthesized primarily by the long-term energy system and the utilization of inspired oxygen.
Type (modality): walking, cycling, jogging are recommended to improve exercise tolerance, can be maintained at a constant velocity, very low
interindividual variability.
Dynamic arm exercise (arm ergometry): uses a smaller muscle mass, results in lower VO2 max (60%-70%lower) than leg ergometry; at a given
workload, HR will be higher, stroke volume lower; systolic and diastolic BP’s will be higher.
Early rehab: activity is discontinuous (interval training), with frequent rest periods; progressing to continuous training. Interval training can also
be incorporated in vigorous training to allow patient to work at higher percentage of V02 max.
Warm and up and cool down: gradually decrease the intensity of exercise, 5-10 minutes.
Resistive exercises: to improve strength and endurance in clinically stable pts. Usually prescribed in later rehab, after a period of aerobic
training. Moderate intensities are typically used (60%-80% of 1 repetition or 10 repetition maximal voluntary contraction. Precautions: monitor
BP, avoid breath holding (Valsalva’s response: may dramatically ↑ BP and work of heart). Contraindicated for patients with: uncontrolled
hypertension or arrhythmias
Intensity: prescribed as % of functional capacity revealed on ETT, within a range of 40%-85% depending upon initial level of fitness; typical
training intensity is 60%-80% of functional capacity; lower training intensities may necessitate an increase in training duration; most clinicians
use a combination of HR, RPE, and METs to prescribe exercise intensity (eliminates problems that may be associated with individual measures)
Heart rate:
1. Percentage of maximum HR achieved on ETT; without ETT 208-0.7 x age. 70%-85% HR max closely corresponds to 60%-80% of functional
capacity or VO2 max.
2. Estimated HR max is used in cases where submax ETT has been given.
3. Heart rate range or reserve (Karvonen’s formula) Can more closely approximate the relationship between HR and VO2 max, but
increased variability in pts on medications. Problems associated with use of HR alone to prescribe exercise intensity. 60%-80% (HR maxresting HR) + resting HR = target HR.
4. Beta blocking: affects ability of HR to rise in response to an exercise stress.
5. Pacemaker: can affect the ability of HR to rise in response to an exercise stress if it is fixed.
6. Environmental extremes, heavy arm work, isometric exercise and valsalva may affect HR and BP responses.
Rating of perceived exertion, the original Borg RPE scale (6-20).
1. Useful along with other measures of pts effort if beta blockers or other HR suppressors are used.
2. Problems with use of RPE alone to prescribe exercise intensity:
Individuals with psychological problems (depression)
Unfamiliarity with RPE scale; may affect selection of ratings
RPE scale 6-20 is linearly associated with HR.
Ex. Multiple by 10. 6x10=60 bpm.
If pt is 42 years old and reports 16 on the scale: 220-42=178 (predicted Max HR) 16x10=160bpm (borg scale) 160/178=89% so answer would be
the one that correlates most with 89%.
METs, or estimated energy expenditure (V02)
1. 40%-85% of functional capacity (maximal METs) achieved on ETT. Without a maximal ETT, this is an estimation of workload.
2. Problems associated with use of METs alone to prescribe exercise intensity:
-With high intensity activities (jogging) need to adopt a discontinuous work pattern: walk 5 minutes, jog 3 minutes to achieve the
desired intensity.
-Varying skill level or stress of competition may affect the known metabolic cost of an activity.
-Environmental stresses (heat, cold, high humidity, altitude, wind, changes in terrain such as hills) may affect the known
metabolic cost of an activity.
Duration: Conditioning phase may vary from 10-60 minutes, depending upon intensity; the higher the intensity, the shorter the duration.
-Average conditioning time is 20-30 minutes for moderate intensity exercise.
-Severely compromised individuals may benefit from multiple, short exercise sessions spaced throughout the day (3-10 min sessions)
-Warm-up and cool-down periods are kept constant 5-10 min each.
Frequency:
-Frequency of activity is dependent upon intensity and duration; the lower the intensity, the shorter the duration, the greater the frequency.
-Average: 3-5 sessions/week for exercise at moderate intensities and duration (>5 METs)
-Daily or multiple daily sessions for low intensity exercise (<5 METs)
Progression:
-Modify exercise prescription if:
-HR is lower than target HR for a given exercise intensity
-RPE is lower (exercise is perceived as easier) for a given exercise
-Symptoms of ischemia (angina) do not appear at a given exercise intensity
-Rate of progression depends on age, health status, functional capacity, personal goals, and preferences.
-As training progresses, duration is increased first, then intensity.
Normal Cardiorespiratory Response
to Acute Aerobic exercise:
-↑ oxygen consumption due to ↑
cardiac output, ↑ blood flow, and
oxygen utilization in the exercising
skeletal muscles
-Linear increase in SBP with
increasing workload (8 to 12 mm Hg
per MET)
-No change or moderate decrease in
DBP
-↑respiratory rate and tidal volume
Consider reduction in
exercise/activity with:
-Acute illness: fever, flu
-Acute injury, orthopedic
complications
-Progression of cardiac disease:
edema, weight gain, unstable angina
-Overindulgence: food, caffeine,
alcohol
-Environmental stressors: extremes
of heat, cold, humidity, air pollution
Consider terminating exercise:
Absolute Indications:
-Drop in systolic BP >10 mm Hg with
increased workload
-Moderate to severe angina
-↑ nervous system symptoms
(ataxia, dizziness, near syncope)
-Signs of poor perfusion
-Technical difficulties in monitoring
EKG or BP
-Subject’s desire to stop
-Sustained VT
-ST elevation > or equal to 1.0 mm
Relative Indications to terminate
exercise:
-ST or QRS changes (excessive ST
depression) or marked axial shift
-Arrhythmias other than sustained
VT (multifocal PVCs, triplets, SVT,
heart block, bradyarrhythmaias)
-Fatigue, SOB, wheezing, leg cramps
or claudication
-Development of bundle branch
block that can’t be distinguished
from VT
-Increasing chest pain
-Hypertensive response (SBP >250
mmHg or DBP >115 mmHg)
•Exercise prescription for post-PTCA (percutaneous transluminal coronary angioplasty):
1. Wait to exercise vigorously approximately 2 weeks post-PTCA to allow inflammatory process to subside. Walking program can be
initiated immediately.
2. Use post-PTCA ETT to prescribe exercise.
•Exercise prescription post-CABG (coronary artery bypass graft):
1. Limit upper extremity exercise while sternal incision is healing
2. Avoid lifting, pushing, pulling for 4-6 weeks postsurgery
_____________________________________________________________________________________
Phase 1: Inpatient Cardiac Rehabilitation (Acute)
Length of hospital stay is commonly 3-5 days for uncomplicated MI (no persistent angina, malignant arrhythmias, or heart failure)
1. Exercise/activity goals out outcomes
-Initiate early return to independence in ADLs, typically after 24 hours or until the patient is stable for 24 hours; monitor activity
tolerance
-Counteract deleterious effects of bed rest: reduce risk of thrombi, maintain muscle tone, reduce orthostatic hypotension, and
maintain joint mobility
-Help allay anxiety and depression
-Provide medical surveillance
-Provide pt & fam education
-Promote risk factor modification
2. Exercise/activity guidelines:
-Program components: ADLs, selected arm and leg exercises, early supervised ambulation
-Initial activities: low intensity (2-3 METs) progressing to > or equal to 5 METs by discharge.
-Post-MI: limited to 70% max HR and/or 5 METs until 6 weeks post-MI.
-Short exercise sessions, 2-3 times a day; gradually duration is lengthened and frequency is decreased.
Post surgical pts:
-Typically are progressed more rapidly than post MI, unless there was a peri-operative MI.
-Lifting activities are restricted, generally for 6 weeks.
Patient and family education goals:
-Improve understanding of cardiac disease, support risk factor modification
-Teach self-monitoring procedures, warning signs of exertional intolerance; (persistent dyspnea, angina pain, dizziness)
-Teach concepts of energy costs, fatigue monitoring, general activity guidelines, activity pacing, energy conservation techniques;
home exercise program
-Provide emotional support and assist with referral to social work as needed
Home Exercise Program (HEP):
-Low risk pts may be safe candidates for unsupervised exercise at home
-Gradual increase in ambulation time: goal of 20-30 minutes, 1-2 times per day at 4-6 weeks post MI.
-Upper and lower extremity mobility exercises.
-Elderly homebound pts with multiple medical problems may benefit from a home cardiac rehab program.
-Pts should be skilled in self-monitoring procedures.
-Recommended family training in CPR, and AED as indicated; emergency lifeline for some pts.
Phase 2: Outpatient Cardiac Rehabilitation (Subacute):
1. Eligible patients
-MI/acute coronary syndrome
-CABG
-PCI
-Stable angina
-Heart valve surgical repair or replacements
-Heart or heart/lung transplantation
-Heart failure and PAD: not covered by insurance but these populations benefit from supervised exercise program
2. Exercise/activity goals and outcomes:
-Improve functional capacity
-Progress towards full resumption of activities of daily living, habitual and occupational activities.
-Promote risk-factor modification, counseling as to lifestyle changes.
-Encourage activity pacing, energy conservation; stress importance of taking proper rest periods
3. Exercise/activity guidelines:
Outpatient Program :
-Pts at risk for arrhythmias with exercise, angina, other medical problems benefit from outpatient programs with availability of EKG monitoring,
trained personnel and emergency support.
-Group camaraderie and support of program participants may assist in risk-factor modification and lifestyle changes
-Frequency: 2-3 sessions/week
-Duration: 30-60 minutes with 5-10 minutes of warm-up and cool down
-Programs may offer a single mode of training (walking) or multiple modes using a circuit training approach (treadmill, cycle ergometer, arm
ergometer); strength training.
-Pts are gradually weaned from continuous monitoring to spot checks and self-monitoring.
-Suggested exit point: 9 MET functional capacity (5 MET capacity is needed for safe resumption of most daily activities)
Strength training in Phase 2 programs:
-Guidelines: after 3 weeks cardiac rehab; 5 weeks post MI or 8 weeks post CABG.
-Begin with use of elastic bands and light hand weights (1-3 lbs)
-Progress to moderate loads, 12-15 comfortable repetitions.
Phase 3: Community Exercise Programs (Post-acute, Postdischarge from Phase 2)
1. Exercise/activity goals and outcomes:
-Improve and/or maintain functional capacity
-Promote self-regulation of exercise programs
-Promote life-long commitment to risk-factor modification
2. Exercise/Activity guideliens:
-Location: community centers, YMCA, or clinical facilities
-Entry level criteria: functional capacity of 5 METs, clinically stable angina, medically controlled arrhythmias during exercise
-Progression is from supervised to self-regulation of exercise
-Progression to 50%-85% of functional capacity, 3-4 times/week, 45 minutes or more/session.
-Regular medical check-ups and periodic ETT generally required
-Utilize motivational techniques to maintain compliance with exercise programs, life-style modifications
-Discharge typically in 6-12 months.
Clinical indications for inpatient
& outpatient cardiac rehab:
-Medically stable post MI
-Stable angina pectoris
-PTCA
-CABG
-Compensated heart failure
-Cardiomyopathy
-Heart transplant
-Other cardiac surgery (valve
repair, pacemaker)
-Peripheral arterial disease
-High risk for coronary artery
disease with diagnosis of DM,
dyslipidemia, HTN, or obesity
-End-stage renal disease
Clinical Contraindications for
inpatient & outpatient cardiac
rehab:
-Unstable angina
-Resting SBP >200 mm Hg or
resting DBP >110 mm Hg
-Orthostatic blood pressure drop
of >20 mm Hg with symptoms
-Critical aortic stenosis
-Acute systemic illness or fever
-Uncontrolled atrial/ventricular
arrhythmias
-Third-degree atrial ventricular
block without pacemaker
-Active pericarditis or
myocarditis
-Recent embolism
-Thrombophlebitis
-Resting ST segment depression
or elevation >2 mm
-Uncompensated congestive
heart failure
-Orthopedic or metabolic
conditions that would prohibit
exercise
Resistance Exercise Training:
Goals: Improve muscle strength and endurance; enhance functional independence; decrease cardiac demands during daily activities
Patient criteria for resistance training:
-Post MI: resistance training permitted if remain under 70% max HR or 5 METs for 6 weeks post MI, be cautious of Valsalva with resistance
training
-Cardiac surgery: LE resistance training can be initiated immediately, in the absence of peri-operative MI. UE resistance training should be
avoided until soft tissue and bony healing has occurred: 6-8 weeks.
-Post-transcatheter procedure (PTCA, other): minimum of 3 weeks following procedure and 2 weeks of consistent participation in a supervised
CR endurance training program.
-No evidence of the following conditions: congestive heart failure, uncontrolled dysrhythmias, severe valvular disease, uncontrolled
hypertension and unstable symptoms.
Exercise Prescription:
-Start with low resistance (one set of 10-15 reps) and progress slowly
-Resistance can include:
-Weights, 50% or more of maximum weight used to complete one repetitition (1RM)
-Elastic bands
-Light (1-5 lb) cuff and hand weights
-Wall pulleys
-Perceived exertion (RPE-Borg scale) should range from 11 to 13 (“light to somewhat hard”), but this needs to be correlated to
hemodynamic response to activity.
-Rate pressure product should not exceed that prescribed during endurance exercise
Rehab Guidelines for Arterial Disease:
1. Risk factor modification
2. Limb protection
a. Avoid excessive strain, protection of extremities from injury and extremes of temperature
b. Bed rest may be required if gangrene, ulceration, acute arterial disease are present
3. Exercise Training for pts with PAD:
a. May result in improved functional capacity, improved peripheral blood flow via collateral circulation and muscle oxidative
capacity.
b. Consider interval training with frequent rests
c. Walking program: intensity such that pt reports 1 on claudication scale within 3-5 minutes, stopping if they reach a 2 (until pain
subsides), total of 30-60 minutes (intervals as necessary), 3-5 days per week.
d. Record time of pain onset and duration
e. Non-weight bearing exercise (cycle ergometry, arm ergometry) may be necessary in some pts; less effective in producing a
peripheral conditioning effect.
f. Well-fitting shoes essential; with insensitive feet, teach techniques of proper foot inspection and care.
g. Beta blockers for treatment of HTN or cardiac disorders may decrease time to claudication or worsen symptoms.
h. Pentoxifylline, dipyridamole, aspirin and warfarin may improve time to claudication.
i. High risk for CAD.
4. Lower extremity exercise:
a. Modified Buerger-Allen exercises: postural exercises plus active plantar and dorsiflexion of the ankle; active exercises improve
blood flow during and after exercise; effects less pronounced in pts with PAD.
b. Resistive calf exercises: most effective method of increasing blood flow.
5. Medical treatment:
a. Medications to decrease blood viscosity, prevent thrombus formation (heparin)
b. Vasodilators: controversial
c. Calcium channel blockers in vasospastic disease
6. Surgical management:
a. Atherectomy, thromboembolectomy, laser therapy
b. Revascularization: angioplasty or bypass grafting
c. Sympathectomy: results in permanent vasodilation, improvement in blood flow to skin
d. Amputation when gangrene is present
_____________________________________________________________________________________
Rehab Guidelines for Venous Disease:
1. Deep vein thrombophlebitis (DVT):
a. Early stages may be asymptomatic; symptomatic pts demonstrate dull ache, pain, tenderness in calf; may also see slight edema
or fever.
b. Acute: activity limited until a dose of low molecular weight heparin, then ambulation permitted. Compression stockings (>30-40
mm Hg) can assist with pain control
c. Anticoagulation medications
2. Chronic venous insufficiency (CVI)
a. Management of edema:
i. Positioning: extremity elevation, minimum of 18 cm above heart. Encourage pts to elevate leg as much as possible and
avoid the dependent position
b. Compression therapy
i. Bandages (elastic, tubular); applied within 20 minutes of rising
ii. Paste bandages (Unna boot). Gauze impregnated with zinc oxide, gelatin and glycerine; applied for 4-7 days (less with
some wounds)
iii. Graduated compression stockings (Jobst), at least 30 mm Hg
iv. Compression pump therapy, used for a 1-2 hour session twice daily
v. Red flag: consider consequences of compression therapy to a limb with an ankle-brachial index (ABI) <0.8 or with
evidence of active cellulitis or infection
3. Exercise
a. Active ankle exercises: emphasis on muscle pump exercises (dorsiflexion/planatarflexion, foot circles)
b. Cycle ergometry in sitting or attached to foot of bed
c. Early ambulation as soon as pt is able to get out of bed, 3-4 times a day.
Patient education: meticulous skin care
Severe conditions with dermal ulceration may require surgery (ligation and vein stripping, vein grafts, valvuloplasty.
_____________________________________________________________________________________
Rehab Guidelines for lymphatic Disease:
1. Phase 1 Management: edema secondary to lymphatic dysfunction
a. Short stretch compression bandages, worn 24 hours/day
b. Manual lymph drainage (MLD) with complete decongestive therapy
i. Massage and passive ROM to assist lymphatic flow (Vodder techniques, modifications by Askonk. Leduc, Fodi)
ii. Emphasis is on decongesting proximal segments first (trunk quadrant), then extremities, directing flow distal to proximal
iii. Compression using multilayered padding and short-stretch bandages
1. Bandages have low resting pressure and high working pressure
2. Bandages maintain limb after techniques applied to reduce limb
3. Decongestive exercises with padding in place. Activate muscles in extremity. Work trunk and limb girdle first,
then limb muscles from proximal to distal. Performed with compression bandages on.
4. Certified specialists (certified lymphedema therapist)
c. Functional activities:
i. Walking program, cycling
ii. Water-based programs: swimming
iii. Tai chi and balance activities
iv. ADL training
v. RED FLAG: strenuous activities, jogging and ballistic movements are contraindicated, as they are likely to exacerbate
lymphedema.
vi. Signs of lymph overload: discomfort, aching or pain in proximal lymph areas (axilla or inguinal areas), change in skin
color. If any of these are present, discontinue activity.
d. Meticulous skin care: hygiene, nail care.
e. Contraindicated modalities:
i. Ice, heat, hydrotherapy, saunas, contract baths, paraffin; all cause vasodilation and increase lymphatic load of water
ii. No electrotherapeutic modalities greater than 30 Hz.
f. Compression garments at end of Phase 1.
g. Red flag: excessively high pressures will occlude superficial lymph capillaries and restrict fluid absorption
2. Phase II Management (self-management)
a. Skin care
b. Compression garments
c. Exercise
d. Lymphedema bandaging at night
e. MLD as needed
f. Compression pumps: use with caution; limited benefits
g. RED FLAG: pressures higher than 45 mm Hg are contraindicated, as they can cause lymphatic collapse; contraindicated with soft
tissue injury
3. Education
a. Skin and nail care
b. Self-bandaging, garment care
c. Infection management
d. Maintain exercise while preventing lymph overload
_____________________________________________________________________________________
Basic Life Support and CardioPulmonary Resuscitation (CPR)
1.
2.
3.
4.
5.
6.
Compressions come first, and then focus on airway and breathing. Only exception is newborn babies.
No more looking, listening, and feeling. Call 911 immediately.
Push a little harder for adult CPR: at least 2 inches deep on chest.
Push a little faster: about 100 compressions/min.
Hands only CPR for untrained lay rescuers.
Don’t stop pushing, no interruptions.
First Aid:
1. External bleeding
a. Minor bleeding:
i. Usually clots within 10 minutes
ii. If pt/client is taking aspirin or nonsteroidal anti-inflammatory drugs, clotting may take longer
b. Severe bleeding characteristics:
i. Blood spurting from a wound
ii. Blood fails to clot even after measures to control bleeding have been taken
iii. Arterial bleed: high pressure, spurting, red
iv. Venous bleed: low pressure, stead flow, dark red or maroon blood
v. Capillary bleed: low pressure, oozing, dark red blood
c. Controlling external bleeding:
i. Use standard precautions such as wearing gloves
ii. Apply gauze pads using firm pressure. If no gauze available, use a clean cloth, towel, a gloved hand or pts own hand. If
blood soaks through, do not remove any gauze, add additional layers.
iii. Elevate the part if possible unless it is deformed or it causes significant pain when elevated.
iv. Apply a pressure bandage, such as roller gauze, over the gauze pads.
v. If necessary, apply pressure with the heel of your hand over pressure points. The femoral artery in the groin and the
brachial artery in the medial aspect of the upper arm are two such points.
vi. Monitor A, B, Cs and overall status of the pt. Administer supplemental oxygen if nearby. Seek more advanced care as
necessary
2. Internal bleeding:
a. The possible result of a fall, blunt force trauma or a fx rupturing a blood vessel or organ.
b. Severe internal bleeding may be life-threatening
c. Severe internal bleeding characteristics:
i. Ecchymosis (black and blue) in the injured area
ii. Body part, especially the abdomen, may be swollen, tender, and firm
iii. Skin may appear blue, gray or pale and may be cool or moist
iv. Respiratory rate in increased
v. Pulse rate is increased and weak
vi. Blood pressure is decreased
vii. Pt may be nauseated or vomit
viii. Pt may exhibit restlessness or anxiety
ix. Level of consciousness may decline
d. Management of internal bleeding
i. If minor, follow RICE procedure
ii. Major internal bleeding
1. Summon advanced medical personnel
2. Monitor A, B, Cs and vital signs
3. Keep the pt comfortable and quiet. Keep them from getting chilled or overheated.
4. Reassure pt or victim
5. Administer supplemental oxygen if available and nearby
3. Shock (hypo-perfusion)
a. Failure of the circulatory system to perfuse vital organs
b. At first, blood is shunted from the periphery to compensate
i. The victim may lose consciousness as the brain is affected
ii. The heart rate increases, resulting in increased oxygen demand
iii. Organs ultimately fail when deprived of oxygen
iv. Heart rhythm is affected, ultimately leading to cardiac arrest and death
c. Types and causes of shock:
i. Hemorrhagic: severe internal or external bleeding.
ii. Psychogenic: emotional stress causes blood to pool in body away from the brain
iii. Metabolic: loss of body fluids from heat or severe vomiting or diarrhea
iv. Anaphylactic: allergic reaction from drugs, food or insect stings
v. Cardiogenic: MI or cardiac arrest results in pump failure
vi. Respiratory: respiratory illness or arrest results in insufficient oxygenation of the blood
vii. Septic: severe infections cause blood vessels to dilate
viii. Neurogenic: traumatic brain injury, spinal cord injury or other neural trauma causes disruption of blood vessel
dilation/constriction
d. Signs and symptoms:
i. Pale, gray or blue, cool skin
ii. Increased, weak pulse
iii. Increased respiratory rate
iv. Decreased blood pressure
v. Irritability or restlessness
vi. Diminishing level of consciousness
vii. Nausea or vomiting
e. Care for shock:
i. Obtain a history if possible
ii. Examine the victim for airway, breathing, and circulation and bleeding
iii. Assess level of consciousness
iv. Determine skin characteristics and perform capillary refill test of finger tips
1. Capillary refill test: squeeze fingernail for 2 seconds
2. In healthy individuals, the nail will blanch and turn pink when pressure is released
3. If nail bed does not refill and turn pink within 2 seconds, the cause could be that blood is being shunted away
from the periphery to vital organs or to maintain core temperature.
4. Treat any specific condition if possible: control bleeding, splint a fx, Epipen for anaphylaxis and so on.
5. Keep the victim form getting chilled or over heated
6. Elevate the legs 12 inches unless there is suspected spinal injury or painful deformities of the lower extremities
7. Reassure the victim and continue to monitor A, B, Cs
8. Administer supplemental oxygen if nearby
9. Do not give any food or drink
o
Bronchial Drainage
 Upper lobes Apical segments
 Bed or drainage table flat
 Pt leans back on pillow at 30-degree angle against therapist.
 Therapist claps with markedly cupped hand over area between the clavicle and top of the scapula on each
side.
 Upper lobes posterior segments
 Bed or drainage table flat
 Pt leans over folded pillow at 30 degrees angle
 Therapist stands behind and claps over upper back on both sides
 Upper lobes anterior segments
 Bed or drainage table flat
 Pt lies on back with pillows under knees
 Therapist claps between clavicle and nipple on each side
 Left Upper lobe Lingular Segments
 Foot of table or bed elevated 16 inches
 Pt lies head down on right side and rotates ¼ turn backward. Pillow may be placed from behind shoulder to
hip. Knees should be flexed
 Therapist claps with cupped hands over left nipple area
 Right Middle Lobe
 Foot of table or bed elevated 16 inches

o
Pt lies head down on left side and rotates ¼ turn backward. Pillow may be placed behind from shoulder to
hip. Knees should be flexed
 Therapist claps over right nipple area
 Lower Lobe anterior basal segment
 Foot of table or bed elevated 20 inches
 Pt lies on side head down, pillow under knees
 Therapist claps with cupped hands over lower ribs.
 Draining left lie on right, Draining right Lie on left
 Lower lobes Posterior Basal segments
 Foot of table or bed elevated 20 inches
 Pt lies on abdomen, head down with pillow under hips.
 Therapist claps over lower ribs close to spine on each side
 Lower Lobes Superior Segments
 Babe or table flat
 Pt lies on abdomen with two pillows under hips
 Therapist claps over middle of back at tip of scapula on either side of spine
 Lower Lobes Lateral basal segments
 Foot of table or bed elevated 20 inches
 Pt lies on abdomen, head down and rotates ¼ turn upward. Upper leg is flexed over pillow for support.
 Therapist claps over uppermost portion of lower ribs
 Drainage of left lie on right, Drainage of right lie on left.
Airway clearance techniques
 Cough: Pt should be asked to cough in the upright position, if possible, after each area of lung has been treated.
 Huffing: more effective in Pt with collapsible airways. Prevents the high intrathoracic pressure that causes
premature airway closure.
 Ask pt to inhale deeply
 Immediately, the pt forcibly expels the air, saying ha, ha
 Assisted cough: the therapist hands or fist become the force behind the pt exhaled air. Used when the pts
abdominal muscles cannot generate an effective cough.
 Position the Pt against a solid surface; supine with head of bed or table flat or in a Trendelenburg position,
or sitting with wheelchair against the wall.
 The therapist’s hand is placed below the pts subcostal angle
 Pt inhales deeply



As the pt attempts to cough, the therapist hand pushes inward and upward, assisting the rapid exhalation of
air.
 Any secretions raised should be removed by a suction catheter if expectoration is problematic
Tracheal stimulation: used with pts who are unable to cough on command.
 The therapist finger or thumb is placed just above the substernal notch, and a quick inward and downward
pressure on the trachea elicits the cough reflex.
Endotrachel suctioning: used only when the above airway clearance techniques fail to adequately remove
secretions. (10-15 seconds)
Airway Clearance Techniques:
Airway clearance techniques are intended to manage or prevent the consequences of impaired mucociliary transport or the inability to protect
the airway (impaired cough). The techniques may include breathing strategies, manual and mechanical techniques, and postural drainage.
Indications for Airway Clearance:
-Restrained secretions in the central airways
-Prophylaxis against postoperative pulmonary complications
-Obtain sputum for diagnostic analysis
-Difficulty clearing secretions
-Atelectasics caused by or suspected of being caused of mucus plugging
Technique:
Active Cycle of
Breathing (ACB)
What is it:
Procedure:
ACB was developed under
the name “forced expiratory
technique” to assist
secretion clearance in pts
with asthma. The name of
the technique was changed
to “active cycle of
breathing” to emphasize
that ACB always couples
breathing exercise with the
•Breathing control: Gentle,
relaxed breathing (may be
diaphragmatic breathing at
pts tidal volume and
resting respiratory rate for
5-10 seconds, or as long as
the pt needs in order to
prepare for the next phase.
•Thoracic expansion
exercise: 3-4 deep, slow,
Precautions/Contraindica
tions:
-Splinting post-operative
incisions to achieve
adequate expiratory force
-Bronchospasm or hyperreactive airways
huff cough. It includes 3
phases: breathing control,
thoracic expansion
exercises, and forced
expiratory technique.
Autogenic Drainage
(AD)
relaxed inhalations to
inspiratory reserve with
passive exhalation –Chest
percussion, vibration or
shaking may be combined
with exhalation
•Forced expiratory
technique:
1 or 2 huffs at mid to low
lung volumes with the
glottis open into the
expiratory reserve volume;
a brisk adduction of the
upper arms may be added
to self-compress the thorax
AD uses controlled
The pt is sitting upright in a
breathing to mobilize
chair with back support.
secretions by varying
Controlled breathing at
expiratory airflow without
three lung volumes:
using postural drainage
-“Unsticking phase”: slowly
positions or coughing. The
breathe in through nose at
theory is to improve airflow low-lung volumes followed
in small airways to facilitate by a 2-3 second breaththe movement of mucus. AD hold to allow collateral
requires patience to learn,
ventilation to get air
so this may not be suitable
behind the secretions, then
for young children and pts
exhale down into the
who are not motivated or
expiratory reserve volume.
easily distracted. Because
-“Collecting phase”:breath
AD does not require the
at tidal volume,
assistance of another person interspersed by 2-3 second
or equipment, it can be
breath holds
performed anywhere and
-“Evacuating phase”:
during activities of daily
deeper inspirations from
Requires motivation and
concentration to learn
living.
Directed cough and
huffing
A directed cough tries to
compensate for the pts
physical limitations to elicit
a maximum forced
exhalation.
Huffing is a forced
expiratory maneuver
performed with the glottis
open. The maneuver is
similar to fogging a pair of
glasses with your breath.
Although a huff does not
produce the same airflow
velocity as a cough, the
potential for airway collapse
is less. Huffing may be
reinforced by a quick
adduction of the arms to
self-compress the chest
wall.
High-frequency
airway oscillation
The Acapella & Flutter are
handheld devices that
combine positive expiratory
low-to-mid inspiratory
reserve volume, with
breath holding followed by
a huff
Exhalation through pursedlips may be used to control
expiratory flow rate
-An average treatment is
30-45 min
Cough: Inhale maximally ,
close the glottis and hold
breath for 2-3 seconds;
contract the expiratory
muscles to produce
increased intrathoracic
pressure against the closed
glottis; cough sharply 2-3
times through a slightly
open mouth; post-surgical
pts may need to splint the
chest or abdomen by
applying pressure over the
incision with a pillow or
blanket roll.
Huff: Inhale deeply through
an open mouth; contract
the abdominal muscles
during a rapid exhalation
with the glottis open,
saying, “Ha, ha, ha.”
-Place the device in the
mouth the lips firmly
sealed around the
-Inability to control
possible transmission of
infection from pts
suspected or known to
have pathogens
transmittable by droplets
-Elevated intracranial
pressure or known
intracranial aneurysm
-Reduced coronary artery
perfusion (acute MI)
-Acute unstable head,
neck or spine injury
-Potential for
regurgitation/aspiration
-Acute abdominal
pathology, abdominal
aortic aneurysm, hiatal
hernia or pregnancy
-Untreated pneumothroax
-Osteoporosis
-Flail chest
-Pt tolerance of increased
work of breathing (acute
asthma, COPD)
pressure and high frequency
airway vibrations to mobilize
mucus secretions in the
airways
Postural drainage,
percussion, and
vibration
Postural drainage consists of
positioning the pt so that
gravity will help drain
bronchial secretions from
specific lung segments
toward the central airways
where they can be removed
by cough or mechanical
aspiration.
Percussion, also known as
cupping & clapping, is the
rhythmic clapping or striking
of the thorax with a cupped
hand or mechanical
percussor directly over the
lung segment being drained.
This rhythmic sequence
should last for several
minutes and should not be
painful.
Vibration is the application
of a fine, tremulous action
on the chest wall over the
mouthpiece
-Inhale slowly to 75% of a
full breath
-Hold the breath for 2-3
seconds
-Exhale through the device
for 3-4 seconds
-Repeat 10-20 breaths
-Remove the device and
perform 2-3 coughs or
huffs to raise secretions
Postural drainage: The pt
assumes the appropriate
position for the affected
lung segment. Standard
positions may be modified
as the pts conditions and
tolerance warrant.
Maintain each position for
2-3 minutes.
Percussion & vibration: Place the pt in the
appropriate postural
drainage position; cover
the skin overlying the
affected segment with a
thin material (towel, t-shirt,
hospital gown); therapist
rhythmically strikes the
chest with a cupped hand
for 2-3 minutes per lung
segment; therapist places
one hand on top of the
other over affected area or
-Intracranial pressure >20
mm Hg
-Recent facial, oral, or
skull surgery or trauma
-hemodynamic instability
-Acute sinusitis
-Nosebleed
-Esophageal surgery
-Active hemoptysis
-Nausea
All positions are
contraindicated for:
-ICP >20 mm Hg
-Head and neck injury
until stabilized
-Active hemorrhage with
hemodynamic instability
-Recent spinal surgery or
acute spinal injury
-Active hemoptysis
-Empyema
-Bronchopleural fistula
-Pulmonary edema
associated with CHF
-Large pleural effusion
-Confused or anxious pts
who do not tolerate
position changes
-Rib fx, with or without fail
chest
-Surgical wound or healing
tissue
Trendelenburg position is
lung segment being drained
in the direction the ribs
move during exhalation. It
may be performed manually
or with a mechanical
vibrator. Vibration should be
performed during
exhalation.
one hand on each side of
the rib cage; vibrate the
chest wall as the pt exhales
by tensing the muscles of
the hands and arms while
applying moderate
pressure downward; the
maneuver is performed in
the direction in which the
ribs move on expiration;
encourage the pt to cough
or huff after 2-3 vibrations
contraindicated for:
-Uncontrolled HTN
-Distended abdomen
-esophageal surgery
-Recent gross hemoptysis
related to lung carcinoma
-Uncontrolled airway at
risk for aspiration )tube
feeding or recent meal)
-Subcutaneous
emphysema
-Recent epidural spinal
infusion or spinal
anesthesia
-Recent skingrafts, or flaps
on the thorax
-Burns, open wounds, and
skin infections
-Recently placed
transvenous or
subcutaneous pacemaker
-Suspected pulmonary
tuberculosis
-Lung contusion
-Bronchospasm
-Osteomyelitis of the ribs
-Osteoporosis
-Complaint of chest wall
pain
Breathing Exercises:
Exercise
Diaphragmatic
Breathing (DB):
involves breathing
predominately
with the
diaphragm while
minimizing the
action of
accessory muscles
and motion of the
upper rib cage
during inspiration
Indications
Precautions/Contra
Procedure
-Post surgical pt
with pain in the
chest wall or
abdomen, or
restricted mobility
-Pt learning active
cycle of breathing
or autogenic
drainage airway
clearance
techniques
-Dysnpea at rest
or with minimal
activity
-Inability to
perform ADLs due
to dyspnea or
inefficient
breathing pattern
-Moderate to
severe COPD &
marked
hyperinflation of
the lungs with
diaphragmatic
movement
-Pts with
paradoxical
breathing patterns
or who
demonstrate
increased
inspiratory muscle
effort, and
increased dyspnea
during DB
-Semi-fowler’s
positions is a good
starting position
-Sniffing can be
used to facilitate
contraction of the
diaphragm
-Have the pt place
one hand on the
upper chest and
the other just
below the rib cage
-Instruct the pt to:
“Breathe in slowly
through your nose
so that your
stomach moves
out against your
hand. The hand on
your chest should
remain as still as
possible. Feel your
abdomen gently
rise into your
hand. Exhale
through pursed
lips, let the hand
on your abdomen
descend, while
the hand on your
upper chest
Expected
Outcomes
-Decreased
respiratory rate
-Decrease use of
accessory muscles
of inspiration
-increase tidal
volume
-Decrease
respiratory flow
rate
-Subjective
improvement of
dyspnea
-Improve
tolerance for
activity
Inspiratory Muscle
training (IMT):
attempts to
strengthen the
diaphragm and
intercostals
muscles. Two
different IMT
devices provide
different modes of
training: flow
resistive breathing
and threshold
breathing. During
flow resistive
breathing, the pt
inspires through a
mouthpiece and
adapter with an
adjustable
diameter.
Decreasing the
diameter
increases the
resistance to
breathing,
provided that
breathing rate,
tidal volume, and
inspiratory time
are kept constant.
Threshold loading
requires a buildup
Impaired
inspiratory muscle
strength and/or a
ventilatory
limitation to
exercise
performance
-Clincal signs of
inspiratory muscle
fatigue
-Tachypnea
-Reduced tidal
volume
-Increased PaCO2
-Bradypnea and
decreased minute
ventilation
remains still.”
Measure the pts
maximum
inspiratory
pressure (MIP)
with a
manometer. Use
the measured MIP
to calculate the
training load.
Using the
threshold
inspiratory muscle
trainer: Place
mouthpiece in
mouth and inhale
with enough force
to open the valve,
the higher the
setting the greater
the effort needed,
begin training
with the setting
that elicits 30% to
40% of the pts
MIP. Pt breathes
at tidal volume for
5-15 min. Using
the PFLEX
Inspiratory muscle
trainer: Place
PFLEX in mouth
and breath at tidal
volume, setting 1
-Increased
inspiratory muscle
strength and
endurance;
decrease dysnpea
at rest and during
exercise; increase
functional
exercise capacity
of negative
pressure before
flow occurs
through a valve
that opens at a
critical pressure.
Threshold
breathing
provides
consistent and
specific pressure
for IMT,
regardless of how
quickly or slowly
pts breathe.
Paced breathing
and exhale with
effort: Paced
breathing is a
strategy to
decrease the work
of breathing and
prevent dyspnea
during activity. It
allows anyone
who experiences
shortness of
breath to become
less fearful of
activity and
exercise.
Exhale with effort
is a breathing
strategy employed
provides the least
resistance, begin
training that elicits
30-40% level MIP
for 10-15 min
daily.
-Pts with dysnpea
at rest or with
minimal activity
-Inability to
perform activity
due to pulmonary
limitation
-Inefficient
breathing pattern
during activity
Avoid valsalva
maneuver during
activity
Perform activity at
a tempo that does
not exceed the pts
breathing
limitations; find a
comfortable
inspiration to
expiration time to
synchronize with
the exertion phase
of activity;
synchronize
breathing with
components of
the activity: inhale
before or during
the easier
component of the
activity, exhale
Complete activity
without dyspnea;
decrease pts fear
of becoming short
of breath during
activity
during activity to
prevent a pt from
holding their
breath. The
technique breaks
any activity into
one or more
breaths with
inhalation during
the resting or less
active phase of
the activity and
exhalation during
the movement or
more active phase
of the activity.
during the more
vigorous
component of the
activity, do not
hold breath or
rush through the
activity.
Walking: Inhale
through the nose
while walking 2
steps and then
pause; exhale
through pursed
lips while walking
4 steps.
Climbing stairs:
inhale through the
nose while
standing, exhale
through pursed
lips while stepping
up (or down) 1 or
2 stairs, remain on
the step until
breathing control
is restored
Lifting: inhale
through the nose
while standing or
sitting; exhale
through pursed
lips while bending
to reach the
object; pause;
Pursed-lip
breathing (PLB) is
a simple
technique to
reduce respiratory
rate, reduce
dyspnea, and
maintain a small
positive pressure
in the bronchioles,
which may help
prevent airway
collapse in pts
with emphysema.
Any pt who is SOB
may use this
technique.
Tachypnea,
dysnpea
Forcing exhalation
Segmental
breathing: also
known as localized
breathing or
thoracic
expansion
-Decreased
intrathoracic lung
volume,
decreased chest
wall lung
compliance,
None
inhale through the
nose while
grabbing the
object; exhale
through pursed
lips while standing
up
Semi-fowlers is a
good position to
initiate the
breathing
technique.
Instruct the pt to:
“breathe in slowly
through your nose
with the mouth
closed for two
counts. Pucker, or
purse your lips as
if you were going
to whistle, then
gently breathe out
through pursed
lips, as if trying to
make a candle
flame flicker, for a
4 count. Do not
blow with force.”
Position the pt:
-sitting position
for basal
atelectasis
-sidelying with
affected lung
-Decrease
respiratory rate,
relieve dyspnea,
reduce arterial
partial pressure of
carbon dioxide,
improve tidal
volume, improve
oxygen saturation,
prevent airway
collapse in pts
with emphysema,
increase activity
tolerance
-Increase chest
wall mobility
-Expand collapsed
alveoli via airflow
through collateral
ventilation
exercises, is
intended to
improve regional
ventilation and
prevent and treat
pulmonary
complications
after surgery. It is
based on the
presumption that
asymmetrical
chest wall motion
may coincide with
underlying
pathology
(pneumonia,
pleuritic chest wall
pain, retained
secretions) and
that inspired air
can be directed to
a particular area
by facilitation or
inhibition of chest
wall movement
through proper
hand placements,
verbal cues or
coordination of
breathing.
Sustained
maximal
inhalation with
incentive
increased flow
resistance from
decreased lung
volume,
ventilation:
perfusion
mismatch
-Decreased
intrathoracic lung
volume
-Decreased chest
-Pt is not
cooperative or is
unable to
understand or
uppermost
-Postural drainage
positions with
affected lung
uppermost to
assist with
secretion removal
-Therapist applies
firm pressure at
the end of
exhalation to the
pts chest wall
overlying the area
to be expanded
-pt inhales deeply
and slowly
expanding the rib
cage under the
therapist hands
-Therapist reduces
hand pressure
during the pts
inhalation
channels
-assist with
secretion removal
-Hold the
incentive
spirometer in a
vertical position
-Absence of or
improve
improvement in
signs of atelectaiss
spirometer: (SMI), wall lung
demonstrate
-Have the pt
-Decreased
a maximal
compliance
proper use of the
exhale
respiratory rate
inspiratory effort
-Increased flow
incentive
completely, then
-Resolution of
is held for 3 or
resistance from
spirometer
seal his lips
fever
more seconds at
decreased lung
-Pt is unable to
around the
-Normal pulse
the point of
volume
deep breathe
mouthpiece
rate
maximum
-ventilation:
effectively (with
-breath in slowly
-Normal chest xinspiration before perfusion (V:Q)
vital capacity less
and deeply
ray
exhalation. Many
mismatch
than 10 mL/Kg or
through the
-Improved paO2
airway clearance
-Atelectasis or risk inspiratory capacity mouth, raising the -Increased forced
techniques
of atelectasis due less than 1/3 of
ball or piston of
vital capacity and
include SMI to
to thoracic and
predicted)
the spirometer
peak expiratory
compensate for
upper abdominal
-Pts with moderate -Encourage the pt flows
asynchronous
surgery
to severe COPD
move the
ventilation, to
-Restrictive lung
with increased
diaphragm and
promote air
defect associated respiratory rate and expand the lower
passage past
with quadriplegia hyperinflation
chest, not the
mucus
and/or
upper chest
obstructions in
dysfunctional
-Hold the breath
airways, and to
diaphragm
for at least 3
maximize alveolar
seconds and note
expansion. SMI is
the highest level
also called
the piston reaches
incentive
-Perform SMI
spirometry when
independently 5using a device that
10 breaths per
provides visual or
hour when awake
other feedback to
encourage the pt
to take long, slow,
deep inhalations.
o Abdominal Breathing
 Used when abdominal muscles are too weak to provide an effective cough. Abdominal splinting: used when the
abdominal muscles cannot provide the necessary support needed for passive exhalation.

Glossopharyngeal breathing (air gulping) can also be taught to assist coughing.
Positions to relieve Dyspnea:
A number of positions may be used to provide relief from dyspnea. The choice of position will depend on the circumstances at the time. The
forward leaning position often provides relief of dyspnea to pts with lung disease.
Forward leaning with arm support optimizes the length-tension relationship of the diaphragm and allows the pectorals minor and pectoralis
major muscles to assist in elevating the rib cage during inspiration. The positions may be combined with other breathing techniques.
Reverse Trendelenburg position:
The opposite of the Trendelenburg position, the reverse Trendelenburg position places a person in supine with their head above their trunk and
lower extremities, decreasing the weight of the abdominal contents on the diaphragm and reducing the resistance to movement during
breathing.
Semi-Fowler’s position:
The semi-fowler’s position places a pt in supine with the head of the bed elevated to 45° and pillows under the knees for support and
maintenance of a proper lumbar curve. This position is used often for pts with congestive heart failure or other cardiac conditions.
Musculoskeletal System—Physical Therapy Examination
1. Anatomy and Physiology of the MS System
Muscle
Deltoid--Clavicular part
Acromial part
Spinal part
Origin
Lateral clavicle
Acromion
Scapular spine
Insertion
Humerus (deltoid
tuberosity)
Action
Flexion, IR, ADD
Abduction
Extension, ER, ABD
Innervation
Axillary n. C5, C6
Supraspinatus
Greater tuberosity
Abduction
Infraspinatus
Supraspinous
fossa
Infraspinous fossa
Greater tuberosity
ER
Teres Minor
Lateral border
Greater tuberosity
Subscapularis
Subscapular fossa
Lesser tuberosity
ER, weak
adduction
IR
Pectoralis Major-Clavicular part
Sternocostal part
Abdominal part
Clavicle
Sternum and
costal cartilages 16
Rectus sheath
Humerus (crest of
greater tuberosity)
Coracobrachialis
Coracoid process
Humerus
Pectoralis Minor
3rd to 5th ribs
Coracoid process
Serratus Anterior
Superior part
Intermediate part
Inferior part
1st to 9th ribs
Scapula (medial
border)
Trapezius
1.Spinous process
1.Clavicle
Entire muscle:
adduction, IR
Clavicular &
sternocostal
parts:flexion;
assist in
respiration when
shoulder is fixed
Flexion, ADD, IR
Draws scapula
downward,
causing inferior
angle to move
posteromedially;
rotates glenoid
inferiorly
Lowers the raised
arm, draws
scapula laterally
forward; elevates
ribs when
shoulder is fixed,
rotates scapula
laterally
1.Upward
Suprascapular n.
C4-C6
Suprascapular n.
C4-C6
Axillary n. C5,C6
Subscapular n. C5,
C6
Medial & lateral
pectoral nn. C5-T1
Musculocutaneous
C6, C7
Medial & lateral
pectoral nn. C6-T1
Long thoracic n
C5-C7
Accessory n (CN
1.Descending part
2.Transverse part
3.Ascending part
C1-C7
2.Spinous process
T1-T4
3.spinous process
T5-T12
2.Acromion
3.Scapular spine
rotation, rotates
gleniod superiorly,
tilts head to SAME
side and rotates to
OPPOSITE
2.Draws scapula
medially
3.Draws scapula
medially
downward
Entire
muscle:steadies
scapula on thorax
XI), cervical plexus
C3, C4
Muscle
Levator Scapulae
Origin
Transverse
process C1-C4
Insertion
Scapula, superior
angle
Innervation
Dorsal scapular n.
C4-C5
Rhomboid minor
Spinous process
C6,C7
Rhomboid major
Spinous process
T1-T4 vertebrae
Steadies scapula,
upward rotation
Dorsal scapular n.
C4-C5
Latissimus Dorsi
Veretbral part
Scapular part
Costal part
Iliac part
Spinous process
T7-T12 vertebrae
Scapula:inferior
angle
9th to 12th ribs
Iliac crest
Scapula (inferior
angle)
Medial border
above scapular
spine
Medial border
below scapular
spine
Crest of lesser
tuberosity of the
humerus
Action
Upward rotation,
inclines neck to
SAME side
Steadies scapula,
upward rotation
IR, ADD,
extension, “cough
muscle”
Thoracodorsal n.
C6-C8
IR, ADD, extension
Lower subscapular
n. C5-C7
Elbow: flexion,
Musculocutaneous
Teres major
Biceps brachii
Supraglenoid
Crest of lesser
tuberosity of the
humerus
Radial tuberosity
Dorsal scapular n.
C4-C5
Long head
Short head
tubercle of scapula
Coracoid process
of scapula
Brachialis
Humerus (distal
half of anterior
surface)
Scapula
(infraglenoid
tubercle)
Posterior humerus
(medial septum)
Posterior humerus
(lateral septum)
Lateral epicondyle
of humerus
Ulnar tuberosity
Triceps brachii
Long head
Medial head
Lateral head
Anconeus
Muscle
Superfical Group
Pronator teres
Flexor carpi
radialis
Palmaris Longus
supination (when
elbow flexed
powerful
supinator)
Shoulder:flex, abd,
and IR of humerus
Flexion of elbow
n. C5, C6
Olecranon of ulna
Elbow: extension
Shoulder-long
head:extension
and ADD
Radial n. C6-C8
Olecranon of ulna
Extends the elbow
and tightens joint
Radial n. C6-C8
Origin
Humeral
head:medial
epicondyle of
humerus
Ulnar head:
coronoid process
Medial epicondyle
Insertion
Lateral radius
(distal to supinator
insertion)
Action
Elbow: weak flexor
Forearm:
pronation
Innervation
Median n. C6, C7
Base of 2nd
metacarpal
Median n. C6, C7
Medial epicondyle
Palmar aponeurois
Wrist: flexion &
ABD (radial
deviation of hand)
Elbow: weak
flexion
Wrist: flexion
tightens palmar
aponeurosis
Musculo. C5,C6 &
radial C7
Median n. C7, C8
Flexor carpi
ulnaris
Intermediate
Group-Flexor digitorum
superficialis
Deep Group-Flexor digitorum
profundus
Flexor pollicis
longs
Humeral head:
medial epicondyle
Ulnar head:
olecranon
Humeral head:
medial epicondyle
Ulnar head:
coronoid process
Ulna
Pisiform; hook of
hamate; base of
5th metacarpal
Wrist: flexion and
ADD (ulnar
deviation)
Ulnar n. C7-T1
Sides of middle
phalanges of 2nd to
5th digits
Elbow: weak flexor
Wrist: MCP, and
PIP joints of 2nd to
5th digits: flexion
Wrist, MCP, PIP,
and DIP of 2nd to
5th digits: flexion
Wrist: flex, abd
CMC of
thumb:flexion
MCP & IP of
thumb:flexion
Hand: pronation
Distal radioulnar
joint: stabilization
Elbow: flexion
Forearm:
semipronation
Elbow: weak
flexion
Wrist: extension &
ABD
Elbow: weak
flexion
Wrist: extension &
ABD
Median n. C8, T1
Action
Wrist: extension
Innervation
Radial n. C7, C8
Radius
(midanterior
surface)
Distal phalanges of
2nd to 5th digits
(palmar surface)
Distal phalanx of
thumb (palmar
surface)
Pronator
quadrates
Distal ulna
(anterior surface)
Distal radius
(anterior surface)
Brachioradialis
Distal humerus
Styloid process of
the radius
Extensor carpi
radialis longus
2nd metacarpal
base
Extensor carpi
radialis brevis
Lateral
supracondylar
ridge of distal
humerus
Lateral epicondyle
of humerus
Muscle
Extensor
Origin
Lateral epicondyle
Insertion
Dorsal digital
3rd metacarpal
base
Median n. C8, T1
Ulanr n. C8, T1
Median n. C7,C8
Median n. C7, C8
Radial n. C5, C6
Radial n. C6, C7
Radial n. C7, C8
expansion of 2nd to
5th digits
digitorum
Extensor digiti
minimi
Lateral epicondyle
5th digit
Extensor carpi
ulnaris
Supinator
Lateral epicondyle,
ulnar head
Olecranon, lateral
epicondyle,
annular ligament
Radius and ulna
Base of 5th
metacarpal
Radius
Extensor pollicis
brevis
Radius (posterior
surface)
Base of proximal
phalanx of thumb
Extensor pollicis
longus
Ulna (posterior
surface)
Base of distal
phalanx of thumb
Extensor indicis
Ulna (posterior
surface)
Lumbricals
Tendons of flexor
digitorum
Posterior digital
extension of 2nd
digit
2nd-5th digits on
dorsal digital
Abductor pollicis
longus
Base of 1st
metacarpal
MCP, PIP, and DIP
of 2nd to 5th digits:
Extension/ABD of
fingers
Wrist: ext, ulnar
abd of hand
MCP, PIP, & DIP of
5th digit: ext and
abd
Wrist: ext, add
Radial n. C7, C8
Radial n. C7, C8
Supination
Radial n. C6, C7
Radiocarpal joint:
abd of hand
Carpometacarpal
joint of thumb:
abd
Radiocarpal joint:
abd
Carpometacarpal
& MCP of thumb:
ext
Wrist: ext, abd
CMC of thumb:
add
MCP & IP of
thumb: ext
Wrist: ext
MCP, PIP, & DIP of
2nd digit: ext
2nd-5th digits—
MCP: flexion
Radial n C7, C8
Radial n. C7, C8
Radial n. C7, C8
Radial n. C7, C8
Median n C8, T1
profundus
Muscle
Iliopsoas
1.Psoas minor
2.Psoas major
3.Iliacus
Origin
1.T12-L1 vertebrae
2.T12-L4 &
associated
vertebral disks; L1L5 vertebrae
3.Iliac fossa
Gluteus maximus
Sacrum, ilium
Gluteus medius
Ilium
Gluteus minimus
Ilium
Tensor fasciae latae
ASIS
Piriformis
Pelvic surface of
expansion
Insertion
1.Iliopectineal
arch
2&3. Lesser
trochanter
PIP and DIP:
extension
Action
1.Assists in upward rotation
of the pelvis
2&3:
Hip joint:flex, ER
Lumbar spine:bends trunk
laterally to same side;
contraction raises the trunk
from the supine position
Upper
Entire muscle: ext, ER of hip
fibers:iliotibial
in sagittal and coronal
tract Lower fibers: planes
gluteal tuberosity
Upper: abd
Lower: add
Greater trochanter ABD, stabilizes pelvis
Ant part: flex, IR
Pos part: ext, ER
Greater trochanter ABD, stabilizes pelvis
Ant part: flex, IR
Pos part: ext, ER
Iliotibial tract
Tenses the fascia lata
Hip joint: abd, flex, IR
Greater trochanter ER, ABD, ext; stabilizes hip
Innervation
1&2: direct
branches from the
lumbar plexus
(psoas) L2-L4
3. Femoral n. L2-L4
Inferior gluteal n.
L5-S2
Superior gluteal n.
L4-S1
Superior gluteal n.
L4-S1
Superior gluteal n.
L4-S1
Direct branches
sacrum
Obturator internus
Medial surface of
greater trochanter
ER, ADD, and ext
Medial surface
greater trochanter
ER, ADD, and ext
Quadratus femoris
Inner surface of
obturator
membrane
Superior: ischial
spine
Inferior: ischial
tuberosity
Ischial tuberosity
Intertrochanteric
crest of femur
ER, ADD of hip
Pectineus
Pecten pubis
Femur
Muscle
Adductor longus
Origin
Superior pubic
ramus
Inferior pubic
ramus
Inferior pubic
ramus
Insertion
Femur
ADD, ER, & slight flexion;
stabilizes pelvis
Action
ADD, flex (up to 70 degrees)
ext (past 80 degress of flex)
ADD, flex (up to 70 degrees)
ext (past 80 degress of flex)
Hip: ADD flex
Knee: flex & IR
Gemelli
Adductor brevis
Gracilis
Obturator externus
Adductor minimus
Adductor magnus
Outer surface of
obturator
membrane
Inferior pubic
ramus
Inferior pubic
ramus; ischial
tuberosity
Sartorius
ASIS
Rectus femoris
AIIS
Femur
Tibia (medial
border of
tuberosity (SGT)
Trochanteric fossa
of femur
Medial lip of linea
aspera
Medial lip of linea
spine; adductor
tubercle of the
femur
Medial to tibial
tuberosity
Tibial tuberosity
from sacral plexus
S1-S2
Direct branches
from sacral plexus
L5, S1
Direct branches
from sacral plexus
L5, S1
Direct branches
from sacral plexus
L5, S1
Femoral n,
obturator n, L2, L3
Innervation
Obturator n. L2-L4
Obturator n. L2, L3
Obturator n. L2, L3
Hip:ADD & ER; stabilizes
pelvis
Obturator n L3, L4
ADD , EXT, slight flexion of
hip
ADD, EXT, slight flexion;
stabilizes pelvis
Obturator n. L2-L4
Hip: flex, abd, ER
Knee: flex, IR
Hip: flex
Femoral n. L2, L3
Obturator L2-L4;
tibial n. L4
Femoral n. L2-L4
Vastus medialis
Both sides of
tuberosity
Both sides of
tuberosity
Tibial tuberosity
Head of fibula
Semimembranosus
Linea aspera
(medial lip)
Linea aspera
(lateral)
Femoral shaft
Iscial tuberosity;
lateral lip of linea
aspera
Ischial tuberosity
Semitendinosus
Ischial tuberosity
Medial to tibial
tuberosity
Fibularis longus
Fibula head
Medial cuneiform
(plantar side); 1st
metatarsal base
Fibularis brevis
Fibula
Tibialis anterior
Upper 2/3 of tibia
Extensor hallucis
longus
Fibula-middle
third
5th metatarsal
base
Medial cuneiform
& 1st metatarsal
base (plantar
surface)
1st toe at base of
DIP
Extensor digitorum
longus
Fibula head; tibia
lateral condyle
2nd to 5th toes at
the base of DIP
Fibularis tertius
Distal fibula
Gastrocnemuis
Femur (medial &
5th metatarsal
base
Calcaneal
Vastus lateralis
Vastus intermedius
Biceps femoris
Medial tibial
condyle
Knee: ext
Knee: ext
Femoral L2-L4
Knee: ext
Femoral L2-L4
Knee: ext
Hip: extends, stabilizes
pelvis
Knee: flex, ER
Hip: extends, stabilizes
pelvis
Knee: flex, IR
Hip: extends, stabilizes
pelvis
Knee: flex, IR
Talocrural joint:PF
Subtalar:eversion(pronation)
Supports transverse arch of
foot
PF; eversion
Femoral L2-L4
Tibial n L5S2/Common
fibular L5-S2
Tibial n. L5-S2
Talocrural: DF
Subtalar: inversion
(supination)
Tibial L5-S2
Superficial fibular
n. L5, S1
Superficial fibular
L5, S1
Deep fibular L4, L5
DF, active in
eversion/inversion, ext of
MTP and IP of big toe
DF, eversion (pronation);
extends MTP and IP of 2nd5th toes
DF, eversion
Deep fibular L5
Talocrural: PF
Tibial S1, S2
Deep fibular L5, S1
Deep fibular L5, S1
Soleus
lateral
epicondyles)
Fibula head, tibia
tuberosity via
Achilles
Calcaneal
tuberosity via
Achilles
Calcaneal
tuberosity via
Achilles
Plantaris
Femur (lateral
epicondyle)
Tibialis posterior
Adjacent borders
of tibia & fibula
Flexor digitorum
longus
Flexor hallucis
longus
Tibia (posterior
surface)
Fibula (posterior
surface)
Popliteus
Masseter
Lateral femoral
condyle
Zygomatic arch
Posterior tibial
surface
Mandibular angle
Temporalis
Temporal fossa
Coronoid process
Navicular
tuberosity,
cuneiforms, 2nd-4th
metatarsal bases
2nd-5th distal bases
1st distal base
Lateral pterygoid
Medial pterygoid
Sternocleidomastoid Sternum
Clavicle
Mastoid process
Occipital bone
Knee: flexion
PF
Tibial S1, S2
Negligible; may prevent
compression of posterior leg
musculature during knee
flex
PF, inversion (supination),
supports the longitudinal
and transverse arches
Tibial S1, S2
PF, inversion, MTP and IP
2nd-5th: PF
PF, inversion, MTP and IP
2nd-5th toes: PF; supports
medial longitudinal arch
Knee: flexion, IR (stabilizes
knee)
Elevates (adducts) and
protrudes mandible
Elevate (adduct) mandible
Retract (retrude) mandible
Unilateral: lateral movement
(chewing)
Bilateral: protrudes
mandible (pulls disk
forward) Unilateral: lateral
movements (chewing)
Elevates (adducts) mandible
Unilateral: Tilts head to
same side, rotates head to
opposite side. Bilateral:
Tibial n. L5-S2
Tibial n. L4, L5
Tibial n. L5-S2
Tibial n L4-S1
Mandibular (CN V)
Mandubualr n.
(CN V)
Mandibular N.
Mandibular n.
Accessory (CN XI)
Longus Capitis,
Longus Colli, Rectus
Capitis anterior,
Rectus capitis
lateralis
Scalenes
Rectus capitis
posterior minor and
major, Obliquus
capitis inferior and
superior
extends head, aids in
respiration
Flexion
C3-C6, C1-C2, C5C7
1st rib, 2nd rib
Elevates upper ribs, bends
cervical spine to same side,
flexes neck
Extends head, rotates head
to same side
Direct brances C3C8
Force Couple- is defined as two forces that act in opposite directions to rotate a segment around its axis of motion.
Ex. Deltoid pulls the humerus up, rotator cuff pulls the humeral head down to allow smooth movement of the humeral head in the glenoid
cavity.
Ex. Trapezius and serratus anterior cause upward rotation of the scapula during arm elevation.
Rhomboids, levator scapulae, and pec minor cause downward rotation with purposeful shoulder extension (chopping wood)
Ex. Serratus anterior and pec minor result in scapular protraction.
Ex. Rhomboids, middle and lower trap cause scapular retraction.
Ex. Upper trap and levator scap create elevation while pec minor and latissimus dorsi cause depression of the scapula.
If the muscle is in a shortened position, the overlap of actin and myosin reduces the number of sites available for cross-bridge formation. Active
insufficiency-occurs when the muscle is incapable of shortening to the extent required to produce full range of motion at all joints crossed
simultaneously. Ex: The finger flexors cannot produce a tight fist when the wrist is fully flexed, as they can when it is in neutral position.
If the muscle is in a lengthened position compared with the optimum length, the actin filaments are pulled away from the myosin heads such
that they cannot create as many cross-bridges.
Passive insufficiency –occurs when the two-joint muscle cannot stretch to the extent required for full range of motion in the opposite direction
at all joints crossed. Ex: a larger range of hyperextension is possible at the wrist when the fingers are not fully extended.
2. MS Tests and Measures
MMT Grades
0 Zero; No evidence of contraction
1 Trace; Slight contraction, no motion
2- Poor minus; Movement through partial test range in gravity eliminated position
2 Poor; Movement through complete test range in gravity eliminated position
2+ Poor plus; Movement through complete test range in gravity eliminated position and through up to one half of test range against gravity
3- Fair minus; Movement through complete test range in gravity eliminated position and through more than half of test range against gravity
3 Fair; Movement through complete test range against gravity
3+ Fair plus; Movement through complete test range against gravity and able to hold against minimum resistance
4 Good; Movement through complete test range against gravity and able to hold against moderate resistance
5 Normal; Movement through complete test range against gravity and able to hold against maximum resistance
Normal ROM
Cervical: Flex/Ext/lateral flex/45 degrees; Rotation-60-70
Lumbar: Flex-90; Ext-25; lateral flexion-35; Rotation-45
Shoulder: Flex-180; Ext-60; Abd-180; IR-70; ER-90
Elbow: Flex-150; Ext-0; Pronation/supination-80
Wrist: Flex-80; Ext-70, RD-20; UD-30
1st CMC: Flex-15; Ext-20
MCP Fingers: Flex-90; Ext-45
MCP thumb: Flex-50; Ext-0
PIP: Flex-100; Ext-0
DIP: Flex-90; Ext-0
Hip: Flex-120; Ext-30; Abd-45; Add-30; IR-45; ER-45
Knee: Flex-135; Ext-0-10
Ankle: DF-20; PF-50; Inv-35; Ev-15
1st MTP: Flex-30; Ext-70
Subtalar: Inverstion-5; Eversion-5
End-Feels:
Firm (stretch)-ankle dorsiflexion, finger extension, hip IR, forearm supination, Knee ext
Hard (bone to bone)-elbow extension
Soft (soft tissue approx.)-elbow flexion, knee flexion
Posture:
Ideal plumb line alignment:
-Slightly posterior to coronal suture
-Through external auditory meatus
-Through axis of the odontoid process
-Midway through the tip of the shoulder
-Through the bodies of the lumbar vertebrae
-Slightly posterior to the hip joint
-Slightly anterior to the axis of knee
-Slightly anterior to the lateral malleolus
-Through the calcaneocuboid joint
Mobilizations:
Grade 1-Small amplitude oscillations performed at beginning of range.
Grade 2-Larger amplitude oscillations performed into mid-range of a joint.
Grade 3-Large oscillations performed through the available range of a joint and into the tissue resistance.
Grade 4-Small amplitude oscillations performed into the tissue resistance.
*Grades 1 and 2 maintain joint mobility, relieve pain, and are indicated in the subacute state of joint inflammation or sprain.
*Grade 3 maintains joint mobility.
* Grade 4 increases joint mobility.
*Grades 3 and 4 are both indicated in more advanced stages of hypomobility or for joint impingement or motion restrictions. These grades
should NOT be used when the joint has inflammation and pain (e.g. with acute exacerbation with RA)
Types of Fractures:
Avulstion fx-a portion of bone becomes fragmented at the site of tendon attachment due to a traumatic and sudden stretch of the tendon.
Closed fx-a break in a bone where the skin over the site remains intact
Comminuted fx-a bone that breaks into fragments at the site of injury
Compound fx-a break in a bone that protrudes through the skin
Greenstick fx-a break on one side of a bone that does not damage the periosteum on the opposite side. This type of fx is often seen in children.
Nonunion fx-a break in a bone that has failed to unite and heal after 9-12 months.
Stress fx- a break in a bone due to repeated forces to a particular portion of the bone.
Spiral fx- a break in a bone shaped like an “S” due to torsion and twisting.
Types of Muscular Contraction:
Concentric-occurs when the muscle shortens while developing tension
Eccentric-occurs when the muscle lengthens while developing tension
Isometric-occurs when tension develops, but there is no change in the length of the muscle
Isotonic-occurs when the muscle shortens or lengthens while resisting a constant load. (hand held weights)
Isokinetic-occurs when the tension developed by the muscle, while shortening or lengthening at a constant speed (variable load), is maximal
over the full range of motion (Cybex, Biodex, and Lido)
Common DTRs:
-Biceps (C5-C6)
-Brachioradialis (C6)
-Triceps (C7)
-Patellar tendon (L3, L4)
-Achilles tendon (S1, S2
Responses: Areflexia (absent) =0
Hyporeflexia (sluggish) = 1+ (LMN)
Normal =2+
Hyperreflexia (brisk) = 3+ (UMN)
Common Neural tension tests:
-Passive SLR =sciatic nerve
•Tibial nerve=passive SLR with DF & eversion
•Fibular nerve=passive SLR with PF & inversion
•Sural nerve=passive SLR with DF and inversion
•Prone knee bend=femoral nerve
•Passive neck flexion=spinal dura
Common Disorders/Pathology of the MS system:
Pathology
What is it
Etiology
1.Arthrogryposis
A non
progressive,
nongenetic,
congenital
disorder
-not inherited
2.Complex
Regional Pain
Syndrome
(CPRS) Formerly
known as
“Reflex
Sympathetic
Dystrophy”
Abnormal
sympathetic
reflex resulting
from a persistent
painful lesion
-
3.Colles fracture
Most common
wrist fx resulting
-Results from
falling onto
Signs &
Symptoms
-Characterized
by rigid joints
of the
extremities
(usually
symmetrical)
-sausage like
shapeless
limbs, and
weak/non
functioning
limbs
-Pain, edema,
decreased
circulation,
osteoporosis,
skin dryness,
decreased
proprioception,
and atrophy of
muscles in
close proximity
to involved
area
-The distal
fragment of the
Treatment
-Surgery, ROM exercises,
splinting, positioning, ADL
training, use of adaptive
devices
Modalities to decrease pain,
joint mobs, weight bearing or
closed chain exercise,
massage, manual lymphatic
drainage, splinting
-Casting, early active ROM
and PROM are essential for
from a fall on an
outstretched
hand
extended
wrist
3A.Smith’s
fracture
Distal fx of the
radius, which
dislocates in the
ventral direction.
