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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 9  |  Issue : 3  |  Page : 439-441

An unusual case of methemoglobinemia resulting from self-administration of nitrobenzene in a psychiatric patient


1 Department of Emergency Medicine, Vinayaka Mission's Kirupananda Variyar Medical College & Hospital, Salem, Tamil Nadu, India

Date of Submission04-Aug-2022
Date of Acceptance29-Aug-2022
Date of Web Publication29-Sep-2022

Correspondence Address:
Dr. Chanjal Koonampadan Sathyan
Department of Emergency Medicine, Vinayaka Mission's Kirupananda Variyar Medical College & Hospital, Salem 636308, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mgmj.mgmj_129_22

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  Abstract 

Nitrobenzene, when consumed in large enough doses, can cause methemoglobinemia. By reducing oxygen unloading and oxygen binding, methemoglobinemia reduces oxygen delivery. This is a case of 55-year-old man who is a known case of psychiatric disorder was brought to the emergency room with an alleged history of deliberate consumption of nitrobenzene liquid approximately 10 mL in the morning of the day at his residence. He also instilled 2 drops in the right ear and was taken to a private hospital where the initial management with gastric lavage, multidose activated charcoal and methylene blue was given. He was then referred to the government tertiary care setting for further management. Prompt intravenous methylene blue treatment increases PaO2 in patients with methemoglobinemia.

Keywords: Acute poisoning, methemoglobinemia, nitrobenzene


How to cite this article:
Sathyan CK, Chidambaram, HS, Dominic M, Sirajudeen SA, Jinka VD. An unusual case of methemoglobinemia resulting from self-administration of nitrobenzene in a psychiatric patient. MGM J Med Sci 2022;9:439-41

How to cite this URL:
Sathyan CK, Chidambaram, HS, Dominic M, Sirajudeen SA, Jinka VD. An unusual case of methemoglobinemia resulting from self-administration of nitrobenzene in a psychiatric patient. MGM J Med Sci [serial online] 2022 [cited 2022 Nov 29];9:439-41. Available from: http://www.mgmjms.com/text.asp?2022/9/3/439/357487




  Introduction Top


Nitrobenzene is an aromatic substance that is frequently found in agricultural fertilizers. When consumed in large enough doses, it can cause methemoglobinemia. By reducing oxygen unloading and oxygen binding, methemoglobinemia reduces oxygen delivery.[1] For the manufacture of artificial solvents such as paint remover, a pale-yellow oily liquid nitrobenzene is used as an intermediary, having an aroma of bitter almonds. The foremost case of the poisoning of nitrobenzene was reported in the year 1886, and numerous reports of fatalities were reported thereafter.[2] Accidental or suicidal intoxication is a possibility, as is intoxication as a side effect of certain medications, such as metoclopromide. Patients who drink well water containing dangerously high levels of nitrites and nitrates are on the risk of accidental poisoning.[3] Inhalation and skin absorption are the two most typical methods of occupational exposure to nitrobenzene. Once nitrobenzene has been metabolized by the body, it is reduced to aniline. Methemoglobinemia is subsequently caused by the oxidation of the blood’s hemoglobin during this process.[4] A modified version of hemoglobin called methemoglobin (MetHb) occurs when the ferrous ion Fe2+ is oxidized to Fe3+ (ferric ion). As MetHb cannot bind to oxygen, it cannot transport oxygen. Less than 1% of MetHb can be tolerated by the human body, but any more is likely to result in methemoglobinemia.[5] We describe a case of self-administrated nitrobenzene poisoning in an old psychiatric male patient.


