rhabdomyolysis causes muscle breakdown and the leakage of intracellular muscle constituents ( e.g. , enzymes , electrolytes , myoglobin ) into the circulation and extracellular fluid3,4 ) . when massive amounts of myoglobin are released , the binding capacity of plasma proteins is exceeded and the myoglobin reaches renal tubules and can cause acute renal failure8 ) . prolonged mental deterioration and convulsive seizures should be included among the neurological conditions in which rhabdomyolysis can develop1 ) . a case is presented in which prolonged mental deterioration with hyperosmolar state and continuous convulsive seizure after head injury led to rhabdomyolysis and acute renal failure . the pathophysiological mechanism of this uncommon entity after severe head injury is discussed and a review of relevant literature is included . a previously healthy 42-year - old man was referred to our emergency department due to a deteriorating mental status after a car accident . there were no associated systemic injuries , muscle contusions , internal organ damage or swelling of the extremities . however , he showed decerebrated rigidity at both arms and legs . on admission , sodium , potassium , and osmolarity were 143 meq / l , 3.5 meq / l , and 335 mmol / l , respectively . computed tomography ( ct ) showed diffuse cerebral swelling consistent with hemorrhagic contusion and epidural hematoma at right temporoparietal area ( fig . 1 ) . 150 ml of mannitol solution ( 20% ) every 4 hours was prescribed . however , despite treatment to lower intracranial pressure ( icp ) , that is , mannitol , mild hyperventilation , and extraventricular drainage ( evd ) , his mental status remained semicomatose and recurrent convulsive generalized tonic - clonic seizures developed , and thus , he was admitted to the neurosurgical intensive care unit for adequate hydration , anticonvulsant and correction of the metabolic derangement . unfortunately , myoglobinuria developed 3 days after admission with a high serum creatine kinase ( ck ) level up to 48 , 837 iu / l ( normal 55 - 215 iu / l ) . at this time , his serum sodium , potassium , and osmolarity were 152 meq / l , 3.0 meq / l and 352 mmol / l . ck level peaked at 52 , 825 iu / l on day 5 , and serum myoglobin exceeded 25 mg / dl ( normally < 2.5 mg / dl ) . despite intensive supportive treatment , no source of muscle breakdown was evident , but his condition deteriorated rapidly , culminating in cardiorespiratory arrest with dilated non - reactive pupils . rhabdomyolysis is a frequent concomitant of multisystem trauma , and the source of muscle breakdown is often apparent from the pattern of injury2 ) . although mechanical damage to muscle is the most common cause of rhabdomyolysis in trauma patients , other causes should not be overlooked . in patients with severe head injury , a prolonged deteriorated mental status , convulsive seizure , and hyperosmolar states importantly predispose significant rhabdomyolysis9,10 ) . our patient had a decreased mental status , which probably played a role in the development of rhabdomyolysis . experiments with human volunteers have demonstrated that sustained lying in a fixed and rigid position can cause sufficient intramuscular pressure to occlude capillaries7 ) . furthermore , mannitol - induced hyperosmolar states have also be known to cause significant rhabdomyolysis . our patient had received mannitol solution ( 20% ) intravenously 150 ml/4 hr for 5 days , which probably aggravated his hyperosmolar state . singhal et al.9 ) reported relations between the hyperosmolar state and the pathogenesis of rhabdomyolysis , and observed that serum sodium and serum osmolarity were both linearly related to serum ck . it was also noted that hypokalemia and hypophosphatemia were present in patients who developed rhabdomyolysis . in our patient , a hyperosmolar state , hypernatremia , and hypokalemia , were all present , and serum ck reached an extremely high level . it is known that the combination of potential potassium and phosphate deficiency in combination with acidosis , hypernatremia , and a hyperosmolar state , can reduce sodium release from muscle cells , and thus , decrease transmembrane potentials , which animal experiments have shown is a crucial precursor of rhabdomyolysis5 ) . in addition , our patient experienced convulsive seizures and intense rigidity , and in our opinion , these factors are also likely to predispose rhabdomyolysis . the cause of muscle injury in exertional rhabdomyolysis has been postulated to be energy deficiency . during maximal exertion , energy is obtained almost solely from muscle glycogen , and if exertional requirements exceed available energy stores , muscle glycogen is depleted10 ) . furthermore , if energy production is deficient , energy rich phosphate compounds are subject to subcellular competition and insufficient energy is available for muscle cell membrane structural maintenance , which results in changes ranging from reversible permeability to cell death . this type of cellular damage results in the release of intracellular potassium , purine , creatinine , myoglobin , and creatine kinase . fever , malaise , weakness , and extremity pain , as well as swelling and tenderness are usually reported when the onset of rhabdomyolysis results from exertion . in patients with a deteriorated mental status however , volume contraction , hypernatremia and the hyperosmolar state in neurosurgical patients treated with osmotic diuretic agents for brain swelling should be done with caution . the most appropriate treatment for hyperosmolar state - induced rhabdomyolysis is adequate hydration and alkaline diuresis . in patients with convulsive seizures or rigidity , sustained muscle contractions may be modified by the use of an anticonvulsant or muscle relaxant . dialysis may be required if renal failure persists ; indications for dialysis include hyperkalemia , uremic pericarditis , or encephalopathy , and evidence of volume overload6 ) . although rare , the possibility of rhabdomyolysis should be kept in mind in patients with severe head injury .
rhabdomyolysis is a rare but potentially life - threatening disorder caused by the release of injured skeletal muscle components into the circulation . 
 the authors report a case of severe head injury , in which a hyperosmolar state and continuous seizure complicated by severe rhabdomyolysis and acute renal failure evolved during the course of treatment resulted in a fatal outcome despite intensive supportive treatment . 
 our bitter experience suggests that rhabdomyolysis should be born in mind in patients with severe head injury who may develop hyperosmolar state and continuous seizure .