Nursing Intervention Synthesis/Patient Summary
Events leading to admission (ER, Direct Admit, Transfer from another facility)
This client, K.R., is a 15-year-old, well-developed Caucasian male. On Sunday,
March 16th, 2013, this young man was riding to church with his mother and two brothers.
There were headed down a two-way 55-mph country road when the mother hit a patch of
black ice and slid into a head on collision with another vehicle. K.R. was seated in the
back seat, likely was ejected from the vehicle during the collision. The remaining 3
passengers all remained within the vehicle. The driver of the other vehicle rushed over to
K.R., who was lying in the road 50 feet from the vehicle unresponsive and bleeding
profusely from his head. Per EMS reports that CPR was performed and the patient was
intubated and transported to St. Mary’s via helicopter. The remaining three passengers
were all admitted to hospitals for varying injuries include one brother to St. Mary’s, the
mother to Covenant Health Care, and the other brother to Mid Michigan Regional
Medical Center.
Presenting Symptoms per ED documentation: The patient arrived at St. Mary’s
unresponsive and with full spinal precautions. At1032. On admission he was quite
hypothermic and was shivering. He also presented with a large laceration in the right
parietal occipital are which was stapled quickly and after being hemodynamically
stabilized he was taken back to the CT scan for a full body scan (See Laboratory/ Test
Results). The following information was obtained from K.R’s medical record prior to my
arrival.
Physical Assessment per ED documentation: This is the initial physical assessment
completed in the emergency department prior to surgery submitted at 1324 on the day of
the accident. Information Presented here is verbatim from a physical assessment
document done by emergency department personnel. See “Physical Assessment” for a
full in depth assessment completed the following morning.
Craniofacial: The client had approximately 8 centimeters laceration to the right parietal
occipital area of the scalp in which staples were applied.
Neck: The client has a C-collar in place that was applied at the scene.
Eyes: Pupils are 3 mm, equal, round, and sluggishly reactive to light.
ENT: The client does have an ET tub in place. Mucous membranes are pink, moist, and
normal in color. External ears are intact. Tympanic membranes are intact.
Respiratory: Equal breath sounds.
Cardiovascular: Regular rate and rhythm. No pericardial friction rubs.
Abdomen: Soft, non-tender, non-distended with active bowel sounds. No peritoneal
signs. No organomegaly.
Back: No tenderness to palpation in the thoracic, lumbar or sacral spine.
Extremities: No cyanosis, no clubbing, no edema. No obvious deformities.
Neurologic: The patient is a Glascow Coma Scale (GCS) of 7T. Some purposeful
movement noted. The patient is intubated.
Psychiatric: Unobtainable.
Glascow Coma Scale: 7
Vital Signs: These are the vital signs for K.R. on the scene and at his arrival in the ED at
1055. Note a pain scale was not provided due to his lack of consciousness. EMS did a
good job of stabilizing his vitals as evidenced by the chart below. Tachycardia was not
present, however, he was hypothermic. Oxygen saturation was poor and then improved as
well as respirations after intubation. Note that the patient minimal respiratory effort, most
of the breathing effort was done by assist-control ventilator. No widened pulse pressure.
Time
1036
1055
BP
134/95
128/99
P
86
90
RR
29
16
GCS
7
7
Osat
86
99%
Temp
95.1
95.7
Lab Results: Lab results obtained in the emergency department submitted at
approximately 1300.
Hemoglobin
Hematocrit
WBC
Platelet
PT
INR
Lactic Acid
Glucose
BUN
Creatinine
Sodium
Potassium
Chloride
13.0
40.0
24.0
183,000
13.5
1.3
3.1
197
13
0.6
142
3.7
107
Low
Low
High
Normal
Normal
High
High
High
Normal
Normal
Normal
Normal
Normal
Predicted Serum Osmolarity
299.6 mOsm/kg
4.6 points above normal
but not high enough to be
considered a gap.
ABG: Results obtain in the emergency department submitted at approximately 1200.
Note that the specific initial ventilator setting were unable to be found via EMR,
however, see “Respiratory Assessment” for ventilator settings and ABGs for the
following day. If the FiO2 was room air (21%) then these values would be fairly close to
normal, however if FiO2 was 100% then these would be far from normal.
PH
pCO2
7.30
46
pO2
Bicarbonate
89
22
Urinalysis: All Normal.
Drug Screen: Negative.
