Introduction: Nitrobenzene, an aromatic nitro-compound, used as dissolver in shoe and metal glosss, pesticide and screen printing in India. Its toxicity is due to its ability to bring on methemoglobinemia. Clinical Picture: A 42 twelvemonth female patient survived a self-destructive ingestion of 250ml of 20 % Nitrobenzene. On presentation to the infirmary, the patient was unconscious and showed typical symptoms of cyanosis, unnatural arterial blood gas ( ABG ) demoing metabolic acidosis with SpO2 of 83 % , and the arterial blood sample was chocolate brown in coloring material. The patient suspected of methemoglobinemia showed the formation of 17.7 % methemoglobin ( normal: 0-3 % of Hb ) , and normalized to the full within 10 yearss due to speedy extended intervention. Result: She underwent supportive intervention and was given 1 % methylene blue and 1gm ascorbic acid which acts as an O scavenger. The patient finally made a complete recovery and the ABG was wholly normalized within 10 yearss due to quick and extended intervention. Decision: Acute Methemoglobinemia is normally associated with high mortality ; hence an early aggressive direction of toxic condition should be attempted. RBC exchange transfusion and hyperbaric O therapy are normally reserved for patients who are immune to standard intervention and for those with terrible symptoms.
Nitrobenzene Poisoning, Acute Methemoglobinemia, Methylene Blue, Ascorbic Acid, Cyanosis
Intentional exposure is a major cause of premature mortality globally and 113914 self-destructions are recorded yearly from India for which a assortment of chemicals have been used.1 Nitrobenzene is a pale xanthous oily liquid, with an smell of acrimonious Prunus dulciss is used in the synthesis of dissolvers, like pigment removers, industry of dyes, lubricating oils and man-made gum elastic. It ‘s besides known as nitrobenzol or oil of mirbane.2 In India, 20 % nitrobenzene emulsion is widely used as pesticides and marketed under the trade name name Synflower offered by Mandar agrotech. The deadly dosage is reported to run from 1 to 10gm by different studies.3-5 Methemoglobinemia is the primary acute consequence that later occurs after nitrobenzene consumption. The toxic dosage ensuing in methemoglobinemia was estimated in one instance survey at 4.3 to 11gm based on urinary p-nitrophenol levels.6
A 42 twelvemonth old adult female was rushed to a local infirmary and given first assistance after a self-destructive effort of devouring 250ml 20 % Nitrobenzene Pesticide an hr ago. After 8 hours she became centrally and peripherally cyanosed, unconscious and gasping, and was rapidly transferred to a mission infirmary. She was intubated ; her arterial blood sample drawn was found to be chocolate brown in coloring material and was suspected of methemoglobinemia. Her blood sample analysis suggested metabolic acidosis with pH -7.10, PaO2 -134mmHg, PaCO2 -42.6mmHg, and HCO3 -12.9meq/L. She was so lavaged via naso-gastric ( NG ) tubing with Na hydrogen carbonate, followed by disposal of activated wood coal ( 1 g/kg of 20 % suspension ) and started with IV fluids. Her blood sample analysis after 4 hours showed respiratory alkalosis with pH-7.49, PaO2-273mmHg, PaCO2 -33mmHg, and HCO3 -20.2meq/L. Her SpO2 was 83 % and had respiratory hurt. Due to non handiness of endovenous methylene blue ; specific counterpoison could non be given and was referred to our infirmary. On scrutiny her pulsation was 106beats/min, blood force per unit area 90/60mmHg, and her SpO2 was still 85 % with FiO2 – 100 % .7 Urine was dark colored, WBC count was 21,500/dL while all the other parametric quantities and trials remained normal. MetHb spectrophotometry values gave the consequence as 17.7 % ( Normal 0-3 % of Hb ) . It was diagnosed as Acute Nitrobenzene Poisoning with Severe Methemoglobinemia and treated with 1 % solution of methylene bluish 2mg/kg intravenously over a period of 5 proceedingss and decelerate endovenous extract of 1gm ascorbic acid in 5 % dextrose thrice a twenty-four hours. MetHb spectrophotometry values on the 6th twenty-four hours gave the consequence as 13.8 % and SpO2 was 90 % . After 3 yearss of ICU stay patient status was stabilized, easy recovered, SpO2 bit by bit increased and was discharged on the tenth twenty-four hours.
