guillain - barre syndrome ( gbs ) is an acute immune - mediated polyradiculopathy that presents as a rapidly progressive , areflexic , symmetric ascending motor paralysis with or without sensory disturbances .
the clinical course of gbs can be complicated by pneumonia , sepsis , pulmonary embolism , respiratory paralysis or cardiac arrest .
diagnosis of gbs is usually based on clinical examination and is supported by nerve conduction studies and cerebrospinal fluid ( csf ) examination .
mild elevation in serum creatine kinase ( ck ) level have been seen in early stage of gbs , but marked elevation of ck in gbs is an extremely rare finding .
we present the case of gbs with marked elevation in serum ck , serum myoglobin levels and persistent hyperkalemia as a result of associated acute rhabdomyolysis , which is a potentially life - threatening condition .
the present case report is about a 24-year - old indian man who presented with 20 days history of weakness of both lower and upper extremities .
the weakness began suddenly in both lower extremities , which progressed to both upper extremities over 2 days .
he had no history of trauma , toxin exposure , illicit drug or alcohol abuse .
on general examination , he was afebrile , with a pulse rate of 106/min , blood pressure of 110/70 mmhg and respiratory rate of 18/min .
on neurological examination , he had flaccid , areflexic , pure motor quadriparesis with strength graded as 2/5 in both lower extremities and 3/5 in both upper extremities .
his laboratory tests on hospital day 1 revealed hyperkalemia , elevated liver enzymes ( aspartate aminotransferase , 274 iu / l ; alanine aminotransferase , 476 iu / l ) , leukocytosis ( 14,100/mm ) and deranged renal profile [ table 1 ] .
his electrocardiogram showed tall t - waves , absent p - waves and widening of qrs complexes consistent with severe hyperkalemia [ figure 1 ] .
he was treated with intravenous infusion of insulin - dextrose and calcium gluconate for hyperkalemia .
serum laboratory test results during patient 's hospital course electrocardiogram showing tall t - waves , absent p - waves and widening of qrs complexes his csf examination revealed a protein of 68 mg / dl , glucose of 90 mg / dl and a csf cell count of 2 leukocytes / mm .
it showed low amplitude of compound muscle action potential and nerve action potential , with near normal conduction velocity and the presence of fibrillation and positive sharp wave potentials consistent with axonal neuropathy .
his serological tests were negative for leptospira , dengue , human immunodeficiency virus , antinuclear antibodies , hepatitis b virus and hepatitis c virus .
immunoglobulins could not be given to him for the treatment of gbs due to financial constraints .
inotropic support ( noradrenalin and dopamine ) was started after adequate fluid repletion . on hospital day 3 , he was not able to lift his head off the pillow and cough out his secretions .
he was put on a mechanical ventilator for respiratory failure . in view of rising renal parameters , oliguria , proteinuria ( 2 + on urine dipstick test ) and persistent hypotension ,
a possibility of coexisting chronic renal insufficiency or acute rhabdomyolysis was kept in view of the presence of persistent hyperkalemia , hyperphosphatemia ( 10.8 mg / dl ) , hyperuricemia ( 14.2 mg / dl ) , hypocalcemia ( 7.4 mg / dl ) and high anion gap metabolic acidosis .
his renal profile prior to admission was normal and there was no evidence of chronic kidney disease on abdominal ultrasonography .
his biochemical analysis on day 3 of admission revealed serum ck of 7002 u / l ( n. 38 - 174 ) , lactate dehydrogenase ( ldh ) of 1250 u / l ( n. 91 - 180 ) , serum myoglobin levels were above 10,000 g / l ( n. 10 - 46 ) and urine myoglobin levels were 25.7 g / l ( n. 0 - 1000 ) .
u / l and 44 u / l on day 2 of admission ( in our hospital ) and 3 days prior to admission ( in other private hospital from where he was referred ) respectively [ table 1 ] .
a final diagnosis of gbs complicated by acute kidney injury ( aki ) and rhabdomyolysis was made .
rhabdomyolysis is a syndrome which results from skeletal muscle injury with the release of intracellular muscle cell contents including electrolytes , myoglobin and other muscle enzymes ( creatinine kinase , aldolase , ldh , aminotransferases ) into the systemic circulation .
the common causes of rhabdomyolysis are trauma , vigorous exercise , burns , alcohol , seizure , metabolic abnormalities , drugs , toxins and infections .
the mechanisms underlying rhabdomyolysis due to infection are direct muscle invasion , toxin production and myotoxic cytokines released in response to viral infection .
post - viral immune - mediated damage to muscle cells leading to acute rhabdomyolysis may be the possible etiology in our case of gbs .
negative history of trauma , illicit drug or alcohol abuse , toxin consumption or recurrent episodes of rhabdomyolysis in the past ruled out the other possible causes of rhabdomyolysis .
volume depletion as a result of influx of extracellular fluid into injured muscles resulting in renal ischemia , tubular obstruction due to heme pigment casts and direct nephrotoxic effects of liberate muscle cell constituents may all contribute to the development of aki in our patient .
the risk of aki in patients with rhabdomyolysis is lower in patients with ck levels at presentation less than 15,000 u / l .
the risk factors for aki in patients with lower ck values include dehydration , sepsis and acidosis .
persistent hyperkalemia not responding to conservative measures in our case might be due to an additive effect of massive release of cellular potassium as a result of rhabdomyolysis , impaired excretion of potassium as a consequence of aki and reduced sodium and water delivery to the sites of potassium secretion in the distal nephron due to reduced effective arterial blood volume .
mild to modest raised levels of ck have been documented in the early stages of gbs , the cause of which is uncertain . the possible mechanism proposed in the literature is rapid extensive denervation due to severe axonal degeneration of motor nerve terminals can result in the release of muscle enzymes ( ck ) .
acute rhabdomyolysis leading to markedly raised ck levels in a gbs patient is extremely rare .
acute rhabdomyolysis should be searched for a possible cause in a patient of gbs presenting with hyperkalemia .
its early recognition and institution of the appropriate management could prevent the fatal complications such as aki , compartment syndrome , disseminated intravascular coagulation , multi - organ failure and death .
 guillain - barre syndrome ( gbs ) is a heterogenous group of peripheral - nerve disorders with similar clinical presentation characterized by acute , self - limited , progressive , bilateral and relatively symmetric ascending flaccid paralysis , which peaks in 2 - 4 weeks and then subsides . 
 the usual complications , which occur in a patient of gbs are pneumonia , sepsis , pulmonary embolism , respiratory insufficiency and cardiac arrest . 
 the clinical course of gbs complicated by acute rhabdomyolysis is extremely rare . 
 we present the case of gbs with marked elevation in serum creatine kinase , serum myoglobin levels and persistent hyperkalemia as a result of associated acute rhabdomyolysis . 
Introduction
Case Report
Discussion
Conclusion