Image Results
1. Chest X-Ray: Moderate opacity involving the right upper lobe. Differential diagnosis
includes pulmonary contusion versus pneumonia.
2. Pelvic X-Ray: Negative, no mention of kidneys.
3. CT of the head: right frontoparietal subdural hemotoma, large scalp hematoma,
parenchymal hemorrhage within the right frontal cortex, left temporal lobe, left thalamus,
arachnoid cyst seen within the right middle cranial fossa and posterior fossa.
4. CT of the maxillofacial: negative
ECG: Normal Sinus Rhythm
Treatment Provided in Emergency Department: The patient was seen and evaluated
in the emergency department immediately upon arrival where all imaging and diagnostic
tests were completed. Access devices included two 18-guage peripheral IV’s (Left A/C
and right A/C), one arterial line in the right radial and a central line. The patient was then
admitted to the NICU after surgery with critical care orders. The plan at this time was to
keep the patient on the ventilator and wean as appropriate, monitor lab values and treat
them according while they wait for further instruction from the neurosurgeon.
Impression: Status is post motor vehicle accident with intracranial hemorrhage including
right frontoparietal subdural hematoma as well as a parenchymal hemorrhage. A large
scalp hematoma is present as well as a large scalp laceration, which was repaired with
staples. A right pulmonary contusion versus aspiration pneumonia and traumatic
respiratory failure, requiring intubation. Lactic Acidosis is also present. Traumatic brain
injury (TBI) is a major cause of morbidity and mortality worldwide. The modern
management of severe TBI has fallen into the area of a multidisciplinary team led by
neurointensivists, neuroanaesthetists, and neurosurgeons. Patient care is based on the
avoidance of secondary injury, maintenance of cerebral perfusion pressure (CPP), and
optimization of cerebral oxygenation. After viewing the information above I can gather
the severity of this case and prepare myself for what to expect as the day progresses.
Guidance by the licensed nurse in addition to my clinical instructor allowed me to be
confident as I began the day caring for K.R.
Patient Information:
Patient Initials: K.R. Age: 15
Height: 5’9”
Weight: 65.3 kg Allergies: NKA
Social and Family Background: Due to immediacy of the situation, the family dynamic,
and the widespread locations of the passengers in the accident there was no information
in his St. Mary’s chart relative to a social and family assessment for K.R. However, his
aunt came in around 1300 during my shift and I had the opportunity to sit down with her
and gather some information regarding his family and social background. She explained
to me that the woman driving the vehicle was, in fact, his biological mother but the two
other boys in the vehicle were his half-brothers. His mother remarried and had 2 boys
with another man, K.R’s stepfather. She also explained to me that K.R’s biological father
had not been around for some time and his whereabouts were unknown to her. She also
described the 3 brothers as very close, displaying good relationships between them. She
stated that the other 2 brothers were extremely worried and upset about K.R. but couldn’t
see him due to their conditions following the accident. K.R’s aunt had just left Covenant
ICU where K.R’s mother was located for 2 broken legs and several other injuries. The
biological father of K.R’s 2 brothers had been upstairs most of the day with one of the
other passengers and did not visit K.R once during my shift. His mother had been in
contact via phone where we had been updating her on the status of her son for most of the
afternoon.
A social assessment revealed that K.R. is a freshman at a local high school where he is an
accomplished wrestler and a beloved student. His aunt also explained that he has had
some behavioral issues throughout childhood and adolescence. She described him as
having anxiety, depression, panic disorder, and some violence towards others.
Past Medical History: K.R’s mother revealed this client’s past medical history via
phone during the morning of March 17th, 2013. This was the only information we had
about his previous history since he was not in St. Mary’s electronic system. Note: the
information regarding his health history was not obtained from his family doctor and the
mother had been in severe emotional and physical distress during this time. During a
brief phone call from the mother on Sunday night she provided the medical staff with
information regarding his medical history. She explained that he has a history of mild
seizures and takes medication to prevent them. She also confirmed his behavioral health
history that the aunt would later explain to me. Known previous medical history by
system:
Neurovascular: Seizures, nonspecific
HEENMT: Migraines, sinusitis
Respiratory: None
Cardiovascular: None
Peripheral Vascular: None
Gastrointestinal: None
Genitourinary: None
Musculoskeletal: Back pain, possible scoliosis
Skin: None
Hematology/Oncology: None
Endocrine: None
Behavioral Health: Anxiety disorder, depression, panic disorder, violence towards others
Infectious Diseases: None
Home Medication: Because of the aforementioned dynamics of this situation it was
unknown the exact medication(s) that he was taking at home during the time of my care.
