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a 56-year - old hispanic male presented to the emergency department for gradually progressive shortness of breath and chest tightness of 4-hour duration .
he was recently diagnosed with stage iv mantle cell lymphoma and had received his first cycle of r - chop ( rituximab , cyclophosphamide , doxorubicin , hydrochloride ( hydroxydaunomycin ) , vincristine sulfate ( oncovin ) , and prednisone ) chemotherapy 2 days prior to presentation .
rituximab infusion was postponed by 1 day due to inclement weather , and he received this 1 day prior to presentation .
he also received one dose of intravenous ( iv ) rasburicase 2 days prior to presentation .
he had been using emla ( eutectic mixture of topical 2.5% lidocaine and 2.5% prilocaine ) cream , 30 gm topically , around his port to minimize pain during infusions , the last application being 1 day prior to the presentation .
he denied any cough , fever , chills , sputum production , headache , or dizziness .
significant past medical history included corneal dystrophy , hyperlipidemia , hypertension , and gastro - esophageal reflux disease .
blood pressure was 146/81 mmhg , pulse rate was 92/min , respiratory rate was 24/min , and temperature was 98.4f .
he was alert and oriented to time , place , and person , and not in respiratory distress .
he had a port - a - cath in the right anterior chest with no erythema or discharge around the catheter entry site .
laboratory investigation showed a white cell count of 77,900/mm ( with differential count of neutrophils  85.9% , lymphocytes  0.8% ,
1.8% ) , platelet count of 394,000/mm , and hb of 9.3 g / dl .
leukocytosis was thought to be secondary to the dexamethasone and pegfilgrastim received 2 days ago .
serum uric acid was 0.6 mg / dl ( 3.47.8 mg / dl ) , creatinine 0.77 mg / dl ( 0.51.5 mg / dl ) , and potassium 3.9 meq / l .
the patient was placed on non - invasive , positive pressure ventilation because of persistent hypoxia via facemask , but his pulse oximetry remained at 86% with 100% fractional inspiration of oxygen ( fio2 ) .
arterial blood gas ( abg ) on 100% fio2 revealed pao2 215.6 ( normal 7590 mmhg ) , ph 7.45 ( normal 7.367.46 ) , pco2 42.6 ( normal 3446 mmhg ) , bicarbonate 29.5 ( normal 2227 meq / l ) , base excess 5 ( normal 2 to 2
t changes and cardiac enzymes were within normal range . computed tomography scan of the chest was negative for pulmonary embolism and other abnormalities .
saturation gap between the oxygen saturation in pulse oximetry and arterial blood gas analysis led to a high suspicion of acquired methemoglobinemia .
methemoglobin level ( methb ) was 8.4% ( normal 0.41.5% ) and carboxyhemoglobin level was 3% ( normal 12% ) . although his symptoms were improved with oxygen therapy , he was given one dose of 100 mg ( 1 mg / kg ) of intravenous methylene blue in the emergency department due to persistent hypoxia , and transferred to intensive care unit .
repeat methb level was still significantly elevated at 7.3% 2 hours later ; hence , a repeat dose of methylene blue was given .
although a third dose was planned , his hemoglobin ( hb ) level dropped to 6.6 g% from 9.3 g% .
iu / l ) , haptoglobin < 1.0 ( normal 36195 mg / dl ) , total bilirubin 2.4 mg / dl ( normal 0.21.1 mg / dl ) , and direct bilirubin 0.5 mg / dl ( normal 00.4 mg / dl ) .
the third dose of methylene blue was held and he was transfused with four units of packed red blood cells . given the clinical situation of methemoglobinemia , unresponsive to iv methylene blue , and hemolysis after iv methylene blue in the background of recent use of rasburicase , occult g6pd deficiency was suspected .
g6pd level was low ( 1.5 /g hb ) ( normal 8.813.4 /g hb ) , which is diagnostic for g6pd deficiency .
methb level normalized the next day and he was transferred out of the intensive care unit and then discharged from the hospital .
methemoglobin ( methb ) is constantly produced in the red blood cells by autoxidation of hemoglobin .
its level is maintained in a steady state of less than 2% of total hemoglobin ( 3 ) .
the major pathway is cytochrome b5 reductase pathway ( also called nicotinamide adenine dinucleotide - dependent methb reductase ) .
the second one is nicotinamide adenine dinucleotide phosphate ( nadph)dependent methb reductase , which requires a cofactor such as methylene blue or riboflavin for activation . the latter is clinically important for the treatment of methemoglobinemia by intravenous methylene blue ( 4 ) .
