A 1-year, 6-month-old boy was presented to us 8 h postexposure with burn of 20% BSA involvement including the lower part of the face and anterior chest wall. After initial resuscitation including intubation and ventilation, he was hyperhydrated assuming the possibility of acute kidney injury (AKI) secondary to pigment nephropathy, but in spite of this, his urine output started falling from day 2 of admission, and hemoglobinuria became obvious along with rising creatinine from 0.28 to 0.98 mg/dl. Furosemide infusion was started to maintain urine output >1.5 ml/kg/h, and slowly with judicious fluid support and furosemide infusion, urine started clearing from 4th day of admission and creatinine normalized. Evaluation of the gastrointestinal tract by endoscopy revealed esophagus Grade 2b and stomach Grade 2a burn injury. He was extubated by day 6 of mechanical ventilation. He was initially kept on total parenteral nutrition for 7 days and thereafter started on clear liquids which were gradually built up to semi-solid. Solids were initiated after 6 weeks, once repeat endoscopy revealed normal esophageal and gastric mucosa. At present, he is doing well without any long-term complication.\nAccording to the parents/onlookers, none of the children ingested significant amount of carbolic acid as they spitted it out immediately, and the majority of the carbolic acid was splattered on their various body parts.
A 35-year-old male was admitted to our emergency department with giddiness as the major complaint following ingestion of an unknown quantity of an unknown poison. Patient was conscious, oriented with stable cardio-respiratory parameters at the time of arrival. After sometime, despite being well oxygenated via face mask, patient started having generalized tonic-clonic seizures. Initial attention to airway, breathing and circulation (ABC) was given, followed by a bolus dose of diazepam. Seizures subsided for a brief period only to recur repeatedly.\nOn repeated enquiry, the patient's relative brought empty bottles of “ALL OUT,” a commercial composition of pyrethroid used as insecticides providing a circumstantial evidence of the nature of the poisoning.\nPatient was given a bolus dose of thiopentone sodium, and soon his trachea was intubated. This was followed by a loading dose of the anti-convulsant phenytoin to control seizures.\nPatient was shifted to the intensive care unit for further management. On examination, he was deeply comatose. There was profuse sweating. His pulse rate was 136 per minute, and the blood pressure was 90/60mmHg. His pupils were dilated bilaterally and sluggishly reacting to light. Examination of the other systems was unremarkable. Hemogram, liver and kidney function tests, X-ray chest, ECG, and arterial blood gases were normal. Patient was put on a ventilator on the SIMV mode.\nAgain the patient started showing tonic–clonic seizures, which were continuous and unresponsive to anti-convulsant therapy. Thereafter, thiopentone sodium and midazolam infusions were administered and titrated clinically as no bedside EEG monitoring was available. Gradually, thiopentone sodium and midazolam infusions were tapered off, and patient was weaned off the ventilator to be extubated after 72 hours. The patient was discharged from the hospital on the 7th day after a psychiatry consultation.