Sir,A 21-year-old female presented with a complaint of dyspnea for the past 6 h. She was tachypneic and in obvious respiratory distress on inspection. Her oxygen saturation was 76% (at room air), pulse rate was 120/min, blood pressure was 150/90, and respiratory rate was 26/min. No adventitious sounds were heard on auscultation. Immediate resuscitative measures were started in the form oxygen supplementation and noninvasive ventilation support to decrease the respiratory distress. Bedside chest radiograph and echocardiography were within normal limits. She was a known case of mononeuritis multiplex and was on treatment with dapsone, methotrexate, and prednisolone apart from some other symptomatic medicines. Her complete blood count and urine examination were unyielding. Arterial blood gas (ABG) analysis was done which showed pH 7.48, pO2 268.1 (on oxygen), pCO2 24.5, bicarbonate levels as 18.9, SpO2 as 96.3%. The blood withdrawn for ABG was brownish. Furthermore, seeing the discrepancy between SaO2 (which was 96.3%) in ABG and SpO2 (76%) in finger pulse oximetry, methemoglobinemia was suspected. A repeat ABG was done for methemoglobin (MetHb) levels, which revealed 28.2% MetHb. As the detailed history was being taken from the family members simultaneously, it was revealed that the girl had ingested around 10 tablets of dapsone a few hours back with intent of suicide. With a working diagnosis of dapsone-induced methemoglobinemia, she was managed with intravenous methylene blue 4 ml 8 hourly along with other resuscitative measures. Gradually, her MetHb levels reduced to 10.3% in the next few days along with improvement in serial ABG reports [Table 1]. She was started on antidepressants after having appropriate consultation with the psychiatrist. The patient was maintaining saturation 96% at room air on the 4th day (pulse oximetry) and was discharged in a satisfactory condition.
Table 1
Serial arterial blood gas measurements
Serial arterial blood gas measurementsMetHb is formed when iron in the hemoglobin (Hb) changes from ferrous (Fe2+) to ferric (Fe3+) state. In healthy adults, 99% Hb is in Fe2+ state and remaining 1% is MetHb.[1] Increased fraction of MetHb impairs the oxygen-carrying capacity of Hb and hence leads to hypoxemia. MetHb concentration above 20% is associated with dizziness, fatigue, palpitations and above 40% is associated with arrhythmias, dyspnea, and seizures.[1] The diagnosis is usually made by a precipitating/trigger factor in history, and a typical “saturation gap” between oxygen saturation noted in pulse oximetry and ABG analysis.[2] Pulse oximetry can detect only oxyhemoglobin and deoxyhemoglobin. In the presence of MetHb, the oxygen saturation falls when detected via pulse oximetry but not when detected through ABG analysis. This saturation gap is very suggestive of the presence of an alternative form of Hb, especially MetHb.[2] In addition, the chocolate brown color of blood (detected while sampling) is again indicative of MetHb.[3] Apart from supportive care, specific treatment includes intravenous methylene blue 1–2 mg/kg body weight. In vivo, methylene blue is converted to leukomethylene blue which subsequently acts as electron donor to MetHb and reduces its concentration.[4] Hemodialysis may be the last resort in refractory cases.[2] Methemoglobinemia is an uncommon side effect of dapsone treatment, incidence reported in around 5% of cases. In addition, other drugs, namely antimalarials, sulfonamides, and prilocaine are also reported to cause similar adverse outcomes which the clinicians should be aware of.[5]
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