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Home Explore Late presentation of secondary cycling - nitrobenzene poisoning: A rare case report

Late presentation of secondary cycling - nitrobenzene poisoning: A rare case report

Published by iaim.editor, 2014-12-24 00:28:05

Description: Virendra Goyal. Late presentation of secondary cycling - nitrobenzene poisoning: A rare case report. IAIM, 2014; 1(3): 39-43.

Keywords: Acute methemoglobinemia, Methylene blue, Nitrobenzene poisoning, Blood transfusion.


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Late presentation of secondary cycling - nitrobenzene poisoning ISSN: 2394-0026 (P)Case Report ISSN: 2394-0034 (O) Late presentation of secondary cycling -nitrobenzene poisoning: A rare case report Virendra Goyal* 142,Taruchaya Nagar, Tonk Road, Jaipur, Rajasthan, India *Corresponding author’s email: [email protected] to cite this article: Virendra Goyal. Late presentation of secondary cycling - nitrobenzenepoisoning: A rare case report. IAIM, 2014; 1(3): 39-43. Available online at www.iaimjournal.comReceived on: 14-10-2014 Accepted on: 20-10-2014AbstractWe presented here a case of acute nitrobenzene poisoning in which effective clinical evaluation andtimely management in form of repeated intravenous methylene blue and blood transfusions playeda vital role to save a life. It is very important to take care of patient who presented late after heavyexposure form the secondary cycling of nitrobenzene from body stores. Clinicians should be awareof this uncommon, but treatable and potential serious poisoning of nitrobenzene.Methemogobinemia can leads to high mortality but effective treatment with methylene blue ispreferential.Key wordsAcute methemoglobinemia, Methylene blue, Nitrobenzene poisoning, Blood transfusion.Introduction change the outcome of a patient in positive manner.Nitrobenzene is also known as nitrobenzol,mirbane oil or essence of mirbane. When Case reportintroduced into the body, it is metabolized by A 30 years old, irritable, anxious male presented to emergency department who referred fromreduction to aniline. Nitrobenzene and aniline other centre on mechanical ventilation with cyanosis and a greyish-brown hue. Onare typical aromatic nitro compounds and examination, he had labored respiration of 26/min, blood pressure was 129/74 mm of Hg,aromatic amino compounds that cause pulse rate was 74/min, pupils with sluggish reaction, and SpO2 of 89% only. There was amethemoglobinemia. Significant history of severe pain in the abdomen, nausea,methemoglobinemia due to acute nitrobenzenepoisoning is uncommon and rare but lifethreatening emergency condition. Oncepoisoning is suspected on clinical evaluation,early and effective management of it mayInternational Archives of Integrated Medicine, Vol. 1, Issue. 3, November, 2014. Page 39Copy right © 2014, IAIM, All Rights Reserved.