As stated above we were able to obtain information relative to K.R’s history of seizures
but the specifics of the diagnosis were unknown at that time including the exact
medication(s) he was taking. However, the mother was able to explain to us that he was
not taking anything currently for his behavior issues and that the only medication(s) he
was taking were for seizure prevention. I was led to believe that someone was in the
process of trying to obtain a pharmacy record, however, I was never notified of the
results.
Past Surgical History: According to the mother, grandmother, and aunt, K.R. has had no
previous surgeries.
Primary Diagnosis: K.R’s primary diagnosis is a severe traumatic Brain injury (TBI)
with a thin right-sided frontoparietal subdural hematoma and bilateral punctate
hemorrhages, suggestive of axonal injury. He also presents with small compound skull
depression with overlying laceration in occipital parietal area.
Pathophysiology:
Traumatic Brain Injury: Traumatic brain injury (TBI) is the result of an external
mechanical force applied to the cranium and the intracranial contents, leading to
temporary or permanent impairments, functional disability, or psychosocial
maladjustment. TBI can manifest clinically from concussion to coma and death. Injuries
are divided into 2 subcategories: (1) primary injury, which occurs at the moment of
trauma, and (2) secondary injury, which occurs immediately after trauma and produces
effects that may continue for a long time. The physical mechanisms of brain injury are
classified using the following categories: Impact loading (Collision of the head with a
solid object at a tangible speed), Impulsive loading (Sudden motion without significant
physical contact), Static or quasistatic loading (Loading in which the effect of speed of
occurrence may not be significant). Impact loading, which is what caused K.R. TBI,
causes trauma through a combination of contact forces and inertial forces. Inertial force
ensues when the head is set in motion with or without any contact force, leading to
acceleration of the head. Contact force occurs when impact injury is delivered to the head
at rest. In this instance it was likely a combination of impact loading, impulsive loading
and contact force that led to K.R’s TBI.
Subdural Hematoma: The usual mechanism that produces an acute subdural hematoma is
a high-speed impact to the skull as seen in this case. This causes brain tissue to accelerate
or decelerate relative to the fixed dural structures, tearing blood vessels. Often, the torn
blood vessel is a vein that connects the cortical surface of the brain to a dural sinus. The
head trauma may also cause associated brain hematomas or contusions, subarachnoid
hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema,
infarction, secondary hemorrhage, and brain herniation.
Diffuse Axonal Injury (DAI): Unlike brain trauma that occurs due to direct impact and
deformation of the brain, DAI is the result of traumatic shearing forces that occur when
the head is rapidly accelerated or decelerated, as may occur in auto accidents, falls, and
assaults. It usually results from rotational forces or severe deceleration. Vehicle accidents
are the most frequent cause of DAI. The major cause of damage in DAI is the disruption
of axons, the neural processes that allow one neuron to communicate with another. Tracts
of axons, which appear white due to myelination, are referred to as white matter.
Acceleration causes shearing injury, which refers to damage inflicted as tissue slides over
other tissue. When the brain is accelerated, parts of differing densities and distances from
the axis of rotation slide over one another, stretching axons that traverse junctions
between areas of different density, especially at junctions between white and grey matter.
(ADD CITATION)
Surgical Intervention:
Name of procedures: Right parietooccipital craniotomy and elevation of depressed skull
fracture, debridement and closure of right occipital parietal laceration, insertion of left
frontal ventriculostomy. Patient tolerated the procedure well and was taken to ICU
recovery room in a stable condition.
Time of procedure: 1600 3-16-2014
My Day of Care:
The following information, assessments and lab values all occurred during the 12
hours in which I was assigned to K.R.
***Diagnostic Testing/Lab Results: Lab results for 3-17-2014 at 1010, my day of care.
Lab
Results
Normal Range
Patient Correlation
Test/other
diagnostic
testing
WBC
14 mm3
5-10 mm3
High. Within minutes of a
traumatic impact, a robust
inflammatory response is elicited
in the injured brain. The
complexity of this post-traumatic
squeal involves a cellular
component, comprising the
activation of resident glial cells,
microglia, and astrocytes, and the
infiltration of blood leukocytes
RBC
4.7
4.5-5.5
WNL. Tells how many red blood
cells you have. Helps diagnose
anemia and other conditions
affecting red blood cells
Hgb
13 g/dl
12-15 g/dL
WNL. Protein found on the RBC
that gives blood its red color. Hgb
is composed of iron and carries
oxygen.
