Refractory Congestive Heart Failure and Modest Renal Failure: II

Abstract

A 47‐year‐old male was admitted to the hospital because of progressive dyspnea leading to orthopnea. He had a history of insulin‐dependent diabetes mellitus for 23 years with nephropathy and mild renal insufficiency for two years. The patient had undergone triple vessel coronary artery bypass surgery five years prior. Ischemic cardiomyopathy was diagnosed two years previously when heart failure led to multiple hospital admissions. During the past year, congestive heart failure (CHF) was treated with increasing doses of furosemide (maximum 160 mg) and metolazone (10 mg), intermittent intravenous dobutamine, and amrinone infusions. A short trial of an angiotensin converting enzyme (ACE) inhibitor (captopril 12.5–50 mg/day) resulted in hyperkalemia and deterioration of renal function. On admission to the hospital, physical examination revealed a well‐developed and well‐nourished male in respiratory distress. Supine blood pressure was 90/60 mmHg. Jugular veins were distended up to the jaw. Heart rate was 90/min, regular. Heart sounds were distant but an S3 gallop was heard. Wet rales were heard bilaterally over the lungs. Liver was enlarged below the costal margin and was tender to touch. Pitting edema was present in both lower extremities up to the knees. Laboratory data: serum sodium was 130 mEq/l, potassium 5.7 mEq/l, blood urea nitrogen (BUN) 59 mg%, serum creatinine 4.9 mg%, hemoglobin 11.2 gm%. Chest X ray revealed cardiomegaly and pulmonary vascular congestion. EKG showed a normal sinus rhythm with first degree heart block and a left bundle branch block. Echocardiogram revealed moderate left ventricular dilation, moderate global hypokinesia, estimated left ventricular ejection fraction of 20%, mild right ventricular dilation, mild right atrial dilation, mitral regurgitation, and no pericardial effusion. The patient exercised for 4 min and 22 sec in a modified Naughton protocol. Heart response to exercise was accentuated and blood pressure response was flat. The patient received 200 mg of IV furosemide and 5 mg of metolazone with an increase in urine output of only 200 cc over a 2‐hr period. In a 24‐hr urine, output was only 950 cc. Urine sodium was 18 mEq/l, potassium 39 mEq/l, and osmolality 310 mOsm/kg. Because of the continued dyspnea and an arterial oxygen saturation of 68% despite 100% oxygen via face mask, the patient was subjected to 3 hr of isolated ultrafiltration using a femoral Quinton catheter. Three liters of fluid were removed with a drop in pulmonary wedge pressure to 20 from 27 mmHg. Subjectively, the patient started breathing better. Oxygen saturation improved. However, no increase in urine output was observed during the next 48 hr. The symptoms of CHF recurred. Isolated ultrafiltration was repeated with good result. Over the next week, it became apparent that the patient was dependent on ultrafiltration to maintain a symptom‐free status. It was decided to put the patient on chronic dialysis because of chronic renal failure and chronic heart failure. Following multiple discussions with the dialysis educator, the patient chose continuous ambulatory peritoneal dialysis (CAPD) as the form of chronic renal replacement therapy.