Outline of Key Learning Areas related to PBL Case
Week 28 – ‘Get a grip’
Relevant Symptoms (incl. relevant negatives)
27 year old male ‘Tony’ presented to ED with a 10 cm laceration to R medial forearm
Complains of numbness and difficulty moving fingers
Other Significant History
Carpenter
Right handed
Had tetanus shot in high school
Examination and Signs
Initially abusive, so examination delayed for an hour
Clean wound, no contamination visible
Negative signs:
 Unable to adduct or abduct fingers of R hand
 Unable to flex middle, ring and little fingers
 No reaction to pinprick stimuli on little and ring fingers
Positive signs:
 Shoulder bruised and tender
Peripheral circulation normal.
Provisional Diagnosis
Differential Diagnoses
Severed R ulnar nerve
Severed R flexor tendons
Risk Factors and Aetiology
Intoxication
Young male
Key Basic Science Learning Issues
1) Anatomy
3) Microbiology
Tetanus
Caused by Clostridium tetani, grampositive obligate anaerobic bacteria
• Spread by deep wounds, leading to
invasion of bacteria into deep tissue
• Incubation period: ~ 8 days
• Pathogenesis of infection
Bacteria release endotoxin
4) Pathophysiology
Nerve injury
Segmental Demyelination
Schwann cell dysfunction or myelin
sheath damage, with the axon
remaining intact
Degenerating myelin is initially
engulfed by Schwann cells and later
by macrophages
Axonal Degeneration
Primary destruction of the axon and
secondary destruction of the myelin
sheath
Wallerian degeneration:
degeneration of a nerve fibre from the
point of damage forwards
Triggered by severe nerve injury –
trauma, transaction, toxins,
inflammation, demyelination
Local Schwann cells break down
myelin and engulf axonal fragments
Nerve damage can also lead to
degeneration of cells that share
synapses with the injured cell –
anterograde or retrograde
transneuronal
Neuron regeneration
Peripheral Nervous System

Axonal sprouting occurs at the
proximal stump within 96 hours
Axon eventually reaches target, and
functional connection(e.g. NMJ) is
reformed
Axonal growth proceeds at a rate of
1mm/day
Central Nervous System
CNS neurons are post-mitotic so are
not able to divide or regenerate
CNS axons are capable of
regenerating, but the surrounding
environment is inhibitory
Glial cells form scar tissue and secrete
inhibitory factors, preventing axonal
growth
Astrocytic proliferation, activation of
microglia, inflammation, and invasion
of immune cells also contribute
to a poor environment for regeneration
Treatment is currently focused on
rehabilitation rather than repairing
injury
2) Physiology/Biochemistry
Mechanism of muscle contraction
Ulnar claw