Late presentation of secondary cycling - nitrobenzene poisoning ISSN: 2394-0026 (P) ISSN: 2394-0034 (O)vomiting, and dizziness, which was treated on 93% and a PaO2 of 112. He improved rapidlyadmission at primary centre. At primary centre, after the 10th day with SpO2 of 90% on room air.oral methylene blue was given (5 ml, 12 hourly), Patient had a single episode of generalized tonicas to non-availability of intravenous therapy. An clonic seizure (GTCS) on 11th day and wasurgent ultrasonography of abdomen was done epsolinised, followed by oral dilantin tabletswhich ruled out any abdominal catastrophe (100 mg TDS). CT head was absolutely normaland showed a generalized mild to moderate but liver enzymes were raised. He washepatic inflammation. Blood samples were discharged on the 14th day on oral iron, folate,drawn for arterial blood gas (ABG) analysis ascorbic acid, and liver enzyme supplements andwhich had a chocolate brown color, which did breathing exercises.not improve on exposure to 100% oxygen andshowed compensated metabolic acidosis. X-ray Discussionof the chest and ECG were within normal limitswhile WBC and liver enzymes were markedly Nitrobenzene is a pale yellow, oily liquid, withraised. Serum creatinine and blood urea were bitter almond odor and it is widely used as anwithin normal range. Hemoglobin at admission intermediate in the production of variouswas 9.4 gm%, which dropped down to 6.3 gm% solvents, like paint remover. Commonon 9th day. Similarly serum bilirubin at admission occupational exposure of nitrobenzene is viawas 2.0 mg% which was raised to 13.0 mg%. A inhalation or through absorption of skin [1, 2]. Inclinical diagnosis of severe acute 1886, first report of nitrobenzene poisoning wasmethemoglobinemia due to nitrobenzene noted [3] and then after various fatality reportspoisoning was made. were come into noticed [3, 4]. Nitrobenzene100 mg of methylene blue (prepared as 1% poisoning can be accidental or suicidal insterile solution) was given intravenously and manner [5]. Accidental exposure may possible inrepeated after 12 hours. This improved patient’s patients who are consuming well water withSpO2 to 92% and then after intravenous vitamin extremely high levels of nitrites and nitrates in itK; vitamin C, 10% dextrose, anxiolytics, oral iron, [6]. Lethal dose of it is varied from 1-10 g, as perand intravenous antibiotic were also given. different scholar authors [7, 8, 9]. A systematicUrine output was maintained above 100 literature review of already published articles onml/hour with proper hydration, maintaining a it does not provide any significant conclusivenormal central venous pressure (CVP). matter regarding fatalities and dose of ingestion [8]. Nitrobenzene poisoning is usually presentedMultiple blood and blood products like fresh as chronic poisoning or as occupational hazardfrozen plasma (FFP) were transfused. Patient at with development of methemoglobinemia [10].admission had severe hypokalemia (2.5 mEq/L), The clinical features of ingestion of such poisonwhich was corrected by intravenous slow are due to the rapid development ofpotassium infusion. Methemoglobin estimation methemoglobinemia [7, 11], which is a conditionin blood was done and it was significantly high of altered hemoglobin formation in which the(11.1 units as compared to normal values of 0.00 iron presented within the hemoglobin isto 2.0). He was extubated at 48 hours and oxidized into ferric (Fe3+) state from the ferrousmaintained on a continuous positive airway (Fe2+) state, resulting in the inability to transportpressure (CPAP) mask, with arterial blood gas oxygen effectively [12, 13, 14] and causes(ABG) analysis which showed a saturation of brownish discoloration of the blood and functional anemia [6]. After formation ofInternational Archives of Integrated Medicine, Vol. 1, Issue. 3, November, 2014. Page 40Copy right © 2014, IAIM, All Rights Reserved.

Late presentation of secondary cycling - nitrobenzene poisoning ISSN: 2394-0026 (P) ISSN: 2394-0034 (O)methemoglobin, it can be reduced enzymatically oxygen therapy without severe cardiopulmonaryeither via an adenine dinucleotide (NADH)- disease, low arterial oxygen saturation, withdependent reaction, which is catalysed by normal ABG (calculated) oxygen saturation arecytochrome b5 reductase, or an alternative very important for diagnosis. Methemoglobinpathway utilizing the nicotine adenine detection can be done bedside by placing fewdinucleotide phosphate [15]. Certain drugs and drops of blood on white filter paper andchemicals can accelerate production of observing for color change in whichmethemoglobin like antimalarial drugs such as deoxyhemoglobin brighten and methemoglobinchloroquine and primaquine; nitrites or nitrates, holds color [23]. Dark brown blood that fails toflutamide, inhaled nitric oxide, metoclopramide, turn bright red on shaking, which suggestslocal anesthetic agents like benzocaine; methaemoglobinaemia and this is supported byacetanilide, nitroprusside, sulfonamides, the chocolate red color of dried blood. Presencephenacetin, phenazopyridine hydrochloride, of nitrobenzene compounds may be confirmedphenytoin, chlorates, probenecid etc. [16]. spectrophotometrically and estimated by the butanone test of Schrenk [1], methemoglobinNormal physiological level of Methemoglobin is levels in the blood, and urinary presence of p-less than 1% of total hemoglobin [17]. At level of nitrophenol and p-aminophenol [3, 21, 24].10-15% of methemoglobin, person is usuallyasymptomatic with mild cyanotic changes. Plan of management is based upon theWhen methemoglobin level is 20-40%, principles of decontamination along withheadache, dyspnea, chest pain, tachypnea, and symptomatic and supportive treatment.tachycardia develop [18]. At 40 – 50% level of Methylene blue is the drug of choice (antidote)methemoglobin, person feels confusion, for the treatment of acquired (toxic)lethargy, and metabolic acidosis which later on methaemoglobinaemia [25]. It is an exogenousleading to coma, seizures, bradycardia, cofactor, which greatly accelerates the NADPH-ventricular dysrythmia, and hypertension [19]. dependant methemoglobin reductase systemMethemoglobin level around 70% is considered and is indicated if the methemoglobin levels,as fatal [20]. More severe symptoms are noted which are more than 30% [7]. It is administeredin patients with anemia or G6PD deficiency [4, intravenously at 1 – 2 mg/kg (up to 50 mg dose7]. In certain cases, leukocytosis has been in adults,) as a 1% solution over five minutes;reported along with relative lymphopenia [8]. with a repeat in one hour, if necessary.Altered liver function tests, hepato- Methylene blue is act as an oxidant at levels ofsplenomegaly, and Heinz body haemolytic more than 7 mg/kg, and therefore, may causeanaemia are other significant features [4, 21, methaemoglobinaemia in susceptible patients22]. Nitrobenzene is metabolized in the body [26]. It is contraindicated in patients with G6PDand converted into p-nitrophenol and deficiency, because it can lead to severeaminophenol and later on excreted in urine (up haemolysis. Ascorbic acid is an antioxidant thatto 65%), and in stools (up to 15%) after five days may also be administered in patients withof ingestion. Liver, stomach, blood, and brain methemoglobin levels of more than 30% [27]. Inmay act as storage house and release it recent studies, N-acetylcysteine has been showngradually [21]. to reduce methemoglobin, but it is not yet an approved treatment for methaemoglobinaemiaHistory of chemical ingestion, characteristic [27]. Exchange transfusion is indicated in severebitter almond smell, persisting cyanosis on cases [7, 27]. Hyperbaric oxygen is reserved onlyInternational Archives of Integrated Medicine, Vol. 1, Issue. 3, November, 2014. Page 41Copy right © 2014, IAIM, All Rights Reserved.

