A 48-year-old male, pharmacist by occupation was found lying unconscious on the floor of his chemist shop with a 50 cc syringe partially filled with carbolic acid (household phenol) by his side. He was immediately rushed to the emergency department of our hospital. On inquiry, his wife said that he was staying aloof for past 1 week. He was otherwise healthy and was not on any regular medication. There was no history of smoking or alcohol intake.\nOn examination, he was irritable, but still following simple command like showing tongue when asked for. His extremities were cold. He was pale but not icteric. He had tachycardia (heart rate 116/min, regular) with blood pressure of 86/56 mmHg. He was tachypnic with a respiratory rate of 40/min. No abnormality was detected in respiratory system and abdominal examination. He was moving all four limbs spontaneously and there was no apparent cranial nerve deficit. His left forearm was swollen with evidence of thrombophlebitis extending up to the arm []. Random Blood Glucose was 95 mg/dl. Initial blood gas revealed hypoxia, lactic acidosis and respiratory alkalosis with a compensated pH (pH 7.35, PO2 75.9 mmHg, on 12 L O2 by mask, PCO2 33.1 mmHg, HCO3 17.8 mmol/L, lactate 5.2 mmol/L). Electrocardiogram was unremarkable except sinus tachycardia. Echocardiogram showed prominent Right Atrium with mild Tricuspid Regurgitation (estimated Pulminary Artery Systolic Pressure 37 mmHg); Inferior Vena Caval diameter of 12 mm with large respiratory variation; no wall motion abnormality and global ejection fraction EF 55%.\nAfter an initial fluid bolus of 1000 ml Normal Saline (NS) over half an hour and 500 ml × 2 of NS over next one and a half hour, he was continued on NS 100 ml/h with intermittent boluses of Furosemide. Oxygen supplementation with 40% Venturi Mask was started to maintain Oxygen saturation SpO2 above 92%. He was also given other supportive therapy in the form of intravenous Pantoprazole as stress ulcer prophylaxis and Ondansetron. After 2 h in the ICU, he had improvement in blood pressure, normalization of serum lactate level (2.3 mmol/L) and sensorium. He confessed to the self-injection of intravenous phenol. He also revealed that he tried to consume “All Out” liquid (Mosquito repellent containing 1.6% Pyrethrin) but immediately vomited out. At this time, he was oliguric and progressively more tachypneic with worsening oxygenation status. Chest X-ray showed bilateral patchy infiltrate []. Initial laboratory investigations revealed normal complete blood count; high blood urea nitrogen (21.1 mg/dl) and S Creatinine 2 mg/dl with normal electrolytes; deranged liver function test (S Bilirubin 3.02 mg/dl, direct Bilirubin 0.14 mg/dl, aspartate aminotransferase AST 211 U/L. alanine aminotransferase ALT 95 U/L, alkaline phosphate ALP 95 U/L. lactate dehydrogenase LDH 2574 U/L); normal serum Amylase; deranged coagulation parameters partial thromboplastin time 63.7 min, control 26 min and prothrombin time 27.8 min, control 12.4 min); high creatine phosphokinase (447 U/L). Urine analysis showed hemoglobinuria and proteinuria 3+. After an initial trial of noninvasive ventilation for half an hour, he was intubated and started on mechanical ventilation support with low tidal volume strategy.\nAfter 6 h, he was still oliguric with 45 ml of dark urine [] (Total intake 3500 ml). There was evidence of intravascular hemolysis with low serum Haptoglobin. His G-6PD level was normal. Abdominal ultrasonography examination was unremarkable. Hemodialysis was initiated in view of oliguria persistent metabolic acidosis and probable fluid overload. On day 2 he developed thrombocytopenia (platelet count 100,000/dl). In the subsequent days in the ICU his hypoxia improved but he continued to remain anuric. He was successfully weaned off the ventilator on day 4. On day 5 he was shifted to the ward on oxygen supplementation with 4 L O2 by nasal prong (maintaining SpO2 of 95%), still anuric on daily hemodialysis. On day 14, he was discharged from the hospital with normalization of all parameters except kidney function. He was advised 3 times a week maintenance hemodialysis, at discharge. His kidney function tests normalized over the subsequent 8 weeks of follow-up.
A 24-year-old female was admitted to our intensive care unit (ICU) with repeated episodes of seizures following deliberate ingestion of an unknown quantity of the anti-lice medication BUTOX (Deltmethrin 1.2%). On arrival in the emergency department, the patient was given a bolus dose of Lorazepam, and soon intubated, and then a loading dose of phenytoin was commenced. Gastric lavage was not performed as patient had repeated convulsions. On examination, she was deeply comatose, and was getting generalized tonic clonic seizures. Her pulse rate was 130/min regular, and her blood pressure was 136/76 mmHg. Her pupils were equal (2 mm in size) bilaterally briskly reacting to light. Other systemic examinations were unremarkable. An arterial blood gas showed mild metabolic acidosis. Hemogram, renal and liver function tests, electrocardiogram, and chest X-ray were normal. After repeat doses of Lorazepam and phenytoin, the patient was put on mechanical ventilatory support. A therapeutic coma was induced using a combination of Midazolam and Thiopentone sodium, as the patient continued to have convulsions. In the next 36 hours, Thiopentone and Midazolam were gradually tapered off after electroencephalography documentation of complete suppression of burst activity. She was gradually weaned off the ventilator after 72 hours. She was discharged from the hospital on Day 5 after psychiatry consultation.