Hct
41%
36-46 %
WNL. Hct is the volume of packed
red blood cells found in 100 ml of
blood. Tells the concentration of
RBC in the blood.
Platelet
152
150-400
WNL. Basic elements in the blood
Count
that promote coagulation.
Neutrophils
73%
50-70 %
High. Most numerous circulating
WBC. Body’s first line of defense.
They respond to inflammatory and
tissue injury.
High. Immune response with T
cells and B cells.
Lymphocyte
37%
25-35 %
Monocyte
5.4%
4-6%
Ingest large particles of debris.
Second line of defense.
Eosinophil
2.8%
1-3%
WNL.
Basophil
1%
0.4-1.0%
Increase during the healing
process.
PT
13.5 seconds
10-12 seconds
High: A limited trauma-induced
coagulopathy as evidence by
prolonged PT levels has been
found in patients hospitalized for
head injury, but PT levels return to
normal after 12 hours and the
clinical importance of this
prolongation is currently unclear
INR
1.4
2-3
PTT
Not provided
BUN
7 mg/dl
20-30 seconds
1.5-2 x normal
value
(40-75 seconds
with a PE)
5-25 mg/dL
Creatinine
0.5 mg/dl
0.5-1.5 mg/dL
WNL. Used to diagnose renal
dysfunction.
GFR
Ca++
Not calculated for
ages <18
7.8 mEq/L
8.5-10.5 mEq/L
Low:
K+
3.8 mEq/L
3.5-5.0 mEq/L
WNL.
Na+
144 mEq/L
135-145 mEq/L
WNL. Sodium (Na+) is the major
cation in the extracellular fluid and
plays a major role in maintaining
osmotic pressure of extracellular
fluid, regulating potassium and
chloride levels, stimulating
neuromuscular reactions, and
maintaining systemic blood
pressure. Alterations in serum
sodium levels are critical in
patients with head injuries
Hyponatremia may be due to the
syndrome of inappropriate
antidiuretic hormone (SIADH) or
cerebral salt wasting. Both
Cl-
114 mmol/L
98-106 mmol/L
Mg
1.5 mg/dl
Glucose
104
60-110 mg/dl
Predicted
Serum
Osmolarity
296.3
285-295
mOsm/kg. The
measured
osmolality should
not exceed the
predicted by more
than 10 mOsm/kg.
A difference of
more than 10
mOsm/kg is
considered an
osmolal gap
.
syndromes involve decreased
serum sodium level in the face of
increased urinary sodium losses.
Elevated sodium levels in head
injury indicate simple dehydration
or diabetes insipidus.
High: Chloride is the most
plentiful extracellular anion in the
body. It carries a negative charge
and serves to maintain electrically
neutrality with cations.
Magnesium is depleted in the
acute phases of both minor and
severe head injuries. Because this
cation blocks the excitotoxic
response and functions as an
antioxidant, careful monitoring of
magnesium may improve
outcomes.
There is substantial evidence
highlighting the adverse effects of
hyperglycemia in critically ill
patients and tight glycemic control
has become a part of the routine
management of general intensive
care patients. Hyperglycemia has
been associated with increased
cerebral lactate resulting in local
brain tissue acidosis.
Slightly high but not high enough
to be considered an osmolal gap.
Serum osmolarity is a good
indicator of dehydration and over
hydration.
Importance of Diagnostic Tests:
Medications:
Medication
Indication
Dose
Route
Frequency
Drip
5mcg/kg/min
10 mg/ml
Continuous
24 hr
Diprivan
(propofol)
Chemical class: 2,6diisopropylphenol
derivative
Therapeutic class:
Sedative-hypnotic
Pregnancy category:
B
To provide
sedation for
critically ill
patients in
intensive care
Sublimaze
(fentanyl)
Indicated for the Drip
management of 1mcg/kg/hr
persistent,
.3ml/hr
Side Effect
Contraindications
Patient
Correlation
Diprivan is not
recommended in
hypothermic patients as
it has a tendency to
accumulate and
precipitate
hyperlipidaemia. Other
reported problems with
propofol include
precipitous
cardiovascular collapse
and the propofol
infusion syndrome of
metabolic acidosis,
rhabdomyolysis, and
bradycardia, first
described in children
but also identified in
adults.
