Acute barium intoxication following ingestion of soap water solution
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. There was no previous history of influenza like illness, diarrhea or alcoholism. Her family history was noncontributory.\nOn 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. There were no external injuries.\nAs 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. The patient was treated symptomatically and vitals were monitoredcontinuously. On admission, her blood sugar was 100 mg/dl and her ABG was normal.\nOne 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. Her respiratory rate was 24 breaths/minute with a paradoxical pattern of respiration. On auscultation of chest air entry was equalbilateraly. 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.\nThe patient's trachea was intubated with a 7 mmI.D. endotracheal tube and ventilation started with 100% oxygen. The patient was then transferred to the ICU. In ICU she was put on ventilatory support with SIMV mode of ventilation and FIO2 100%. 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.\n200 mEq of sodium bicarbonate infusion was started for correction of metabolic acidosis. Meanwhile, her ECG began showing frequent ventricular ectopy. Intravenous lidocaine 60 mg was given intravenously. 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.\nWhen contacted,the manufacturer revealed that the soap contained barium sulfide. 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. Simultaneously, potassium correction was continued with 40 mEqof potassium per hour. 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.\nOver the next 24 hours there was a dramatic improvement of her muscle power coincident with the rise in serum potassium levels and acidosis. She subsequently made a complete recovery with no residual neurological deficit.