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CASE REPORT
Year : 2012  |  Volume : 56  |  Issue : 4  |  Page : 397-400  

Acute methaemoglobinaemia initially treated as organophosphate poisoning leading to atropine toxicity


Department of Anaesthesiology, Mahadevappa Rampure Medical College, Gulbarga, Karnataka, India

Date of Web Publication8-Sep-2012

Correspondence Address:
Srinivas Kakhandki
Department of Anaesthesiology, Mahadevappa Rampure Medical College, Gulbarga, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5049.100836

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A case of unknown compound poisoning is presented. It was initially treated as organophosphate poisoning with lack of response. A timely diagnosis of acute methaemoglobinaemia and iatrogenic atropine toxicity was made based on clinical evaluation. Treatment of methaemoglobinaemia using oral methylene blue and of atropine toxicity with supportive measures could save the patient.

Keywords: Acute methaemoglobineamia, atropine toxicity, methylene blue


How to cite this article:
Kakhandki S, Yahya M, Praveen M. Acute methaemoglobinaemia initially treated as organophosphate poisoning leading to atropine toxicity. Indian J Anaesth 2012;56:397-400

How to cite this URL:
Kakhandki S, Yahya M, Praveen M. Acute methaemoglobinaemia initially treated as organophosphate poisoning leading to atropine toxicity. Indian J Anaesth [serial online] 2012 [cited 2020 Apr 4];56:397-400. Available from: http://www.ijaweb.org/text.asp?2012/56/4/397/100836


   Introduction Top


Suicide is a major cause of premature mortality globally, for which a variety of chemicals are used. The treatment of poisoning due to an unknown compound becomes a challenge. It becomes more difficult when laboratory support to detect a certain specific poison is unavailable. Inj. Atropine and inj. PAM (pralidoxime) are used as the universal antidotes by some physicians for all pesticides poisoning. The consequences of misusing these drugs are rarely reported in the literature. Hence, timely diagnosis and treatment of acute methemoglobinaemia and iatrogenic atropine toxicity based on clinical evaluation is reported.


   Case Report Top


A 40-year-old female was referred from a peripheral hospital as a case of organophosphate (OP) poisoning. She had consumed poison the previous night and was admitted in the afternoon of the next day, after a lapse of 12 h, to our hospital. She had vomited once, and had loss of consciousness for some time. She had received stomach wash, inj. Atropine and inj. PAM as treatment for presumed OP poisoning.

At the time of admission to our hospital, she was drowsy and cyanosis of nails and lips were present. The tongue was bitten and the patient was afebrile. Pulse rate was 84/min and blood pressure (BP) was 130/80 mmHg, respiratory rate (RR) was 10/min and the pupils were normal sized and reacting to light. SpO2 2 was 82-84% on room air. Oxygen (O2 2 ) supplementation was given with face mask. Inj. Atropine 3 mg IV stat was given and again 6 mg was repeated after 5 min, and then 1.8 mg hourly was continued. Inj. PAM 1 g IV and antibiotic were given. The serum cholinesterase level was 7850 U/L and the chest X-ray was normal.

After 2 h, the patient became irritable and tachypnoeic. SpO 2 was 82% with 8 L O 2 by mask. Pulse rate was 120/min and blood pressure was 130/80 mmHg, respiratory rate was 30/min and cardiovascular and respiratory systems were normal. Arterial blood gas (ABG) analysis showed pH of 7.39, PaCO 2 of 36.2 mmHg, PaO 2 of 68 mmHg and base excess of -2.4.

Based on clinical condition and ABG analysis, the patient was sedated and intubated and put on ventilatory support. The patient's condition remained the same over the next 24 h. Later, on Day 2, the patient became agitated and was febrile. The pupils were dilated and reacting to light and cyanosis was present. The pulse rate was 140/min and blood pressure was 140/92 mmHg. Cardiovascular and respiratory systems were normal. Abdomen was distended. SpO 2 was 84% with FiO 2 0.8 on SIMV mode. ABG was repeated and showed pH of 7.44, PaCO 2 of 37 mmHg, PaO 2 of 269 mmHg and base excess of -1.7.