Adequate
sedation
minimizes pain,
anxiety, and
agitation,
reduces the
cerebral
metabolic rate
of oxygen
consumption,
and facilitates
mechanical
ventilation.
This is
achieved with
sedative drugs.
Propofol is
preferred
because of its
superior
metabolic
suppressive
effects, and
favorable short
half-life. 46
CNS:
Agitation, amnesia,
anxiety, asthenia,
As an adjunct
to sedation
therapy,
Chemical class:
Opioid,
phenylpiperidine
derivative
Therapeutic class:
Analgesic, anesthesia
adjunct
Pregnancy category:
C
Controlled substance
schedule: II
norepinephrine
(Levophed)
Chemical class:
Catecholamine
Therapeutic class:
Cardiac stimulant,
vasopressor
Pregnancy category:
C
moderate to
severe chronic
pain in opioid
tolerant patients
Continuous
24 hour
To treat acute
hypotension,
cardiogenic
shock, and
septic shock
1mg/ml at
4ml/hr
titrate for
MAP>80
ataxia, confusion,
delusions
CV:
Asystole, bradycardia
GI:
Anorexia, constipation
RESP:
Apnea, depressed
cough reflex
Contraindicated: Under
age 2, asthma,
myasthenia gravis,
opioid hypersensitivity
or intolerance,
significant respiratory
depression, upper
airway obstruction;
transmucosal form:
acute or chronic pain
Contraindicated:
Concurrent use of
hydrocarbon inhalation
anesthetics,
hypersensitivity to
norepinephrine or its
components,
hypovolemia,
mesenteric or
peripheral vascular
thrombosis
Side effects:
CV:
Angina, bradycardia,
ECG changes
GI:
Nausea, vomiting
GU:
Decreased renal
perfusion
RESP:
Apnea, dyspnea
SKIN:
Pallor
Sliding Scale Insulin
To treat acute
Maintaining
Side effects:
fentanyl is
provided in
regular doses,
which has
minimal effects
on cerebral
hemodynamics
in adequately
resuscitated
patients.
Important
component in
maintaining
blood pressure
to a level
adequate
enough to
profuse the
body but more
importantly the
brain. Also note
that fentanyl is
a hypotensive
agent so
caution must be
taken with
order changes.
The stress
mannitol
(Osmitrol)
Chemical class:
Hexahydroxy alcohol
Therapeutic class:
Antiglaucoma,
diagnostic agent,
osmotic diuretic,
urinary irrigant
Pregnancy category:
B
hyperglycemia
related to body
response to
accident
glucose rates
between 80120
-Hypoglycemia
To reduce
intracranial or
intraocular
pressure
30g IVPB
every 6
hours
150ml/hr
Contraindications:
Active intracranial
bleeding (except during
craniotomy), anuria,
hepatic failure,
hypersensitivity to
mannitol or its
components,
pulmonary edema,
severe dehydration,
severe heart failure,
severe pulmonary
congestion, severe
renal insufficiency
Side effects:
CNS:
Chills, dizziness, fever,
headache, seizures
CV:
Chest pain, heart
failure, hypertension,
tachycardia,
thrombophlebitis
EENT:
Blurred vision, dry
mouth, rhinitis
GI:
Diarrhea, nausea, thirst,
vomiting
GU:
Polyuria, urine
retention
RESP:
response in
trauma patients,
including those
with severe
TBI, generates
a
hypercatabolic
state leading to
rapid muscle
protein
breakdown and
hyperglycaemia
Hyperosmolar
therapy is a key
intervention for
the
management of
cerebral edema
and raised ICP
after TBI. It is
particularly
indicated for
acute rises in
ICP as it has a
rapid effect.
Mannitol, an
osmotic
diuretic, is
commonly
employed and
the immediate
efficacy is
likely to result
from a plasmaexpanding
effect and
improved blood
rheology due to
a reduction in
hematocrit.
