Furosemide
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Anuria and azotaemia: case report A 48-year-old man developed anuria and azotaemia during treatment with furosemide. The man, who had dilated cardiomyopathy, chronic heart failure and metabolic syndrome, had developed myocardial infarction two times in 1998 and 1999, respectively. This was followed by coronary angioplasty and stenting of the left anterior descending artery of the left coronary branch. For his ventricular tachycardia, an implantable cardioverter defibrillator (ICD) was placed in 2001. In May 2003, he was upgraded to a biventricular (BiV) ICD. Due to early dysfunction of left ventricular pacing and technical difficulties with reimplantation, the revision ended in August 2003 only with bifocal (BiF) pacing. He was scheduled for an orthotopic heart transplantation. However, orthotopic heart transplantation was abandoned in October 2003 due to a weight of 124kg (required weight 100kg). He had been receiving treatment with furosemide 125mg, spironolactone, isosorbide mononitrate, quinapril, hydrochlorothiazide, carvedilol and digoxin. Also, diet modification was performed. He underwent elective coronary angioplasty and stenting on the circumflex branch. In the meantime, he was repeatedly hospitalised for circulatory decompensation and ventricular tachycardia. In April 2004, he was again admitted for severe dyspnoea. A rapid weight gain, low diuresis, swelling, ventricular tachycardia and blood pressure 90/60mm Hg, hyperglycaemia, hepatopathy, hypokalaemia and hyponatraemia were noted. He was continued on IV furosemide 500 mg/day, which led to a negative fluid balance and drop in body weight. Repeat monomorphic VT at 145 /min was below the ICD detection limit before ICD reprogramming. It always ended spontaneously before the application of an external electric shock, once it caused a short unconsciousness. He was gradually switched to oral furosemide, which resulted in anuria and azotaemia [duration of treatment to reactions onsets not stated]. At the same time, hypotension was also noted. Therefore, he was started on levosimendan [Simdax] infusion 12.5 mg/24h. Within several hours, his diuresis restored. Levosimendan increased myocardial contractility and cardiac output. However, asynchrony of left ventricular myocardial contraction still persisted. Due to this partial success of the levosimendan infusion, an attempt to reposition the LV electrode into the coronary sinus and improve the contractile synchrony of the left ventricle by BiV pacing was made. A further reduction in the size of the left ventricle, left atrium, and a reduction in mitral regurgitation as measured immediately after BiV implantation was noted. Thereafter, no IV diuretics were administered, yet the diuresis lasted around two liters per day. Consequently, his weight decreased to 94kg. He was stabilised. Blood pressure of 120/80mm Hg was achieved. His metabolic condition improved. Therefore, he was transferred to transplant cardiocentre with a new proposal for orthotopic heart transplantation. During the next ten months, he was a
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