The patient is a 57-year-old African-American man with a history of well-controlled asthma treated with mometasone. He had a positive PPD test in the 1970s and presented to the pulmonary clinic for evaluation of chronic, progressive cough and abnormal chest imaging. The patient’s cough began approximately 2 months ago. His cough was initially nonproductive but progressed to become productive with thick, tenacious yellow-green sputum. He denied any weight loss, fevers, chills, or hemoptysis.
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Puzzler Answer and Case Report
An ABG. In this case, ABG showed: pH 7.35, paCO2 46 mmHg, paO2 324 mmHg. Methemoglobin reading was 38%.
Methemoglobinemia
CASE REPORT : a 35 year old Caucasian man was admitted for elective fusion of C5-C6, C6-C7 with an allograft and plating due to pain and left arm weakness. Past medical history was significant for exercise-induced asthma, gastroesophageal reflux disease, fibromyalgia, depression, and long-term narcotic use for his chronic neck pain. Medications on admission were quetiapine, sertraline, montelukast, gemfibrozil, omeprazole, otodolac, lortab, fentanyl patch, and cyclobenzaprine as needed. Following the procedure he received a patient-controlled infusion of morphine, valium, and oxycodone as needed in addition to his out-patient medications.
He was noted to have increasing oxygen requirements over the next several days. On hospital day 3 he complained of chest pain and shortness of breath, and was noted to have perioral and peripheral cyanosis. Pulse oximetry showed an oxygen saturation of 80%. The patient was placed on oxygen through a non rebreather mask. Basic metabolic panel, complete blood count, EKG and chest radiograph were all within normal limits. An arterial blood gas showed pH 7.35, paCO2 46 mmHg, paO2 324 mmHg, with a methemoglobin level of 38%. A bottle of benzocaine spray was noted at his bedside.
The patient was transferred to the intensive care unit and a single dose of methylyne blue 1 mg/kg was administered with rapid resolution of his symptomatic methemoglobinemia. He was discharged from the hospital without further complications.
DISCUSSION: Methhemoglobinemia was first described with nitrate pollution in the well water of New York in 1949.[1] In the following decades it was noted to be associated with hereditary G6PD deficiency.[2,3] It was first described in 1977 with the use of cetacaine spray (a topical anesthetic).[4] Methemoglobinemia results from the oxidation of ferrous (Fe2+ to ferric (Fe3+)which results in an increased O2-binding affinity shifting the oxygen dissociation curve to the left, thus decreasing O2 delivery. Clinical effects at high levels can result in cardiac arrythmias and ischemia, metabolic acidosis, coma, and even death. Treatment involves 1% methylene blue 1-2 mg/kg IV and supportive care.[5]
[1] Wood IR, Well water methemoglobinemia, NY State J Med 1949;49(21):2576.
Puzzler and case report submitted by:
Antonio Salud II, M.D.
Reviewed by:
MAJ Alexander Niven, MC, USA, FCCP
John Shigeoka, M.D.