Pulmonary edema
pantoprazole
(Protonix)
peptic ulcer
disease
prophylaxis
40mg iv
push once
daily
Side effects:
CNS:
Anxiety, asthenia,
confusion, dizziness,
headache, hypertonia,
hypokinesia, insomnia,
malaise, migraine,
speech disorder vertigo
CV:
Chest pain,
hypercholesterolemia,
hyperlipidemia
EENT:
Anterior ischemic optic
neuropathy, blurred
vision, increased
salivation, pharyngitis,
rhinitis, sinusitis,
tinnitus
ENDO:
Hyperglycemia
GI:
Abdominal pain,
atrophic gastritis,
constipation, diarrhea,
elevated liver function
tests results, flatulence,
gastroenteritis,
hepatotoxicity,
indigestion, nausea,
pancreatitis, vomiting
GU:
Elevated serum
creatinine level,
interstitial nephritis
Chemical class:
Substituted
benzimidazole
Therapeutic class:
Antiulcer, gastric acid
proton pump inhibitor
Pregnancy category:
B
Potassium Chloride
Contraindications:
Hypersensitivity to
pantoprazole,
Electrolyte
balance/
20mEg IV in
NS at
Contraindications:
Urinary retention,
Peptic ulcer
disease
prevention due
to increased
medication load
on stomach.
In the TBI
patient with
hydration
100ml/hr via
central line
hyperkalemia.
Side effects:
· confusion, anxiety,
feeling like you might
pass out;
· uneven heartbeat;
· extreme thirst,
increased urination;
· leg discomfort;
· muscle weakness or
limp feeling;
cefazolin
(Ancef)
To treat
pneumococcal
pneumonia
1000 mg IV
push every
12 hours
Chemical class: Firstgeneration
cephalosporin, 7aminocephalosporanic
acid
Therapeutic class:
Antibiotic
Pregnancy category:
B
levetiracetam
(Keppra)
Contraindications:
Hypersensitivity to
cephalosporins or their
components
Side effects:
CNS:
Chills, fever, headache,
seizures
CV:
Edema
EENT:
Hearing loss
GI:
Abdominal cramps,
diarrhea, elevated liver
function test results,
hepatic failure,
hepatitis,
hepatomegaly, nausea,
oral candidiasis,
pseudomembranous
colitis, vomiting
GU:
Elevated BUN and
serum creatinine levels,
nephrotoxicity, renal
failure, vaginal
candidiasis
As adjunct to
treat partial
seizures
500 mg IV
every 12
hours
Contraindications:
Hypersensitivity to
levetiracetam or its
raised ICP,
sudden changes
in serum
sodium
concentration
and osmolarity
must be
avoided since
these factors
impact on the
nature and
degree of
cerebral edema
With the
possibility that
K.R. aspirated
he is at an
increased risk
to develop
pneumonia.
Anti-epileptics
should not be
prescribed
components
Chemical: Pyrrolidine
derivative
Therapeutic:
Anticonvulsant
Pregnancy category:
C
Normal Saline Drip
Side Effects:
CNS:
Abnormal gait,
aggression, agitation
EENT:
Amblyopia,
conjunctivitis
GI:
Anorexia, constipation,
diarrhea
MS:
Neck pain
RESP:
Asthma, cough
SKIN:
Alopecia, ecchymosis
Hydration
1000 ml at
100ml/hr
Side effects:
Febrile response,
infection at the site of
injection, venous
thrombosis or phlebitis
extending from the site
of injection,
extravasation, and
hypervolemia.
unless there is
documented
clinical or EEG
evidence of
seizures, which
in this case
there is a
previous
medical history
of seizures.