Late presentation of secondary cycling - nitrobenzene poisoning ISSN: 2394-0026 (P) ISSN: 2394-0034 (O)for those patients who have a methemoglobin Referenceslevel > 50% or those who do not respond to 1. Min JW, Park SY, Lee GR, Jeon YD, Jungstandard treatment. Exchange transfusion is JY, Cho YJ, Nam HW. Case of acutemore widely and rapidly available compared to methemoglobinemia caused byhyperbaric oxygen. Exchange transfusion nitrobenzene ingestion. Korean J Med,involves replacement of the patient's red cells 2013; 84(3): 442–445.with donor cells and has been used in thetreatment of various hemoglobinopathies [15]. 2. Martinez MA, Ballesteros S, Almarza E, Sanchez de la Torre C, Bua S. AcuteIn this case, we repeated low dose methylene nitrobenzene poisoning with severeblue and blood transfusions helped in tidingover the fluctuating symptoms due to the associated methemoglobinmeia:release of nitrobenzene from the body stores,without exceeding the maximum dose. Fresh Identification in whole blood by GF-FIDblood transfusion improved the oxygen carryingcapacity and haemoglobin content, improving and GC-MS. J Anal Toxicol, 2003; 27(4):the patient symptomatically. Oral charcoal andpurgation up to five days helped to eliminate the 221–5.body stores of nitrobenzene and preventedsecondary deterioration in the patient .Taking 3. Gupta G, Poddar B, Salaria M, Parmar of nutrition, adequate urine output, andhepatoprotection prevented kidney and liver Acute nitrobenzene poisoning. Indianfailure, which have been cited as late effects [3,21]. Regular use of charcoal and purgation by Pediatr., 2000; 37: 1147–8.peglag during hospital stay may be of some helpaccording to some centers. Forced diuresis can 4. Dutta R, Dube SK, Mishra LD, Singh AP.lead to a rapid fall in methemoglobin levels andimproved discoloration [8]. Ascorbic acid Acute methemglobinemia. Internet Jsupplements are useful for follow-upmanagement of methaemoglobinaemia [28]. Emerg Intensive Care Med., 2008; 11: 1092–4051. 5. R. Ewert, E Buttgereit, M. PrCigel, R Reinke. Intravenous injection of India ink with suicidal intent. Int.J. Med. LegalMed., 1998; 111: 91-92. 6. Michelle, Kumar M. Methemoglobinemia overview. e medicine from web med. Available from: article/956528-overview. Accessed in 2010.Conclusion 7. Chongtham DS, Phurailatpam, Singh MM, Singh TR. Methemglobinemia inClinicians should be aware of this uncommon, nitrobenzene poisoning. J Postgradbut treatable and potential serious poisoning of Med., 1997; 43: 73–4.nitrobenzene with secondary cycling from the 8. International Program on Chemicalbody tissues. Methemogobinemia can leads to safety (IPCS) – 2003 (8.11)high mortality but effective treatment with Nitrobenzene. Environmental healthmethylene blue is preferential. criteria 230. Geneva: WHO. Available from:Acknowledgement author is highly thankful to Jeevanrekha /ehc/ ehc230.htm#8.1.1;#7.8. AccessedCCTH, Jaipur team for their kind cooperation in 2003.and wholehearted support in. 9. Harris JC, Rumack BH, Paterson RG, Mc Guire BM. MethaemoglobinemiaInternational Archives of Integrated Medicine, Vol. 1, Issue. 3, November, 2014. Page 42Copy right © 2014, IAIM, All Rights Reserved.

