Successful treatment of an apparently terminal stage of heart failure with anasarca resulting in achieved cardiac compensation: A case report

Introduction: Chronic heart failure (CHF) represents the end stage of various cardiovascular diseases and is one of the leading causes of hospitalization and mortality in the elderly population. Decompensated chronic heart failure (DCHF), with or without acute exacerbation, often leads to circulatory congestion and fluid accumulation, with anasarca (generalized edema)being one of the most severe manifestations, along with cardiac cachexia. In addition to the four “pillars” of CHF treatment across different severity stages according to the New York Heart Association (NYHA) classification, diuretic therapy remains the cornerstone of treatment in the terminal stage with severe systemic congestion, such as anasarca. Diagnostic and therapeutic challenges are frequently present due to comorbidities such as chronic kidney disease and anemia. Case report: An 88-year -old male patient with a history of chronic heart failure with reduced left ventricular ejection fraction (HFrEF), permanent atrial fibrillation, and significant comorbidities: stage 3b chronic kidney disease and severe iron-deficiency anemia. On admission, the patient presented with dyspnea at rest, tachypnea, bilateral hydrothorax, severe edema of the lower legs and forearms (anasarca), and marked general weakness. Laboratory findings showed elevated NT-proBNP levels, markedly reduced hemoglobin (68 g/L), aggravated by hemodilution, and impaired renal function (glomerular filtration rate, GFR = 44 mL/min/1.73 m²). Echocardiography revealed left ventricular dilation (end-diastolic diameter, EDD= 59mm) and left atrial enlargement (left atrial volume index, LAVI = 45 mL/m²), an inferior wall scar with an aneurysm of the basal inferior segment, and anteroseptal -apical dyskinesia. The left ventricular ejection fraction was significantly reduced (EF = 37%). The right ventricular systolic pressure (RVSP) was 64 mmHg, global longitudinal strain (GLS) was 11.6%, and there were signs of grade II diastolic dysfunction (E/e’ = 15.0). The therapeutic approach included urgent parenteral administration of high-dose furosemide over three days in a day-hospital setting (the patient refused hospitalization and blood transfusion). Optimization of chronic therapy was performed, including the introduction of sacubitril/valsartan (ARNI) and sodium glucose co-transporter 2 (SGLT2) inhibitors, along with restriction of salt and fluid intake and more intensive correction of iron-deficiency anemia. During outpatient follow-up, significant improvement was achieved: marked diuresis, body weight reduction of 14 kg, excellent regression of edema, normalization of lung findings with a significant reduction in hydrothorax, improvement in EF to 47%, improvement in diastolic function (E/e’ = 13.6), and reduction of RVSP to 25 mmHg. Renal function normalized (GFR = 64 mL/min/1.73 m²), and hemoglobin increased to 128 g/L. Conclusion: This case report highlights the importance of individualized intravenous diuretic therapy in combination with contemporary pharmacological strategies in patients with the most severe form of decompensated chronic heart failure (NYHA class IV) with anasarca. Timely initiation of parenteral diuretics, optimization of baseline therapy, and correction of associated disorders led to significant clinical, echocardiographic, and laboratory improvement. This report emphasizes the importance of continuous monitoring of critically ill patients using ECG monitoring and other vital parameters, as well as therapy adjustment according to diuresis, body weight, blood pressure, heart rate, and echocardiographic parameters, to achieve optimal outcomes alongside the management of comorbidities in consultation with other specialties