TBI patients are
susceptible to
disorders of salt
and water
balance. Causes
include central
diabetes
insipidus
(CDI), cerebral
salt wasting
(CSW)
syndrome, and
syndrome of
inappropriate
anti-diuretic
hormone
(SIADH)
secretion
Physical Assessment: 1200 on 3-17-2014 my day of care
Time
0700
0800
0900
1000
1100
BP
129/58
130/61
144/63
124/60
143/57
HR
62
67
72
66
63
RR
16
16
16
16
16
Temp
96.8
96.8
96.7
97.5
97.3
O2 Sat
100
100
100
100
100
MAP
81
84
90
81
85
CPP
66
66
71
65
70
ICP
15
18
19
16
15
1200
154/64
68
16
97.5
100
94
73
21
Neurological Assessment: K.R was unresponsive; sedated and ventilated during my
entire shift. He remained in a calm state throughout the day. His pupils were round, 3mm
in size and sluggish when presented with light. During my Glascow Coma Scale he
presented with no verbal response, no eye opening and a bilateral flexion withdraw to
pain for a score of 6. His motor ability was minimal but he did present with both upper
and lower flexion withdrawal on both sides. When prompted to squeeze my fingers there
was no response bilaterally, however, damage to his temporal lobe cannot be ruled out as
he may be able to hear me but his auditory center for sound interpretation could be
damaged. Muscles of the extremities were flaccid. Throughout the morning K.R. showed
no signs of voluntary movement, however, towards the later afternoon his left arm moved
spontaneously several times. As shown in the vitals chart above his Cerebral Perfusion
Pressure (CPP) remained above near 70. After brain injury, cerebral blood flow may be
lowered to the ischaemic threshold. To prevent further neuronal death (the secondary
brain injury), this flow of well-oxygenated blood must be restored. Cerebral Perfusion
Pressure may be maintained by raising the Mean Arterial Pressure (MAP, which
remained above 80 via norepinephrine) or by lowering the Intracranial Pressure (ICP,
which remained below 20mmHg). In addition to controlling CPP, adequate sedation
minimizes pain, anxiety, and agitation, reduces the cerebral metabolic rate of oxygen
consumption, and facilitates mechanical ventilation. This is achieved with sedative drugs
and opioids. Propofol is preferred because of its superior metabolic suppressive effects,
and favorable short half-life. Analgesia was provided with fentanyl, which has minimal
effects on cerebral hemodynamics in adequately resuscitated patients.
Cardiovascular Assessment: Normal sinus rhythm on patient’s telemetry monitor (Lead
II). Regular rate and rhythm of S1 and S2 heart sounds. Left and right radial, brachial,
femoral and dorsalis pedis 2+ bilaterally. No clubbing, pink nail beds, capillary refill <2
seconds in toes and hands. Jugular venous distention absent. Upper and lower extremities
were warm to the touch bilaterally. Murmur or rub not present. Blood pressure was high
in response to norepipenephrine. Hypertensive readings in this case are okay because
higher blood pressure may be maintaining cerebral blood flow. No cardio-related changes
occurred throughout the day.
Pulmonary Assessment: K.R. was mechanically ventilated via endotrachial tube by
EMS. He remained mechanically ventilated on assist-control mode throughout the day
with orders to wean, however, his settings remained the same throughout the day. The
ventilation settings were as follows: Vent Humidifier Temp: 35 degrees Celsius, FiO2:
50%, Tital Volume: 450ml, Set Rate (Breath/min): 16/min, Peak Inspiratory Pressure:
15cm H2O, Flow Rate: 40L/min, PEEP: 5. His breath sounds were clear bilaterally with a
productive cough presenting with small amounts of thin, white sputum, which was
suctioned intermittently throughout the day. He did not breath over the ventilator at all
which may indicate a minimal to no respiratory effort. His pulse oximetry never dropped
below 99%. Patients with severe head injury require mechanical ventilation to maintain
an arterial Po2 and Pco2 between 4.5. No changes in respiratory status occurred during my
shift.
GI: No symptoms. Abdomen rounded, soft, symmetric and non-tender. Bowel sounds
active x 4. His last bowel movement was unknown. No bowel movements during shift.
Note that the patient is taking protonix once daily for peptic ulcer disease prophylaxis. At
the time of assessment K.R. was NPO, however, it had been suggested that he start
enternal feedings via O/G tube with osmolite at 30ml/hr and increase with tolerance by
10 ml increments every 8 hours until 55ml/hr to reach goal of 1980 kcals/day and 83
grams of protein/day. Total caloric intake including propofol would be 2112 kcals/day.
It’s important to remember that as he is weaned off the propofol in the future his enteral
feeding rate with need to increase to make up for the kcals. Enternal feeding started at
approximately 1300 during my day of care. No changes in GI throughout the day.
GU: Foley catheter: patent with urine yellow and clear. Secured via tape on his thigh.
Bladder distention was absent. Due to his traumatic brain injury and heavy sedation a
Foley catheter is needed to prevent urinary retention. The prior 12 hours before my
assessment his intake was 3485 ml and his output was 2,965 ml for a net of 520 ml. He
continued to display adequate voiding patterns throughout the day. No urinary changes
occurred throughout my shift.
