Lower extremity injuries causing significant neurovascular compromise can be an iatrogenic or traumatic complication.
Early diagnosis and intervention is the key to restoration of neurologic function of the affected lower extremity. The
authors present a case of gluteal hematoma, due to a fall, causing a common causing a common peroneal nerve compression
and foot drop. Common peroneal nerve palsy is usually caused by compression at the femoral head. In our case
common peroneal nerve palsy was caused due to compression by hematoma at both the femoral head as well as at the
level of the gluteus muscle. It was also unusual to see this diagnosis in a patient with blunt trauma due to a fall.Lower extremity injuries causing significant neurovascular
compromise can be a iatrogenic or traumatic complication.
Common peroneal nerve palsy is usually caused by compression
at the femoral head. In this case common peroneal nerve
palsy was caused due to compression by hematoma at both
the femoral head as well as at the level of the gluteus muscle.
A previously healthy 22-year-old male presented to an Emergency
Department (ED) via Emergency Medical Services (EMS)
for the evaluation of a suspected overdose. The patient was
found on the ground by his mother. Multiple bags of suspected
heroin were in the vicinity of the patient. The patient’s
mother called 911. His mother had Narcan at home and administered
it. The patient subsequently became responsive.
Per EMS patient was unable to move his right lower extremity
in the field. Patient did not have any significant past medical
history. He did not take any medications at home. He denied
having any surgeries in the past. Patient denied any history of
smoking or alcohol use. He did admit to using drugs including
marijuana and heroin. He did admit to injecting drugs but stated
he used clean needles. Patient denied any significant family
history. The patient had nausea and a few episodes of vomiting
prior to arrival.
He noted a loss of sensation of his right
lower extremity below his knee. On physical exam, the patient
was tachycardic at 110 bpm, respiratory rate 16 breaths per
minute. He was noted to be hypotensive at 85/60 torr but was
alert, awake and oriented X 3. He was afebrile. His O2 sat was
98% on 2L nasal cannula. Upon inspection of his back he was
noted to have a large gluteal hematoma measuring 4 cm x 4
cm on his right gluteal region. The area was severely tender
to palpation. His neurologic exam showed decreased muscle
strength of 2/5 at his right thigh area and 0/5 on dorsiflexion
and plantar flexion of his right foot. He had no sensation to
light touch on his right lower extremity below his right knee.
Lab studies showed WBC: 45.5 g/dL, Hgb 15.1 g/dL, Hct 42.9g/dL, and platelet count of 456. His basic metabolic profile
showed (mEq/L): sodium of 134, potassium of 6.4, chloride
of 99, bicarbonate of 16, BUN of 22 (mg/dL), Creatinine of
2.87 (mg/dL) with an anion gap of 26.4. His lactate was 7.0.
His liver function test showed a total bilirubin of 0.9μmol/L,
AST of 159, ALT of 365. His CK was 41,154 U/L. His toxicology
screening was negative for alcohol, positive for opiates
and cannabinoids. A computed tomography (CT) scan without
contrast of his chest, abdomen and pelvis with thoracic and
lumbar 2-Dimensional reconstruction was performed. The CT
showed patchy ground glass densities in both upper lobes,
right greater than left, possibly secondary to aspiration. There
was also an asymmetric enlargement of right gluteal muscle
with underlying areas of decreased attenuation significant for
possible myositis versus gluteal hematoma.
Due to his significant leukocytosis, elevated creatinine, elevated
lactate level, hypotension and tachycardia, the patient
was treated as sepsis secondary to possible aspiration pneumonia.
The patient also had underlying rhabdomyolysis, acute
renal failure and hyperkalemia. The LFTs were also elevated.
The patient was given antibiotics and an intravenous (IV) fluid
bolus of 30 cc/kg in the ED and was admitted to the ICU. His
tachycardia and hypotension improved with the fluid bolus.
His neurologic deficits were discussed with the neurologist on
call. No acute neurological intervention was recommended.
On Day 1 of his hospital stay, the patient’s clinical condition
was suggestive of severe sepsis with end organ dysfunction
as indicated by his LFTs and elevated creatinine levels. His
lactate, creatinine and LFT function improved with IV fluid
boluses. He was placed on IV antibiotics for possible aspiration
pneumonia. His rhabdomyolysis improved with IV fluids.
An orthopedic consult was obtained to address the patient’s
right lower extremity weakness and gluteal hematoma. At the
time of their consult, the patient’s neurologic exam showed
2/5 muscle strength on dorsiflexion and plantar flexion of the
right ankle. He continued to demonstrate decreased sensation
to light touch below his right knee. On exam, the right
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