A 13-year-old girl was admitted in our accident emergency with history of Bilbo 505 ingestion. The patient had ingested approximately 20 mL of Bilbo (chlopyrifos 50% and cypermethrin 5%) which was found to be a combination of OP and pyrethriod compound, with alkyl benzene sulfuric acid as emulsifier []. On arrival, the patient had difficulty in breathing which was accompanied by multiple episodes of vomiting. On examination, she was drowsy and had pinpoint pupils with an up-rolling of eye balls. There was no associated neck rigidity. Her heart rate was 92/min; peripheral oxygen saturation was 50%–70%, and auscultation of chest revealed bilateral crepitations, with excessive oral secretions. A chest radiograph revealed bilateral pulmonary infiltrates []. In view of her deteriorating clinical condition, the patient was intubated and mechanically ventilated. Gastric lavage was done to facilitate gastrointestinal decontamination. The patient received four doses of intravenous atropine, each of 6 mg. This was followed by administering atropine infusion at 6 mg/h till signs of atropinization were evident. Pralidoxime 2 g was administered intravenously in 100 mL of normal saline over 20 min, followed by repeat doses of 1 g pralidoxime four times a day. After an improvement in clinical course, tracheal extubation was done after 72 h of atropinization and pralidoxime administration. Her atropine dose was gradually tapered over the next 2 days and stopped thereafter.\nHowever, on day 7, she developed cough, breathlessness, and diarrhea for which she received oxygen supplementation, darolac sachet (containing lactobacillus sporegens), dextromethorphan hydrobromide, and chlorpheniramine maleate syrup. However, after 48 h (day 10), there was an increase in excessive frothy secretions from mouth, severe breathlessness, and diarrhea. It was accompanied by tachycardia and bilateral crepitations in both lung fields. She was immediately intubated, and considering the cholinergic symptoms of poisoning, atropine was restarted at an infusion of 3 mg/h. She responded rapidly to the antidote and was extubated uneventfully after 24 h. The dose of atropine was weaned-off by day 15. However, on day 18, the patient again had cholinergic symptoms characterized by miosis, excessive salivation, lacrimation, diarrhea, blurring of vision, and up-rolling of eyeballs. Atropine was restarted at low dose of 1.6 mg/h and the patient was asymptomatic. Simultaneously we sent her plasma and red blood cell cholinesterase and it was is in normal range. The patient was observed for prolonged poisoning effects and was kept under observation in a high dependency unit. She had few episodes of urinary incontinence, blurring of vision, and cough on day 25 of poisoning, which subsided without any further need of atropine administration. She had no new symptoms of lacrimation, bronchorrhea, and miosis. The patient was observed for few more days to look for delayed intermediate symptoms or rebound cholinergic symptoms. She was discharged after a month of poisoning and was being followed telephonically. Since the last telephonic contact, the patient was not known to have any symptoms and was living a healthy life.
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.