exposure to oxidizing agents can result in excessive formation of methb , which can lead to clinically significant methemoglobinemia , resulting in tissue hypoxia and death ( 4 , 5 ) .
patients usually develop cyanosis without any symptoms in levels of 1020% , with confusion starting above these levels and progressively worsening symptoms as the level increases resulting in coma , cardiovascular collapse , and death in levels above 70% ( 1 , 6 ) .
the most common oxidizing agents are dapsone , topical anesthetic agents ( benzocaine , lidocaine , and prilocaine ) , nitrites , and aniline dyes ( 7 ) .
rasburicase is a recombinant uric acid oxidase and converts uric acid to water - soluble allantoin , and hydrogen peroxide , which is responsible for methemoglobinemia and hemolysis , especially with concurrent g6pd deficiency ( 8) .
onset can be as early as 90 min from administration of rasburicase to beyond 6 hours ( 9 ) . as our patient did not have any evidence of tumor lysis syndrome , and as rituximab is not listed as an oxidizing agent , a combination of application of emla and recent use of rasburicase might have precipitated methb .
the lack of improvement in oxygen saturation with high - flow oxygen without any apparent causes and the gap in oxygen saturation > 5% between abg and pulse oximetry ( saturation gap ) are considered to be the diagnostic clues .
the diagnosis is confirmed by the level of methemoglobin in blood ( 1 , 6 ) . the treatment with specific antidote is usually recommended in patients with blood methemoglobin level of > 20% in symptomatic patients and > 30% in asymptomatic patients .
patients with significant other comorbid conditions , including severe anemia , heart disease , lung disease , or carbon monoxide poisoning , should be treated even if the blood methemoglobin level is as low as 10% .
however , symptoms may not always correlate with the level and clinical judgment is important for decision making ( 1 , 2 ) .
our case had occult g6pd deficiency and developed hemolysis after a second dose of iv methylene blue .
although the patient had received rasburicase almost 60 hours prior to the hemolytic episode , the long half - life of rasburicase might have played a role in the setting of occult g6pd deficiency .
screening for g6pd deficiency before rasburicase therapy would have cautioned against the use of methylene blue and subsequently prevented hemolysis .
it could have encouraged physicians to use an alternative therapy such as high - dose vitamin c , especially in the setting of methemoglobinemia .
in fact , it is the drug of choice in g6pd deficiency , acting independent of the nadph pathway ( 9 ) .
the diagnosis of g6pd deficiency in the suspected patient would require repeat testing in 23 months after the acute hemolysis episode resolves , if initial test is normal or borderline ( 10 ) .
the food and drug administration has a black box warning for both hemolysis and methemoglobinemia as contraindications to the use of rasburicase .
it is suggested that high - risk ethnicity for g6pd deficiency , including people of african american , african , mediterranean , and south asian descent , should be screened for g6pd deficiency before the administration of rasburicase ( 10 ) .
however , it may not be practical in an emergency situation , such as severe tumor lysis syndrome and severe methemoglobinemia , because it takes 2448 hours for test results to be available ( 8) . as our patient 's symptoms were improved on oxygen even before the first dose of iv methylene blue , he could have been simply observed with oxygen .
the decision was based on the basis of pulse oximetry , even though he did not have any tissue hypoxia and did not have any symptoms .
this would have avoided the treatment - related complications , including hemolysis and blood transfusion , which can be devastating .
non - improvement in oxygenation with high - flow oxygen without apparent causes and the saturation gap of > 5% between abg and pulse oximetry are considered to be the diagnostic clues .
the diagnosis is made by blood methemoglobin level . in patients with mild asymptomatic methemoglobinemia without any comorbid conditions
, it would be reasonable to simply observe and treat symptomatically to avoid severe treatment - related complications , especially in patients with suspected g6pd deficiency .
if we opt to treat these patients , treating with vitamin c would be a better choice .
the authors have not received any funding or benefits from industry or elsewhere to conduct this study .
acquired methemoglobinemia is a medical emergency , and its prompt recognition and treatment can avoid catastrophic complications including death 
 . however , in mild asymptomatic cases without any comorbid conditions , it would be reasonable to simply observe and treat symptomatically to avoid severe treatment - related complications , especially in patients with suspected glucose-6-phosphate dehydrogenase ( g6pd ) deficiency . 
 we present a case of mild methemoglobinemia in occult g6pd deficiency in which the patient developed hemolysis after treatment with intravenous methylene blue , requiring transfusion .