(reverse colles fx)
-Results from
a fall onto a
flexed wrist
4.DJD
(Osteoarthritis)
Chronic disease
that causes
deneneration of
articular
cargilage,
thickening of
subchondral
bone often
affecting weight
bearing joints
5.Fibromyalgia
An immune
system disorder
-Unknown,
typically
appears
during middle
age & affects
nearly all
individuals to
some extent
by age 70.
Occurs more
common in
men than
women up to
age 55. Risk
factors:
overweight,
fxs or other
joint injuries,
athletic
overuse
-Unknown
origin; often
radius has a
dorsal
displacement
with a radial
shift of the
wrist and hand
-Fragment
dislocates in
the ventral
direction
-Gradual onset
of pain present
at the affect
joint, increased
pain after
exercises,
increased pain
with weather
changes,
enlarged joints,
crepitus,
stiffness,
limited joint
ROM,
Heberden’s
nodes, &
Bouchard’s
nodes.
-Characterized
by aching or
functional recovery,
progressive resistive
exercises, mobs, closed-chain
stabilization exercises
-Casting, early active ROM
and PROM are essential for
functional recovery,
progressive resistive
exercises, mobs, closed-chain
stabilization exercises
-Reduce pain, promote joint
function, and protect the
joint.
NSAIDS/acetaminophen, and
corticosteroids.
Viscosupplementation which
is administered into the knee
to improve lubrication. PT:
PROM/AROM, heating and
cooling agents, pt education,
strengthening, e-stim, energy
conservation, bracing.
Surgical intervention can
include arthroscopic surgery
to total joint replacement.
-Holistic and multidisciplinary
approaches are necessary.
that causes
tenderness, pain,
and stiffness in
the muscles.
11/18 points
throughout the
body
related to
stress,
anxiety,
fatigue, and
sleeplessness
in women
more than
men.
6.Osteogenesis
Imperfecta
A connective
tissue disorder
that affects the
formation of
collagen during
bone
development.
There are 4
classifications of
imperfects that
vary in level of
severity.
7.Osteochondriti
s dissecans
Seperation of the
articular cartilage
from the
underlying bone
-The cause is
genetic
inheritance
with types I
and IV
considered
autosomal
dominant
traits and
types II and III
considered
autosomal
recessive
traits.
Osteochondra
l fracture
burning of the
muscles “a
migraine
headache of
the muscles”
diffuse pain, or
tender points
on both sides
of the body.
-Pathological
fractures,
osteoporosis
(brittle bones),
hypermobile
joints, bowing
of the long
bones,
weakness,
scoliosis,
impaired
respirator
function
ADL education and training,
Stress management training,
analgesics and
antidepressants, local
modalities and techniques
for muscle pain relief,
aerobic/conditioning
exercises, improve sleeping
patterns
-Management begins at birth
with caregiver education on
proper handling and
facilitation of movement. PT
will focus on AROM
emphasizing symmetrical
movements, positioning,
functional mobility, fracture
management, and the use of
orthotics. In severe cases,
wheelchair prescription.
-Usually
involving the
medial femoral
condyle near
the
intercondylar
notch and
observed less
frequently at
the femoral
head and talar
-If fracture is displaced then
surgery is indicated. PT after
surgery: gait training,
functional strengthening,
conditioning.
8.Osteomalacia
Decalcification of
bones
-Results from
vitamin D
9.Osteomyelitis
Acute or chronic
bone infection
-Commonly
the result of
combined
traumatic
injury and an
acute
infection.
10.Osteoporosis
Most common
metabolic bone
disease
-Affects white
females most
commonly,
depletes bone
mineral
density, which
may
predispose
the indivudal
to fracture
dome
-May cause
deformities,
fractures, and
severe pain
-In children:
most common
site includes
the distal femur
and proximal
tibia, humerus,
and radius. In
adults, the
disease
commonly
localizes in the
pelvis and
vertebrae and
is usually a
result of
contamination
related to
surgery or
trauma
-Common sites
of fx: thoracic
and lumbar
spine, femoral
neck, proximal
humerus,
proximal tibia,
pelvis, distal
radius
-Pain control, functional
mobility training
-High doses of IV antibiotics,
the infected extremity is
immobilized by a cast,
traction or bed rest.
-Pain management, postural
reeducation, , breathing
exercises, general
conditioning, pectoral
stretching, abdominal
strengthening(with caution—
do not want excessive and
repeated flexion of spine as
this can lead to wedge
fractures in these pts)
11.Paget’s
disease(osteitis
deformans)
A slowly
progressive
metabolic bone
disease
characterized by
an initial phase of
excessive bone
reabsorption
followed by a
reactive phase of
excessive
abnormal bone
formation. The
new bone
structure is
fragile and weak
and causes
painful
deformities of
the external
contour and the
internal
structures.
-Unknown
12.Patellofemor
al syndrome
The patella fails
to properly track
in the trochlear
groove of the
-Repetitive
overuse
disorder,
decreased
-Usually affects
several skeletal
areas including
spine, pelvis,
femur, and
skull. The
disease can be
fatal when
associated with
congestive
heart failure
(widespread
disease creates
a continuous
need for high
cardiac output),
bone sarcoma,
or giant cell
tumors.
Involved sites
can fx easily
and heal slowly
and usually
incompletely.
Vertebral
collapse or
vascular
changes can
lead to
paralysis.
-Anterior knee
pain, q-angle
greater than
18°, instability
-If pt is asymptomatic,
treatment is not needed. If
symptoms are present, pt
will require drug therapy.
-Modalities to decrease pain
& inflammation, McConnell’s
taping technique, stretching
of the iliotibial band and
femur
13.Scleroderma
A chronic
disorder
characterized by
fibrosis and
changes in the
internal organs
and skin
quad
strength,
decreased
lower
extremity
flexibility,
patellar
instability,
increased
tibial torsion
or femoral
anteverison.
Increased risk
for
developing:
females,
growth
spurts,
runners who
have
increased
mileage,
overweight,
Positive
chondromalac
ia test (Clark’s
sign)
-Frequently
accompanied
by Raynaud’s
phenomenon
or pain usually
occurs in the
first 30° of knee
flexion, stair
climbing,
prolonged
sitting,
squatting, or
jumping
tensor fascia latae,
strengthening of the VMO,
shoe inserts to decrease
genu valgum and pes planus,
On-Track Brace to reposition
patella, transverse friction
massage over the lateral
retinaculum, patellar
mobilization: medial patellar
glide and stretching deep
fibers of lateral retinaculum
to decrease patellar tilt.
-Polyarthalgia is
a prominent
early symptom,
heartburn and
dyspnea
occasionally are
the first
-Maintain joint ROM,
medications, strengthening
exercises
14.Pronator
teres syndrome
Median nerve
entrapment in
the pronator
teres muscle
15.Rheumatoid
Arthritis (RA)
Chronic, systemic
inflammatory
disorder, the
disease presents
with a chronic
inflammatory
reaction in the
synovial tissues
-Unknown.
Women more
affected than
men (40-60
years age)
May initially
occur at any
joint, but it is
manifestations
of the disease.
Positive
rheumatoid
factor test,
other blood
tests
-DD via
pronator teres
test: The
clinician
strongly resists
pronation of
the elbow as
the pts elbow is
extended from
90° of flexion
toward full
extension, test
is + if tingling or
paraesthesia is
provoked in the
forearm and
hand in a
median nerve
distribution
Onset may be
gradual or
immediate,
symmetrical
involvement,
pain and
tenderness of
affected joints,
-Manual nerve glides,
stretching exercises, AROM
exercises, Ultrasound, NMES
for nerve healing
Reduce inflammation and
pain, promote joint function,
and prevent joint destruction
and deformity. NSAIDS,
DMARDS are slow acting and
take weeks or months to
become effective but can
slow the progression. PT:
of a joint that
results in erosion
of cartilage and
supporting
structures within
the capsule.
16.Juvenile RA
Most common
chronic
rheumatic
disease in
children and
presents with
inflammation of
the joints and
connective
tissues.
Classification of
JRA includes
systemic,
polyarticular, and
oligoarticular.
Onset is prior to
age 16 with
common in
the small
joints of the
hand, foot,
wrist, and
ankle. It has
periods of
exacerbation
and
remission. It is
diagnosed
based on
clinical
presentation
of involved
joints & blood
RA factors.
-Unknown, is
theorized that
an external
source such as
a virus,
infection or
trauma may
trigger an
autoimmune
response
producing JRA
in a child with
a genetic
predisposition
.
morning
stiffness, warm
joints, decrease
in appetite,
malaise,
increased
fatigue, swan
neck deformity
(DIP flexion, PIP
hyperextension
) boutonniere
deformity (DIP
ext, PIP flexion,
low grade fever
PROM/AROM, heating and
cooling agents, splinting, pt
education, energy
conservation, body
mechanics, and joint
protection techniques.
Fever and Rash.
-Systemic JRA
occurs in 1020% of cases
and presents
with acute
onset, high
fevers, rash,
enlargement of
the spleen &
liver, and
inflammation
of the lungs
and heart.
Polyarticular
JRA accounts
for 30-40% of
-Pharmacological
management to relieve pain
and inflammation through
NSAIDS, corticosteroids,
antirheumatics, and
immunosuppressive agents.
PT: PROM/AROM,
positioning, splinting,
strengthening, endurance
training, weight bearing
activities, postural training,
functional mobility. Pain
management includes the
use of modalities such as
paraffin, ultrasound, warm
water, and cryotherapy.
Surgical intervention may be
complete
remission in 75%
of children.
17.Gout (gouty
arthritis)
Metabolic
disease marked
by elevated level
of serum uric acid
and deposition of
urate crystals in
the joints, soft
tissue, and
kidneys.
cases and
presents with
high female
incidence,
significant
rheumatoid
factor, and
arthritis in
more than four
joints with
symmetrical
involvement.
Oligoarticular
accounts for
40-60% of
cases and
affects less
than five joints
with
asymmetrical
involvement.
Most often
affects the feet,
especially the
great toe,
ankle, and midfoot. There is
severe joint
pain commonly
at night with
warmth,
erythema, and
extreme
tenderness/
indicated secondary to pain,
contractures or irreversible
joint destruction.
Anti-inflammatory
medications, daily use of
colchicines, lowering the
urate concentration in body
fluids with diet, weight loss,
and moderation of alcohol
intake, allopurional to
reducehyperuricemia, rest,
elevation, and joint
protection during acute
phase.
18.Hemophilia
19.Iliotibial band
friction
syndrome
20.Myositis
Ossfifcans
hypersensitivity
.
Hemorrhagic
-Results from -Can cause
disorder that is
a deficiency of pain, swelling,
hereditary
specific
extreme
clotting
tenderness,
factors
and possibly
permanent
deformity.
Bleeding near
peripheral
nerves can
cause
peripheral
neuropathies,
pain
parathesia, and
muscle
atrophy.
An irritation
-Often occurs -Positive Ober’s
caused by the
in runners
test, excessive
rubbing of the
from an
hip IR in stance,
ITB over the
overuse
palpation over
lateral epicondyle syndrome
ITB insertion,
of the femur
positive Noble
compression
test
Often caused by
-Can be
-Frequent
trauma to a
induced by
locations:
muscle resulting
early
quads,
in hematoma
mobilization
brachialis, and
that may calcify
and stretching biceps brachii.
or ossify
with
Radiological
aggressive PT studies will
-Splinting, Ice, rest, and
elevation are needed in
acute stage. In chronic
situations, joint protection,
maintaining joint function,
daily exercises for ROM,
endurance and strength, ADL
training, and the use of
appropriate splints and Ads
should be addressed.
-Stretching exercise program,
modalities for pain and
inflammation, soft tissue
mobilization techniques,
shoe orthosis may be
necessary.
-Conservative with gentle
active and active assisted
ROM, passive stretching is
not indicated, NO manual
stretching with overpressure
at end-range.
21.Scoliosis
Lateral curvature
of the spine.
Most often
quantified using
the Cobb method
with a standing
radiograph.
Classified as
functional
(nonstructural)(r
esults from leg
length
discrepancy,
muscle
imbalance, poor
posture) can be
corrected
w/lateral
bending.
Neuromuscular
scoliosis results
w/developmental
pathology
resulting in
alterations within
the structure of
the spine.
Observed in pts
w/CP or Marfan
syndrome.
Degenerative
following
trauma to the
muscle
-Typically
idiopathic. It
is most
commonly
diagnosed
between 10
and 13 years
of age. Girls
and boys have
a similar risk
of developing
a mild curve
(10°or less),
however, girls
have a
significantly
greater risk of
acquiring a
curve greater
than 30°
show calcium
deposits
-Shoulder level
asymmetry w/
or w/out the
presence of a
rib humb. Pain
is not typically
associated w
the spinal
curvature,
rather it is a
result of the
abnormal
forces placed
on other tissues
of the body.
-Based on magnitude of
curve and degree of
progression. If curve not
progressing no formal action
is taken. PT: muscle
strengthening, and flexibility
exercises, shoe lifts, and
bracing. A spinal orthosis is
often warranted with a curve
that ranges between 25-40°.
Surgical intervention may be
required with curves greater
than 40°.
Ankylosing
spondylitis
scoliosis occurs
due to the
normal aging
process and is
facilitated by
changes such as
osteophyte
formation, bone
demineralization,
and disk
herniation.
Neuromuscular
and degenerative
scoliiosis are
considered to be
forms of
structural
scoliosis since the
curves are
inflexible and do
not reduce
w/lateral
bending.
Progressive
inflammatory
disorder of
unknown
etiology that
initially affects
axial skeleton
Initial onset
(usually mid
and low back
pain for 3
months or
greater)
before fourth
decade of life
First symptoms
include mid and
low back pain,
morning
stiffness, and
scaroiliitis.
Results in
kyphotic
deformity of
the cervical &
thoracic spine
NSAIDS, corticosteroid
therapy. PT: implementation
of flexibility exercises for
trunk to maintain/improve
normal joint motion & length
of muscles in all directions,
especially extension.
22.Sjogren’s
syndrome
A rheumatoidlike disorder
characterized by
dryness of the
mucous
membranes, joint
inflammation,
and anemia.
-More
common than
systemic
lupus
erythematosu
s (SLE) and
less common
than RA.
23.Achilles
Tendonitis
Is a repetitive
disorder resulting
in microscopic
tears of collagen
fibers on the
surface or in the
substance of the
Achilles tendon.
The tendon is
most often
impacted in an
avascular
zonelocated two
to six centimeters
above the
insertion of the
tendon.
-Repetitive
overload of
the tendon
caused by
changes in
training
intensity or
faulty
techniques.
Pts w/limited
flexibility and
strength in
the
gastroc/soleu
s and pts w a
pronated or
cavus foot are
at increased
& a decrease in
lumbar
lordosis.
-Dryness of the
eyes and
mouth along
with joint
inflammation.
Arthritis occurs
in about 33% of
the pts & is
similar in
distribution to
RA, but milder
& without joint
destruction.
-aching or
burning in the
posterior heel,
tenderness of
the Achilles
tendon, pain w
increased
activity,
swelling, and
thickening in
the tendon
area, muscle
weakness due
to pain,
morning
stiffness
-Sipping fluids throughout
the day, chewing surgarless
gum, using a mouthwash for
mouth dryness, medications
for pain and inflammation
occasionally needed,
maintain mobility and
function through a regular
exercise program.
-Initially RICE, NSAIDS, as
needed. A heel lift and cross
training may be used to limit
the amount of tensile loading
through the tendon.
Prevention includes heel cord
stretching exercises, use of
appropriate soft-soled
footwear, eccentric
strengthening of the
gastroc/soleus, and avoiding
sudden changes in intensity
of training programs.
24.Adhesive
Capsulitis
Results in a loss
of ROM in active
and passive
shoulder motion
due to soft tissue
contracture. The
condition is
caused by
adhesive fibrosis
and scarring
between the
capsule, rotator
cuff, subacromial
bursa, and
deltoid.
25.Anterior
cruciate
ligament sprain
ACL runs from
the anterior
intercondylar
area of the tibia
to the medial
aspect of the
lateral femoral
condyle in the
intercondylar
risk.
-May be
related to a
direct injury
to the
shoulder or
may being
insidiously.
Peak
incidence
occurs in
individuals 40
and 60 years
of age w
females being
affected
more. Pts w
diabetes have
increased
incidence. The
condition is
self-limiting
and typically
resolves in 1-2
years.
-Noncontact
twisting injury
associated
with
hyperextensio
n, varus or
valgus stress
to the knee.
An ACL sprain
-Insidious onset
of localized
pain often
extending
down the arm,
subjective
reports of
stiffness, night
pain, restricted
motion in a
capsular
pattern. (ER
most limited)
-Increase ROM with
glenohumeral mobilization,
ROM exercises, and palliative
modalities. The therapist and
pt should AVOID
overstretching and elevating
pain since this can result in
further loss of motion.
Surgical options include
suprascapular nerve block
and closed manipulation
under anesthesia.
-The pt may
report a loud
pop or feeling
of the knee
“giving way” or
“buckling”
followed by
dizziness,
sweating, and
-Initially RICE, NSAIDS, and
analgesics as needed.
Conservative treatment
includes lower extremity
strengthening exercises
emphasizing the quads and
hamstrings. Surgery if often
warranted for a complete
tear. A de-rotation brace may
26.Posterior
cruciate
ligament sprain
notch. The
ligament
prevents anterior
displacement of
the tibia in
relation to the
femur. The
extent of the
sprain is classified
according to the
extent of
ligament
damage. A grade
I sprain involves
microscopic tears
of the lig, while a
grade III indicates
a completely torn
ligament.
PCL runs from
the posterior
intercondylar
area of the tibia
to the lateral
aspect of the
medial femoral
condyle in the
intercondylar
notch. The PCL
prevents
posterior
displacement of
the tibia in
relation to the
often involves
injury to other
knee
structures
such as the
medial
capsule, MCL,
and menisci.
swelling.
Special tests:
Lachman’s &
lateral pivot
shift test
be beneficial for a pt with
ACL deficient knee, but has
limited benefit for a pt
following surgical
reconstruction. (90°-40°flex)
-Most
common
cause of
injury are
landing on the
tibia with a
flexed knee or
hitting a
dashboard in
a MVA w a
flexed knee.
Isolated PCL
tears are not
common and
often involve
-The pt may
report feeling
as if the femur
is sliding off the
tibia. Swelling
and mild pain
may be
present, but
often the pt is
asymptomatic.
Special tests:
posterior
drawer,
posterior sag
sign
-Initially RICE, NSAIDS, PT:
lower extremity
strengthening and functional
progression. If surgery is
performed, isolated
hamstrings exercises are
often AVOIDED for a
minimum of six weeks.
femur
27.Medial
collateral
ligament sprain
MCL runs from
slightly above the
medial femoral
epicondyle to the
medial aspect of
the shaft of the
tibia. A MCL
sprain often
ivolves injury to
other knee
structures
(ACL/medial
meniscus)
28.Meniscus
Tear
The medial &
lateral menisci
are attached to
the proximal
surface of the
tibia. The menisci
are thick at the
periphery and
thinner at their
internal
other knee
structures
such as the
ACL, MCL,
LCL, and
menisci
-A contact or
noncontact,
fixed foot,
tibial
rotational
injury
associated
with valgus
force and
external tibia
rotation can
damage MCL.
Often
associated w
activities such
as football,
skiing, and
soccer.
-Associated
with fixed
foot rotation
while weight
bearing on a
flexed knee.
This action
produces
compression
and rotational
-Clinical
presentation
includes knee
pain, swelling,
anatlgic gait,
decreased
ROM, and a
feeling of
instability. A
valgus stress
test can be
used to assess
the integrity of
the MCL.
-Initially RICE, NSAIDS.
Conservative treatment
includes decreasing
inflammation, protecting the
knee joint and ligament,
ROM, and strengthening
exercise as tolerated.
Strengthening exercises
gradually become more
aggressive and functional
activities are introduced.
Surgery is rarely required
since the MCL is well
vascularized.
-Joint linepain,
swelling,
catching or a
locking
sensation.
Special tests:
Apley’s
compression
test, bounce
home test, and
-Initially RICE, NSAIDS.
Conservative treatment
consists of palliative
modalities and strengthening
exercise. Surgery ranging
from a partial meniscectomy
to a meniscal repair is often
warranted for active
individuals. Meniscal repairs
are typically performed on
29.Lateral
epicondylitis
“tennis elbow”
unattached
edges. The
medial meniscus
is more
commonly
injured than the
lateral bc it is less
mobile due to its
attachment to
the joint capsule.
The incidence of
medial tears
increases
significantly over
time with ACL
deficiency.
Mensical injuries
are definitively
diagnosed w
arthroscopy or
MRI.
Refers to an
irritation or
inflammation of
the common
extensor muscles
at their origin on
the lateral
epicondyle of the
humerus.
Individuals who
take part in
racquet sports
are at greatest
forces on the
meniscus
McMurray test.
tears located on the outer
edges of the meniscus due to
the increased vascularity.
-Caused by
eccentric
loading of the
wrist extensor
muscles,
usually the
extensor carpi
radialis brevis,
resulting in
microtrauma.
Lateral
epicondylitis
can be
-Pain is present
immediately
anterior or
distal to the
lateral
epicondyle of
the humerus.
Pain typically
worsens with
repetition and
resisted wrist
extension.
-Initially RICE, NSAIDS, and
activity modification. PT:
attempt to increase
strength(initial emphasis on
eccentric phase of ex),
flexibility, and endurance of
the wrist extensors. A strap
placed 2-3 inches distal to
the elbow joint can reduce
muscular tension placed on
the epicondyle and may
diminish or eliminate pt
symptoms. *Resist wrist
risks
30.Medial
epicondylosis
“golfers elbow”
Usually a
degenerative
condition of the
pronator teres &
flexor carpi
radialis tendons
at their
attachment to
the medial
epicondyle of the
humerus.
31.Congenital
Hip dysplasia
Also known as
developmental
dysplasia, is a
condition
characterized by
malalignment of
the femoral head
within the
precipitated
by poor
mechanics or
faulty
equipment
such as too
small of a
handle on a
tennis raquet.
Most
common in
individuals
between 3050.
-Occurs w
overuse in
sports, such
as baseball,
swimming, or
jobs that
require a
strong hand
grip and
excessive
pronation of
the formearm
-Cultural
predisposition
, malposition
in utero,
environmenta
l and genetic
influences
extension, wrist radial
deviation, and forearm
pronation with fingers fully
flexed (fist) simultaneously
=Cozen’s test.
Clinician:
passively
supinate
forearm,
extend elbow,
and extend
wrist.
Reproduces
pain at medial
epicondyle.
Same as lateral
-Clinical
presentation
includes
asymmetrical
hip abduction
with tightness
and apparent
femoral
-Dependent on age, severity,
and initial attempts to
reposition the femoral head
w/in the acetabulum through
the constant use of a
harness, bracing, splinting, or
traction. Open reduction w/
subsequent application of a
acetabulum. The
condition
develops during
the last trimester
in utero.
32.Congenital
Limb
Deficiencies
A congenital limb
deficiency is a
malformation
that occurs in
utero, secondary
to an altered
developmental
course.
Congenital limb
deficiencies are
classified as
longitudinal or
transverse. A
longitudinal limb
deficiency refers
to a reduction or
absence of an
element or
elements within
the long axis of
the bone. A
transverse limb
deficiency refers
to a limb that has
developed to a
-The majority
of congenital
limb
deficiencies
are idiopathic
or genetic in
origin. Other
possible
etiologies
include poor
blood supply,
constricting
amniotic
bands,
infection, and
maternal drug
exposure.
shortening of
the involved
side. Testing for
this condition
may include
Ortolani’s test,
Barlow’s test,
and diagnostic
ultrasound.
-structural or
acquired
abnormality of
a limb,
phantom limb
pain.
hip spica cast may be
required if conservatice
treatment fails. PT:
stretching, strengthening,
and caregiver education.
-Symmetrical movements,
strengthening, ROM, weight
bearing activities, and
prosthetic training when
appropriate.
33.Congenital
torticollis “wry
neck”
particular level
beyond which no
skeletal elements
exist.
Characterized by
a unilateral
contracture of
the
sternocleidomast
oid muscle. The
condition is most
often identified
in the first 2
months of life.
34.Glenohumera Refers to
l instability
excessive
translation of the
humeral head on
the glenoid
during active
rotation.
Subluxation
refers to joint
laxity, allowing
for more than
50% of the
humeral head to
passively
translate over the
glenoid rim
w/out
dislocation.
Dislocation is the
-Cause is
unknown,
may be
associated
with
malpositionin
g (breech) in
utero and
birth trauma.
A
combination
of forces
stress the
anterior
capsule,
gelenhumeral
ligament, and
rotator cuff,
causing the
humerus to
move
anteriorly out
of the glenoid
fossa. An
anterior
dislocation is
the most
common and
-Clinical
presentation
includes lateral
cervical flexion
to the SAME
side as the
contracture,
rotation toward
the opposite
side, and facial
asymmetries.
Subluxation:fee
ling the
shoulder
“popping” out
and back into
place, pain,
paresthesias,
sensation of
the arm feeling
“dead” positive
apprehension
test, capsular
tenderness,
swelling;
Dislocation:
severe pain,
paresthesias,
limited ROM,
-Initially-treatment is
conservative with emphasis
on stretching (ex. Right
torticollis: to stretch, perform
left side bending & right
rotation), AROM, positioning,
and caregiver education.
Surgical management is
indicated when conservative
options have failed and the
child is over one year of age.
-Initial immobilization with a
sling for 3 to 6 weeks. RICE
and NSAIDS. Following
immobilization, ROM, and
isometric strengthening
should be initiated followed
by progressive resistive
exercises emphasizing the
internal and external
rotators, as well as the large
scapular muscles.
35.Impingement
Syndrome
36.Legg-CalvePerthes Disease
complete
separation of the
articular surfaces
of the glenoid
and the humeral
head. Approx
85% of
dislocations
detach the
glenoid labrum
(Bankart lesion)
Is one of the
most common
injuries of the
shoulder. It is
often caused by
repetitive
microtrauma
from upper
extremity activity
performed above
the horizontal
plane.
is usually
associated
with shoulder
abd and LR.
weakness,
visible shoulder
fullness, arm
supported by
contralateral
limb.
-Caused by
the humeral
head and the
associated
rotator cuff
attachments
migrating
proximally
and becoming
impinged on
the
undersurface
of the
acromion and
the
coracoacromi
al igament
Characterized by
degeneration of
the femoral head
due to a
disturbance in
-Trauma,
genetic
predisposition
, synovitis,
vascular
-discomfort or
mild pain deep
within the
shoulder, pain
with overhead
activities,
painful arc of
motion (70-120
abduction),
positive
impingement
sign,
tenderness
over the
greater
tuberosity and
the bicipital
groove
-gradual onset
of ‘aching” pain
at hip, thigh,
and knee.
AROM limited
-Initially RICE, NSAIDS, and
activity modifications. Once
tolerated, treatment includes
rotator cuff strengthening
and scapular stability
exercises. Long-term
prevention includes
continued strengthening of
the rotator cuff and scapula
stabilizers, along with
improved biomechanics
related to sport specific or
relevant work activity.
-Activities are variable based
on the clinical presentation,
but primary focus is to
relieve pain, maintain the
femoral head in the proper
36A.Slipped
capital femoral
epiphysis (SCFE)
37.OsgoodSchlatter
Disease
the blood supply
(avascular
necrosis). The
disease is selflimiting and has
four distinct
stages:
condensation,
fragmentation,
re-ossification,
and remodeling.
Most common
hip disorder
observed in
adolescents
abnormalities,
infection (Age
of onset:2 &
13 years avg.6
yrs) Males
have 4x
greater
incidence
AKA traction
apophysitis, is a
self-limiting
condition that
results from
-Caused by
repetitive
tension to the
patellar
tendon over
-Unknown;
onset in
males: 10-17
years, avg 13.
Onset in
females: 8-15
years, avg 11.
Males have 2x
the incidence
of females.
in ABDuction &
ext.
Characteristic
psoatic limp
due to
weakness of
psoas major;
affected LE
moves in ER,
flex, and
adduction
-pt describes
pain as vague
at knee, thigh,
& hip. AROM is
restricted in
ABD, FLEX & IR.
With chronic
conditions, pt
may
demonstrate a
Trendelenburg
gait. Diagnostic
tests: plain film
shows
displacement
of upper
femoral
epiphysis.
-Point
tenderness
over the patella
tendon at the
insertion on the
position & improve ROM. PT:
may be required
intermittently for stretching,
splinting, crutch training,
aquatic therapy, traction, and
exercise. Orthoics and
surgical intervention may
benecessary.
NSAIDS for pain, joint bone
protection strategies,
maintain/improve joint
mechanics, implementation
of aerobic
capacity/endurance (aquatic
programs)
Post surgical interventions
include regaining functional
flexibility, improving
strength/endurance/cooridn
ation, and gait training.
-Conservative treatment
focuses on education, icing,
flexibility exercises, and
eliminating activities that
place strain on the patella
repetitive
traction on the
tibial tuberosity
apophysis.
38.Plantar
fasciitis
Refers to
inflammation of
the plantar fascia
at the proximal
insertion on the
medial tubercle
of the calcaneus.
The plantar fascia
is a broad
structure
comprised of
connective tissue
which spans from
the calcaneus to
the metatarsal
heads. The
structure is
designed to
provide support
to the arch of the
foot. Excessive
tension over time
creates chronic
the tibial
tuberosity in
young
athletes. This
can result in a
small avulsion
of the
tuberosity
and
subsequent
swelling.
-Often
associated
with an acute
injury from
excessive
loading of the
foot or
chronic
irritation from
an excessive
amount of
pronation or
prolonged
duration of
pronation.
The condition
is most
common in
pts between
40-60 years of
age.
tibial tubercle,
anatalgic gait,
pain with
increasing
activity
tendon such as squatting,
running, or jumping.
-Clinical
presentation
includes
tenderness at
the insertion of
the plantar
fascia, presence
of a heel spur,
pain that is
worse in the
morning or
after periods of
prolonged
inactivity,
difficulty with
prolonged
standing, &
pain when
walking in bare
feet.
-Initially RICE, NSAIDS. A heel
cup, massage using a tennis
ball or rolling pin, medial
longitudinal arch taping, and
joint mobs may be helpful.
Prevention includes heel cord
stretching exercises, use of
appropriate soft-soled
footwear, & avoiding sudden
changes in the intensity of
training programs. Orthotics
may be used to minimize
hyperpronation (resting night
splints)
39.Talipes
Equinovarus
“clubfoot”
40.Rotator cuff
tear
inflammation and
microtears at the
proximal
insertion.
Is a deformity
characterized by
the heel pointing
downward and
the forefoot
turning inward.
Can be torn due
to an acute
traumatic
incident or as a
result of a
chronic
degenerative
pathology. Pts 50
-Unknown,
theories
postulate
familia
tendency,
positioning in
utero or a
defect in the
ovum. This
condition
accompanies
other NM
abnormalities
including
spina bifida
and
arthrogryposi
s, & may
result from
the lack of
movement in
utero.
-Intrinsic
factors
associated
with rotator
cuff tears
include
impaired
blood supply
-Clinical
presentation
includes
adduction of
the forefoot,
varus
positioning of
the hindfoot,
and equines at
the ankle (PF)
-Medical management begins
shortly after birth and
includes splinting and serial
casting. The goal of
intervention is to restore
proper positioning of the
foot and ankle. Failed
management or severe
involvement may require
surgical intervention &
subsequent casting.
-arm positioned
in internal
rotation and
adduction,
point
tenderness at
the greater
tubercle and
-Conservative management:
RICE, NSAIDS. Primary focus
of therapy is to prevent
adhesive capsulitis and
strengthen UE musculature.
Surgical management to
repair the tendon can be
arthroscopic, mini-open with
41.Total Hip
years of age and
older are
particularly
susceptible to
tears due to
chronic
degenerative
pathology.
Rotator cuff tears
are classified as
partial thinkness
or full thickness.
A partialthickness tear
extends through
only a portion of
the tendon. A
full-thickness tear
is a complete tear
of the tendon.
The size of the
tear can range
from small (1cm
or less) to large
(more than 5cm)
Refers to removal
of the proximal &
distal surfaces of
the hip with
subsequent
replacement by
an acetabular
component and a
femoral implant.
to the tendon,
resulting in
degeneration.
Extrinsic
factors
include
trauma,
repetitive
microtrauma,
and postural
abnormalities.
acromion,
marked
limitation in
shoulder
flexion and
abduction w
upper trap
recruitment
evident,
increased tone
in anterior
shoulder
structures.
arthroscopic assist or a
traditional open approach.
Following surgery, the pt will
be immobilized in a sling. The
amount of immobilization
time will vary depending on
surgeon preference,
procedure, and size of tear.
A large tear may require 4-6
weeks of immobilization. PT
beings with PROM, gradually
to AAROM. Active motion &
isometric exercises begin
once approved by the
surgeon. The pt will gradually
become functional w ADLS
and progress to more
aggressive strengthening
activities. Return to
functional activities requiring
dynamic over head motion
occurs in 9-12 months.
-Elective
surgical
procedure.
Needs include
OA, RA,
osteomyelitis,
and avascular
necrosis.
-Prior to
surgery, severe
pain with
weight bearing,
loss of mobility,
gross instability
or limitation in
ROM, failure of
non-operative
-Initially PT focuses on
decreasing inflammation and
allowing tissues to heal,
emphasizing adherence to
hip precautions, minimizing
muscle atrophy, and
regaining full PROM. Tx can
include ankle pumps, quad
and glut sets, active hip
Surgical
procedure can be
anterolateral,
direct lateral or
posterolateral.
Fixation can be
cemented or
cementless.
Cemented
fixation allows
weight bearing as
tolerated often
immediately.
Cementless and
hybrid fixation
rely on bone
growth and may
dictate partial
weight bearing or
NWB initially.
Cementless is
normally for
young, active
individuals (less
than 65
years)Average
lifespan of a total
hip is 15-20
years.
42.Total knee
Elective
surgery
management
or a previous
surgical
procedure.
flexion w/in available range,
assistive device training, and
progressive ambulation. As
the pt progresses, treatment
moves toward regaining full
strength & endurance and
attaining independence in
the home setting.
Anterolateral approach:
AVOID-hip flexion greater
than 90, hip ext, adduction.
Direct lateral
approach:AVOID-hip flexion
beyond 90, hip ext, ER, and
adduction.
Posterolateral
approach:AVOID-hip flexion
beyond 90, IR, adduction
Severe pain w
weight bearing,
loss of mobility,
gross instability
or limitation in
Initially, PT treatment
focuses on decreasing
inflammation & allowing
tissues to heal, emphasizing
adherence to knee
ROM, marked
deformity of
the knee,
failure of nonoperative
management.
43.Temporoman
dibular joint
syndromes
Can be divided
into 3 diagnostic
categories: 1.
Joint
abnormalitiestrauma arthritis,
disease or
neoplasm.
2.Congenital
structural
defects. Can
include meniscus,
ligaments that
control
movement of the
disc, the
condyles, the
fossa, or the
articular
tubercles. 3. Loss
-Joint noise,
joint locking,
AROM of the
jaw, lateral
deviation of the
mandible
during
depression or
elevation,
decreased
strength,
tinnitus,
headaches,
forward head
posture, and
paint
w/movement.
precautions, minimizing
muscle atrophy, and
regaining full PROM. Knee
flexion requires a minimum
of 90° for ADLS & 105° to rise
comfortably from sitting.
Theraputic activities include
ankle pumps, quads and glut
sets, AROM, CPM, assistive
device training, & progressive
ambulation. Advanced
activities include wall slides,
controlled lunges, stationary
cycling, & step ups.
-Postural reeducation,
modalities for pain,
inflammation reduction,
biofeedback, joint
mobilization, AROM and
muscle strengthening
exercises, pt education for
eating soft foods and
decreasing habits that stress
the TMJ(biting nails or
pencils), instruct the pt in
maintaining the rest position
of the tongue (upright
postural position of the
tongue on the hard palate).
of functional
mobility of
unknown
etiology. May
result from
increased activity
in the muscles of
mastication as
the result of
stress & anxiety.
*Specific conditions of TMJ:
1. Synovitis & capsulitis-pain located anterior to ear area, unable to fully close back teeth together, opening less than 40 mm secondary to pain,
pain decreases w rest.
2.TMJ hypermobility-pt reports “my jaw feels like it goes out of place,” may report joint noises, short term episodes of jaw “catching” in fully
opened position. Mandibular depression is greater than 40mm and deviates toward the NONinvolved (contralateral) side, palpable irregularities
during closure.
3. Disc displacement w/reduction-Pt reports joint noises with opening and closing equal to “pops” or “clicks.” Palpation over lateral poles
reveals an opening click (the reduction of the disc) and a closing click (the disc displacing anterior to the condyle). These noises equal the
“reciprocal click.”
4. Disc displacement w/out reduction-Pt reports intermittent locking without joint noises. Opening of mandible is limited to 20-25 mm with
deflection toward INVOLVED side. Limited lateral excursion toward the opposite side of the involved joint.
*primary glide is inferior, which gaps joint, stretches the capsule, and allows relocation of anteriorly displaced disc.
Musculoskeletal Pathologies:
Pathology
Achilles
Tendon
Rupture
Diagnosis
Contributing
Factor
Normally occurs
within 1-2
inches above its
tendinous
Occurs most
frequently
when
pushing off a
Clinical
Presentatio
n
Pt will
present with
swelling
over the
Lab/Imaging
Management/Outco
me
X-ray to rule
out avulsion
fx or bony
injury. MRI
Immobilization
through casting or
surgical repair.
Pharmacological
insertion on the
calcaneus.
weight
bearing
extremity
with an
extended
knee,
through
unexpected
DF while
WBing or
with a
forceful
eccentric
contraction
of the PFors.
Poor
stretching
routine,
improper
shoe wear. A
person over
30 is at
higher risk,
average 3050 years who
participate in
recreational
activities.
distal
tendon, a
palpable
defect in the
tendon
above the
calcaneal
tuberosity,
pain &
weakness
with PF. Pt
will limp
and often
complain
that there
was a snap
or pop
associated
with severe
pain during
the inury. A
pt will not
be able to
stand on
their toes.
Thompson
test will
result in no
movement
into PF. A
complete
rupture will
result in a
palpable
can be used
to located
the presence
& severity of
the tear or
rupture.
management is not
necessary except to
relieve pain. Serial
casting for approx 10
weeks followed by
the use of a heel lift
to ensure maximal
healing without
stress on the tendon
for 3-6 months. If pt
requires surgical
intervention then a
cast or brace is
required for 6-8
weeks. PT includes
ROM, stretching,
icing, gait training,
strengthening,
plyometrics, and skill
specific training.
Modalities, pool
therapy, may assist
in recovery. Pt
should return to
their previous
functional level
within 6-7 months.
Adhesive
Capsulitis
“frozen
shoulder” is
characterized by
inflammation
and fibrotic
thickening of
the anterior
joint capsule of
the shoulder.
The capsule
becomes
adherent to the
humeral head
and under goes
contracture.
This condition
causes
symptoms of GH
limitations and
pain.
Primary
adhesive
capsulitis has
no known
etiology, it is
associated
with DM,
hypothyroidi
sm or
cardiopulmo
nary
conditions.
Secondary
adhesive
capsulitis can
result from
trauma,
immobilizatio
n, reflex
sympathetic
dystrophy,
RA,
abdominal
disorders,
and
psychogenic
disorders.
Occurs more
in the middle
aged
gap in the
tendon prior
to the
insertion.
Restricted
active and
passive
ROM at the
GH joint.
Pain that
radiates
below the
elbow and
awakens the
pt at night.
PROM is
limtied
during this
acute phase
due to pain
& guarding.
Pain is
present with
a loss of GH
motion,
restricted
elevation,
and ER.
An
arthrogram
can assist
with the
diagnosis by
detecting a
decreased
volume of
fluid within
the joint
capsule.
Greatest
restriction in
ER and
abduction.
Self-limiting process
that can take over
12 months to run its
course. A physician
can inject
corticosteroids to
assist with recovery.
Surgical intervention
to break up
adhesions or release
adhered muscles. PT
during acute phase
includes icing or
superficial heat,
gentle joint mobs,
progressive
strengthening,
pendulum exercises,
& isometrics. During
the chronic phase:
ultrasound, grade III
and IV mobs, PNF to
restore painless
ROM. PT is usually
prescribed on an
outpatient basis 3-5
months after
diagnosis. Follows a
nonlinear pattern of
recovery.
Ankylosing
Spondylitis
Is a systemic
condition that is
characterized by
inflammation of
the spine and
larger
peripheral
joints. The
chronic
inflammation
causes
destruction of
the ligamentous
osseous
junction with
subsequent
fibrosis and
ossification of
the area.
population
with females
having a
greater
incidence
than males.
Genetic
inheritance.
Typically
seen
between 2040 years of
age, and men
are at a 2-3x
greater risk
than women.
More
common in
Caucasians.
Spontaneous
recover is said to
take 12-24 months.
Will present
with
recurrent &
insidious
epidoses of
low back
pain,
morning
stiffness,
impaired
spinal
extension,
and limited
ROM in the
affected
joints for
over a 3
month
period of
time. Other
manifestatio
ns include
kyphosis,
fatigue,
weight loss,
and
peripheral
joint
X-ray of the
spine may be
negative in
the initial
stage of AS
but with
progression
will revel
areas of
erosion,
demineraliza
tion,
calcification,
and
syndesmopht
ye
formation. In
later stages,
X-ray will
reveal fusion
of the SI joint
and a
bamboo
appearance
of the spine.
Lab work can
be used to
rule out
Reduce
inflammation,
maintain functional
mobility and relieve
pain. PT should
include postural
exercises
emphasizing
extension, general
ROM, pain
management, and
energy conservation.
Low impact and
aerobic exercise
with emphasis on
extension and
rotation are
appropriate for a pt
with AS. High impact
and flexion exercises
are contraindicated.
Swimming is highly
recommended. AS
slowly progresses
over a 15-25 year
period and may
remain isolated to
the spine and SI joint
ACL sprain—
Grade III
Extends from
the anterior
intracondylar
region of the
tibia to the
medial aspect of
the lateral
femoral
condyle. The
ligament
prevents
anterior
translation of
the tibia on the
fixed femur and
posterior
translation of
the femur on
the fixed
tibia.Permits up
to 500 lbs of
pressure prior
to rupture.
Ligament has
poor blood
supply and does
not have the
ability to heal a
complete tear.
Injuries to the
ACL most
commonly occur
Participation
in athletic
activities
requiring
high levels of
agility
(soccer,
basketball)
and contact
sports.
Women have
higher
incidence of
ACL injury
than males.
involvement
.
The peak
incidence of
ACL injury
occurs
between 14
and 29
years. A
grade III is
characterize
d by
significant
pain,
effusion,
and edema
that
significantly
limits ROM.
Pt may be
unable to
WB.
other
diseases.
MRI is the
preferred
imaging tool
to identify
the presence
of an ACL
tear. X-rays
may be used
to rule out a
fracture.
Subjective
reports such
as hearing a
pop.
or spread to larger
joints.
Control edema,
increase ROM,
strengthening.
Patellar tendon graft
is the most
commonly used. Pts
often initially
present with a knee
immobilizer and
crutches to protect
the graft. Treatment
begins to focus on
strengthening
focusing on closed
chain exercises.
Closed chain is
considered more
desirable than openchain since they
minimize anterior
translation of the
tibia. Pts electing to
have surgery can
expect to return to
their previous
functional level in 46 months.
Bicipital
Tendonitis
during
hyperflexion,
rapid
deceleration,
hyperextenion,
or landing in an
unbalanced
position
Is an
inflammatory
process of the
tendon of the
long head of the
biceps.
Impingement or
an inflammatory
injury can result
in symptoms of
shoulder pain.
Repeated full
abduction and
ER of the
humeral head
can lead to
irritation that
produces
inflammation,
edema,
microscopic
tears within the
tendon, and
degeneration of
the
tendon.Commo
Often caused
through
repetitive
overhead
activity and
motion.
There is
usually direct
trauma to
the tendon
as the
shoulder
motion
approaches
excessive
abduction
and ER. High
risk:baseball
pitchers,
tennis
players,
gymnastics,
rowers, and
swimmers.
Can also be
caused
Pts report a
deep ache
directly in
the front
and on top
of the
shoulder.
The ache
may spread
down into
the biceps
muscle and
is usually
made worse
with lifting
heavy
objects.
Resting the
shoulder
typically
reduces the
pain.
Bicipital
tendinopath
y, pain to
palpation
No lab tests
to assist with
diagnosis.
Plain x-rays
do not
diagnosis
bicipital
tendonitis,
but may
show
calcification
the groove
or
subacromial
spurring. MRI
can view the
tendon, but
is expensive
and not
usually used
unless the pt
is not
responding
to
conservative
treatment.
Generally the pt
should avoid all
overhead
movement,
reaching, and lifting
of objects. Active PT
is not often initiated
immediately,
however, the pt may
be referred for
instruction in
general education of
the pathology,
guidelines for
restrictions,
pendulum exercises,
and the use of TENS.
Pt may benefit from
iontophoresis or
phonophoresis. As
pt progresses out of
acute stage therapy
should focus on an
exercise program
that stretches and
strengthens the
Carpal Tunnel
Syndrome
n in overhead
activities.
Individuals who
throw, swim, or
swing a racquet
or club are at
greatest risk.
secondary to
rotator cuff
disease,
impingement
, labral tears.
The carpal
tunnel is
created by the
transverse
carpal ligament,
the scaphoid
tuberosity and
trapezium, the
hook the
Any
condition
such as
edema,
inflammation
, tumor or
fibrosis, may
cause
compression
over the
anterior
sholulder in
the area of
the biciptial
groove, pain
with the
biceps
resistance
test
(shoulder
flexion
against
resistance
with the
elbow
extended
and forearm
supinated)
and a
positive
Yerganson’s
or Speed’s
are positive
indicators.
Most pts are
diagnosed
between 3555 years
with a
greater
prevalence
in women. A
pt will
affected muscle
groups. This can
restore the tendon’s
ability to function
properly, improve
healing, and prevent
future injury. Once
pt doesn’t
experience pain they
can slowly return to
activity. Most pts
can return to their
activities after an
average of 6-8
weeks of PT.
Electromyogr
aphy and
electroneuro
graphic
studies can
be used to
diagnose a
motor
conduction
Local corticosteroid
management,
splinting, and PT. Pt
includes splinting,
carpal mobilization,
and gentle
stretching. May
require surgery if
conservative
hamate and
pisiform, and
the volar
radiocarpal
ligament and
volar
ligamentous
extensions
between the
carpal bones.
The median
nerve, for flexor
digitorum
profundus
tendons, and
the flexor
polllicis longus
tendon pass
through the
carpal
tunnel.Carpal
tunnel
syndrome
occurs as a
result of
compression of
the median
nerve. The
increase in
pressure
produces
ischemia in the
nerve and
results in
of the
median
nerve.
Repetitive
use, RA,
pregnancy,
DM, trauma,
tumor,
hypothyroidi
sm, and wrist
sprain or
fracture.
present with
sensory
changes
along the
median
nerve
distribution
in the hand.
Night pain,
weakness of
the hand,
muscle
atrophy, ↓
grip
strength,
clumsiness
and ↓ wrist
mobility.
delay along
the median
nerve. MRI is
sometimes
used to
identify
inflammation
of the
median
nerve,
altered
tendon or
nerve
positioning.
Positive
Tinel’s sign,
Positive
Phalen’s
treatment fails. Post
surgical should
include heat with estim, iontophoresis,
cryotherapy, gentle
ROM. Pt should
initially avoid wrist
flexion and a
forceful grasp. After
4 weeks, a pt can
progress with active
wrist flexion, gentle
stretching, putty
exercises, light
progressive resistive
exercise, and
modification of body
mechanics. Radial
deviation against
resistance should be
avoided due to the
tendency for
irritation. Rehab
usually lasts 6-8
weeks.
Congenital
Torticollis
sensory and
motor
disturbances.
Is a condition
that causes the
neck to
involuntarily
unilaterally
contract to one
side secondary
to contraction
of the
sternocleidomas
toid muscle. The
head is laterally
flexed toward
the contracted
muscle, the chin
faces the
opposite
direction, and
there may be
facial
asymmetries.
May be
caused by
local trauma
to the soft
tissues of the
neck just
before or
during
delivery.
Malpositioni
ng in utero.
Pts head is
laterally
flexed
towards the
shortened
muscles side
and chin is
pointed
toward the
opposite
shoulder.
Cervical
spine X-rays
are used to
assess
potential
fracture or
subluxation.
A CT scan or
MRI of the
cervical spine
can identify
the presence
of a potential
neck mass.
Electromyogr
aphy study
may be
useful in
defining the
degree of
muscle or
nerve
involvement.
Typically treated
with non-operative
intervention for 1224 months before
considering surgical
intervention. PT
includes
family/caregiver
education and
teaching, passive
stretching, local
heat, analgesics,
sensory
biofeedback, and
TENS. AROM with
subsequent
strengthening is also
indicated to correct
the infants
positioning of their
head. PT is indicated
after surgery and
should include
manual stretching of
the neck to maintain
the overcorrected
position. Manual
stretching should be
continued 3x daily
for 3-6 months. A
cervical collar may
Degenerative
Spondylolisthe
sis (DS)
Is the forward
slippage of one
vertebra on the
vertebra below.
Classifications
include
congenital,
isthmic,
degenerative,
post-traumatic,
and pathologic.
Degenerative is
caused by the
weakening of
joints that
allows for
forward
slippage one
vertebral
segment on the
one below due
to degenerative
changes. Can
result in
stenosis of the
spinal canal.
Most
common site
is L4-L5 level.
DS is caused
by arthritis
and
degenerative
changes in
the spine.
Usually
affects
individuals
over 50.
More
common in
African
females.
Back pain is
a primary
symptom
that is said
to increase
with
exercise,
lifting
overhead,
prolonged
standing,
getting out
of bed or
car, walking
up stairs on
an incline,
and
positioning
in
extension.
Pain maybe
severe and
radiate
depending
on the area
of stenosis.
Sensory and
motor loss
may be
significant
and follow a
myotomal
Plain
radiographs
of the
vertebral
column are
adequate to
confirm the
diagnosis of
DS. CT scan
or MRI may
be indicated
to rule out
any other
contributing
conditions or
to further
assess nerve
impingement
.
be used for first 6-12
weeks after surgery.
Management should
initially include
education,
medication, activity
modification, and
PT. Activity
modification and
rest should be
instituted to further
allow inflammation
to subside and
improve overall
symptoms. William’s
flexion exercises
should be
performed to
strengthen the
abdominals and
reduce lumbar
lordosis. External
support may relive
intradiscal pressure.
Majority of pts with
DS are successful
with conservative tx.
Fibromyalgia
Syndrome
(FMS)
Is classified as a
rheumatology
syndrome or a
nonartiicular
rheumatic
condition. Pain
the primary
symptom
caused by
tender points
within muscles,
tendons, and
ligaments.
Diet, sleep
disorders,
viral
infections,
psychological
distress,
occupational
&
environment
al factors,
hypothyrodis
m, trauma,
and
hereditary
links.
Juvenile RA
JRA is a form of
arthritis found
in children less
Develops in
children with
a genetic
or
dermatomal
distribution.
Greater
incidence in
females and
can affect
any age but
most
frequently
diagnosed
between 1468 years.
Widespread
hx of pain,
11/18
tender
points.
Fatigue,
memory
and visual
impairment,
sleep
disturbance
s, irritable
bowel
syndrome,
headaches,
and
anxiety/dep
ression.
3 types of
JRA and
classified by
No specific
tests to
diagnose
FMS.
Radiographs
are negative
and blood
work often
appears
normal
except for a
possible
alteration in
the levels of
substance P.
this
substance is
a chemical
involved with
pain
transmission.
There is not
a single test
to identify
Education, medical
management, and
exercises. Physicians
must address
hormonal
imbalances, sleep
disturbances.
Psychotherapy may
be warranted for
anxiety/depression.
PT includes
relaxation, heat,
ultrasound, posture
and body mechanics,
biofeedback,
improve a pts fitness
level. These pts
require short
exercise sessions
initially (3-5
minutes) due to a
low tolerance for
exertion. FMS is not
curable, likely to
experience these
symptoms for years
or even their entire
lifetime.
A pediatric
rheumatologist is
ideal to direct a
Lateral
Epicondylitis
than 16. Causes
inflammation &
stiffness to
multiple joints
for a period of
greater than 6
weeks. An
autoimmune
disorder occurs
when the
immune cells
mistakenly
being to attack
the joints and
organs.
predispositio
n for the
disease. May
be triggered
by
environment
al factors or a
viral/bacteria
l infection.
Girls have a
higher
incidence of
JRA and most
commonly in
the toddler
or
adolescent.
number of
joints
involved,
symptoms,
presence of
RF.
Symptoms
include
persistent
joint
swelling,
pain, and
stiffness.
the presence
of JRA. Blood
tests may
include
serum
evaluation to
measure
inflammation
and detect
RF.
Tennis elbow, is
characterized by
inflammation or
degenerative
changes at the
common
extensor tendon
that attatches to
the lateral
epicondlye of
the elbow.
Repetitive
wrist action
against
resistance
during
extension
and
supination
appear to
produce this
condition.
Unilateral
involvement
, pain along
the lateral
aspect of
the elbow
and
sometimes
radiates into
the dorsum
of the hand.
No lab or
imaging
studies are
required to
diagnose. Xray or MRI to
rule out
other
conditions.
team in the complex
care of JRA. Primary
goals are to maintain
a high level of
physical functioning
and quality of life. PT
should include ROM,
exercise, pain
control, functional
mobility,
strengthening,
endurance, aerobic
trainng. Modalities,
splints and orthotics,
pt/family education
will optimize the
quality of life.
Surgical intervention
is sometimes
warranted. Some pts
outgrow JRA while
others will be on a
long term basis.
RICE, avoid all
activities that
aggravate the injury.
NSAIDS. Modalities
or iontophoresis
with
dexamethasone.
Phonophoresis with
hydrocortisone.
Resting splints may
be used during acute
MCL Sprain—
Grade II
Primary
symptom is
pain.
Continued
microtrauma
Men are
more likely
to develop
lateral
epicondylitis
and in
individuals in
their late
30’s & 40’s.
Resists medially
directed force at
the knee.
Primary
stabilizer
against valgus
force and ER of
the tibia
(especially
during knee
flexion). A grade
II is
characterized by
partial tearing
of the
ligament’s fibers
resulting in joint
Individuals
participating
in contact
activities
requiring a
high level of
agility or
susceptible.
MOI is
usually a
blow to the
outside of
the knee
joint. Can
also be
injured by
twisting of
Pain will
increase
with wrist
flexion with
elbow
extension,
resisted
wrist
extension,
and resisted
radial
deviation.
The pain
usually ↑
with activity
and is noted
at night.
Will present
with an
inability to
fully extend
and flex the
knee, pain
and
significant
tenderness
along the
medial
aspect of
the knee,
possible
decrease in
strength,
potential
stage to relieve
tension in the
involved muscles. PT
should use
stretching &
strengthening. All
exercise must
remain pain free.
Counter-force
bracing may be
indicated. Overall
outcome is favorable
and should return to
previous activities.
MRI is
extremely
expensive
and
therefore
may not be
commonly
employed
with a
suspected
MCL injury
without
other
extenuating
circumstance
s. A valgus
stress test
Conservative
management
including RICE.
Pharm intervention
for pain
management. May
utilize a full length
knee immobilizer or
a hinge brace and
crutches to limit
WBing. PT should
increase ROM, light
resistive exercises.
Heel slides,
stationary cycling
without resistance.
Resistive exercises
Osteoarthritis
laxaity when the
ligament is
stretched.
the knee.
loss of
propriocepti
on, and an
antalgic
gait. Slight
to moderate
swelling
around the
knee.
will help
detect
medial
instability. A
pt with a
grade II MCL
sprain may
exhibit 5-15°
of laxity with
valgus stress
at 30° of
flexion.
OA is a
degenerative
chronic disorder
resulting from
the biochemical
breakdown of
articular
cartilage in the
synovial joints.
Primary OA is
idiopathic
occurring
within intact
joints and no
history that
supports the
initiation of
this
condition.
Primary OA is
related to
the aging
process and
typically
occurs in
older adults.
Joints of the
hands,
knees, hips,
and spine.
Decrease in
ROM,
crepitus,
deep and
aching pain.
Pts have
pain during
activity that
is alleviated
by rest and
respond to
analgesics.
Morning
OA is
typically
diagnosed on
the basis of
clinical
examination
and x-ray
findings. Lab
tests will not
diagnose OA.
should be directed
towards the quads
and may include
isometrics and
closed kinetic chain
ex. Gait and stair
climbing. E-stim,
transverse friction
massage to the
healing ligament so
it doesn’t adhere
down. Pt should be
able to return to
previous functional
level within 4-8
weeks following
injury.
Pharm
intervention,k
glucocorticoid intraarticiular injections
may improve
symptoms.
Nutritional
education and
weight reduction
may be indicated to
reduce stress on
joints. Posture
retraining, work site
eval, strengthening,
relaxation and
hydrotherapy,
modalities, pt
Osteogenesis
Imperfecta
(OI)
A rare
congenital
disorder of
collagen
synthesis that
affects all
connective
tissue in the
body. Reduces
collagen from
20-50%.
Secondary
OA results
from trauma
that has
adversely
affected the
cartilage. In
pts greater
than 55, the
prevalence of
OA I higher in
women then
men.
Most
children
inherit OI
from parents
as either an
autosomal
dominant or
autosomal
recessive
trait. 25% of
the time the
genetic
defect occurs
by
spontaneous
mutation of
the genes.
stiffness,
deviated
gait pattern,
muscle
atrophy.
4 types that
have a wide
range of
clinical
presentatio
ns. Type I is
the mildest
form &
presents
with easy
bruising,
triangular
face, and
possible
hearing loss.
Type II is
most severe
form where
a child dies
in utero or
early
education, aquatic
therapy, and
functional activities.
If conservative
magnt fails, joint
replacement therapy
may be indicated.
A skin biopsy
is used to
examine the
collagen and
determine
what type of
OI is present.
X-rays and
bone scans
may be used
for evidence
of
deformities
and old fxs.
Bone
densitometry
may also be
used to
measure
bone mass
and estimate
Goals include
maximizing
independence with
mobility, improving
optimal bone mass
and muscle strength,
and prevention of
fxs. Pharm
intervention has no
strong effect.
Children should not
be given steroids
since it may deplete
bone and increase
fragility. Light weight
orthotics may be
indicated early to
support the
extremities and
assist with
ambulation. Pt
childhood.
Type III is
severe,
presents
with
retardation,
progressive
deformties,
ongoing fxs,
severe
osteoporosi
s, triangular
face,
significicant
limitations
in functional
mobility.
Type IV is
usually
milder and
experience
fxs easily
prior to
puberty,
shorter
stature,
bowing of
long bones,
possible
hearing loss,
brittle
teeth.
the risk of fx.
initially focuses on
parent handling
techniques,
recognition of fxs,
positioning, and
activities that
facilitate safe
movement.
Swimming is agood
alternative for
strengthening and
exercise. All
strengthening
exercises should
avoid rotational
forces, placing
weights/resistance
near a joint, and
using long lever
arms. Surgical
procedures known
as “rodding’ may
also be indicated if
child has more than
2 fxs to the same
bone within 6
months. PT may be
required
intermittently over
the pts childhood. A
strong predictor of a
child’s ability to
ambulate in the
future also lies in the
Osteoporosis
Metabolic bone
disorder where
the rate of bone
resorption
accelerates
while the rate of
bone formation
slows down;
osteoclast
activity exceeds
osteoblast
activity. This
decreases the
overall bone
density and
strength.
Primarily affects
trabecular bone
in
postmenopausal
pt.
Risk factors
include
inadequate
dietary
calcium,
smoking,
excessive
caffeine, high
intake of
alcohol or
salt, small
stature,
Caucasian
race, inactive
lifestyle,
family history
or chronic
disease.
Postmenopa
usal
osteoporosis
targets
women 5060 years.
Senile
osteoporosis
targets men
and women
Low
thoracic or
lumbar pain,
experience
compressio
n fxs of the
vertebrae
and
complain of
back pain.
Pain is acute
and ↑ with
WBing and
palpation.
Pt may also
present with
deformities
such as
kyphosis,
Dowager’s
hump, a
decrease in
height.
No accurate
measure of
overall bone
strength, Xrays are
taken to
investigate
the amount
of
degeneration
and the
decrease in
density. A
bone mineral
test accounts
for 70% of
bone
strength and
is the easiest
way to
determine
osteoporosis.
child’s ability to sit
by 10 months. Some
have minimal
involvement while
others use power
wheelchairs.
Vitamin &
supplemental
management.
Hormone
replacement therapy
is recommened. PT
should include pt
education regarding
exercise, positioning,
pain management,
nutrition, and fall
prevention. A PT
may require a corset
our lumbar support
if at risk for fxs.
Aquatic tx will help
but should not
replace WBing
activity. Surgical
intervention may be
required for fxs. Pts
should be educated
to avoid heavy
resistance, excessive
flexion during
exercise, or use of
ballistic movements.
Patellofemoral
Syndrome
Is caused by
abnormal
tracking of the
patella between
the femoral
condyles. Most
commonly
occurs when the
patella is pulled
too far laterally
during knee
extension.
Damage can
range from
softening of the
cartilage of
complete
cartilage
destruction
resulting in
exposure of
subchrondral
bone.
>70 years.
Adolescence,
More
prevalent in
females than
males, and
has a direct
associated
with the
activity level
of the pt.
Patella alta,
insufficnet
lateral
femoral
condyle,
weak vastus
medialis
obliquus,
excessive
pronation,
excessive
knee valgus,
and tightness
in LE
muscles
(iliopsoas,
hamstrings,
gastroc, and
vastus
lateralis.
Often
describes a
gradual
onset of
anterior
knee pain
following an
increase in
physical
activity.
Located
behind the
patella and
may be
exacerbated
with
activities
that
increase
compressive
forces (stair
climbing,
jumping)
and also
sitting with
knee flexed
90° for
prolonged
period.
Point
tenderness
is common
over the
Laboratory
or imaging
studies are
not
commonly
used to
diagnose PF
syndrome. Xrays are used
to rule out a
fx.
Arthrogram
and
arthroscopy
can used to
examine the
articular
cartilage.
Clarke’s sign
can be
useful. Pts
often have
an increased
Q angle (13°
in males, 18°
in females) Q
angle is
measured
using the
ASIS,
midpoint of
patella, and
tibial
Conservative
maganment is
usually successful,
surgery is rare. PT
includes controlling
edema, stretching
(hams, IT band, TFL
and rectus femoris),
strengthening (VMO
in WBing and nonWBing positions;
quad setting, SLR
and mini squats)
Deep squats should
be avoided),
improving ROM, and
activity modification.
Mob activity to
↑medial glide can
be beneficial to
increase the
flexibility of the
lateral fascia.
Patellar taping can
improve position
and tracking. An
active pt must ↓
their level of activity
to relieve additional
stress. Pt that
undergoes
conservative mangt
can return to
Plantar
Fasciitis
Imflammatory
process at its
origin on the
calcaneus. PF is
a chronic
overuse
condition that
develops
secondary to
repetitive
stretching of the
PF through
excessive foot
pronation
during the
loading phase of
gait.
Excessive
pronation
during gait,
tightness of
the foot calf
muscles,
obesity, and
possessing a
high arch.
Running or
dancing,
prolonged
walking or
standing are
at an
increased
risk.
lateral
border of
the patella
and crepitus
may be
elicted
when the
patella is
manually
compressed
into the
trochlear
groove.
Severe pain
in the heel
when first
standing up
in the
morning.
Pain
typically
subsides for
a few hours
during the
day, but
increases
with
prolonged
activity.
Described as
pain “that
moves
around”
Point
tubercle.
previous activities
within 4-6 weeks.
Prognosis is a full
recovery unless
failure to adequately
address the cause of
PF syndrome.
Initially
treated
based on
symptoms
and physical
exam. If pain
persists after
6-8 weeks of
PT, MRI may
be used to
confirm the
diagnosis.
Medical and pharm
mangt. Requires
corticosteroid
injections or antiinflammatory
medications. PT
consists of ice
massage, deep
friction massage,
shoe modification,
heel insert, foot
orthotic
prescription,
modifications of
activity, gentle
stretching. Muscle
strengthening for
the intrinsic and
extrinsic muscles
should be
implemented once
tenderness,
usually
unilateral
and
tightness in
the Achilles
tendon.
Reflex
Sympathetic
Dystrophy
Also known as
complex
regional pain
syndrome. Type
I (occurring
subsequent to
trauma) type II
(associated with
peripheral nerve
injury) is usually
found in an
extremity that
has experience
some form of
trauma.
Symptoms
result from a
disturbance in
the functioning
of the
sympathetic
nervous system.
This causes a
Trauma,
surgery, CVA,
TBI,
repetitive
motion
disorders,
and LMN and
periperhal
nerve
injuries.
Most likely
found in 3560 years of
age with
females 3x
more likely
to be
affected than
males.
Intense
burning and
chronic pain
in the
affected
extremity
that will
eventually
spread
proximally.
Edema,
thermal
changes,
discoloratio
n, stiffness,
and dryness
are seen
during stage
I (acute
stage).
Progression
to stage II
(dystrophic
X-rays may
reveal bone
less,
osteoporosis,
erosion.
Thermograp
hic studies,
laser Doppler
flowmetry.
the acute symptoms
have subsided. Night
tension splints may
be indicated is
symptoms persist. Pt
should return to
functional level
within 8 weeks.
Total resolution of
symptoms can take
up to 12 months.
RSD requires
prolonged medical
management. Tx is
based on identifying
the underlying cause
and stage of RSD at
the time of
diagnosis. Surgical
interventions such
as sympathetic
blocks, or a
sympathectomy are
used to alleviate
pain. PT includes
pain control, pt
education, skin care,
joint mob,
desensization,
functional activity
training. Overall
prognosis is better
for a pt that beings
tx early in the cycle.
release of
norepinephrine
in the periphery
and subsequent
vasoconstriction
of blood vessels.
This results in
pain and ↑ in
sensitivity to
peripheral
stimulation
RA
Rheumatoid
Arthritis is an
autoimmuine
disorder of the
connective
tissue that is
characterized by
chronic
inflammation
within the
synovial
membranes,
Genetic
predispositio
n with viral
or bacterial
triggers. The
incidence of
RA in women
is 3x greater
than in men.
Diagnosed
most
frequently
stage) is
characterize
d by
worsening
and
constant
pain, tropic
skin
changes.
Stage III
(atrophic
stage) is
characterize
d by
continued
pain,
hardened
edema,
atropic
changes to
fingertips or
toes.
RA will vary
in onset and
progression
from pt to
pt. May be
sudden or
develop
over a
period of
weeks. Early
signs
include
RSD can
spontaneously
resolve, continue
with ongoing
symptoms that can
last for years or
follow a pattern of
remissions. Research
indicates a better
prognosis if
treatment is
initiated within the
first 6 months of the
disease.
Blood work
assists with
the diagnosis
of RA
through
evaluation of
the RF, white
blood cell
count,
erythrocyte
sedimentatio
n rate,
Early medical mangt
is critical to improve
the long term
outcomes of the
disease. It will focus
on pain relief,
reduction of edema,
and preservation of
joint integrity. PT
includes pt
education regarding
regular rest, pain
Rotator Cuff
Tendonitis
tendon sheaths,
& articular
cartilage.
Smaller
peripheral joints
are usually the
first to be
affected.
between 3050 years of
age.
Repetitive
overload can
produce
impingement of
the
supraspinatus
tendon
Individuals
participating
in activities
that require
excessive
overhead
activity such
fatigue,
bilateral
involvement
, tenderness
of smaller
joints, & low
grade fever.
