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Letters to the Editor Indian Pediatrics 2000;37: 1147-1148 |
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Acute Nitrobenzene Poisoning |
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The first report of poisoning due to nitrobenzene was in 1886 and subsequently several cases have been reported(1). Here we report a case fatality due to accidental ingestion of screen printing material, which contains nitrobenzene. A 5-year-old boy was brought with history of screen printing material ingestion following which vomiting was induced. Altered senso-rium developed 6 hours later. At admission, he was drowsy with localization to pain, had cyanosis, respiratory rate 30/min with hyperpnea, and was hemodynamically stable. Systemic examination was normal. A diagnosis of toxic methemoglobinemia due to screen printing material poisoning was entertained. His oxygen saturation at 6 liters/min oxygen via mask was 75-80%. Investigation revealed a normal hemogram. ABG showed at pH of 7.5, PaCO2 of 28 mmHg, HCO3 24 mEq/L, PaO2 90 mmHg and SaO2 of 99%. Blood taken on a filter paper turned dark brown on drying. X-ray chest was normal. Analysis of the substance ingested revealed nitrobenzene. Following gastric lavage and supportive management, he became conscious, cyanosis reduced and saturation improved (97%). As methylene blue was not available, he was put on vitamin C 500 mg orally. Eighteen hours after admission he was fully conscious but started having headache and occasional vomiting. Eight hours later, he became pale, sick, drowsy and had a seizure. He sustained a cardiorespiratory arrest, from which he could not be revived. Nitrobenzene, a pale yellow oily liquid with an odor of bitter almonds is used as intermediate in the synthesis of aniline dyes, and as a solvent, for the manufacture of cellulose ethers and acetate, as a flavoring agent, as a perfume for soap and in rubber industry(2). Nitrobenzene induces methemoglobinemia and this is responsible for the manifesta-tions(13). At levels of methemoglobin of 10-15%, cyanosis alone is obvious, though asymptomatic. Beyond 20%, headache, dyspnea, chest pain, tachypnea and tachycardia develop. At 40-50%, confusion, lethargy and metabolic acidosis occur leading to coma, seizures, bradycardia, ventricular dysrhythmia and hypertension. Fractions around 70% are fatal. Anemic patients and those with G6PD enzyme deficiency suffer more severe symptoms(3,4). The other effects include hepatosplenomegaly, altered liver functions, Heinz body hemolytic anemia and contact dermatitis(12). Clues for diagnosis are a history of chemi-cal ingestion(13). The characteristic smell of almonds, central cyanosis with no apparent respiratory distress, low pulse oximeter (observed) oxygen saturation with normal ABG (calculated) oxygen saturation(4,6) and persisting cyanosis on oxygen therapy, without severe cardiopulmonary disease(3,5,6). Dark brown blood that fails to turn bright red on shaking suggests methemoglobinemia(4) and this is supported by chocolate red color of dried blood(3). Presence of nitrobenzene compounds may be confirmed spectrophoto-metrically(7) and estimated by the butanone test of Schrenk(6). The management includes induction of vomiting, use of activated charcoal and high flow oxygen. Artificial ventilation may be required(3,7). In symptomatic patients, intra-venous 1% methylene blue (2 mg/kg over 5-10 minutes) is the first-line antidote and results in a dramatic decrease in cyanosis. A repeat dose (1 mg/kg) may be given after 15-20 minutes, the total dose not exceeding 5-7 mg/kg as this may aggravate hemolysis without further lowering methemoglobin content(3,7). Methy-lene blue causes an accelerated reduction of oxidized hemoglobin by acting as a co-enzyme in alternate NADPH-dependent reductase pathways(3,4). Methylene blue therapy is ineffective and can trigger hemolysis in patients with G6PD deficiency. In such patients and where methylene blue is un-successful, exchange transfusion should be considered. If methemoglobin fraction exceeds 50%, exchange transfusion should be consi-dered(3,4). Vitamin C, in oral or parenteral route, and dialysis are ineffective in acute methemoglobinemia(3,4), the former because of the slow rate at which it reduces methemoglobin. Our patient had severe poisoning and had secondary deterioration leading to fatality probably due to the delayed release of nitrobenzene from stores in the adipose tissue and gastrointestinal tract. Early exchange transfusion may have altered the outcome in this patient. Gaurav Gupta,
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