SUBASH MOHAN THULASI,ASHA GOPAN G P,SORNAVALLI VALLIAPPAN,S.T.SAKTHI SUGANYA,ANANTHAKUMAR P.K.,DR. MADHUMITHA M
DOI: https://doi.org/Chemotherapy-induced cardiomyopathy spans asymptomatic LV dysfunction to fulminant heart failure. We report a 42-year-old woman with metastatic caecal adenocarcinoma who received two fortnightly cycles of fluoropyrimidine-platinum chemotherapy. She remained well after the first cycle but developed progressive dyspnea and edema seven days after the second, presenting one week later in shock and hypoxemic respiratory failure. On arrival: pulse 130/min, unrecordable blood pressure, SpO₂ 88% on room air, elevated JVP, peripheral edema, and basal crepitations. ECG showed sinus tachycardia without ischemic changes. NT-proBNP was 32,300 and troponin-I 2.89; labs revealed hyponatremia and azotemia. Chest radiography demonstrated bilateral infiltrates with mild pleural effusions. Echocardiography showed severe global LV systolic dysfunction (LVEF ~15%) with moderate RV dysfunction and a plethoric non-collapsing IVC. Arterial blood gas confirmed type 1 respiratory failure (PaO₂ 58 mmHg). Thyroid function was normal; blood and urine cultures were negative. She received non-invasive ventilation, vasopressors, low-dose furosemide infusion, low-dose digoxin and spironolactone, and empiric antibiotics; she subsequently required intubation and intra-aortic balloon pump for refractory shock. Coronary and CT pulmonary angiography were not feasible due to instability. Despite escalation, she suffered cardiac arrest and could not be revived. This case underscores the potential for rapid, fatal cardiotoxicity after fluoropyrimidine-based therapy—even with a normal baseline evaluation—highlighting the need for early recognition, immediate drug cessation, phenotype-directed management, and cardio-oncology pathways.