Pts
experience
pain with
motion,
stiffness,
progression
of
symptoms
to larger
synovial
joints. In
later stages
the heart
can become
affected and
deformities,
subluxations
and
contracture
s can occur.
Often
reports
difficulty
with
overhead
activities
and a dull
hemoglobin,
and
hematocrit
values. A
synovial fluid
analysis
evaluates the
content of
synovial fluid
within the
joint. X-rays
can be used
to evaluate
the joint
space and
the extent of
decalcificatio
n.
relief, relaxation,
positioning, joint
protection
techniques, gentle
massage,
hydrotherapy, hot
pack, paraffin, or
cold modalities,
gentle isometrics,
and instruction in
use of assistive
devices. Low impact
conditioning,
endurance and
strength during
remission. PT cannot
halt RA but can
improve a pts ability
to function. No
known cure that
creates irreversible
damage and
deformity and
results in disability.
MRI can be
used to
identify the
presence of
rotator cuff
tendonitis,
however,
Early PT:
cryotherapy, activity
modification, ROM,
& rest. After pain
subsides pt is
instructed in
strengthening
immediately
proximal to the
greater tubercle
of the humerus.
The
impingement is
caused by an
inability of a
weak
supraspinatus
muscle to
adequately
depress the
head of the
humerus in the
glenoid fossa
during elevation
of the arm. As a
result the
humerus
translates
superiorly due
to the
disproprotionat
e action of the
deltoid.
as swimming,
tennis,
baseball,
painting, and
other manual
labor.
Individuals
from 25-40
years of age
are the most
likely to
develop this
condition.
ache
following
periods of
activity. The
pt may
experience
a feeling of
weakness
and identify
the
presence of
a painful arc
of motion
most
commonly
occurring
between 60120° of
active
abduction.
Pt usually
presents
with pain
with
palpation of
the
musculoten
dinous
junction of
the involved
muscle or
with
stretching
or resisted
due to the
high cost is
not
commonly
employed
prior to
formal
treatment. Xrays with
the shoulder
laterally
rotated can
be used to
identify the
presence of
calcific
deposits or
other bony
abnormalitie
s. Special
tests
including the
empty can,
jobe test,
neer’s,
Hawkinskennedy can
be used to
confirm.
exercise. All ROM
should be pain free.
ROM using a pulley
system or a cane can
serve as an effective
intervention. Elastic
tubing and hand
held weights are
often preferred.
Shoulder shrugs and
push-ups with arms
abducated to 90°
can effectively be
used to strengthen
the upper trap and
serraus anterior. Pt
should be able to
return to previous
level of functioning
within 4-6 weeks.
Also depends on
classification of
stage. Stage I is
population less than
25 years. Stage II is
25-40 years. Stage III
end stage and likely
over 40.
Sciatica
A herniated disk
Secondary to a is an
herniated Disk intervertebral
disk that bulges
and protrudes
posterolaterally
against a nerve
root. Sciatica is
the diagnosis of
compression of
The natural
aging
process. Each
decade the
composition
of the
annulus
fibrosus and
nucleus
pulposus is
contraction
of the
muscle. Pain
often
increases at
night
resulting in
difficulty
sleeping on
the affected
side.
Difficulty
with
dressing,
and
repetitive
motions
such as
lifting,
reaching,
throwing,
swinging or
pushing and
pulling.
Low back &
gluteal pain
that
typically
radiates
down the
back of the
thigh along
the sciatic
nerve
Radiologic
testing of the
spine and
electrophysi
ologic
studies are
initially
performed to
assist with
diagnosis.
Short-term bed rest,
overall reduction of
intradiskal pressure,
pt education, PT,
meds and in rare
instances surgical
intervention. PT will
include pain mangt,
traction, heat,
lumbar endurance
the sciatic nerve
(L4, L5, S1, S2,
S3) secondary to
a herniated disk
causing pts
symptoms.
Other causes of
sciatica include
tumor,
infection,
spondyloisthesis
, narrowing of
the canal, and
blood clots.
altered and
decreases in
overall
stability.
Once there is
adequate
structural
breakdown
within the
disk, a pt
becomes
high risk for
injury. As
expected,
sciatica
secondary to
a hearniated
disk is most
often seen in
pts between
40 and 60
years.
distribution.
Sciatic pain
occurs from
nerve root
compressio
n and can
be dull,
aching or
sharp. Pain
may have a
sudden
onset or
develop
gradually
over time.
Early
sciatica may
involve
discomfort
or pain
limited to
the low
back and
gluteal
region. Leg
pain can
become
greater than
the back
pain and
can radiate
the entire
length of
the nerve to
Other
imaging may
include
myelogram,
discography,
CT scan or
MRI. Blood
work may
assist with
differential
diagnosis.
The SLR will
reproduce
symptoms in
the case of a
herniated
disk.
activities, mckenzie
exercises, stretching,
and walking are
indicated with
tolerance. Lifting,
squatting, and
climbing are
contraindicated due
to the significant ↑
in intradiskal
pressure.Most
herniations will
spontaneously
decrease in size with
conservative
treatment. Research
indicates majority of
pts will improve with
2-4 months of
conservative tx,
however 2%
undergo surgery. Pts
needs stabilization
exercises at home.
This condition can
be corrected
through rest and PT.
Healing of the disk
can also occur and
scarring can
reinforce the
posterior aspect and
annular fibers so
that it is protected
Scoliosis
Pt presents with
lateral curvature
of the spine.
The curve is
usually found in
the thoracic or
lumbar area.
The curve of the
spine may be
towards the
right or left &
Idiopathic
scoliosis,
accounts for
80% of all
cases.
Upwards of
1:10 children
are affected
by some
form of
scoliosis with
the toes.
The pt may
also
experience
intermittent
numbness
and tingling
localized to
the
dermatomal
distribution,
limited
thoracolum
bar range of
motion in all
planes,
tenderness
to palpation
at the
segment of
herniation
and muscle
guarding.
A pt with a
structural
curve will
present with
asymmetrie
s of the
shoulders,
scapulae,
pelvis, and
skinfolds.
Juvenile
from further
protrusion.
X-ray should
be taken in
an anterior
and lateral
view with
the pt
standing and
with the pt
bending
over. A
device called
Based on the type
and severity of the
curve. E-stim to
alleviate pain and
biofeedback for
education with
proper posture and
positioning. A pt
with scoliosis that is
less than 25° should
be monitored every
with our
without
rotation.
Typically, the
rotation will
occur towards
the convext side
to the major
curve.
1:4 requiring
treatment for
the curve.
Infantile (03), juvenile
(4-puberty),
adolescent
(12 for girls,
14 for boys),
or adult
(skeletal
maturation)
scoliosis.
Nonstructural
scoliosis is a
reversible
curve that
can change
with
repositioning
. Thisi type of
curve is non
progressive
and is usually
cased by
poor posture
or leg length
discrepancy.
Structural
scoliosis
cannot be
corrected
with
idiopathic
scoliosis is
characterize
d by a
thoracic
curve with
convexity
towards the
right. As the
curve
progresses
there will be
a rib hump
posteriorly
over the
thoracic
region on
the convex
side of the
curve.
Adolescent
scoliosis of
greater than
30° is seen
more in
females
than males.
Curves that
are less than
20° rarely
cause a
person to
experience
significant
a
scoliometer
can be used
to measure
the angle of
trunk
rotation. The
Cobb
method can
be used to
determine
the angle of
curvature. A
bone scan or
MRI can be
used to
determine
and rule out
conditions
such as
infections,
neoplasms,
spondylosis,
disk
herniations,
or
compression
fractures.
3 months. Breathing
exercises & a
strengthening
program for the
trunk and pelvic
muscles are
indicated. A pt with
scoliosis that ranges
beween 25 & 40°
requires a spinal
orthosis and PT for
posture, flexibility,
strengthening,
respiratory function,
and proper
utilization of the
spinal orthosis. A pt
with scoliosis
greater than 40°
usually requires
surgical spinal
stabilization. One
method is spinal
fusion and
stabilization with a
Harrington Rod.
Prognosis for
structural scoliosis is
based on the age of
onset and severity of
the curve. Early
intervention results
in the best possible
outcome. If the
Spondylolisthe
sis
Refers to
forward
slippage of one
vertebral body
with respect to
the vertebral
body below it.
In many cases
there can be
symptoms that
range from
localized or
radiating pain to
significant nerve
compression,
radiculopathy or
neurogenic
claudication.
Spondylosis has
a 2:1 male to
female
predominance
compared to all
forms of
spondylolisthesi
s, which
movement
and can be
caused by
congenital,
musculoskele
tal, and
neuromuscul
ar reasons.
A defect in
the pars
interarticulari
s that may
produce the
forward
slippage of a
vertebrae as
found with
spondylolisth
eiss. High risk
activities
include
gymnastics,
wrestling,
football, and
weight
lifting.
problems or
impairment
s.
Pain is the
most
common
symptom. If
the pt is
young, pain
is usually
confined to
the area of
slippage and
may
occasionally
radiate.
Progression
involves
neurological
, motor,
sensory, and
reflex
changes.
Pain is
usually
provoked
with activity
especially
when it
curvature is over 50°
there likely will be
ongoing progression
of the curve each
year of life.
Lateral and
anteroposter
ior plain xrays of the
lumbar spine
should be
obtained.
The oblique
view can
show the
pars as
having the
appearance
of a “Scottie
dog with a
collar” when
a spondylosis
is present.
Other studies
may include
a bone scan,
CT scan and
myelogram.
Lab studies
will not assist
with
Initially treated
conservatively
regardless of the
type or causative
factors. PT is
indicated with
emphasis on activity
modification, pt
education on
disease process,
bracing, and
therapeutic
stretching and
strengthening.
Exercise protocols
should include
exercise and activity
that reduces stress
with spinal
extension.
Conservative
treatment is very
successful especially
with the younger pt,
however, surgery
may be indicated for
indicated a
female to male
predominance
of 2:1. Overall,
females tend to
me more prone
to progressive
spondyloisthesis
and require
surgery.
Temporomand TMJ is a
ibular Joint
complex joint
Dysfunction
that is classified
as a condylar,
hinge, and
synovial joint.
The TMJ
contains
fibrocartilaginou
s surfaces &
articular discs.
TMJ dysfunction
occurs due to a
change in the
joint structure
that can cause
multiple
symptoms and a
limitation in
function. In
many instances
inflammation &
muscle spasm
surrounding the
Predisposing
factors,
triggering
factors, and
perpetuation
/sustaining
factors. Can
occur due to
injury or
trauma to
the joint,
congenital
abnormalitie
s, internal
derangement
of joint
structure,
arthritis,
dislocation,
disk
degeneration
, metabolic
conditions or
stress. Habits
involves
extension of
the spine.
diagnosis.
unsuccessful pts.
A pt will
present with
symptoms
that include
pain, muscle
spasm,
abnormal or
limited jaw
motion,
headache,
and tinnitus.
Pt will often
complain of
feeling and
hearing a
“clicking or
popping”
sound with
motion at
the TMJ.
May include
x-ray, MRI,
mandibular
kinesiograph
y, CT scan,
and a dental
examination.
Pharm management,
splint to assist with
realignment of the
joint and a guard or
bite plate to
maintain proper
position. PT is based
on the exact etiology
of the dysfunction. It
includes pt
education, postural
retraining, moist
heat, ice,
biofeedback,
ultrasound, e-stim,
TENS, stretching,
joint mobs, ROM
and relaxation. PT
intervention should
improve a pts
condition and
decrease the
symptoms. If
conservative
joint produces
symptoms for
the pt.
Total Hip
Warranted
secondary to
progressive and
severe
osteoarthritis or
RA,
developmental
dysplasia,
tumors,
nonuntion fx,
avascular
necrosis.
Destruction of
cartilage resuls
in bone to bone
contact.
of gum
chewing and
nail biting
may increase
the incidence
of injury. Pts
are typically
between 2040 years with
a greater
incidence in
women.
Intraarticular
disease or
the
destruction
of articular
cartilage may
come for
arthritis,
repetive
microtrauma,
obesity,
nuturitional
imbalances,
falls or
abnormal
joint
mechanics.
treatment fails,
surgery may be
required.
Pt will
present with
decreased
ROM,
impaired
mobility
skills, and
persistent
pain that
increases
with motion
and weight
bearing. The
pt is usually
over 55
years of age
and has
experienced
consistent
pain that is
not relieved
through
X-ray, CT and
MRI
procedures
may be used
to view the
integrity of
the joint.
These
procedures
are also used
to rule out a
fx or tumor.
Contraindicat
ions for
surgery
include
active
infection,
severe
obesity,
arterial
insufficiency,
A THA that utilizes a
posteriorlateral
approach allows the
abductor muscles to
remain intact,
however there may
be a higher
incidence of joint
instability due to the
interruption of the
posterior capsule.
Management will
include pharm
(anticoagulant), hip
precautions, ankle
pumps, quad sets,
gluteal sets, heel
slides, and isometric
abduction, scar
management. At the
time of hospital
discharge the pt
Total Knee
May be
warranted
secondary to
progressive and
disabling pain
within the knee
joint.
Destruction
of articular
cartilage
secondary to
OA.
conservativ
e measures.
NM disease,
and certain
mental
illness.
Severe knee
pain that
worsens
with motion
and weight
bearing,
limited
ROM,
possible
deformity
and
impaired
mobility.
X-ray, CT,
and MRI
imaging are
used to
determine
the extent of
deterioration
. A pain
assessment
scale and the
Arthritis
Impact
Measuremen
t tool may be
used.
should be able to
extend the hip to
neutral and flex the
hip to 90°. The pt
should have
diminished to no
pain, increased
strength and
endurance, and
improved mobility
within 6-8 weeks
after surgery.
Post-operative care
includes a knee
immobilizer,
elevation of the
limb, crotherapy,
CPM, and initiation
of knee protocol
exercises. A
noncemented knee
requires toe touch
weight bearing for
up to 6 weeks to
allow the bone to
grow and affix to the
prosthesis. PT
should focus on
mobility training
with the AD. Early
ambulation is
encouraged in order
to avoid
Deconditioning and
Total Shoulder
Sever pain and
impaired
shoulder motion
due to
deterioration of
the GH joint.
These
Degenerative
joint disease,
pain and
limited ROM
secondary to
OA, RA,
avascular
Pt will
exhibit
impaired
ROM at the
shoulder,
may lack
independen
X-ray will
reveal the
level of
degeneration
within the
shoulder
complex.
the risk of DVT. PT
should include ankle
pumps, quad sets,
and hamstring sets
as well as ROM and
stretching. A goal of
90° of knee flexion
and 0° knee
extension is often
established prior to
discharge.
Precautions follow
surgery for several
months: avoid
squatting, avoid
quick pivoting, do
not use pillows
under the knee
while in bed, and
avoid low seating.
The pt should
experience relief of
pain that will allow a
full return to
previous functional
activities within 8-12
weeks after surgery.
A pt status post TSA
will remain
hospitalized for an
average of 2-5 days.
A CPM may be
prescribed by the
surgeon for the use
candidates have
undergone
conservative
treatment
measures that
have failed to
improve their
condition.
necrosis,
fracture or
rotator cuff
arthropathy.
Others are
bone tumor,
Paget’s
disease or
with
recurrent
dislocations.
ce with
functional
mobility and
ADLs, and
severe pain.
It is this
unremitting
pain (with
failed
conservatice
treatment)
that is the
primary
indication
for TSA.
Usually
performed
on pts
between 5570 years.
MRI or CT
will allow the
physician to
assess the
integrity of
the rotator
cuff and
deltoid
muscles
surrounding
the joint.
during the pts
hospitalization. PT is
initiated the day
after surgery and
should follow the
shoulder rehab
protocol designed by
the surgeon. The
shoulder usually
remains immobilized
using a sling during
initial rehab. The
Neer shoulder
protocol advocates
initiating isometric
shoulder exercise
approx. 3 weeks
after surgery and
active shoulder
exercises 6 weeks
after surgery. PROM
and AAROM are
indicated but AROM
at the shoulder is
contraindicated
during the first
phase of rehab. PT
includes pain mgnt,
AROM, therapeutic
ex, edema
management, pt
education in selfROM and
wand/pendulum ex
Transfemoral
Amputation
due to
Osteosarcoma
Osteosarcoma is
the 2nd most
common
primary bone
tumor and is a
highly malignant
cancter that
begins in the
medullary cavity
of a bone and
leads to the
formation of a
mass. It usually
affects bones
with an active
growth phase
such as the
femur or tibia
and is often
located in the
metaphysic.
Osteosacrom
as can occur
as a primary
or secondary
cancer and
the etiology
is unknown.
This form of
tumor
primarily
affects young
children
(especially
males),
adolescents,
and young
adults under
30 years of
age. A peak
time for
incidence is
and use of
modalities. A pt
must not perform
any form of medial
rotation or lateral
rotation beyond 3540° during the first
2-3 weeks post
surgery. PT should
assist the pt to meet
goals of relieving
pain and regaining
functional motion.
Found most X-ray, MRI
Physical &
often in long and
occupational
bones at the scintigraphy
therapies should
site of the
allow the
begin immediately
most active physician to
after the
epiphyseal
determine
transfemoral
growth
the
amputation.
plate, the
presence,
Preprosthetic
distal femur, location, and intervention should
proximal
size of a
focus on ROM,
tibia,
tumor. The
positioning,
proximal
“Codman’s
strengthening,
humerus,
triagle” can
desensitization, and
and pelvis.
be seen on x- pt education for care
The knee
ray indicating of the residual limb.
region
reactive
Pts with a
accounts for bone at the
transfemoral
approx 50% site where
amputation should
of
the
lie prone for period
osteosarco
periosteum
of time each day to
mas. Pts
has been
prevent a hip flexion
Transtibial
Amputation
due to
Arteriosclerosi
s Obliterans
Amputation
may be
necessary to
remove the
tumor and
surrounding
tissues to avoid
metastic
disease.
during a
growth spurt.
Arteriosclerosis
obliterans (AKA
peripheral
arterial disease;
PAD) is a form
of peripheral
vascular disease
that produces
thickening,
hardening, and
eventual
narrowing and
Risk factors
associated
with
arteriosclero
sis obliterans
include age,
diabetes, sex,
HTN, high
serum
cholesterol
and lowdensity lipid
that require
amputation
secondary
to an
osteosarco
ma will
present with
a mass
often found
in the tibia
or femur.
Most
common
symptoms
are pain and
swelling,
pain worse
at night or
with
exercise a
lump may
develop.
The pt that
requires a
transtibial
amputation
secondary
to this
condition is
typically an
individual
over 45
years that
smokes and
elevated by
the
neoplasm.
Definitive
diagnosis for
an
osteosarcom
a is made
through
tissue biopsy
of the tumor.
contracture.
Modalties may be
used to improve
ROM and decrease
pain. Serial casting
may be indicated if a
contracture
develops. Without
complication the pt
should be able to
return home with
support and receive
short term physical
therapy for
prosthetic training.
Arteriosclero
sis obliterans
can be
diagnosed
using
Doppler
ultrasonogra
phy, MRI or
arteriograph
y. These
diagnostic
tests
A pt should be a
candidate for
inpatient PT services
immediately after
the transtibial
amputation.
Preprosthetic
intervention should
focus on strength,
ROM, functional
mobility, use of Ads,
desensitization, and
occlusion of the
arteries. This
results in
ischemia and
subsequent
ulceration of the
affected tissues.
The affected
area may
become
necrotic,
gangrenous, and
require
amputation.
levels,
smoking,
impaired
glucose
tolerance,
obesity, and
sedentary
lifestyle.
Unsuccessful
mangt of
PVD may
ultimately
lead to
uncontrolled
infection,
gangrene,
necrosis, and
amputation.
Males have
an overall
higher
incidence of
arteriosclero
sis than
females.
will present
with
intermittent
claudication
that
produces
cramps and
pain in the
affected
areas.
Resting
pain,
decreased
pulses,
ischemia,
pallor skin,
and
decreased
skin temp.
examine the
degree of
blood flow
throughout
the
extremities.
pt education. A pt
should be able to
achieve estabilished
goals and function
with a prosthesis
and an AD if
warranted.
Pharmacological Management of the MS System:
Drug
Nonopiod
Agents
Opioid Agents
Action
Indications
Side Effects
Provide
analgesia and
pain relief,
produce antiinflammatory
effects, and
initiate antipyretic
properties.
These drugs
promote a
reduction of
prostaglandin
formation that
decreases the
inflammatory
process,
decreases
uterine
contractions,
lowers fever,
and minimizes
impulse
formation of
pain fibers.
Opioid agents
Mild to
moderate pain
of various
origins, fever,
headache,
muscle ache,
inflammation
(except
acetaminophen
), primary
dysmenorrheal
, reduction of
risk of
myocardial
infaction
(aspirin only)
Nausea,
vomiting,
vertigo,
abdominal
pain,
gastrointestin
al distress or
bleeding,
ulcer
formation,
potential for
Reye
syndrome in
children
(aspirin only)
Moderate to
Mood swings,
Implications
for PT
Pts are at
increased risk
for masked
pain that
would allow
for movement
beyond
limitation or
false
understanding
of their level
of mobility.
Complaints of
stomach pain
should be
taken
seriously with
a subsequent
referral to a
physician.
A therapist
Examples
Tylenol
(acetaminoph
en);
Nonsteroidal
antiinflammatorie
s (NSAIDS):
Aspirin
(acetylsalicylic
acid), Aleve
(naproxen),
Advil
(ibuprofen,
Celebrex
(celecoxib)
Roxanol
(narcotics)
provide
analgesia for
acute severe
pain
management.
The medication
stimulates
opioid
receptors
within the CNS
to prevent pain
impulses from
reaching their
destination.
Certain drugs
are also used
to assist with
dependency
and withdrawal
symptoms.
severe pain of
various origins,
induction of
conscious
sedation prior
to a diagnostic
procedure,
management
of opiod
dependence,
relief of severe
and persistent
cough
(codeine)
sedation,
confusion,
vertigo, dulled
cognitive
function,
orthostatic
hypotension,
constipation,
incoordination
, physical
dependence,
tolerance
Glucocorticoid
Agents
(Corticosteriods)
Glucocorticoids
provide
hormal, antiinflammatory,
and metabolic
effects
including
suppression of
articular and
Replacement
therapy for
endocrine
dysfunction,
anti
inflammatory
and
immunosuppre
ssive effects;
Muscle
atrophy, GI
distress,
glaucoma,
adrenocortical
suppression,
drug induced
Cushing
syndrome,
must monitor
the pt for
potential side
effects,
especially
signs of
respiratory
depression.
Treatment
that is
otherwise
painful should
be scheduled
approximately
2 hours after
administration
to maximize
the analgesic
benefit. A pt
may not
accurately
report if a
particular
technique is
painful.
A therapist
must wear a
mask when
working with
pts on
glucocorticoid
therapy since
their immune
system is
(morphine),
Demerol
(meperidine),
Oxycontin
(oxycodone),
Sublimaze
(fentanyl),
Paveral
(codeine)
Deermacort
(hydrocortison
e or cortisol),
Cordrol
(prednisone),
Prediapred
(prednisolone)
, Medrol
(methylpredis
Diseasemodifying
Antirheumatic
Agents
systemic
diseases. These
agents reduce
inflammation
in chronic
conditions that
can damage
healthy tissue
through a
series of
reactions.
Vasoconstrictio
n results from
stabilizing
lysosomal
membranes
and enhancing
the effects of
catecholamines
.
treatment of
rheumatic,
respiratory,
and various
other diseases
weakening
with
breakdown of
supporting
tissue (bone,
ligament,
tendon, skin)
mood
changes, HTN
DMARDS slow
or halt the
progression of
rheumatic
disease. They
are used early
during the
disease process
to slow the
progression
Rheumatic
disease,
preferably
during early
treatment
Nausea,
headache,
joint pain and
swelling,
toxicity, GI
distress, sore
throat, fever,
liver
dysfunction,
hair loss,
weakened. A
therapist must
be aware of
signs of
toxicity
including
moon face,
buffalo hump,
and
personality
changes. Pts
are at risk for
osteoporosis
and muscle
wasting.
Treatment of
an injected
joint will
require
special care
due to
ligament and
tendon laxity
or weakening.
Therapists
should
recognize that
many of the
gents have a
high incidence
of toxicity.
olone),
Decadrol
(dexamethaso
ne), Nasonex
(mometasone)
Rheumatrex
(methotrexate
), Arava
lefunomide),
Antimalaria:
Aralen
(chloroquine),
Plaquenil
(hydroxychlor
oquine); Gold
prior to
widespread
damage of the
affected joints.
They act to
induce
remission by
modifying the
pathology and
inhibiting the
immune
response
responsible for
rheumatic
disease.
potential for
sepsis, retinal
damage
Individual Joints MS:
Shoulder:
Upward rotators: Upper trap, lower trap, serratus anterior
Downward rotators: Levator scapulae, rhomboids
External rotators: Infraspinatus, teres minor, deltoid
Internal rotators: Subscapularis, Latissimus, teres major, pec major & minor
Abductors: deltoid, supraspinatus
Adductors: subscapularis, pec major, lat, teres major & minor
ROM:
FLEX/ABD: 180
ER: 90
IR: 90
EXT: 60
compounds:
Ridaura
(auranofin),
Solganal
(aurothiogluco
se); Tumor
necrosis
factor
inhibitors:
Humira
(adalimumab),
Enbrel
(etanercept)
Arthrokinematics:
Motion to Increase
Abduction
Early flexion (0-45)
Internal rotation
Horizontal adduction
Extension/lateral rotation
Horizontal abduction
Late flexion (120-180)
Mobilization Glide
Inferior or caudal glide
Posterior glide
Posterior glide
Posterior glide
Anterior glide
Anterior glide
Anterior glide
Degree of Abduction:
First 20 degrees: Supraspinatus
90-150 degrees: serratus anterior and trapezius
Degree of Elevation:
0-60 degrees: anterior delt, coracobrachialis, pec major
60-120 degrees: serratus anterior, and trap
Force couple of the shoulder:
-Downward rotation: levator and rhomboids vs. lat, pec major and minor
-Upward rotation: serratus (most effective rotator) and upper trap vs. lower trap that contributes during later phase of shoulder abduction
Peripheral Nerve Tests:
•Spinal Accessory nerve-Inability to abduct the arm beyond 90 degree, Pain in shoulder with abduction
•Musculocutaneous nerve- Weak elbow flexion with forearm supinated
•Long thoracic nerve- Pain on flexing fully extended arm, inability to flex fully on extended arm, winging of scapula at 90 degree of forward
flexion
•Suprascapular nerve- Increased pain on forward shoulder flexion, pain increased with scapular abduction, pain increased with cervical rotation
to opposite side
*Painless weakness is usually due to neurologic problems or myopathies.
* Shoulder weakness may be caused by a rotator cuff tear or nerve injury.
* Symptoms that are not associated with movement should alert the clinician to a more serious condition.
* Pain that is worse at night, but increased when rolling onto the shoulder, points to periarticualr mechanical problems.
* Pain that occurs between 70-110 degrees of abduction is deemed a “painful arc” and may indicate rotator cuff impingement, or tearing, or
subacromial bursitis. Pain which occurs in the 120-160/160-180 degrees range, may indicate involvement of the A-C joint.
* Loss of ACTIVE motion with preservation of PASSIVE motion is likely caused by rotator cuff tear.
* A severely restricted active abduction pattern with NO pain is suggestive of a rupture of the supraspinatus or deltoid.
* Loss of BOTH active AND passive motion is usually caused by adhesive capsulitis.
* A loss of passive OR active ROM may be associated with a loss of flexibility in the passive restraints to motion.
Muscles prone to tightness-Upper trap, levator, pec major and minor, upper cervical extensors, sternocleidomastoid, scalene, teres major and
minor, subscapularis
Muscles prone to lengthening-Middle and lower trap, rhomboids, serratus anterior, deep neck flexors, supraspinatus, infraspinatus
Closed packed position-90 degress of GH ABD & full ER
Capsular pattern: Most limited: ER, ABD, & IR (least)
Common MMT for the shoulder:
1. Scapular Elevation (Upper trap, Levator Scap): Sitting, apply resistance over superior aspect of shoulders in inferior direction. Gravity
Eliminated: Pt prone
2. Scapular Adduction (Middle trap): Pt prone and performs active scapular adduction. Examiner applies resistance over lateral aspect of
scapula in direction of scapular abduction. Gravity eliminated: Seated c shoulder abducted to 90 degrees and full lateral rotation.
3. Scapular adduction and depression (Lower trap): Prone c upper extremity in ~130 abd and 0 degrees elbow extension. Apply resistance
over lateral aspect of scapula. Gravity eliminated: No separate test.
4. Scapular adduction and downward rotation (Rhomboid major and minor): Pt prone with upper extremity behind back. Shoulder in
medial rotation and adduction (dorsum of hand on gluteal region). Apply resistance on vertebral border of scapula in direction of
scapular abduction and upward rotation. Gravity eliminated: Pt seated with arm behind back.
5. Scapular abduction and upward rotation (Serratus Anterior): Pt supine with UE in 90 degrees shoulder flexion and elbow extension.
Apply resistance by grasping wrist and pushing down. Gravity eliminated: Seated with UE in 90 degrees shoulder flexion with arm
supported on flat surface.
6. Shoulder flexion (anterior delt, coracobrachialis): Pt seated with UE in 0 degrees flexion and adduction, palm facing trunk. Apply
resistance proximal to elbow. Gravity eliminated: Side-lying with arm to be tested uppermost and supported.
7. Shoulder extension (Lat, Teres major, pos delt): Pt prone, with palm facing ceiling. Pt raises arm through range, apply resistance just
proximal to elbow. Gravity eliminated: Side-lying with arm to be tested uppermost and supported.
8. Shoulder abduction (Middle delt, supraspinatus): Seated. Apply resistance proximal to elbow. Gravity eliminated: Supine on firm
surface.
9. Shoulder horizontal abduction (posterior delt): Pt prone with upper extremity in 90 degree shoulder abduction, 90 degree elbow
flexion, arm hanging off table. Apply resistance over distal humerus. Gravity eliminated: Seated
10. Shoulder horizontal adduction (Pec major): Supine with UE in 90 degrees shoulder abd, 90 degree elbow flexion. Have pt horizontally
adduct shoulder; apply resistance just proximal to elbow in direction of abduction. Gravity eliminated: Seated
11. Shoulder Internal rotation (Subscapularis, Pec major, Lat, Teres major): Prone with UE in 90 degrees shoulder abduction, 90 degrees
elbow flexion, arm hanging down. Pt moves through full range of IR, apply resistance just proximal to wrist in direction of ER. Gravity
eliminated: Prone, with arm hanging off side of table, rotate humerus along long axis.
12. Shoulder external rotation (Infraspinatus, teres minor): Prone with UE in 90 degrees shoulder abduction, 90 degrees elbow flexion, arm
hanging down. Pt moves through full range of ER, apply resistance just proximal to wrist in direction of IR. Gravity eliminated: Prone,
with arm hanging off side of table, rotate humerus laterally along long axis.
Special tests for the Shoulder:
Dislocation:
1. Apprehension test for anterior shoulder dislocation: The pt is positioned in supine with arm in 90 degrees abduction. Therapist laterally
rotates pts shoulder. A positive test is indicated by a look of apprehension or a facial grimace prior to reaching end point.
2. Apprehension test for posterior dislocation: The pt is positioned in supine with the arm in 90 degrees of flexion and medial rotation. The
therapist applies a posterior force through the long axis of humerus. A positive test is indicated by a look of apprehension.
Biceps tendon Pathology:
1. Ludington’s test: The pt is positioned in sitting and is asked to clasp both hands behind the head with the fingers interlocked. The pt is
then asked to alternately contract and relax the biceps muscles. A positive test is indicated by absence of movement in the biceps
tendon and may be indicative of a rupture of the long head of the biceps.
2. Speed’s test: The pt is positioned in sitting or standing with the elbow extended and the forearm supinated. The therapist places one
hand over the bicipital groove and the other hand on the volar surface of the forearm. The therapist resists active shoulder flexion. A
positive test is indicated by pain or tenderness in the bicipital groove region.
3. Yeargason’s test: The pt is positioned in sitting or standing with the arm in 90 degrees of elbow flexion and forearm pronated. The
humerus is stabilized against the pts thorax. The therapist places on hand on the patient’s forearm and the other hand over the bicipital
groove. The patient is directed to actively supinate and laterally rotate against resistance. A positive test is indicated by pain or
tenderness in the bicipital groove and may be indicative of bicipital tendonitis.
Rotator Cuff Pathology/Impingement:
1. Drop arm test: The pt is positioned in sitting or standing with the arm in 90 degrees of abduction. The pt is asked to slowly lower the arm
to their side. A positive test in indicated by the patient failing to slowly lower the arm to their side or by the presence of severe pain and
may be indicative of a tear in the rotator cuff.
2. Hawkins-Kennedy Impingement test: The pt is positioned in sitting or standing. The therapist flexes the pts shoulder to 90 degrees and
then medially rotates the arm. A positive test is indicated by pain and may be indicative of shoulder impingement involving the
supraspinatus tendon.
3. Neer impingement test: The pt is positioned in sitting or standing. The therapist positions one hand on the posterior aspect of the
patient’s scapula and the other hand stabilizing the elbow. The therapist elevates the patients arm through flexion. A positive test is
indicated by a facial grimace or pain and may be indicative of shoulder impingement involving the supraspinatus tendon.
4. Supraspinatus test(empty can): The pt is positioned with the arm in 90 degrees of abduction followed by 30 degrees of horizontal
adduction with the thumb pointing downward. The therapist resists the patient’s attempt to abduct the arm. A positive test is indicated
by weakness or pain and may be indicative of a tear of the supraspinatus tendon, impingement, or suprascapular nerve involvement.
Thoracic Outlet Syndrome:
1. Adson maneuver: The pt is positioned in sitting or standing. The therapist monitors the radial pulse and asks the pt to rotate their head
to face the test shoulder. The pt is then asked to extend their head while the therapist laterally rotates and extends the pts shoulder. A
positive test is indicated by an absent or diminished radial pulse and may be indicative of thoracic outlet syndrome.
2. Allen test: The pt is positioned in sitting or standing with the test arm in 90 degrees of abduction, lateral rotation, and elbow flexion. The
pt is asked to rotate the head away from the test shoulder while the therapist monitors the radial pulse. A positive test is indicated by an
absent or diminished pulse when the head is rotated away from the test shoulder. A positive test may be indicative of thoracic outlet
syndrome.
3. Costoclavicular syndrome test (military brace): Pt positioned in sitting. The therapist monitors the pts radial pulse and assists the pt to
assume a military posture. A positive test is indicated by an absent or diminished radial pulse and may be indicative of thoracic outlet
syndrome caused by compression of the subclavian artery between the first rib and the clavicle.
4. Roos test: The pt is positioned in sitting or standing with the arms positioned in 90 degrees of abduction, lateral rotation, and elbow
flexion. The pt is asked to open and close their hands for three minutes. A positive test is indicated by the inability to maintain the test
position, weakness of the arms, sensory loss or ischemic pain. A positive test may be indicative of thoracic outlet syndrome.
5. Wright (hyperabduction test): The pt is positioned in sitting or supine. The therapist moves the pts arm overhead in the frontal plane
while monitoring the pts radial pulse. A positive test is indicated by an absent or diminished radial pulse and may be indicative of
compression in the costoclavicular space.
Miscellaneous:
1. Glenoid Labrum tear test “clunk test”: The pt is positioned in supine. The therapist places one hand on the posterior aspect of the pts
humeral head while the other hand stabilizes the humerus proximal to the elbow. The therapist passively abducts and laterally rotates
the arm over the patient’s head and then proceeds to apply an anterior directed force the humerus. A positive test is indicated by a
clunk or grinding sound and may be indicative of a glenoid labrum tear.
2. Upper limb tension tests: Neural provocation maneuvers. Symptoms and relevant changes in symptoms should be identified after each
step. Non-involved side tested first.
Joint position
ULTT 1
Shoulder depression
with 110° abd, elbow
ext, forearm
supination, wrist ext,
finger and thumb ext
“yay position”
ULTT 2
Shoulder depression
with 10° abd, elbow
ext, forearm
supination, wrist ext,
finger and thumb ext,
shoulder lateral
rotation
ULTT 3
Shoulder depression
with 10° abd, elbow
ext, forearm
pronation, wrist
flexion, ulnar
deviation, finger and
thumb flexion,
shoulder medial
ULTT 4
Shoulder depression
with 10-90° abd,
elbow flexion,
forearm supination,
wrist ext, radial dev,
finger and thumb
ext, shoulder lateral
rotation “waiter’s
Sensitization
Test
Contralateral cervical Contralateral cervical
lateral flexion
lateral flexion
Nerve Bias
Median nerve,
anterior
interosseous nerve
Median nerve,
musculocutaneous
nerve, axillary nerve
rotation “waiter’s
tip”
Contralateral cervical
lateral flexion
Radial nerve
tray position”
Contralateral
cervical lateral
flexion
Ulnar nerve
Shoulder conditions:
1. Glenohumeral subluxation and dislocation:
•Most dislocations (95%) occur in anterior-inferior direction.
•Anterior-inferior dislocation occurs when abducted upper extremity is forcefully, externally rotated, causing tearing of the inferior
glenohumeral ligament, anterior capsule, and occasionally glenoid labrum.
•Posterior dislocations are rare, and occur with multidirectional laxity of glenohumeral joint.
•Posterior dislocation occurs with horizontal adduction and internal rotation of glenohumeral joint.
•Complications include compression fracture of posterior humeral head (Hill-Sachs lesion), tearing of superior glenoid labrum from
anterior (front) to posterior (back) (aka SLAP superior labrum, anterior to posterior) lesion, an avulsion of anteroinferior capsule and
ligaments associated with glenoid rim (Bankart’s lesion), and bruising of axillary nerve.
•Following surgical repair for dislocation/chronic subluxation, pts should avoid apprehension position (flexion to 90 or greater,
horizontal abduction to 90 or greater, and ER to 80)
•Diagnostic tests utilized: plain film, CT, or MRI
•Diagnosis made by clinical examination. Apprehension tests will be positive.
Goals, outcomes, interventions: PT intervention is varied, depending on if surgery is indiciated. Biomechanical faults caused by joint
restriction should be corrected with joint mobs.
2. Instability:
•Divided into two categories: traumatic (common in young throwing athletes), and atraumatic (individuals with congenitally loose
connective tissue around the shoulder).
•Characterized by popping/clicking and repeated dislocation/subluxation of the GH joint.
•Unstable injuries require surgery to reattach the labrum to the glenoid.
•Bankart’s lesions require surgery.
•Diagnosis made by clinical exam by comparing results of pt history with the AROM, PROM, resistive tests, and palpation.
•MRI arthrograms are VERY effective in identifying labral tears.
•Meds: acetaminophen for pain, NSAIDS for pain/inflammation
Goals, outcomes, interventions: Intervention emphasizes return of function without pain. Functional training and restoration of muscle
imbalances using exercise to normalize strength.
• For patients requiring surgery, the shoulder is usually kept in a sling for 3-4 weeks. After 6 weeks, more sports-specific training can
be done, although full fitness may take 3-4 months.
3. Labral tears:
• Glenoid labrum injuries are classified as either superior (toward the top of the glenoid socket) or inferior (toward the bottom of the
glenoid socket). A SLAP lesion is a tear of the rim above the middle of the socket that may also involve the biceps tendon. A tear of the
rim below the middle of the glenoid socket is called a Bankart’s lesion, and also involves the inferior glenohumeral l igament. Tears of
the glenoid labrum may often occur with other shoulder injuries, such as a dislocated shoulder.
• Characterized by the following signs and symptoms:
-Shoulder pain that cannot be localized to a specific point
-Pain is made worse by overhead activities or when the arm is held behind the back
-Weakness
-Instabilitiy in the shoulder
-Pain on resisted flexion of the biceps
-Tenderness over the front of the shoulder
• Unstable injuries require surgery to reattach the labrum to the glenoid. Bankart’s lesions require surgery.
• Diagnosis made by clinical exam, through comparing results of AROM, PROM, resistive tests, and palpation.
•MRI arthrograms are very effective in identifying labral tears.
• The gold standard for identifying a labral tear is through arthroscopic surgery of the shoulder.
•Meds: acetaminophen, NSAIDS
Goals, Outcomes, Interventions: Return to function without pain, normal strength, endurance, coordination, and flexibility.
•Following surgery, the shoulder is usually kept in a sling 3-4 weeks. After 6 weeks, more sports specific training can be done.
4. Thoracic Outlet Syndrome (TOS):
•Compression of neurovascular bundle (brachial plexus, subclavian artery and vein, vagus and phrenic nerves, and the sympathetic
trunk) in thoracic outlet between bony and soft tissue structures.
•Compression occurs when size or shape of thoracic outlet is altered.
•Common areas of compression: Superior thoracic outlet, Scalene triangle, between clavicle and first rib, between pectoralis minor and
thoracic wall.
•Surgery may be performed to remove a cervical rib or a release of anterior and/or middle scalene muscle.
•Diagnostic tests utilized: plain film imaging to identify abnormal bony anatomy and MRI to identify abnormal soft tissue anatomy.
Electro diagnostic test to assess nerve dysfunction.
•Clinical exam of special tests will be helpful to make diagnosis: Adson’s, Roos test, Wright test, Costoclavicular test.
•Medications: acetaminophen, NSAIDS
Goals, Outcomes, Interventions: Postural reeducation, functional training of muscle imbalance, flexibility. Joint mobs, Manipulations (1st
rib articulation)
5. Acromioclavicular and sternoclavicular joint disorders:
•Mechanism of injury is a fall onto shoulder, with UE adducted, or a collision with another individual during a sporting event.
•Traditionally, degree of injury is grated from first to third degree. Rockwood classification scales uses grades from I to IV, with grades
IV-VI as variations of the traditional grade III.
•UE is positioned in neutral with use of sling in acute phase. AVOID shoulder elevation during the acute phase of healing.
•Diagnostic tests: plain film imaging
•Special test useful in making diagnosis: Shear test
•Surgical repair is rare, due to tendency of acromioclaviculr joint degeneration following the repair.
•Meds: acetaminophen, NSAIDS
Goals, Outcomes, Interventions: Return of function without pain. Functional training and restoration of muscle imbalances using
exercise to normalize strength, endurance, coordination, and flexibility.
•Manual therapy techniques to AC and SC joints such as soft tissue/massage, joint oscillations, and mobilizations to normalize soft tissue
and joint biomechanics.
*Arthrokinematics for Sternoclavicular joint: (Protraction=same direction)( Elevation=opposite)
Motion to Increase
Mobilization Glide
SC elevation
Inferior glide
SC protraction
Anterior glide
6. Subacromial/subdeltoid bursitis:
•Subacromial and subdeltoid bursae (which may be continuous) have a close relationship to rotator cuff tendons, making them
susceptible to overuse.
•Palpable by extending the humerus.
•The bursa is located over the bicipital groove under the deltoid muscle, separating this muscle from the rotator cuff and allowing for
free motion of the deltoid over the humerus.
•They can also become impinged beneath the acromial arch.
•Diagnosis made by clinical exam. Differentiate from contractile condition by comparing results of AROM, PROM, and resistive tests
7. Rotator cuff tendonosis/tendonopathy:
•Tendons of the rotator cuff are susceptible to tendonitis, due to relatively poor blood supply near insertion of muscles.
•Results from mechanical impingement of the distal attachment of the rotator cuff on the anterior acromion and/or coracoacromial
ligament with repetitive overhead activities.
•Diagnostic tests utilized: MRI may be used, but sometimes not sensitive enough for accurate assessment.
•Clinical exam include the following special tests: Supraspinatus test, Neer’s impingment test
8. Impingement syndrome:
•Characterized by soft tissue inflammation of the shoulder from impingement against the acromion with repetitive overhead AROM.
•Diagnostic tests utilized: arthrogram or MRI
•Clinical exam will include the following: Neer’s, Supraspinatus test, Drop arm test
•Surgical repair of shoulder impingement. The pt should avoid shoulder elevation greater than 90°.
Goals, Outcomes, Interventions: Restoration of posture, correction of muscle imbalance
9. Bicipital tendonosis/tendonopathy:
•Most commonly an inflammation of the long head of the biceps.
•Results from mechanical impingement of the proximal tendon, between the anterior acromion and the bicipital groove of the humerus.
•Diagnostic tests utilized: MRI may be used, but sometimes not sensitive enough.
•Clinical exam will include Speed’s test.
•Meds: acetaminophen and NSAIDS
10. Proximal humeral fractures:
•Humeral neck fractures frequently occur with a fall onto an outstretched UE among older osteoporotic women. Generally does not
require immobilization or surgical repair, since it is a fairly stable fx.
•Greater tuberosity fractures are more common in middle-aged and elder adults. Usually related to a fall onto the shoulder, and does
not require immobilization for healing.
•Diagnostic tests utilized: plain film radiographs.
•Early PROM is important in preventing capsular adhesions.
11. Adhesive Capsulitis (frozen shoulder):
•Characterized by a restriction in shoulder motion as a result of inflammation and fibrosis of the shoulder capsule, usually due to disuse
following injury or repetitive microtrauma.
•Restriction follows a capsular pattern of limitation: Greatest limitation in ER, followed by abduction, and flexion, and least restricted in
IR.
•Commonly seen in association with diabetes mellitus.
Elbow:
Supination: (Supinator, biceps) C5-C6
Pronation: (Pronator quadrauts, pronator teres, flexor carpi radialis) C8-T1, C6,C7
Extension of wrist: (ECRL, ECRB, ECU) C6-C7, C7-C8
Flexion of wrist: (FCR, FCU) C6-C7, C7-C8
UD of wrist: (FCU, ECU) C7-C8, C7-C8
RD of wrist: (FCR, ECRL, abd pollicis longus, ext pollicis brevis) C6-C7, C7-C8
Ext of fingers: (Extensor digitorum communis, ext indicis, extensor digiti minimi) C7-C8
Flexion of fingers: (flex digit profundus, superficialis, lumbricals, interossei, flexor digit minimi): C8-T1
Abduction of fingers: (Doral interossei, abductor digiti minimi) C8-T1
Adduciton of fingers: (palmar interossei) C8, T1
Ulnar nerve (C8-T1) *Largest branch of the medial cord of the brachial plexus. Entrapment site: cubital tunnel and Guyon’s canal. Intervention:
splint wrist in neutral position at night, elbow pad. Education-positioning in elbow ext and decreasing direct pressure on nerve; stretch flexor
carpi ulnaris
Median nerve (C5-T1) *AIN branches off median nerve and supplies motor innervation to the index and middle flexor digitorum profundus, the
flexor pollicis longus, and the pronator quadrates. Entrapment site: carpal tunnel, proximal forearm. Intervention: splint wrist in neutral position
at night, stretching exercises for pronator teres, rest periods in supination.
Radial nerve (C5-T1) Entrapment site: arcade of froshe, forearm. Intervention: positioning in supination and avoid repetitive pronation and
supination activities.
ROM:
Flexion: 5° hyperextension to 145° flexion
Extension: 0° to 5-10° hyperextension
Arthrokinematics:
Joint
Ulnohumeral (same)
Proximal radioulnar (opposite)
Distal radioulnar (same)
Motion to Increase
Elbow flexion
Elbow extension
Pronation
Supination
Pronation
Supination
Mobilization Glide
Anterior
Posterior
Posterior (lateral)
Anterior (medial)
Anterior (medial)
Posterior (lateral)
Force couples:
•The triceps/biceps during elbow extension and flexion
•pronator teres and pronator quadratus/supinator during forearm pronation and supination
•FCR, FCU, flexor digitorum communis/ERCL, ECRB, and extensor communis during wrist flexion and extension
•triceps/biceps and brachioradialis; pronator teres/supinator/ and FCR, FCU/ECRB, and ECRL during activities requiring elbow stabilization
Closed-pack position: Humeroulnar-full extension and maximum forearm supination;
open-packed position: 70° of flexion with 10° supination
Capsular pattern: flexion more limited than extension
Common MMT for the elbow:
1. Elbow flexion (biceps brachii): Seated, with UE in 0° shoulder add, 0° elbow ext, forearm supination. Apply resistance just proximal to
wrist in direction of elbow extension. Gravity eliminated: seated w arm supported on table.
2. Elbow flexion (brachialis): Seated, same position except forearm PRONATION. Apply resistance just proximal to wrist in direction of
elbow extension. Gravity eliminated: seated with arm supported (hand thumb side down)
3. Elbow flexion (brachioradialis): Seated, same position except NEUTRAL forearm rotation. Gravity eliminated: Seated, with arm
supported (palm face down on table)
4. Elbow extension (triceps, anconeus): Supine w UE in 90° shoulder flexion, full elbow flexion, full forearm supination. Flex pts elbow
slightly, then apply resistance just proximal to wrist in direction of elbow flexion. Gravity eliminated: Seated w arm supported, shoulder
abducted to 90°, elbow full flexed, forearm supinated (pinky on table)
5. Forearm supination (supinator, biceps): Seated w UE in 0° shoulder abd, 90° elbow flexion, full forearm pronation. Apply resistance over
volar surface of ulna and dorsal surface of radius in direction of pronation. Gravity eliminated: Seated w UE in 90° shoulder flex, 90°
elbow flexion, full forearm pronation
6. Forearm pronation (pronator quadraus, pronator teres): Seated, w UE in 0° shoulder abd, 90° elbow flex, full forearm supination. Apply
resistance over volar surface of radius and dorsal surface of ulna in direction of supination. Gravity eliminated: Same except full forearm
supination.
Special tests for the elbow:
Ligamentous Instability
1. Varus stress test: The pt is sitting w the elbow in 20-30° of flexion. Therapist places one hand on the elbow and the other proximal to the
pts wrist. The therapist applies a varus force to test the LCL while palpating lateral joint line. A positive test is indicated by increased
laxity in the LCL when compared to the contralateral limb, apprehension or pain. A positive test may be indicative of a LCL sprain.
2. Valgus stress test: Same position as varus, except therapist applies a valgus force to test the MCL while palpating the medial joint line. A
positive test is indicated by increased laxity in the MCL when compared to the contralateral limb, apprehension or pain. A positive test
may be indicative of a MCL sprain.
Epicondylitis
1. Cozen’s test: Pt is positioned in sitting w the elbow in slight flexion. Therapist places his/her thumb on the patient’s lateral epicondyle
while stabilizing the elbow joint. The pt is asked to make a fist, pronate the forearm, radially deviate, and extend the wrist against
resistance. A positive test is indicated by pain in the lateral epicondyle region or muscle weakness and may be indicative of lateral
epicondylitis.
2. Lateral epicondylitis test: The pt is positioned in sitting. The therapist stabilizes the elbow w one hand and places the other hand on the
dorsal aspect of the pts hand distal to the proximal interphalangeal joint. The pt is asked to extend the third digit against resistance. A
positive test is indicated by pain in the lateral epicondlye region or muscle weakness and may be indicative of lateral epicondylitis.
3. Medial epicondylitis test: Pt positioned in sitting. The therapist palpates the medial epicondyle and supinates the pts forearm, extends
the wrist, and extends the elbow. A positive text is indicated by pain the medial epicondyle region and may be indicative of medial
epicondylitis.
4. Mill’s test: Pt positioned in sitting. The therapist palaptes the lateral epicondyle, pronates the pts forearm, flexes the wrist, and extends
the elbow. A positive test is indicated by pain in the lateral epicondyle region and may be indicative of lateral epicondylitis.
Neurological Dysfunction
1. Tinel’s sign: Pt positioned in sitting w the elbow in slight flexion. Therapist taps with the index finger between the olecranon process and
the medial epicondyle. A positive test is indicated by a tingling sensation in the ulnar nerve distribution of the forearm, hand, and
fingers. A positive test may be indicative of ulnar nerve compression or compromise.
2. Pronator teres syndrome test: Pt sitting w elbow in 90° flexion and supported. Therapist resists forearm pronation and elbow extension
simultaneously. A positive test reproduces a tingling or parestheisa within the median nerve distribution. A positive test may be
indicative of median nerve entrapment within pronator teres. Occurs with repetitive gripping activities.
Elbow conditions: (See chart for common MS diagnosis)
1. Distal humeral fractures:
•Complications can include loss of motion, myositis ossificans, malalignment, neurovascular compromise, ligament injury, and CRPS.
•Supracondylar fxs must be examined quickly for neurovascular status, due to high number of neurological (typically radial nerve
involvement) and vascular structures that pass through this region (may lead to Volkmann’s ischemiaI. In youth, it is important to assess
growth plate as well. These fxs have a high incidence of malunion.
*Volkmann’s Contracture=severe pain in forearm, sensation of pressure if compartment syndrome. Onset is nerve and muscle ischemia,
secondary to arterial compromise. Pt has pain w/in 2 hrs increase by passive finger ext, pallor, paresis, pulselessness, pt has wrist ext,
and finger flex contractures.
•Lateral epicondyle fxs are fairly common in young people, and typically require an open reduction internal fixation (ORIF) to ensure
absolute alignment.
•Diagnostic tests utilized: plain film
Goals, outcomes, Interventions: pain reduction and limiting the inflammatory response following trauma/surgery. Improving flexibility of
shortened structures, strengthening, and training to restore functional use of UE.
2. Osteochondrosis of humeral capitellum:
•Osteochondritis dissecans affects central and/or lateral aspect of capitellulm or radial head. An osteochondral bone fragment becomes
detached from articular surface, forming a loose body in joint. Caused by repetitive compressive forces between radial head and
humeral capitellum. Occurs in adolescents between 12 and 15 years of age.
3. Panner’s disease:
•Is a localized avascular necrosis of capitellum leading to loss of subchondral bone, with fissuing and softening of articular surfaces of
radiocapitellar joint. Etiology is unknown, but occurs in children age 10 or younger.
•Diagnostic tests: plain film
Goals, outcomes, Interventions: PT includes rest with avoidance of any throwing or upper extremity loading activities (gymnastics) When
pt is pain-free, initiate flexibility and strengthening/endurance/coordination ex. During late phases of rehab, a program to slowly
increase load on joint it initiated. If symptoms persist, surgical intervention is necessary. After surgery initial focus of rehab is to
minimize pain and swelling using modalities.
4. Radial nerve entrapment:
•Occurs within radial tunnel as a result of overhead activities and throwing. Clinical signs include lateral elbow pain that can be confused
with lateral epicondylitis, pain over supinator muscle, and presthesias in a radial nerve distribution. Tinel’s sign may be positive.
•Diagnostic tests utilized: electrodiagnositc tests.
Goals, outcomes, and interventions: Early intervention includes rest, avoiding exacerbating activities, use of NSAIDS, modalities and soft
tissue massage. If abnormal neurotension is present, neurodynamic mobilization may be indicated. Protective padding and night splints
to maintain slackened position of involved nerves.
5. Elbow dislocations:
•Posterior dislocations account for most dislocations occurring at the elbow. Posterior dislocations are defined by position of olecranon
relative to the humerus.
•Posterolateral dislocations are most common, and occur as the result of elbow hyperextension from a fall on the outstretched UE.
•Posterior dislocations frequently cause avulsion fxs of medial epicondyle secondary to traction pull of medial collateral ligament.
•Anterior and radial head dislocations account for only 1-2% of all elbow dislocations. With a complete dislocation, ulnar collateral
ligament will rupture, with possible rupture of anterior capsule, lateral collateral ligament, brachialis muscle, and/or wrist flexor and
extensor muscles.
•Clinical signs include rapid swelling, severe pain at the elbow, and a deformity with the olecranon pushed posteriorly
Goals, outcomes, and interventions: Initial intervention includes reduction of the dislocation. If elbow is stable, there is an initial phase
of immobilization, followed by rehab focusing on regaining flexibility within limits of stability and strengthening.
*Nurse-maid’s (pulled) Elbow-pain localized to superior radioulnar joint, caused by longitudinal pull on forearm, a partial slippage of the
annular ligament over the head of the radius pt will avoid use of arm, arm held in pronation, pt has inability to supinate w/out pain.
Special tests: palpate sulcus proximal to radial head.
Wrist & Hand
*The wrist is positioned in slight extension to allow effective hand function.
*Wrist extension of 20°-30° is needed for optimal use of the hand.
*The most active muscle in grasping is the extensor carpi radialis brevis, which holds the wirst in extension.
Two types of functional grasp:
1. The power grip is used to exert force on an object and maintain it against the palm. This requires finger flexion and wrist extension
with ulnar deviation.
2. The precision (prehension) grip is used for accurate functions with the object held between the fingertips.
Four stages of gripping: Opening the hand, closing the fingers, exerting force, and releasing the object. The thumb, wrist, hand, and
fingers control the gripping actions with varying ranges of precision or power.
ROM:
Flex-80
Ext-70
RD-20
UD-30
MCP flex-90
DIP hyperextension-10
MCP hyperextension-45
PIP flex-100
DIP flex-90
The wrist joint comprises the distal radius & ulna, 8 carpal bones, and the bases of 5 metacarpals. The carpal bones lie in two transverse
rows. The proximal row contains (lateral to medial) scaphoid (navicular), lunate, triquetrum, and pisiform. The distal row holds the
trapezium, trapezoid, capitate, and hamate.
Arthrokinematics:
Joint
Radiocarpal (opposite)
Mid carpal (same)
Metacarpophalangeal (same)
Motion to increase
Wrist extension
Wrist flexion
Wrist ulnar deviation
Wrist radial deviation
Wrist extension
Wrist flexion
Finger flexion
Finger extension
Mobilization glide
Anterior
Posterior
Lateral
Medial
Anterior
Posterior
Anterior (Ventral)
Posterior (Dorsal)
Closed pack position: Extension with radial deviation
Loose pack position: neutral with slight ulnar deviation
Capsular pattern: (wrist)=Flexion and extension equally limted (MCP and IP)=flexion more limited than extension
Common MMT for the wrist/hand:
1. Wrist flexion and radial deviation (flexor carpi radialis): Seated w forearm supinated and supported on a flat surface. Pt flexes and
deviates wrist to radial side while examiner maintains stabilization of forearm. Apply resistance along volar aspect of bases of first
and second metacarpals in direction of wrist ext and ulnar deviation. Gravity eliminated-seated w arm in neutral (halfway between
pronation and supination)
2. Wrist flexion and ulnar deviation (flexor carpi ulnaris): Seated w forearm supinated and supported. Pt flexes and deviates wrist to
ulnar side while examiner maintains stabilization of forearm. Apply resistance along volar aspect of 5th MC bone in direction of wrist
ext. Gravity eliminated-Same as other.
3. Wrist extension and radial deviation (extensor carpi radialos longus and brevis): Seated with forearm pronated and supported on a
flat surface. Pt extends and deviates wrist to radial side. Apply resistance along dorsal aspect of 1st and 2nd metacarpals in direction
of wrist flexion and ulnar deviation. Gravity eliminated-seated w forearm in neutral rotation, wrist in neutral position, forearm
supported.
4. Wrist extension and ulnar deviation (extensor carpi ulnaris): Seated with forearm pronated and supported. Pt extends and deviates
wrist to ulnar side. Apply resistance along dorsal aspect of 5th metacarpal in direction of wrist flexion and radial deviation. Gravity
eliminated-Seated w forearm in neutral rotation, and supported on surface.
5. Finger flexion(lumbricals, palmar and dorsal interossei): Seated with forearm fully supinated and supported, wrist in neutral,
fingers extended. Pt flexes MCP joints while extending IP joints. Apply resistance with one finger along volar surface of proximal
phalanx of 2nd-5th digits individually in direction of MCP extension. Gravity eliminated-Seated w forearm in neutral rotation and
supported on flat surface.
Special tests for the wrist/hand:
Ligamentous Instability
1. Ulnar collateral ligament instability test-The pt is positioned in sitting. The therapist holds the pts thumb in extension and applies a
valgus forace to the metacarpophalangeal joint of the thumb. A positive test is indicated by excessive valgus movement and may be
indicative of a tear of the ulnar collateral and accessory collateral ligaments. This type of injury is referred to as gamekeeper’s or skier’s
thumb.
Vascular Insufficiency
1. Allen test-Pt is positioned in sitting or standing. Pt is asked to open and close the hand several times in succession and then maintain the
hand in a closed position. Therapist compresses the radial and ulnar arteries. Pt is then asked to relax the hand and the therapist
releases the pressure on one of the arteries while observing the color of the hand and fingers. A positive test is indicated by delayed or
absent flushing of the radial or ulanr half of the hand and may be indicative of an occlusion in the radial or ulnar artery.
Contracture/Tightness
1. Bunnel-Littler test-Pt is positioned in sitting with the metacarpophalangeal joint held in slight extension. Therapist attempts to move
the PIP joint into flexion. If the PIP joint does not flex with the MCP joint extended, there may be a tight intrinsic muscle or capsular
tightness. If the PIP joint fully flexes with the MCP joint in slight flexion, there may be intrinsic muscle tightness without capsular
tightness.
2. Tight retinacular ligament test-The PIP joint is held in a neutral position while the therapist attempts to flex the DIP joint. If the
therapist is unable to flex the DIP joint, the retinacular ligaments or capsule may be tight. If the therapist is able to flex the DIP joint
with the PIP joint in flexion, the retinacular ligaments may be tight and the capsule may be normal.
Neurological Dysfunction
1. Froment’s sign-Pt is positioned in sitting or standing and is asked to hold a piece of paper between the thumb and index finger. The
therapist attempts to pull the paper away from the pt. A positive test is indicated by the pt flexing the distal phalanx of the thumb
due to adductor pollicis muscle paralysis. If at the same time, the pt hyperextends the metacarpophalangeal joint of the thumb, it is
termed Jeanne’s sign. Both objective findings may be indicative of ulnar nerve compromise or paralysis.
2. Phalen’s test-Pt is positioned in sitting or standing. Therapist flexes the pts wrists maximally and asks the pt to hold the position for
60 seconds. A positive test is indicated by tingling in the thumb, index finger, middle finger, and lateral half of the ring finger and
may be indicative of carpal tunnel syndrome due to median nerve compression.
3. Tinel’s sign-Pt is positioned in sitting or standing. Therapist taps over the volar aspect of the pts wrist. A positive test is indicated by
tingling in the thumb, index finger, middle finger, and lateral half of the ring finger distal to the contact site at the wrist. A positive
test may be indicative of carpal tunnel syndrome due to median nerve compression.
Miscellaneous
1. Finkelstein test-Pt is positioned in sitting or standing and is asked to make a fist with the thumb tucked inside the fingers. Therapist
stabilizes pts forearm and ulnarly deviates the wrist. A positive test is indicated by pain over the abductor pollicis longs and extensor
pollicis brevis tendons at the wrist and may be indicative of tenosynovitis in the thumb (De Quervain’s disease)
2. Grind test- Pt positioned in sitting or standing. The therapist stabilizes the pts hand and grasps pts thumb on the metacarpal.
Therapist applies compression and rotation through the metacarpal. A positive test is indicated by pain and may be indicative of
degenerative joint disease in the CMC.
3. Murphy sign-Pt is positioned in sitting or standing and is asked to make a fist. A positive test is indicated by the pts third metacarpal
remaining level with the second and fourth metacarpals. A positive test may be indicative of a dislocated lunate.
Wrist/hand conditions: (See chart for common MS pathologies)
1. Dupuytren’s Contracture:
•Observed as banding on palm and digit flexion contractures, resulting from contracture of palmar fascia that adheres to skin.
•Affects men more than women
•Contracture usually affects the MCP and PIP joints of 4th and 5th digits in nondiabetic individuals and affects 3rd and 4th digits most often
in individuals with diabetes.
Goals, outcomes, and Interventions-flexibility ex, splint application, promote restoration of normal hand function
2. Boutonniere deformity:
•Results from rupture of central tendinous slip of extensor hood.
•Observed deformity is extension of MCP and DIP with flexion of PIP.
•Commonly occurs following trauma, or in rheumatoid arthritis with degeneration of the central extensor tendon.
3. Swan neck deformity:
•Results from contracture of intrinsic muscles with dorsal subluxation of lateral extensor tendons.
•Observed deformity is flexion of MCP and DIP with extension of PIP.
•Commonly occurs following trauma, or with RA following degeneration of lateral extensor tendons.
4. Ape hand deformity:
•Observed as thenar muscle wasting, with first digit moving dorsally until it is in line with second digit.
•Results from median nerve dysfunction.
5. Mallet finger:
•Rupture or avulstion of extensor tendon at its insertion into distal phalanx of digit.
•Observed deformity is flexion of DIP joint.
•Usually occurs from trauma, forcing distal phalanx into a flexed position.
6. Gamekeeper’s thumb:
• A sprain/rupture of ulanr collateral ligament of MCP joint of first digit.
•Results in medial instability of thumb.
•Frequently occurs during a fall wile skiing, when increasing forces are placed on thumb through ski pole.
•Immobilized for 6 weeks.
7. Boxer’s fx:
•Fx of neck of 5th metacarpal
•Frequently sustained during a fight, or from punching a wall in anger
•Casted for 2-4 weeks
Hip:
Flexors: Psoas, Iliacus, Pectineus, Rectus femrois
Extensors: Glut max, semitendinosus, semimembranosus, biceps femoris (long head)
Abductors: glut med. Assist movers: glut min, TFL, Sartorius, rectus, piriformis (at 90° hip flex)
Adductors: Adductor magnus, adductor longus, adductor brevis, gracilis, pectineus
ER: Glut max, gemellus inferior & superior, obturator externus & internus, quadratus femoris, piriformis (at less than 60° hip flexion)
IR: TFL, glut min Assist movers: semitendinosus, semimembranosus, gracilis, piriformis (at 90° hip flexion)
ROM:
Flex-110-120°
Ext-10-15°
Abd-30-40°
Add-25-30°
ER-40-60°
IR-30-40°
Arthrokinematics:
Joint
Hip
Motion to increase
Abduction
ER/extension
IR/flexion
Mobilization Glide
Inferior
Anterior
Posterior
Closed packed position: full ext, medial rotation
Loose packed position: 30° flex, 30°abd, slight lateral rotation
Capsular pattern: most limited flexion, abduction, and medial rotation (sometimes medial rotation is most limited)
End-feels for the hip: Tissue stretch/approximation (flexion and adduction)
Common MMT of the hip:
1. Hip flexion (Iliacus and Psoas Major)-Seated with legs off side of treatment table, holding on to table edge with hands. Pt flexes hip
through range while keeping knee flexed. Apply resistance over anterior aspect of distal thigh in direction hip ext. Gravity eliminatedSidelying on side of lower extremity to be tested.
2. Hip flex, abd, and external rotation(Sartorius)-Seated with legs off side table, holding on to table. Pt will slide heel of limb being tested
up shin of opposite leg. Pt flexes, abducts, and externally rotates hip while flexing knee. Apply resistance. Gravity eliminated-Supine with
heel of lower extremity to be tested on ventral surface of contralateral ankle, contralateral lower extremity extended.
3. Hip extension (glut max, semitendinosus, semimembranosus, and biceps femoris)-Prone with lower extremities extended. Apply
resistance over posterior aspect of distal thigh in direction of hip flexion. Gravity eliminated-Sidelying on side of lower extremity to be
tested.
4. Hip abduction (glut med and min)-Sidelying with limb to be tested uppermost. Apply resistance over lateral aspect of distal thigh in
direction of hip adduction. Gravity eliminated-Supine with hips fully adducted.
5. Hip abduction with flexion (tensor fascia lata)-Sidelying with limb to be tested uppermost, hip or upper limb in 45° flexion an neutral
rotation, lower limb flexed for balance. Abduct pts hip 30°, maintaining hip in flexion, apply resistance over lateral aspect of distal thigh
in direction of hip adduction. Gravity eliminated-Long sitting, hips flexed to 45°, knees extended. Pt supports trunk by learning back on
extended arms.