The presence of clinical cyanosis with normal PaO 2 and low SPO 2 was highly suggestive of methemoglobinaemia, which was further corroborated by the bed side test, which showed the presence of dark brown colour in patient's blood that failed to turn bright red on shaking and later not turning to chocolate red on drying. [1]

A total of 50 mL of 1% methylene blue solution was given in two divided doses at an interval of half an hour through the Ryles tube as an IV preparation was not available. After 1.5 h, the SpO 2 increased to 94%. The patient's consciousness level improved and ventilatory support was continued.

The next day, on Day 3, the patient was conscious, alert and haemodynamically stable. Ventilatory support weaned off and the trachea was extubated and put on face mask. After about 6 h of extubation, the patient became restless, irritable and tachypnoeic and the pulse rate was 120/min, blood pressure was 130/100 mmHg and SpO 2 came down to 84%. ABG was done and showed pH 7.4, PaCO 2 36.8 mmHg, PaO 2 79 mmHg and base excess of -1.8.

The patient was reintubated and put on SIMV mode. This hypoxic state was suspected to be due to either atropine toxicity or due to methaemoglobinaemia as a result of release of poison from tissue stores. [1] Hence, atropine was stopped and a repeat dose of 50 mL of 1% methylene blue was given through the Ryle's tube. Ventilator support was continued overnight.

On the morning of Day 4, the patient was conscious, oriented and haemodynamically stable. SpO 2 was 98% with FIO 2 0.4. The patient was put on "T" piece for 2 h. ABG was done, which showed pH 7.42, PCO 2 37.6 mmHg, PaO 2 299 mmHg and base excess of -2.4. The patient was extubated and put on face mask. The patient was monitored for 48 h and then discharged from the Intensive Care Unit. Further recovery was uneventful.


   Discussion Top


Hospitals in rural areas bear the brunt of problems of poisoning, with case fatalities of 15-30%. These hospitals are not adequately staffed or equipped to deal with very sick patients. Intensive care beds and ventilators are in short supply and even unconscious patients are managed in open wards, with antidotes being poorly used or unavailable. Atropine and PAM are used as universal antidotes by some physicians for all pesticides poisoning. The consequences of misusing these drugs are rarely discussed in the literature. [2]

Atropine is the drug of choice for the treatment of OP nerve agent and insecticide intoxication. Adverse reactions to atropine may occur, and are of two types: toxic and allergic. [3],[4] Toxic reactions are the most common, which result from anti-muscarinic effects of the drug. For treatment, Inj. physostigmine IV is preferred, along with monitoring of respiratory functions, level of consciousness and ECG. In few case reports, toxicity was reversed without the use of antidotes, with respiratory and haemodynamic support. [5] In our case, which was a case of methaemoglobinaemia, inappropriate atropine therapy resulted in iatrogenic atropine toxicity, which was timely recognized, and the patient improved with stoppage of atropine, along with respiratory and haemodynamic support.

Methaemoglobin is a derivative of normal haemoglobin in which iron of the haem complex has been oxidized from ferrous to ferric form. It does not combine with O 2 and thus will not take part in O 2 transport. Concentration of methemoglobin in the blood is less than 1% normally. This reduction of methemoglobin is accomplished by two mechanisms. One is the hexose-monophosphate shunt pathway within the RBC and the second uses two enzyme systems: Diaphorase-I, which requires NADH and Diapharease-II, which requires NADPH enzyme. The term methaemoglobinemia is used to describe excess accumulation of methaemoglobin in RBC. [6]

Causes of methaemoglobinemia include ingestion of phenacetine, sulphonamide, primaquine, dapsone, nitrates, nitrites, nitrobenzene compounds, aniline dyes, deficiency of NADH/NADPH-haemoglobin reductase enzyme, abnormal haemoglobin with tendency to oxidize, etc. [6] [Table 1].
Table 1: Signs and symptoms that are correlated with methemoglobin percentage[7]

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Diagnosis is based on definite cyanosis in the absence of cardiorespiratory disease, which persist on O 2 therapy and low SpO 2 with normal PaO 2 on ABG (calculated SaO 2 ). [8] The blood has a chocolate-brown colour, which does not disappear on O 2 therapy. It can also be identified spectrophotometrically by its absorption band part of the spectrum at 630 nm. [6] Pulse oximetry behaves differently in methaemoglobinemia. Methaemoglobin causes optical interference to the pulse oximeter by falsely absorbing light, which leads to a plateau in the oxygen saturation at 85%. In methaemoglobinemia, the severity of the cyanosis or the percentage of methaemoglobin in the blood does not correspond to the pulse oximetry reading. The diagnosis can be confirmed by measurement of methaemoglobin by a multiple wavelength co-oximeter.