Interossei do DAB and PAD – and
work with lumbricles to extend
the PIP and DIP while flexing the
MCP
Extensor digitorum tendon
extends down dorsum of hand –
attaches with lumbricles and
interossi.
 Pincer/writing position =
interosseus muscle action –
flexion of proximal and extension
of distal two.
 Without this you get the opposite
– extension MCP and flexion of
DIP and PIP
 This will compromise his ability to
work as a carpenter – pincer grip
to power grip.
 He also appears to have muscle
wasting
 Resting muscle tone in dorsal and
palmar interossei is gone
The paired muscles on the other side of
the hand are unopposed
Complex regional pain
Acute and dramatic autonomic effects
persist beyond expected limits
Prevalent in distal extremities – affects
pain perception in response to smaller
stimuli. It may also cause hyper-inflated
sweat response, hirsutism, abnormal
control of vasculature.
Absence of sweating
ANS damage – sympathetic nerve input is
compromised
Mechanism of nerve conduction
Steps in the Generation of an Action Potential
1. Resting state (before stimulation)
Na+ and K+ voltage- gated ion channels (primarily located in axon hillock and axon) are closed
2. Beginning of stimulation
Na + arrives at axon hillock, depolarizing the membrane at that point (steadily rising LP). For
anything more to happen, this LP must rise to a critical voltage called the threshold (about 60mV) in order to open voltage gates at trigger zone.
3. Depolarisation Phase:
At threshold the neuron “fires” producing an AP.
Here voltage-gated Na + gates open quickly while K+ gates open more slowly.
Positive feedback were more and more Na+ gates open, causing membrane voltage to rise
rapidly.
3. Repolarisation Phase:
As rising MP passes 0 mV, Na+ gates begin to slowly close and by time they are fully closed the
voltage peaks at +35 mV. Membrane now positive on inside and negative on out (reversed to
RMP).
By this peak, the Na+ gates are closed and the slow K+ gates are fully open and there is an
efflux of K+ as they are repelled by the positive ICF. This causes the repolarisation (shifting
back to negative numbers)
4. Hyperpolarisation:
K+ gates stay open longer than Na+ gates, so the amount of K+ leaving is greater than amount
of Na+ that entered. Thus membrane voltage drops 1-2 mV. This is restored by Na+/K+ pump
and simple diffusion of K+ back into the cell.
Continuous conduction occurs along unmyelinated axons. It is a step=by-step depolarization
where the resulting depolarization excites voltage-regulated gates immediately distal to the AP
Saltatory conduction occurs in neurons that are myelinated. These neurons have gaps
in between the myelin sheaths called Nodes of Ranvier. These gaps contain the
highest concentration of voltage-gated Na+ and K+ channels. Therefore, impulse jumps
from node to node.
Functional features of forearm manual anatomy
 Free Motion
 Power grasping
 Precision handling
 Pinching
Investigations and Results
Other possible
investigations
1) Blood tests
1) Blood tests
2) Imaging
X-rays of upper limb including shoulder showing no fracture or foreign body
2) Imaging
X-ray would show glass it reflects the rays
3) Other
3) Other
Management Plan
Problem
Goal/desired outcome
Method (incl. patient
actions)
Severed ulnar nerve and flexor tendons
Damaged artery
Wound thoroughly debrided before
suturing
Surgery
Resources/health
professional s
involved
Surgeon…
Small artery ligated
Hand vulnerable while regeneration occurring
Relief of tensile load upon tissues
undergoing repair. You don’t want to
challenge these tissues by extra loading
Forearm and hand
immobilized in a brace
in the flexed position
Potential exposure to C. tetanii
Immunity
Inability to use dominant hand
Rehabilitation
Financial strain – four dependent children
Medications
Financial aid
Return to work facilitated
Mode of action
Vaccination
administered
Stimulation of
neuromuscular
pathways through
passive and active
exercises
Centrelink /Community
assistance
Side effects
Antibiotics
Prevent spread of bacterial infection
Analgesia
Various, previously outlined
Saline administered intravenously
Blood loss replacement (?)
Occupational
therapist
Physiotherapist
GP
Rehab team
Social worker
Any specific
monitoring
required?
Other Psychosocial/ethical/legal/patient-centred considerations
Depression common following disabling injury – inability to function or work as previously able
Mental assessment
+ 12 months still ulnar claw and weakened grip in R hand – after 12 months you’re unlikely to get much more improvement
PPH implications
Tetanus immunisation programme
1. Infancy: DTPw (diphtheria, tetanus, pertussis) is given at 2 months with boosters at 4, 6 and 18 months
2. Childhood: the DTPw vaccination is given before school entry (4-5 years)
3. Adulthood: ADT (adult tetanus/diphtheria) is given before leaving school and once every 10 years
If patient hasn’t had received immunisations, and exposure to bacterium is considered a possibility, passive immunity should be administered
via immunoglobulin.
Alcohol and injury
1 in 5 Australians drink at short-term/high risk (binge drinking) levels at least once a month (this goes to about 1 in 4 in young adults aged 2029)
Approximately 10-18% of all injured patients arrive at the emergency room due to alcohol-related causes




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Most are males under 35 (mostly late teens/young adults) of middle socioeconomic status
Alcohol-related injuries mostly occur in public places, during leisure activities and intentionally
caused by a friend/acquaintance
Responsible for 5% of male injuries and 1.5% injuries in females
Most common cause of death due to intoxication is road crash and among chronic condition alcohol-related liver cirrhosis accounts
for majority of deaths
Prevention
Ineffective Strategies (though often popular)
 Voluntary Industry Codes e.g. of bar practice
 Alcohol education and persuasion
 Public service messages
 Non-specific warning labels
 Promoting alternativeness e.g. alcohol free activities
 Designated drivers and ride services
Effective Strategies
 Regulating physical availability of alcohol – restricting hours and days of sale, restriction on density of outlets, restricting availability by
alcohol strength, sales bans (e.g. cask wines and cask fortified wines in indigenous population), Minimum legal purchase age
 Government monopoly of retail sales
 Increase taxes and pricing for alcohol
 Drink driving countermeasures – lower BAC limits, RBT’s, license suspension
 Treatment and intervention for hazardous drinkers – can be at the level of health setting and workplace. Pharmacotherapy has also
been proven to be effective
Resources used/discovered