6. Hip adduction (magnus, longus, brevis, pectineus, and gracils)-Sidelying on side of limb to be tested, pt may hold table for support. Pt
adducts hip of test limb, apply resistance on medial aspect of distal thigh in direction of hip abduction. Gravity eliminated-Supine with
non-test limb in full abduction.
7. Hip medial rotation(TFL, glut min and med)-Seated with legs hanging over table, with towel under knee of limb to be tested. Medially
rotate pts hip by moving foot laterally; resistance is applied in medial direction on lateral aspect of distal leg. Gravity eliminated-Supine
with limb to be tested in full hip lateral rotation.
8. Hip lateral rotation(piriformis, gemellus superior & inferior, obturator internus & externus, and quadratus)-Seated with legs off table,
towel under knee of test limb. Laterally rotate pts hip by moving foot medially. Apply resistance in lateral direction on medial aspect of
distal leg. Gravity eliminated-Supine with limb to be tested in full medial rotation.
Special tests for the hip:
Contracture/Tightness
1. Ely’s test-Pt is prone while the therapist passively flexes the pts knee. A positive test is indicated by spontaneous hip flexion occurring
simultaneously with knee flexion and may be indicative of a rectus femoris contracture.
2. Ober’s test-Pt is positioned in side-lying with the lower leg flexed at the hip and knee. The therapist moves the test leg into hip extension
and abduction and then attempts to slowly lower the test leg. A positive test is indicated by an inability of the test leg to adduct and
touch the table and may be indicative of a tensor fasciae latae contracture.
3. Piriformis test-Pt is positioned in sidelying with the test leg positioned toward the ceiling and the hip flexed to 60°. Therapist places one
hand on the pts pelvis and the other hand on the pts knee. While stabilizing the pelvis, the therapist applies a downward (adduction)
force on the knee. A positive test is indicated by pain or tightness, and may be indicative of piriformis tightness or compression on the
sciatic nerve caused by the piriformis.
4. Thomas test-Pt is positioned in supine with the legs fully extended. The pt is asked to bring one of their knees to the chest in order to
flatten the lumbar spine. The therapist observes the position of the contralateral hip while the pt holds the flexed hip. A positive test is
indicated by the straight leg rising from the table and may be indicative of a hip flexion contracture.
5. 90-90 straight leg raise test-The pt is positioned in supine and asked to stabilize the hips in 90° of flexion with the knees relaxed. The
therapist instructs the pt to alternately extend each knee as much as possible while maintaining the hips in 90° of flexion. A positive test
is indicated by the knee remaining in 20° or more of flexion and is indicative of hamstrings tightness.
Pediatric Tests
1. Barlow’s test-The pt is positioned in supine the hips flexed to 90° and knees flexed. The therapist tests each hip individually by stabilizing
the femur and pelvis with one hand while the other hand moves the test leg into abduction while applying forward pressure posterior to
the greater trochanter. A positive test is indicated by a click or clunk and may be indicative of a hip dislocation being reduced. The test is
considered to be a variation of Ortolani’s test.
2. Ortolani’s test-The pt is positioned in supine with the hips flexed to 90° and knees flexed. The therapist grasps the legs so that their
thumbs are placed along the pts medial thighs and the fingers are placed on the lateral thighs toward the buttocks. The therapist
abducts the pts hips and gentle pressure is applied to the greater trochanters until resistance is felt at approx 30°. A positive test is
indicated by a click or a clunk and may be indicative of a dislocation being reduced.
Miscellaneous
1. Craig’s test-Pt is positioned in prone with the test knee flexed to 90°. The therapist palpates the posterior aspect of the greater
trochanter and medially and laterally rotates the hip until the greater trochanter is parallel with the table. The degree of femoral
anteversion corresponds to the angle formed by the lower leg with the perpendicular axis of the table. Normal anteversion for an
adult is 8-15°.
2. Patrick’s test (FABER test)-The pt is positioned in supine with the test leg flexed, abducted, and externally rotated at the hip onto the
opposite leg. The therapist slowly lowers the test leg through abduction toward the table. A positive test is indicated by failure of the
test leg to abduct below the level of the opposite leg and may be indicative of iliopsoas, sacroiliac or hip joint abnormalities.
3. Quadrant scouring test-The pt is positioned in supine. The therapist passively flexes and adducts the hip with the knee in maximal
flexion. The therapist applies a compressive force through the shaft of the femur while continuting to passively more the pts hip. A
posistive test is indicated by grinding, catching or crepitation in the hip and may be indicative of pathologies such as arthritis,
avascular necrosis or an osteochondral defect.
4. Trendelenburg test-Pt is positioned in standing and is asked to stand on one leg for approx 10 seconds. A positive test is indicated by
a drop of the pelvis on the unsupported side and may be indicative of weakness of the gluteus medius muscle on the supported side.
Conditions of the hip (see MS chart):
1. Avascular necrosis (AVN)
•Multiple etiologies resulting in an impaired blood supply to the femoral head.
•Hip ROM is decreased in flexion, IR, and abduction
•Diagnositc tests utilized: plain film imaging, bone scans, CT, and MRI
•Symptoms include pain in the groin and/or thigh, and tenderness with palpation at the hip joint
•Coxalgic gait
•Corticosteriods contraindicated since they may be causative factor
Goals, outcomes, interventions-Joint/bone protection strategies, maintain joint mechanics and connective tissue functions.
Implementation of aerobic capacity/endurance conditioning, such as aquatics. Post surgical intervention includes regaining
functional flexibility, improving strength, and gait training.
2. Piriformis Syndrome
•Piriformis muscle is an external rotator of the hip and can become overworked with excessive pronation of the foot, causing
abnormal femoral internal rotation.
•Considered a tonic muscle that is active with motion of sacroiliac joint, particularly sacrum
•Tightness or spasm of the piriformis muscle can result in compression of sciatic nerve and/or sacroiliac dysfunction.
•Diagnostic tests utilized: possibly electrodiagnostic tests for sciatic nerve
•Signs & symptoms include: restriction in internal rotation, pain with palpation of piriformis muscle, referral of pain to the posterior
thigh, weakness in external rotation, positive piriformis test, uneven sacral base
•Perform lower extremity biomechanical examination to determine if abnormal biomechanics are the cause. Must rule out
involvement of lumbar spine and or SI joint.
•NSAIDS and neurontin
Goals, outcomes, interventions-Reduction of pain using modalities and manual therapy techniques, such as soft tissue massage to
piriformis, joint oscillations to hip or pelvis to inhibit pain, correction of muscle imbalances and biomechanical faults using
strengthening. Restore muscle balance and pt education regarding protection of the SI joint (instruction not to step off a curb onto
the dysfunctional LE)
Knee
“Screw home mechanism”-describes the 5° of tibial external rotation, which occurs during terminal knee extension. Occurs as closed-chain
internal femoral rotation during weight bearing to provide increased stability of knee joint during weight-bearing activities. Can also occur as
open-chain external tibial rotation. Unlocking occurs through action of popliteus. Open-chain unlocking occurs primarily with popliteal action.
Internal rotation of femur is the same as external rotation of tibia.
ROM:
Flex-135°
Closed pack position-full extension, lateral rotation of tibia
Loose-pack position-25° flex
Capsular pattern: flexion more limited than extension
Arthrokinematics:
Joint
Tibiofemoral (knee)
Patellofemoral
Motion to increase
Knee extension
Knee flexion
Knee extension
Knee flexion
Mobilization glide
Anterior/medial/lateral
Posterior
Superior
Inferior
Common MMT of the knee:
1. Knee extension (quadriceps femoris)-Seated with legs off side of table and towel under knee of test limb. Pt extends knee through full
range, apply resistance over anterior aspect of distal leg in direction of knee flexion. Gravity eliminated-Side lying on side to be tested,
knee fully flexed.
2. Knee flexion(biceps femoris, semitendinosus, and semimembranosus)-Prone with lower extremities extended. Flex pts knee to 90°,
rotating knee laterally. Apply resistance over posterior aspect of distal leg in direction of knee extension.(Biceps femoris) Prone with
lower extremities extended, flex pts knee to 90°, rotating knee medially (semitendinous and semimembranosus) Gravity eliminatedSidelying on side to be tested.
Special tests for the knee:
Ligamentous Instability
1. Anterior drawer test-Pt is positioned in supine with the knee flexed to 90° and the hip flexed to 45°. The therapist stabilizes the lower leg
by sitting on the forefoot. The therapist grasps the pts proximal tibia with two hands, places their thumbs on the tibial plateau, and
administers an anterior directed force to the tibia on the femur. A positive test is indicated by excessive anterior translation of the tibia
on the femur with a diminished or absent end-point and may be indicative of an anterior cruciate ligament injury.
2. Lachman test-Pt is positioned in supine with the knee flexed to 20-30°. The therapist stabilizes the distal femur with one hand and places
the other hand on the proximal tibia. The therapist applies an anterior directed force to the tibia on the femur. A positive test is
indicated by excessive anterior translation of the tibia on the femur with a diminished or absent end-point and may be indicative of an
ACL injury.
3. Lateral pivot shift test-Pt is positioned in supine with the hip flexed and abducted to 30° with slight medial rotation. The therapist grasps
the leg with one hand and places the other hand over the lateral surface of the proximal tibia. The therapist medially rotates the tibia
and applies a valgus force to the knee while the knee is slowly flexed. A positive test is indicated by a palpable shift or clunk occurring
between 20 and 40° of flexion and is indicative of anterolateral rotator instability. The shift or clunk results from the reduction of the
tibia on the femur.
4. Posterior drawer test-Pt is positioned in supine with the knee flexed to 90° and the hip flexed to 45°. The therapist stabilizes the lower
leg by sitting on the forefoot. The therapist grasps the pts proximal tibia with two hands, places their thumbs on the tibial plateau, and
administeres a posterior directed force to the tibia on the femur. A positive test is indicated by excessive posterior translation of the
tibia on the femur with a diminished or absent end-point and may be indicative of a PCL injury.
5. Posterior sag sign-Pt is positioned in supine with the knee flexed to 90° and the hip flexed to 45°. A positive test is indicated by the tibia
sagging back on the femur and may be indicative of a PCL injury.
6. Slocum test-Pt is positioned in supine with the knee flexed to 90° and the hip flexed to 45°. Therapist rotates the pts foot 30° medially to
test anterolateral instability. The therapist stabilzes the lower leg by sitting on the forefoot. Therapist grasps the pts proximal tibia with
two hands, places their thumbs on the tibial plateau, and administers an anterior directed force to the tibia on the femur. A positive test
is indicated by movement of the tibia occurring primarily on the lateral side and may be indicative of anterolateral instability. The test
can also be performed to assess anteromedial instability by rotating the pts foot 15° laterally.
7. Valgus stress test-Pt is positioned in supine with the knee flexed to 20-30°. The therapist positions one hand on the medial surface of the
pts ankle and the other hand on the lateral surface of the knee. The therapist applies a valgus force to the knee with the distal hand. A
positive test is indicated by excessive movement and may be indicative of a MCL sprain. A positive test with the knee in full extension
may be indicative of damage to the MCL, PCL, posterior oblique ligament, and posteromedial capsule.
8. Varus stress test-Pt is positioned in supine the knee flexed to 20-30°. The therapist positions one hand on the lateral surface of the pts
ankle and the other hand on the medial surface of the knee. The therapist applies a varus force to the knee with the distal hand. A
positive test is indicated by excessive varus movement and may be indicative of a LCL sprain. A positive test with the knee in full
extension may be indicative of damage to the LCL, PCL, arcuate complex, and posterolateral capsule.
Meniscal Pathology
1. Apley’s compression test-The pt is positioned in prone with the knee flexed to 90°. The therapist stabilzes the pts femur using one hand
and places the other hand on the pts heel. The therapist medially and laterally rotates the tibia while applying a compressive force
through the tibia. A positive test is indicated by pain or clicking and may be indicative of a meniscal lesion.
2. Bounce home test-The pt is positioned in supine. The therapist grasps the pts heel and maximally flexes the knee. The pts knee is
extended passively. A positive test is indicated by imcomplete extension or a rubbery end-feel and may be indicative of meniscal lesion.
3. McMurray test-The pt is positioned in supine. The therapist grasps the distal leg with one hand and palpates the knee joint with the
other. With the knee fully flexed, the therapist medially rotates the tibia and extends the knee. The therapist repeates the same
procedure while laterally rotating the tibia. A positive test is indicated by a click or pronounced crepitation felt over the joint line and
may be indicative of a posterior meniscal lesion.
Swelling
1. Brush test-Pt is positioned in supine. The therapist places one hand below the joint line on the medial surface of the patella and strokes
proximally with the palm and fingers and far as the suprapatellar pouch. The other hand then strokes down the lateral surface of the
patella. A positive test is indicated by a wave of fluid just below the medial distal border of the patella and is indicative of effusion in the
knee.
2. Patellar tap test-Pt is positioned in supine with knee flexed or extended to a point of discomfort. The therapist applies a slight tap over
the patella. A positive test is indicated if the patella appears to be floating and may be indicative of joint effusion.
Miscellaneous
1. Clarke’s sign-The pt is positioned in supine with the knees extended. The therapist applies slight pressure distally with web space of their
hand over the superior pole of the patella. The therapist then asks the pt to contract the quads muscle while maintaining pressure on
the patella. A positive test is indicated by failure to complete the contraction without pain and may be indicative of patellofemoral
dysfunction.
2. Hughston’s plica test-The pt is positioned in supine. The therapist flexes the knee and medially rotates the tibia with one hand while the
other hand attempts to move the patella medially and palpate the medial femoral condyle. A positive test is indicated by a popping
sound over the medial plica while the knee is passively flexed and extended.
3. Noble compression test-Pt positioned in supine with the hip slightly flexed and the knee in 90° of flexion. The therapist places the thumb
of one hand over the lateral epicondyle of the femur and the other hand around the pts ankle. The therapist maintains pressure over the
lateral epicondyle while the pt is asked to slowly extend the knee. A positive test is indicated by pain over the lateral femoral epicondlye
at approximately 30° of knee flexion and may be indicative of iliotibial band friction syndrome.
4. Patellar apprehension test-The pt is positioned in supine with the knees extended. The therapist places both thumbs on the medial
border of the patella and applies a laterally directed force. A positive test is indicated by a look of apprehension or an attempt to
contract the quads, in an effort to avoid subluxation and may be indicative of patella subluxation or dislocation.
Knee conditions (see MS chart)
1. Classification of ligament injuries:
Tissue Healing:
Acute Inflammatory Phase (2-3 days)
Proliferative/Repair Phase (Day 3-Week 8)
Remodeling Phase (Week 6-Month 12)
Grades of sprain:
Grade I-Mild stretch, no macroscopic tear, no functional instabililty; Healing time: 1-2 weeks
Grade II-Moderate stretch, partial tear, some functional instabililty; Healing time: 2-3 weeks
Grade III-Severe, complete tear/rupture; Healing time: 3-6 weeks (requires external bracing)
Repairs:
(Depending on the choice of graft, these healing times will follow these general guidelines)
•0-2 weeks-Maximum protection phase
-Focus on muscular control/proprioception
-Inflammatory/proliferative phase
•2-6 weeks-Moderate protection phase
-Restore normal gait, ROM
-Protect graft
-Proliferatieve phase
•6-12 weeks-Gradually-less-protection phase
-Improve confidence
-Progress strength, power, and proprioception
-Maturation phase
•12-24 weeks-Graded return to sport phase
-Return to former levels of function in a graded fashion
-Continue strength/flexibility/power
-Maturation p hase
•24 weeks-Return to sport
2. Tendon Healing:
Inflammatory phase-3-7 days
Proliferative phase-day 5-week 5
Remodeling phase-week 6-month 6
Tendonitis/overuse injuries:
-Remove offending activity
-Follow tissue healing guidelines
●Days 1-7
•PROM, AAROM (if tolerated), no loading
•Modalities (“stop the bleeding”)
●Days 7-Week 5
•Progressive addition of load from PROM to AAROM to AROM as tolerated
•Avoid adhesions between tendon and paratenon
•Provide cardiovascular perfusion to area (train well-leg/arm, increase heart rate and perfusion)
●Weeks 6-Month 6
•Progressively load tendon from AROM to resisted ROM
•This can include isometric, isotonic, isokinetic, and eccentric work
•GRADUAL and progressive loading as tolerated
3. Genu varum & valgum
•Normal tibiofemoral shaft angle is 6° of valgum
•Genu varum is an excessive medial tibial torsion, commonly referred to as “bowlegs”
•Genu varum results in excessive medial patellar positioning and the pigeon-toed orientation of the feet
•Genu valgum is an excessive lateral tibial torsion commonly referred to as “knock knees”
•Genu valgum results in excessive lateral patellar positioning
4. Anterior compartment syndrome
•Increased compartmental pressure resulting in a local ischemic condition
•Multiple etiologies: direct trauma, fracture overuse, and/or muscle hypertrophy
•Symptoms of chronic or exertional compartment syndrome are produced by exercise or exertion and descriped as a deep, cramping,
feeling
•Symptomes of acute ACS are produced by sudden trauma causing swelling within the compartment
•Diagnosis made by clinical exam
•Acute ACS is considered a medical emergency and requires immediate surgical intervention with fasciotomy.
5. Anterior tibial periostitis (shin splints)
•Musculotendinous overuse condition
•Three common etiologies:
1. Abnormal biomechanical alignment
2. Poor conditioning
3. Improper training methods
•Muscles involved include anterior tibialis and extensor hallucis longus
•Pain elicited with palpation of lateral tibia and anterior compartment
Goals, outcomes, interventions: correction of muscle imbalances and biomechanical faults using strengthening, endurance, and
coordination exercises. Flexibililty exercises for anterior compartment muscles, as well as the tricpes surae, to gain restoration of normal
function
Ankle/foot
-The talocrural joint is formed between the talus and the distal tibia.
-The posterior talofibular ligament (PTFL) is the strongest of the lateral ligament complex. It is rarely injured except in severe ankle sprains.
-The strength of the ankle ligaments from weakest to strongest is the ATFL, PTFL, CFL, and deltoid complex.
-The fibular (peroneal) muscles serve as both plantar flexors and evertors of the foot. The peroneus longus also abducts the forefoot in the
transverse plane, thereby serving as a support for the medial longitudinal arch.
ROM (ankle):
DF-0-20
PF-0-50
INV-0-35
EVR-0-15
ROM (subtalar):
INV-0-5
EVR-0-5
Closed pack position (talocrural): maximum DF
Loose pack position: 10° PF, midway between maximum inversion and eversion
Capsular pattern: Plantar flexion more limited than dorsiflexion
Closed packed position of (Subtalar, Midtarsal, and tarsometatarsal): Supination
Loose packed position: midway between extremes of range of movement
Capsular pattern of subtalar: limitation of varus range of movement
Capsular pattern of midtarsal: DF, PF, ADD, MR
Closed packed position of metatarsophalangel and interphalangeal: full extension
Loose packed position: Neutral(MTP); slight flexion (IP)
Arthrokinematics:
Joint
Talocrural
Subtalar
Motion to Increase
Plantarflexion
Dorsiflexion
Inversion
Eversion
Mobilization Glide
Anterior
Posterior
Lateral
Medial
Common MMT of the Ankle/foot:
1. Ankle plantarflexion: Weight-bearing test (Gastrocnemius and Soleus)-Standing on one leg (test limb), knee extended, foot flat on
floor. Pt rises on toes of weight bearing leg through range of plantar flexion, keeping knee extended. Pt repeats motion until
fatigued or stopped by examiner. (Soleus)-pt is standing on one limb, knee flexed, foot flat on floor. Pt demonstrates movement of
rising on toes with knee flexed. Gravity eliminated-side-lying on side to be tested.
2. Ankle plantarflexion: Non-weight bearing test (Gastroc & Soleus)-Prone with knee extended, foot off end of table, ankle neutral. Pt
plantarflexes ankle through ROM, apply resistance on superoposterior aspect of calcaneus in direction of ankle DF. Soleus-prone
with knee flexed to 90°, ankle neutral.
3. Ankle dorsiflexion and subtalar inversion-Seated with legs off table, ankle neutral. Dorsiflex and invert pts ankle through ROM,
apply resistance over dorsal surface of medial side of foot in direction of PF and eversion. Gravity eliminated-Supine with LE’s
extended, ankle of test limb in neutral, foot extended beyond edge of table.
Special tests of the ankle/foot:
Ligamentous Instability
1. Anterior Drawer test-Pt is positioned in supine. The therapist stabilizes the distal tibia and fibula with one hand, while the other
hand holds the foot in 20° of plantar flexion and draws the talus forward in the ankle mortise. A positive test is indicated by
excessive anterior translation of the talus away from the ankle mortise and may be indicative of an anterior talofibular ligament
(ATFL) sprain.
2. Talar tilt-Pt is positioned in sidelying with knee flexed to 90°. The therapist stabilizes the distal tibia with one hand while grasping the
talus with the other hand. The foot is maintained in a neutral position. The therapist tilts the talus into abduction and adduction. A
positive test is indicated by excessive adduction and may be indicative of a calcaneofibular ligament sprain.
Miscellaneous
1. Thompson test-Pt is positioned in prone with the feet extended over the edge of a table. The therapist asks the pt to relax and proceeds
to squeeze the muscle belly of the gastrocnemius and soleus muscles. A positive test is indicated by the absence of plantar flexion and
may be indicative of a ruptured Achilles tendon.
2. Tibial torsion test-Pt is positioned in sitting with the knees over the edge of a table. The therapist places the thumb and index finger of
one hand over the medial and lateral malleolus. The therapist then measures the acute angle formed by the axes of the knee and ankle.
Normal lateral rotation of the tibia is considered to be 12-18° in an adult.
3. True leg length discrepancy test-Pt is positioned in supine with the hips and knees extended, the legs 15-20 cm apart, and the pelvis in
balance with the legs. Using a tape measure, the therapist measures from the distal point of the ASIS to the distal point of the medial
malleoli. A positive test is indicated by a bilateral variation of greater than 1 cm and may be indicative of a true leg length discrepancy.
Conditions of the Foot/ankle (see MS chart):
1. Ligament sprains:
•95% of all ankle sprains involve lateral ligaments
•With lateral sprains, foot is plantar flexed and inverted at time of injury
2.
3.
4.
5.
6.
7.
•Diagnostic test utilized: MRI
Tarsal tunnel syndrome:
•Entrapment of the posterior tibial nerve or one of its branches within the tarsal tunnel
•Over/excessive pronation, overuse problems resulting in tendonitis of the long flexor and posterior tibialis tendon, and trauma may
compromise space in the tarsal tunnel
•Symptoms include pain, numbness, and paresthesias along the medial ankle to the plantar surface of the foot
•Diagnostic tests utilized: electrodiagnostic tests
•Positive Tinel’s sign at the tarsal tunnel
Goals, Outcomes, interventions: Use of orthoses to maintain neutral alignment, neurodynamic mobilization may be indicated
Charcot-Marie-Tooth Disease:
•Peroneal muscular atrophy that affects motor and sensory nerves
•May begin in childhood or adulthood
•Initially affects muscles in lower leg and foot, but eventually progresses to muscles of hands and forearm
•Slowly progressive disorder with varying degrees of involvement, depending on degree of genetic dominance.
•No specific treatment to prevent, since it is an inherited disorder.
Rearfoot varus (subtalar varus, calcaneal varus):
•Etiology-abnormal mechanical alignment of tibia, shortened rearfoot soft tissues, or malunion of calcanus.
•Deformity observed: rigid inversion of calcaneus when subtalar joint is in neutral position
Rearfoot valus:
•abnormal alignment of the knee (genu valgum) or tibial valgus
•Deformity observed: eversion of calcaneus with a neutral subtalar joint
Forefoot varus: inversion of forefoot
Forefoot valgus: eversion of forefoot
Cervical Spine
ROM:
Flex-45
Ext-45
Lateral flex-45
Rotation-60
Capsular pattern: Full flexion most limited followed by limited extension, and symmetric limitation of rotation and sidebending.
*Limitation of or pain on cervical rotation usually suggests pathology at the C1-C2 (atlantoaxial) segment, because most rotation occurs here.
Special tests of cervical region:
1. Foraminal compression test (Spurling’s)-Pt is positioned in sitting with the head laterally flexed. The therapist places both hands on top
of the subject’s head and exerts a downward force. A positive test is indicated by pain radiating into the arm toward the flexed side and
may be indicative of nerve root compression.
2. Vertebral artery test-Pt is positioned in supine. The therapist places the pts head into extension, lateral flexion, and rotation to the
ipsilateral side. A positive test is indicated by dizziness, nystagmus, slurred speech or loss of consciousness and may be indicative of
compression of the vertebral artery. **Performing mobilization/manipulation within cervical region w/out performing this test
beforehand would be considered a breach in standard care.
3. Hautant’s test-Differentiates vascular versus vestibular causes of dizziness/vertigo.
Two steps to this test:
1. Pt sitting with shoulders at 90° and palms up. Have pt close eyes and remain in this position for 30 seconds. If arms lose their
position, there may be a vestibular condition.
2. Pt sitting with shoulders at 90° and palms up. Have pt close eyes, and cue pt into head and neck ext with rotation right, then left,
remaining in each position for 30 seconds. If arms lose their position, the condition may be vascular in nature.
4.Transverse Ligament stress test (sharp-purser)-Tests integrity of transverse ligament. Pt supine, with head supported on table. Glide C1
anterior. Should be firm end-feel. Positive findings: soft end-feel, dizziness, nystagums, lump sensation in throat, nausea.
5. Lhermitte’s sign-Identifies dysfunction of spinal cord and/or an upper motor neuron lesion. Pt in long sitting on table. Passively flex pts
head and one hip, while keeping knee in extension. Repeat with other hip. Positive finding is pain down the spine and into the upper or lower
limbs.
6. Romberg test-Identifies upper motor neuron lesion. Pt standing, and closes eyes for 30 seconds. Excessive swaying during test indicates
positive finding.
Conditions of the cervical spine:
1. “Whiplash” acceleration/deceleration injury-occurs when excess shear and tensile forces are exerted on cervical structures. Structures
injured may include facets/articular processes, facet joint capsules, ligaments, disc, anterior/posterior muscles, fracture to odontoid
process and spinous processes, TMJ, sympathetic chain ganglia, spinal and cranial nerves.
Signs and symptoms-early include headaches, neck pain, limited flexibility, reversal of lower cervical lordosis and decrease in upper
cervical kyphosis, vertigo, change in vision and hearing, irritability to noise and light, dysesthesias of face and bilateral upper UEs,
nausea, difficulty swallowing, and emotional lability.
Late include chronic head and neck pain, limitation in flexibility, TMJ dysfunction, limited tolerance to ADLs, disequilibrium, anxiety, and
depression.
Common clinical findings include postural changes, excessive muscle guarding with soft tissue fibrosis, segmental hypermobility, and
gradual development of restricted segmental motion, crainial and caudal to the injury.
Medications: NSAIDS, muscle relaxants, trigger point injections, corticosteroid injection or by mouth
Goals, outcomes, interventions: Spinal manipulation, correction of muscle imbalance, joint mobs, pt education on elimination of harmful
positions, postural education. Manual or mechanical traction: cervical spine positioned at 15° of flexion to provide optium intervertebral
foraminal opening. Contraindications: joint hypermobility, pregnancy, RA. Down syndrome, or any other systemic disease that affects
ligamentous integrity.
Thoracic and Lumbar Spine
ROM:
Flex-80
Ext-25
Lateral flex-35
Rotation-45
Capsular pattern for both: lateral flexion and rotation equally limited, extension
Lumbar special tests:
1. Stork standing test-Identifies sponlylolisthesis. Pt standing on one leg, cue pt into trunk extension. Repeat with opposite leg on
ground. Positive finding is pain in low back with ipsilateral leg on ground.
2. McKenzie’s slide glide test-Differentiates between scoliotic curvature versus neurological dysfunction causing abnormal curvature
(lateral shift) of trunk. Test is performed if “lateral shift” of trunk is noted. Pt standing, stand on one side of pt so that upper trunk is
shifted toward you. Place your shoulders into pts upper trunk and wrap your arms around pts pelvis. Stabilize upper trunk and pull
pelvis, to bring pelvis and trunk into proper alignment. Positive test is reproduction of neurological symptoms as alignment of trunk
is corrected.
3. Bicyle (van Gelderen’s test)-Differentiates between intermittent claudication and spinal stenosis. Pt seated on stationary bike. Pt rides bike
while witting erect. Time how long they can ride at a set pace/speed. After a sufficient rest period, have pt ride bike at same speed while in a
slumped position. Determination is based on length of time pt can ride bike in sitting upright vs sitting slumped. If pain is related to spinal
stenosis, pt should be able to ride bike longer while slumped.
4. Standing flexion test-Tests the iliosacral motion and determines if there is a joint dysfunction and the side of involvement. The clinician palpates
both the PSISs and asks the pt to bend forward. The PSIS that either moves cranially first or farthest is considered the blocked or positive side.
Spinal conditions:
1. Spondyloysis/spondyloisthesis: Thought to congenitallyl defective pars interarticularis.
Spondylolysis is a fracture of the pars interarticularis with positive “Scotty dog” sign on oblique radiographic view of spine.
Spondylolisthesis is the actual anterior or posterior slippage of one vertebra on another, following bilateral fracture of pars
interarticularis. It can be graded according to amount of slippage from 1 (25% slippage) to 4 (100% slippage).
Diagnostic tests utilized: plain film (oblique to see fracture and lateral views to see slippage)
Clinical exam including stork test, helps identify this condition.
Goals, outcomes, and interventions: Dynamic stabilization of trunk, with particular emphasis on abdominals. AVOID EXTENSION
and/or other positions that add stress to the defect (extension, ipsilateral side-bending, and contralateral rotation). Braces such as
Boston brace and TLSO. Spinal manipulation may be contraindicated for this condition, particularly at the level of defect.
2. Spinal or intervertebral stenosis-Congenital narrow spinal canal or intervertebral foramen, coupled with hypertrophy of the spinal
lamina and ligamentum flavum or facets, as the result of age-related degenerative processes or disease. Results in vascular and/or
neural compromise.
Signs and symptoms: Bilateral pain and paresthesia in back, buttocks, thighs, calves, and feet. Pain decreases in spinal flexion,
increases in extension. Pain increases with walking. Pain relieved with prolonged rest.
Diagnostic tests utilized: plain films, MRI, and/or CT scan
Clinical exam including bicycle.
Goals, outcomes, and interventions: Perform flexion-based exercise, and exercises that promotes dynamic stability throughout the
trunk and pelvis. Avoid extension and/or other positions that narrow the spinal canal (ipsilateral sidebending or rotation)
3. Disc Conditions-Internal disc disruption: Internal structure of disc annulus is disrupted; however, external structures remain normal.
Most common in lumbar region.
Symptoms include constant deep, achy pain, and increased pain with movement. No objective neurological findings, although pt
may have referred pain in LE.
Regular CT or myelogram will not demonstrate any abnormal findings. Can be diagnosed by CT discogram or an MRI.
Goals, outcomes, interventions: Spinal manipulation may be contraindicated for this condition. Limit repetitive bending and twisting
movements, limiting UE overhead and sitting activities, and carrying heavy loads.
Posterolateral bulge/herniation-Most commonly observed disc disorder of lumbar spine due to three structural deficiencies:
Posterior disc is narrower in height than anterior disc, Posterior longitudinal ligament is not as strong and only centrally located in
lumbar spine, posterior lamellae of annulus are thinner.
Etiology-overstretching and/or tearing of annular rings, vertebral endplate and /or ligament structures, from high compressive
forces or repetitive microtrauma.
Results in loss of strength, radicular pian, paresthesia and inability to perform ADLS.
Goals, outcomes, interventions-exercise program to promote dynamic stability throughout trunk and pelvis and to provide optimal
stimulus for regeneration of disc. Positional gapping for 10 minutes to increase space within region of space occupying lesion.
If left posterolateral lumbar herniation is present:
-Have pt side-lying on right side, with pillow under right trunk, flex both hips and knees, rotate trunk to left (or pelvis to right), pt can
be taught to perform this at home.
Spinal manipulation may be contraindicated for this condition.
Sacroiliac Joint:
Special tests:
1. Gillet’s test (march test)-After palpating the PSISs, the pt stands on one leg and pulls the opposite knee toward the chest. The blocked or
dysfunctioning joint will not move while the normal joint will move inferiorly.
2. Long-sitting test-Used to determine if there is a posteriorly or anteriorly rotated innominate based on apparent leg length differences. If
the lower limb on the affected side appears longer with a pt lies supine, but shorter when sitting, the test is positive, indicating an
anterior innominate rotation on the affected side.
Long to short=anterior
If the lower limb is shorter in supine and appears to get longer when sitting, then a posterior innominate rotation exists on the affected
side.
Short to long=posterior
3. Sitting flexion test-therapist localizes the PSISs as the pt, in a sitting position, bends forward with arms across the chest and passes
elbows between the knees as if to touch the floor. The pts feet should be in contact with the floor or resting on a stool. A positive test
occurs when a blocked joint moves first and/or farther cranially.
4. Straight leg raise-Used to evaluate low back pain and can indicate the unilateral dysfunction of the SI joint. The test is positive if pain
extends from the back down the leg in the sciatic nerve distribution.
The cluster of 5 tests (3/5 to be positive) have a sensitivity of .91 and specificity of .87 related to SI joint pain. The tests are:
1. Distraction (applies cross arm pressure to both ASIS, + if increased pain)
2. Thigh thrust (pt supine with hip flexed to 90°, examiner applies posteriorly directed force through the femur, + if pain or symptoms
reproduced)
3. Gaenslen’s test (pt supine with one leg hanging over edge of table, other if flexed toward chest. Examiner applies firm pressure to both
the hanging leg and flexed, + if symptoms increase or reproduced)
4. Sacral thrust (pt lies prone and examiner applies a force vertically downward to the center of the sacrum, + if symptoms increased or
reproduced)
5. Compression test (pt positioned in sidelying with affected side up, hips are flexed approx 45° and knees flexed to 90°. Examiner applies a
force vertically downward on ASIS, + if symptoms increase or reproduced)
TMJ (see MS chart)
Capsular pattern: limitation of mouth opening
Closed packed position: Clenched teeth
Loose packed position: mouth slightly open
ROM:
Opening: 40mm
Rotation: 25mm
Translatory glide:15mm
GAIT:
Stance Phase (60% of gait cycle)
Swing Phase (40% of gait cycle)
Standard Terminology
Heel strike
Foot flat
Midstance
Heel off
Toe Off
Acceleration
Midswing
Deceleration
Rancho Los Amigos Terminology
Initial Contact
Loading response
Midstance
Terminal Stance
Pre-Swing
Initial Swing
Midswing
Terminal Swing
• = Standard terminology
( ) =Rancho terminology
Stance Phase:
•Heel strike: is the instant that the heel touches the ground to begin stance phase.
(Initial Contact): is the beginning of the stance phase that occurs when the foot touches the ground
•Foot flat: is the point in which the entire foot makes contact with the ground and should occur directly after heel strike.
(Loading response): corresponds to the amount of time between initial contact and the beginning of the swing phase for the other leg.
•Midstance: is the point during the stance phase when the entire body weight is directly over the stance limb.
(Midstance): corresponds to the point in stance phase when the other foot is off the floor until the body is directly over the stance limb.
•Heel off: is the point in which the heel of the stance limb leaves the ground.
(Terminal stance): begins when the heel of the stance limb rises and ends when the other foot touches the ground.
•Toe off: is the point in which only the toe of the stance limb remains on the ground.
(Pre-swing): begins when the other foot touches the ground and ends when the stance foot reaches toe off.
Swing phase:
•Acceleration: beings when toe off is complete and the reference limb swings until positioned directly under the body.
(Initial swing): beings when the stance foot lifts from the floor and ends with maximal knee flexion during swing.
•Midswing: is the point when the swing limb is directly under the body.
(Midswing): begins with maximal knee flexion during swing and ends when the tibia is perpendicular with the ground.
•Deceleration: begins directly after midswing, as the swing limb begins to extend, and ends just prior to heel strike.
(Terminal swing): beings when the tibia is perpendicular to the floor and ends when the foot touches the ground.
Phase
Heel Strike
Hip
Knee
Begins to
extend
from a
position of
20-40° of
flexion. Hip
in slight
add & ER.
Full knee
extension
before
heel
contact,
but
flexing as
heel
makes
contact.
Tibia
ER
Ankle
Moving into
PF
Foot
Supination
(rigid at heel
contact)
Muscle
Activity
Ant tib:
eccentric (to
control
pronation)
EHL & ED:
eccentric
(decelerate
PF)
Pos tib, soleus,
gastroc:
eccentric
(decelerate
pronation)
G max &
hams:
eccentric
(resist flexion)
Erector
spinae:
eccentric
Foot Flat
Hip moving
into ext,
add & IR.
20°
flexion,
moving
towards
extension.
IR
Midstance
Neutral
position,
pelvis
rotates
posteriorlly.
15°
Neutral
flexion
(moving
toward
extension)
PFDF
Pronation
(adapting to
support
surface)
3° DF
Neutral
(control trunk
flexion).
G max &
hams:
concentric (to
move hip into
extension).
After foot is
flat, quads
activity
becoming
concentric to
bring femur
over.
Pos tib,
soleus, FHL,
FDL: eccentric
to decelerate
movement
Pos tib,
soleus, &
gatroc:
concentric (to
supinate
subtalar and
metatarsal
joint)
Iliopsoas:
eccentric. Glut
med: creating
reverse action
to stabilize
opposite
pelvis. Quad
Heel Off
Toe Off
10-15°
extension,
abd, & ER.
Moving
towards
10° ext,
abd, & ER.
4° flexion
ER
15° DF
Moving
from full
ext to 40°
flexion.
ER
20° PF
Supination
(rigid for
push-off)
Supination
activity
decreasing
Quads activity
decreasing
Peroneus
longus & abd
hallucis:
concentric (to
PF 1st ray)
Peronus
brevis:
antagonist to
supinators of
subtalar and
metatarsal
joints. FHL,
EHL, EHB, &
intrinsics:
concentric
stability.
Adductor
magnus:
eccentric (to
control pelvis)
Reaction
forces moving
posterior to
knee. Quadseccentric
Phase
Acceleration to
Midswing
Hip
Slight flexion (015°) moving at 30°
flexion and
external rotation
to neutral
Knee
30°-60° knee
flexion and
external rotation
of tibia moving
toward neutral.
Ankle& Foot
20° DF and slight
pronation
Midswing to
Deceleration
Continued flexion
at about 30° to 40°
Moving to near
full extension &
slight lateral tibial
rotation
Ankle in neutral;
foot in slight
supination
Muscle Activity
Hip: flexors
working
concentrically to
bring limb
through;
contralateral glut
med concentrically
contracting to
maintain pelvis
position.
Hamstrings
concentrically
contracting.
Dorsiflexors
contracting
concentrically.
Glut max
contracting
eccentrically to
slow hip flexion.
Quads contracting
concentrically &
hamstrings
eccentrically.
Dorsiflexors
contracting
isometrically.
Peak Muscle Activity During the Gait cycle:
Tibialis anterior:
Peak activity is just after heel strike. Responsible for eccentric lowering
of the foot into plantar flexion.
Gastroc-soleus
Peak activity is during late stance phase. Responsible for concentric
group:
raising of the heel during toe off.
Quadriceps group: Two periods of peak activity. In periods of single support during early
stance phase and just before toe off to initiate swing phase.
Hamstrings group: Peak activity is during late swing phase. Responsible for decelerating
the unsupported limb.
ROM Requirements for Normal gait:
Hip flexion
0-30°
Hip extension 0-10°
Knee flexion
0-60°
Knee
0°
extension
Ankle DF
0-10°
Ankle PF
0-20°
Gait terminology:
•Base of support-the distance measured between the left and right foot during progression of gait. The distance decreases as cadence increases.
The average base of support for an adult is 2-4 inches.
•Cadence-the number of steps an individual will walk over a period of time. The average value for an adult is 110-120 steps per minute.
•Degree of toe-out-the angle formed by each foot’s line of progression and a line intersecting the center of the heel and second toe. The
average degree of toe-out for an adult is 7°
•Step length-the distance measured between right heel strike and left heel strike. The average for an adult is 28 inches.
•Stride length-the distance measured between right heel strike and the following right heel strike. The average for an adult is 56 inches.
Abnormal gait patterns:
•Antalgic-a protective gait pattern where the involved step length is decreased in order to avoid weight bearing on the involved side, usually
secondary to pain.
•Ataxic-a gait pattern characterized by staggering and unsteadiness. There is usually a wide base of support and movements are exaggerated.
•Cerebellar-a staggering gait pattern seen in cerebellar disease.
•Circumduction-a gait pattern characterized by a circular motion to advance the leg during swing phase; this may be used to compensate for
insufficient hip or knee flexion or dorsiflexion.
•Double step-a gait pattern in which alternate steps are of a different length or at a different rate.
•Equine-a gait pattern characterized by high steps; usually involves excessive activity of the gastrocnemius.
•Festinating-a gait pattern where a pt walks on toes as though pushed. It starts slowly, increases, and may continue until the pt grasps an object
in order to stop.
•Hemiplegic-a gait pattern in which pts abduct the paralyzed limb, swing it around, and bring it forward so the foot comes to the ground in front
of them.
•Parkinsonian-a gait pattern marked by increased forward flexion of the trunk and knees; gait is shuffling with quick and small steps; festinating
may occur.
•Scissor-a gait pattern in which the legs cross midline upon advancement
•Spastic-a gait pattern with stiff movement, toes seeming to catch and drag, legs held together, and hip and knee joints slightly flexed.
Commonly seen in spastic paraplegia.
•Steppage-a gait pattern in which the feet and toes are lifted through hip and knee flexion to excessive heights; usually secondary to dorsiflexor
weakness. The foot will slap at initial contact with the ground secondary to the decreased control.
•Tabetic-a high stepping ataxic gait pattern in which the feet slap the ground.
•Trendelenburg-a gait pattern that denotes gluteus medius weakness; excessive lateral trunk flexion and weight shifting over the stance leg.
•Vaulting-a gait pattern where the swing leg advances by compensating through the combination of elevation of the pelvis and plantar flexion of
the stance leg.
MS Interventions:
Orthopaedic Surgical Repairs:
1. Surgical repairs of upper extremity:
a. Rotator Cuff tears
i. Usually degenerative and occur over time, with impingement of supraspinatus tendon between the greater tuberosity
and acromion.
ii. Signs and symptoms include:
-Significant reduction in AROM into abduction
-No reduction of PROM
-Drop arm test is positive
-Poor scapulothoracic and glenohumeral rhythm
b. Diagnostic tests utilized: arthrogram traditionally had been the “gold standard” test. MRI may be done, but may not be as
sensitive.
c. PT goals, outcomes, and interventions:
-Rehab is initiated, following a period of immobilization with surgical intervention
-PT intervention emphasizes return or normal strength/endurance/coordination of muscles, joint mechanics, flexibility
(AROM/PROM), and scapulothoracic and glenohumeral rhythm with overhead function.
2. Tendon injuries and repairs of the hand:
a. Flexor tendon repairs
i. First 3-4 weeks, distal extremity is immobilized with a protective splint, with wrist and digits flexed. Rubber band
traction is applied to maintain interphalangeal joints in 30-50° of passive flexion.
ii. PT goals, outcomes and interventions:
1. Pt can perform resisted extension and passive flexion with constraints of splint. AROM to tolerance is initiated at
4 weeks.
2. Goal is to manage all soft tissues through wound-healing phases by providing collagen remodeling, which
preserves free tendon gliding.
3. Early intervention consists of wound management, edema control, and passive exercises.
4. Active extension exercises are initiated first followed by flexion.
5. Resistive and functional exercises are introduced when full AROM is achieved.
b. Extensor tendon repairs
i. Distal repairs are immobilized such that the distal interphalangeal joints are in neutral for 6-8 weeks.
ii. PT goals, outcomes, and interventions:
1. AROM is initiated at 6 weeks, with PIP joints in neutral
2. Goal is to manage all soft tissues through wound-healing phases by providing collagen remodeling, which
preserves free tendon gliding
3. Early intervention consists of wound management, edema control, and passive exercises.
4. Active extension exercises are initiated first, followed by flexion.
5. Resistive and functional exercises are introduced when full AROM is achieved.
6. Proximal repairs are immobilized, with the wrist and digital joints in extension for 4 weeks.
7. PT goals, outcomes, and interventions: Early AROM/PROM in flexion with MCP joint in extension. At 6 weeks,
full AROM is initiated into flexion and extension.
3. Surgical repairs of lower extremity:
a. Total hip replacement/arthroplasty (THR):
This info may vary, depending on surgical procedure and/or MD preference/protocol. Must be familiar with
postoperative protocol for each patient relative to procedure and/or MD.
b. Cemented vs. non-cemented.
i. Cemented hips can tolerate full weight bearing immediately following surgery.
ii. Cement may crack with aging, causing a loosening of prosthesis. Noncemented technique is more stressful on bones
during the surgical procedure.
iii. Noncemented procedures are typically used with younger and/or more active individuals. Cemented technique may be
better for those who will benefit from immediate ability to weight bear e.g. those with dementia or significant
debilitation.
iv. Bed positioning with a wedge to prevent adduction
v. Pt should avoid the position of hip flexion >90° with adduction and IR.
vi. Partial weight bearing to tolerance is initiated on the second post-surgery day, using crutches or a walker with typical
surgical procedures.
vii. PT goals, outcomes, and interventions: PT focuses on bed mobility, transitional movements, ambulation, and return to
premorbid ADLs.
c. Open reduction internal fixation (ORIF) following femoral fx:
i. Pt will typically be non-weight bearing for 1-2 weeks, using crutches or a walker. Thereafter, the pt will be partial weight
bearing as tolerated.
ii. PT goals, outcomes, and interventions: Pt focus on bed mobility, transitional movements, ambulation, and return to
premorbid ADLs. Important to note that guidelines/precautions can vary significantly.
d. Total knee replacement/arthroplasty (TKR):
i. TKR surgery is typically performed as a result of severe DJD of the knee joint, which has lead to pain and impaired
function.
ii. PT goals, outcomes, interventions: Goals of early rehab (1-3 weeks) include muscle reeducation, soft tissue mobilization,
lymphedema reduction, and initiation of PROM (CPM), AROM, and reduction of postsurgical swelling.
iii. Goals of the second phase of rehab include regaining endurance, coordination, and strength of the muscles surrounding
the knee. Functional activities include progressive ambulation stair climbing, as well as transitional training based on
healing and the type of prosthesis used.
iv. Goals and outcomes of the last phase of rehab include returning the pt to premorbid ADLs. Functional and endurance
training and proprioceptive exercises introduced during this phase.
v. The weight bearing status of pts with a cemented prosthesis is at the level of the pts tolerance. Pts with cementless
prostheses are progressed according to the time frame for fx healing. Weight bearing is 25% at 1-7 weeks, 50% by week
8, 75% by week 10, and 100% without an AD by week 12.
vi. Avoidance of forceful mobilization and PROM into flexion >90° is important, because of the mechanical restraints of the
prosthesis.
vii. Biomechanical faults caused by joint restrictions should be corrected with joint mobilizations to the specific restrictions
identified during the exam.
e. Ligamentous repairs of the knee
i. Six phases of rehab are followed with ACL and PCL reconstructive surgery.
Anterior cruciate ligament reconstruction:
-Immediately following surgery, a CPM unit is utilized, with PROM from 0°-70° of flexion.
-Motion is increased to 0°-120° by the 6th week.
-Reconstruction is usually protected with a hinged brace set at 20°-70° of flexion initially.
-Pt is non-weight bearing for approx 1 week.
-Weight-bearing progresses as tolerated to full weight bearing
-Pt is weaned from brace between the 2nd and 4th weeks
Posterior cruciate ligament reconstruction:
-Generally similar to ACL repair, except is often initially in hinged brace at 0° during ambulation.
-6 phases of rehab for ACL/PCL are as follows: Preoperative, maximum protection, controlled motion, moderate protection,
minimum protection, and return to activity.
-Specific interventions:
-Soft tissue massage to quad/hams to reduce muscle guarding; joint oscillations to inhibit joint pain and muscle
guarding; correction of muscle imbalances and biomechanical faults; progress to functional training based on pts occupation and
recreation.
Lateral retinacular release:
-Typically performed as a result of patellofemoral pain syndrome (PFPS). Purpose of procedure is to restore normal tracking of the patella during
contraction of the quads muscle.
PT intervention:
1. Should emphasize closed kinetic chain exercises to strengthen quadriceps muscle and regain dynamic balance of all structures
(contractile and noncontractile) surrounding knee.
2. Normalize the flexibility of the hamstrings, triceps surae, and ITB will help restore mechanical alignment.
3. Mobilization of patella is important to maintain nutrition and decrease the likelihood of adhesions.
Meniscal arthoscopy:
1. Partial meniscectomy:
a. Partial weight bearing as tolerated when full knee extension is obtained
b. PT goals, outcomes, and interventions:
i.
ii.
iii.
iv.
Initial goals focus on edema/effusion control
AROM is urged after surgical day 1.
Isotonic and isokinetic strengthening by day 3.
Jogging on the ball of the foot or toes is recommended to decrease the loading of the knee joint.
2. Repairs
a. Pt will be non-weight bearing for 3-6 weeks
b. Rehab of the joint begins within 7-10 days of procedure.
c. PT goals, outcomes, interventions: Soft tissue/massage to quad/hams, joint oscillations, correction of muscle imbalances,
biomechanical faults, progression to functional training
3. Surgical repairs of spine:
a. Rehab varies according to the type of surgery performed.
b. A back protection program and early mobilization exercises should be initiated prior to surgery.
c. Pts should avoid prolonged sitting, heavy lifting, and long car trips for approx 3 months.
d. Repetitive bending with twisting should always be avoided.
e. With microdiscetomies, rehab time is decreased bc the fibers of the annulus fibrosus are not damaged.
f. With laminectomy/discectomy, early movement and activation of paraspinal musculature (especially mulitfidus) is necessary.
g. Multilevel vertebra fusion:
i. Typically requires 6 weeks of trunk immobility with bracing
ii. Once brace is removed and movement is allowed, important to regain as much normal/functional movement as
possible, while restoring functional activation of muscles.
iii. With combined anterior/posterior surgical approach, bracing is seldom used.
h. With Harrington rod placement for idiopathic scoliosis, rehab goals focus on early mobilization in bed and effective coughing.
i. The pt can begin ambulation between the 4th and 7th postoperative days
j. The pt should avoid heavy lifting and excessive twisting and bending.
k. PT goals, outcomes, and interventions: Soft tissue/massage to paraspinal muscles; joint oscillations to inhibit joint pain,
correction of muscle imbalances, make sure that multifidus function is restored.
Interventions for Patients/clients with Acute Conditions
o Acute Phase
 Immobilization with limited (1-2 days) bed rest. Use of braces, slings, corsets, cervical collars, assistive devices, and taping
 Control inflammatory response (RICE)
 Physical agents: ice and electrical stimulation
 Compression and elevation to reduce and prevent effusion and swelling.
 NSAIDs
 Rest/relaxation to reduce pain
 Soft tissue/massage techniques
 Assisted movement of injured tissue
 Joint oscillations (grade 1-2) for pain relief
 Therapeutic exercise
 Dose of 40-60% of one rep max to stimulate regeneration of tissue and revascularization.
 Exercise should be nontraumatic, meaning no pain and/or increased edema as a result of the exercise.
 Educate Pt/client on joint protection strategies
o Subacute phase
 Avoidance of continued irritation and repetitive trauma.
 Modify activities at home/work/recreation
 Modify use of equipment or type of equipment at home/work/recreation
 Correct biomechanical faults, such as leg length discrepancy, abnormal foot biomechanics, abnormal throwing motion.
 Joint mobilization
 Continued therapeutic exercises, including flexibility/endurance/coordination exercise.
 Postural reeducation
 Biomechanical education
o Functional restoration phase
 Maintain or return to optimal level of Pt function
 Normalize flexibility of joints and related soft tissues
 Restore loading capacity of connective tissues to normal strength
 Functional strengthening exercise
 Functional stabilization of the involved joint/region.
Interventions for Patients/Clients with a Chronic Condition
o Determine possible causative factors
 Abnormal remodeling of injured tissues
 Chronic low-grade inflammation due to repetitive stresses of tissues.
o Reduce stresses to tissues
 Identify/eliminate magnitude of loading
 Identify/eliminate direction of forces
 Identify and eliminate any biomechanical barriers that are preventing haling
 Pt education regarding protection of joints and associated soft tissues.
o Regain structural integrity
 Improving flexibility
 Postural reeducation
 Increasing tissue capacity to tolerate loading
 Functional strengthening, endurance, and coordination exercises.
o Resume optimal patient function and prevention of reoccurrence
 Pt education regarding causative factors in dysfunction
 Work conditioning
Specific Interventions:
o Soft tissue/myofascial techniques
 Aid in reduction of metabolites for muscle, reactivating a muscle that has not been functioning secondary to guarding and ischemia,
revascularization of muscle, and also decreased guarding in a muscle
 Autonomic: stimulation of skin and superficial fascia to facilitate a decrease in muscle tension.
 Mechanical: movement of skin, fascia, and muscle causes histological and mechanical changes to occur in soft tissue to produce improved
mobility and function.
 Goals: decrease pain, edema, and muscle spasm, increase metabolism and cutaneous temp, stretch tight muscles and other soft tissues,
improve circulation, strengthen weak muscles, and mobilize joint restrictions.
 Indications: Pt with soft tissue and joint restrictions that result in pain and limits in ADLs
 Contraindications
 Absolute- soft tissue breakdown, infection, cellulitis, inflammation, and or neoplasm.
 Relative- hypermobility and sensitivity
 Traditional massage techniques such as effleurage and petrissage
 Functional Massage
 Three techniques used to assist in reactivation of a debilitated muscle and/or to increase vascularity to a muscle.
o Soft tissue without motion
 Traditional technique; however hands do not slide over skin; instead, they stay in contact with the skin while hands and skin move together
over the muscle.
 Direction of force is parallel to muscle fibers, and total stroke time should be 5-7 seconds.
o Soft tissue with passive pumping
 Place muscle in shortened position and with one hand place tension on muscle parallel to muscle fibers.
 Other hand passively lengthens muscle and simultaneously gradually releases tension of hand in contact with muscle.
o Soft tissue with active pumping
 Place muscle in lengthened position, and with one hand place tension on muscle, perpendicular to muscle fiber.
 Other hand glides limb as Pt actively shortens muscle. As muscle shortens, gradually release tension of hand in contact with muscle.

Transverse Friction Massage
o Used to initiate an acute inflammatory response for a tissue that is in metabolic stasis, such as a tendonosis.
o Involved tendon is briskly massaged in a transverse fashion
o Performed for 5-10 min and tends to be very uncomfortable for the pt
 Movement approaches require the pt to actively participate in treatment.
Examples include:
o Feldenkrais
 Facilitates development of normal movement patterns
 The practitioner uses skillful, supportive, gentle hands to create a sense of safety, maintain supportive contact, while introducing new
movement possibilities in small, easily available increments.
o Muscle energy techniques
 Include voluntary contraction in a precisely controlled direction, at varying levels of intensity, against an applied counterforce from the
clinician.
 Purpose is to gain motion that is limited by restrictions of the neuromuscular system.
 Modification of PNF technique
o PNF hold-relax-contract technique
 Antagonist of the shortened muscle is contracted to achieve reciprocal inhibition and increased range
o Articulatory techniques
 Joint oscillations
 Inhibit pain and/or muscle guarding
 Lubricate joint surfaces
 Provide nutrition to the joint structure
 Grades 3-4 are beneficial to stretch tight connective tissue
 Five grades of joint play in neutral
 Grade I oscillations are small amplitude at the beginning of the range of joint play.
 Grade II oscillations are large amplitude at the midrange of joint play.
 Grade III oscillations are large amplitude at the end range of joint play.
 Grade IV oscillations are small amplitude at the end of joint play.
 Grade V is a manipulation of high velocity and low amplitude to the anatomical endpoint of a joint.
 Indications for use of oscillation grades, per Maitland
 Grade I and II are used to improve joint lubrication/nutrition, as well as decrease pain and muscle guarding.
 Grades III and IV are used to stretch tight muscles, capsules, and ligaments
 Grade V is used to regain normal joint mechanics, as well as decrease pain and muscle guarding.
 Contraindications
 Absolute: joint ankylosis, malignancy involving bone, disease that affects the integrity of ligaments, arterial insufficiency, and active
inflammatory and/or infective process.
 Relative: arthrosis (DJD), metabolic bone disease, hypermobility, total joint replacement, pregnancy, spondylolisthesis, use of steroids, and
radicular symptoms.
 Joint mobilization (nonthrust)
 To stretch/lengthen/deform collagen and normalize the arthrokinematic glide of joint structures.
 Grades of translatoric glide, as described by Kaltenborn:
o Grade I
 Loosening translatoric glide
 Movement is very small amplitude traction force
 Used to relieve pain and/or decompress a joint during joint glides, performed within examination or intervention.
o Grade II
 Tightening translatoric glide.
 Movement takes up slack in tissues surrounding joint.
 Used to alleviate pain, assess joint play, and/or reduce muscle guarding.
o Grade III
 Stretching translatoric glide
 Movement stretches tissue crossing joint
 Used to assess end-feel, or to increase movement (stretch tissue)
 Traction: manual, mechanical, and self or auto traction
 Vertebral bodies separating
 Distraction and gliding of facet joints
 Tensing of the ligamentous structures of the spinal segments
 Intervertebral foramen widening
 Spinal muscle stretching
 Contraindications
 Absolute: joint ankylosis, malignancy involving bone, disease that affect the integrity of ligaments, arterial insufficiency, and active
inflammatory and/or infective process.
 Relative: arthrosis (DJD), metabolic bone disease, hypermobility, total joint replacement, pregnancy, spondylolisthesis, use of steroids, and
radicular symptoms.
 Manipulation thrust
 Inhibit pain and/or muscle guarding
 Improve translatoric glide in cases of joint dysfunction due to restriction.
 Health-care practitioners who commonly perform manipulative thrusts include physical therapist, osteopaths, chiropractors, and medical
doctors.
 Types of manipulations
o Generalized
 Fairly forceful, long lever techniques intended to include as many vertebral segments as possible.
 More commonly performed by chiropractors
o Specific
 Aimed at having an effect on either a specific segment or only a few vertebral segments.
 Uses minimal force with short lever arms
 Often include locking techniques based on biomechanics to ensure that a specific vertebral segment receives the manipulative thrust.
 More commonly performed by a PT.
o Mid-range
 Vary gently, short lever arm technique
 Barrier is created in mid-range by specific positioning of patient as well as creating tautness in surrounding soft tissues.
 More commonly performed by osteopathic practitioners.
 Contraindications
 Absolute: joint ankylosis, malignancy involving bone, disease that affect the integrity of ligaments, arterial insufficiency, and active
inflammatory and/or infective process.
 Relative: arthrosis (DJD), metabolic bone disease, hypermobility, total joint replacement, pregnancy, spondylolisthesis, use of steroids, and
radicular symptoms.
 Common mistakes in performing a thrust manipulation
 Not communicating clearly with the pt regarding the technique.
 Taking too long to position the pt
 Not performing the trial thrust prior to the actual thrust
 Not allowing the person to bottom out with their breath prior to performing the thrust.
 Taking up the slack as the Pt exhales and then letting off with pressure prior to the thrust
 Velocity too slow/amplitude to great.

Suggested algorithm to perform a manipulation
 Consider indications and contraindications
 Explain the intensions and implications regarding manipulation to the Pt
 Describe the actual technique to the Pt
 Place the Pt into position and assess for Pt comfort
 Perform a pre-thrust force into the rage to determine Pt comfort.
 Ask Pt to inhale and then exhale. Take up the slack into the range as they exhale.

When they reach the end of exhalation perform the thrust.
o Neural tissue mobilization
 Movement of neural structures to regain normal mobility.
 Tension test for upper and lower extremities
 Movement of soft tissues that may be restricting neural structures
 Indications: used for pts who have some type of restriction in neural mobility, anywhere along the course of the nerve.
 Postural reeducation: to open up the intervertebral foramen and decrease tension to tissue.
 Contraindications: extreme pain and/or increase in abnormal neurological signs
Determine whether managing irritated or nonirritated neurologic tissue:
1. Irritated tissue
a. Utilize grade II mobilizations (based on Maitland scale): should be nonpainful
2. Nonirritated tissue:
a. Utilize garde III mobilizations to engage the barrier but remain nonpainful.
Therapeutic exercise for ms conditions:
1. Therapeutic exercise is indicated to:
a. Decrease muscle guarding
b. Decrease pain
c. Increase vascularity of tissue
d. Promote regeneration and/or speed up recovery of connective tissues, such as cartilage, tendons, ligaments, capsules,
intervertebral discs
e. Mobilize restricted tissue to increase flexibility
f. Increase endurance of muscle
g. Increase coordination of muscle
h. Sensitize muscles to minimize joints going into excessive range, in cases of hypermobility
i. Develop dynamic stability and functional movement patterns, allowing for optimal function within the environment
2. Home exercise program for pts with ms conditions:
a. Pts home program will consist of exercsies to reinforce clinical program
b. Necessary to perform enough repetitions for desired physiological effect on appropriate tissues, as well as to develop coordination
and endurance in order to promote dynamic stability within functional patterns.
3. Dry Needling
a. Also referred to intramusuclar manual therapy (IMT)
b. Utilized to break up trigger points in myofascial pain syndrome
c. A solid filiform needlel is inserted into the trigger point (within the muscle)
Manual Therapy Approaches in Rehab:
1. All approaches proved a philosophical basis, subjective evaluation, objective examination, a diagnosis, and a plan of care.
2. Approaches can be divided into three categories:
a. Physician generated.
i. Mennell believed the joint is the dysfunctional unit.
ii. Osteopaths suggest that any component of the somatic system is responsible for dysfunction.
iii. Cyriax contends that dysfunction is due to interplay between contractile and noncontractile tissues.
b. Physical Therapist Generated
i. Mckenzie feels that postural factors preciptiate discal dysfunction. Treatment emphasizes the use of extension
exercises.
ii. Maitland proposes that the subjective evaluation should be integrated with objective measures to determine the
dysfunctional area
iii. Kaltenborn believes that abnormal joint mobility and soft tissue changes account for dysfunction
c. Chiropractic generated
i. Focus is to restore normal joint function through soft tissue and joint manipulation. Chiropractics believe that
restoration of normal biomechanical function affects other systems of the body as well, thus improving the state of
health in many ways.
Psychosocial Considerations:
1. Malingering (symptom magnification syndrome)
a. Defined as a behavioral response where displays of symptoms control the life of the patient, leading to functional disability.
b. There may be psychological advantages to illness.
i. The pt may feel protected from the threatening world.
ii. Uncertainty or fear about the future.
iii. Social gain
iv. Reduces stressors
c. Therapist needs to recognize symptoms and respond to the pt
i. Tests to evaluate malingering back pain may include Hoover test, Burn’s test, and Waddell’s signs.
ii. Hoover test involves the therapists evaluation of the amount of pressure the pts heels place on the therapists hands
when the pt is asked to raise one lower extremity while in a supine position.
iii. Burn’s test requires the pt to kneel and bend over a chair to touch the floor.
iv. Waddell’s signs evaluate tenderness, simulation tests, distraction tests, regional disturbances, and overreaction.
Waddell’s scores can be predictive of functional outcome.
v. Functional capacity evaluations are used to evaluate psychosocial as well as physical components of disability.
vi. Emphasize regaining functional outcomes, not pain reduction.
d. Secondary gain.
i. Usually some type of financial gain for staying ill.
ii. Workers compensation
iii. Larger settlement for injury claims
iv. Frequently seen in clinics that manage industrial injuries
v. May not want to return to work for various reasons associated with the work environment (stress, disliking
coworkers)
MS Imaging:
Tissue
Air
Fat
Bone Cortex
Radiograph
Black
Poorly visualized
White
CT
Black
Black
White
TI MRI
Black
White
Black
T2 MRI
Black
Gray
Black
Bone Marrow
White
Gray
White
Gray
Neuromuscular Examination:
Blood Supply to the Brain:
Blood Supply to the Brain
Anterior cerebral artery (ACA): anterior frontal lobe; medial surface of
frontal & parietal lobes
Middle Cerebral artery (MCA): most of outer cerebrum, basal ganglia,
posterior and anterior internal capsule, putamen, pallidum, lentiform
nucleus
Posterior cerebral artery (PCA): portion of midbrain, subthalamic
nucleus, basal nucleus, thalamus, inferior temporal lobe, occipital and
occipitoparietal cortices
Expected Possible Impairment
-Contralateral LE motor and sensory involvement
-Loss of bowel and bladder control
-Loss of behavioral inhibition
-Significant mental changes
-Neglect
-Aphasia
-Apraxia & agraphia
-Perservation
-Akinetic mutism with significant bilateral involvement
-Most common site of CVA
-Wernike’s aphasia in dominant hemisphere
-Homonymous hemianopsia
-Apraxia
-Flat affect with right hemisphere damage
-Contralateral weakness and sensory loss of face and upper extremity
with lesser involvement in the lower extremity
-Impaired spatial relations
-Anosognosia in non-dominant hemisphere
-Impaired body schema
-Contralateral pain & temp sensory loss
-Contralateral hemiplegia (central area), mild hemiparesis
-Ataxia, athetosis or choreiform movement
-Quality of movement is impaired
-Thalamic pain syndrome
-Anomia
-Hemiballisums
-Visual agnosia
Vertebral-basilar artery: lateral aspect of pons and midbrain together
with superior surface of cerebellum, cerebellum, medulla, pons,
midbrain
-Homonymous hemianopsia
-Memory impairment
-Alexia, dyslexia
-Cortical blindness form bilateral involvement
-Loss of consciousness
-Hemiplegia
-Comatose or vegative state
-Inability to speak
-Locked in syndrome
-Vertigo
-Nystagmus
-Dysphagia
-Dysarthria
-Syncope
-Ataxia
Spinal Cord tracts:
Ascending tracts-Sensory tracts ascending in the white matter of the spinal cord arise either from cells of spinal ganglia or from intrinsic neurons
within the gray matter that receive primary sensory input. Relay sensory feedback to the cerebrum and cerebellum.
Descending tracts-Involved with voluntary motor function, muscle tone, reflexes and equilibrium, visceral innervation, and modulation of
ascending sensory signals.
Ascending Tracts
Fasciculus cuneatus (posterior or dorsal column): sensory tract for
trunk, neck, UE proprioception, vibration, two-point discrimination,
and graphesthesia.
Descending Tracts
Anterior corticospinal tract-pyramidal motor tract responsible for
ipsilateral voluntary, discrete, and skilled movements
Fasciculus gracilis (posterior or dorsal column): sensory tract for trunk
and LE proprioception, two-point tract discrimination, vibration, and
graphesthesia
Spinocerebellar tract (dorsal): sensory tract that ascends to the
cerebellum for ipsilateral subconscious proprioception, tension in
muscles, joint sense, and posture of the trunk and LEs.
Spinocerebellar tract (ventral): sensory tract that ascends to the
cerebellum, some fibers crossing with subsequent recrossing at the
level of the pons for ipsilateral subconscious proprioception, tension in
muscles, joint sense, and posture of the trunk, UEs, and LEs.
Sino-olivary tract-ascends to the cerebellum and relays info from
cutaneous and proprioceptive organs
Spinoreticular tract: the afferent pathway for the reticular formation
that influences level of consciousness
Lateral corticospinal tract-pyramidal motor tract responsible for
contralateral voluntary fine movement •Damage to the corticospinal
tracts results in a positive Babinksi sign, absent superficial abdominal
reflexes and cremasteric reflex, and the loss of fine motor or skilled
voluntary movement.
