A 66-year-old woman hospitalized for acute pulmonary edema presents with dyspnea, orthopnea, and bibasilar crackles. Vital signs: BP 168/94 mmHg, HR 118 bpm, RR 28/min, SpO2 88% on room air. Chest X-ray shows pulmonary edema. She receives aggressive intravenous furosemide therapy and subsequently develops tinnitus and bilateral high-frequency hearing loss. Serum creatinine is 1.8 mg/dL. She denies recent aminoglycoside or NSAIDs use. Which mechanism best explains this ototoxic adverse effect?
- A)Blue gray skin discoloration from antiarrhythmic therapy
- B)Immune hemolysis from central alpha 2 agonism
- C)Bronchospasm from muscarinic agonism
- D)Ototoxicity from loop diuretic therapyGABARITO
- E)Myopathy from HMG CoA reductase inhibition
Explicação
High dose loop diuretics can cause ototoxicity, especially when given rapidly intravenously or combined with other ototoxic drugs. The temporal association with aggressive furosemide therapy and tinnitus is classic. Ver explicação completa e trilha adaptativa →