  Case report Top


A 55-year-old man who is a known case of psychiatric disorder was brought to the emergency room with an alleged history of deliberate consumption of nitrobenzene liquid approximately 10 mL in the morning of the day at his residence and instilled 2 drops in his right ear and was taken to a private hospital where the initial management with gastric lavage, multidose activated charcoal and methylene blue was given and referred to the government tertiary care setting for further management. The patient had a history of auditory hallucination and there is no history of breathlessness, seizures, nausea, vomiting, abdominal pain, chest pain, palpitation, and loss of consciousness. On arrival at the government hospital, the patient was alert, with a pulse rate of 78 per min, blood pressure of 130/90 mm Hg, and oxygen saturation (SpO2) of 93% at room air. His Glasgow coma scale reading was 15/15, respiratory rate was 16/min, and the airway was patent. Laboratory studies revealed an unremarkable complete blood count and comprehensive metabolic profile. Initial arterial blood gas measured pH, 7.51 (7.35– 7.45); pCO2, 31 mm Hg (35–45); pO2, 86 mm Hg (83–108); HCO3−, 24.5 mEq/L (22–26); SaO2, 97.6%; total calculated hemoglobin, 17.6 g/dL [Table 1] and [Table 2]. Patient was started on intravenous fluids, injection methylene blue, one proton pump inhibitor, multidose activated charcoal, enema, and other measures. Two sets of exchange transfusions were done. A psychiatry opinion was obtained. The patient improved symptomatically and was discharged.
Table 1: Arterial blood gas analysis of the patient

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Table 2: Various laboratory parameters of the patient

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  Discussion Top


According to several sources, the fatal dose of nitrobenzene is in the range of 1–10 g. There are no consistent data involving fatalities and dose of ingestion, according to a review of published reports.[6] The rapid onset of methemoglobinemia impairs the ability of the hemoglobin to transport oxygen and results in a brownish discoloration of the blood. This effect of methemoglobinemia causes the toxic effects after nitrobenzene ingestion. Methemoglobinemia is a condition in which the iron in hemoglobin is oxidized from the ferrous (Fe2+) state to the ferric (Fe3+) state. Adenine dinucleotide (NADH)-dependent reaction, catalyzed by cytochrome b5 reductase, or an alternative pathway using the nicotine adenine dinucleotide phosphate (NADPH)-dependent MetHb reductase system are two ways that methemoglobin can be reduced enzymatically after it has been formed.[7] A history of chemical intake, the distinctive aroma of bitter almonds, the persistence of cyanosis while receiving oxygen therapy without serious cardiopulmonary disease, low arterial SpO2, and a normal ABG (calculated) SpO2 are all diagnostic indicators.[8] Blood that is dark brown and does not shake brilliant red suggests methemoglobinemia, which is corroborated by the dried blood’s chocolate red color. The Schrenk butanone test, blood levels of methemoglobin, and the presence of p-nitrophenol and p-aminophenol in the urine can all be used to confirm and estimate the existence of nitrobenzene compounds.[9]

The ideas of decontamination and symptomatic and supportive management provide the foundation for the suggested course of treatment. The preferred treatment for acquired (toxic) methemoglobinemia is methylene blue. If the methemoglobin levels are greater than 30%, it is an external cofactor that dramatically accelerates the NADPH-dependent methemoglobin reductase mechanism. It is injected intravenously at 1 to 2 mg/kg (up to 50 mg dosage in adults) over 5 min, with the option of repeating the procedure in an hour, if necessary.[10] At concentrations greater than 7 mg/kg, methylene blue is an oxidant and may result in methemoglobinemia in patients. Patients with G6PD deficiency should not use it because it may cause severe hemolysis. Antioxidant ascorbic acid may also be given to patients whose methemoglobin levels are more than 30%. N-acetylcysteine has been found to lower methemoglobin in recent research; however, it has not yet been licensed as a treatment for methemoglobinemia. In serious situations, exchange transfusion is recommended.[11]

Without going above the allowed dose, repeated little doses of methylene blue in this example were able to control the varying symptoms brought on by the body’s release of nitrobenzene from its storage.[12] A fresh blood transfusion increased the patient’s hemoglobin content and oxygen-carrying capability, which helped with their symptoms. In other cases, oral charcoal and purgation lasting up to 5 days helped to clear the body’s nitrobenzene stockpiles and stop the patient from further deteriorating. The prevention of kidney and liver failure, which have been mentioned as late effects, required a proper diet, enough urine output, and hepatoprotection. Forced diuresis improved discoloration and caused MetHb levels to drop quickly. Supplemental ascorbic acid is helpful in the ongoing therapy of methemoglobinemia.