Reticulospinal tract: extrapyramidal motor tract responsible for
facilitation or inhibition of voluntary and reflex activity through the
influence on alpha and gamma motor neurons.
Rubrospinal tract: extrapyramidal motor tract responsible for motor
input of gross posture tone, facilitating activity of flexor muscles, and
inhibiting the activity of extensor muscles.
Tectospinal tract: extrapyramidal motor tract responsible for
contralateral postural muscle tone associated with auditory/visual
stimuli
Vestibulospinal tract: extrapyramidal motor tract responsible for
ipsilateral gross postural adjustments subsequent to head movements;
facilitating activity of the extensor muscles and inhibiting activity of the
flexor muscles •Damage to the extrapyramidal tracts results in
significant paralysis, hypertonsicity, exaggerated deep tendon reflexes,
and clasp-knife reaction.
Spinotectal tract-sensory tract providing afferent information for
spinovisual reflexes and assists with movement of eyes and heads
towards a stimulus
Anterior spinothalamic tract-sensory tract for light touch and pressure
Lateral spinothalamic tract-sensory tract for pain and temperature
sensation
Cranial Nerves:
Nerve
I-Olfactory
Afferent (sensory) function
Smell
II-Optic
Eye
Efferent (motor) function
How to test
Identify familiar objects, close off
other nostril
Test visual fields (Snellen eye
III-Oculomotor
IV-Trochlear
V-Trigeminal
Skin of face, mucous membranes
of nose, sinuses, mouth, anterior
tongue
VI-Abducens
VII-Facial
Taste: anterior tongue
VIII-Vestibulocochlear
Hearing & balance (ear)
IX-Glossophyaryngeal
Touch, pain: posterior tongue,
pharynx
Taste: posterior tongue
Touch,pain: pharynx, larynx,
bronchi
Taste: tongue, epiglottis
X-Vagus
XI-Spinal Accessory
XII-Hypoglossal
Voluntary: Elevation of eyelid,
superior, medial, and inferior
recti, inferior oblique muscle of
eyeball. Turns eye up, down & in
Autonomic: smooth muscle of
eyeball
Turns adducted eye down
Temporal & masseter muscles
(mastication)
Turns eye out (lateral rectus
muscle)
Facial expressions. Autonomic:
lacrimal, submandibular, and
sublingual glands
Select muscle of pharynx; parotid
gland
Muscles of palate, pharynx, and
larynx Thoracic and abdominal
viscera
Sternocleidomastoid & trapezius
Tongue movements
chart), 20 ft away, test peripheral
vision
Up, down, and in (medial gaze)
Pupillary size/shape, reaction to
light
Downward & lateral gaze
Corneal reflex, face sensation,
clench teeth; push down on chin
to separate jaws
Lateral gaze
Close eyes tight, smile and show
teeth, whistle and puff cheeks
Identify familiar tastes
Eye-head coordination, vestibular
ocular reflex, auditory acuity.
Weber’s test: place tuning fork on
top of head. Rinne’s test-place on
mastoid process
Gag reflex, ability to swallow,
listen to voice quality
Examine for difficulty in
swallowing, ability to say “ahhh”
Resisted shoulder shrug
Tongue protrusion (if injured,
tongue deviates toward injured
side)
Upper Motor Neuron (UMN) VS. Lower Motor Neuron (LMN)
UMN Lesion
Central Nervous System
Cortex, brainstem, corticospinal tracts, spinal
cord
CP, hydrocephalus, ALS, CVA, birth injuries,
MS, Huntington’s chorea, TBI, Pseudobulbar
palsy, brain tumors
Location of Lesion:
Structures involved:
Disorders:
Tone:
Reflexes:
Involuntary movements:
Strength:
Muscle Bulk:
Hypertonia; velocity dependent
Increased: hyperreflexia, clonus, + Babinski
Muscle spasms: flexor or extensor
Stroke: weakness or paralysis on one side of
the body
Disuse atrophy
Voluntary movements:
Impaired or absent: dyssynergic patterns
LMN Lesion
Peripheral nervous system
Anterior horn cell, spinal roots, peripheral
nerves, cranial nerves
Poliomyelitis, ALS, Guillain-Barre syndrome,
tumors involving the spinal cord, trauma,
progressive muscular atrophy, infection, Bell’s
palsy, carpal tunnel syndrome, muscular
dystrophy, spinal muscular atrophy
Hypotonia, flaccidity; not velocity dependent
Decreased or absent, hyporeflexia
With denervation: fasciulations
Segmental or focal pattern
Neurogenic atrophy: rapid focal severe
wasting
Weak or absent if nerve interruped
Reflexes:
Superficial Reflex Testing:
Reflex
Abdominal Reflex
Spinal Level
T8-L1
Corneal “blink” reflex
Trigeminal and facial nerves
Procedure
Stoke briskly & lightly with a blunt
object from each quadrant of the
abdomen in a diagonal manner
towards the umbilicus
Ask the pt to look up and away
from you; stroke the cornea using
a piece of cotton
Normal response
Contraction of the abdominals
and deviation of the umbilicus in
the direction of the stimulus
Both eyes will blink with contact
to one eye
Cremasteric reflex
L1-L2
Gag Reflex
Glossopharyngeal & vagus nerves
Plantar reflex
L5-S1
Scratch the skin of the upper
medial thigh
The therapist lightly stimulates
each side of the back of the throat
and notes the reaction
A brisk and brief elevation of the
testicle on the ipsilateral side
A gag will occur post stimulation;
may be absent in some
percentage of the normal
population
Stroke the lateral aspect of the
Flexion of the toes *Babinski
sole of the foot with the blunt end reflex is the abnormal response
of a reflex hammer from theheel
that indicates CNS lesion
to the ball of the foot and
medially to the base of the great
toe
Reflex Grading Scale:
Reflex Grading
0=no response
1+=diminished response
2+=active normal response
3+=exaggerated resonse
4+=hyperactive; very brisk
Interpretation
Always abnormal
May or may not be normal
Normal
May or may not be normal
Always abnormal
Stroke: Ceberovascular accident-is a specific event that results in a lack of oxygen supply to a specific area of the brain secondary to either
ischemia or hemorrhage.
Types of Cerebrovascular Accidents:
Transient Ischemic Attack (TIA):
Completed Stroke:
Stroke in Evolution:
Is usually linked to an atherosclerotic thrombosis which causes a
temporary interruption of blood supply to an area of the brain.
Symptoms resolve typically between 24-48 hrs.
A CVA that presents with total neurological deficits at the onset.
A CVA, usually caused by a thrombus that gradually progresses. Total
neurological deficits are not seen for one to two days after onset.
Ischemic Stroke:
Once there is a loss of perfusion to a portion of the brain (within just
seconds), there is a central area of irreversible infarction surrounded
by an area of potential ischemia.
•Embolus (20% of ischemic CVAs): associated with cardiovascular
disease, can be a solid liquid or gas and originate in any part of the
body. Occurs rapidly with no warning, and presents with a headache.
•Thrombus: atherosclerotic plaque develops in an artery and occludes
the artery causing an infarct. Symptoms can appear in minutes or over
several days. Usually occurs during sleep or upon awakening after a MI
or post surgical procedure.
Abnormal bleeding in the brain due to a rupture in blood supply. HTN
is usually a precipitating factor causing rupture of an aneurysm.
Characteristics include: headache, vomiting, high BP. Approx. 50% of
deaths from hemorrhagic stoke occur within the first 48 hours.
Hemorrhage (10-15% of CVAs):
Characteristics of a CVA:
Left Hemisphere
Weakness, paralysis of the right
side
↑ frustration
↓ processing
Possible aphasia (expressive,
receptive, global)
Possible dysphagia
Right Hemisphere
Weakness, paralysis of the left
side
↓attention span
Left hemianospia
↓awareness and judgment
Possible motor apraxia
(ideomotor and ideational)
↓discrimination between left and
r ight
Right hemianopsia
Left inattention
Memory deficits
↓abstract reasoning
Emotional lability
Impulsive behaviors
Brainstem
Unstable vital signs
↓consciousness
↓ ability to swallow
Weakness on both sides of the
body
Paralysis on both sides of the
body
Cerebellum
↓balance
Ataxia
↓coordination
Nausea
↓ability for postural adjustment
Nystagmus
↓spatial orientation
Left hemisphere (right hemiplegia): Slow, cautious, and insecure. Give frequent feedback and support. Use appropriate communication:
words, gestures, assess level of understanding. Don’t underestimate ability to learn.
Right Hemisphere (left hemiplegia): Quick, impulsive, poor judgment. Use verbal cues (demonstrations or gestures may confuse pts). Give
frequent feedback: focus on slowing down and controlling movement. Focus on safety, avoid clutter. Do not overestimate ability to learn.
Synergy Patterns:
Upper Limb
Scapula
Shoulder
Elbow
Forearm
Wrist
Fingers
Thumb
Flexor synergy
Elevation & retraction
Abduction & ER
Flexion
Supination
Flexion
Flexion with adduction
Flexion and adduction
Extensory synergy
Depression & Protraction
IR & adduction
Extension
Pronation
Extension
Flexion with adduction
Adduction and flexion
Flexor synergy
Abduction and ER
Flexion
Dorsiflexion with supination
Extension
Extenor synergy
Extension, IR, and adduction
Extension
Plantar flexion with inversion
Flexion and adduction
Lower limb
Hip
Knee
Ankle
Toes
CVA tests and measures:
National Institue of Health (NIH) Stroke Scale:
Functional Independce Measure (FIM):
Stroke Impact Scale:
Assessment of an acute CVA relative to impairment
Provides a level of burden through assessment of mobility and ADL
management
Assessment of physical and social disability or level of impairment
Fugl-Meyer Assessment of Physical Performance:
secondary to CVA
Motor, sensory, and balance impairment; also assesses pain and ROM
NM & nervous system Terminology
Agnoisa: the inability to interpret information.
Agraphesthesia: the inability to recognize symbols, letters, or numbers traced on the skin.
Agraphia: the inability to write due to a lesion within the brain and is typically lfound in combination with aphasia.
Alexia: the inability to read or compreheand written language secondary to a lesion within in the dominant lobe of the
brain.
Anosognosia: the denial or unawareness of one’s illness; often associated with unilateral neglect.
Aphasia: the inability to communicate or comprehend due to damage to specific areas of the brain.
Apraxia: the inability to perform purposeful learned movements or activities even though there is no sensory or motor
impairment that would hinder completion of the task.
Asterognosis: the inability to recognize objects by sense of touch.
Body schema: having an understanding of the body as a whole and the relationship of its parts to the whole.
Constructional apraxia: the inability to reproduce geometric figures and designs. A person is often unable to visually
analyze how to perrom a task.
Decerebrate rigidity: a characteristic of a cortiospinal lesion at the level of the brainstem that results in extension of
the trunk and all extremities.
Decorticate rigidity: a characteristic of a cortiospinal lesion at the level of the diencephalon where the trunk and lower
extremities are positioned in extension and the upper extremities are positioned in flexion.
Dilopia: double vision
Dysarthria: slurred and impaired speech
Dysphagia: inability to properly swallow
Dysprosody: impairment in the rhythm and inflection of speech.
Emotional lability: a characteristic of a right hemisphere infarct where there is an inability to control emotions and
outbursts of laughing or crying that are inconsistent with the situation.
Fluent aphasia (Wernike’s aphasia/temporal): characteric of receptive aphasis where speech produces functional
output regarding articulation, but lacks content and is typically dysprosodic using neologisic jargon.
Hemiparesis: condition of weakness on one side of the body
Hemiplegia: condition of paralysis on one side of the body
Homonymous hemianopsia: the loss of the right or left half of the visual field of vision in both eyes.
Ideational apraxia: the inability to perform an initial motor plan and sequence tasks where the proprioceptive input
necessary for movement is impaired.
Ideomotor apraxia: a condition where a person plans a movement or task, but cannot volitionally perform it.
Automatic movement may occur, however a person cannot imose additional movement on command.
Neologism: substitution within a word that is so severe that it makes the word unrecognizable.
Non-fluent aphasia (Broca’s aphasia/frontal lobe): characteristic of expressive aphasia where speech is nonfunctional, effortful, and contains paraphasias. Writing is also impaired.
Perservation: the state of repeatedly performing the same segment of a task or repeatedly saying the same
word/phrase without a purpose
Synergy: mass movement patterns that are primitive in nature and coupled with spasticty due to brain damage
Unilateral neglect: the inability to interpret stimuli and events on the contralateral side of a hemispheric lesion. Leftsided neglect is most common with a lesion to the right inferior parietal or superior temporal lobes.
Spinal Cord Injuries:
Anterior Cord Syndrome:
Brown-Sequard’s Syndome:
Cauda Equina Injuries:
An incomplete lesion that results from compression and damage to the
anterior part of the spinal cord. The MOI is cervical flexion. There is a
loss of motor function and pain and temperature sense below the
lesion due to damange of the corticospinal and spinothalamic tracts.
Usually caused by a stab wound, which produces hemisection of the
spinal cord. There is paralysis and loss of vibratory and postion sence
on the ipsilateral side as the lesion due to the damage of the
corticospinal tract and dorsal columns. There is a loss of pain and temp
sense on the contralateral side of the lesion from damage to the lateral
spinothalamic tract.
Occurs below the L1 spinal level where the long nerve roots transcend.
Can be complete, however they are frequently incomplete due to the
large number of nerve roots in the area. A cauda equine injury is
considerd a peripheral nerve injury. Characterics include flaccidity,
arelexia, and impairment of bowel and bladder function. Full recovery
Central Cord Syndome:
Poserior Cord Syndrome:
is not typical due to the distance needed for axonal regeneration.
An imcomplte lesion that results from compression and damage of the
central portion of the spinal cord. The MOI is usually cervical
hyperextension that damages the spinothalamic t tract, corticospinal
tract, and dorsal columns. The UEs present with greater involvement
than the LEs, and greater motoer deficts exist as compared to sensory
deficits.
A relatively rare syndrome that is caued by compression of the
posterior spinal artery and is characterized by a loss of pain
perception, proprioception, two-point discrimination, and
stereognosis. Motor function is preserved.
Classification of Level of Injury:
Motor level: determined by the most caudal key muscles that have muscle strength of 3 or greater with the superior segment tested as normal
(5).
Sensory level: determined by the most caudal dermatome with a normal score of 2/2 for pinprick and light touch.
Terminology:
Myelotomy:
Neurectomy:
Neurogenic bladder:
Nonreflexive bladder:
Paradoxical breathing:
Paraplegia:
A surgical procedure that severs certain tracts within the spinal cord in
order to decrease spastic and improve function.
A surgical removal of a segment of nerve in order to decrease
spasticity and improve function.
The bladder empties reflexively for a pt with an injury above the level
of S2.
The bladder is flaccid as a result of a cauda equine or conus medullaris
lesion. Sacral reflex arc is damanged.
A form of abnormal breathing that is common in tetraplegia where the
abdomen rises and the chest is pulled inward during inspiration. On
expiration the abdomen falls and the chest expands.
Used to describe injuries that occur at the level of the thoracic, lumbar,
or sacral spine.
A physiologic response that occurs between 30 and 60 minutes after
trauma to the spinal cord and can last up to several weeks.
Describes injuries that occur at the level of the cervical spine.
Spinal shock:
Tetraplegia:
Spinal Cord tests and measures:
ASIA Impairment Scale
A=
B=
C=
D=
E=
Complete: no sensory or motor function is preserved in sacral segments S4-S5.
Sensory Incomplete: Sensory but not motor function is preserved below the neurologic level and extends through sacral segments S4S5.
Motor Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a
muscle grade less than 3.
Motor Incomplete: Motor function is preserved below the neurologic level, and most key muscles below have a muscle grade greater
than or equal to 3.
Normal: sensory and motor functions are normal.
Traumatic Brain Injury:
Types of brain injury:
Open Injury:
Closed Injury:
Primary Injury:
Secondary
Injury:
Direct penetration through the skull to the brain. Ex: gunshot wounds, knife, or shart objects, skull fx, direct trauma.
Without penetration through the skull. Ex: Concussion, contusion, hematoma, hypoxia, drug overdose, near drowning,
acceleration/deceleration injuries
Initial injury to the brain sustained by impact. Ex: skull penetration, skull fx, and contusions. Coup lesion: a direct lesion of the
brain under the point of impact. Contracoup lesion: results on the opposite side of the brain. Rebound effect of the brain after
impact.
Brain damage that occurs as a response to the initial injry. Ex: increase pressure, hypoxia, ischemia
Levels of Consciousness:
Coma:
Stupor:
Obtundity:
Delirium:
Clouding of
consciousness:
Consciousness:
A state of unconsciousness and a level of unresponsiveness to all interal and external stimuli.
A state of general unresponsiveness with arousal occurring from repeated stiumuli.
A state of consciousness that is characterized by a state of sleep, reduced alertness to arousal, and delayed responses to
stimuli.
A state of consciousness that is characterized by disorientation, confusion, agitation, and loudness.
A state of consciousness that is characterized by quiet behavior, confusion, poor attention, and delayed responses.
A state of alertness, awareness, orientation, and memory.
Traumatic Brain Injury Tests and Measures:
Ranchos Los Amigos Levels of Cogntive Functioning:
I.
II.
No response
Generalized Response
III.
Localized Response
IV.
Confused-agitated
V.
Confused-inappropriate
VI.
Confused-appropriate
Pt appears to be in a deep sleep and is completely unresponsive to any stimuli.
Pt reacts inconsistently and non-purposefully to stimuli in a nonspecific manner. Responses are
limited and often the same regardless of stimulus presented.
Pt reacts specifically, but inconsistently to stimuli. Responses are directly related to the type of
stimulus presented. May follow simple commands such as closing the eyes or squeezing the hand in
an inconsistent, delayed manner.
Pt is in a heightned state of activity. Behavior is bizarre and non-purposeful relative to the immediate
behavior. Does not discriminate among persons or objects, is unable to cooperate directly with
treatment effors. Verbalizations frequently are incoherent and/or inappropriate. Gross attention to
environment is very brief. Pt lacks short and long term recall.
Pt is able to respond to simple commands fairly consistently. However with increased complexity of
commands or lack of any external structure, responses are non-purposeful, randome, or fragmented.
Memory is severly impaired, inappropriate use of objects may perform previously learned taks with
structure but is unable to learn new info.
Pt shows goal-directed behavior, but is dependent on external input or direction. Follow simple
directions consistently and shows carryover for relearned tasks such as self-care. Responses may be
incorrect due to memory problems, but they are approparite to the situation. Past memories show
VII.
Automatic-appropriate
VIII.
Purposeful-appropriate
more depth and detail than recent memory.
Pt appears appropriate and oriented with the hospital and home setting. Goes through daily routine
automatically, but frequently robot-like. Pt shows minimal to no confusion and has shallow recall of
activities. Shows carryover for new learning, but a decreased rate. With structure is able to initiate
social or recreational activityes, judgment remains impaired.
Pt is able to recall and integrate past and recent events and is aware of and responsive to
environment. Shows carryover for new learning and needs no supervision once tasks are learned. May
continue to show a decreased ability relatively to premorbid abilities, abstract reasoning, tolerance for
stress, and judgment in emergencies or unusually circumstances.
Glasgow Coma Scale: Eye opening, Best motor response, Verbal response
Severe brain injury/coma: 8 or less
Moderate brain injury: 9-12
Mild brain injuries: 13-15
NM and Nervous System Patholody:
Pathology
Alzheimer’s Disease
What is it
A progressive
neurodegenerative
disorder that results in
deterioration and
irreversible damange
within the cerebral cortex.
Etiology
Unknown, however
hypothesized causes
unclude lower levels of
neurotransmitters, higher
levels of aluminum within
brain tissue, genetic
inheritance, autoimmune
disease. Risk of developing
increases with age, higher
incidence in women.
Signs & Symptoms
Difficulty with new
learning and subtle
changes in memory and
concentration. Progression
includes a loss of
orientation, word finding
difficulty, depression, poor
judgment, rigidity,
bradykinesia, shuffling
gait, impaired ability to
perform self-care skills.
Later stages include
Treatment
There is no curative
treatment for the disease
process. Medications are
administered to inhibit
acetylcholinesterase,
alleviate cognitive
symptoms, and control
behavioral changes. PT:
should focus on
maximizing pts remaining
function and providing
family and caregiver
incontinence, functional
dependence, and an
inability to speak.
Amyotrophic Lateral
Sclerois (ALS)
A chronic degenerative
disease that produces
both upper and lower
motor neuron
impairments. Produces
weakness and muscle
atrophy. The rapid
degeneration causes
denervation of muscle
fibers, mustly atrophy, and
weakness.
Unknown. Theories
include genetic
inheritance, virus,
metabolic disturbances,
and toxicity of lead and
aluminum. Higher
incidence in men and
beings ages 40-70.
Bell’s Palsy
A temporary unilateral
facial paralysis secondary
to trauma with
demyelination and/or
axonal degeneration of
the facial nerve. This is a
common clinical condition
with the highest incidence
in individuals between 1545 years of age.
Unclear, however may be
secondary to viral
infection, specifically the
herpes simplex/herpes
zoster virus. Inflammation
and subsequenet pressure
injure the nerve with
varying degress of
damage.
Diabetic Neuropathy
A complication and direct
Primary diagnosis is result
Lower motor neuron signs
include asymmetric
muscle weakness,
cramping, and atrophy
within the hands.
Weakness spreads in a
distal to proximal path.
Upper motor neuron
symptoms can include
spasticity, clonus, +
Babinski. A pt with ALS will
exhibit fatigue, oral motor
impairment, motor
paralysis, and eventual
respiratory paralysis.
Asymmetrical facial
appearanace with
“drooopoing” of the eyelid
and mouth, potential for
drooling, dryness of the
eye, and inability to close
the eyelid due to
weakness.
Weakness and sensory
education. Many pts
require a long term care
secondary to personality
changes, aggressive
behavior, and end stage
complications.
Effective management of
ALS is based on supportive
care and symptomatic
therapy. Pharmacological
intervention may include
riluzole. Physical,
occupational, speech,
respiratory, and
nutritional therapies may
be warranted with the
focus on quality of life and
caregiver training.
The sooner the person is
diagnosed and treated,
the better the outcome.
Some pts have very mild
involvement and their
symptoms typically resolve
within 2 weeks with
formal medical
intervention. PT may be
indicated for stimulation
of the facial nerve, facial
massage, and exercise.
Pts require strict
Epilepsy
Guillain-Barre Syndrome
effect of diabetes. Nerve
ischemia results from
microvascular disease
combined with the direct
effects of hyperglycemia
on neurons resulting in the
impairment of nerve
function.
of DM.
Chronic condition where
there is temporary
dysfunction of the brain
that results in
hypersynchronus electrical
discharge of cortical
neurons and seizure
activity that is typically
unprovoked and
unpredictable. A seizure is
a transient even that is a
symptom of interrupted
brain functioning. A
seizure is the hallmark sign
of epilepsy, however, one
seizure does not signal
epilepsy.
Acute polyneuropathy,
that is a temporary
inflammation and
Various classifications of
seizures, many cases are
idiopathic. Other
associated conditions:
genetic influence, head
trauma, dementia, CVA,
cerebral palsy, down
syndrome, and autism.
Unknown, however, it is
hypothesized to be an
autoimmune response to a
disturbances occur distally
in a symmetrical pattern.
Initial symptoms include
tingling, numbness or
pain, especially in the feet.
Additional symptoms may
include wasing of muscles
in the feet or hands
“stocking glove” sensory
distribution imparitmens,
orthostatic hypotension,
weakness, urinary
impairments, and
significant pain.
Seizure symptoms vary,
depending on type and
extent. Loss of awareness
or consciousness and
disturbances of
movement, sensation,
mood or mental function
may occur.
-Stay calm & prevent
injury
-Remove all objects that
could cause harm
-Do not restrain
-Avoid placing anything in
pts mouth
-Call 911 if seizure lasts
longer than 5 minutes
Motor weakness in a distal
to proximal progression,
sensory impairment, and
monitoring of blood
glucose levels to prevent
further nerve pathology.
PT is typically indicated to
address the various
symptoms including pain
management, foot care,
and overall fitness.
Antiepileptic medication
to manage seizures. No
cure.
Typically requires
hospitalization for
treatment of symptoms.
demyelination of the
peripheral nerves’ myelin
sheaths, potentially
resulting in axonal
degeneration. The
autoantibodies of GBS
attack segments of the
myelin sheath of the
peripheral nerves. Can
occur at any age, however
there is a peak in
frequency in young adult
population and again in
adults between their 5th
and 8th decades.
previous respiratory
infection, influenze,
immunization or surgery.
Viral infections, EpsteinBarr syndrome,
cytomegalovirus, bacterial
infections, surgery, and
vaccinations.
Huntington’s Disease
(chorea)
Is a neurological disorder
of the CNS and is
characterized by
degeneration and atrophy
of the basal ganglia and
cerebral cortex within the
brain. The
neurotransmitters become
deficient and are unable to
modulate movement.
Is genetically transmitted
as an autosomal dominant
trait with the defect linked
to chromosome 4 and to
the gene identified as IT15. The disease is usually
perpetuated by a person
that has children prior to
diagnosis. The average age
for developing symptoms
is between 35-55 years,
however can develop at
any age.
Multiple Sclerosis
Produces patches of
demyelination of the
myelin sheaths that
surround nerves within
Genetics, viral infections,
and environment all have
a role in the development
of MS. MS can oocur at
possible respiratory
paralysis. Will initially
present with distal
symmetrical motor
weakness, mild distal
sensory impairments, and
transient paresthesias that
progress towards the
upper extremities and
head. Level of disability
peaks within 2-4 weeks
after onset. Muscle and
respiratory paralysis,
inability to speak or
swallow may also occur.
Can be life threatening.
HD is a movement
disorder that included
affective dysfunction and
cognitive impairment. The
pt may present with
involuntary choeric
movements, mild
alteration in personality,
grimacing, protrusion of
the tongue, and ataxia
with choreoathetoid
movements. Late stage HD
includes mental
immobility, and rigidity.
Vary based on the type.
Initial symptoms include
visual problems,
paresthesias and sensory
Cardiac monitoring and
mechanical ventilation
may be required. PT may
include pulmonary rehab,
strengthening, mobility
training, wheelchair and
orthotic prescription, AD
training.
Medical management
requires genetic,
psychological, and social
counceling for the pt and
family. Pharmacological
mangt is initiated once
choreiform movement
impairs a pts functional
capacity. PT should
maximize endurance,
strength, balance, postural
control, and functional
mobility.
Pharmacoligcal, medical,
and therapeutic
interventions. The goal is
to lessen the length of
the brain and spinal cord.
This decreases the
efficiency of nerve impulse
transmission and
symptoms will vary based
on the location and the
extent of demyelination.
There is subsequent
plaque development and
eventual failure of impulse
transmission.
any age with the highest
incidence between 20-35
years of age.
Myasthenia Gravis
Autoimmune disease
resulting in neuromuscular
junction pathology. There
is a defect specifically in
the transmisstion of nerve
impulses to the muscles at
the NM junction.
Antibodies block or
destroy the receptors that
are needed for
acetylcholine uptake and
this prevents muscle
contraction.
Autoiummune disease
process that also has an
association with an
enlarged thyms. There is
also an associated with
DM, RA, lupus and other
immune disorders. There
are multiple forms of
gravis that range from
mild to severe
involvement.
Parkinsons’ Disease
Primary degenerative
disorder and is
characterized by a
decrease in production of
dopamine
Unknown. Contributing
factors that can produce
symptoms include genetic
defect, toxicity from
carbon monoxide,
changes, clumsiness,
weakness, ataxia, balance
dysfunction, and fatigue.
The clinical course usually
consists of periods of
exacerbations and
remissions, with the
degree of neurologic
dysfunction.
exacerbations and
maximize the health of the
pt. Pharmacological
intervention is indicated
along with physical,
occupational, and speech
therapies throughout the
disease process. PT
includes regulation of
activity level, relaxation
and energy conservation
techniques, normalization
of tone, balance and gait
training, core stabilization,
and AD training.
The cardinal signs include
Myasthenia gravic “crisis”
extreme fatiguability and
is a medical emergency
skeletal muscle weakness
where there is an
that can fluctuate within
exacerbation that includes
minutes or over an
the respiratory muscles
extened period. The ocular and requires a ventilator.
muscles are typically
PT will focus on obtaining
affected first and approx.
a respiratory baseline and
half of the pts experience
pulmonary intervention as
ptosis and diplopia,
needed. Energy
Dysphagia, dysarthria, and conservation and
cranial nerve weakness are strengthening using
also common.
isometric contractions are
appropriate for most pts.
A resting tremor in the
Relies heavily on
hands (sometimes called
pharmacolocial
pill rolling tremor), or feet intervention. Dopamine
that increases with stress
replacement therapy is
and disappears with
most effective in reducing
Post-polio Syndrome
(neurotransmitter) within
the corpus striatum of the
basal ganglia. The basal
ganglia stores the majority
of dopamine and is
responsible for
modulation and control of
voluntary movement.
excessive copper,
encephalitis, and other
neurodegenerative
diseases such as HD or
Alzheimer’s. The majority
of pts are between 50 and
79.
A viral infection resulting
in neuropathy that
includes focal and
asymmetrical motor
impairments. This virus
was all but eradicated in
the 1960s with the
development of a vaccine.
Post-polio is a LMN
A previous diagnosis of
polio is essential to
diagnose PPS. Approx 2550% of persons with polio
experience PPS decades
after their initial recovery
(interval approx 25 years)
movement or sleep. Early
symptoms: balance
disturbances, difficuly
rolling over and rising from
bed, and impairment with
fine manipulataive
movements seen in
writing, bathing and
dressing. Progression of
the disease includes
hypokinesia. Sluggish
movement, difficulty with
initiating and stopping
movement, festinating and
shuffling gait,
bradykinesia, poor
posture, cogwheel and
lead pipe rigidity of
skeletal muscles. Pts may
also experience freezing
during ambulatin, speech,
blinking, and movements
of the arms. Mask like
appearance with no
expression.
Commonly there is slow
and progressive weakness,
fatigue, muscle atrophy,
pain, and swallowing
issues.
movement disorders,
rigidity and tremor. PT
should include maximizing
endurance, strength, and
functional mobility. Verbal
cueing and visual feedback
are also effective tools to
use with this population.
No pharmacological
intervention to alter the
progression of PPS.
Emphasis of treatment
surrounds lifestyle
modification and
symptomatic intervention.
PT should emphasize
supervised exercise,
pathology that affects the
functional independence,
anterior horn cells of
adaptive equipment, and
those previously affected
education to assit pts to
with polio. Surviving axons
maintain as much
were originally able to
independence as possible.
increase the size of ther
innervation ratio to assist
denervated muscle. PPS
occurs when the
compensated
reinnervation fails and
results in ongoing muscle
denervation.
Peripheral nerve lesions: A lesion of the nerve can occur through many MOIs. Ex. Compression, fx, compartment syndrome
Double crush syndrome:
Mononeuropathy:
Neuroma:
Peripheral neuropathy:
Polyneuropathy:
Wallerian degeneration:
Existence of two separate lesions along the same nerve that create more severe symptoms that in only one lesion
existed.
An isolated nerve lesion, associated condtions include trauma and entrapment
Abnormal growth of nerve cells; associated conditions include vasculitis, AIDS, entrapment
Impairment or dysfunction of the peripheral nerves; associated conditions include diabetic peripheral neuropathy,
trauma, alcoholism
Diffuse nerve dysfunction that is symmetrical and typically secondary to pathology and not trauma, associated
conditions include GBS, peripheral neuropathy, use of neurotoxic drugs, and HIV
Degeneration that occurs distally, specifically to the myelin sheath and axon.
Classification of Acute Nerve Injuries:
Neurapraxia:
(Class I)
-Mildest form of injury
-conduction block usually due to myelin dysfunction
-Axonal continuity preserved
-Nerve conduction is preserved
-Nerve fibers are not damaged
-Symptoms include pain, minimal muscle atrophy, numbness or greater loss of motor and sensory function,
diminished proprioception
Axonotmesis:
(Class II)
Neurotmesis:
(Class III)
-Recovery is rapid and complete and will occur within 4-6 weeks
-Pressure injuries are the most common
-A more severe grade of injury to a peripheral nerve
-Reversible injury to damaged fibers since they maintain an anatomical relationship to each other
-Damage occurs to the axons with preservation of the endoneurium, epineurium, Schwann cells, and supporting
structures
-Distal Wallerian degeneration can occur
-The nerve can regenerate distal to the site of the lesion at rate of 1mm per day
-Recovery is spontaneous and varies from spotty to no recovery; surgery may be required for repair
-Traction, compression, and crush injuries are most common
-The most severe grade of injury to a peripheral nerve
-Axon, myelin, connective tissue components are all damaged or transected
-Irreversible injury, no possibility of regeneration
-Flaccid paralysis and wasting of muscles occur, total loss of sensation to area supplied by the nerve
-All motor and sensory loss distal to the lesion becomes permantely impaired
-No spontaneous recovery ; with surgical reattachment potential regenerating axons may grow at 1 mm per day
-Complete transaction of the nerve trunk
Pediatrics & Development
Concepts of Development
Cephalic to Caudal:
Gross to fine:
Mass to specific:
Proximal to distal:
A person develops head and UE control prior to trunk and LE control. There is a general skill acquisition from the
direction of head to toe.
A general trend for large muscle movement acquisition with progression to small muscle skill acquisition.
A general trend for a person to acquire simple movements and progress towards complex movements.
A concept that uses the midline of the body as the reference point. Trunk control (midline stability) is acquired first
with subsequent gain in distal control (extremities).
Infant Reflexes and Possible Effects if Reflex Persists Abnormally:
Reflex:
Normal:
Interferes with:
Asymmetrical Tonic Neck Reflex (ATNR)
Stimulus: Head position
Response: Arm & leg on face side are
extended, arm & leg on skull side are flexed
with convexity toward face side
Normal age of response: Birth to 6 months
Symmetrical Tonic Neck Reflex (STNR)
Stimulus: Head position, flexion or extension
Response: When head is in flexion, arms are
flexed legs extended. When head is in
extension, arms are extended, legs are flexed.
Normal age of response: 6-8 months
Tonic Labyrinthine Reflex (TLR)
Stimulus: Position of labyrinth in inner ear—
reflected in head position
Response: in the supine position, body and
extremities are held in extension; in the prone
position, body and extremities are held in
flexion
Normal age of response: Birth to 6 months
Stimulus: Touch to skin along spine from
shoulder to hip
Response: Lateral flexion of trunk to side of
stiumuls
Normal age of response: 30 weeks of
gestation to 2 months
Stimulus:Pressure in palm on ulnar side of
hand
Response: Flexion of fingers causing a strong
grip
Normal age of response: Birth to 4 months
Stimulus: Pressure to base of toes
Galant Reflex
Palmar grasp reflex
Plantar grasp reflex
-Feeding
-Visual tracking
-Midline use of hands
-Billateral hand use
-Rolling
-Development of crawling
-Can lead to skeletal deformities (scoliosis, hip
subluxation, hip dislocation)
-Ability to prop on arms in prone position
-Attaining and maintaining hands and knees
position
-Crawling reciprocally
-Sitting balance when looking around
-Use of hands when looking at object in hands
in sitting position
-Ability to initiate rolling
-Ability to prop on elbows with extended hips
when prone
-Ability to flex trunk and hips to come to
sitting position from supine position
-Often causes full body extension, which
interferes with balance in sitting or standing
-Development of sitting balance
-Can lead to scoliosis
-Ability to grasp and release objects
voluntarily
-Weight bearing on open hand for propping,
crawling, protective responses
-Ability to stand with feet flat on surface
Rooting reflex
Moro reflex
Startle reflex
Positive support reflex
Walking (stepping) reflex
Response: Toe flexion
Normal age of response: 28 weeks gestation
to 9 months
Stimulus: Touch on cheek
Response: turning head to same side with
mouth open
Normal age of response: 28 weeks gestation
to 3 months
Stimulus: Head dropping into extension
suddenly for a few inches
Response: Arms abduct with fingers open,
then cross trunk into adduction, cry
Normal age of response: 28 weeks gestation
to 5 months
Stimulus: Loud, sudden noise
Response: similar to Moro response, but
elbows remain flexed and hands closed
Normal age of response: 28 weeks gestation
to 5 months
Stimulus: Weight placed on balls of feet when
upright
Response: Stiffening of legs and trunk into
extension
Normal age of response: 35 weeks of
gestation to 2 months
Stimulus: Supported upright position with
soles of feet on firm surface
Response: Reciprocal flexion/extension of legs
Normal age of response: 38 weeks of
gestation to 2 months
-Balance reactions and weight shifting in
standing
-Oral-motor development
-Development of midline control of head
-Optical righting, visual tracking, and social
interaction
-Balance reactions in sitting
-Protective responses in sitting
-Eye-hand coordination, visual tracking
-Sitting balance
-Protective responses in sitting
-Eye-hand coordination
-Social interaction, attention
-Standing and walking
-Balance reactions and weight shift in standing
-Can lead to contractures of ankles into PF
-Standing and walking
-Balance reactions and weight shifting in
standing
-Development of smooth, coordinated
reciprocal movements of lower extremities
Developmental Gross & Fine Motor Skills:
Age
Gross motor skills
Fine motor skills
Newborn to 1 month:
2-3 months
4-5 months
6-7 months
8-9 months
Prone: physiological flexion, lifts head briefly,
head to side
Supine: physiological flexion, rolls partly to
side
Sitting: head lag in pull to sit
Standing: Reflex standing and walking
Prone: Lifts head 90° briefly, chest up in prone
position with some weight through forearms,
rolls prone to supine
Supine: ATNR influence is strong, legs kick
reciprocally, prefers head to side
Sitting: Head upright, but bopping, variable
head lag in pull to sitting position, needs full
support to sit
Standing: poor weight bearing, hips in flexion,
behind shoulders
Prone: Bears weight on extended arms, pivots
in prone to reach toys
Supine: Rolls from supine to side position,
plays with feet in mouth
Sitting: head steady in supported sitting
position, turns head in sitting position, sits
alone for brief periods
Standing: bears all weight through legs in
supported standing
Prone: Rolls from supine to prone, holds
weight on one hand to reach for toy
Supine: Lifts head
Sitting: Lifts head and helps when pulled to
sitting position, gets to sitting position without
assistance, sits independently
Mobility: may crawl backward
Prone: gets into hands-knees position
Supine: does not tolerate supine position
-Regards objects in direct line of sight
-Follows moving onject to midline
-Hands fisted
-Arm movements jerky
-Movements may be purposeful or random
-Can see farther distances
-Hands open more
-Visually follows through 180°
-Grasp is reflexive
-Uses palmar grasp
-Grasps and releases toys
-Uses ulnar-palmar grasp
-Approaches objects with one hand
-Arm in neutral when approaching toy
-Radial-palmar grasp “rakes” with fingers to
pick up small objects
-Voluntary release to transfer onjects
between hands
-Develops active supination
-Uses inferior pincer grasp
10-11 months
12-15 months
16-24 months
2 years
Sitting: moves from sitting to prone position,
sits without hand support, pivots
Standing: stands at furniture
Mobility: crawls forward, walks along
furniture (cruising)
Standing: stands without support briefly, picks
up object from floor
Mobility: walks with both hands held, walks
with one hand held, bear walk
-Walks without support
-Fast walking
-Walks backward, sideways
-Bends to look between legs
-Creeps or hitches upstairs
-Squats in play
-kicks ball
-Throws ball
-Extends wrist actively
-Points with index finger
-Rides tricycle
-Walks backward
-Walks on tiptoe
-Runs on toes
-Hops on one foot
-Turns knob
-Opens and closes jar
-12-15 piece puzzle
-Fine pincer grasp developed
-Marks paper with crayon
-Builds tower
-Folds paper
-Strings beads
-Holds crayon with thumb and fingers
NM and Nervous Systems Pediatric Pathology
Pathology
Cerebral Palsy (CP)
What is it
Is an umbrealla term used
to describe movement
disorders due to brain
damage that are nonprogressive and are
acquired in utero, during
birth or infancy. The brain
Etiology
CP can occur before or
during birth secondary to
a lack of oxygen, maternal
infections, drug or alcohol
abuse, placental
abnormalities, toxemia,
prolonged labor,
Signs & Symptoms
Spastic-indicating a lesion
in the motor cortex of the
cerebrum; upper motor
neuron damage
Athetoid-indicating a
lesion involving the basal
ganglia; cerebellum and
Treatment
Tx of CP is a life long
process. Intervention
includes ongoing family
and caregiver education,
normalization fo tone,
stretching, strengthening,
motor learning and
damage decreases the
brain’s abilility to monitor
and control nerve and
voluntary muscle activity.
prematurity, and Rh
imcompatibility. The
etiology of acquired CP
includes meningitis, CVA,
seizures, and brain injury.
Down Syndrome
Is a genetic abnormality
consisting of an extra 21
chromose, termed trisomy
21.
Includes incomplete cell
division of the 21st pair of
chromosomes due to
nondisjunction,
translocation or mosaic
classficiation. Advanced
maternal age increases the
risk of genetic imbalance.
Duchenne Muscular
Dystrophy
Is a progressive disorder
caused by the absence of
the gene required to
produce the musle
proteins dystrophin and
nebulin. Without
dystrophin and nebulin,
cell membranes weaken,
myofibrils are destored,
and muscle contractility is
lost. Fat and connective
The causative factor is
inheritance as an X-linked
recessive trait. The child’s
mother is a silent carrier
and only male offspring
will manifest the disease.
cerebellar pathways
Distribution of
Involvement:
-Monoplegia-one
extremity
-Diplegia-bilateral LE
involvement, however UE
may be affected
Hemiplegia-unilateral
involvement of the upper
and lower exremties
Quadriplegia-involvment
of the entire body
Mental retardation,
hypotonia, joint
hypermobility, flattened
nasal bridge, narrow
eyelids with epicanthal
folds, small mouth,
feeding impairments, flat
feet, scoliosis, congenital
heart disease, and visiual
and hearing loss.
Characteristics usually
manifest between 2-5
years of age. Progressive
weakness, disinterest in
running, falling, toe
walking, excessive
lordosis, and
pseudohypertorphy of
muscle groups (calves).
Progressive impairment
with ADLs and mobility
developmental
milestones, positioning,
weight bearing activities,
and mobility skills.
Splinting, assistive devices,
and specialized seating
may be indicated. Surgical
intervention may be
required for orthopedic
management or reduction
of spasticity.
Should emphasize exercise
and fitness, stability,
maximizing respiratory
function, and education
for caregivers. Surgical
intervention may be
indicated for cardiac
abnormaities.
Intervention focuses on
family/caregiver
education, respiratory
function, submax exercise,
mobility skills, splinting,
orthotics, and adaptive
equipment. Medical
management includes the
use of
immunosuppressants,
steroids, and surgical
Spina Bifida
tissue eventually replace
muscle, and death usually
occurs from
cardiopulmonary failure
prior to age 25, usually in
the teenage years.
Is a developmental
abnormality due to
insufficnet closure of the
neural tube by the 28th day
of gestation.
Causative factors include:
genetic predisposition,
environmental influence,
low levels of maternal folic
acid, maternal
hyperthermia, and certain
classifications of drugs.
Classifications of spinal
bifida include:
Spina bifida Occultaimpairment and nonfusion of the spinous
processes of a vertebrae,
however, the spinal cord
and meninges remain
intact. No associated
disabilitiy. Spina bifida
cystic-presents with a cyst
like protrusion through the
non-fused vertebrae,
which results in
impairment.
2 types of Cystica:
1. Meningoceleherniation of
meninges and CSF
into a sac that
protrudes through
begins around age 5 and
the ability to ambulate
slows. *Gower’s sign
Proximal weakness first
intervention for
orthopedic impairments.
Motor loss below the level
of the defect, sensory
deficits, hydrocephalus,
Arnold-Chiari Type II
malformation,
osteoporosis, clubfoot,
tethered cord syndrome,
latex allergy, bowel and
bladder dysfunction, and
learning disabilities.
PT emphasizes significant
family teaching regarding
positioning, handling,
ROM, and therapeutic
exercises. Skin care,
strengthening, AD,
splinting, wheelchair
prescription.
the vertebral
defect.
2. 2.
Myelomeningocel
e-a severe form
with herniation of
meninges, CSF,
and spinal cord
extending through
the defect in the
vertebrae. Cyst
may or may not be
covered by skin.
Neuromuscular Pathologies:
Disease
Alzheimer’s
Disease
Diagnosis
Is a progressive
neurological
disorder that
results in
deterioration &
irreversible
damage within
the cerebral
cortex and
subcortical
areas of the
brain. The loss
of neurons
results from the
breakdown of
several
Contributing
Factors
Hyopthesized
causes
include lower
levels of
neurotransmi
tterse, higher
levels of
aluminum
within brain
tissue,
genetic
inheritance,
autoimmune
disease,
abnormal
processing of
Clinical
Presentation
Initially noted
by a change in
higher cortical
functions
characterized
by subtle
changes in
memory,
impaired
concentration
, and difficulty
with new
learning.
During the
middle stages,
pt will
Lab/Imaging
Alzheimer’s
disease
presently
cannot be
confirmed
until a
postmortem
biopsy revels
the
neurofibrillary
tangles and
amyloid
plaques. MRI
can be used to
assess any
abnormalities
Management/Out
come
Drug therapies are
usually short term
in effect lasting 69 months. PT
should focus on
maximizing the pts
remaining
function and
providing family
and caregiver
education. The
therapist should
attempt to create
an emotional &
physical
environment that
Amyotrophic
Lateral
processes that
would normally
sustain the
brain cells.
the
substance
amyloid, and
virus. The risk
of developing
↑ with age
and a higher
incidence in
women.
develop
behavioral
and motor
problems
such as
aphasia,
apraxia,
perseveration,
agitation and
violent or
socially
unacceptable
behavior that
can include
wandering.
Eventually all
ability to learn
is lost and
long-term
memory also
disappears.
or signs of
atrophy
within the
brain that is
associated
with
Alzheimer’s
disease or to
rule out other
medical
conditions.
Is a chronic
degenerative
Exact
etiology
Both upper
and lower
There are
multiple tests
provides the pt
with the
opportunity to
experience
success. Safety
with functional
mobility and gait
training may be
indicated in the
early stages. Many
pts require a long
term care facility
due to personality
changes,
aggressive
behavior, and endstage
complications.
This is a chronic
and progressive
disorder and is the
4th leading cause
of death of adults.
The typical course
of the disease
averages between
7-11 years. The
leading cause of
death of a pt with
Alzheimer’s
disease is infection
or dehydration.
Management is
based on
Sclerosis
(ALS)
disease that
produces both
upper and lower
motor neuron
impairments.
Demyelination,
axonal swelling,
& atrophy
within the
cerebral cortex,
premotor areas,
sensory cortex,
and temporal
cortex cause the
symptoms of
ALS.
unknown,
theories of
causative
factors that
include
genetic
inheritance
as an
autosomal
dominant
trait, a slow
acting virus,
metabolic
disturbances,
and theories
of toxicity of
lead &
aluminum.
Familial ALS
occurs in 510% of all
cases. Risk
for ALS is
higher in men
& usually
occurs
between 4070 years of
age.
motor neuron
involvement.
Lower motor
neuron signs
include
asymmetric
muscle
weakness,
cramping, and
atrophy that
are usually
found within
the hands.
Muscle
weakness due
to
denervation
eventually
causes
significant
fasiculations,
atrophy, and
wasting of the
muscles. The
weakness
spreads
throughout
the body over
the course of
the disease
and generally
follows a
distal to
proximal
used to assist
with
diagnosing
ALS.
Electromyogra
phy assesses
fibrillation and
muscle
fasciculations.
Muscle biopsy
verifies LMN
involvement
rather than
muscle
disease and a
spinal tap may
reveal a
higher protein
content in
some pts with
ALS.
supportive care
and symptomatic
therapy. PT should
focus on quality of
life, low level
exercise, ROM,
mobility training,
assistive/adaptive
devices,
wheelchair
prescription,
bronchial hygiene,
and energy
conservation
techniques. ALS is
usually a rapidly
progressing
neurological
disease with an
average course of
2-5 years with 2030% surviving
longer than 5
years. Death
usually occurs
from respiratory
failure.
path. Upper
motor neuron
symptoms
occur due to
the loss of
inhibition of
the muscle.
Incoordinatio
n of
movement,
spasticity,
colnus, and a
positive
Babinski
reflex are
some of the
indicators of
UMN
involvement.
Bulbar
involvement
is
characterized
by dysarthria,
dysphagia,
and emotional
lability. A pt
will ALS will
exhibit
fatigue, oral
motor
impairment,
fasciulations,
spasticity,
Central Cord
Syndrome
(CCS)
Is an incomplete
SCI that most
often results
from a cervical
hyperextension
injury.
Symptoms are
secondary to
damage to the
central aspect of
the spinal cord.
CCS usually
occurs from a
fall but can
occur from
other forms of
trauma such as
MVA.
Most
common MOI
is a
hyperextensi
on injury of
the cervical
spine. Other
potential
contributing
factors in the
development
of CCS
include
cervical
spondylosis,
narrowing or
congenital
defect of the
spinal canal,
tumor
rheumatoid
arthritis or
syringomyeli
a. CCS
predominatel
y affects the
population
over 50 and
greater
motor
paralysis, &
eventual
respiratory
paralysis.
CCS presents
with motor
loss that is
greater in the
UEs than in
the LEs and is
most severe
distally in the
UEs. This
presentation
is due to the
damage that
occurs within
the central
location of
the spinal
cord. Sensory
loss found
below the
level of the
lesion is
usually
limited, but
can be
variable.
Sacral
segments are
usually
unaffected.
MRI is used to
assess spinal
cord
impingement
form bone or
disk. CT scan
of the spine
will assess
spinal canal
compromise
and the
degree of
impingement.
X-rays can be
utilized to
assess
potential
fractures,
dislocations,
and degree of
spondylotic
deterioration.
Rehab is initiated
once the pt is
medically stable.
PT intervention
should include pt
and caregiver
education, ROM,
strengthening,
endurance,
balance, proximal
stabilization ex,
and functional
mobility based on
current function. If
a pt ambulates, a
platform
attachment walker
may be initially
indicated since
hand function is
usually poor for
grasp. Surgical
intervention is
rare. CCS is the
most common
incomplete SCI
and accounts for
~30% of overall
tetraplegia.
incidence in
men.
Cerebral
Palsy
Is an umbrealla
term used to
describe a group
of nonprogressive
movement
disorders that
result from
brain damage.
Most common
cause of
permanent
disability in
children.
Multifactorial
& sometimes
unknown.
Risk factors
are
categorized
as prenatal
(80%), or
perinatal and
postnatal
(20%).
Factors can
include
maternal
malnutrion,
hypothyroidis
m, infection,
diabetes, and
chromosome
abnormalities
. Perinatal
factors
include
multiple or
premature
births,
breech
Bowel &
bladder
functions
resolve in 5585% of pts
with CCS after
6 months.
CP is a NM
disorder of
posture and
controlled
movement. A
child may
present with
high tone, low
tone, or
athetoid
movement.
CP is classified
as monoplegia
(one involved
extremity),
hemiplegia
(unilateral
involvement
of the upper
and lower
extremities),
and
quadriplegia
(all
extremities).
General
characteristics
Statistics indicated
77% of pts with
CCS will ambulate.
Older pts do not
recover as well as
younger ones.
If CP is
suspected
through
clinical
findings,
including
seizures, an
electroenceph
alography
(EEG) may be
performed. Xray of the hp
may rule out
hip
dislocation;
blood and
urine tests can
be sued to
investigate a
metabolic
cause of CP.
Observation
usually will
diagnose CP
secondary to
the observed
outward
Life long team
approach. PT for
CP often uses
neurodevelopmen
tal treatment and
sensory
integration
techniques.
Treatment should
include
normalization of
tone, family
education,
developmental
milestones,
positioning,
stretching,
strengthening,
balance, mobility,
specialized
wheelchair seating
and orthotic
prescription. If a
pt is going to
ambulate, this will
usually occur by
the age of 8. CP is
delivery, low
birth weight,
prolapsed
cord. Post
natal include
CVA, head
trauma,
infection and
brain tumor.
The most
common
cause of CP is
prenatal
cerebral
hypoxia.
Down
Syndrome
(DS)
(Trisomy 21)
occurs when
there is an error
in cell division
either through
nondisjunction
(95%),
translocation
(4%), or
mosaicism (1%)
and the cell
nucleus results
in 47
chromosomes.
include motor
delays,
abnormal
muscle tone,
poor postural
control, reflex
abnormalities,
high risk for
hip
dislocations,
and
perceptual
skills. Pt may
also have
mental
retardation
(50-60%),
hearing
impairments,
constipation.
Some
DS is the most
theories
common
suggest than cause of MR.
an increase in Pt will present
maternal age with
(and age of
hypotonia,
the oocyte)
flattened
may cause
nasal bridge,
predispositio almondn to errors in shaped eyes,
meiosis.
abnormally
Environment shaped ears.
al factors
Simian line
such as virus, (palmar
characteristics
.
a non-progressive
but permanent
condition.
Prognosis for mild
to moderate CP is
a near normal
lifespan. 50% of
children with
severe CP die by
the age of 10.
During
pregnancy a
female can be
tested for
Alphafetoprotein,
human
chorionic
gonadotropin,
and
unconjugated
estrogen
levels (the
triple screen).
Team approach
that requires life
long intervention.
PT intervention
play a role in
developmental
delay, hypotonia,
laxity of ligaments,
and poor strength
are key areas of tx.
Positioning and
handling are key
components in
order to maximize
paternal age,
medical
exposure,
reproductive
medications,
and intrinsic
predispositio
ns have been
associated
with DS.
crease),
epicanthal
folds,
enlargement
of the tongue,
congenital
heart disease,
developmenta
l delay, and a
variety of MS
disorders.
Three
diagnostic
studies
include
chorionic
villsu
sampling,
amniocentesis
or
percutaneous
umbilical
blood
sampling.
Detection of
DS occurs in
~60-70% in
the women
tested that
are carrying a
baby with DS.
After birth a
chromosome
analysis called
a karyotype
can be
performed to
confirm the
suspected
diagnosis. Pt
will have AA
(atlantoaxial)
instability,
sensory,
hearing and
proper alignment
and to minimize
pathological
reflexes,
malalignment, and
instability.
Individual with DS
today have a
longer life
expectancy
secondary to
advances in
medical care,
however, it is still
less than standard.
Approx 80% reach
the age of 55.
Duchenne
Muscular
Dystrophy
(DMD)
Is a progressive
NM
degenerative
disorder than
manifests
symptoms once
fat and
connective
tissue being to
replace muscle
that has been
destroyed by
the disease
process. The
mutation of the
dystrophin gene
causes the
symptoms of
DMD.
Inheritance
as an X-linked
recessive
trait. The
mother is the
silent carrier
of this
disorder.
Since it is a
recessive
trait, only
male
offspring will
manifest the
disorder
while female
offspring
become
carriers.
Diagnosis
occurs
between 2-5
years of age
of only males.
The first
symptoms
include
waddling gait,
proximal
muscle
weakness,
clumsiness,
toe walking,
excessive
lordosis,
pseudohypert
rophy of the
calf and other
muscle
groups, and
difficulty
climbing
stairs. DMD
primarily
affects the
shoulder
girdle
musculature,
pects, delts,
rectus
abdominis,
visual
impairments.
Electromyogra
phy is used to
examine the
electrical
activity within
the muscles. A
muscle biopsy
can be
performed to
determine the
absence of
dystrophin
and evaluate
the muscle
fiber size. DNA
analysis and
high serum
creatinine
kinase levels n
the blood also
assist with
confirming the
diagnosis.
Treatment focuses
on maintaining
function of the
unaffected
musculature for as
long as possible.
PT is initially
indicated to assist
a young child with
progression
through the
developmental
milestones. PT
should focus on
maintaining
available strength,
encouraging
mobility, adapting
to the loss of
function. And
promoting family
involvement in a
home program.
MMT and ROM
should be
evaluated on a
consistent basis to
determine the
pattern and rate
of disability.
Orthotics, Ads,
and wheelchair
Erb’s Palsy
A term used to
denote an upper
brachial plexus
injury or palsy
that usually
results from a
difficult birth.
One side of
the baby’s
neck is
stretched
which
damages the
nerves. If the
gluteals,
hamstrings,
and calves. Pt
initially has
difficulty
getting off the
floor, needing
to use the
Gowers’
maneuver.
Approx 1/3 of
pts have some
form of
learning
disability
secondary to
the
dystrophin
abnormalities.
There is
usually rapid
progression of
this disease
with the
inability to
ambulate by
10-12 years.
There are 4
types of
brachial
plexus
injuries:
avulsion,
rupture,
prescription are
areas that will
require attention.
Respiratory care
will also become a
vital part. DMD is
a progressive
disorder and
progresses rapidly.
Death occurs
primarily from
cardiopulmonary
complications.
Death usually
takes place by the
time a pt is a
teenager or less
frequently into
their 20s.
An x-ray or
MRI may be
performed to
see if there is
any damage
to the bones
and joints of
PT is recommened
for a pt with Erb’s
palsy with focuses
on increasing
active & passive
movement and
promoting use to
This type of
injury is the
most common
palsy related to
the brachial
plexus. It
primarly affects
the muscles of
the shoulder
and elbow. The
muscles
affected are
those supplied
by cervical roots
C5 & C6;
axillary, lateral
pectoral, upper
and lower
subscapular,
suprascapular,
and partial
paralysis of the
long thoracic
and
musculocutaneo
us nerves. The
result is loss of
rotator cuff,
deltoid,
brachialis,
coracobrachials,
and biceps.
upper nerves
are affected
the condition
is termed
Erb’s palsy.
One theory
suggests that
congenital
chicken pox
or amniotic
bands may
also produce
this
condition.
When it
occurs in
adults, the
cause
typically is an
injury that
has caused
stretching,
tearing, or
other trauma
to the upper
brachial
plexus
network. The
chance of an
infant having
a brachial
plexus palsy
is equally
distributed
neuroma, and
neurapraxia,
The clinical
presentation
is a flaccid
paralysis that
is nicknamed
the “Waiter’s
tip deformity”
characterized
by a loss of
shoulder
function, loss
of elbow
flexion,
forearm
pronation,
and the hand
positioned in
a pinch grip
manner.
the neck and
shoulder. The
physician may
also use an
EMG or nerve
conduction
studies to see
if any nerve
signals are
present.
the weak UE for
functional
activities. If a pt
has spontaneous
recovery of active
movements within
3-4 months, the
caregivers are
given a home
program. If
conservative tx
fails, surgery is
indicated. Surgery
will not restore
normal function.
After surgery, the
infant will wear a
splint for ~3-4
weeks. Caregiver
education is very
important
regarding
positioning and
handling to avoid
further traction.
Approx. 9 out of
10 infants with
brachial plexus
palsy can recover
with conservative
treatment. Since
nerves grow at a
rate of 1 inch per
month, it may
according to
gender,
gestational
age, and
race.
Guillain-Barre
Syndrome
(GBS)
Or acute
polyneuropathy
is a temporary
inflammation
and
demyelinaton of
the peripheral
nerves’ myelin
sheaths,
potentially
resulting in
axonal
degeneration.
GBS results in
motor weakness
and in a distal to
proximal
progression,
sensory
impairment, and
possible
respiratory
paralysis.
Unknown,
however it is
hypothesized
to be an
autoimmune
response to a
previous
respiratory
infection,
influenza,
immunization
, or surgery.
Viral
infections,
cytomegalovi
rus, bacterial
infections,
surgery and
vaccinations
have been
associated
with the
development
of GBS.
Can occur at
any age, there
is a peak in
frequency in
the young
adult
population
and again in
adults that
are between
their 5th and
8th decades.
Incidence is
slightly
greater in
males than
females and
in Caucasians
than African
Americans. Pt
will initially
present with
distal
symmetrical
weakness and
will
experience
GBS can be
diagnosed
through a
cerebrospinal
fluid sample
that contains
high protein
levels and
little to no
lymphocytes.
Electromyogra
phy will result
in abnormal
and slowed
nerve
conduction.
take several
months or even
years for nerves
repaired at the
cervical spine to
reach the muscles
of the hand.
May require
hospitalization for
treatment of
symptoms. A
tracheostomy may
be performed for
ventilation. PT
should be initiated
upon admission to
the hospital with
focus on PROM,
positioning, and
light exercise.
During the acute
stage a therapist
must limit over
exertion and
fatigue to avoid
exacerbation of
symptoms. As the
pt progresses,
intervention may
include orthotic,
wheelchair or AD
prescription,
family teaching,
gait training. The
sensory
impairments
& transient
paresthesias.
The weakness
will progress
towards the
upper
extremities
and head. The
level of
disability
usually peaks
within 2 to 4
weeks after
onset. Muscle
& respiratory
paralysis,
absence of
DTRs. GBS can
be life
threatening if
there is
respiratory
involvement.
Huntington’s
Disease (HD)
AKA
Huntington’s
Chorea, is a
neurological
disorder of the
CNS and is
HD is
genetically
transmitted
as an
autosomal
dominant
The average
age for
developing
symptoms
ranges
between 35 &
MRI or CT
scan may
indicate
atrophy or
abnormalities
within the
pool may be
indicated to
initiate movement
without the
effects of gravity.
PT may assist with
recovery, but it
can’t alter the
course of the
disease. PT may
be required on an
ongoing basis to
assist w recover
that can last from
3-12 months.
Recover is slow
and can last up to
2 years after
onset. Although
most pts
experience full
recovery, statistics
indicated that 20%
have remaining
neurologic deficits
and 3-5% die from
respiratory
complications.
PT should
maximize
endurance,
strength, balance,
postural control,
and functional
characterized by
degerneration &
atrophy of the
basal ganglia
(specifically the
striatum) and
cerebral cortex
within the brain.
trait with the
defect linked
to
chromosome
four and to
the gene
identified as
IT-15. The
disease is
usually
perpetuated
by a person
that has
children prior
to the normal
onset of
symptoms &
without
knowledge
that he/she
possesses the
defective
gene. Genetic
testing is able
to identify
the defective
gene for HD
prior to the
onset of
symptoms.
55. HD is a
disease that
produces a
movement
disorder,
affective
dysfunction,
and cognitive
impairment.
Pt will initially
present with
involuntary
choreic
movements
and a mild
alteration in
personality.
Unintentional
facial
expressions
such as a
grimace,
protrusion of
the tongue,
and elevation
of the
eyebrows are
common. As
the disease
progresses
gait will
become ataxic
and a pt
experiences
cerebral
cortex as well
as the basal
ganglia. PET
may be used
to augment
other testing
and obtain
info regarding
blood flow,
oxygen
uptake, and
metabolism of
the brain. A
DNA marker
sutyd may be
administered
to determine
if the
autosomal
dominant trait
is present for
HD.
mobility. Pt
education should
include prone
lying, stretching,
prevention of
deformity and
contracture, and
safety with
mobility. As the
disease progresses
the degree of
dementia will
influence
treatment and
goals. HD is a
chronic
progressive
genetic disorder
that is fatal within
15-20 years after
clinical
manifestation.
Late stages of the
disease result in
total physical and
mental
incapacitation.
The pt usually
requires an
extended care
facility due to the
burden of care &
physical, cognitive,
and emotional
Multiple
Sclerosis
MS produces
patches of
demyelination
that decreases
the efficiency of
nerve impulse
transmission.
Symptoms vary
Genetics,
viral
infections,
and
environment
all have a
role in the
development
choreoathetoi
d movement
of the
extremities
and trunk.
Speech
disturbances
& mental
deterioration
are common.
Late stage HD
is
characterized
by a ↓ in IQ,
dementia,
depression,
dysphagia,
incontinence,
inability to
ambulate or
transfer, and
progression
from
choreiform
movements
to rigidity.
Differs by
geographic
area, sex, and
race. MS can
be classified
as relapsingremitting
(85%),
dysfunction.
There is not a
single testing
procedure to
diagnose MS
early in the
disease. MRI
may assist
with
The goal of
medical treatment
is to lessen the
length of
exacerbations and
maximize the
health of the pt.
PT includes
based on the
location &
extent of
demyelination
of MS. It is
theorized
that a slow
acting virus
initiates the
autoimmune
response in
individuals
that have
environment
al and
genetic
factors of the
disease. The
incidence of
MS is higher
in Caucasians
between 20
& 35 years
and is nearly
twice as
common in
women as in
men. There is
also a higher
incidence of
MS in
temperate
climates.
secondary
progressive,
primary
progressive,
or progressive
relapsing.
Initial
symptoms
include visual
problems,
paresthesias,
and sensory
changes,
clumsiness,
weakness,
ataxia,
balance
dysfunction,
and fatigue.
observation
and
establishing a
baseline for
lesions,
evoked
potentials
may
demonstrate
slowed nerve
conduction,
and
cerebrospinal
fluid can be
analyzed for
an elevated
concentration
of gamma
globulin and
protein levels.
regulation of
activity level,
relaxation and
energy
conservation
techniques,
normalization of
tone, balance
activities, gait
training, core
stabilization, &
adaptive/assistive
device training. Pt
and caregiver
education
regarding safety,
energy
conservation,
patterns of
fatigue, and the
use of AD is vital
to the quality of
life. Exercise in the
morning when the
pt is rested and to
avoid fatigue.
Factors that
influence
exacerbations
include heat,
stress, infection,
trauma, and
pregnancy. Most
pts live with MS
Parkinson’s
Disease
This syndrome
occurs as a
secondary effect
or disorder from
another disease
process.
Parkinsons’
Contributing
factors that
can produce
symptoms of
Parkinson’s
include
genetic
The risk for
developing
increases with
age, 1:100 are
affected over
the age of 75.
Majority of
There are no
laboratory or
imaging
studies that
initially
diagnose
Parkinson’s.
for many years
and die from
secondary
complications
such as disuse
atrophy, pressure
sores,
contractures,
fractures, renal
infection, and
pneumonia. If left
untreated 50% of
pts will require a
w/c within 15
years post
diagnosis. Overall
mortality rate and
long-term
outcome
correlates to age
at diagnosis,
number of attacks
& exacerbations,
frequency &
duration of
remissions & type
of MS
The medical
management of
Parkinson’s
disease relies
heavily on
pharmacological
intervention.
disease is a
primary
degenerative
disorder and is a
characterized by
a decrease in
production of
dopamine
(neurotransmitt
er) within the
corpus striatum
portion of the
basal ganglia.
The
degeneration
bof the
dopaminergic
pathways
creates an
imbalance
between
dopamine and
acetylcholie.
This produces
the symptoms
of Parkinsons’s.
defect,
toxicity from
carbon
monoxide,
excessive
manganese
or copper,
carbon
disulfide,
vascular
impairment
of the
striatum,
encephalitis,
and other
neurodegene
rative
diseases such
as
Huntington’s
disease or
Alzheimer’s
disease.
pts are
between 5079 years.
Initially pts
will notice a
resting tremor
in the hands
(pill rolling) or
feet that
increases with
stress and
disappears
with
movement or
sleep. Early in
the disease
process a pt
may attribute
symptoms to
“old age” such
as balance
disturbances,
difficulty
rolling over
and rising
from bed, and
impairment
with fine
manipulative
movements
seen in
writing,
bathing, &
dressing. A
CT scan or
MRI may be
used to rule
out other
neurodegener
ative disease
and obtain a
baseline for
future
comparison.