Treatment mainly involves gastric lavage, stopping further exposure through skin and respiratory tract and ventilator support may be required. Methylene blue is the antidote of choice for methaemoglobinaemia. It accelerates the NADPH-dependent methaemoglobin reductase system by acting as a co-factor. The initial dose is 1-2 mg/kg IV over 5 min. Response will occur within 1 h. [7] It can also be given orally. [7],[8] High absolute bioavailability of aqueous oral formulation makes it equally effective when administered orally. [9] Methylene blue is absorbed from the gastrointestinal tract. It is believed to be reduced in the tissues to leucomethylene blue. It is slowly excreted, mainly in the urine, together with some unchanged drug. In large doses, methylene blue can itself produce methaemoglobinemia. It should be used with caution in a renal impairment patient and in patients with G6PD deficiency and in pregnancy. [9]

A rapid disappearance of cyanosis in response to methylene blue would be expected within 1 hour, but may not occur if a patient has erythrocyte G6PD or NADPH-diaphorase deficiency or if methaemoglobin is due to ingestion of large amounts. A second dose may be required in these patients. [9]

In this case, the initial suspicion of OP poisoning made by the referral hospital and absence of clear signs due to the treatment initiated by them made us continue the same treatment as there was no facility to detect specific poisoning. Lack of response to treatment and clinical suspicion of methaemoglobinemia made us treat the patient with methylene blue. There was dramatic improvement in the patient's condition following this intervention, which was followed by deterioration. This deterioration was initially suspected to be due to atropine toxicity. Stopping of atropine and repeat dose of methylene blue improved the patient's condition.


   Conclusion Top


Cases of methaemoglobinaemia due to agricultural (nitrobenzene) compounds' poisoning can be mistakenly treated as OP compound poisoning using inj. Atropine and inj. PAM as universal antidote in the periphery, resulting in fatal outcome. Timely diagnosis of methaemoglobinaemia based on clinical findings and treatment with oral methylene blue and also recognizing atropine toxicity due to its inappropriate use can prevent complications.

 
   References Top

1.1. Gupta G, Poddar B, Salaria M, Parmar V. Acute nitrobenzene poisoning. Indian Pediatr 2000;37:1147-8.  Back to cited text no. 1
    
2.2. Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorous pesticide poisoning. Lancet 2008;371:597-607.  Back to cited text no. 2
    
3.3. Aguilera L, Martinez-Bourio R, Cid C, Arino JJ, Saez de Eguilaz JL, Arizaga A. Anaphylactic reaction after atropine. Anaesthesia 1988;43:955-7.  Back to cited text no. 3
    
4.4. O'Connor PS, Mumma JV. Atropine toxicity. Am J Ophthalmol 1985;99:613-4.  Back to cited text no. 4
    
5.5. Martinez-Mora B, Cristobo-Sáinz P, Nevado-Portero J, Domínguez-Petit A. A case of acute iatrogenic atropine poisoning. Rev Esp Cardiol 2011;64(Suppl 4):345.(single page,hence no page range)  Back to cited text no. 5
    
6.6. deGruchy's. Clinical hematology in medical practice. In: Frank F, Chesterman C, David P, Bryan R, editors. Disorders of hemoglobin.5 th ed. Berlin: Blackwell; 1998. p. 166-7.  Back to cited text no. 6
    
7.7. Abhishek S, Amrita C, Surender KG, Agarwal GR, Verma RK. Acute nitrobenzene poisoning: Case fatality and importance of methylene blue. Sri Lankan J Anaesthesiol 2010;18(Suppl 2):91-3. Available from: http://www.sljol.info/index.php/SLJA/article/view/1319/1998.  Back to cited text no. 7
    
8.8. Hema S, Anand P. Acute methemoglobinemia due to ingestion of nitrobenzene. Indian J Anaesth 2010;54:160-2.  Back to cited text no. 8
    
9.9. Walter-Sack, Jens R, Heike O, Juergen B, Olaf M, Peter M, et al. High absolute bioavailability of methylene blue given as an aqueous oral formulation. Eur J Clin Pharmacol 2009;65(1, Suppl 2):179-89.  Back to cited text no. 9
    



 
 
    Tables

  [Table 1]


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