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Rhabdomyolysis, a rare
complication of head injury
– a case
report.
Dr. Manoj Kumar
Majhi,
Dept. Neurosurgery,
Apollo Hospitals, Chennai, India.
Rhabdomyolysis in a case
of closed head injury, not associated with any extracranial
compressive injury is a rare entity . There is marked by high levels
of serum creatinine kinase and myoglobinuria. Resultant acute
renal failure may further complicate the clinical course as in our
case. Intensive supportive treatment dictates the outcome.
To our present knowledge
rhabdomyolysis and such high levels of creatine kinase in a case of
head injury without any associated extracranial crush injury have
earlier been reported only in four cases.
Case
report:
A 12-year-old boy
sustained a closed head injury due to fall from the bicycle.The
patient, who was unresponsive at the scene of the accident, was
transferred to the local hospital where he became combative.
CT scan done there showed brain stem contusion. He was started on
antiedema drugs (mannitol and lasix). His neurological condition
further deteriorated, whereupon he was transferred to our facility
on the 4th post trauma day.
On admission to our
hospital, he was semiconscious, flexing to pain and opening eyes to
pain. He also had left hemiparesis. Systemic examination was normal,
including absence of extremity injury and vascular compromise. His
abdominal and extremity compartments were soft.
A CT scan of the cranium
revealed brainstem contusion at the level of pons.
In view of the low GCS,
he was intubated, shifted to the ICU and connected to
ventilator.
His urine was having a
brownish discoloration and his billurubin was high as revealed by
the routine investigations. Associated with this the serum uric
acid, GOT and LDH were also raised. From the above metabolic
derangements along with discolored urine, a suspicion of
rhabdomyolysis and myoglobinuria was made.
The following investigations confirmed our
diagnosis--
Serum CPK-10,940(nor-20 to
200)
Urine myoglobin-3,86,000
ng/ml(nor<25 ng/ml)
Serum myoglobin-30,100 ng/ml
(nor<90 ng/ml)
Increased bilateral renal
cortical echos on ultrasonogram.
Nephrologists opinion
was sought and he was treated with hemodilution and alkalinisation
of serum with sodium bicarbonate infusion.
Repeat CPK values the
next day was 53,714 iu per litre. But with continuation of
treatment, the rhabdomyolysis and renal failure gradually
resolved.
His neurological status
also gradually improved. After 2 weeks, the boy was transferred to
the ward. His renal function improved gradually. The patient has
continued to make a slow, but steady, neurologic
recovery.
Discussion:
Rhabdomyolysis is a syndrome usually, resulting
from damage to skeletal muscle with the resultant appearance of free
myoglobin in the circulation. Myoglobin is then filtered by the
glomerulus and appears in the urine. Elevated urinary levels of
myoglobin can lead to acute renal failure.
This condition should be suspected in a comatose
patient with fever, brown discoloration of the urine, and edema of
the extremities. Laboratory results will show orthotoluidine
positive urine with a clear serum, elevated serum creatine
phosphokinase, and serum creatinine elevation out of proportion to
blood urea nitrogen. Management consists of fluids and diuretics
with dialysis if necessary.
The hyperosmolal state, which may cause
rhabdomyolysis, can occur in critically ill neurosurgical patients.
This state may be secondary to central diabetes
insipidus or to dehydration from osmotic diuretics such as mannitol.
Monitoring a patient's serum creatinine levels
and administering fluids and sodium bicarbonate may be crucial in
preventing renal failure. It was assumed that the rhabdomyolysis in
this case, had occurred secondary to the hyperosmolar state caused
by the over enthusiastic diuretic therapy.
Several reports describe rhabdomyolysis secondary
to a hyperosmolal state. Hyperosmolality results in a decrease of
sodium extrusion from muscle cells and a subsequent decrease in
transmembrane potential. Animal models suggest that the decrease in
transmembrane potential is a precursor to rhabdomyolysis. The
loss of cell membrane integrity results in muscle injury and muscle
cell lysis, or rhabdomyolysis. The injured muscle cell releases
myoglobin, which is about a quarter of the size of hemoglobin.
Myoglobin is not protein-bound and is filtered rapidly by the
glomerulus.
The 3 most common causes of nontraumatic
rhabdomyolysis are drug ingestion, alcohol intoxication, and muscle
compression or ischemia.
Nephrotoxin-induced acute tubular necrosis
develops when myoglobin precipitates in the proximal renal
tubule.
In the presence of acidic urine, myoglobin is
converted to acid ferrihematin, which reacts with tubular protein
and precipitates, resulting in nephrotoxicity. Myoglobin-induced
acute tubular necrosis is more likely in an intravascularly depleted
neurosurgical patient treated with osmotic diuretics or fluid
restriction.
An increase in the serum sodium level should
alert you to consider hyperosmolality, and one should seek signs of
rhabdomyolysis with the use of serial CK level monitoring and
measurement of urinary myoglobin. If rhabdomyolysis is highly
suspected or if the diagnosis of rhabdomyolysis is made, the patient
should receive adequate fluid infusion to maintain a high urinary
output (200 to 300 mL/h) for at least the first 24 hours. This must
be undertaken judiciously in neurosurgical patients with altered
cerebral vascular auto regulation
Rhabdomyolysis is characterized by an elevated
serum concentration of CPK and myoglobinuria.
Maintenance of adequate intravascular volume
increases the excretion of substances that can injure or obstruct
the renal tubules. In addition, the patient's urine should be
alkalized with intravenous sodium bicarbonate. This limits the toxic
effects of myoglobin and the crystallization and precipitation of
uric acid that develops in acidic urine. Diuretics may be given if
the patient has acute renal failure or decreased urinary output. If
the patient does not respond to therapy, dialysis may be
required.
Hypokalemia and/or hypophosphatemia are strongly
implicated as causes of rhabdomyolysis. Experimental
hypokalemia has been associated with both reduced transmembrane
electrical potential and histologic damage to muscle cells. A
deficiency of intracellular phosphate can lead to a fall in
transmembrane potential, reduced adenosine triphosphate levels, and
inhibition of the energy dependent sodium pump.
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