RESUMEN
Introduction: Though acetaminophen overdoses are common, acetaminophen induced methemoglobinemia is rare and it is thought to be due to oxidative stress from reactive metabolites. However, few prior cases of sulfhemoglobinemia in the setting of acetaminophen overdose have been reported. We report a case of mixed methemoglobinemia and sulfhemoglobinemia in the setting of a large, isolated acetaminophen ingestion. Case report: A 30-year-old African American male presented after intentionally ingesting 50 tablets of 500 mg acetaminophen two days prior. He was cyanotic and tachypneic. Peripheral oxygen saturation was 78 % on room air and minimally improved with high-flow oxygen. He was noted to have leukocytosis, thrombocytopenia, anion gap metabolic acidosis with lactic acidemia, acute kidney injury, transaminitis, hyperbilirubinemia, and coagulopathy. Arterial partial pressure of oxygen was normal. Methemoglobin and sulfhemoglobin concentrations were 8.5 % and 5.2 %, respectively. Along with intravenous N-acetylcysteine, methylene blue was administered without clinical improvement. Hemolytic anemia was subsequently noted. Glucose-6- phosphate dehydrogenase (G6PD) deficiency was then confirmed with a quantitative assay and genetic testing. He also received one dose of intravenous metoclopramide. The patient ultimately required eight units of packed red blood cells and several weeks of hemodialysis before discharge on hospital day 43. Discussion: Acetaminophen is structurally related to compounds known to cause methemoglobinemia and sulfhemoglobinemia. We hypothesize that these dyshemoglobinemias were triggered by acetaminophen-induced oxidative stress. The role of G6PD deficiency in the formation of sulfhemoglobinemia is unclear. Acetaminophen overdoses presenting with methemoglobinemia should prompt concern for underlying G6PD deficiency. Coincidental sulfhemoglobinemia should be considered if the clinical presentation is more severe than the methemoglobin concentration alone would suggest. Use of methylene blue in this case, despite the low measured methemoglobin percentage, which likely triggered hemolytic anemia; methylene blue use in a similar circumstance should be weighed carefully against the risk of harm.
RESUMEN
OBJECTIVE: To investigate 5 years' experience with fine needle aspiration (FNA) of salivary glands at a single academic center. STUDY DESIGN: A total of 191 salivary gland FNAs were performed at Louisiana State University Health Science Center from 2003 to 2007, and all were done on major salivary glands except for 1 case. RESULTS: The cytologic diagnoses included 17 malignancies, 6 atypia, 73 neoplasms, 87 negative and 18 nondiagnostic. Eighty-six cases had histologic follow-up (45.0%). There were 5 false negatives: 2 adenoid cystic carcinomas, 1 acinic cell carcinoma, 1 polymorphous low grade adenocarcinoma and 1 metastatic basaloid squamous cell carcinoma. The only false positive was a pleomorphic adenoma misdiagnosed as adenoid cystic carcinoma. Four reactive processes were diagnosed as benign neoplasms, including 2 granulomatous inflammation and 2 chronic sialadenitis. Five benign neoplasms were interpreted as reactive processes, including 2 Warthin's tumors, 2 sebaceous lymphoadenomas and 1 pleomorphic adenoma. The overall accuracy in distinguishing benign from malignant lesions was 79.1%, and the sensitivity for salivary neoplasia was 89.4%. CONCLUSION: Our results are consistent with the literature that salivary gland FNA has good sensitivity, specificity and accuracy in the diagnosis of salivary neoplasms. FNA can play a significant role in triaging patients with onsite cytologic interpretation and can reduce many unnecessary surgeries.