Dopamine
replacement
therapy
(Levadopa,
Siinemet,
Madopar) is the
most effective
treatment in
reducing
symptoms. PT
should include
maximizing
endurance,
strength, and
functional
mobility. Verbal
cueing and
oral/visual
feedback are
effective tools to
use with this
population. PT is
recommened on
an intermittent
basis. Parkison’s
disease does not
significantly alter a
pts lifespan if the
pt is diagnosed
with a generalized
form between 5060 years. As the
disease
progresses,
Spina BifidaIncomplete
Myelomening fusion of the
ocele
posterior
vertebral arch
with both
meninges and
spinal cord
pts symptoms
slowly
progress and
often include
hypokinesia,
sluggish
movement,
difficulty with
initiating
(akinesia) and
stopping
movement.
Festinating
and shuffling
gait,
bradykinesia,
poor posture,
dysphagia,
and
“cogwheel” or
“lead pipe”
rigidity of
skeletal
muscles.Mask
like with no
facial
expression.
The incidence Impairments
varies by
associated
socioeconomi include motor
c status,
and sensory
geographic
loss below the
area, and
vertebral
ethnic
defect,
however, there
will be an
exacerbation of all
symptoms and
significant loss of
mobility. The
inactivity &
Deconditioning
allows for
complications and
eventual death.
Prior to birth a
fetal
ultrasound
may identify
the
myelomening
ocele defect in
Immediate
surgical
intervention to
repair and close
the defect and for
placement of
shunt to alleviate
protruding
outside the
neural arch.
Characterized
by a sac or cyst
that protrudes
outside the
spine.
background.
The overall
incidence is
declining due
to improved
prenatal
care.
Prenatal care
including
recommende
d amounts of
folic acid,
especially in
the first 6
weeks of
pregnancy,
appears to be
the most
effective way
to prevent
neural tube
defects.
hydrocephalu
s, ArnoldChiari type II
malformation,
clubfoot,
scoliosis,
bowel &
bladder
dysfunction,
and learning
disabilities.
The higher
the lesion the
worse the
prognosis is
for survival. In
90% of the
cases a shunt
is required for
hydrocephalu
s. Approx 2/3
of children
with
myelomening
ocele and
shunted
hydrocephalu
s have normal
intelligence
and the other
third
demonstrate
only mild
retardation.
the spine.
Prenatal
testing of
alphafetoprot
ein (AFP)in
the blood will
show and
elevation in
levels that
indicate a
probably
neural tube
defect at
approx. week
16 of
gestation. At
birth an
obvious sac
will be
present over
the spinal
defect.
hydrocephalus. PT
is initiated
immediately and
focuses on family
education
regarding
positioning,
handling
techniques, ROM,
and therapeutic
play. Long term PT
attempts to
maximize
functional
capacity, skin care,
strength, blance,
and mobility, w/c
prescription,
orthotics. A pt
with
myelomeningocle
has a near normal
life expectancy as
long as the pt
receives
consistent and
thorough health
care. Functional
outcome of the pt
depends on the
level of injury, the
amount of
associated
impairments, and
Spinal Cord
Injury—
Complete C7
Tetraplegia
After injury, C7
is the most
distal segment
of the spinal
cord that both
the motor and
sensory
components
remain intact.
Motor
Vehicle
Accidents,
violence &
falls are the
top causes.
Higher ratio
of injury in
men (80%)
and
Caucasians.
The highest
incidence of
occurs
between 1530 years of
age.
Regardless of
intelligence,
children
exhibit
difficulties
with
perceptual
abilities,
attention,
problem
solving, and
memory.
Spinal shock
which is the
total
depression of
all nervous
system
function
below the
level of the
lesion occurs
immediately
following
injury and
may last for
days. Include
flaccid
paralysis and
loss of all
reflexes &
sensation.
Surgical
intervention
the caregiver
support that is
provided.
X-rays of the
cervical spine
observe the
positioning
and damage
of the
involved
vertebrae. The
results of
imaging
determine
subsequent
medical
intervention
including
stabilization of
the spine.
The acute phase
begins at injury
and includes
medically
stabilizing the pt.
Inpatient rehab
(typically 6-8
weeks) should
initially focus on
ROM, positioning
in bed, and cough,
clearance of
secretions,
bronchial
drainage, and
incentive
spirometry.
Compensatory
techniques,
strengthening,
muscle
substitution, and
may be
required after
injury in order
to stabilize
the spinal
cord through
decompressio
n and fusion
at the site of
injury. A Halo
device is
commonly
used with
cervical
injuries to
stabilize the
spine. As sock
subsides, a pt
will
experience an
↑ in muscle
tone below
the level. A pt
with C7
tetraplegia
will also
present with
impaired
cough and
ability to clear
secretions,
altered
breathing
pattern and
the use of
momentum and
the head-hips
relationship
should be utilized
during all
activities. Ongoing
intervention
should include
mat skills, selfROM, transfer
skills, and
community
reintegration.
Typical outcomes
at this level
include
independence
with feeding,
grooming, and
dressing, selfROM,
independent
manual
wheelchair
mobility,
independent
transfers, and
independent
driving with an
adapted
automobile.
Independent living
with adaptive
poor
endurance.
Spinal Cord
Injury—
Complete L3
Paraplegia
A pt sustains
primary damage
to the spinal
cord and
surrounding
tissues at the L3
level through
the disruption
of the
membrane,
displacement or
compression of
the spinal cord,
& subsequent
hemorrhage and
vascular
damage. After a
complete injury
at this level, L3
is the most
distal segment
Motor
Vehicle
Accidents,
violence &
falls are the
top causes.
Higher ratio
of injury in
men (80%)
and
Caucasians.
The highest
incidence of
occurs
between 1530 years of
age.
Pts specifically
with a
complete
lesion at the
L3 level
typically have
a least partial
innervation of
the gracilis,
iliopsoas,
quadratus
lumborum,
rectus
femoris, and
Sartorius. Pts
have full use
of their UEs
and have hip
flexion,
adduction,
and knee
The
evaluation of
a pt with an
acute lumbar
spine fracture
should include
routine lab
tests, such as
CBC, and
electrolytes.
X-rays, CT
scan, and MRI
allows for
bony and
ligamentous
injury
diagnosis.
equipment is
possible. The
triceps, extensor
pollicis longs and
brevis, extrinsic
finger extensors,
and flexor carpi
radialis will remain
the lowest
innervated
muscles. Life
expectancy over
45 years of age.
Stabilization of the
pts airway in order
to secure
adequate
oxygenation. All
pts with spinal
cord injury should
immediately
receive
intravenous
methylprednisolo
ne since it has
proven to control
the amount of
secondary damage
and improve the
neurological
outcome. The pt
may be placed in a
thoracolumbar
orthosis (TLSO)
of the spinal
cord that both
the motor and
sensory
components
remain intact.
extension.
with restriction of
activities or
undergo
stabilization
surgery followed
by the use of a
TLSO. Orthotic
prescription
(KAFOs or AFOs) is
recommended
once the pt has
gained strength to
assist with
ambulation using
crutches. A pt with
L3 SCI will usually
participate in 4-8
weeks of inpatient
rehab immediately
after injury and
stabilization. The
pt should be able
to function
independently
from a w/c level
and ambulation
level. Outcome is
based on the
degree of injury,
the pts mental
capacity, outside
support,
emotional
stability, and co-
Thoracic
Outlet
Syndrome
Is a term used
to describe a
group of
disorders that
presents with
symptoms
secondary to
neurovascular
compression of
fibers of the
brachial plexus.
This usually
occurs between
the points of the
interscalene
triangle and the
inferior border
of the axilla.
Compression of
the nerves and
blood supply
can occur as
they pass over
the first rib.
Results from
compression
and damage
the brachial
plexus nerve
trunks,
subclavian
vascular
supply,
and/or the
axillary
artery.
Contributing
factors in the
development
of TOS
include the
presence of a
cervical rib,
an abnormal
first rib,
postural
deviations or
changes,
body
composition,
chronic
hyperabducti
on of the
arm,
hypertrophy
or spasms of
the scalene
Will present
with
symptoms
based on
nerve and/or
vascular
compression.
Typical
symptoms
include
diffuse pain in
the arm most
often at night,
paresthesias
in the fingers
and through
the upper
extremities,
weakness &
muscle
wasting, poor
posture,
edema, and
discoloration.
If the upper
plexus is
involved, pain
will be
reported in
the neck and
may radiate
to the face
and follow the
X-ray will
confirm the
presence of a
cervical rib or
other bony
abnormality.
Nerve
conduction
velocity
testing may
be valuable if
a neuropathy
exists.
Otherwise,
diagnosis
relies solely
on a through
history of a
pts symptoms,
provocative
testing, and
physical exam.
Adson’s,
wright, roos,
sallen,
Halstead
maneuver,
hyperabductio
n.
morbidities.
Initially
management
takes a
conservative
approach, it that
fails its followed
by surgical
intervention. PT
require
intervention to
assist with
modification of
posture, breathing
patterns,
positioning in bed
and at the work
site, and gentle
stretching. Should
focus on pain
magnt,
strengthening
(trap, levator, and
rhomboids) joint
mobs, body
mechanics,
flexibility. If a pt
has positive result
from PT there will
not be any long
term impairments,
however if they
persist for 3 to 4
months, surgery
muscles,
degenerative
disorders,
and an
elongated
cervical
transverse
process.
Traumatic
Brain Injury
(TBI)
Injury where the
brain makes
contact with the
skull secondary
to a sudden
violent
acceleration or
deceleration
impact. Can also
occur secondary
to anoxia as
with cardiac
arrest or near
drowning.
lateral aspect
of the
forearm into
the hand. If
the lower
plexus is
involved, pain
is reported in
the back of
the neck and
shoulder,
which will
radiate over
the ulnar
distribution of
the hand.
Falls and
Altered
motor vehicle consciousness
accidents are (coma,
the leading
obtundity,
causes. High
delirium),
risk groups
cognitive and
include ages
behavioral
0-4, 15-19,
deficits,
and greater
changes in
than 65.
personality,
Males are at
motor
a greater risk. impairments,
alterations in
tone, speech
and
swallowing
issues.
may be
warranted. PT
should allow pts
to return to
previous activity
within 4-8 weeks.
CT scan or
MRI should be
performed
immediately
in order to
rule out
hemorrhage,
infarction, and
swelling. Xrays taken of
the cervical
spine can be
used to rule
out fx and
potential for
subluxation.
An EEG, PET,
and cerebral
Medical mangt
initiated at the site
of injury or in the
emergency room
for life preserving
measures. Once
stable, PT rehab in
initiated and
treatment
includes PROM for
a comatose pt or
pathfinding and
high-level balance
for a pt with mild
injury. Mobility
tranining,
behavior
modification,
blood flow
mapping may
also be
utilized for
diagnosis and
baseline data.
serial casting,
compensatory
strategies,
vestibular rehab,
task specific
activities, w/c
seating. Outcome
is based on the
degree of primary
and secondary
damage. Many pts
experience long
term deficits that
don’t allow them
to return to their
pre-injury lifestyle.
NM Medications:
Drug
Action
Indications
Side effects
Antiepileptic
Agents
Reduce or
eliminate seizure
activity within the
brain. These agents
attempt to inhibit
the firing of certain
cerebral neurons
through various
Seizure
activity
(partial,
generalized,
and
unclassified
seizures)
Ataxia, skin
issues,
behavioral
changes, GI
distress,
headache,
blurred vision,
weight gain
Implication
s for PT
Therapists
must have
adequate
knowledge
of
established
protocols
for
Examples
Seconal
(secobarbital),
Klonopin
(clonazepam),
Depakote
(valproic acid),
Dilantin
(phenytoin),
effects on the CNS.
Chemical
classifications
include
barbiturates,
benzodiazepines,
carboxylic acids,
hydantoins,
iminostilbenes,
succinimides, and
second generation
drugs.
Antispasticity
Agents
Promote relaxation
in a spastic muscle.
Spasticity is an
exaggerated
stretch reflex of the
muscle that can
occur after injury
to the CNS.
Spasticity is not a
primary condition,
but a secondary
effect from CNS
damage. Agents
Increased
tone,
spasticity, SCI,
CVA, MS
Drowsiness,
confusion,
headache,
dizziness,
generalized
muscle
weakness,
hepatotoxicity
potential with
Dantrium,
tolerance,
dependence
responding
to a seizure
as well as
potential
side effects
of
antiepilepti
c
medication
s. Pts with
epilepsy
may show
greater
sensitivity
to
environme
ntal
surroundin
gs such as
light or
noise level.
Therapists
must
balance the
need to
decrease
spastic
muscles
with the
loss of
function
that a pt
may
experience
Tegretol
(carbamazepine0
, Celontin
(methsuximide),
Neurontin
(gabapentin)
Lioresal
(baclofen),
Valium
(diazepam),
Dantrium
(dantrolene),
Zanaflex
(tizanidine)
bind selectively
within the CNS or
within the skeletal
muscle cells to
reduce spasticity.
Cholinergic
Agents
Cholinergic direct
stimulant agents
mimic
acetylcholine and
bind directly to the
Glaucoma,
dementia due
to Alzheimer’s
disease,
postoperative
GI distress,
impaired
visual
accommodati
on,
with the
reduction
of
hypertonici
ty. Once
spasticity is
reduced,
therapists
should
focus on
therapeutic
handling
techniques,
facilitation,
and
strengtheni
ng to
promote
overall
mobility.
Sedation
may also
alter the
scheduling
of therapy
to allow for
maximal
participatio
n.
Pts may
experience
a ↓ in HR
and
dizziness.
Direct: Duvoid
(bethanechol),
Pilocar
(pilocarpine)
Indirect: Aricept
Dopamine
cholinergic
receptor to activate
& create a
response at the
cellular level.
Indirect acting
cholinergic
stimulants increase
cholinergic synapse
activity through the
inhibition of
acetylcholinesteras
e (which normally
destroys
acetylcholine). The
increase of
acetylcholine at the
synapse increases
cholinergic synaptic
transmission.
↓in GI
motility,
myasthenia
gravis,
reversal of
anticholinergi
c toxicity
bronchoconstr
iction,
bradycardia,
flushing, other
parasympathe
tic effects
Assist to relieve the
Parkinsons’
Arrhythmias
Therapist
would be
aware of
characterisi
cs of both
sympatheti
c and
parasympa
thetic
systems
and notify
the
physician if
pt begins
to exhibit
unexpected
side
effects. Pts
with
Alzheimer’s
disease and
myasthenia
gravis may
be better
able to
participate
in
therapeutic
activities
when
taking
cholinergic
agents.
Therapists
(donepezil),
Tensilon
(endrophonium),
Prostigmin
(neostigmine),
Cognex (tacrine)
Sinemet or
Replacement
Agents
symptoms of
Parkinson’s disease
secondary to the ↓
in endogenous
dopamine. These
agents are able to
cross the bloodbrain barrier
through active
transport and
transform to
dopamine within
the brain.
disease,
Parkinsonism
(levadopa), GI
distress,
orthostatic
hypotension,
dyskinesias,
mood and
behavioral
changes,
tolerance
& pts attain
maximal
benefit
from
scheduling
therapy
one hour
after
administrat
ion of
levadopa.
Therapist
must
understand
the
debilitating
effects of
drug
holidays
and should
monitor
the pts BP
frequently
due to the
potential
for
orthostatic
hypotensio
n.
Madopar
(levadopa),
Symmetrel
(amantadine)
Muscle
Relaxant
Agents
Promote relaxation
in muscles that
typically present
with spasm that is
Muscle spasm
Sedation,
drowsiness,
dizziness,
nausea,
Therapists
must be
aware of
the
Valium
(diazepam),
Flexeril
(cyclobenzaprine)
a continuous, tonic
contraction.
Spasms typically
occur secondary to
a MS or peripheral
nerve injury rather
than CNS injury.
vomiting,
headache,
tolerance,
dependence
potential
side
effects,
however,
maximize
the
potential
for
relaxation
through
therapeutic
techniques
and the use
of
modalities
during
treatment.
Prevention
of reinjury
through
stretching,
posture
retraining,
and
education
should
assist the
pt to
achieve
desired
outcomes.
, Paraflex
(chlorzoxazone)
Neuromuscular Rehab:
Grading Spasticity: Modified Ashworth Scale
Grade
0
1
1+
2
3
4
Description
No increase in muscle tone
Slight increase in muscle tone,
minimal resistance at the end
of ROM
Slight increase in muscle tone,
minimal resistance through
less than half of the ROM
More marked increase in
muscle tone, through most of
ROM, but affected part easily
moved
Considerable increase in
muscle tone, passive
movement difficult
Affected part rigid in flexion or
extension
Balance:
•Somatosensory Input:
Somatosensory receptors are located in the joints, muscles, ligaments, and skin to provide proprioceptive information regarding length, tension,
pressure, pain, and joint position. Proprioceptive and tactile input from the ankles, knees, hips, and neck provide balance information to the
brain.
Challenging the somatosensory system: examination of pressure and vibration; observation of a pt when changing the surface they are standing
on. Examples would be slopes, uneven surfaces, standing on foam.
•Visual Input:
Visual receptors for perceptual acuity regarding verticality, motion of objects and self, environmental orientation, postural sway, and
movements of the head/neck. Children rely heavily on this system for maintenance of balance.
Challenging the visual system: examination of quiet standing with eyes open, observing balance strategies to maintain center of gravity with
and without visual input. Assessment of potential visual field cuts, hemianopsia, pursuits, saccades, double vision, gaze control, and acuity is
necessary.
•Vestibular Input:
The vestibular input provides the CNS with feedback regarding the position and movement of the head with relation to gravity. The labyrinth
consists of three semicircular canals filled with endolymph and two otolith organs. Semicircular canals respond to the movement of fluid with
head motion. Otoliths measure the effects of gravity and movement with regard to acceleration/deceleration.
Challenging the vestibular system: examination of balance with movement of the head; testing such as Dix-hallpike maneuver, bithermal caloric
testing, assessment for nystagmus, head thrust sign; testing of the vestibulocular reflex.
Balance Reflexes:
Vestibuloocular reflex (VOR)
Vestibulospinal reflex (VSR)
VOR allows for head/eye movement coordination. This reflex supports
gaze stabilization through eye movement that counters movements of
the head. This maintains a stable image on the retina during
movement.
VSR attempts to stabilize the body and control movement. The reflex
assists with stability while the head is moving as well has coordination
of the trunk during upright postures.
Automatic Postural Strategies: Are automatic motor responses that are used to maintain the center of gravity over the base of support. These
responses always react or respond to a particular stimulus.
Ankle strategy:
Hip strategy:
The ankle strategy is the first strategy to be elicited by a small range and slow
velocity perturbation when the feet are on the ground. Muscle groups contract in
a distal to proximal fashion to control postural sway from the ankle joint.
The hip strategy is elicited by a greater force, challenge or perturbation through
the pelvis and hips. The hips will move (in the opposite direction from the head) in
Suspensory
strategy:
Stepping strategy:
order to maintain balance. Muscle groups contract in a proximal to distal fashion
in order to counteract the loss of balance.
The suspensory strategy is used to lower the center of gravity during standing or
ambulation in order to better control the center of gravity. Examples of this
include knee flexion, crouching or squatting. This strategy is often used when both
mobility and stability are required during a task (such as surfing)
Is elicited through unexpected challenges or perturbations during static standing
or when the perturbation produces such a movement that the center of gravity is
beyond the base of support. The lower extremities step and/or upper extremities
reach to regain a new base of support.
Vertigo is used to describe a sense of movement and rotation of oneself or the surrounding environment. It typically is a sensation of spinning,
but can also present as liner motion or falling. Vertigo may have a peripheral or central origin.
Characteristics of Central Vs. Peripheral Vertigo:
Peripheral
Episodic and short
duration
Autonomic
symptoms present
Precipitating factor
Central
Autonomic symptoms
less severe
Loss of consciousness
can occur
Neurological symptoms
present including:
-diplopia
-hemianopsia
-weakness
-numbness
-ataxia
-dysarthria
Pallor, sweating
Nausea and
vomiting
Auditory fullness
(fullness within the
ears)
Tinnitus
Etiology of Central Vs. Peripheral Vertigo
Peripheral
Benign paroxysmal
positional vertigo
(BPPV)
Meniere’s disease
Infection
Trauma/tumor
Metabolic disorders
(DM)
Acute alcohol
intoxication
Central
Meningitis
Migraine headache
Complications of
neurologic origin post
ear infections
Trauma/tumor
Cerebellar degeneration
disorders (alcoholism)
Multiple Sclerosis
Benign paroxysmal positional vertigo (BPPV): this condition is comprised of repeated episodes of vertigo that occur subsequent to changes in
head position. BPPV only lasts a few seconds and is typically first noted while in a recumbent position since it most commonly affects the
posterior semicircular canal. The etiology is usually otoconia (canalith) that loosens and travels into the posterior semicircular canal, causing
vertigo. Nystagmus is present and can be noted when assessing a patient using the Dix-Hallpink test. Pts with BPPV typically find it self-limiting
and can be successfully treated with canalith repositioning maneuvers which are passive movements used to remove the otoconia from the
canals, thus remediating the vertigo.
Dix-Hallpike test: This maneuver is a vertiginous position test used in assessment and treatment. This test stimulates the posterior semicircular
canal and attempts to determine if otoconia exist within the canal. If the pt experiences nystagmus and vertigo, the test is performed to
determine if a pt presents with BPPV or a central lesion.
Procedure:
The initial positioning for the Dix-hallpike test where the pt starts in sitting with the legs extended on the table and head rotated 45° to one side.
The pt is rapidly moved to a supine position with the head (still in 45° rotation) extended 30° beyond horizontal off the end of the table.
The therapist continues to hold the pts head in this position for 20-30 seconds observing the potential for nystagmus. If nystagums exists, the
direction of the eyes and appearance of the nystagmus can determine inner ear versus CNS lesion.
Balance Tests and Measures:
•Berg Balance Scale: this is a tool designed to assess a pts risk for falling. There are 14 tasks, each scored on an ordinal scale from 0-4. These
tasks include static activities, transitional movements, and dynamic activities in sitting and standing positions. The maximum score is a 56 with a
score less than 45 indicating an ↑ risk for falling. This tool can be used as one time examination for as an ongoing tool to monitor a pt who may
be at risk for falls.
•Fregley-Graybiel Ataxia Test Battery: A tool that consists of 8 test conditions used in the battery with each leg measured on 2 accounts, the
time spent in each test position and the number of steps that a pt takes without falling. 5 trials of each condition are performed. The test
conditions include:
-stand on beam with eyes open
-Stand on beam with eyes closed
-walk on beam with eyes open
-sharpened Romberg (heel-toe static positioning)
-standing with eyes open
-standing with eyes closed
-standing on one leg with eyes closed
-walking on the floor with eyes closed
The therapist scores each condition on a pass/fail basis with normative data for comparison. This tool is best suited for pts with high level motor
skills since each condition is challenging. Therapists use this tool to assess and treat balance dysfunction, however, pt performance does not
assist the therapist to diagnose the cause of balance dysfunction.
•Fugl-Meyer Sensorimotor Assessment of Balance performance Battery: this tool is designed as a subset of the Fugl-Meyer Physical
Performance Battery and is designed to assess balance specifically for pts with hemiplegia. Each of the 7 items assessed is scored from 0-2,
specific to each item with the maximum score being 14. Even though 14 is the best score that a person can receive, the pt still may not have
normal balance.
•Functional Reach Test: a single task screening tool used to assess standing balance and risk of falling. A person is required to stand upright with
a static base of support. A yardstick is positioned to measure the forward distance that a pt can reach without moving the feet. Three trials are
performed and averaged together.
The following are age-related standard measurements for functional reach:
20-40 years: 14.5-17 inches
41-69 years: 13.5-15 inches
70-87 years: 10.5-13.5 inches
A pt that falls below the age appropriate range for functional reach has an increased risk for falling. The outcome measure demonstrates high
test-retest correlation and intrarater reliability
•Romberg Test: this is an assessment tool of balance and ataxia that initially positions the pt in unsupported standing, feet together, upper
extremities folded, looking at a fixed point straight ahead with eyes open. With the eyes open, 3 sensory systems (visual, vestibular,
somatosensory) provide input to the cerebellum to maintain standing stability. If there is a mild lesion in the vestibular or somatosensory
systems, the pt will typically compensate through the visual sense.
Next the pt maintains the same standing posture, but closes the eyes. A pt receives a grade of “normal” if they are able to maintain the position
for 30 seconds. An abnormal response occurs with the inability to maintain balance when standing erect with the feet together and the eyes
closed. Pts may exhibit excessive sway or begin to fall. When the visual input is removed, instability will be present if there is a larger
somatosensory or vestibular deficit producing the instability. If a pt demonstrates ataxia and has a positive Romberg test, this indicates sensory
ataxia and not cerebellar ataxia.
There is also a sharpened Romberg test where the pts balance is further assessed by performing in the same manner but with a heel-to-toe
stance, typically with the non-dominant foot in front. The pt would first be tested with eyes open and then with the eyes closed. This
modification increases the challenge to the vestibular and somatosensory systems.
•Timed Get Up and Go Test: this is a functional performance screening tool used to assess a person’s level of mobility and balance. The person
initially sits in a supported chair with a firm surface, transfers to a standing position, and walks approximately 10 feet. The pt must then turn
around without external support, walk back towards the chair, and return to a sitting position. The pt is scored based on amount of postural
sway, excessive movements, reaching for support, side-stepping or other signs of loss of balance. The 5 point ordinal rating scale designates a
score of 1 as normal and a score of 5 as severely abnormal. In an attempt to increase overall reliability the use of time was implemented. Pts
who are independent can complete the multi-task process in 10 seconds or less. Pts that require over 20 seconds to complete the process are at
the limit for functional independence and may be at an increased risk for falling. Pts that require 30 seconds are at high risk for a fall.
•Tinetti Performance Oriented Mobility Assessment: a tool used to screen pts and identify if there is an increased risk for falling. The first
section assesses balance through sit to stand and stand to sit from an armless chair, immediate standing balance with eyes open and closed,
tolerating a slight push in the standing position, and turning 360°. A pt is scored form 0-2 in most categories with a maximum score of 16. The
second section assess gait at normal spend and at a rapid, but safe speed. Items scored in this section include initiation of gait, step length, and
height, step asymmetry and continuity, path, stance during gait, and trunk motion. A pt is scored 0-2 for each with a maximum score of 12. The
tool has combined maximum total of 28 with the risk of falling increasing as the total score decreases. A total score less than 19 indicates a high
risk for a fall.
Vestibular Rehab:
Vestibular rehab is a therapeutic intervention that can be highly successful for pts with vestibular or central balance system disorders. Exercise
protocols for vestibular retraining utilize compensation, adaption, and plasticity to increase the brain’s sensitivity, restore symmetry, improve
vestibulocular control, and subsequently increase motor control and movement.
Goals for vestibular Rehab:
-Improve balance
-Improve trunk stability
-↑ strength and ROM in
order to improve ms balance
responses and strategies
-↓the rate and risk of falls
-Minimize dizziness
Vestibuloocular Retraining Therapeutic Guidelines:
-Vestibuloocular reflex (VOR) and vestibulospinal reflex (VSR)
stimulation exercises
-Ocular motor exercises
-Balance exercises
-Gait exercises
-combination exercises (obstacle courses, functioning in a public
place)
-Habituation training exercises (use only with appropriate pts)
-Individualize each program based on the pts specific impairments
(rehab vs. compensation training)
-Use of practice, feedback, and repetition are vital for skill
refinement
-Use of gravity, varying surface conditions, visual conditions, and
environmental cues should be included in therapeutic planning
-The center of gravity must be controlled at each stage of
treatment
-Strategy (hip, ankle, stepping, suspense) training should be
implemented during treatment so that strategies become
automatic responses
-Force plate systems, electromyographic biofeedback, optokinetic
visual stimulation, and videography are all technical systems that
can provide feedback to motor learning during vestibular rehab
-Foam, mirrors, rocker boards, BAPS boards, Swiss balls, foam
rollers, tramplines, and wedges are lower “tech” treatment tools
that are successfully used to vestibular rehab
CVA Tests and Measures:
There are various tests and measures to assess the different impairments secondary to CVA. Pts are administered specific tests based on clinical
diagnosis and pt presentation.
•National Institute of Health (NIH) stroke scale: assessment of an acute CVA relative to impairment
•Functional Independence Measure (FIM): provides a level of burden through assessment of mobility and ADL management
•Stroke Impact Scale: assessment of physical and social disability or level of impairment secondary to CVA
•Fugl-Meyer Assessment of Physical Performance: motor, sensory, and balance impairment; also assesses pain and ROM
Neurological Rehabilitation:
Neuro rehab may incorporate a variety of treatments based on the pts pathology, problem list, and deficits. There are many forms of
neurological rehab based on each construct’s beliefs regarding motor control and motor learning. A therapist must use therapeutic techniques
that meet the individual pts therapeutic objectives and goals. The following are various theories of neurological rehab based on each theory’s
interpretation of motor control and motor learning.
Motor Control: is the study of the nature of movement; or the ability to regulate or direct essential movement. Historically, control was thought
to arise from reflex or hierarchical models where the cortex was perceived as the highest functioning component of the system and spinal level
reflexes were the lowest functioning components. New models of motor control challenge these theories and believe that there is a greater
distribution of control and that the cortex is not solely at the top of the hierarchy.
Theories in general should provide a framework to interpret the issue or behavior, guide clinical action and treatment, provide new ideas, and
utilize working hypotheses for examination and intervention. There are multiple theories of motor control that each embrace abstract ideas
regarding the actual control of movement and are based on a specifc interpretation of how the brain functions and interacts with other body
systems. Some of the motor control theories include the Reflex theory, Hierarchical theory, Motor programming theory, Task-oriented theory,
and ecological theory.
●Motor Learning:
Motor learning is the study of the acquisition or modification of movement. Motor learning differentiates learning versus performance, provides
guidelines for appropriate use of feedback, prioritizes the impact of practice as it relates to skill and movement, and also focuses on the transfer
of learning across tasks and environments of practice. Two of the initial theories of motor learning include:
•Adam’s closed loop theory: The first attempt at the creation of a comprehensive motor learning theory with the premise of sensory
feedback as an ongoing process for the nervous system to compare current movement with stored information on memory of past movement;
high emphasis on the concept of practice.
•Schmidt’s schema theory: this theory was created in response to the limitations of the closed loop theory. Its main construct relies on
open loop control processes and a motor program concept; promotes clinical value to feedback and importance of variation with practice.
●Three Stage Model of Motor Learning:
Cognitive Stage: This is the initial stage of learning where there is a high concentration of conscious processing of information. The person will
acquire information regarding the goal of the activity and being to problem solve as to how to attain the goal. A controlled environment is ideal
for learning during this stage and participation is a must for the person to progress.
Characterized by:
-large amount of errors
-inconsistent attempts
-repetition of effort allows for improvement in strategies
-inconsistent performance
-high degree of cognitive work: listening, observing, and processing feedback
Associative Stage: This is the intermediate stage of learning where a person is able to more independently distinguish correct versus incorrect
performance. The person is linking the feedback that has been received with the movement that has been performed and the ultimate goal. A
controlled environment is helpful but at this stage, the person can progress to a less structured or more open environment. Avoid excessive
external feedback as the person should have improved internal or proprioceptive feedback for the task at hand.
Characterized by:
-decreased errors with new skill performance
-decreased need for concentration and cognition regarding the activity
-skill refinement
-increased coordination of movement
-large amount of practice yields refinement of the motor program surrounding the activity
Autonomous Stage: this is the final stage of learning or skilled learning where a person improves the efficiency of the activity without a great
need for cognitive control. The person can also perform the task with interference from a variable environment.
Characterized by:
-automatic response
-mainly error-free regardless of environment
-distraction does not impact the activity
-the person can simultaneously perform more than one task if needed
-extrinsic feedback should be very limited or should not be provided
-internal feedback or self-assessment should be dominant
Feedback: is imperative for the progression of motor learning. A pt will rely on both intrinsic and extrinsic feedback as it relates to movement.
Feedback allows for correction and adaptation within the environment. Current research supports reducing the extrinsic feedback (fading of
feedback) in order to ultimately enhance learning.
Intrinsic (inherent
Represents all feedback that comes to
feedback):
the person through sensory systems
as a result of the movement including
visual, vestibular, proprioceptive, and
somatosensory inputs.
Extrinsic
Represents the information that can
(augmented)
be provided while a task or movement
feedback:
is in progress or subsequent to the
movement. This is typically in the form
of verbal feedback or manual
contacts.
Knowledge of
Is an important form of extrinsic
results:
feedback and includes terminal
feedback regarding the outcome of a
movement that has been performed
in relation to the movement’s goals.
Knowledge of
Is extrinsic feedback that relates to
performance:
the actual movement pattern that
someone used to achieve their goal of
movement.
Practice: refers to repeated performance of an activity in order to learn or perfect a skill. Physical practice allows for direct physical experience
and kinesthetic stimulation to assist with acquisition of the skill. Mental practice is the cognitive rehearsal of a task or experience without any
physical movement.
Massed practice:
The practice time in a trial is greater than the amount
Distributed
practice:
Constant
practice:
Variable practice:
Random practice:
Blocked practice:
Whole training:
Part training:
of rest between trials
The amount of rest time between trials is equal to or is
greater than the amount of practice time for each trial
Practice of a given task under a uniform condition
Practice of a given task under differing conditions
Varying practice amongst different tasks
Consistent practice of a single task
Practice of an entire task
Practice of an individual component or selected
components of a task
Key terminology:
Closed system model:
Compensation:
Habituation:
Learning:
Non-associative:
Associative:
Procedural:
Declarative:
Motor learning:
This is characterized by transfer of information that incorporates multiple
feedback loops and larger distribution of control. In this model, the nervous
system is seen as an active “participant” with the ability to enable the initiation
of movement as opposed to solely “reacting” to stimuli.
The ability to utilize alternate motor and sensory strategies due to an
impairment that limits the normal completion of a task.
The decrease in response that will occur as a result of consistent exposure to
non-painful stimuli.
The process of acquiring knowledge about the world that leads to a relatively
permanent change in a person’s capability to perform a skilled action.
A single repeated stimulus (habituation, sensitization)
Gaining understanding of the relationship between two stimuli, causal
relationships or stimulus and consequence (classical, operant conditioning)
Learning tasks that can be performed without attention or concentration to
the task; a task is learned by forming movement habits (developing a habit
through repetitive practice)
Requires attention, awareness, and reflection in order to attain knowledge
that can be consciously recalled (internal practice)
The ability to perform a movement as a result of internal processes that
Motor program:
Open system model:
Performance:
Plasticity:
Postural control:
Recovery:
Sensitization:
Strategy:
interact with the environment and produce a consistent strategy to generate
the correct movement. It is the acquisition of, or modification of movement.
A concept of a central motor pattern that can be activated by sensory stimuli
or central processes. Motor programs are seen as containing the rules for
creating spatial and temporal patterns of motor activity needed to carry out a
given motor task.
This is characterized by a single transfer of information without any feedback
loop (reflexive hierarchial theory). In this theory, the nervous system is seen as
awaiting stimuli in order to react.
A temporary change in motor behavior seen during a particular session of
practice that is a result of many variables, however, only one variable is
focusing on the act of learning. Performance is not an absolute measure of
learning since there are multiple variables that potentially affect performance.
The ability to modify or change at the synapse level either temporarily or
permanently in order to perform a particular function.
The ability of the motor and sensory systems to stabilize position and control
movement.
The ability to utilize previous strategies to return to the same level of
functioning.
The increase in response that will occur as a result of a noxious stimuli.
A plan used to produce a specific result or outcome that will influence the
structure or system.
●Carr & Shepherd: Motor Relearning Approach:
An approach developed by Janet Carr and Roberta Sheperd in the 1970’s that targets normal movement and how it is relearned after
neurological insult. Carr and Shepherd’s construct is that factors that are involved with learning are also involved with relearning and should
include:
•Identification of a goal
•inhibition of any unnecessary activity that does not relate to normal movement
•the ability to adjust during activity to the effects of gravity and balance
•proper body alignment
•proper motivation
•incorporate internal or mental practice as well as external or physical practice
•feedback
•knowledge of results
A significant construct of this approach is centered around a therapist’s observation of the pt during examination in order to identify the
variations in normal movement. Through critical assessment, the therapist is able to identify components of movement that are missing or
abnormal and the corresponding interventions. Treatment relies on techniques inherent to this approach as well as other various approaches to
neurological rehab. Intrinsic feedback through sensory, visual, proprioceptive or tactile channels as well as external feedback through an
observer is necessary for the pt to influence their progress towards their goals.
Key terminology:
Closed motor skill: a skill that is performed under a stable and unchanging environment
Knowledge of results: providing the pt with external feedback regarding a pts performance of a task. This can include observations as well as
objective data and can be positive or negative in nature with the goal of influencing the learner.
Open motor skill: a skill that is performed under a consistently changing environment
Transfer of learning: An action cannot be separated from the environment that is performed in. A pt must be able to transfer the skill or motor
task into different environments.
●Bobath: Neuromuscular Development Treatment (NDT):
An approach developed by Karl and Berta Bobath based on the hierarchical model of neurophysiologic function. Abnormal postural reflex
activity and abnormal muscle tone are caused by the loss of central nervous system control at the brainstem and spinal cord levels. The concept
recognizes that interference of normal function within the brain caused by central nervous system dysfunction leads to a slowing down or
cessation of motor development and the inhibition of righting reactions, equilibrium reactions, and automatic movements. The pt should learn
to control movement through activities that promote normal movement patterns that integrate function.
New assumptions that have been incorporated into NDT resulting from current motor control research include:
•Postural control can be learned and modified through experience
•Postural control uses both feedback and feed-forward mechanisms for execution of tasks
•Postural control is initiated from a pts base of support
•Postural control is required for skill development
•Postural control develops by assuming progressive positions in which there is an increase in the distance between the center of gravity and
base of support; the base of support should also decrease
Key Terminology:
Facilitation: a technique utilized to elicit voluntary muscular contraction
Inhibition: a technique utilized to decrease excessive tone or movement
Key points of control: specific handling of designated areas of the body (shoulder, pelvis, hand, and foot) will influence and facilitate posture,
alignment, and control
Placing: the act of moving an extremity into a position that the pt must hold against gravity
Reflex inhibiting posture: Designated static positions that Bobath found to inhibit abnormal tone influences and reflexes.
●Brunnstrom: Movement therapy in Hemiplegia
Movement therapy in hemiplegia developed by Singe Brunnstrom is based on the hierarchical model by Hughlings Jackson. This approach
created and defined the term synergy and initially encouraged the use of synergy patterns during rehab. The belief was to immediately practice
synergy patterns and subsequently develop combinations of movement patterns outside of the synergy. Synergies are considered primitive
patterns that occur at the spinal cord level as a result of the hierarchial organization of the central nervous system. Reinforcing synergy patterns
is rarely utilized now as research has indicated that reinforced synergy patterns are very difficult to change. Brunnstrom developed the seven
stages of recovery, which are used for evaluation and documentation of pt progress.
Key Terminology:
-Associated reaction: an involuntary and automatic movement of a body part as a result of an intentional active or resistive movement in
another body part
-Homolateral synkinesis: a flexion pattern of the involved upper extremity facilitates flexion of the involved lower extremity.
-Limb synergies: a group of muscles that produce a predictable pattern of movement in flexion or extension patterns.
-Raimiste’s phenomenon: the involved LE will abduct with applied resistance to the uninvolved LE in the same direction
-Souque’s phenomenon: Raising the involved UE above 100° with elbow extension will produce extension and abduction of the fingers
Seven Stages of Recovery:
Stage 1:
No volitional movement initiated
Stage 2:
The appearance of basic limb
Stage 3:
Stage 4:
Stage 5:
Stage 6:
Stage 7:
synergies. The beginning of spasticity.
The synergies are performed
voluntarily; spasticity increases
Spasticity beings to decrease.
Movement patterns are not dictated
solely by limb synergies.
A further decrease in spasticity is
noted with independence form limb
synergy patterns.
Isolated joint movements are
performed with coordination
Normal motor function is restored.
●Kabat, Knott, and Voss: Proprioceptive Neuromuscular Facilitation (PNF)
PNF was introduced in the early 1950s using the hierarchial model as its framework. The original goal of treatment was to establish gross motor
patterns within the central nervous system. This approach is based on the premise that stronger parts of the body are utilized to stimulate and
strengthen the weaker parts. Normal movement and posture is based on a balance between control of antagonist and agonist muscle groups.
Development will follow the normal sequence through a component of motor learning. This theory places great emphasis on manual contacts
and correct handling. Short and concise verbal commands are used along with resistance throughout the full movement pattern. The PNF
approach utilizes methods that promote or hasten the response of the NM mechanism through stimulation of the proprioceptors. Movement
patterns follow diagonals or spirals that each possess a flexion, extension, and rotary component and are directed toward or away from midline.
Key Terminology:
-Chopping: a combination of bilateral UE asymmetrical patterns performed as a closed chain activity
-Developmental sequence: a progression of motor skill acquisition. The stages of motor control include mobility, stability, controlled mobility,
and skill.
-Mass movement patterns: the hip, knee, and ankle move into flexion or extension simultaneously
-Overflow: muscle activation of an involved extremity due to intense action of an involved muscle or group of muscles
Upper Extremity:
D1 Flexion: flexion/adduction/external rotation; verbal cues:”close your hand, turn, and pull your arm across your face.” (grabbing earring)
D1 Extension: extension/abduction/internal rotation; verbal cues: “open your hand, turn, and push your arm down and out.” (throwing earring
away)
D2 Flexion: flexion/abduction/external rotation; verbal cues: “open your hand, turn and lift your arm up and out. (sword drawn)
D2 Extension: extension/adduction/internal rotation; verbal cues: “close your hand, turn, and pull your arm down and across your body.” (put
sword in holder)
Lower Extremity:
D1 Flexion: flexion/adduction/external rotation; verbal cues: “bring your foot up, turn, and pull your leg up and across your body” (frog sit)
D1 Extension: extension/abduction/internal rotation; verbal cues: “push your foot down, turn, and push your leg down and out.”
D2 Flexion: flexion/abduction/internal rotation; verbal cues: “lift your foot up, turn, and lift your leg up and out.”
D2 Extension: extension/adduction/external rotation; verbal cues: “push your foot down, turn, and pull your leg down and in.”
Levels of Motor Control:
Mobility:
The ability to initiate movement through a
functional range of motion
Stability:
The ability to maintain a position or posture
through co- contraction and tonic holding around
a joint. Unsupported sitting with midline control is
an example of stability.
Controlled
The ability to move within a weight bearing
mobility:
position or rotate around a long axis. Activities in
prone on elbows or weight shifting in quadruped
are examples of controlled mobility.
Skill:
The ability to consistently perform functional tasks
and manipulate the environment with normal
postural reflex mechanisms and balance reactions.
Skill activities include ADLs and community
locomotion.
PNF Therapeutic Exercise Descriptions:
Agonistic Reversals
Controlled mobility, skill: An isotonic concentric
(AR)
Alternating Isometrics
(AI)
Contract-Relax (CR)
Hold-relax (HR)
Hold-Relax Active
Movement (HRAM)
contraction performed against resistance
followed by alternating concentric and eccentric
contractions with resistance. AR requires use in
a slow and sequential manner, and may be used
in increments throughout the range to attain
maximum control.
Stability: Isometric contractions are performed
alternating from muscles on one side of the joint
to the other side without rest. AI emphasizes
endurance or strengthening.
Mobility: a technique used to increase ROM. As
the extremity reaches the point of limitation,
the pt performs a maximal contraction of the
antagonistic muscle group. The therapist resists
movement for 8-10 seconds with relaxation to
follow. The technique is repeated until no
further gains in ROM are noted during the
session.
Mobility: an isometric contraction used to
increase ROM. The contraction is facilitated for
all muscle groups at the limiting point in the
ROM. Relaxation occurs and the extremity
moves through the newly acquired range to the
next point of limitation until no further increases
in ROM occur. The technique is often used for
pts that present with pain.
Mobility: a technique to improve initiation of
movement to muscle groups tested at 1/5 or
less. An isometric contraction is preformed once
the extremity is passively placed into a
shortened range within the pattern. Overflow
and facilitation may be used to assist with the
contraction. Upon relaxation, the extremity is
immediately moved into a lengthened position
Joint Distraction
Normal Timing (NT)
Repeated contractions
(RC)
Resisted Progression
(RP)
Rhythmic Initiation
(RI)
of the pattern with a quick stretch. The pt is
asked to return the extremity to the shortened
position through an isotonic contraction.
Mobility: a proprioceptive component used to
increase ROM around a joint. Consistent manual
traction is provided slowly and usually in
combination with mobilization techniques. It can
also be used in combination with a quick stretch
to initiate movement.
Skill: a technique used to improve coordination
of all components of a task. NT is performed in a
distal to proximal sequence. Proximal
components are restricted until the distal
components are activated and initiate
movement. Repetition of the pattern produces a
coordinated movement of all components.
Mobility: a technique used to initiate movement
and sustain a contraction through the ROM. RC
is used to initiate a movement pattern,
throughout a weak movement pattern or at
point of weakness within a movement pattern.
The therapist provides a quick stretch followed
by isometric or isotonic contractions.
Skill: a technique used to emphasize
coordination of proximal components during
gait. Resistance is applied to an area such as the
pelvis, hips, or extremity during the gait cycle in
order to enhance coordination, strength or
endurance.
Mobility: a technique used to assist in initiating
movement when hypertonia exists. Movement
progresses from passive “let me move you” to
active assistive “help me move you”, to slightly
resistive “move against the resistance”.
Rhythmical Rotation
(RR)
Rhythmic Stabilization
(RS)
Slow Reversal (SR)
Slow Reversal Hold
(SRH)
Timing for Emphasis
(TE)
Movements must be slow and rhythmical to
reduce the hypertonia and allow for full ROM.
Mobility: a passive technique used to decrease
hypertonia by slowly rotating an extremity
around the longitudinal axis. Relaxation of the
extremity will increase ROM.
Mobility, stability: a technique used to increase
ROM and coordinate isometric contractions. The
technique requires isometric contractions of all
muscles around a joint against progressive
resistance. The pt should relax and move into
the newly acquired range and repeat the
technique. If stability is the goal, RS should be
applied as a progression from AI in order to
stabilize all muscle groups simultaneously
around the specific body part.
Stability, controlled mobility, skill: A technique
of slow and resisted concentric contractions of
agonists and antagonists around a joint without
rest between reversals. This technique is used to
improve control of movement and posture.
Stability, controlled mobility, skill: Using slow
reversal with the addition of an isometric
contraction that is performed at the end of each
movement in order to gain stability.
Skill: used to strengthen the weak component of
a motor pattern. Isotonic and isometric
contractions produce overflow to weak muscles.
●Rood:
This theory is based on Sherrington and the reflex stimulus model. Rood believed that all motor output was the result of both past and present
sensory input. Treatment is based on sensorimotor learning. It takes into account the autonomic nervous system and emotional factors as well
as motor ability. Rood used a developmental sequence, which was seen as “key patterns” in the enhancement of motor control. A goal of this
approach is to obtain homeostasis in motor output and to activate muscles to perform a task independent of a stimulus. Exercise is seen as a
treatment technique only if the response is correct and if it provides sensory feedback that enhances the motor learning of that response. Once
a response is obtained during treatment, the stimulus should be withdrawn. Rood introduced the use of sensory stimulation to facilitate or
inhibit responses such as icing, and brushing in order to elicit desired reflex motor responses.
Sensory Stimulation techniques:
Facilitation
Inhibition
-Approximation
-Deep pressure
-Joint compression -Prolonged stretch
-Icing
-Warmth
-Light touch
-Prolonged cold
-Quick stretch
-Resistance
-Tapping
-Traction
Key Terminology:
Heavy work: a method used to develop stability by performing an activity (work) against gravity or resistance. Heavy work focuses on the
strengthening of postural muscles.
Light work: a method used to develop controlled movement and skilled function by performing an activity (work) without resistance. Light work
focuses on the extremities.
Key patterns: a developmental sequence designed by Rood that directs pts mobility recover from synergy patterns through controlled motion.
Integumentary Examination:
Foundational Science: Integ is the body’s largest organ. The avascular epidermis is the most superficial layer of skin. The dermis, known as the
true skin, is well vascularized, and is characterized as elastic, flexible, and tough.
Key functions: Protection, sensation, thermoregulation, excretion of sweat, vitamin D synthesis
Phases of Normal wound Healing: Normal wound healing occurs as damaged tissues move through distinct yet overlapping phases of repair. In
chronic wounds, this progression is either interrupted or delayed causing the wound to become “stuck” in a particular phase of healing.
Inflammatory Phase (1-10 days)
Inflammation is the immune system’s initial
Proliferative Phase (3-21 days)
Maturation Phase (7 days - 2 years)
response to a wound. Temporary repair
mechanisms rapidly re-establish hemostasis
through platelet activation and the clotting
cascade. Debris and necrotic tissue are removed
and bacteria are killed by mast cells, neutrophhils,
and leukocytes. Processes occurring in the
inflammatory phase establish a clean wound bed
which signals tissue restoration and permanent
repair processes to begin. Re-epithelialization
typically begins within 24 hours at the wound
borders, though visible signs are usually not
observed earlier than 3 days after injury.
The formation of new tissue signals the beginning
of the proliferative phase. Capillary buds and
granulation tissue begin to fill the wound bed
creating a support structure for the migration of
epithelial cells. Keratinocytes, endothelial cells,
and fibroblasts are active and the collagen matrix
is formed. Skin integrity is restored in the
proliferative phase with wound closure occurring
through epithelialization and wound contraction.
The maturation, or remodeling phase is initiated
when granulation tissue and epithelial
differentiation being to appear in the wound bed.
As the maturation phase progresses, mechanisms
of fiber reorganization and contraction shrink and
thin the scar. An immature scar will appear red,
raised, and rigid while a mature scar will appear
pale, flat, and pliable. Scar tissue is remodeled and
strengthened though the processes of collagen
lysis and synthesis. Newly repaired tissues have
approximately 15% of pre-injury tensile integrity
and should be protected to prevent re-injury. Over
time, tensile integrity may increase as much as
80% of the pre-injury strength. Hypertrophic
scarring, especially in relation to burn injuries, can
significantly impact maturation phase progression.
A burn without hypertrophic scarring will typically
mature within 4-8 weeks; burns with hypertrophic
scarring, however, may require up to two years to
reach maturity.
Wound Types:
Acute wounds
Abrasion
Avulsion
Incisional
wound
Laceration
Penetrating
Puncture
Skin tear
Is a wound caused by a combination of friction and shear forces, typically over a rough
surface, resulting in the scraping away of the skin’s superficial layers.
A soft tissue avulsion, sometimes referred to as degloving, is a serious wound resulting
from tension that causes skin to come detached from underlying structures.
Is most often associated with surgery and is created intentionally by means of a sharp
object such as a scalpel or scissors.
Is a wound or irregular tear of tissues often associated with trauma. Lacerations can
result from shear, tension, or high force compression with the resultant wound
characteristics dependent on the mechanism of injury.
Can result from various mechanisms of injury and is described as a wound that enters
the interior of an organ or cavity.
Is made by a sharp pointed object as it penetrates the skin and underlying tissues.
Typically, there is relatively little tissue damage beyond the wound tract, however, the
risks of contamination and infection can be significant.
Often results from trauma to fragile skin such as bumping into an object, adhesive
removal, shear or friction forces. The severity of a skin tear can range from a flap like
tear, that may or may not remain viable, to full-thickness tissues loss.
Ulcers:
Type
Description
Recommendations
Arterial Insufficiency Ulcers
Wounds resulting from arterial
insufficiency occur secondary to
inadequate circulation of
oxygenated blood (ischemia)
often due to complicating factors
such as atherosclerosis.
Venous Insufficiency Ulcers
Wounds resulting from venous
insufficiency occur secondary to
impaired functioning of the
venous system resulting in
inadequate circulation and
eventual tissue damage and
ulceration.
Neuropathic Ulcers
Are a secondary complication
usually associated with a
combination of ischemia and
neurophathy. Neuropathic ulcers
are often associated with
diabetes mellitus, however, any
form of peripheral neuropathy
poses an increased risk of wound
development
Also referred to as decubitus
ulcers, result from sustained or
prolonged pressure on tissue at
levels greater than that of
capillary pressure. Skin covering
bony prominences is particulary
susceptible to localized ischemia
and tissue necrosis due to
Pressure Ulcers
-Rest, limb protection, risk
reduction education, inspect legs
and feet daily, avoid unnecessary
leg elevation, avoid using
heating pads or soaking feet in
hot water, wear appropriately
sized shoes with clean, seamless
socks
-Limb protection, risk reduction
education, inspect legs & feet
daily, compression to control
edema, elevate legs above the
heart when resting or sleeping,
attempt active exercise including
frequent ROM, wear
appropriately sized shoes with
clean, seamless socks
-Limb protection, risk reduction
education, inspect legs and feet
daily, inspect footwear for debris
prior to donning, wear
appropriately sized off-loading
footwear with clean, cushioned,
seamless socks
-Repositioning every 2 hours in
bed, management of excess
moisture, off-loading with
pressure relieving devices,
inspect skin daily for signs of
pressure damage, limit shear and
friction forces over fragile skin
pressure. Pressure injury risk
assessment tools (Braden Scale,
Norton Scale)
Characteristics of LE Ulcers:
Arterial Ulcers
Lower one third of leg,
toes, web spaces, dorsal
foot, lateral malleolus
Venous Ulcers
Proximal to the medial
malleolus
Appearance
Smooth edges, well
defined, lack of
granulation tissue, tend
to be deep
Irregular shape, shallow
Exudate
Pain
Minimal
Severe
Moderate/heavy
Mild to moderate
Pedal pulses
Diminished or absent
Normal
Edema
Skin Temp
Tissue changes
Normal
Decreased
Thin and shiny, hair
loss, yellow nails
Increased
Normal
Flaking, dry skin,
brownish discoloration
Miscellaneous
Leg elevation increases
pain
Leg elevation lessens
pain
Location
Neuropathic Ulcers
Areas of the foot
susceptible to pressure
or shear forces during
WBing
Well-defined oval or
circle, callused rim;
cracked periwound
tissue; little to no
wound bed necrosis
with good granulation
Low/moderate
None, however
dysesthesia may be
reported
Diminished or absent,
unreliable anklebrachial index with
diabetes
Normal
Decreased
Dry, inelastic, shiny
skin, decreased or
absent sweat and oil
production
Loss of protective
sensation
Wound Assessment
Wound Classification by depth of injury:
*Wounds that are not categorized as pressure or neuropathic ulcers (skin tears, surgical wounds, venous statisis ulcers) are classified based on
the depth of tissue loss.
Superficial wound:
Partial-thickness
wound:
Full-thickness wound:
Subcutaneous wound:
Causes trauma to the skin with the epidermis remaining intact, such as with a
non-blistering sunburn. A superficial wound will typically heal as part of the
inflammatory process.
Extends through the epidermis and possibly into, but not through the dermis.
Examples include abrasions, blisters, and skin tears. A partial thickness wound
will typically heal by re-epithelialization or epidermal resurfacing depending
on the depth of injury.
Extends through the dermis into deeper structures such as subcutaneous fat.
Wounds deeper than 4 mm are typically considered full thickness and heal by
secondary intention.
Subcutaneous wounds extend through integumentary tissues and involve
deeper structures such as subcutaneous fat, muscle, tendon or bone.
Subcutaneous wounds typically require healing by secondary intention.
Primary intention: Most common in acute wounds with minimal tissue loss. Smooth clean edges are reapproximated and closed with sutures,
staples, or adhesives. Typically have minimal scarring, and heal quickly in uncomplicated progression. Examples: surgical incision, laceration,
puncture, and superficial & partial thickness wounds.
Secondary Intention: Permits wounds to close on their own without superficial closure. Wounds with characteristics such as significant tissue
loss or necrosis, irregular on nonviable wound margins that can’t be reapproximated, infection or debris contamination. Require ongoing wound
care and have larger scars. Examples: neuropathic, arterial, venous or pressure ulcers, most full thickness wounds, and chronically inflamed
wounds.
Tertiary Intention: AKA delayed primary intention. Wounds at risk for developing complications such as sepsis or dehiscence, may be temporarily
left open. Once risk factors have been alleviated, the wound is closed by the usually primary intention methods.
Wagner Ulcer Grade Classification Scale
Grade
0
1
2
3
4
5
Description
No open lesion, but may possess pre-ulcerative lesions; healed ulcers; presence of bony
deformity
Superficial ulcer not involving subcutaneous tissue
Deep ulcer with penetration through the subcutaneous tissue, potentially exposing bone,
tendon, ligament or joint capsule
Deep ulcer with osteitis, abscess or osteomyelitis
Gangrene of digit
Gangrene of foot requiring disarticulation
Pressure Ulcer Staging
*A pressure ulcer describes a localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure or
pressure in combination with shear/friction forces.
Stage I
StageII
Stage III
Stage IV
Intact skin with non-blanchable redness of a localized area usually over a bony prominence.
Darkly pigmented skin may not have visible blanching, but instead present as local coloration
differing from the surrounding area. The area may be painful, firm, soft, warmer or cooler as
compared to adjacent tissue. Stage 1 may be difficult to detect in individuals with dark skin
tones.
Partial-thickness tissue loss of the dermis presenting as a shallow open ulcer with red or pink
wound bed. May present as an intact or ruptured serum filled blister or presents as a shiny or
dry shallow ulcer without slough or bruising. This stage should not be used to describe skin
tears, tape burns, perineal dermatitis, maceration or excoriation.
Full-thickness tissue loss. Subcutaneous fat may be visible but tone, tendon or muscle are not
exposed. Slough may be present, but does not obscure the depth of tissue loss. May include
undermining and tunneling. Bone and tendon are not visible or directly palpable. The depth
of a stage III pressure ulcer varies by anatomical location. For example, a stage III ulcer on the
bridge of the nose, ear, occiput, and malleolus, where there is not significant subcutaneous
tissue, can be quite shallow. In contract, areas with significant adipose tissue can develop
extremely deep stage III pressure ulcers.
Full-thickness tissue loss with exposed bone, tendon or muscle that is visible or directly
palpable. Slough or eschar may be present on some parts of the wound bed. Undermining
and tunneling may be present. Stage IV ulcers can extend into muscle and supporting
structures (fascia, tendon, joint capsule) making osteomyelitis possible.
Suspected
Purple or maroon localized areas of intact skin or blood-filled blister due to damage of
Deep tissue underlying soft tissue from pressure/and or shear forces. The area may be preceded by tissue
injury
that is painful, firm, mushy, boggy, warmer or cooler compared to adjacent tissue. Deep
tissue injury may be difficult to detect in individuals with dark skin tones. The evolution may
include a thin blister over a dark wound bed. The wound may further evolve and become
covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with
optimal treatment.
Unstageable Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, gray,
green, or brown) and or eschar (tan, brown, or black) in the wound bed. Until enough slough
and/or eschar is removed to expose the base of the wound, the true depth, and therefore
stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuating
appearance) eschar on the heels serve as “the body’s natural (biological) cover” and should
not be removed.
Exudate Classification:
Serous
Presents with a clear, light color and a thin, watery consistency. Serous exudates is
considered to be normal in a healthy healing wound and is observed during the
inflammatory and proliferative phases of healing.
Sanguineous
Presents with a red color and a thin, watery consistency. The red appearance of
sanguineous exudates is due to the presence of blood which may become brown if allowed
to dehydrate. Sanguineous exudates may be indicative of new blood vessel growth or the
disruption of blood vessels.
Serosanguineous Presents with a light red or pink color and a thin, watery consistency. Serosanguineous
exudates is considered to be normal in a healthy healing wound and is typically observed
during the inflammatory and proliferative phases of healing.
Seropurulent
Presents as cloudy or opaque, with a yellow or tan color and a thin, watery consistency.
Seropurulent exudates may be an early warning sign of an impending infection and is always
considred an abnormal finding.
Purulent
Presents with a yellow or green color and a thick, viscous consistency. Purulent exudates is
generally an indicator of wound infection and is always considered an abnormal finding.
Necrotic Tissue Types:
*Necrotic tissue is dead tissue resulting from the localized physiological and enzymatic changes associated with cell death. Necrotic tissue is
often documented and named by the specific type observed, and may also be referred to as devitalized or nonviable tissue.
Eschar
Described as dark or leathery, black/brown, dehydrated tissue that tends to be firmly adhered
to the wound bed.
Gangrene
Refers to death and decay of tissue resulting from an interruption of blood flow to an area of
the body. Some types of gangrene are also characterized by the presence of bacterial
infection. Gangrene most commonly affects the extremities, but can also occur in muscles and
internal organs.
Hyperkeratosis Also referred to a callus, is typically white/gray in color and can vary in texture from firm to
soggy depending on the moisture level in surrounding tissue.
Slough
Described as moist, stringy or mucinous, white/yellow tissue that tends to be loosely attached
in clumps to the wound bed.
Red-Yellow-Black System
Red
Color
Wound Description
Pink granulation tissue
Yellow
Most, yellow slough
Black
Black, thick eschar firmly
attached
Goals
Protect wound, maintain moist
environment
Remove exudates and debris;
absorb drainage
Debride necrotic tissue
Wound Terminology:
Contusion
An injury, usually caused by a blow, that does not disrupt skin integrity. The injury is
characterized by pain, edema, and discoloration which appears as a result of blood
seepage under the surface of the skin.
Dehiscence
The separation, rupture or splitting of a wound closed by primary intention. This disruption
of previously approximated surfaces may be superficial or involve all layers of tissue.
Dermis
The vascular layer of skin located below the epidermis containing hair follicles, sebaceous
glands, sweat glands, lymphatic and blood vessels, and nerve endings.
Desiccated
The drying out or dehydration of wound. Desiccation often results from poor dressing
selection that does not control the evaporation of wound bed moisture.
Desquamation
The peeling or shedding of the outer layers of the epidermis. Desquamation normally
occurs in small scales, although certain injuries and conditions, and medications may cause
peeling in larger scales or sheets and extend to deeper layers of skin.
Ecchymosis
The discoloration occurring below intact skin resulting from trauma to underlying blood
vessels and blood seeping into tissues. The discoloration is typically blue-black, changing in
time to a greenish brown or yellow color. An area where ecchymosis is present is
commonly referred to as a bruise.
Epidermis
The superficial, avascular epithelial layer of the skin that includes flat, scale-like squamous
cells, round basal cells, and melanocytes which produce melanin and give skin its color.
Erythema
A diffuse redness of the skin often resulting from capillary dilation and congestion or
inflammation.
Friable
Tissue that readily tears, fragments or bleeds when gently palpated or manipulated.
Hematoma
A localized swelling or mass of clotted blood confined to a tissue, organ or space usually
caused by a break in a blood vessel.
Hypergranulation
Increased thickness of the granular layer of the epidermis that exceeds the surface height
of the skin.
Hyperpigmentation An excess of pigment in a tissue that causes it to appear darker than surrounding tissues.
Hypertrophic scar
An abnormal scar resulting from excessive collagen formation during healing. A
hypertrophic scar is typically raised, red, and firm with disorganized collagen fibers.
Keloid
An abnormal scar formation that is out of proportion to the scarring required for normal
tissue repair and is comprised of irregularly disturbed collagen bands. A keloid scar
typically exceeds the boundaries of the original wound appearing red, thick, raised, and
firm.
Maceration
The skin softening and degeneration that results from prolonged exposure to water and
other fluids.
Normotrophic scar Characterized by the organized formation of collagen fibers that align in a parallel fashion.
Turgor
The relative speed with which the skin resumes its normal appearance after being lightly
Ulcer
pinched. Turgor is an indicator of skin elasticity and hydration and normally occurs more
slowly in older adults.
An open sore or lesion of the skin accompanied by sloughing of inflamed necrotic tissue.
Types of Burns:
Thermal burns
Electrical burns
Chemical burns
Radiation burns
Caused by conduction or convection. Ex: hot liquid, fire or steam
Caused by the passage of electrical current through the body. Typically there is an
entrance and an exit wound. Complications can include cardiac arrhythmias,
respiratory arrest, renal failure, neurological damage, and fractures. Ex. Lightning
Occurs when certain chemical compounds come in contact with the body. The
reaction will continue until the chemical is diluted at the site of contact. Sulfuric
acid, lye, hydrochloric acid, and gasoline are examples.
Occurs most commonly with exposure to external beam radiation therapy. DNA is
altered in exposed tissues and ischemic injury may be irreversible. Complications
may include severe blistering and desquamation, non-healing wounds, tissue
fibrosis, permanent discoloration, and new malignancies.
Zones of Injury:
Zone of coagulation
Zone of stasis
Zone of hyperemia
The area of the burn that received the most severe injury with irreversible cell
damage.
The area of less severe injury that possesses reversible damage and surrounds the
zone of coagulation.
The area surrounding the zone of stasis that presents with inflammation, but will
fully recover without any intervention or permanent damage.
Burn Classification:
Superficial Burn
Superficial PartialThickness Burn
Involves only the outer epidermis, Area may be red with slight edema. Healing
occurs without peeling or evidence of scarring in 2-5 days.
Involves the epidermis and the upper portion of the dermis. The involved area may
be extremely painful and exhibit blisters. Healing occurs with minimal to no
Deep PartialThickness Burn
Full thickness burn
Subdermal Burn
scarring in 5-21 days.
Involves complete destruction of the epidermis and the majority of the dermis. The
involved area may appear to be discolored with broken blisters and edema.
Damage to nerve endings may result in only moderate levels of pain. Hypertrophic
or keloid scarring may occur. In the absence of infection, healing will occur in 21-35
days.
Involves complete destruction of the epidermis and dermis along with partial
damage to the subcutaneous fat layer. Healing varies within weeks, with or
without grafting, and/or months to heal.
Involves the complete destruction of the epidermis, dermis, and subcutaneous
tissue. Subdermal burns may involve muscle and bone and as a result, often
require multiple surgical interventions and extensive healing time.
Rule of Nines:
Head and neck
Anterior trunk
Posterior trunk
Bilateral anterior
arm, forearm &
hand
Bilateral posterior
arm, forearm, &
hand
Genital region
Bilateral anterior
leg and foot
Bilateral posterior
leg and foot
9%
18%
18%
9%
9%
1%
18%
18%
Integumentary Pathology:
Pathology
Cellulitis
What is it
Is a fast spreading
inflammation that
occurs as a result
of a bacterial
infection of the
skin and
connective tissues.
It can develop
anywhere under
the skin, but will
typically affect the
extremities.
Etiology
Caused by a
particular bacterial
infections including
strep or staph.
Predisposing factors
to cellulitis include
an increased age,
immunosuppression,
trauma, the
presence of wounds
or venous
insufficiency.
Signs & Symptoms
Localized redness
that may spread
quickly, skin that is
warm or hot to
touch, local
abscess of
ulceration,
tenderness to
palpation, chills,
fever, and malise
Contact dermatitis
Is a superficial
irritation of the
skin resulting from
localized irritation
(poison ivy, latex,
soap, jewelry,
sensitivity). This
condition can be
acute or chroic
Occurs with
exposure to
mechanical,
chemical,
environmental or
biological agents.
Nickel, rubber, latex
and topical
antibiotics are
Intense itching,
burning and red
skin in areas
corresponding to
the location of the
irritation.
Treatment
Should be
immediately
referred to a
physician for
further
assessment.
Cellulitis requires
pharmacological
intervention using
systemic
antibiotics.
Differential
diagnosis should
attempt to rule
out DVT and
contact dermatitis.
PT may be
warranted for
wound care.
Cellulitis can lead
to sepsis or
gangrene if not
properly treated.
Focus should be
on identifying and
removing the
source of
irritation. Topical
steroid application
is commonly
employed.
based on exposure
to the
precipitating
agent. Contact
dermatitis is a very
common skin
disease that can
occur at any age.
