Rhabdomyolysis, a rare complication of head injury – a case report.
By Dr. Manoj Kumar Majhi,
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.
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.
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.