The emergency medical service (EMS) brought a 26-year-old Asian man to the emergency department (ED) approximately 2 hours after ingesting Clorox (sodium hypochlorite) and Dettol from two separate 1-l bottles. His workmate had found him “shaking” in the bathroom and had called for an ambulance. He was distressed and confused, with increased oral secretion and drooling. The EMS started him on intravenous normal saline and oxygen via a nonbreather mask. On examination in the ED, the patient complained of abdominal pain and headache. His initial vital signs were respiratory rate of 22 breaths per minute, oxygen saturation 98% on a non-rebreather mask, heart rate of 84 beats per minute, blood pressure (BP) 182/102 mmHg, and Glasgow Coma Scale (GCS) was 13/15 (E4, V4, M5). The patient’s oral mucosa and oropharynx were erythematous with slough and moderate swelling. He was drooling but had no stridor. He had drug-assisted endotracheal intubation using direct laryngoscopy and a size 7.5 mm tube, based on suspicion of an impending airway compromise. He was put on a mechanical ventilator in continuous mandatory ventilation (CMV) mode. A blood sample was collected for venous gas, full blood count (FBC), urea and electrolytes (U and E), clotting screen, liver functions, and drug toxicology screen. Bedside and admission blood tests showed venous blood gas (VBG) pH 7.26 (7.35–7.45), CO2 36.9 kP (33–45), HCO3 16 mEq/l (22–28), Base excess (BE) −10 (−2 to +2), lactate 4.5 (< 2). White blood cell count (WBC) was 16.9 (4–9) with neutrophilia. International normalized ratio (INR) was I.4 (1.0–1.1), with prothrombin time (PT) and activated partial thromboplastin clotting time (APTT) of 14.3 (11.5–15.55) and 39.7 (30–40), respectively. There was evidence of hepatic and pancreatic injury with raised aspartate aminotransferase (AST) 122 mEq/l (0–20 mEq/l) and alanine transaminase (ALT) 74 mEq/l (0–20 mEq/l). His amylase and lipase levels were 1137 U/l (25–125 U/l) and 3000 U/l (25–60 U/l). Urine and serum toxicology screens, including phosphatidyl ethanol levels, were negative. A chest X-ray confirmed the correct position of the endotracheal tube and a right middle lobe consolidation, suggestive of aspiration pneumonitis. A contrast computed tomography scan of the head, neck, thorax, and abdomen showed (a) significant soft tissue edema of the larynx and pharynx, (b) ground glass opacity right lower and middle lobes, and (c) blotch of contrast in the stomach fundus, peripancreatic and perigastric streaks with contrast substance extravasation in the stomach, and hypodensity of the periphery of the liver in mainly the right lobe and periportal edema. Figure a–c show the computed tomography of the larynx, chest, and abdomen. An esophagogastroduodenoscopy (OGD) showed severe erosive esophagitis with blood oozing throughout. The gastric lumen was filled with blood, obscuring the view of the stomach wall and duodenum. The patient was admitted to the intensive care unit. On the 2nd day of admission, the patient’s heart rate was 147 beats per minute, and his BP was 76/55 mmHg. Repeated laboratory results showed worsening hepatic and renal functions and raised procalcitonin levels. The patient was diagnosed with sodium hypochlorite and Dettol-induced corrosive gastrointestinal mucosa injury on the basis of the OGD findings. His laboratory test results showed a high anion gap metabolic acidosis and hyperkalemia, indicating acute kidney injury. He developed multiorgan failure involving the lungs, pancreas, and liver and disseminated intravascular coagulopathy (DIC). The patient received a loading dose of intravenous pantoprazole 80 mg, followed by a continuous infusion at a rate of 8 mg per hour. Intravenous normal saline was continued, and he was started on intravenous piperacillin/tazobactam 4 g/0.5 g. The patient was catheterized to monitor urine output, and frank hematuria was noted. His DIC was treated with transfusion with factor VIIa recombinant, fresh frozen plasma, and cryoprecipitate. He was placed on sodium bicarbonate infusion and continuous renal replacement therapy due to worsening metabolic acidosis and hyperkalemia. Intravenous vancomycin 1 g was added for broader antimicrobial coverage. The patient had persistent hypotension, which was treated with norepinephrine, vasopressin, and packed red blood cells (RBC) transfusion. In total, he was transfused with 12 units of packed RBCs, 23 packs of fresh frozen plasma, three packs of cryoprecipitate, and three units of platelets. He had persistent metabolic acidosis and hyperlactatemia, despite renal replacement therapy and continuous bicarbonate infusion. On day 5 of post-hospital admission, the patient’s condition remained critical with worsening bradycardia (heart rates of 30–47 beats per minute) and invasive mean arterial blood pressure of 30–40 mmHg. His laboratory values on day 5 were creatinine 100 mmol/l, alkaline phosphatase 441 IU/l, AST > 7000 IU/l, ALT 2820 IU/l, N-terminal (NT)-pro hormone brain natriuretic peptide 32 (NT pro-BNP) 477 ng/l, troponin > 10,000, hemoglobin (Hb) 83 g/l, platelets 24 × 109/l, pH 7.19, base excess −17.30, HCO3 12, and lactate 18 mmol/l. The patient was placed on a do not attempt resuscitation (DNAR) order in case of cardiac arrest following a review by the ICU multidisciplinary team comprising intensivists, renal physicians, gastroenterologists, and representatives of the patient’s family. The patient subsequently went into cardiac arrest and was pronounced dead.