Late presentation of secondary cycling - nitrobenzene poisoning ISSN: 2394-0026 (P) ISSN: 2394-0034 (O)resulting from absorption of nitrates. 20. Eisen Kraft JB. Pulse oximeterJAMA, 1979; 242: 2869-2871. desaturation due to10. Aruna Dewan, Ashwin Patel, Habibullah methaemoglobinemia. Anaesthesiology,Saiyed. Acute Methemoglobinemia - A 1988; 68: 279-282.Common Occuptional Hazard in an 21. Wakefield JC. Nitrobenzene toxicologicalIndustrial City in Western India. J Occup overview file format. AvailableHealth, 2001; 43: 168-171. form: Schimelman MA, Soler JM, Muller HA. webFile/HPAweb_C/1222068850334 paMethaemoglobinem: Nitrobenzene ge 1-10. Accessed in 2008.ingestion. J Am Coll Emerg Phys, 1978; 7: 22. David C Lee. Methemoglobinemia.406-408. eMedicine from web med. Accessed in12. Bradberry SM, Aw TC, Williams NR, Vale 2012.JA. Occupational methemoglobinaemia. 23. Mary Denshaw-Burke, John Schofstall.Occup Environ Med, 2001; 58(9): 611– Methhemoglobinemia. eMedicine from616. web med. Accessed in 2012.13. Park SS, Nam EM, Kim IH, Kim JS, Lim YJ, 24. Verive M, Kumar M.Ahn SJ. A case of methemoglobinemia Methemglobinemia: Differentialcaused by hair dyeing with henna. diagnoses and workup, e medicine fromKorean J Med, 2007; 72(2): 314–317. web med. Available14. Shin JH, Lee JK, Park SS, Na SJ, Park JS. from: http://www.emedicine.medscape.Indoxacarb pesticide poisoning with com/article/956528-diagnosis. Accessedmethemoglobinemia. J Korean Soc Clin in 2010.Toxicol, 2006; 4(2): 158.–160. 25. Curry S. Methaemoglobinemia. Ann15. Michael A. Pritchett, Nathalie Celestin, Emerg Med, 1982; 11: 214-221.Nicole Tilluckdharry, Katherine Hendra, 26. Whitwan JG, Taylor AR, White JM.Peter Lee. Successful Treatment of Potential hazard of methylene blue.refractory methemoglobinemia with red Anaesthesia, 1979; 34: 181-182.blood cell exchange transfusion. Chest 27. Verive M, Kumar M.Meeting Abstracts, 2006; 130(4): 294. Methemglobinemia: Treatment and16. Ferraro-Borgida MJ, Mulhern SA, DeMeo Medication, e medicine from web med.MO, Bayer MJ. Methemoglobinemia Availablefrom perineal appliction of an anesthetic from: http://www.emedicine.medscape.cream. Ann Emerg Med, 1996; 27: 785- com/article/956528-8. treatment. Accessed in 2010.17. Mansouri A. Review: 28. Kaushik P, Zuckerman SJ, Campo NJ,Methaemoglobinemia. Am J Med Sci, Banda VR, Hayes SD, Kaushik R.1985; 29: 200-209. Celecoxib Induced18. Walley T, Flangan M. Nitrite-induced Methemoglobinemia. Annmethaemoglobinemia. Postgrad Med J, Pharmacother., 2004; 38: 1635–8.1987; 63: 643-644. Source of support: Nil19. Piotrowski. Further investigations on the Conflict of interest: None declared.evaluation of exposure to nitrobenzene.Br. J. Ind. Med., 1967; 24: 60-67.International Archives of Integrated Medicine, Vol. 1, Issue. 3, November, 2014. Page 43Copy right © 2014, IAIM, All Rights Reserved.

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