Integumentary: Skin was warm, dry, pink, elastic and intact. Mucus membranes were
pink and moist. Elastic skin turgor and hydration as evidence by minimal tenting on the
back of his hands. Braden scale: limited response to painful stimuli, occasionally moist
skin, confined to bed, very limited mobility, inadequate nutrition. Braden scale score of
12. Patient has several minor scrapes on legs that do not require attention. Overall his
skin was in remarkable shape given the circumstances of the accident. Patient position
was changed every 2 hours to provide adequate profusion. No integumentary changes
occurred during my shift.
IV Assessment: Access devices included two 18-guage peripheral IV’s (Left A/C and
right A/C), one arterial line in the right radial and a central line. All devices were inserted
the day before in the emergency department. All insertion points were dry, intact, non
edematous and warm. No changes in IV assessments throughout the day.
Activity: Patient is unresponsive and heavily sedated; activity type is bed rest. Orthotics
included a hard cervical collar as precaution for re-injury and intermittent pneumatic
compression devices for blood circulation and DVT prevention. Patient spontaneously
moved a handful of times but otherwise he was completely motionless. No changes in
activity during my shift.
Psychosocial/Spiritual: Unable to asses due to unresponsiveness and heavy sedation.
Family support was minimal but the aunt showed genuine concern and was very
supportive of the nursing staff.
Educational Needs: Once again this area was impossible to assess due to the patient’s
status. It is apparent that the family as a whole needs education regarding seatbelt safety.
I was not in contact with the mother therefore I could not assess her educational needs
specifically. The aunt understood the plan of care and was supportive of our efforts.
Prevention/Plan: As previously stated the general plan for TBI is based on the
avoidance of secondary injury, maintenance of cerebral perfusion pressure, and
optimization of cerebral oxygenation. In this case there are several steps to the plan for
K.R. The patient had displayed a pattern of optimal cerebral perfusion via MAP and ICP
measures throughout the day. Therefore, part one of the plan is to continue this trend to
prevent secondary injury and other complications. Part two of the plan is to wean him off
of the ventilator slowly by decreasing the FiO2 by 5 every 2-4 hours while closely
monitoring arterial blood gases to insure appropriate reading relation to specific FiO2
measures. Part three of the plan includes continuing protonix therapy for PUD prevention
and antibiotic therapy while the patient has drains. Infection avoidance is important in
any ICU case but it is extremely important with brain injuries due to the detrimental
effects of the inflammatory response on a recovering brain. Part four of the plan includes
the nutritional outline previously mentioned in the “GI Assessment”. Lastly, there is a
need for family support. Within the coming weeks they expect the number of visitors to
increase dramatically. It is important to allow K.R. a quiet, cool, non-stimulating
environment while his brain begins to heal. Increasing numbers of visitors could
stimulate K.R. to the point of raising his ICP to dangerous levels. Balancing patient
advocacy and family visitation will be a topic that must be discussed amongst the nursing
staff.
Priority NANDAs, NICs, and NOCs:
NANDA 1: Fall risk related to altered level of consciousness and limited mobility as
evidenced by impaired judgment.
NIC: Assess safety needs, bed in low position/side rails up, call bell within reach, initiate
precautions, floor uncluttered, restraints as needed.
NOC: No falls or injuries to self or staff
NANDA 2: Acute pain related to diagnostic/surgical procedure, medical treatment, and
trauma as evidenced by changes in vital signs and restlessness.
NIC: Assess for causes of pain, evaluate response to pain, monitor signs and symptoms
associated with pain.
NOC: Stable vital signs, no restlessness, no symptoms associated with pain, exhibits
increased comfort.
NANDA 3: Disturbed sensory perception related to neurological trauma as evidenced by
altered communication patterns, altered thought process, disorientation.
NIC: Assess sense of touch, eliminate extra stimuli, promote safe environment, reorient
frequently.
NOC: Improved sensory perception, no anxiety related to orientation, successful
alternatives to communication.
NANDA 4: Impaired gas exchange related to altered delivery of oxygen, altered oxygen
carrying capacity of blood as evidenced by cyanosis, dyspnea, hypoxia, tachycardia.
NIC: Administer medications as ordered, auscultate breath sounds at least every 2-4
hours or as needed, change position every 2 hours, monitor ABGs.
NOC: Demonstrates improved ventilation and oxygenation of tissues, baseline respiratory
rate for patient, ABGs and pulse oximetry in normal range.