a 24-year - old female was brought to the casualty department of our hospital with an alleged history of ingestion of a soapy solution 4 hours prior to admission . her chief complaints were a sudden onset of severe cramping abdominal pain , vomiting and diarrhea . her family history was noncontributory . on examination , she was conscious and oriented with a blood pressure of 110/70 mmhg , a pulse rate of 92 beats/ minute and respiratory rate of 16/minute . as the chemical composition of the soap was not mentioned on the label , a prompt gastric lavage was done and the contents preserved for chemical analysis . one hour after admission she started complaining of increased difficulty in breathing and there was progressive deterioration of her level of consciousness . on examination by the icu team in the casuality her gcs was 7 ( e2 v1 m4 ) , her pupils were dilated and sluggishly reacting . her pulse rate was 100/minute , irregularly irregular and systolic blood pressure was 90 mmhg . an ecg done in casualty revealed prolongation of pr interval , st segment depression and t wave inversion in leads ii , iii , avf and lateral chest leads with a normal rhythm . her abg revealed severe metabolic acidosis with a ph of 6.97 , pco2 , 40.2 mmhg , hco3 8.4 and base excess of -25.2 . laboratory examination revealed a serum potassium level of 1.6 meq / l , serum bilurubin , ast and alt , blood urea and serum creatinine were within normal range . potassium supplementation was started immediately under strict cardiovascular monitoring and 80 meq potassium was infused over the next 2 hours via central venous line . however , her motor paralysis progressed inspite of potassium correction at the rate of 40 meq per hour . saline diuresis was initiated with 0.9% saline and spironolactone 6 milligrams bd through ryel 's tube . magnesium levels were ( 1.7 mg/ dl ) intravenous magnesium supplementation 1 gm single dose was administered . an additional 280 meqwas given in the first 24 hours and further 140 meqgiven over the next 24 hours after which the potassium levels were 4 meq / l . over the next 24 hours there was a dramatic improvement of her muscle power coincident with the rise in serum potassium levels and acidosis . barium sulfide is utilized as a constituent of various facial depilatory creams and hair - removing soaps . it is well known to physicians as a benign radio - opaque contrast agent and its insoluble sulfate salt has been utilizedfor x - ray diagnosis of colorectal and upper gastrointestinal conditions . most of the cases reported in literature of acute toxicity due to barium are those due to ingestion of soluble salts of barium like barium carbonate ( rodenticide ) which allowsfor absorption of free barium ions.[26 ] these free barium ions are severe irritants of the gastrointestinal tract and ingestion leads to excessive salivation , intractable vomiting , severe abdominal pain and diarrhea within 2 - 3 hours . progressive toxicity causes muscle twitching , periorbital and extremity paraesthesias , weakness progressing to convulsions and flaccid paralysis , as well as life - threatening arrhythmias . gastric lavage was done even 4 hours after ingestion as it is a protocol in our hospital to lavage all poisoning patients and to collect the samples for toxicological examination . the administration of activated charcoal has no role in barium toxicity as it does not bind barium and should not be used unless other agents are ingested or suspected . however , oral administration of magnesium sulfate or sodium sulfate leads to precipitation of ionic barium in gut to form insoluble barium sulfate and catharsis . we initiated a saline diuresis with intravenous normal saline 0.9% and utilized sprinolactone as a diuretic agent as it is a potassium - sparing diuretic to maintain a urine output of 200 ml / hr . intravenous magnesium sulfate has also been used as an antidote of barium and also for correction of profound refractory hypokalemia . this was our rationale for administration of magnesium though theoretically magnesium sulfate can precipitate barium in the kidneys leading to acute renal failure . aggressive respiratory assistance and bicarbonate administration are essentialto manage the life threatening respiratory paralysis and acidosis . intravenous potassium administration reverses the hypokalemia as well as displaces barium from potassium channels , allowing it to be excreted in the urine . immediate administration of up to 400 m eqof potassium evenly and over 24 hours , which might prove dangerous in other situations , is essential for rapid management of barium intoxication and for protection against fatal barium - induced arrhythmias . phelan , have emphasized on the value of early hemodialysis for the reduction in serum barium levels as they found a strong correlation between serum barium levels and the degree of weakness . however , we found a good correlation between the degree of paralysis and serum potassium levels . we could not do serum barium levels as facility to do this investigation was not available in our hospital . but respiratory assistance , aggressive intravenous potassium supplementation and saline diuresis may result in successful outcome .
we present a rare case in which a young girl ingested a solution of a hair - removing soap . 
 the ingestion resulted in profound hypokalemia and severe acidosis leading to flaccid paralysis , respiratory arrest and ventricular arrhythmias . 
 ultimately the patient made complete recovery . 
 the soapwas found to contain barium sulfide . 
 the degree of paralysis and acidosis appeared to be directly related to serum potassium levels .