AKA dermatitis. Is
used to describe a
group of disorders
that cause chronic
skin inflammation
typically due to an
immune system
abnormality,
allergic reaction or
external irritant.
common agents.
Gangrene (Dry)
When there is a
loss of vascular
supply resulting in
local tissue death.
Fingers, toes, and
limbs are most
affected. Typically
develops slowly
and results in
auto-amputation.
Occurs most
commonly in blood
vessel disease, such
as DM or
atherosclerosis. It
develops when
blood flow to an
affected area is
impaired, typically
as a result of poor
circulation.
Gangrene (wet)
If there is an
Can develop after a
Eczema
Is based on the
particular form of
the disorder. Infants
and children are at a
high risk for eczema
but may outgrow it.
Red or browngray, itchy,
lichenified skin
plaques that may
be exacerbated by
some topical
agents such as
soaps and lotions.
Oozing and
crusting of the
patchy occurs in
younger
population.
Dark brown or
black nonviable
tissue that
eventually
becomes a
hardened mass. Pt
will complain of
cold or numb skin
and they may
present with pain.
Swelling and pain
Pharmacological
interventions are
variable from
topical to oral.
Cold compresses
and other
modalities may
assist with
reducting the
itching. Extreme
temps should be
avoided.
Serious medical
condition and
requires
immediate
medical
intervention. Tx
includes
pharmacolocial
intervention,
surgery, and
hyperbaric oxygen
therapy.
Serious medical
associated
bacterial infection
in the affected
tissue. Swelling
resulting from the
bacterial infection
causes a sudden
stoppage of blood
flow.
severe burn,
frostbite or injury
and requires
immediate
treatment since it
tends to spread very
quickly and can be
fatal.
at the site of
infection, change
in skin color from
red to brown to
black, blisters that
produce pus,
fever, and general
malaise
Onychomycosis
Refers to a fungal
infection that
primarily affects
the toenails &
nailbeds.
Yellow or brown
nail discoloration;
hyperkeratosis
and hypertrophy
of the nail causing
it to partially
detach from the
nailbed.
Plaque psoriasis
Autoimmune
disease of the skin
and is most
common of the 5
types of psoriasis.
T cells trigger
inflammation
within the skin
Acquiring a fungal
infection is a
common
occurrence. Risk
factors include
manicures and
pedicures with
unsterile utensils,
possessing nail
injuries or
deformities, excess
skin moisture,
wearing closed toe
shoes, and an
impaired immune
response.
Genetic
predisposition to
plaque psoriasis.
Other factors may
trigger psoriasis,
such as injury to the
skin, insufficient or
excess sunlight,
Red raised
blotches that
typically present in
a bilateral fashion
(over both knees
or elbows). Tend
to itch and flake.
condition and
requires
immediate
intervention.
Surgical
debridement and
intravenous
antibiotic
treatment are
typical.
Manual
debridement of
the nail and
topical antifungal
medications are
primary.
Control symptoms
and prevent
secondary
infection. Lifelong
condition that can
be effectively
managed and
controlled through
Tinea pedis
and produce an
accelerated rate of
skin cell growth.
The skin cells
accumulate in
raised red patches
on the surface of
the skin.
Athlete’s foot. Is a
superficial fungal
infection which
causes epidermal
thickening and a
scaly skin
appearance. This
fungus is
opportunistic and
will rapidly
multiply in a warm
and most
environment
(between the
toes)
stress, excessive
alcohol, HIV
infection, smoking,
and certain
medications.
Wearing closed toed
shoes that don’t
allow airflow,
prolonged periods of
moisture or
wetness, excessive
sweating, and
possessing small nail
or skin abrasions.
This infection is
contagious through
direct contact.
the various stages
and exacerbations.
Itching, redness,
peeling skin
between the toes,
pain, odor, and in
more severe cases
breaks in skin
continuity
Pharmacological
management
includes topical or
oral antibiotics
depending on the
severity of
symptoms. May
persist or recur
and more longterm management
may be required.
Prevention
includes drying of
the feet when
bathing or
swimming,
wearing sandals
around public
pools or showers,
changing socks
frequently, proper
hygiene, and
avoiding shoe
wear that creates
a moist
environment.
Integumentary Pathologies:
Pathology
Diagnosis
FullThickness
Burn
This severe
burn causes
immediate
cellular and
tissue death
and
subsequent
vascular
destruction.
Indicates
complete
destruction
of the
epidermis,
dermis, hair
follicle, and
nerve
endings,
within the
dermis; and
also affects
the
subcutaneo
us fat layer
and
underlying
muscles,
resulting in
red blood
Contributing
Factor
75% of burns
are a direct
result from
the pts
actions.
Higher risk
for burns in
children
between 1 &
5 years as
well as
individuals
over 70.
Burns are
currently the
third leading
cause of
accidental
death in all
age
categories
with males
having a
higher overall
frequency of
injury.
Clinical
Presentation
Characterized by
a variable
appearance of
deep red, black
or white
coloring. Eschar
form from
necrotic cells and
creates a dry and
hard layer that
requires
debridement.
Edema is present
at the site of
injury and in
surrounding
tissues. Hairs
within this region
of the burn are
easily pulled
from the follicle
due to the
destruction. An
area of fullthickness burn
does not have
sensation or pain
due to
destruction of
Lab/Imaging
Blood work
should
include a
complete
blood count,
electrolytes,
blood urea
nitrogen,
creatinine,
bilirubin, and
arterial blood
gases. This
will indicate
baseline data,
systemic
changes, level
of shock, and
metabolic
complications
.
Bronchoscopy
& pulmonary
function tests
may be
indicated to
assess airway
damage and
pulmonary
insufficiency.
Management/Outcom
e
Initial management
includes medically
stabilizing the pt. This
emergent phase lasts
48-72 hours and
concludes with
regaining capillary
permeability and
hemodynamic stability.
An autograft
procedure is usually
required for fullthickness burns. The
rehab phase is a long
term commitment that
includes all aspects of
functional recover. PT
begins immediately
following skin grafting
and includes wound
care, pulmonary
exercises, positioning,
splinting, and
immobilization for the
first 3-5 days. Early
ambulation and
mobility activities
should be incorporated
as soon as possible in
cell
destruction.
free nerve
endings,
however there
may be pain
from adjacent
areas that
experience
partial-thickness
burns. During the
initial stages the
pt will
experience
thermoregulatio
n impairment,
SOB, electrolyte
disturbances,
poor urine
output, and
variation in level
of consciousness.
order to decrease
complications.
Continued PT should
involve edema control,
monitoring of any
elastic garments,
massage, stretching,
hydrotherapy, ROM,
debridement,
relaxation techniques,
progressive exercise,
ambulation, and
functional mobility
training. The mortality
rate has decreased
over the last 2 decades
due to improvement in
burn care. Mortality
rates are highest for
children under 4 and
adults over 65. Overall
prognosis is dependent
on factors such as
cardiac pathology,
alcoholism, PVD, and
obesity. Garments may
be worn up to 2 years
after injury. Without
significant
complications a pt
should achieve
independence within a
few months post
injury.
Pressure
Ulcer
Ischemia to
the site,
subsequent
cell death,
and tissue
necrosis. A
definition of
unrelieved
pressure is
>32mm Hg
of pressure
to an area
for more
than 2
hours.
Can occur at
any time
secondary to
unrelieved
pressure, but
there are
certain
populations
and risk
factors that
are
associated
with its
development
. Immobility
is a leading
factor and
seen in pts
with SCI,
paralysis,
hemiplegia,
impaired
cognition,
poor
nutrition,
altered
sensation,
incontinence,
decreased
lean body
mass, and
infection.
A pt will usually
develop a
pressure ulcer
over a bony
prominence with
common sites
including the
greater
trochanter,
ischium, sacrum,
and heel. A stage
I is classified as
an area of
nonblanchable
erythema of
intact skin. State
II is classified as a
partial thickness
wound involving
the epidermis,
dermis, or both.
Does not extend
through the
entire dermis.
Stage III is
classified as an
ulcer that
extended into
subcutaneous
tissue, but not
through fascia.
Stage IV is
classified as an
ulcer that
A diagnosis is
made from
visual
inspection,
however,
blood studies
such CBC,
electrolyte,
and protein
levels, as well
as tests for
baceremia or
sepsis may be
indicated.
Urinalysis and
stool samples
may be
indicated to
determine
contributing
factors in the
development
of the ulcer.
Coagulation
studies and
tissue
sampling may
also be
indicated. The
Braden Scale,
Gosnell Scale,
or Norton
Scale along
with baseline
Pt and caregiver
education for the
prevention of
subsequent pressure
ulcers is very
important and should
include skin inspection,
positioning, and
pressure relief
techniques. Seat
cushions, multipodus
boots or specialized
mattresses is also an
important aspect of
care of ulcers. Dressing
for the ulcer may
include nonocclusive
or occlusive types.
Nonocclusive include
dry to dry, wet to wet,
wet to dry or
composite dressings.
Occlusive dressings
include semipermeable
films, hydrocollooids,
hydrogels,
semipermeable foams,
and alginates. A
general exercise
program should be
provided daily. Pts
should avoid the use of
hot water and the use
of massage
extends through
the fascia and
deeper. It is a
full-thickness
wound that may
damage muscles,
bones, ligaments
and/or tendons.
measurement
of size and
depth of the
ulcer.
surrounding the site.
Therapist should
promote proper
positioning techniques
(such as positioning of
the bed at less than
45° angle) in order to
decrease friction and
shear. Approx 60,000
pts die annually due to
secondary
complications from
ulcers. However, many
people that develop a
pressure ulcer
completely recover
with no residual
impairments.
Types of Dressings:
Dressings may be defined as either primary or secondary. A primary dressing is one that comes into direct contact with a wound. A number of
primary dressings include a self-adhesive backing and not require a secondary dressing. Secondary dressings are placed directly over the primary
dressing to provide additional protection, absorption, occlusion, and/or to secure the primary dressing in place.
Type
Hydrocolloids: Consist
of gel-forming polymers
(carboxymethylcellulose,
gelatin, pectin) backed
by a strong film or foam
adhesive. The dressing
does not attach to the
wound itself but instead
Indications
Hydrocolloids are useful
for partial and fullthickness wounds. The
dressings can be used
effectively with granular
or necrotic wounds.
Advantages
-Provides a moist
environment for wound
healing
-Enables autolytic
debridement
-Offers protection from
microbial
contamination
Disadvantages
-May traumatize
surrounding intact skin
upon removal
-May tend to roll in
areas of excessive
friction
-Cannot be used on
infected wounds
anchors to the intact
surrounding skin. The
dressings absorb
exudates by swelling
into a gel-like mass and
vary in permeability,
thickness, and
transparency.
Hydrogels: Consist of
varying amounts of
water and gel-forming
materials such as
glycerin. The dressings
are typically available in
both sheet and
amorphous forms.
Foam Dressings: Are
comprised of a
hydrophilic
polyurethane base that
contacts the wound
surface and a
hydrophobic outer layer.
The dressings allow
exudates to be absorbed
into the foam through
the hydrophilic layer.
The dressings are most
-Provides moderate
absorption
-Does not require a
secondary dressing
-Provides a waterproof
surface
Hydrogels are moisture
retentive and
commonly used on
superficial and partialthickness wounds
(abrasions, blisters,
pressure ulcers) that
have minimal drainage.
Foam dressings are
used to provide
protection and
absorption over partial
and full-thickness
wounds with varying
levels of exudates. They
can also be used as
secondary dressings
over amorphous
hydrogels.
-Provides a moist
environment for wound
healing
-Enables autolytic
debridement
-May reduce pressure
and diminish pain
-Can be used as a
coupling agent for
ultrasound
-Minimally adheres to
wound
-Some products have
absorptive properties
-Provide a moist
environment for wound
healing
-Available in adhesive
and non-adhesive forms
-Provides prophylactic
protection and
cushioning
-Encourages autolytic
debridement
-Provides moderate
absorption
-Potential for dressing
to dehydrate
-Cannon be used on
wounds with significant
drainage
-Typically requires a
secondary dressing
-May tend to roll in
areas of excessive
friction
-Adhesive form may
traumatize periwound
area upon removal
-Lack of transparency
makes inspection of
wound difficult
commonly available in
sheets or pads with
varying degrees of
thickness.
Semipermeable foam
dressings are produced
in adhesive and nonadhesive forms. Nonadhesive forms require a
secondary dressing.
Transparent Film: Film
dressings are thin
membranes made from
transparent
polyurethane with
water-resistant
adhesives. The dressings
are permeable to vapor
and oxygen, but are
largely impermeable to
bacteria and water. They
are highly elastic,
conform to a variety of
body contours, and
allow easy visual
inspection of the wound
since they are
transparent.
Gauze: Manufactured
from yarn or thread and
are the most readily
available dressing used
in inpatient
environments. Gauze
Film dressings are
useful for superficial or
partial-thickness
wounds with minimal
drainage (scalds,
abrasion, lacerations)
-Provides a moist
environment for wound
healing
-Enables autolytic
debridement
-Allows visualization of
the wound
-Resistant to shearing
and frictional forces
-Cost effective over
time
-Excessive exudates
accumulation can result
in periwound
maceration
-Adhesive may
traumatize periwound
area upon removal
-Cannot be used on
infected wounds
Gauze dressings are
commonly used on
infected or non-infected
wounds of any size. The
dressings can be used
for wet-to-wet, wet-to-
-Readily available and
cost effective shortterm dressings
-Can be used alone or in
combination with other
dressings and topical
-Has a tendency to
adhere to the wound
bed traumatizing viable
tissue on removal
-Highly permeable
-Requires frequent
dressings come in many
shapes and sizes (sheets,
squares, rolls, packing
strips). Impregnated
gauze is a variation of
woven gauze in which
various materials such
as petroalatum, zinc or
anitmicrobials have
been added).
Alginates: Are derived
from a seaweed
extraction, specifically,
the calcium salt
component of alginic
acid. Alginates are highly
absorptive, but are also
highly permeable and
non-occlusive. As a
result, they require a
secondary dressing.
Alginate dressings act as
a hemostat and create
hydrophilic gel through
the interaction of
calcium ions in the
dressing and sodium
ions in the wound
exudate.
moist or wet-to-dry
debridement.
agents
-Can modify number of
layers to accommodate
for changing wound
status
-Can be used on
infected or non-infected
wounds
dressing changes
-Prolonged use
decreases cost
effectiveness
-Increased infection
rate compared to
occlusive dressings
Alginates are typically
used on partial or fullthickness draining
wounds such as
pressure or venous
insufficiency ulcers.
Alginates are often used
on infected wounds due
to the likelihood of
excessive drainage.
-High absorptive
capacity
-Enables autolytic
debridement
-Offers protection from
microbial
contamination
-Can be used on
infected or non-infected
wounds
-Non-adhering to
wound
-May require frequent
dressing changes based
on level of exudates
-Requires a secondary
dressing
-Cannot be used on
wounds with an
exposed tendon, joint
capsule or bone
Dressings from Most
Occlusive to NonOcclusive
Hydrocolloids
Hydrogels
Semipermeable foam
Semipermeable film
Impregnated gauze
Alginates
Traditional gauze
Dressings from Most to
Least Moisture Retentive
Alginates
Semipermeable foams
Hydrocolloids
Hydrogels
Semipermeable films
Topical Agents Used in Burn Care:
Topical Agent
Silver Sulfadiazine
Silver Nitrate
Povidone-iodine
Mafenide Acetate
Advantages
-Can be used with or without
dressings
-Painless
-Can be applied to wound
directly
-Broad-spectrum
-Effective against yeast
-Broad-spectrum
-Non-allergenic
-Dressing application is painless
-Broad-spectrum
-Penetrates burn eschar
-May be used with or without
occlusive dressings
-Broad-spectrum
-Penetrates burn eschar
Disadvantages
-Does not penetrate into eschar
-Poor penetration
-Discolors, making assessment
difficult
-Can cause severe electrolyte
imbalances
-Removal of dressings is painful
-Not effective against
pseudomonas
-May impair thyroid function
-Painful application
-May cause metabolic acidosis
-May compromise respiratory
-May bused with or without
occlusive dressings
Gentamicin
Nitrofurazone
-Broad-spectrum
-May be covered or left open to
air
-Bacteriocidal
-Broad-Spectrum
function
-May inhibit epithelizlization
-Painful application
-Has caused resistant strains
-Ototoxic
-Nephrotoxic
-May lead to overgrowth of
fungus and pseudomonas
-Painful application
•Selective Debridement- involves the removal of only nonviable tissue.
• Sharp Debridement- requires the use of a scalpel, scissors, and/or forceps to selectively remove devitalized tissue, foreign material or debris
from a wound. Sharp debridement is most often used for wounds with large amounts of thick, adherent, necrotic tissue; however, it may be
used in the presence of cellulitis or sepsis.
• Enzymatic Debridement- refers to the topical application of an enzymatic preparation to necrotic tissue. Enzymatic debridement can be used on
infected and non-infected wounds with necrotic tissue. Enzymatic debridement can be slow to establish a clean wound bed and should be
discontinued once devitalized tissue is removed to avoid damage to adjacent healthy tissue.
• Autolytic Debridement- refers to the use of the body’s own mechanisms to remove nonviable tissue. Common methods of autolytic
debridement include the use of transparent films, hydrocolloids, hydrogels, and alginates. Autolytic debridement develops a moist wound
environment that rehydrates necrotic tissue and eschar, facilitating enzymatic digestion of the nonviable tissue.
•Non-selective Debridement- involves the removal of viable and nonviable tissue.
•Wet-to-dry Dressings- refers to the application of moistened gauze dressing over an area of necrotic tissue. The dressing is allowed to dry
completely and is later removed, along with any necrotic tissue that has adhered to the gauze. Wet to dry dressing are most commonly used on
moderate amounts of exudate and necrotic tissue. This type of debridement should be used sparingly on wounds containing both necrotic and
viable tissue since granulation tissue will be traumatized during the process.
•Wound irrigation- Removes necrotic tissue from the wound bed using pressurized fluid. Pulsatile levage is an example of wound irrigation that
uses a pressurized stream of irrigation solution. This type of debridement is most desirable for wounds that are infected or have loose debris.
• Hydrotherapy- is most commonly employed using a whirlpool tank with agitation directed toward a wound requiring debridement. This process
softens and loosens adherent necrotic tissue. PT must be aware of potential hydrotherapy side effects such as maceration of viable tissue,
edema from dependent lower extremity positioning, and systemic effects such as hypotension.
-
Skin Care Products
Therapeutic Moisturizers- Lotions are largely water-based and best used to replace skin moisture that has been lost either to the air or as a
result of frequent hand washing. Creams are thicker water-based substances with higher concentrations of solids and oils than lotions.
-
Moisture Barriers- (e.g., ointment) Moisture barriers are designed to adhere to the skin and repel excess moisture from protected areas. They
are frequently used to protect surrounding skin from a heavily draining wound or perineal tissue from exposure to incontinence.
-
Liquid Skin Portectants- (e.g., skin sealant) Liquid skin protectant is applied to skin and when dry it creates a thin plastic film protecting the skin
from adhesive-related tissue damage. This thin barrier also offers some degree of moisture protection.
-
Skin Cleansers- skin cleansers are liquid agents typically intended for use on the skin of patients at risk of breakdown. Ingredients often have
pH-balancing component that is especially beneficial for perineal cleansing in patients who are incontinent.
-
Wound Cleansers- Wound cleansers vary from simple saline solutions to more complex compositions with cytotoxicity. Many wound cleansers
have the potential to cause inflammation; however, this quality is product dependent. Wound cleansers are not typically designed to remove
necrotic tissue, but rather associated wound substances such as foreign materials, exudate and dried blood.
Integumentary Interventions:
Selective debridement: removal of only the nonviable tissues from a wound.
Sharp Debridement:
Requires the use of a scalpel, scissors, and/or forceps to
selectively remove devitalized tissue, foreign material or
debris from a wound. Sharp debridement is most often used
for wounds with large amounts of thick, adherent, necrotic
tissue, however, it may also be used in the presence of
cellulitis or sepsis. Sharp debridement is the most expedient
form of removing necrotic tissue. PTs are permitted to
perform sharp, selective debridement as a procedural
intervention.
Enzymatic Debridement: Refers to the topical application of an enzymatic preparation
Autolytic Debridement:
to necrotic tissue. Enzymatic debridement can be used on
infected and non-infected wounds with necrotic tissue. This
type of debridement may be used for wounds that have not
responded to autolytic debridement or in conjunction with
other debridement techniques. Enzymatic can be slow to
establish a clean wound bed and should be discontinued once
devitalized tissue is removed to avoid damage to adjacent
healthy tissue.
Refers to the use of the body’s own mechanism to remove
nonviable tissue. Common methods include the use of
transparent films, hydrocolloids, hydrogels, and alginates.
Autolytic debridement establishes a moist wound
environment that rehydrates necrotic tissue and eschar,
facilitating enzymatic digestion of the nonviable tissue. This
type of debridement can be used with any amount of necrotic
tissue, however, requires a longer healing period and should
be not be performed on infected wounds.
Non-selective Debridement (mechanical): involves the removal of both viable and nonviable tissue from a wound.
Wet-to-dry dressings
Refer to the application of a moistened gauze dressing over an
area of necrotic tissue. The dressing is allowed to dry
completely and is later removed, along with any necrotic
tissue that has adhered to the gauze. Wet to dry dressings are
most often used to debride wounds with moderate amounts
of exudates and necrotic tissue. This type of debridement
should be used sparingly on wounds containing both necrotic
and viable tissue since granulation tissue will be traumatized in
the process. Removal of dry dressings from granulation may
cause bleeding and be extremely painful.
Wound Irrigation
Removes necrotic tissue from the wound bed using
pressurized fluid. Pulsatle lavage is an example of wound
irrigation that uses a pressurized stream of irrigation solution.
This type of debridement is most desirable for wounds that
are infected or have loose debris. Many devices permit
Hydrotherapy
variable pressure settings and provide suction for the removal
of exudates and debris.
Is most commonly employed using a whirlpool tank with
agitation directed toward a wound requiring debridement.
This process softens and loosens adherent necrotic tissue. PTs
must be aware of potential hydrotherapy side effects such as
maceration of viable tissue, edema from dependent LE
positioning and systemic effects such as hypotension.
Modalities & Physical Agents:
Modality
Indications
Negative Pressure Chronic or acute
Wound Therapy
wounds which
(NPWT): also
cannot be closed
referred to as
by primary
vacuum-assisted
intention such as
closure (V.A.C) is a dehisced surgical
non-invasive
incisions, fullwound care
thickness wounds,
modality used to
partial-thickness
facilitate healing
burns, heavily
and manage
draining granular
drainage. A sterile wounds, flaps,
foam dressing is
grafts, and most
placed in the
ulcer types.
wound and sealed
with an airtight
secondary
dressing which
attaches via tubing
to a vacuum pump
with a reservoir
container.
Treatment
Contraindications
Malignancy within
the wound,
insufficient
vascularity to
sustain wound
healing, large
amounts of
necrotic tissue
with eschar
present, untreated
osteomyelitis,
fistulas to organs
or body cavities,
exposed arteries
or veins, and
uncontrolled pain
Advantages
-Provides
management of
wound drainage
-Maintains a moist
wound
environment
-Decreases
interstitial edema
-Decreasees
bacterial
colonization
-Increases
capillary blood
flow
-Increases
granular tissue
formation
-Enhances
epithelial cell
migration
Disadvantages
-Requires special
supplies and
training
-Treatment can be
painful
-Not reimbursed in
acute or long-term
care settings
protocols vary
depending on
wound
characteriscis.
Hyperbaric
Oxygen: refers to
the inhalation of
100% oxygen
delivered at
pressures greater
than one
atmosphere.
Hyperbaric oxygen
treatment is
delivered in a
closed chamber
typically at
pressures 2-3x
that of the
atmosphere,
effectively
reducing edema
and
hyperoxygenating
tissues.
Growth Factors:
used in wound
healing and are
derived from
naturally occurring
protein factors.
Osteomyelitis,
diabetic wounds,
crush injuries,
compartment
syndromes,
necrotizing soft
tissue infections,
thermal burns,
radiation necrosis,
and compromised
flaps and grafts.
Terminal illness,
untreated
pneumothorax,
active malignancy,
pregnancy, seizure
disorder,
emphysema, and
use of certain
chemotherapy
agents
-Antibiotic effects
-Stimulation of
fibroblast
production and
collagen synthesis
-Stimulation of
growth factor
release and
epithelialization
-Specialized
equipment is not
widely available
-Cannot be used
with active
malignancy
Neuropathic ulcers
extending into or
through
subcutaneous
tissue with
adequate
Wounds closed by
primary intention,
pts with known
hypersensitivity to
any component of
the product or a
-Adjunct to
promote wound
healing
environment
-Increases growth
rate of new tissue
-Costly
-Poor
reimbursement
-Additional
research is needed
-Secondary
These substances
facilitate healing
by stimulating the
activity of specific
cell types
(neutrophils,
endothelial cells,
fibroblasts).
Currently, only a
limited number of
growth factors
have been
approved by the
FDA for topical
wound healing
applications.
circulation to
sustain wound
healing.
history of
neoplasm at the
application site.
-Promotes cell
division
dressing required
-Requires
refrigeration
-Limited number
of products
Burns:
Pathophysiology:
1. Burn Injury: results from thermal, chemical, electrical, or radioactive agents
2. Burn wound, consists of 3 zones:
a. Zone of coagulation: cells are irreversibly injured, cell death occurs
b. Zone of stasis: cells are injured; may die without specialized treatment, usually within 24-48 hours
c. Zone of hyperemia: minimal cell injury; cells should recover
3. Degree of burn: Burns are classified by severity, layers of skin damage
Rule of 9’s:
-Head and neck: 9%
-Anterior trunk: 18%
-Posterior trunk: 18%
-Arms: 9% each
-Legs: 18% each
-Perimeum: 1%
Classification by percentage of body area burned:
1. Critical: 10% of body with third degree burns and 30% or more with second degree burns; complications common (respiratory
involvement, smoke inhalation)
2. Moderate: less than 10% with third-degree burns and 15% to 30% with second degree burns.
3. Minor: less than 2% with third degree burns and 15% with second degree burns.
Complications of burn injury:
1. Infection: leading cause of death; gangrene may develop
2. Shock
3. Pulmonary complications: Smoke inhalation of hot smoke results in pulmonary edema and airway obstruction; suspect with burns of the
face, singed nose hairs; pneumonia
4. Metabolic complications
5. Cardiac and circulatory complications
6. Integumentary scars
Burn Management:
1. Emergency care: Immersion in cold water. If less than half the body is burned and injury is immediate; cold compresses may also be
sued. Cover burns with sterile bandage or clean cloth; no ointments or creams.
2. Medical management
a. Asepsis and wound care:
b. Removal of charred clothing
c. Wound cleansing
d. T
e. Topical medications reapplied one to 3 times daily (Ointments: bacitracin, polymyxin B, and Neomycin); Silver sulfadiazine:
common topical agent, avoid at term pregnancy, on infants less than 2 months, and those with sulfa drug allergies.
f. Dressings: prevents bacterial contamination, prevents fluid loss, and protects the wound. May additionally limit ROM. Dressings
include: silver-impregnated, and gauze dressing
g. Estabiilsh and maintain airway, adequate oxygenation, and respiratory function
h. Monitor: arterial blood gases, serum electrolyte levels, urinary output, vital signs
i.
j.
k.
l.
m.
GI function: provide nutritional support
Pain relief: morphine sulfate
Prevention and control of infection: tetanus prophylaxis, antibiotics, standard precatution
Fluid replacement therapy: prevention and control of shock. Post shock fluid and blood replacement
Surgery: Grafts closure of the wound
i. Allograft (homograft)-use of other human skin; cadaver skin; temporary grafts for large burns, used until autograft is
available
ii. Xenograft (heterograft)-use of skin from other species (pig skin) a temporary graft
iii. Biosynthetic grafts: combination of collagen and synthetics
iv. Cultured skin: laboratory grown form pts own skin
v. Autograft: use of pts own skin
vi. Split-thickness graft: contains epidermis and upper layers of dermis from donor site
vii. Full-thickness graft: contains epidermis and dermis from donor site
Rehab: Prevent or reduce the complications of immobilization.
1. Exercises to promote deep breathing and chest expansion; ambulation to prevent pneumonia
2. Positioning and splinting to prevent or correct deformities.
a. Anterior neck: common deformity is flexion; stress hyperextension; position with firm (plastic) cervical orthosis
b. Shoulder: common deformity is adduction and internal rotation; stress abduction, flexion, and external rotation; position
with an axillary splint (airplane splint).
c. Elbow: common deformity is flexion and pronation in extension with posterior arm splint.
d. Hand: common deformity is a claw hand (intrinsic minus position); stress extension (15°), MP flexion (70°), PIP, and DIP
extension, thumb abduction (intrinsic plus position) with resting hand splint.
e. Hip: common deformity is flexion and adduction; stress hip extension and abduction; position in extension, abduction,
neutral rotation.
f. Knee: common deformity is flexion; stress extension; position in extension with posterior knee splint.
g. Ankle: common deformity is plantar flexion; stress dorsiflexion; position with foot-ankle in neutral with splint or plastic
ankle-foot orthosis.
3. Edema control: elevation of extremities, active ROM.
4. Active and passive exercise to promote full ROM.
a. Combine with dressing changes, hydrotherapy; medication doses
b. Post grafting: discontinue exercise for 3-5 days to allow grafts to heal
c. Massage to help reduce scar formation; eg deep friction massage
d. Resistive and strengthening exercises to correct loss of muscle mass and strength.
e. Increase activity tolerance and cardiovascular endurance (ambulation)
f. Promote independence in ADLs, all functional mobility skills
g. Elastic supports to help control edema; pressure garments to help prevent hypertrophic scarring or keloid formation
h. Management of chronic pain.
5. Provide emotional support
1. Edema management:
a. Leg elevation and exercise (ankle pumps)
b. Compression therapy; to facilitate movement of excess fluid from lower extremity
c. Compression wraps: elastic or tubular bandages
d. Paste bandages; Unna boot is a pliable, nonstretchable dressing impregnanted with ainc or calamine and gelatin
e. Compression stockings, e.g. Jobst
f. Compression pump therapy
2. Electrical Stimulation for wound healing:
a. Used to improve circulation, facilitate debridement, and enhance tissue repair
b. Continuous waveform application with direct current
c. High-voltage pulsed current
d. Pulsed biphasic current
3. Nutritional considerations:
a. Delayed wound healing associated with malnutrition and poor hydration
b. Albumin: normal is 3.5-5.5 mg/dl; less than 3.5=malnutrition
c. BMI <21 with weight loss increased risk for pressure ulcer
d. Provide adequate hydration
e. Individuals with wounds require approximately 3 or more liters of water a day
f. Pts on air-fluidized beds require greater hydration (40-60 ml/Kg a day)
g. Provide adequate nutrition: frequent high calorie/high-protein meals; energy intake (25-35 kcal/kg/bodyweight) and protein 1.52.5 gm/kg body weight)
h. Patients with trauma stress and burns require higher intakes.
4. Injury prevention or reduction
a. Daily, comprehensive skin inspection, paying particular attention to bony prominences (sacrum, coccys, trochanter, ischial
tuberosities, medial and lateral malleolus)
b. Therapeutic positioning to relieve pressure and allow tissue reperfusion.
i. In bed: turning or repositioning every 2 hours during acute and rehab phases
ii. In wheelchair: wheelchair pushups every 15 minutes
c. Use techniques to ensure skin protection, avoid friction, shear, or abrasion injury
i. Lifting, not dragging
ii. Use of turning and draw sheets; trapeze, manual, or electric lifts
iii. Use of corn starch, lubricants, pad protectors, thin film dressings, or hydrocolloid dressings over friction risk sites.
iv. Use of transfer boards for sliding wheelchair transfers
d. Pressure-relieving devices (PRDs):
i. Reduce tissue interface pressures
ii. Static devices: use if pt can assume a variety of positions, examples: foam, air, or gel mattress overlays; whater-filled
mattresses; pillows or foam wedges, protective padding (heel relief boots)
iii. Dynamic devices: use if pt cannot assume a variety of positions; examples: alternating pressure air mattresses, fluidized
air or high-air-loss bed.
iv. Seating supports: use for chair-bound or wheelchair bound pts; examples: cushions made out of foam, gel, air, or some
combination
e. Avoid restrictive clothing; e.g. with rough textures, hard fasteners, and studs. Avoid tight-fitting shoes, socks, splints, and
orthoses.
f. Avoid maceration injury
i. Prevent moisture accumulation and temperature elevation where skin contacts support surface.
ii. Incontinence management strategies: use of absorbent pads, brief or panty pad, scheduled toileting, and prompted
voiding, ointments, creams, and skin barriers prophylactically in perineal and perianal areas.
g. Pt and caregiver education:
i. Mechanisms of pressure ulcer development
ii.
iii.
iv.
v.
vi.
vii.
Daily skin inspection and hygiene
Avoidance of prolonged positions
Repositioning, weight shifts, lifts
Safety awareness during self-care
Safety awareness with use of devices and equipment
Importance of ongoing activity/exercise program
Metabolic and Endocrine Systems:
The metabolic system governs the chemical and physical changes that take place within the body enabling it to grow and function. Metabolism
involves breakdown of the body’s complex organic compounds in order to generate energy for all bodily processes. It also generates energy for
the synthesis of complex substances that form tissues and organs. During metabolism, organic compounds are broken down by a process called
catabolism, while anabolism is the process that combines simple molecules for tissue growth. Many metabolic processes are facilitated by
enzymes. The overall speed at which an organism carries out its metabolic processes is termed its metabolic rate (or when the organism is at
rest, its basal metabolic rate).
Metabolic System Pathology:
Metabolic disorders are classified by the particular building block that is affected. An enzyme deficiency leads to accumulation of the substrate
and a subsequent deficiency in the intended enzyme’s product. There are many different disorders that can occur genetically and these are
grouped according to the substrate that has been affected (carbohydrates, amino acids). Inherited metabolic disorders can be diagnosed in
utero via aminocentesis or chorionic villus sampling. Many inherited metabolic disorders will produce symptoms in a newborn including
lethargy, apnea, poor feeding, tachypnea, vomiting, hypoglycemia, urine changes, and seizures. Symptoms that are immediately apparent
indicate a more dangerous disorder.
Pathology
Phenylketonuria
(amino
acid/organic acid
What is it
Phenylketonuria
(PKU) is a
syndrome that
Etiology
This is an
autosomal
recessive inherited
Signs & Symptoms
Symptoms will
typically present
within a few
Treatment
Treated through
dietary restriction
of phenylalaine
metabolic disorder
consist of mental
retardation as well
as behavioral and
cognitive issues
secondary to an
elevation of serum
phenylalanine.
There is a
deficiency in the
enzyme
phenylalanine
hydroxylase.
Normally,
excessive
phenlalanine is
converted to
tyrosine by
phenylalanine
hydroxylase.
When this process
does not occur
and there is an
excess of
phenylalanine, the
brain is the
primary organ that
becomes affected.
Children in the US
are tested at birth
for PKU and levels
greater than
6mg/dl of
phenylalanine
require some form
trait and is most
common in
Caucasian
populations
months of birth as
the phenylalanine
accumulates. If
left untreated,
severe mental
retardation will
occur. These
children may also
experience gait
disturbances,
hyperactivity,
psychoses,
abnormal body
order, and display
features that are
lighter in coloring
when compared to
other family
memberse.
throughout the
person’s lifetime.
Adequate
prevention will
avoid all
manifestations of
the disease.
Tay-Sachs Disease
(lysosomal storage
disorder)
Mitochondrial
Disorders
of treatment.
Is the absence or
deficiency of
hexosaminidase A.
This produces an
accumulation of
gangliosides
(GM2) within the
brain.
There are over 100
different forms of
mitochondrial
disease and each
produces a
different spectrum
of disability and
clinical
manifestations.
This disease is an
autosomal
recessive inherited
trait and carried
primarily in the
Eastern European
(Ashkenazi) Jewish
population.
Result from
genetically
inherited or
spontaneous
mutations in the
DNA that lead to
impaired function
of proteins found
within the
mitochondria.
At approx. 6
months of age, the
child will start to
miss
developmental
milestones and
will continue to
deteriorate in
motor and
cognitive skills. As
symptoms
progress, the pt
develops
significant mental
retardation and
paralysis, and will
usually die by the
age of 5.
Symptoms vary
depending on the
type of
mitochondrial
disorder, however,
can include loss of
muscle
coordination,
muscle weakness,
visual and hearing
problems, learning
disabilities, hear,
liver and kidney
disease,
respiratory,
There is currently
no effective
treatment for this
condition. Genetic
testing in high risk
populations to
identify the
carriers prior to
pregnancy is
important in order
to avoid this
disorder.
These diagnoses
are relatively new
and treatment is
varied as the
symptomatology
and presentation
of the disease.
Treatment is
aimed at
alleviating the
current symptoms
and slowing the
progression of the
disease process.
Wilson’s Disease
(hepatolenticular
degeneration)
Wilson’s disease is
a rare inherited
disorder that is
most common in
eastern
Europeans,
Sicilians, and
southern Italians,
but may occur in
any group.
Wilson’s disease
typically appears
in people under 40
years old and
symptoms can
develop in
children typically
between 4-6 years
of age.
An autosomal
recessive inherited
trait that produces
a defect in the
body’s ability to
metabolize
copper. The
copper
accumulates over
time within the
brain, liver,
cornea, kidney,
and other tissues.
neurological, and
GI disorders, and
dementia.
Symptoms
typically appear
between the ages
of 4 and 6 and
include KayserFleischer rings
surrounding the
iris of the eye
secondary to
copper deposits,
degenerative
changes in the
brain (especially
with the basal
ganglia), hepatitis,
cirrhosis of the
liver, athetoid
movements, and
ataxic gait
patterns. There
may also be
emotional and
behavioral
changes as the
copper continues
to accumulate.
Overtime, and
with severe
disease, there will
be deformities of
the MS system,
Treatment consist
of continual
pharmacological
intervention using
vitamin B6 and Dpenicillamine as
both promote the
excretion of
excess copper
form the body.
Treatment will
also focus on
prevention of
hepatic disease
since a pt will die
from hepatic
failure if the
condition is left
untreated.
pathologic
fractures,
osteomalacia,
muscle atrophy,
and contractures.
Acid-Base Metabolic Disorders:
The process of metabolism is regulated by the endocrine and nervous systems. The rate of metabolism can be influenced by body temperature,
exercise, hormone activity, and digestion activity. If proper fluid or acid-base balance is compromised, it can alter metabolic function and cause
many signs and symptoms of the dysfunction.
Disorder
Metabolic
Alkalosis
What is it
Is a condition that
occurs when there
is an increase in
bicarbonate
accumulation or
an abnormal loss
of acids. As a
result, the pH rises
above 7.45.
Etiology
Commonly occurs
when there has
been continuous
vomiting,
ingestion of
antacids or other
alkaline
substances or
diuretic therapy. It
may also be
associated with
hypokalemia or
nasogastric
suctioning.
Metabolic
Acidosis
Is a condition that
occurs when there
is an accumulation
Commonly occurs
with conditions
such as renal
Signs & Symptoms
Nausea, diarrhea,
prolonged
vomiting,
confusion, muscle
fasciculations,
muscle cramping,
neuromuscular
hyperexcitability,
convulsions,
paresthesias, and
hypoventilation. If
left untreated the
pt can become
comatose,
experience
seizures, and
respiratory
paralysis.
Symptoms include
compensatory
hyperventilation,
Treatment
The most
important
interventions
include managing
the underlying
cause, correcting
coexisting
electrolyte
imbalances, and
administering
potassium
chloride to the pt.
Managing the
underlying cause,
correcting any
of acids due to an
acid gain or
bicarbonate loss.
As a result, the pH
drops below 7.35.
failure, lactic
acidosis,
starvation,
diabetic or
alcoholic
ketoacidosis,
severe diarrhea or
poisoning by
certain toxins.
vomiting,
diarrhea,
headache,
weakness, and
malaise,
hyperkalemaia,
and cardiac
arrhythmias. If left
untreated the
continued
increase in acid
can induce coma
and eventual
death.
coexisting
electrolyte
imbalances, and
administering
sodium
bicarbonate.
Other Metabolic conditions: Osteomalacia, Osteoporosis, Paget’s Disease (SEE Other chart)
Metabolic System Terminology:
Aerobic
metabolism:
Anabolism:
Adenosine
Triphosphate
(ATP):
Catabolism:
The ATP producing metabolic processes that are dependent on oxygen transported
via the circulatory system. Aerobic metabolic functions typically provide energy for
low intensity and/or longer duration activities.
The metabolic process in which simple molecules (nucleic acids, polysaccharides,
amino acids) are combined to create the complex molecules (proteins) needed for
tissue and organ growth.
The molecular unit within the body which transports the chemical compounds used
for cellular metabolism.
The metabolic process in which complex materials (proteins, lipids) are broken down
in the body for the purpose of creating and releasing heat and energy.
DNA
A double helix molecule that contains the genes that provide the blueprint for all of
(deoxyribonucleic the structures and functions of a living bening.
acid):
Gene:
Metabolism:
Mitochondria:
Osteopenia:
Osteopetrosis:
pH:
Pathology
Breast Cancer
A fundamental unit of heredity.
The physical and chemical processes of cells burning fuel to produce and use energy.
Examples include digestion, elimination of waste, breathing, thermoregulation,
muscular contraction, brain function, and circulation.
The part of the cell that is responsible for energy production. The mitochondria are
also responsible for converting nutrients into energy and other specialized tasks.
A condition presenting with low bone mass that is not severe enough to qualify as
osteoporosis. Individuals with osteopenia may not have actual bone loss, but a
naturally lower bone density than established norms.
A group of conditions characterized by impaired osteoclast function which causes
bone to become thickened but fragile. Osteopetrosis is an inherited condition that
can vary widely in symptoms and severity.
A measure of the hydrogen ion concentration in body fluid.
Diagnosis
Contributing
Factor
A mass that is
Estrogen is
composed of
believed to
malignant
have some
altered cells
relationship to
that proliferate the disease
and spread
process. Risk
without
factors include
control. A
gender, age,
malignancy can young
occur
menarche, late
anywhere
menopause,
within the
family history,
breast tissue,
high alcohol
however, the
intake, high fat
lump is usually diet, radiation
found directly
exposure, and
behind the
past history of
areola in men
cancer. Males
Clinical
Presentation
Breast cancer
makes up
approx. 30% of
all female
cancers and is
the 2nd leading
cause of death
in female
cancers.
Approx 70% of
all breast
cancer occurs
in women over
the age of 50.
A pt will
present with a
lump in the
breast that is
Lab/Imaging
Management/Outcome
Mammography
is used to
detect the
location and
growth of a
mass, however
definitive
diagnosis of
breast cancer
is made only
after
microscopic
examination of
a suspected
mass by needle
or excision
biopsy.
Ultrasound can
Surgical management
may range from
excision of the mass
(lumpectomy) to total
radical mastectomy
with axillary dissection.
Chemotherapy,
radiation therapy, and
hormone therapies may
used. PT may be
indicated to assist with
lymphedema
management, postsurgical breathing
exercises, positioning,
pain management,
strengthening and
exercises, ROM,
and is usually
located behind
the areola or in
the outer
upper
quadrant of
the breast in
women. There
may or may
not be
generalized
discomfort in
the area.
account for
less than 1% of
all breast
cancer cases.
noticed by a
physician
(10%), or by
the pt through
self
examination
(90%). Breast
cancer is
initially
otherwise
asymptomatic.
The breast may
become
painful, change
shape, bleed
from the
nipple, and
dimple over
the area of the
mass.
Metabolic/Endocrine System Rehab:
Rehab Considerations for pts with Inherited Metabolic
disorders:
-Must have an awareness of dietary restrictions
-Pt and family training to prevent deleterious effects
from the metabolic disease
-Adapt treatment to facilitate developmental milestones
within pt tolerance
Rehab Considerations for pts with Acid-base disorders:
-Recognize higher risk populations for imbalances such
as pts with renal, cardiovascular, pulmonary disease;
also be used to
detect if a
lump is filled
with fluid or a
solid mass.
Sentinel lymp
node mapping
is used upon
diagnosis to
identify exact
lymph node
involvement.
massage, intermittent
compression, and pt
education. The risk of
recurrence is always
present and should be
monitored closely.
Overall prognosis and
ten-year survival rates
for women are over
85% for stage I disease;
66% for stage II; 36%
for stage III; and 7% for
stage IV disease.
burns, fever and sepsis; pts on mechanical ventilation;
diabetes mellitus; pts currently vomiting with diarrhea or
enteric drainage
-Recognize signs of dehydration in a diabetic pt
-Injury prevention during involuntary muscular
contractions secondary to metabolic alkalosis
-Recognize that pts using diuretic therapy may be at risk
for potassium depletion
-Recognize that Trousseau’s sign during blood pressure
measurements may indicate calcium deficiency and the
early stages of tetany
Rehab considerations for pts with metabolic bone
disease:
-Must have awareness of signs of compression fx and of
pts at higher risk for all forms of fx
-Focus on both resistance training and endurance
training to build bone density and increase strength
-Avoid treatments that exacerbate the condition or place
pts at risk for fx
Rehab considerations for pts with Pituitary Dysfunction:
-Ambulation/exercise encouraged within 24 hours of
surgery (post tumor/gland removal)
-Must demonstrate increased awareness for signs of
hypoglycemia
-Bilateral carpal tunnel syndrome, arthritis, osteophyte
formation are common with hyperpituitarism
-Orthostatic hypotension may be present with
hypopituitarism
-Bilateral hemianopsia that can occur with
hypopituitarism requires special consideration during
treatment
Rehab considerations for pts with adrenal dysfunction:
-Recognize signs of stress or exhaustion and avoid
treatments that exacerbate the condition
-Notify the physician with any signs of illness or
increased intracranial pressure (papilledema),
medications may need to be altered
-Orthostatic hypotension is common secondary to long
term cortisol therapy
-Report sleep disturbances to the physician
-Increased incidence of osteoporosis, bone fx,
degenerative myopathy, tendon ruptures, ataxic gait
-delayed wound healing may be common
Rehab considerations for pts with thyroid dysfunction:
-Recognize reduced exercise capacity and fatigue are
typical
-Avoid treatments that exacerbate the condition such as
exercise in a hot acquatic or gym setting due to heat
intolerance (Graves’ disease)
-Avoid cardiovascular stress to eliminate secondary
complications from hypotension, goiter, Graves’ disease
-Provide close monitoring of vital signs
-Recognize the effects of radioiodine therapy
-Recognize the risk of rhabdomyolysis (hypothyroidism)
Rehab considerations for pts with parathyroid
dysfunction:
-Must be familiar with all signs and symptoms of
parathyroid dysfunction in order to refer pts to a
physician if a change in their status occurs
-Recognize symptoms of excessive or inadequate
pharmacological treatment and side effects of the
agents
-Avoid treatments that exacerbate the condition
-Recognize effects of hypercalcemia
(hyperparathyroidism) and hypocalcemia
(hypoparathyroidism)
-Recognize the increased risk for fractures and effects
form osteogenic synovitis (Achilles, triceps, and
obturator tendons most affected)
Rehab considerations for pts with DM:
-Recognize the risk for peripheral neuropathies, small
vessel angiopathy, tissue ischemia and ulcerations,
impaired wound healing, tissue necrosis, and
amputation
-Recognize acute metabolic changes
-Recognize the signs of sudden hypoglycemia and
necessary treatment
-Focus on consistent management of insulin intake, diet,
and physical activity
-Provide education on proper skin care, shoe evaluation,
and shoe wear
Endocrine System
The endocrine system consists of endocrine glands (specialized ductless glands) that secrete hormones that travel through the bloodstream to
signal specific target cells throughout the body. The hormones travel throughout the body to the target organs upon which they act. They will
bind selectivity to receptor sites on the surface of the receptor cells. The endocrine system and nervous system both function to achieve and
maintain stability of the internal environment (homeostasis). The systems are capable of working alone or in concert with each other. The
endocrine and nervous systems work together to regulate metabolism, response to stress, sexual reproduction, blood pressure, and water & salt
balances.
Endocrine System
-Secreting cells send hormones throught the
bloodstream to signal specific target cells
-Hormones diffuse into the blood and travel long
distances to virtually every area of the body
-Endocrine effectors consist of virtually all tissues
-Regulatory effects are slow and tend to last for
long periods
Nervous System
-Neurons secrete neurotransmitters to signal
nearby cells that have an appropriate receptor site
-Neurotransmitters are sent very short distances
across a synapse
-Nervous effectors are limited to muscle and
glandular tissue
-Regulatory effects appear rapidly and are often
short lived
Glands of the Endocrine System:
Hypothalamus
Is part of the diencephalon located below the thalamus and cerebral hemisphere.
The hypothalamus connects to the pituitary gland through the infundibular or
pituitary stalk. If it responsible for regulation of the autonomic nervous system (body
temp, appetite, sweating, thirst, sexual behavior, rage, fear, blood pressure, sleep)
and other endocrine glands thorough its impact on the pituitary gland.
Pituitary Gland
Normally the size of a pea and is located at the base of the brain just beneath the
hypothalamus. The pituitary gland consists of two separate glands, the
adenophypophysis (anterior) and the neurohypophysis (posterior). The pituitary
gland is considered the most important part of the endocrine system since it releases
hormones that regulate several other endocrine glands. This “master gland” is
influenced by factors such as seasonal changes or emotional stress. The pituitary
gland secrets endorphins that act on the nervous system and reduce a person’s
sensitivity to pain. It also controsl ovulation and works as a catalyst for the testes and
ovaries to create sex hormones.
Thyroid Gland
Is located on the anterior and lateral surfaces of the trachea immediately below the
larynx and is shaped like a “bow tie” or butterfly with two halves (lobes); a right lobe
and left lobe joined by an isthmus. The thyroid produces thyroxine and
triiodothyronine that act to control the rate at which cells burn the fuel from food.
An increase in thyroid hormones will increase the rate of the chemical reactions
within the body.
Parathyroid
There are 4 parathyroid glands found on the posterior surface of the thyroid’s lateral
Glands
Adrenal Glands
Pancreas
Ovaries
Testes
lobes. These glands produce parathyroid hormone, which functions as an antagonist
to calcitonin and is important for the maintenance of normal blood levels of calcium
and phosphate. Parathyroid hormone increases the reabsorption of calcium and
phosphate from bones to the blood. Secretion of parathyroid hormone is stimulated
by hypocalcemia and inhibited by hypercalcemia. Normal clotting, neuromuscular
excitability, and cell membrane permeability are dependent on normal calcium
levels.
The two adrenal glands are located on top each kidney; the outer portion is called
the adrenal cortex and the inner portion is called the adrenal medulla. The adrenal
cortex and the adrenal medulla secrete different hormones. The adrenal cortex
produces corticosteroids that will regulate water and sodium balance, the body’s
response to stress, the immune system, sexual development and function, and
metabolism. The adrenal medulla produces epinephrine that increases heart rate
and blood pressure when there is an increase in stress.
The pancreas is located in the upper left quadrant of the abdominal cavity, extending
from the duodenum to the spleen. The pancreas includes both endocrine and
exocrine tissues. The islets of Langerhans are the hormone-producing cells of the
pancreas. Alpha cells produce glucagon and beta cells produce insulin. These
hormones work in combination to ensure a consistent level of glucose within the
bloodstream and properly maintain stores of energy within the body.
The ovaries are located in the pelvic cavity on each side of the uterus. The ovaries
provide estrogen and progesterone that contribute to regulation of the menstrual
cycle and pregnancy. Estrogen is secreted by the ovarian follicles that is responsible
for the development and maintenance of female sex characteristics such as breast
development and the cycles of the female reproductive system. Progesterone is
produced by the corpus luteum and functions to maintain the lining of the uterus at
a level necessary for pregnancy.
The testes are located in the scrotum between the upper thighs. The testes secrete
androgens (most importantly testosterone) that regulate body changes associated
with sexual development and support the production of sperm.
Endocrine System: Hormone, Function, & Regulation of Secretion
Hypothalamus:
Hormone
Function
Growth hormone-releasing
Increases the release of growth
hormone Target: pituitary gland
hormone
Growth hormone-inhibiting
Decreases the release of growth
hormone Target: pituitary gland
hormone
Gonadotropin-releasing
Increases the release of
hormone Target: pituitary gland
luteinizing hormone and folliclestimulating hormone
Thyrotropin-releasing hormone
Increases the release of thyroid
Target: pituitary gland
stimulating hormone
Corticotropin-releasing hormone Increases the release of
Target: pituitary gland
adrenocorticotropic hormone
Prolactin-releasing hormone
Stimulates the release of
Target:pituitary gland
prolactin
Prolactin-inhibitory factor;
Decreases the release of
dopamine Target: pituitary gland prolactin
Regulation of Secretion
CNS feedback; circulating levels
of hormones
CNS feedback; circulating levels
of hormones
CNS feedback; circulating levels
of hormones
CNS feedback; circulating levels
of hormones
CNS feedback; circulating levels
of hormones
CNS feedback; circulating levels
of hormones
CNS feedback; circulating levels
of hormones
Pituitary:
Hormone
Growth Hormone
Target: bone and muscle
Follicle-stimulating hormone
Target: ovaries and testes
Luteinizing hormone
Target: ovaries and testes
Function
Promotes growth and
development; increases the rate
of protein synthesis
Promotes follicular development
and the creation of estrogen in
females; promotes
spermatogenesis in males
Promotes ovulation along with
estrogen/progesterone synthesis
from the corpus lutem in
females; promotes testosterone
synthesis in males
Regulation of Secretion
Hypothalamus
Hypothalamus
Hypothalamus
Thyroid-stimulating hormone
Target: thyroid gland
Adrenocorticotropic hormone
Target: adrenal cortex
Prolactin Target: mammary
glands
Oxytocin Target: uterus and
mammary glands
Antidiuretic hormone Target:
kidneys
Adrenal Cortex:
Hormone
Adrogen Target: ovaries and
testes
Aldosterone (mineralocorticoid)
Target: kidneys
Cortisol (glucocorticoid)
Target:GI system
Adrenal Medulla:
Hormone
Epinephrine Target:
cardiovascular and metabolic
systems
Increases the synthesis of
thyroid hormones T3 and T4
Increases cortisol synthesis
(adrenal steroids)
Allows for the process of
lactation
Increases contraction of uterine
muscles; promotes release of
milk from mammary glands
Increases water reabsorption;
conserves water; increases blood
pressure through stimulating
contraction of muscles in small
arteries
Hypothalamus
Function
Increases masculinization;
promotes growth of pubic hair in
males and females
Increases reabsorption of
sodium ions by the kidneys to
the blood; increase excretion of
the potassium ions by the kidney
into the urine
Influences metabolism of food
molecules; anti-inflammatory
effect in large amounts
Regulation of Secretion
Influenced by the hypothalamic
production and release of GnRH
and Luteinizing hormone (LH)
Low blood sodium level; high
blood potassium level
Function
Increases heart rate and force of
contraction; increases energy
production; vasodilation in
skeletal muscle
Regulation of Secretion
Sympathetic impulses form the
hypothalamus in stress situation
Hypothalamus
Hypothalamus
Nerve impulses from the
hypothalamus; stretching of the
cervix; nipple stimulation
Decreased water content
Adrenocorticotrophic hormone
Norepinephrine Target:
cardiovascular and metabolic
systems
Vasoconstriction in skin, viscera,
and skeletal muscles
Sympathetic impulses form the
hypothalamus in stress situation
Function
Involved in the regulation of the
female reproductive system and
female sexual characteristics
Regulation of Secretion
Cyclical rise and fall of hormone
levles
Function
Increases blood glucose by
stimulating the conversion of
glycogen to glucose
Decreases blood glucose and
increases the storage of fat,
protein, and carbs
Regulation of Secretion
Hypoglycemia
Function
Increases blood calcium
Regulation of Secretion
Influenced by pituitary release of
LH
Function
Involved in the process of
spermatogeneiss and male
sexual characteristics
Regulation of Secretion
Influenced by pituitary release of
LH
Function
Involved with normal
Regulation of Secretion
Thyroid-stimulating hormone
Ovaries:
Hormone
Estrogen, progesterone Target:
uterus and mammary glands
Pancreas:
Hormone
Glucagon
Targets: liver
Insulin
Targets: all body systems
Parathyroids:
Hormone
Parathormone Targets: bone,
kidney, intestinal mucosa
Hyperglycemia
Testes:
Hormone
Testosterone Target: pituitary
gland
Thyroid:
Hormone
Thyroxine (T4), Triiodothyronine
(T3) Targets: all tissues
Calcitonin Targets: plasma
development, increases cellular
level metabolism
Increases calcium storage in
bone; decreases blood calcium
levels
Hypercalcemia
Endocrine System Pathology:
The endocrine system is multifaceted and can develop pathology in one or more areas due to hyperfunction or hypofunction or one or more
glands. In many instances, it is the hypothalamus or the pituitary gland that affects the function of other endocrine glands when they experience
direct or indirect dysfunction.
Hyperfunction of an endocrine gland: usually secondary to overstimulation of the pituitary gland. This can also occur due to hyperplasia or
neoplasia of the gland itself.
Hypofunction of an endocrine gland: usually secondary to understimulation of the pituitary gland. This can also occur from congenital or
acquired disorders.
Hypopituitarism: This condition occurs when there is a decreased or absent hormonal secretion form the anterior pituitary gland. This is a rare
disorder and symptoms are dependent on the age of the effected person and deficit hormones. Typical disorders may include short stature
(dwarfism), delayed growth and puberty, sexual and reproductive disorders, and diabetes insipidus. Treatment is also based on the deficit
hormones and usually includes pharmacolocial replacement therapy.
Hyperpituitarism: This condition occurs when there is an excessive secretion of one or more hormones under the pituitary gland’s control
(frequently growth hormone that produces acromegaly in adults). Disorders and symptoms are dependent on the hormone(s) that are affected.
Some disorders include gigantism or acromegaly, hirutism galactorrhea (abnormal lactation in males or females), amenorrhea, infertility, and
impotence. Treatment is hormone and site dependent and can include tumor resection, surgery, radiation therapy, and hormone suppression or
replacement (if gland becomes dysfunctional after treatment)
Pathology
Addison’s Disease
What is it
Is a form of
adrenal
dysfunction that
presents with
Etiology
When the adrenal
cortex produces
insufficient cortisol
and aldosterone
Signs & Symptoms
Symptoms include
a widespread
metabolic
dysfunction
Treatment
Primarily consists
of long-term
pharmacolocial
intervention using
Cushing’s
Syndrome
hyopfunction of
hormones it is
the adrenal cortex. termed Addison’s
Subsequently,
disease
there is decreased
production of both
cortisol
(glucocorticoid)
and aldosterone.
secondary to
cortisol deficiency
as well as fluid and
electrolyte
imbalances
secondary to
aldosterone
dysfunction. The
person may
experience
hypotension,
weakness,
anorexia, weight
loss, altered
pigmentation, and
if left untreated
this condition will
result in shock and
possible death.
When the pituitary
Symptoms evolve
gland produces
over years and can
excessive
include persistent
adrenocorticotrophic hyperglycemia,
hormone (ACTH)
growth failure,
with subsequent
truncal obesity,
hyper cortisolism, it
purple abdominal
is termed Cushing’s
striae, moon
disease.
shaped face,
buffalo hump
posteriorly at the
base of the neck,
weakness, acne,
hypertension, and
male
synthetic
corticosteroids and
mineralocorticoids.
Is a form of
adrenal
dysfunction that
presents with
hyperfunction of
the adrenal gland,
allowing for
excessive amounts
of cortisol
(glucocorticoid)
production.
Treatment may
include
pharmacological
intervention to
block production
of the hormones,
radiation therapy,
chemo or surgery.
Graves’ Disease
Is the most
specific cause of
hyperthyroidism.
Graves’ disease is
most common in
women over the
age of 20,
however, it occurs
in men as well and
can affect any age
group
Is caused by an
autoimmune disease
in which certain
antibodies produced
by the immune
system stimulate the
thyroid gland
causing it to become
overactive
gynecomastia.
Mental changes
can include
depression, poor
concentration, and
memory loss.
Symptoms are
consistent with
hyperthyroid
presentation. The
classic signs of
Graves’ disease
include mild
enlargement of
the thyroid gland
(goiter), heat
intolerance,
nervousness,
weight loss,
tremor, and
palpitations. Also
seen, enlargement
in the area of the
Adam’s apple
resulting in
difficulty eating
and episodes of
dyspnea,
Abnormal
protrusion of the
eyes.
Management
includes
pharmacological
intervention
and/or removal of
the thyroid gland
using radiation or
surgical
intervention.
Hypothyroidism
Depression/anxiety, increased
lethargy, fatigue, headache, slowed
speech, slowed mental function,
impaired short-term memory
Proximal muscle weakness, carpal
tunnel syndrome, trigger points,
myalgia, increased bone density, cold
intolerance, paresthesias
Dyspnea, bardycardia, CHF, respiratory
muscle weakness, decreased
peripheral circulation, angina, increase
in cholesterol
Anorexia, constipation, weight gain,
decreased absorption of food and
glucose
Infertility, irregular menstrual cycle,
increased menstrual bleeding
Hyperthyroidism
Tremors, hyperkinesis, nervousness,
increased DTRs, emotional lability,
insomnia, weakness, atrophy
Hypoparathyrodism
↓bone resorption
Hypocalcemia
Elevated serum phosphate levels
Shortened 4th and 5th metacarpals
Hyperparathyroidism
↑ bone resorption
Hypercalcemia
Decreased serum phosphate levels
Osteitis fibrosa, subperiosteal resorption,
arthritis, bone deformity
Nephrocalcinosis, renal hypertension,
and significant renal damage
Compromised breathing due to
intercostal muscle and diaphragm
spasms
Cardiac arrhythmias and potential
heart failure
Increased NM activity that can result
in tetany
Chronic periarthritis, heat intolerance,
flushed skin, hyperpigmentation,
increased hair loss
Tachycardia, palpitations, increased
respiratory rate, increase in blood
pressure, arrhythmias
Hypermetabolism, increased appetite,
increased peristalsis, nausea, vomiting,
diarrhea, dysphagia
Polyuria, infertility, increased first
trimester miscarriage, amenorrhea
Gout
Decreased NM irritability
Pancreas Dysfunction:
Pathology
Diagnosis
Diabetes
Mellitus Type 1
Persistent
hyperglyce
mia due to
diminished
or absent
production
of insulin. In
type 1 DM,
insulin is
functionally
absent due
to the
destruction
of beta cells
of the
pancreas
where the
insulin
would
normally be
produced.
Contributing
Factor
Unknown,
however
there are
several
theories. It is
an
autoimmune
process with
strong
genetic
component.
It is also
believed that
the genetic
predispositio
n in
combination
with an
unknown
factor,
potentially
environment
al, triggers
the ongoing
cycle of
destruction
of the beta
cells of the
pancrease.
Clinical
Presentatio
n
Usually
starts in
children
ages 4 or
older, with
the peak
incidence of
onset at 1113 years. A
relatively
high
incidence
also exists in
people in
their late
30s and
early 40s.
Common
symptoms
are polyuria,
polydipsia,
and
polyphagia,
along with
nausea,
weight loss,
fatigue,
blurred
vision and
dehydration
Lab/Imaging
Management/outco
me
A test of blood
glucose levels
will be
necessary. Other
testing includes
urinalysis for
glucose,
ketones, and
protein and a
white blood cell
count as well as
blood and urine
cultures to rule
out infection.
Usually require
insulin via
continuous pump or
self-administered
injection. Exercise is
an important aspect
in management of
DM. Pts should
exercise at 50-60%
of their predicted
maximum HR. Type
1 DM is associated
with a high
morbididty and
premature mortality
rate due to
complications such
as ischemic heart
disease, PVD,
chronic renal
disease, reduced
visual acuity and
blindness.
Type II DM
This form of
DM typically
occurs in
the
population
over the age
of 40,
however,
there has
been an
increase in
children
diagnosed
with type 2
secondary
to a rise in
obesity. This
form of DM
typically
retains the
ability to
Type 2 DM
occurs
secondary to
an array of
dysfunctions
resulting
from the
combination
of resistance
to insulin
action and
inadequate
insulin
secretion.
This disorder
is
characterize
d by
hyperglycem
ia when the
body cannot
. A fasting
glucose
reading of
126 mg/dl is
also a sign
of DM. This
disease
onset is
usually
sudden or
within a
short period
of time.
Obesity is
found to
contribute
to this
condition by
increasing
insulin
resistance.
Symptoms
are
relatively
the same as
with type 1,
however,
ketoacidosis
does not
occur since
insulin is still
typically
produced.
Treatment of type 2
DM includes blood
glucose control
through diet,
exercise, oral meds,
or insulin injections
when necessary.
Systemic Lupus
Erythematosus
produce
some
endogenous
insulin.
SLE is a
connective
tissue
disorder
caused by
an
autoimmun
e reaction in
the body.
The primary
manifestatio
n of the
condition is
the
production
of
destructive
antibodies
that are
directed in
the
individual’s
own body.
The chronic
inflammator
y disorder
produces a
variety of
symptoms
depending
properly
respond to
insulin.
Genetic,
environment
al, viral, and
hormonal
contributing
factors.
Environment
al include
ultraviolet
light
exposure,
infection,
antibodies
(penicillin
and sulfa
drugs),
extreme
stress,
immunizatio
n, and
pregnancy.
SLE can
occur at any
age, but the
most
common age
group is 1540 years.
More
common in
Diverse
symptoms
based on
the
involvement
of the
connective
tissue
throughout
the body.
Symptoms
such as
arthralgias,
malaise and
fatigue may
persist even
during a
remission
period.
Common
clinical
presentatio
n is butterfly
rash across
the cheeks
and nose,
red rash
over light
exposed
areas,
Microscopic
fluorescent
techniques are
indicated to
detect the
presence of the
antinuclear
antibody (ANA)
within the
blood. A positive
ANA test
warrants an
additional test
for
antideoxyribonu
cleic acid
antibodies.
These two tests
in combination
with physical
presentation
support the
presence of SLE.
Focuses on revering
the autoimmune
response in order to
avoid complications
and exacerbations
of symptoms. PT
intervention is
usually indicated
after a period of
exacerbation and
includes a slow
resumption of
physical activities,
energy conservation
techniques, gradual
endurance activities,
and significant pt
education regarding
skin care, pacing,
exercise, and
strengthening.
Human
Immunodeficie
ncy Virus
on the
severity and
extent of
involvement
.
women.
Is a
retrovirus
that initially
invades and
destroys
cells within
the immune
system;
specifically
CD4+ Tlymphocytes
(t-cells). This
virus also
affects
monocytes,
macrophage
s, and Bcells. Once
the T-cells
decrease
beyond a
specific level
a pt will
HIV is
transmitted
through
contact with
blood,
semen,
vaginal
secretions,
and breast
milk. Contact
can be
sexual,
perinatal or
through
contact with
blood or
body fluids
that carry
infected
cells. Risk
factors for
contracting
HIV include
arthralgias,
alopecia,
pleurisy,
kidney
involvement
, seizures,
depression,
fibromyalgia
, and cardiac
involvement
.
A pt will not
immediately
present with
symptoms
after the
initial
transmission
of the
infection. A
pt can be
symptom
free for 1-2
years post
infection or
may exhibit
flu-like
symptoms
including
rash and
fever. HIV
immediately
begins a
latent phase
HIV is diagnosed
through various
blood tests such
as the enzymelinked
immunosorbent
test or Western
blot test. Once
diagnosed the
lab results can
also assist with
classifying the
stage of HIV
infection.
