A 16-year-old girl was admitted to the ICU with a history of consuming poison (20 ml of deltamethrin containing 12.5mg/ml, total dose = 250mg) following a domestic dispute. She presented with status epilepticus. As per the details gathered from the relatives, the patient was having continuous generalized tonic clonic seizures (GTCs) (status) since one hour prior to admission and was even convulsing during her transfer to the hospital. On arrival the patient was immediately intubated and ventilated and resuscitation started.\nThe convulsions were treated with injection Lorazepam, but there was no response. Further, doses of IV Midazolam/ Valproate/Phenobarbitone were given, but the convulsions continued. A bolus does of Thiopentone was then given, after which she stopped convulsing. She was started on a thiopentone infusion. Despite the thiopentone infusion, she had four episodes of GTCs in the next six hours, which were managed with further boluses of thiopentone (200mg) and increase in rate of the infusion. Inotropes were started and IV fluids were continued which were guided by CVP and arterial BP monitoring. Her rhythm on ECG was normal and lungs were clinically dry. CNS examination was not possible because she was sedated with thiopentone. Her pupils were dilated (6mm) and fixed.\nAn EEG showed 80% suppression of the brain. CT scan showed diffuse cerebral edema with effacement of sulci and chinking of lateral ventricles.\nLab reports showed normal S. cholinesterase levels (4340 IU/L), normal serum electrolytes and urine negative for myoglobin.\nAfter 48 hours of being on thiopentone infusion (24 hours without convulsions), she was weaned off thiopentone infusion. The patient was triggering the ventilator well by the next day (day 4). Supports were hence taken off gradually. The patient's pupils became reactive by day 5.\nIn the following days, the patient was tracheostomized (in view of anticipated prolonged mechanical ventilation) and T-piece trials were initiated soon. By day 11, she was opening eyes to call and was moving all four limbs, but with reduced power. Tracheostomy was decannulated on day 14 [].\nNerve conduction studies were done in view of her poor muscle strength which showed “severe, generalized, predominantly motor axonal polyneuropathy”.\nThe patient was shifted to the ward after 18 days of ICU stay, on supportive care. Wheelchair ambulation was started on day 21 and the patient was discharged on day 26.
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.