hypokalemic paralysis and guillain  barr syndrome ( gbs ) are common differential diagnoses in patients presenting with acute flaccid paralysis . urgent recognition of hypokalemia is needed to prevent potentially lethal complications including cardiac arrhythmias and respiratory insufficiency . hypokalemia can be caused by acquired or inherited metabolic disorders of muscle ion channels and renal tubules . coexistence of hypokalemia , hypomagnesemia , and hypocalciuria occurs in gitelman syndrome ( gs ) , an inherited renal tubular disorder . a 41-year - old male presented with rapidly progressive symmetrical predominantly proximal quadriparesis of 4 days duration with tingling paresthesiae in limbs for 2 days . there was no history of alcohol consumption or exposure to drugs , bites , stings , and inoculations . he had no past history of similar symptoms , muscle aches , or thyroid dysfunction . heart rate was 88 beats / minute and blood pressure was 130/80 mmhg without respiratory insufficiency . he was awake , alert with symmetrical proximal muscle weakness ( shoulders 2/5 , elbow and lower limbs 4/5 , wrist and fingers 5/5 by medical research council [ mrc ] grading ) . sensations , cranial and neck muscles were normal ; muscle stretch reflexes sluggish and plantars flexor . meq / l over 12 hours at which time nerve conduction studies ( ncs ) revealed increased distal motor latencies , partial conduction block along with nonlength - dependent reduction of amplitudes [ table 1 ] . lumbar cerebrospinal fluid ( csf ) revealed albuminocytological dissociation with 250 mg / dl protein and 20 cells / mm ( lymphocytes 75% , polymorphs 25% ) . serial nerve conduction studies ( right side ) with serum potassium and magnesium levels on 5 and 40 day from onset of weakness and during follow - up at 18 months quadriparesis progressed with appearance of asymmetric lower motor neuron facial weakness and on fourth hospital day he required mechanical ventilation . plasmapheresis was initiated on the third hospital day with 10 l removed over the next 9 days . although patient could be weaned from ventilator after 12 days with moderate improvement of quadriparesis , he continued to have persistent hypotension and bradycardia requiring vasopressor support . the serum cortisol , thyroid hormones , ck - mb , echocardiography , and abdominopelvic imaging by ultrasound and contrast enhanced computerized tomography were normal . repeat nerve conductions before discharge revealed persistence of the abnormalities with increase in the latencies along with persistent dyselectrolytemia [ table 1 ] . at discharge 42 days after admission , the muscle power was 4/5 and he walked with minimal assistance . he was discharged on potassium supplements , spiranolactone , and dietary modification for hypomagnesemia . during follow - up the last follow - up 30 months after discharge , patient has persistent hypomagnesemia ( 1.5 mg / dl ) with hypocalciuria ( 90 mg / day ; normal 100 - 300 mg / day ) . nerve conductions revealed significant improvement of distal latencies , amplitudes , and conduction velocities at 18 months [ table 1 ] . gbs and hypokalemia are commonly encountered causes of acute flaccid paralysis ; other less common causes being hyperkalemia , botulism , porphyria , diphtheria , etc . , common subtypes of gbs consist of acute inflammatory demyelinating polyneuropathy ( aidp ) and acute motor axonal neuropathy ( aman ) based on clinicopathological and electrophysiological findings . when the initial conduction studies are inconclusive , repeating the study after an interval would help in the differentiation between the subtypes . our patient had persistent hypokalemia and hypomagnesemia with clinical profile of aidp supported by ncs findings and csf showing albuminocytological dissociation . hypokalemia can result from excessive loss of potassium in the urine or from the gut , poor intake , increased translocation into cells or inherited tubular disorders . the latter is an autosomal recessive renal tubular disorder due to mutations in the solute carrier family 12 , member 3 gene slc12a3 , which encodes the thiazide sensitive sodium chloride cotransporter . diagnosis of gs is based on biochemical abnormalities characterized by hypokalemia , hypomagnesemia , hypocalciuria , and metabolic alkalosis . the prevalence of gs is estimated to be approximately 1:40,000 and is the most frequent inherited renal tubular disorder . though hypomagnesemia has been considered obligatory for the diagnosis of gs , few patients with severe hypokalemia without hypomagnesemia or hypocalciuria were proved to be suffering from gs by genetic studies . barter 's syndrome is associated with hypokalemia and hypercalciuria and presence of hypertension suggests hyperaldosteronism . hypomagnesemia occurs in malnutrition , alcoholism , and with parenteral nutrition due to inadequate intake . increased losses via kidneys , skin , gastrointestinal tract , or sequestration in the bone compartment inherited renal magnesium wasting disorders include gs , bartter 's syndrome , isolated familial hypomagnesemia , hypomagnesemia with hypocalcaemia and hypomagnesemia with hypercalciuria . our patient had severe hypokalemia with mild metabolic alkalosis when he was admitted with quadriparesis resulting from clinical , electrophysiological , and csf features consistent with gbs . reversible abnormalities in ncs with reduced amplitudes in motor and sensory conductions occur in patients with hypokalemic periodic paralysis . during the course of the hospital stay , patient had recurrence of hypokalemia and hypomagnesemia that persisted during the follow - up despite the use of spiranolactone and potassium supplementation suggesting the presence of underlying metabolic dysfunction . plasmapheresis can cause transient hypomagnesemia and possibly contributed to worsening of the already existing hypomagnesemia . however , presence of persistent hypomagnesemia and hypokalemia with hypocalciuria up to 30 months after completion of plasmapheresis suggests the presence of underlying abnormality of magnesium metabolism . the constellation of spontaneous hypomagnesemia , hypokalemia , hypocalciuria , and metabolic alkalosis is strongly suggestive of gs . autonomic nervous system involvement in gbs can manifest with cardiac arrhythmia , blood pressure fluctuations , and is a relatively frequent occurrence . acute flaccid paralysis due to either hypokalemia or gbs manifesting as isolated entities may not perturb the clinician in diagnosis or management . combination of both these conditions along with another comorbid dyseletrolytemia could be life - threatening . it is challenging to treat complex dyselectrolytemia like severe hypokalemia and hypomagnesemia , which can complicate the clinical burden of autonomic and neurological dysfunction in gbs . we report one such rare coexistence of complex dyselectrolytemia in a patient with gbs . while it is essential to prove gs by using genetic studies , the same could not be done due to lack of facility and remains a possible comorbid clinical entity .
guillain  barr syndrome ( gbs ) and hypokalemic paralysis are common causes of acute flaccid quadriparesis and specific therapeutic interventions differ . simultaneous occurrence of severe hypokalemia in patients with gbs at the time of presentation can cause diagnostic and therapeutic dilemma . 
 presence of hypomagnesemia with hypokalemia in patients with gbs can be perplexing and pose further challenges . 
 evaluation for preexisting inherited or other associated metabolic disturbances is needed in the presence of such complex dyselectrolytemia . 
 we report the rare association of gbs with severe hypokalemia and hypomagnesemia in a 41-year - old male presenting with acute flaccid quadriparesis and the therapeutic challenges faced .