Early detection is
important so that
pharm intervention
can be initiated and
slow the
progression of the
virus. There is no
cure for HIV,
however, proper
medical intervention
can allow the virus
to remain a
manageable chronic
condition. PT may
be indicated during
the course of
HIV/AIDS due to
secondary
impairments. PT
goals & intervention
should include
fitness, flexibility,
stress management,
begin to
demonstrat
e symptoms
of the HIV
infection.
unprotected
sexual
relations,
intravenous
drug use or
mother to
fetus
transmission
. The largest
risk factors
for
contracting
HIV are
homosexual
male sex
(46%),
intravenous
drug use
(25%), and
heterosexual
sex (11%).
where
replication
of the virus
is minimal.
The three
phases of
this disease
process
include
asymptomat
ic HIV,
symptomati
c HIV, and
acquired
immunodefi
ciency
syndrome
(AIDS).
relaxation, aquatic
therapy, pain
management,
breathing exercises,
and neuro rehab.
Studies indicate that
psychosocial factors
influence
progression of the
virus as well as
survival. Presently,
the leading cause of
death is kidney
failure secondary to
the extended drug
therapies.
Spotlight on safety:
According to the American Diabetes Association, recommended blood glucose levels include 70-130 mg/dl prior to a meal and <180 mg/dl
after a meal.
Hyperglycemia: Early signs is blood glucose >180-200 mg/dl, increased thirst and frequent urination. Recognition of these early signs is crucial in
preventing the dangerous onset of ketoacidosis, often referred to as a “diabetic come.” Symptoms include dyspnea, fruity breath odor, dry
mouth, nausea, vomiting, confusion, and an eventual loss of consciousness.
Hypoglycemia: Early signs is when blood glucose is <70 mg/dl, hunger, sweating, shaking, dizziness, clumsiness, and headache. If unaddressed,
pts who become hypoglycemic may lose consciousness, at which point immediate medical attention is necessary. Hypoglycemia is often
counteracted simply by ingestion of a glucose or carb rich substance (sugar, honey, juice, crackers). Pts with significant hypoglycemic issues may
be advised by their physician to carry a glucose source of injectable glucagon with them at all times.
Pharmacology of the Endocrine System:
Drug
Action
Indications
Hormone
Replacement
Therapy
Hyperfuntio
n Agents
Bone
mineral
regulating
Agents
These agents
restore normal
endocrine
function when
endogenous
production of a
particular
hormone is
deficient or absent
These agents
manage
hyperactive
endocrine
function to allow
for inhibition of
hormone function.
This is
accomplished
through negative
feedback loops or
through hormone
antagonists
Attempt to
enhance and
maximize bone
mass along with
preventing bone
loss or rate of
Side effects
Implications
for PT
Must be aware
of side effects
Examples
↓ in endogenous
hormone
secretion
Vary by
exogenous or
synthetic
hormone
replacement
used for
treatment
See specific
hormone
categories
Hyperactive or
excessive
endocrine
function,
excessive
hormone levels
Vary
depending
on the use of
hormone
therapy
Must be aware
of signs of
hyperfunction
of particular
hormones and
side effects
See specific
hormones
Paget’s disease,
osteoporosis,
hyperparathyrodi
dism, rickets,
hypoparathyroidi
sm, osteomalacia
GI distress,
dyspepsia,
dysphagia,
anorexia,
bone pain,
cardiac
Pts with bone
mineralization
deficit are at
risk for fracture
and side effects
from drug
Estrogens:
Premarin;
Calcium and
vitamin D:
Tums,
Calderol;
bone
reabsorption.
Typical agents can
include estrogens,
calcium and
vitamin D,
bisphosphonantes
, calcitonin, and
anabolic agents
arrhythmias
therapy.
Should attempt
to augment
drug therapy
through
ambulation
and other
weight bearing
activities that
stimulate bone
formation.
Bisphospho
nates:
Fosamax,
Boniva;
Calcitonin:
Cibacalcin
Genitourinary System PT examination: (Consists of all the reproductive organs and the urinary organs. These are often considered together due
to their common embryological origin)
Anatomy and Function:
Muscles of the Pelvic
Floor
Pelvic diaphragm
Urogenital diaphragm
Urogenital triangle
Anal triangle
Description
Levator ani: pubococcygeus, puborectalis, iliococcygeus, & coccygeus
(ischiococcygeus)
Deep transverse perineal, urethrae sphincter
Female:bulbocavernosus, ischiocavernosus, superficial transverse perineal
Male: bulbospongiosus, ischiocavernosus, superficial transverse perineal
Internal and external anal sphincter
Genital System
Female:
External genitalia: Mons publis, labia majora, labia
•Provides protection and hydration of vaginal
minora, clitoris, vestibule of vagina, bulbs of
vestibule, greater vestibular (Bartholin’s) glands,
Skene’s gland
Vagina: Musculomembranous tube connected to
the cervis
Uterus: hollow muscular organ
Uterine tubes: Extend laterally from the ovaries to
the uterus
Ovaries: almond shaped glands suspended in the
broad ligaments
tissue and urethra
•Receptacle for male sperm
•Birth canal
•Excretory duct for menstrual fluid
•Houses the fetus during development
•Provides transport for the ovum from the ovary
for fertilization and implantation within the uterus
•Produce hormones such as estrogen and
progesterone
•Storage of oocytes prior to ovulation
Male:
Penis
Scrotum
•External genitalia that expels urine during voiding and semen during the act of copulation
•Cutaneous fibromuscular external sac for the testes, ductus deferens, epididymis, nerves,
and blood vessels
Testes
•Produce sperm and hormones such as testosterone
Dustus/vas •Carries sperm from the testes to the seminal vesicle to form the ejaculatory duct
deferens
Epididymis •Encased within the scrotum, stores sperm
Seminal
•Internal tubes that secrete a thick fluid to combine with sperm within the ejaculatory duct
vesicles
Prostate
•Internal organ lying inferior to the bladder
•Produces and secretes fluid to combine with sperm, seminal vesicle fluid, and bulbourethral
gland fluid to create semen
Renal System: two kidneys, two ureters, the urinary bladder, and the urethra that function to form and eliminate urine.
Kidneys
•Remove water, salt, and metabolic waste from the blood through excretion of urine
Ureters
Urinary
bladder
Urethra
•Contribute to homeostasis including: acid-base balance, regulation of electrolyte
concentrations, control of blood volume, and regulation of blood pressure through the
control of hormones secreted into the blood stream.
•Muscular tubes connecting the kidneys to the urinary bladder to transport urine
•Temporary muscular reservoir for urine
•Muscular tube for excretion of urine
•Semen transport during ejaculation in males
Genitourinary System Pathology
Genital Components
Uterus
Vagina
Prostate
Penis
Renal Components
Kidneys
Bladder
Common Pathologies
Cervical cancer, endometriosis, uterine prolpase
Dyspareunia, vulvodynia, vulvovaginal candidasis (yeast infection)
Prostatitis, prostate cancer
Erectile dysfunction
Common Pathologies
Glomerulonephritis, nephrolithiasis, renal failure
Cystocele, dysuria, hematuria, interstitial cystitis, neurogenic
bladder, nocturia, polyuria, urgency, frequency, urinary
incontinence, urinary tract infections
Genitourinary Conditions/Pathology:
Pathology
Uterus:
Endometriosis
What is it
Is the
development of
endometrial
tissue, which
normally lines the
uterus, in
extrauterine
locations within
Etiology
Unknown. During
each menstrual
cycle the
endometrial tissue
bleeds causing
subsequent
scarring and
adhesions.
Signs & Symptoms
Typically include
moderate to
severe lower
abdominal, pelvic,
or low back pain
before or during
menstruation,
irregular
Treatment
PT may include
manual
techniques such as
myofascial
release, visceral
mobilization and
soft and deep
tissue massage to
the abdomen and
pelvis. The most
common location
of growth occurs
at the uterosacral
ligaments. The
level of pain does
not always
correlate with the
severity of tissue
growth.
Uterine Prolapse
Is the descent of
the uterus and
cervis into the
vagina. The
Baden-Walker
System is the most
widespread
classification of
prolapsed using a
5 point grading
system ranging
from no prolapsed
to maximum
descent of vaginal
menstrual cycles,
premenstrual
spotting,
dyspareunia, pain
during defecation,
and infertility.
Typically consists
of genetics,
denervation or
direct muscle
trauma (labor &
delivery)
Primary symptoms
include pelvic
pressure that
increases with
exertion, urgency,
frequency, urinary
incontinenece,
incomplete
bladder empyting,
discomfort,
vaginal dryness or
irritation,
dysparenunia, and
lower back pain
break up scar
tissue and
adhesions.
Mobility exercises
are performed to
sustain elongation
of tissues.
Relaxation
exercises such as
breathing routines
and restorative
poses are
performed to
regulate the pain
cycle. TENS is also
indicated. Surgery
to remove scarring
and a total
hysterectomy may
be recommended.
PT may include
pelvic floor muscle
training using
biofeedback, Kegel
exercises, core
strengthening
exercises, body
mechanics, and
symptom
dependent
lifestyle
modifications. In
severe cases, an
intravaginal
tissue outside the
body.
that is relieved by
lying down.
Prostate:
Prostatitis
An inflammation
of the prostate
gland
Most common
include bacterial
infection or the
backup of prostate
secretions within
the gland.
Penis: Erectile
Dysfunction
Also known as
impotence, is
estimated to
range from 2585% in men with
diabetes, which
makes this
population 3x
more likely than
the general
population. Onset
of ED in individuals
Diabetes is a
primary etiology,
while other risk
factors include
CAD, HTN,
hypothyroidism,
hypopituitarism,
multiple sclerosis,
psychiatric
disorders,
excessive alcohol
consumption,
mechanical
support device
called a pessary
may be indicated.
Pt may require
reconstructive
surgery.
Common
Management
symptoms include includes lifestyle
watery urethral
modifications,
discharge,
biofeedback
urgency,
training, stretching
frequency,
exercises,
discomfort with
myofascial
urination, and pain techniques, and
with ejaculation.
bladder retraining.
Pharmacological
intervention such
as antibiotics,
alpha blockers or
NSAIDS may be
indicated.
Primary symptom Pharmacological
is the consistent
intervention,
inability to
surgical
maintain an
intervention,
erection adequate injections directly
for sexual
to the penis, and
intercourse.
Kegel exercises.
with diabetes
usually occurs 1015 years earlier
than in men
without diabetes.
Kidneys: Renal
Failure
Renal failure is a
condition where
the kidneys
experience a
decrease in
glomerular
filtration rate and
fail to adequately
filter toxins and
waste from the
blood. There are
two forms: acute
and chronic renal
failure.
smoking, vessel
disease, kidney
disease,
pharmacological
side effects, &
hormonal
imbalances.
Renal pathology
typically occurs
sencondary to DM
or HTN, but can
also occur from
poison, trauma,
and genetics. The
nephrons are
usually damaged
and lose their
ability to filter the
blood. Renal
failure can be
classified as: Acute
(damage occurs
quickly) Chronic
(damage occurs
slowly) End-stage
(nearly total or
total renal failure,
dialysis required)
Acute: Sudden
decline in renal
function, increase
in BUN and
creatinine,
oliguria,
Nausea, vomiting,
lethargy,
weakness, hiccups,
anorexia,
ulceration within
the GI tract, sleep
disorders,
headache,
peripheral
neuropathy,
anemia, pruritis,
osteomalacia,
ecchymosis,
pulmonary edema,
seizures, and
coma
Includes
management of
primary etiology,
pharmacological
intervention,
diuretics,
nutritional
etiology,
hydration,
hemodialysis
and/or
transfusions if
applicable. Tx of
chronic failure
includes
conservative
management
(slowing the
process and
assisting the body
in its
compensation).
Nutritional
support,
hydration,
avoidance of
protein. Renal
hyperkalemia,
sodium retention
Chronic:
progressive
deterioration in
renal function,
DM, HTN,
interstitial
nephritis,
polycystic kidney
disease
Bladder:
Neurogenic
Bladder
Is a dysfunction
where there is
damage to the
cerebral control
that allows for
urinary
dysfunction. If the
urine cannot be
properly released,
there may be an
increase in urinary
tract infections
and kidney
damage.
Diabetes,
diminished
bladder capacity,
hyperactive
detrusor muscle,
CVA, other disease
processes,
infection, and
nerve damage
Frequent urinary
tract infections,
leakage of urine,
inability to empty
the bladder or loss
of the urge to
urinate when the
bladder is full.
Diagnosis should
include an
evaluation by a
physician, X-rays,
and urodynamics
to assist with
diagnosis.
replacement
therapy includes
some form of
hemodialysis
and/or organ
transplant.
Peritoneal dialysis
is a form of renal
replacement
therapy that uses
the peritoneal
cavity as a semipeermeable
membrane
between the
dialysate fluid and
blood vessels of
the abdominal
cavity.
Dependent on the
actual etiology
with a goal of
preventing
bladder
overdistention,
UTIs, and renal
damage. Pt
education, bladder
techniques, lower
abdominal
massage,
temporary
catheterization,
pharmacological
intervention, and
a timed urination
program may be
indicated.
Stress Urinary
Incontinence (SUI)
Urge Urinary
Incontinence (UUI)
Overflow Urinary
Incontinence (OUI)
Loss of urine due
to activities that
increase
intraabdominal
pressure, such as
sneezing,
coughing,
laughing, running,
and jumping.
Loss of urine after
a sudden, intense
urge to void due
to the detrusor
muscle of the
bladder
involuntarily
contracting during
bladder filling. UUI
is the most
common
incontinence in
the geriatric
population and
among residents
in long-term care
facilities.
Loss of urine when
the intra-bladder
pressure exceeds
the urethra’s
See page 686 in
scorebuilders
Detrusor muscle
overactivity,
overactive bladder
syndrome,
changes in the
smooth muscle of
the bladder,
increased afferent
activity, increased
sensitivity of the
detrusor to
acetylcholide, and
idiopathic. Also
associated with
MS, SCI, CVA, and
parkinson’s.
Triggered by
certain events dut
to a conditioned
reflex. Two of the
most common
triggers are “key in
the lock” when
arriving home and
running water.
Behavior
modification is the
primary goal of
treatment for this
condition.
Biofeedback,
pelvic floor
strengthening, and
bladder retraining.
(scheduled
voiding) are key
components.
Caused by outflow
obstruction
secondary to a
narrowed or
Difficulty initiating
the urine stream.
One stream is
initiated, its weak
Surgical
intervention if
there is an
obstruction. If
capacity to remain
closed due to
urinary retention.
Functional Urinary
Incontinence (FUI)
Is the loss of urine
due to the inability
or unwillingness of
a person to use
the bathroom
facilities prior to
involuntary
bladder release.
Urinary Tract
Infections (UTI)
Very common and
occur within the
general
population,
however there is a
higher incidence in
women and the
geriatric
population.
obstructed urethra
that results from a
prolapsed pelvic
organ, a stricture,
an enlarged
prostate, chronic
constipation or
neurological
disease.
A decreased level
of mental
awareness or a
decrease in
mobility.
Occur when
bacteria infiltrate
the urethra or
further into the
bladder itself.
Untreated, this
type of infection
and spread and
cause a kidney
infection
(pyelonephritis).
and presents with
post void dribble.
there is weakness
of the detrusor
muscles, double
voiding is
recommened for
these pts as well
as other
strengthening
measures.
Impaired cognition Treatment should
and/or mobility
be directed to
alleviate the
underlying tissue.
Improving
mobility,
modifying clothing
style, increasing
independence.
Frequency of
Early treatment
urination, pain and has the best
or burning with
results.
urination, cloudy
Pharmacological
urine, pressure
treatment includes
above the public
bacteria-specific
bone in women,
antibiotics based
shakiness, fever,
on the bacteria
back pain, and
found in the
fatigue.
bladder. Pts are
also encouraged
to drink an excess
of fluids to assist
with treatment of
the infections.
Stages of Kidney Disease:
Stage 1:
Stage 2:
Stage 3:
Stage 4:
Stage 5:
Kidney damage with normal BFR (90 or greater)
Mild decrease in GFR (60-89)
Moderate decrease in GFR (30-59)
Severe reduction in GFR (15-29)
Kidney failure (GFR less than 15)
Hemodialysis:
-Treatment process for pts with advanced and permanent kidney failure
-Kidney failure creates excess toxic waste, increase BP, retention of excess body fluids, and a decrease in red blood cell production.
-Hemodialysis removes the blood from the body along with waste, excess sodium, and fluids.
-The process cleanses the blood and returns it to the body.
-A patient requires this process on average 3x per week and each visit requires 3-5 hours to complete the treatment.
-Side effects that may be associated with dialysis include anemia, renal osteodystrophy, pruritus (itching), sleep disorders, (restless legs), and
dialysis-related amyloidosis.
Rehab considerations for pts with renal failure/dialysis:
•Modify treatment plan based on fluid and electrolyte staus
•Standard precautions should be followed at all times for protection
•Recognize pts abilities post dialysis and potential for dehydration and hypotension
•Monitor vital signs closely, however, avoid placement of the blood pressure cuff over the fistula
•Avoid mobilization activities as they are contraindicated during dialysis
•Energy conservation techniques and pacing skills should be incorporated into therapy
Genitourinary System Terminology:
Anuria
Inadequate urine output in a 24 hour period; less than 100 ml (severe dehydration, shock,
endstage renal disease)
Benign
A non-cancerous enlargement of the prostate gland that is progressive. Common in males
prostatic
over 60 and can interfere with normal voiding.
hypertrophy
Cystocele
Ectopic
Entometrium
Glomerular
filtration rate
(GFR)
Glomerulus
Bulging of the bladder into the vagina
Implantation of a fertilized ovum outside of the uterus (fallopian) tube is the most
common site of an ectopic pregnancy)
The inner lining of the uterus that is shed monthly in response to hormonal influence
An estimate of the filtering capacity of the kidneys; volume of filtrate produced per
minute by the kidneys
The specialized tuft of capillaries that are needed for the filtration of fluid as blood passes
through the arterioles of the kidneys
Hematuria
Presence of blood in the urine (cancer, faulty catheterization, serious disease)
Impotence
Impairment with ejaculation, orgasm, erection, and/or libido
Myometrium
The muscular outer layer of the uterus
Nephrolithiasis The condition of developing kidney stones. There are various types of crystal formations
that create stones.
Nocturia
Urinary frequency at night (DM, congestive heart failure)
Oliguria
Inadequate urine output in a 24 hour period; less than 400ml (acute renal failure, DM)
Polyuria
Large volume of urine excreted at one time (DM, chronic renal failure)
Perimetrium
The serous peritoneal coat of the uterus
Radical
A surgical procedure in which the entire breast, pectoral muscles, axillary lymph nodes,
mastectomy
and some skin are removed usually secondary to breast cancer
Rectocele
The bulging of the anterior wall of the rectum into the vagina secondary to weakening of
the pelvic supporting structures
Seminiferous
Coiled tubes found within each lobe of the testes where spermatogenesis takes palce
tubules
Urea
Major nitrogen-containing end product of protein metabolism normally cleared from the
blood by the kidney into the urine
Urinary
Voiding more than 8x in a 24 hour period
frequency
Urinary
Sudden desire to urinate that is stronger than usually and difficult to defer
urgency
1st Practice Exam (3rd exam in Scorebuilders) 130.
Gastrointestinal System:
GI Anatomy and Function
Upper GI
Mouth
Esophagus
Stomach
Initiation of mechanical and chemical digestion
Transports food from the mouth to the
stomach
Grinding of food, secretions of hydrochloric
acid and other exocrine functions, Secretions
of hormones that release digestive enzymes
from the liver, pancreas, and gallbladder to
assist with digestion
Lower GI-Small Intestine
Duodenum
Jejunum
Ileum
Neutralizes acid in food from stomach and
mixes pancreatic and biliary secretions with
food
Absorbs water, electrolytes, and nutrients
Absorbs bile and intrinsic factors to be
recycled
Lower GI-Large Intestine
Ascending Colon
Transverse Colon
Descending Colon
Sigmoid
Rectus
Anus
Continues to absorb water and electrolytes;
stores and eliminates undigested food as feces
Gland Organs
Gallbladder
Liver
Pancreas
Stores and releases bile into the duodenum to
assist with digestion
Bile is produced and is necessary for
absorption of lipid soluble substances, assists
with red blood cell and vitamin K production,
regulates serum levels of carbohydrates,
proteins, and fats
Exocrine-secretes bicarbonate and digestive
enzymes into the duodenum;
Endocrine-secretes insulin, glucagon, and
other hormones into the blood to regulate
serum glucose level.
Gastrointestinal Pathology
Pathology
What is it
Etiology
Gastroesophageal
Reflux Disease
(GERD)
GERD is the
result of an
incompetent
lower
esophageal
sphincter (LES)
that allows
reflux or
gastric
contents.
Erosive Gastritis
Is the
Weakness of
the LES,
Intermittent
relaxation of
the LES, Direct
damage to the
LES through
NSAIDS,
alcohol,
infectious
agents,
smoking, and
certain RX
medications.
Bleeding from
Signs &
Symptoms
Heartburn,
regurgitation of
gastric content,
belching, chest
pain, hoarseness
and coughing,
esophagitis, and
hematemesis.
Symptoms
Treatment
Treatment is
usually through
pharmacological
intervention.
Is supportive
Non-erosive Gastritis
Peptic ulcer Disease
inflammation
of the gastric
mucosa or
inner layer of
the stomach.
Symptoms are
similar to
GERD,
however, they
tend to have a
higher
intensity.
Is the
inflammation
of the gastric
mucosa or
inner layer of
the stomach.
Symptoms are
similar to
GERD,
however, they
tend to have a
higher
intensity.
the gastric
mucosa
secondary to
stress, NSAIDS,
alcohol
utilization, viral
infection or
direct trauma.
include
dyspepsia,
nausea,
vomiting and
hematemesis. At
times, the Pt
may be
asymptomatic
with removal of
the stimulus of
the disease
process and
pharmacological
interventions.
This condition
is usually a
result of
helicobacter
Pylori infection
The Pt is usually
asymptomatic
but will show
symptoms if the
gastritis
progresses
H. pylori is a
carcinogen and
must be treated
aggressively.
Pharmacological
interventions
are most
common and
typically include
a proton pump
inhibitor and
antibiotics.
Is a condition
where there is
a disruption or
erosion in the
GI mucosa.
There is an
imbalance
between the
Many ulcers
are caused by
the H. pylori
infection and
chronic NSAID
use, Irritants
that increase
risk of ulcer
Symptoms are
dependent on
the location and
severity of
ulceration and
can include
epigastric pain,
burning or
Treatment is
usually through
pharmacological
intervention,
however, in
more severe
cases, surgical
intervention
protective
mechanisms of
the stomach
and the
secretions of
acids within
the stomach.
Diarrhea/constipation
Malabsorption
Syndrome
Is defined as
an abnormal
frequency or
volume of
stool and can
appear as a
symptom of
certain GI
pathologies.
Constipation is
defined as the
infrequent or
difficult
passage of
stool,
secondary to
an increase in
the hardness
of the stool.
Is a condition
characterized
by a group of
pathologies
where there is
reduced
include stress,
alcohol,
particular
medications,
foods, and
smoking.
heartburn,
nausea,
vomiting,
bleeding, bloody
stools and pain
that comes in
waves that is
relieved by
eating
may be
required.
Malabsorption
syndrome
occurs
secondary to
defects in
digestion
Weight loss,
chronic
diarrhea,
anemia, fatigue,
abdominal
bloating,
Once diagnosed,
treatment
includes
avoidance of the
underlying
cause for the
intestinal
absorption
and
inadequate
nutrition
and/or the
inability of the
intestinal
mucosa to
absorb the
nutrients from
digested food.
steatorrhea,
abdomal
cramps,
indigestion,
bone pain, and
excessive gas.
Irritable Bowel
Syndrome
Consists of
recurrent
symptoms of
the upper and
lower GI
system that
interfere with
the normal
functioning of
the colon.
The etiology is
unknow but
one theory
believes that
the colon or
large intestine
may be
sensitive to
certain foods or
stress.
Diverticulitis
Is a condition
of having
inflamed or
infected
diverticula.
This occurs in
approx. 2025% of the
population
that has
The exact
etiology of
diverticulitis is
unknown;
however, a
dominant
theory is that
the disease
results from a
low fiber diet.
Abdominal pain,
bloating or
distention of the
abdomen,
nausea,
vomiting,
anorexia,
changes in form
and frequency
of stool, and
passing of
mucus in the
stool.
Abdominal pain
is the primary
symptom,
tenderness over
the left side of
the lower
abdomen,
cramping,
constipation,
nausea, fever,
malabsorption,
probiotics,
antibiotics,
dietary
modification,
and nutritional
support
including
vitamins,
minerals and
electrolytes.
Changes in life
style and
nutrition,
decrease in
stress,
pharmacological
interventions,
adequate sleep,
exercise, and
psychotherapy
may all assist in
alleviating
symptoms.
Diet
modification,
controlling the
underlying
infection, and
lowering
internal colonic
pressure
through
increased fiber
diverticulosis.
Hepatitis
Is an
inflammation
process within
the liver. Viral
hepatitis is
most common
and is
classified as
hepatitis
A,B,C,D,E, or G
Cirrhosis of the Liver
Is a condition
where the
healthy tissue
of the liver is
replaced with
scar tissue that
blocks the flow
of blood
through the
organ and
prevents the
liver from
properly
functioning.
Many instances
of hepatitis are
viral in nature.
Other
etiologies
include a
chemical
reaction, drug
reaction or
alcohol abuse.
Other viruses
that can cause
hepatitis
include
Epstein-Barr
virus.
The etiology is
usually
alcoholism or
hepatitis C.
Alcohol tends
to block the
normal
metabolism of
protein, fats,
and carbs.
chills, and
vomiting can
also occur.
Fever, flu
symptoms,
abrupt onset of
fatigue,
anorexia,
headache,
jaundice,
darkened urine,
lighter stool,
enlarged spleen,
and liver and
intermittent
pruritus
intake
Acute viral
hepatitis usually
resolves wit
medical
treatment, but
can become
chronic in some
cases. Chronic
hepatitis may
result in the
need of a liver
transplant.
Fatigue,
Treatment cant
decreased
reverse the
appetite,
process or
nausea,
damage, but can
weakness,
slow the
abdominal pain,
process.
spider angiomas,
Treatment is
ascites, edema
based on the
in the LE,
causative factors
jaundice,
and is
gallstones,
implemented
increased
until symptoms
itching,
cannot be
ecchymosis,
controlled, A
bleeding , and
liver transplant
Cholecystitis and
Cholelithiasis
Refers to
inflammation
of the
gallbladder
that may be
acute or
chronic
The most
common
etiology is
gallstones that
have become
impacted
within the
cystic duct.
Gallstones
develop from
hypomobility of
the gallbladder,
supersaturation
of bile with
cholesterol or
crystal
formation.
increase in
sensitivity to
medications.
Many times
gallstones are
asymptomatic,
however, the
most common
symptom is right
upper quadrant
pain.
Abdominal Pain Quadrant and Potential Etiologies
Left upper Quadrant Right upper Quadrant Left lower Quadrant
Gastric ulcer
Hepatomegaly
Perforated colon
Perforated colon
Duodenal ulcer
Ileitis
Pneumonia
Cholecystitis
Sigmoid Diverticulitis
Spleen injury
Pneumonia
Kidney stone
Spleen rupture
Hepatitis
Ureteral stone
Aortic aneurysm
Biliary stones
Intestinal Obstruction
may be
necessary to
sustain life.
Treatment is not
recommended
for the patient
with
asymptomatic
gallstones, but a
low fat diet can
decrease
gallbladder
stimulation if
mild symptoms
are present.
Right lower Quadrant
Kidney stone
Ureteral stone
Meckel diverticulum
Appendicitis
Cholecystitis
Intestinal obstruction
Gastrointestinal Pharmacology
Name
Antacid agents
Action
Are used to
chemical
neutralize
gastric acid
and increase
the
intragastric
PH.
Indication
Episodic
minor
gastric
indigestion
or
heartburn,
peptic
ulcer,
GERD
Side effect
Acid rebound
phenomenon,
constipation, or
diarrhea, may
effect
metabolism of
other
medications.
Implication
Since these
agents are
well tolerated
there are no
side effects
that interfere
with physical
therapy.
H2 receptor
blockers
Bind
specifically
to histamine
receptors to
prevent the
istamineactivated
release f
gastric acid
normally
stimulated
during food
intake.
Inhibit the
H+K+ATPase
Dyspepsia,
acute and
long term
treatment
of peptic
ulcer, or
GERD
Headache,
dizziness, mild
GI distress,
tolerance,
arthralgia, acid
rebound with
dicontinuation
of medicine.
Since these
agents are
well tolerated
there are no
side effects
that interfere
with physical
therapy.
Dyspepsia,
GERD
Acid rebound
when
discontinued
Since these
agents are
well tolerated
Proton Pump
Inhibitors
Examples
Aluminumcontaining:
basaljel,
Calcuim
carbonatecontaining:
tums,
Magnesiumcontaining:
Milk of
magnesia,
Sodium bicar.
Containing:
Bromo seltzer
Tagament,
Pepcid, Zantac
Prevacid,
nexium,
prilosec,
enzyme that
blockes
secreations
of acid from
gastric cells
into the
stomach
Anticholinergics Block the
effects of
acetylcholine
on parietal
cells in the
stomach and
decrease the
release of
gastric acid.
Antibiotics
Are
prescribed
to treat H.
pylori
infection
with the goal
of facilitating
more rapid
healing of
associated
gastric
ulcerations.
Antidiarrheal
Are used to
Agents
slow the
serious
debilitating
effects of
dehydration
after prolonged
use
there are no
side effects
that interfere
with physical
therapy.
protonix,
acipHex
Gastric
ulcers
Dry mouth,
confusion,
constipation,
urinary
retention
PT should be
aware of
potential side
effects in
order to
respond
appropriately.
Gastrozepin,
Muscarinic
cholinergic
antagonist.
H. pylori
bacteria
Hypersensitivity, PT should be
nausea
aware of
potential side
effects in
order to
respond
appropriately.
Metronidazole,
tetracycline,
clarithromycin,
amoxicillin
Prolonged
diarrhea
Constipation,
Abdominal
discomfort
Donnagel,
Kapectolin,
peptpBismol,
Motofen,
Imodium
Since these
agents are
well tolerated
there are no
side effects
that interfere
Laxative Agents
associated
with
prolonged
diarrhea.
Are used to
facilitate
bowel
evacuation
and should
be used
sparingly
Emetic agents
Are used to
induce
vomiting
Antiemetic
Agents
Are used to
decrease
symptoms of
nausea and
vomiting
with physical
therapy.
To
promote
defecation
Nausea,
abdominal
discomfort,
cramping,
electrolyte
imbalance,
dehydration,
dependence,
with prolonged
use
If the laxative
was recently
ingested
physical
discomfort
may
temporarily
limit patient
participation
in therapy
interventions.
To induce
With
Therapy
vomiting,
inappropriate or should be
usually
prolonged usage deferred if a
after
dehydration,
patient is
ingestion
electrolyte
actively
of a toxic
imbalance, and
vomiting
substance upper GI
erosion may
occur
Nausea
Agent
Antihistamine
associated dependent, but antiemetic
with
can include
agents
motion
sedation,
frequently
sickness,
dysrhythmias,
cause
anesthesia, and pain
sedative
pain or
effects which
oncology
can be
treatment
limiting to PT
interventions
Citrucel,
Metamucil,
colace, fleet
Glycerin
suppository,
senokot
Apomorphine,
Ipecac
Scopolamine,
meclizine,
dolasetron,
phenergan.
Gastrointestinal System Interventions/Rehab:
Rehab considerations for pts with GI disease:
-Recognize electrolyte imbalances from diarrhea,
vomiting, and weight loss
-Recognize the potential for orthostatic hypotension
secondary to electrolyte imbalances
-Increased risk for muscle cramping secondary to
alteration in the sodium-potassium pumps
-Potential for difficulty swallowing secondary to disk
protrusion or esophageal pathology
-Recognize that back pain and/or shoulder pain may be
secondary to an acute ulcer or GI bleed
-Observation of Kehr’s sign indicates free air or blood
within the abdominal cavity
Rehab considerations for pts with GERD:
-Avoid certain exercise secondary to an increase in
symptoms with activity; recumbency will induce
symptoms
-Recognize increased incidence of neck and head
discomfort secondary to perception of a lump in the
throat and subsequent compensation
-Left sidelying preferred since right sidelying may
promote acid flowing into the esophagus
-Recognize conditions such as chronic bronchitis,
asthma, and pulmonary fibrosis may all present with
GERD
-Consider that certain positioning during postural
drainage may encourage acid to move into the
esophagus
Rehab considerations for pts with Gastritis:
-pts with gastritis secondary to chronic NSAID use may
be asymptomatic
-Knowledge of blood in the stool should result in physical
referral
-Educate each pt to take medications with food and
avoid certain types of food and drink
-The pt should avoid all aspirin-containing compunds
Rehab considerations for pts with Peptic Ulcer Disease:
-Asymptomatic pts with history of ulcer should be
monitored for signs of bleeding
-Fatigue level, pallor, and exercise tolerance must be
monitored for signs of bleeding
-Recognize that heart rate increase or blood pressure
decrease may be sings of bleeding
-Recognize that back pain is a sign of perforated ulcer
located on the posterior wall of the stomach and
duodenum
-Recognize that pain that radiates form the midthoracic
area to the right upper quadrant and shoulder may
signify blood and acid within the peritoneal cavity
secondary to a perforated and bleeding ulcer
Rehab considerations for opts with malabsorption
syndrome:
-Recognize increased risk for osteoporosis and
pathologic fractures
-Monitor fatigue level, pallor, bone pain, and exercise
tolerance
-Recognize weight loss and abdominal bloating
-Recognize increased risk for muscle spasms secondary
to electrolyte imbalances
-Recognize increased risk for generalized swelling
secondary to protein depletion
Rehab considerations for pts with Irritable bowel
syndrome:
-Emphasize physical activity to assist with bowel function
and relieve stress
-Emphasize breathing techniques to assist in stress
reduction and with breath holding patterns
-Recognize that biofeedback training may be beneficial
Rehab considerations for pts with diverticular disease:
-Physical activity assists the bowel function and is
extremely important during periods of remission
-Breathing techniques will assist in stress reduction and
with breath holding patterns
-Avoid any increase in intra-abdominal pressure with
exercise or activity
-Back pain and/or referred hip pain must be examined
for possible medical diseases
Rehab considerations for pts with Hepatitis:
-Heath care workers that are at risk for contact with
hepatitis should receive all immunizations for HBV, and if
exposed to blood or body fluids of an infected person
must receive immunoglobulin therapy immediately
-Standard precautions should be followed at all times for
protection
-Enteric precautions are required for pts with hepatitis A
and E
-Recognize that arthralgias may be noted, especially in
older pts, and will not typically respond to traditional
therapeutic intervention
-Energy conservation techniques and pacing skills should
be incorporated into therapy
-Balance activities along with periods of rest, avoid
prolonged bed rest, and provide pt education regarding
signs of relapse or chronic hepatitis
Rehab considerations for pts with cirrhosis of the liver:
-Recognize that ascities may develop as well as fluid
accumulation in the ankles and feet
-Report any blood loss through nose bleeds, gum bleeds,
tarry stools or excessive bruising
-Avoid all activities that produce the valsalve maneuver
(increase in intra-abdominal pressure)
-Adequate rest is required to lower the demands on the
liver and improve circulation; avoid unnecessary fatigue
with therapeutic or daily activities
Rehab considerations for pts with cholecystitis and
cholelithiasis:
-Must be familiar with all signs and symptoms of
cholecystitis in order to refer pts to a physican if a
change in their status occurs
-Post surgical exercises and ambulation are appropriate
post laparoscopic cholecystectomy such as breathing
exercises, splinting while coughing, and mobility training
Genitourinary System:
Pathology
Diagnosis
Urinary Stress
Involuntarily
Contributing
Factor
Occurs from
Clinical
presentation
Dribbling of
Lab/Imaging
Cystometry is
Management/outco
me
Usually consists of
Incontinence
loss of urine.
May occur
during
activities
when there is
an increase in
abdominal
pressure
through
straining,
sneezing,
coughing or
lifting.
a loss of
strength and
or integrity of
the tissues
that maintain
bladder
control. It is
caused by
weakness of
the pelvic
floor
muscles. Risk
factors
include
pregnancy,
vaginal
delivery,
episiotomy,
prostate or
pelvic
surgery,
aging, DM,
recurrent
UTIs. Obesity
(due to
increased
intraabdominal
pressure)
urine,
urgency,
frequency,
nocturia, and
a weak
stream while
voiding.
used to
evaluate
bladder
capacity,
control,
contractility,
and sensation.
During this
procedure
provocative
stress testing
will be
performed
when stress
incontinence is
suspected.
Urodynamic
testing
observes the
stability of the
bladder and
electromyogra
phy observes
bladder
contractions.
Urinalysis is
used for DD to
rule out
infection,
diabetes, and
other
conditions.
convervative
measures (PT) as a
first line of defense
followed my
pharmacological and
surgical
interventions. PT
intervention for
pelvic floor muscle
weakness that is
ststed as 0/5-2/5
includes biofeedback,
e-stim, bladder
retraining, and
therapeutic exercise.
Pelvic floor muscle
strengthing at this
level includes
facilitation and
tapping of the pelvic
floor muscles,
overflow exercises
uring the buttocks,
adductors, and lower
abdominals, and
implementation of
Kegel exercises. PT
for muscle weakness
graded 3-5-5/5
includes continued
biofeedback and
bladder retraining,
weighted vaginal
bones for resistance
training, and
implementation of
pelvic floor muscle
exercises during
activities. Outpatient
PT for urinary stress
incontinence should
alleviate pelvic floor
weakness and
involuntary leakage
of urine within 8-12
weeks.
Obstetric Musculoskeletal Pathology:
Pathology
What is it
Coccydynia
After childbirth
the joint between
the coccyx and
sacrum can
become
hypermobile
causing the soft
tissue surrounding
the coccyx to
become painful.
Etiology
Subluxation during
delivery,
adherence to tear
or episiotomy scar
Signs & Symptoms
Difficulty sitting on
hard surfaces,
referred pain to
the low back,
sacroiliac joint,
hip, buttock, groin
or rectum areas,
pain with bowel
movements,
dyspareunia, and
formation of
hemorrhoids
Treatment
Heat, external
joint mobilization,
myofascial
release, muscle
energy
techniques,
biofeedback for
pelvic floor muscle
relaxation,
postural training,
abdominal
strengthening
exercises,
stretching
exercises for
surrounding
muscles and the
use of a cushion
for sitting.
Diastasis Recti
Is a separation of
the rectus
abdominis muscle
along the linea
alba that can
occur during
pregnancy. Testing
for diastasis recti
should be
performed on all
pregnant women
prior to
prescribing
exercises that
require the use of
the abs.
Hormonal changes
in women may
cause the
separation. The
therapist must
note how many
fingers fit into the
separation and
modify treatment
accordingly.
A pt is considered
to have diastasis
recti if the
therapist detects a
separation greater
than the width of
two fingers when
the woman lifts
her head and
shoulders off the
plinth.
Piriformis
Syndrome
Refers to a
persistent, severe
radiating low back
and buttock pain
spanning from the
sacrum to the hip
and posterior
thigh. However,
controversy exits
over piriformis
syndrome’s
efficacy as an
accurate
diagnosis.
During pregnancy
the piriformis may
shorten or spasm
due to postural
changes and hip
lateral rotation
while walking.
The primary
symptom is sciatic
paresthesia due to
nerveentrapment
as the sciatic
nerve passes
under or through
the pirifiormis
muscle.
Stabilization and
support with
abdominal
strengthening
exercises, postural
awareness
exercises, and
body mechanic
training. A
newborn can also
have diastatis recti
secondary to
incomplete
development,
however, in
infants this
condition usually
resolves itself
without
intervention.
Manual
techniques for
correcting pelvic
or sacral
alignment such as
METs, joint mobs,
self-correction
techniques for
alignment, heat
application, deep
tissue massage,
myofascial
release, straincounterstrain, ab
Symphysis Pubis
Pain
To prepare for
delivery, the
symphysis pubis
joint become
mobile in order to
allow the joint to
slightly separate
during delivery.
Postural
adaptations,
ligamentous laxity
and complications
during delivery or
birthing of a large
infant can result in
more sever injury
Sever pain in the
symphysis pubis
and SI joint as well
as blood in the
urine due to injury
to the urethra or
bladder neck.
strengthening,
stretching for
piriformis, body
mechanics, and
postural
education.
Pharm
intervention for
pain, surgical
intervention based
on the degree of
separation. Heat
or ice if acute,
manual
techniques for
correcting
pelvic/sacral
alignment. Lumbar
stabilization and
the use of a
lumbo-pelvic
brace or binder.
•Women should not exercise in the supine position after the first trimester.
•Prolonged periods of motionless standing should be avoided.
•Left sidelying is the position of choice to reduce the pressure on the inferior vena cave, maximize cardiac output to enhance maternal and
fetal circulation, and reduce the risk if incompetent cervix.
Relative Contraindications to
terminate exercise during
pregnancy:
-Severe anemia
-Unevaluated maternal cardiac
dysrhythmia
-Chronic bronchitis
-Poorly controlled type 1 DM
-Extreme morbid obesity
-Extreme underweight (BMI <12)
-History of sedentary lifestyle
-Poorly controlled HTN
-Orthopedic limitations
-Poorly controlled seizure disorder
-Poorly controlled
hyperthyroidism
-Heavy smoker
Absolute Contraindications to
terminate exercise during
pregnancy:
-Hemodynamically significant
heart disease
-Restrictive lung disease
-Incompetent cervix/cerclage
-Multiple gestation at risk for
premature labor
-Persistent 2nd or 3rd trimester
bleeding
-Placenta previa after 26 weeks of
gestation
-Premature labor during the
current pregnancy
-Ruptured membranes
-Preeclampsia/pregnancy-induced
hypertension
Pharmacology of the Genitourinary System:
Pharm intervention is used for treating bladder symptoms related to urgency, frequency, infection, and pain.
Drug
Action
Overactive
bladder agents
Relive the
symptoms of
an overactive
bladder. This
condition is
noted by
involuntary
contractions of
the bladder
(detrusor
muscle)
Treat urinary
tract
infections, but
are not
traditional
antibiotics or
sulfonamide
agents. These
agents can be
used
independently
or in
combination to
treat urinary
infections.
Urinary AntiInfective
Agents
Indications
Urinary
urgency,
frequency,
incontinence,
nocturia
Cystitis,
urinary
urgency,
burning with
urination, UTI,
nocturia
Side Effects
Implications
for PT
GI distress,
These agents
nausea,
do not typically
dizziness,
interfere with
photosensitivity, rehab
headache,
constipation,
pulmonary
reactions
GI distress,
nausea,
dizziness,
photosensitivity,
headache,
constipation,
rash
These agents
typically do not
interfere with
rehab
Examples
Ditropan
(oxybutynin
chloride),
Detrol
(tolterodine
tartrate)
Cinobac
(cinoxacin),
Furadantin
(nitrofurantoin)
System Interactions:
Oncology-Cancer, malignancy, neoplasm, and tumor are all terms referring to abnormal uncontrolled cell growth within the body. There are
more than one hundred different cancers of various types and tissue origins currently recognized, including lymphoma and hematologic cancers.
Malignant cancer cells are characterized by their ability to grow uncontrollably, invade other tissues, remain undifferentiated, initiate growth at
distant sites, and avoid detection and destruction by the body’s immune system. The origins of malignant cells vary widely from environmental
factors and lifestyle choices to genetic predisposition.
Carcinoma is a malignancy originating from the epithelial cells of organs. Carcinomas in specific organs may be named more specifically
depending on the characteristics present. For example, large cell carcinoma, adenocarcinoma, and squamous cell carcinoma are all subsets of
lung carcinoma. The American Cancer Society reports that at least 80% of all cancers in the US are carcinomas.
Risk factors:
Increasing Age
Tobacco Use
Alcohol Use
Gender
Virus exposure
Environmental
influence
Poor diet
Stress
Occupational
Hazards
Ethnic Background
Genetic influence
Sexual/reproductive
behavior
General Signs & Symptoms of Cancer
C-Change in bowel/bladder routine
A-A sore that will not heal
U-Unusual bleeding/discharge
T-Thickening/lump develops
I-Indigestion or difficulty swallowing
O-Obvious change in wart/mole
N-Nagging cough/hoarseness
Cancer Prevention:
Primary Prevention
-Screening for high
population
-Elimination of
modifiable risk factors
Secondary
Prevention
Tertiary Prevention
-Use of natural agents
(teas, vitamins) to
prevent cancer
-Cancer vaccine
-Early detection
-Selective preventative
pharmacological agents
(Tamoxifen)
-Multifactorial risk
reduction
-Prevent disability that
can occur secondary to
cancer and its
treatment
-Manage symptoms
-Limit complications
Tissue & Tumor Classification:
Tissue Classification
Epithelium: Protect, absorb, and
excrete
Pigmented Cells
Connective Tissues: elastic,
collagen, fibrous
Examples
-Skin, Lines internal cavities,
Mucous membrane, Lining of
bladder
-Moles
-Striated muscle, blood vessels,
bone, cartilage, fat, smooth
muscle
Nerve Tissues: neurons, nerve
fibers, dendrites, glial cells
-Brain, nerves, spinal cord, retina
Lymphoid Tissues
-Wherever lymph tissue is
Tumor Classification
Carcinoma; Adenocarcinoma
(glandular tissue)
Malignant Melanoma
Sarcoma, fibrosarcoma,
liposarcoma, chondrossarcoma,
osteosarcoma,
hemangiosarcoma,
hemangiosarcoma,
leiomyosarcoma,
rhabdomyosarcoma
-Astrocytoma, Glioma,
Neurilemic sarcoma,
neuroblastoma, retinoblastoma
Lymphoma
Hematopoietic Tissues
present throughout the body,
lymph nodes, spleen, can appear
in stomach, intestines, skin, CNS,
bone and tonsils
-Bone marrow, plasma cells
Diagnostic tools:
Family history
Physical exam
Pap smear
Blood tests
Radiography
CT scan
Bone scan
Stool guaiac
Biopsy
Mammography
Endoscopy
Isotope scan
Genitourinary System Intervention/ Rehab:
Rehab considerations for pts with renal failure/dialysis:
-Modify treatment plan based on fluid and electrolyte
status
-Standard precautions should be followed at all time for
protection
-Recgonize pts abilities post dialysis and potential for
dehydration and hypotension
-Monitor vital signs closely, however, avoid placement of
the blood pressure cuff over the fistula
-Avoid mobilization activities as they are contraindicated
during dialysis
-Energy conservation techniques and pacing skills should
be incorporated into therapy
-Leukemia, Myelodysplasia,
Myeloproliferative syndromes,
multiple myeloma
Lifestyle Modifications to address bladder symptoms:
-Daily fluid intake should be 2,500 mL, or 10 cups, to regulate excessively high or low fluid intake
-Reduce bladder irritants including carbonated, caffeinated, and alcoholic beverages, spicy foods, citric juices, and artificial sweeteners. Caffeine
reduction should be tapered slowly to avoid severe headaches.
-Schedule voiding for every 3-4 hours to reduce bladder distension. An average person voids 6-8 times in a 24 hour period. A bladder diary
assists with baseline measurements and goal setting
-Regulate bowel function to prevent constipation and straining during bowel movements by monitoring dietary fiber, fluid intake, and exercise.
-Avoid fluid intake 2-3 hours prior to bedtime to reduce nocturia.
-A smoking cessation program may decrease the occurrence of coughing and subsequent bladder leakage.
-A weight loss program, if moderately obese, may decrease pressure on the pelvic tissues and organs.
Spotlight on Safety: Rehab Considerations for pts undergoing chemotherapy and radiation:
-Strenuous activity should be initially avoided following implantation of radioactive seeds utilized for brachytherapy. Communication with the
radiation oncologist and/or referring physician is imperative as further activity contraindications or precautions may be advised depending on
the individual care.
-Skin tattoos are used to guide beam alignment with external beam radiation. PTs must be cautious and defer interventions which may alter the
position of alignment tattoos (taping interventions, certain soft tissue or myofascial mobilizations)
-Irradiated skin requires special care to protect tissues prone to erythema, rash, and dry desquamation, as well as more painful wet
desquamation and superficial burns.
-Massage and heat are contraindicated over irradiated areas for a minimum of 12 months.
-Certain chemotherapy agents may cause the pt to have a level of toxicity that requires staff and visitors to take additional precautions before
making physical contact.
-Pt vomiting during therapy should be reported to the nurse/physician, especially if the pt it taking antiemetic medications to control nausea and
vomiting.
Stage
Stage 0
Stage I
Stage II
Stage III
Stage IV
Definition
Early malignancy that is present only in the
layer of cells in which it began. For most
cancers, this is referred to as carcinoma in
situ. Not all cancers have a stage 0.
Malignancy limited to the tissue to origin
with no lymph node involvement or
metastatis.
Malignancy spreading into adjacent tissues,
lymph nodes may show signs of
micrometastases.
Malignancy that has spread to adjacent
tissue showing signs of fixation to deeper
structures. The likelihood of metastatic
lymph node involvement is high.
Malignancy that has metastasized beyond
the primary site, for example, to bone or
another organ.
Oncology Pathology:
Pathology
What is it
Brain Cancer
May occur as a
primary tumor
arising from
astrocytes,
meninges, nerve
cells, or tissues
within the brain.
Metastatic brain
cancer occurs
when a brain
Etiology
Most primary
cancers outside of
the brain
metastasize to the
brain during
progression of the
cancer.
Signs & Symptoms
Dependent on the
tumor and
typically
progresses rapidly.
Symptoms include
headache,
seizures, ↑
intracranial
pressure, cognitive
and emotional
Treatment
Surgical resection
along with
radiation or other
combined
therapies are
typically indicated.
Cervical Cancer
Colorectal Cancer
tumor develops as
a consequence of
cancer in another
primary area of
the body.
Starts in the cells
on the surface of
the cervix,
typically
squamous cells.
This precancerous
condition is called
dysplasia and is
easily treatable.
Annual cervical
screening is
recommended;
diagnosis is made
through a Pap
smear. Prognosis
is good with timely
intervention. If
dysplasia goes
undetected,
changes can
develop into
cervical cancer
and metastasize to
the bladder,
intestines, lungs,
and liver.
Accounts for
approx 15% of
cancer deaths
impairment, and
↓ motor and
sensory function.
The human
papilloma virus
(HPV) is the primary
cause of cervical
cancer; it is slow
growing. Risk factors
include smoking,
maternal use of
diethylstilbestrol
(DES), African
American ethnicity,
oral contraceptive
use, and certain
sexually transmitted
dieases.
Asymptomatic
during the early
stages, however,
symptoms can
include abnormal
bleeding, pelvic
and low back pain,
impairment with
bladder and bowel
function.
Dependent on
staging of the
cancer and may
include laser
therapy, excision,
cryotherapy or
hysterectomy with
adjunct
chemotherapy or
radiation.
Risk factors include
increasing age,
history of polyps,
Colon cancer does
not provide early
signs of disease
Based on type and
stage and may
include surgical
Lung Cancer
Lymphoma
(Hodgkin’s, nonHodgkin’s disease)
annually.
Adenocarcinoma
and primary
lymphoma
accoudnt for the
majority of
intestinal cancers.
ulcerative colitis,
Crohn’s disease, fam
history, and a diet
high in fat and low in
fiber.
and the most
prominent
symptom is a
continuous change
in bowel habits.
Bright red blood
from the rectum is
another
prominent sign of
colon caner. The
pt may experience
symptoms of
fatigue, weight
loss, anemia, and
overt rectal
bleeding.
Is cancer of the
epithelium within
the respiratory
tract. It is the most
frequent cause of
death from all
cancers. Rapid
metastasis can
occur through the
pulmonary
vascular system,
adrenal gland,
brain, bone, and
liver.
Lymphoma is
classified as cancer
found in the
Risk factors include
smoking,
environment,
geography,
occupational
hazards, age, and
fam history.
Early symptoms
include cough,
sputum, and
dyspnea.
Progression may
include
adventitious
breath sounds,
chest pain, and
hemoptysis.
Risk factors for
Hodgkin’s disease
include association
A painless lump is
typically the first
sign. Hodgkin’s
resection of the
tumor and
potentially a
portion of the
bowel, with
subsequent
radiation therapy
or chemo.
Colostomy may be
required.
Prognosis is good
for early diagnosis
if the cancer is
contained;
prognosis is poor if
it has
metastasized.
There is a poor
prognosis
secondary to
expedited
metastaiss (less
than 14% for a 5
year survival rate).
Surgical
intervention along
with combination
therapies may be
required.
Hodgkin’s disease
is one the most
curable cancers
Pancreatic Cancer
lymphatic system
and lymph tissues;
lymphomas are
categorized as
Hodgkin’s disease
or non-Hodgkin’s
lymphoma.
with Epstein-Barre
virus, drug abuse,
immunosuppressant
use, obesity, chronic
or autoimmune
diseases. Risk factors
for non-Hodgkin’s
lymphoma include
exposure to benzene
(cigarette smoke),
auto emissions, and
pollution.
disease is
distinguished by
the presence of
Reed-sternberg
cells and
Hodgkin’s disease
can metastasize to
extralympthatic
sites including the
liver, spleen, and
lungs.
Prominent type of
cancer with an
extremely high
mortality rate.
Cancer of the
exocrine cells
within the ducts is
the most common
form of pancreatic
cancer. It will
metastasize to the
liver, lungs, pleura,
colon, stomach,
and spleen.
Risk factors include
tobacco use, gender,
increasing age, and
cholecystectomy.
Symptoms are
very vague during
the initial stages of
the disease which
often results in
delayed diagnosis.
Common
symptoms include
weight loss,
jaundice, and
epigastic pain that
can radiate to the
thoracic region.
Advanced cancer
depending on age,
disease stage,
overall health, and
responsiveness to
treatment.
Treatment options
are based on the
pts age and
staging
classification and
include chemo,
radiation, stem
cell transplant,
and highly active
antiretroviral
therapy. NonHodgkin’s
progression varies
based on
classification.
Usually directed to
assist in the relief
of symptoms.
Pancreatic cancer
has a very poor
survival rate with
a mortality rate of
almost 100%.
Surgical resection
along with
chemotherapy and
radiation assist to
relieve symptoms.
Prostate Cancer
Skin Cancer
Adenocarcinoma
is the most
common type of
prostate cancer.
Typically affects
men over 50, it is
the second highest
cause of death
from cancer in
men. Diagnosis is
found through
prostate biopsy
and prognosis is
good with
appropriate
treatment. There
is an approximate
10% fatality from
this diagnosis.
Basal cell
carcinoma is a
slow growing form
of skin cancer that
rarely
metastasizes. It
originates from
the epidermis and
is the most
common form of
Risk factors include
age, high fat diet,
genetic
predisposition,
African American
descent, and
exposure to
cadmium.
Sun exposure is a
common cause, with
risk factors including
frequent sun
exposure, light eyes,
and fair skin.
may present with
severe pain that
may indicated the
cancer has
metastasized.
Most times this is
asymptomatic
until the cancer
reaches the
advanced stages.
Symptoms include
urinary
obstruction, pain,
urgency, and
decreased
stream/flow of
urine.
Open sores that
can bleed or curst
and remain for
three or more
weeks, reddish
patches of skin, a
shiny bump on the
skin that is often
pink, or a scar-like
area that has
Treatment varies
and may include
surgical incision of
the prostate
gland, radiation,
or hormonal
therapy; can
metastasize to the
bladder, MS
system, lungs and
lymph nodes.
Prognosis is good,
basal cell
carcinoma can
routinely be cured.
Surgical excision
may be required
to remove the
cancer cells.
skin cancer.
Malignant
Melanoma
Originates from
melanocytes and
can be classified
as: superficial
spreading,
nodular, lentigo
maligna or acral
lentiginous
melanomas. Peak
incidence is
between 40-60
years of age. Early
diagnosis is vital to
prognosis, as it
can spread and
metastasize
quickly. Areas of
metastases
include the brain,
lungs, liver, bone,
and skin.
poorly defined
borders.
Risk factors for
Lesions can be
malignant
elevated on the
melanoma include a surface of the skin
history of blistering
and appear
sunburns prior to 20 keratotic or scaly.
years of age, family
Other symptoms
history,
when observing
immunosuppression, the skin or a mole
light eyes, fair skin,
may include
and a previous
asymmetry,
history of cancer.
irregular borders,
varied color, and a
diameter of
greater than 6mm.
Pharmacology—Oncology Management:
Drug
Action
Indications
Alkylating
Agents
Bind the DNA
strands
together to
prevent
replication. If
the DNA
cannot
Various
malignancies
Side Effects
Vary by class of
drugs and by
specific agent;
multisystem
involvement with
mild to severe
side effects,
This form of
cancer is 100%
curable with early
diagnosis. Excision
may solely be
required with
early treatment. If
melanoma has
metastasized,
surgical
intervention along
with combination
therapies may be
required.
Implications
for PT
Therapists
must be aware
of the chemo
regimen and
modify
treatment
based on the
Examples
Mustargen,
Busulfex,
Leukeran
untwist, then it
cannot divide
and replicate
its genetic
code. These
agents initiate
cell death by
disrupting DNA
function and
releasing
enzymes that
destroy the
cell.
Anitmetabolite
Agents
Impair
biosynthesis of
genetic
material and
interrupt the
cellular
pathways that
synthezise the
DNA and RNA.
These agents
create an
imposter to
the
endogenous
metabolites
within the
however,
potential risks are
typically
warranted
secondary to the
diagnosis of
malignancy
Various
malignancies,
particularly
rapidly dividing
neoplastic cells
Vary by class of
drugs, potential
risks are typically
warranted
secondary to the
diagnosis of
malignancy
pts symptoms
and side affects
from cancer
treatment.
Extreme
fatigue, GI
distress, cancer
pain and blood
disorders are
common.
Therapists
must provide
support and
encouragement
without
pushing the pt
beyond their
abilities.
Therapists
must be aware
of the chemo
regimen and
modify
treatment
based on the
pts symptoms
and side affects
from cancer
treatment.
Extreme
fatigue, GI
distress, cancer
pain and blood
disorders are
Leustatin,
Adrucil,
Fludara, Trexall
(methotrexate)
body to form a
nonfunctional
genetic
product that is
incapable of
reproduction.
Antibiotic
Agents
Certain
antibiotic
agents are
used with
treatment of
cancer due to
their high
toxicity and
ability to
interfere with
DNA & RNA
synthesis and
subsequent
cell division.
Plant Alkaloid
Agents in this
Agents (Mitotic classification
Inhibitors)
are nitrogen
based and
largely derived
from plants.
They directly
target the
replication
process prior
to and during
Various
malignancies
SOB,
dysrhythmias,
blood disorders,
myelosuppression,
pedal edema
Various
malignancies
Vary by class of
drugs, potential
risks are typically
warranted
secondary to the
diagnosis of
malignancy
common.
Therapists
must provide
support and
encouragement
without
pushing the pt
beyond their
abilities.
Same as
Adriamycin,
previous
Mithracin,
Cosmegen
Same as
previous
Oncovin,
Taxotere, Taxol
Hormones
Biologic
Response
Modifier
mitosis to
inhibit cell
division. This
limits cell
division and
cancer growth
in various
types of
malignancy.
Certain
hormones can
exacerbate or
facilitate
proliferation of
particular
forms of
cancer while
other
hormones can
attenuate
particular
cancers.
Hormones are
typically used
as adjunct
therapy along
with other
form of
treatment
specific to the
malignancy.
Include
interferons,
interleukin-2,
Various
malignancies,
particularly
hormone
sensitive
neoplasms
Masculinization in
women, hot
flashes, general
catabolic effects
Same as
previous
Nolvadex,
Lupron,
Casodex
Various
malignancies,
particularly
Vary by class of
drugs, potential
risks are typically
Same as
previous
Proleukin,
Avastin,
Intron-A
Agents
Heavy metal
compounds
and
monoclonal
antibodies that
are responsible
for enhancing
the body’s own
ability to
respond to
neoplastic
growth. These
agents are not
cytotoxic, but
facilitate the
pts immune
response to
destroy
malignant
tissues.
Used as
antineoplastic
agents are also
known as
platinum
coordination
complexes.
They act as
askylating
agents that
inhibit DNA
translation are
replication.
leukemias,
lymphomas,
Kaposi
sarcoma,
organ and
tissue
malignanicies
warranted
secondary to the
diagnosis of
malignancy
Various
malignancies,
particularly
epithelial
malignancies,
ovarian,
testicular and
bladder cancer
Vary by class of
drugs, potential
risks are typically
warranted
secondary to the
diagnosis of
malignanc
Oncology Terminology:
Adjuvant
Treatment provided, in addition to other cure-
Same as
previous
Platinol,
Paraplatin,
Eloxatin
Benign neoplasm
Cancer
Differentiated
Cells
Dysplasia
Hyperplasia
Malignant
neoplasm
Metaplasia
Neoadjuvant
Tumor
(neoplasm)
focused inverventions, with the intension of
preventing cancer recurrence
An abnormal cell growth that is usually slow growing
and harmless, closely resembling the composition of
adjacent tissues
A group of diseases characterized by uncontrolled
cell proliferation with mutation and spreading of the
abnormal cells. The etiology is based on the type
and location of the cancer. The most common
causes include cigarette smoking, diet and nutrition,
chemical agents, physical agents, environmental
causes, viral causes, and genetics.
Cells that have matured from a less specific to a
more specific cell type
An abnormal development of cells or tissue that is
often an early sign of neoplasia
An increase in cell number that may be normal or
abnormal depending on additional characteristics
An abnormal uncontrolled cell growth that invades
and destroys adjacent tissues and may metastasize
to other sites and systems of the body
A change in a cell from one type to another that may
be normal or abnormal
Chemotherapy or radiation given prior to surgical
oncology intervention
An abnormal new growth of tissue that increases the
overall tissue mass. Tumors are benign (noncancerous) or malignant (cancerous) as well as
primary or secondary. Primary tumors form from
cells that belong to the area of the tumor. Secondary
tumors grow from cells that hae metastasized
(spread) from another affected area within the
body. Tumor classification is defined by cell type,
tissue of origin, amount of differentiation, benign
Undifferentiated
cells
versus malignant, and anatomic site.
Cells which have not differentiated into a specific
into a specific type (primitive, embryonic) or have no
special structure or function.
Psychological Disorders:
Affective Disorders: are classified by disturbances in mood or emotion. States of extreme
happiness or sadness occur and mood can alternate without cause. These extreme emotions can
become intense and unrealistic.
Depression:
-Slower mental and physical activity; poor self-esteem
-Immobilized from everyday activities; sadness, hopelessness, and helplessness
-Desire to withdraw; delusions in severe cases
Mania:
-Constantly active
-impulses immediately expressed
-Unrealistic activity
-Elation and self-confidence
-Disagreement with a patient may produce patient aggression
-Disorganized thoughts and speech
-Very few pts are diagnosed with only manic disorder
Bipolar:
-Alternating periods of depression and mania
-Females are at a greater risk; typically begins in a pts twenties
Neuroses Disorders: refer to a group of disorders that are characterized by individuals exhibiting
fear and maladaptive strategies in dealing with stressful or everyday stimuli. Pts with neuroses are
not dealing with psychosis, do not have delusions, and usually realize they have a problem.
Obsessive-Compulsive Disorder:
-Obsessions-persistent thoughts that will not leave
-Compulsions-repetitive ritual behaviors the pt cannot stop performing
-Thoughts or ritual behaviors that interfere with daily living
-Unable to control irrational behavior
-Most commonly beings in young adulthood
Anxiety Disorder:
-Constant high tension; overreacts in certain instances
-Presents with apprehension and chronic worry
Acute anxiety attacks:
-Lasts a few minutes in duration
-Excitation of the sympathetic autonomic nervous system
-Fear of impending doom or death
-Shortness of breath, heart palpitations, dizziness, nausea
-Initiated by unconscious and internal mechanisms
Phobia Disorder:
-Excessive fear of objects, occurrences or situations that is considerably out of proportion/irrational
-Fear creates difficulty in everyday life
-Subclassifications include agoraphobia, social phobia, and simple phobia; simple phobia is easiest
to treat
-May develop from traumatic experiences, observation, classical conditioning
Dissociative Disorders: Develop when a person unconsciously dissociates (separates) one part of
the mind from the rest.
Psychogenic Amnesia:
-Produced by the mind with no physical causes
-Forgets all aspects of the past
Multiple Personality:
-A rare dissociative disorder; includes two or more independent personalities
-Each personality may or may not know about the other
-Causative factors are not understood; believed to allow a person to engage in behaviors that are
against the pts morality and normally produce guilt
Somatoform Disorders: are classified based on the physical symptoms present in each disorder.
Somatization Disorder:
-Primarily in women, has familial association, and often chronic and long lasting
-Complaints of symptoms with no physiological basis
-Symptoms usually lead to medications and medical visits and alter the pts life
-Resembles hypochondriasis disorder
Conversion disorder:
-Physical complaints of neurological basis with no underlying cause
-Paralysis is the most common finding; other findings include deafness, blindness, paresthesia
-Frued believed this is mental anxiety transformed into physical symptoms
-Diagnosis can be made once testing is negative for physical ailments
Hypochondriasis Disorder:
-Excessive fear of illness
-Believes that minor illnesses or medical problems indicate a serious or life threatening disease
Schizophrenia Disorders: Psychotic in nature and present with disorganization of thought,
hallucinations, emotional dysfunction, anxiety, and perceptual impairments. Causative factors
include traumatic events, genetic inheritance, biochemical imbalances, and environmental
influence.
Catatonic Schizophrenia:
-Motor disturbances with rigid posturing
-Episodes consist of uncontrolled movements, however, pts remain aware during episodes
Paranoid Schizophrenia:
-Delusions of grandeur; delusions of persecution
-May believe they possess special powers
Disorganized Schizophrenia:
-Usually progressive and irreversible with inappropriate emotional responses; mumbled talking
Personality disorders: is classified by observing a pts pattern of behavior, dysfunctional view of
society, and level of sadness. Personality disorders are usually ongoing patterns of dysfunctional
behavior.
Psychopathic Personality:
-Low morality, poor sense of responsibility, no respect for others
-Impulsive behavior for immediate gratification; high frustration
-Little guilt or remorse for all actions; inability to alter behavior, even with punishment
-Expert liar
Antisocial Behavior:
-Results from particular causes (need for attention or involvement in a gang)
-Typically has some concern for others
-Blames other institution (family, school) for their actions
-Symptoms are typically seen before 16 years of age
-Violates the rights of others; lacks responsibility and emotional stability
Narcissistic Behavior:
-Incapable of loving others
-Self-absorbed; obsessed with success and power
-Unrealistic perception of self-importance
Borderline Behavior:
-Instability in all aspects of life
-Can identify self from others
-Uses projection, denial, defensiveness; unpredictable mood or behavior
-Intense and uncontrolled anger; chronic feelings of emptiness
Tips for interaction with an escalating patient:
-Be empathetic when setting boundaries
-Use a low, calm tone of voice when speaking
-Do not respond defensively to pt comments
-Offer choices, options or small concessions if appropriate
-Do not force constant eye contact, allow the pt to look away
-Be respectful and acknowledge the pts complaints or frustration
-When speaking, wait for the pt to pause rather than raising your voice to be heard
-Be aware of your supportive resources, including the option to leave the area if necessary
-Avoid physical contact
-Do not turn your back to an agitated or escalating pt
-Do not allow an agitated or escalating pt to block your exit route
-Maintain more space than usual between yourself and the pt for safety
-Stand at an angle facing the pt so that it is easier to sidestep if necessary
-Always stay at the same eye level as the pt (both standing, both sitting)
-Keep hands out of your pockets both for self-protection and to avoid the appearance of concealment