  Conclusion Top


A successful patient outcome was made possible by prompt intravenous methylene blue treatment based on a clinical diagnosis of declining SpO2 unresponsive to oxygen with chocolate cyanosis and surprisingly increased PaO2. Symptoms may not manifest for several hours after exposure to methemoglobinemia-causing compounds such as nitrobenzene and aniline, which can be absorbed in a variety of ways. Businesses or persons handling such substances must implement a stringent maintenance system as well as a personal protection system, and have an access to prompt diagnosis and treatment at a connected medical facility.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Lee CH, Kim SH, Kwon DH, Jang KH, Chung YH, Moon JD Two cases of methemoglobinemia induced by the exposure to nitrobenzene and aniline. Ann Occup Environ Med 2013;25:31.  Back to cited text no. 1
    
2.
Al-Lawati A, Murch N Acquired methemoglobinemia. SQU Med J 2012;25:237-41.  Back to cited text no. 2
    
3.
Dutta R, Dube SK, Mishra LD, Singh AP Acute methemoglobinemia. Internet J Emerg Intensive Care Med 2008;11:1092-4051.  Back to cited text no. 3
    
4.
Gupta G, Poddar B, Salaria M, Parmar V Acute nitrobenzene poisoning. Indian Pediatr 2000;37:1147-8.  Back to cited text no. 4
    
5.
Martínez MA, Ballesteros S, Almarza E, Sánchez de la Torre C, Búa S Acute nitrobenzene poisoning with severe associated methemoglobinemia: Identification in whole blood by GC-FID and GC-MS. J Anal Toxicol 2003;27:221-5.  Back to cited text no. 5
    
6.
Pizon AF, Schwartz AR, Shum LM, Rittenberger JC, Lower DR, Giannoutsos S, et al. Toxicology laboratory analysis and human exposure to p-chloroaniline. Clin Toxicol (Phila) 2009;47:132-6.  Back to cited text no. 6
    
7.
Saxena H, Prakash Saxena A Acute methemoglobinaemia due to ingestion of nitrobenzene (paint solvent). Indian J Anaesth 2010;54:160-2.  Back to cited text no. 7
    
8.
Kaushik P, Zuckerman SJ, Campo NJ, Banda VR, Hayes SD, Kaushik R Celecoxib-induced methemoglobinemia. Ann Pharmacother 2004;38:1635-8.  Back to cited text no. 8
    
9.
Cefalu JN, Joshi TV, Spalitta MJ, Kadi CJ, Diaz JH, Eskander JP, et al. Methemoglobinemia in the operating room and intensive care unit: Early recognition, pathophysiology, and management. Adv Ther 2020;37:1714-23.  Back to cited text no. 9
    
10.
do Nascimento TS, Pereira RO, de Mello HL, Costa J Methemoglobinemia: From diagnosis to treatment. Rev Bras Anestesiol 2008;58:651-64.  Back to cited text no. 10
    
11.
Yildirim B, Karagoz U, Acar E, Beydilli H, Nese Yeniceri E, Tanriverdi O, et al. A case report of prilocaine-induced methemoglobinemia after liposuction procedure. Case Rep Emerg Med 2015;2015:282347.  Back to cited text no. 11
    
12.
Sahu KK, Dhibar DP, Gautam A, Kumar Y, Varma SC Role of ascorbic acid in the treatment of methemoglobinemia. Turk J Emerg Med 2016;16:119-20.  Back to cited text no. 12
    



 
 
    Tables

  [Table 1], [Table 2]



 

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