Methemoglobinemia is a status in which the Fe within hemoglobin is oxidized from the ferric ( Fe2+ ) province to the ferric ( Fe3+ ) province, ensuing in the inability to transport O and ensuing in chocolate-brown stain of blood.8 The low degree of methemoglobin is maintained by two of import mechanisms. One that occurs within the red blood cell is the hexose-monophosphate shunt tract which reduces oxidising agents by glutathione prior to the formation of methemoglobin. The 2nd mechanism against methemoglobin formation uses two enzymes systems: diaphorase -I and diaphorase -II which requires NADH and NADPH enzymes severally to cut down methemoglobin to its original ferric province. The NADH-dependent reaction is catalysed by cytochrome b5 reductase enzyme.9, 10
Normal degree of methemoglobin is 0 to 3 % and acute poisoning shows 10 to 15 % methemoglobin which is normally symptomless sometimes with lone cyanosis. Beyond 20 % concern, dyspnoea, thorax hurting, tachypnea, and tachycardia develops and above 40 % confusion, lassitude, and metabolic acidosis taking to coma, ictuss, bradycardia, ventricular dysrythmia, and high blood pressure. More than 70 % is extremely fatal and leads to death.4, 10
It besides causes hepatosplenomegaly, elevated liver map, and hemolytic anemia. Tools of diagnosing include characteristic odor of acrimonious Prunus dulciss, prevailing cyanosis on uninterrupted O therapy without preexistent cardiorespiratory disease, low arterial O impregnation, and unnatural arterial blood gas ( ABG ) analysis. Chocolate brown coloring material that fails to turn bright ruddy on shaking is the chief distinguishing characteristic proposing methemoglobinemia. Presence of nitrobenzene compound can be detected spectrophotometrically by different techniques like pulse-oximeter, co-oximetry, Evelyn- Malloy method and enzyme assay.9, 11, 12
Methemoglobinemia can be inborn or acquired ; counterpoison of pick for acquired ( toxic ) methemoglobinemia is methylene bluish, 1-2 mg/kg administered as a 1 % solution undiluted as direct IV over 3-5 proceedingss, repeated at 1 mg/kg in 1 hr as necessary to command fluctuating symptoms. Toxic dosage of methylene blue is more than 7mg/kg which can do dyspnoea, thorax hurting, and hemolysis.4,13 It is known to do erroneous SpO2 measurements.14 NADPH-dependent methemoglobin reductase system is effectual in cut downing methemoglobin to ferric signifier and methylene blue accelerates it by moving as an negatron donating exogenic cofactor. At higher doses even methylene blue has reverse action doing methemoglobinemia. It should non be given in patients with G6PD ( glucose-6-phosphate dehydrogenase ) lack as it leads to severe hemolysis. Other utilizations of methylene bluish include intervention of urolithiasis, cystitis, herpes simplex infection and counterpoison of pick in nitrile poisoning.4, 9, 10
Other intervention includes ascorbic acid which is an antioxidant ; free group scavenger which reduces the NAD+ at doses of 0.5-1gm given 8th hourly.5, 9 There is really less grounds from recent surveies that suggested N-acetyl cysteine is effectual in change by reversaling methemoglobin. RBC exchange transfusion and hyperbaric O therapy are normally reserved for patients who are immune to standard intervention and for those with terrible symptoms. 10 Dextrose is the major beginning of NADH in the ruddy blood cells which catabolises sugar through glycolysis and besides a beginning of NADPH through the hexose-monophosphate shunt, which is necessary for enhanced effectivity of methylene blue. Hence, dextroglucose should besides be administered.15
The intervention of poisoning caused by an uncommon compound is a challenge and the state of affairs becomes graver when the patient does non react decently on intervention. Acute Methemoglobinemia is normally associated with high mortality ; hence an early aggressive direction of toxic condition should be attempted.11, 13 Methylene blue and ascorbic acid are the intervention of pick, while RBC exchange transfusion and hyperbaric O therapy are normally reserved for patients who are immune to standard intervention and for those with terrible symptoms. The writers wish to indicate out the non handiness of endovenous methylene blue should non be a hinderance, as methylene bluish pulverization is available and can be made into 1 % solution and sterilized in CSSD.10