Motivation: Ever been stuck with diuresis? Every morning you are drawing even with fluid balance, and metolazone plus bumex is making no progress on the crackly lungs. Short of sending the patient to the ICU for ionotropes, is there anything else? Recently one of my fellow interns pointed out that prednisone may actually help with diuresis. I was at first skeptical. After all, with the mineralocorticoid activity of prednisone, I would expect prednisone to worsen diuresis. But, turns out that there is more to steroids. Prednisone also has renal vasodilatory effects and increases renal plasma flow and GFR. So, some data?
Paper: Zhang, H., Liu, C., Ji, Z. et. al. Prednisone Adding to Usual Care Treatment for Refractory Decompensated Congestive Heart Failure. Int. Heart J. (2008) 49: 587-95
Methods: The authors conducted an observational study in which patients were recruited who had been been hospitalized for at least one week for decompensated heart failure and had failed to respond to IV diuretics. Exclusion criteria included infection, cardiogenic shock, SBP<80 or >140, HFpEF, or myocarditis. Patients could receive IV ionotropes so long as they were maintaining blood pressure. Prednisone (1 mg/kg/day with max dose of 60 mg) was added to therapy for nine days. Primary end-points were urine volume, patient assessed dyspnea, changes in renal function, and physician assessed clinical status.
Results:
Cohort: The authors recruited 35 patients with median age of 52.3 years and gender distribution of 48.6% male. All patients were in class IV heart failure with all patients having LVEF less than 30%. Besides IV diuretics, 74% of patients (26/35) were also receiving IV ionotropes with the majority also getting IV nitroglycerine (91.4%, 32/35) and digoxin (82.9%, 29/35).
Outcomes: After nine days of prednisone therapy, mean urine output increased from 1400 mL/day to 2400 mL/day (statistically significant). Interestingly, the main jump in urine output occurred at day 3 when urine output jumped to about 2100 ml/day. Patient assessed dyspnea improved in 80% of patients (p<0.01). All but one patient were transitioned entirely to PO medications (off IV diuretics, ionotropes, or nitroglycerin) by day nine. GFR increased from baseline of 63.4 mL/min to 74.1 mL/min (p<0.05). Average weight loss was 3.17 kg.
Safety: There were no deaths. Prednisone therapy increased fasting glucose levels in diabetic patients but did not affect fasting levels in non-diabetic patients. There were no new infections noted in the cohort.
Discussion: This study could really benefit from a control group! The patients improved remarkably with prednisone administration, but one could also argue that if you stick with diuresis long enough, you will eventually make some headway. The argument made by the authors is that the patients had received conventional therapy for the week prior without improvement in clinical status. A concurrent control group or even a historical control group in the second week of therapy for CHF would make the case more convincing. On the flip side, 34 out of 35 patients progressed from decompensated CHF dependant on IV therapy to PO therapy. The progress was quite dramatic and may suggest benefit from prednisone. So, how does this change therapy? I would still not add prednisone to usual therapy for CHF, but if a patient presents with dyspnea along with the usual CHF/COPD combination, I would be less hesitant to add on the steroids. Also, this topic is a great mini research project for a retrospective outcomes analysis for CHF patients who got steroids (likely for COPD) compared to CHF patients who did not get steroids.
Paper: Zhang, H., Liu, C., Ji, Z. et. al. Prednisone Adding to Usual Care Treatment for Refractory Decompensated Congestive Heart Failure. Int. Heart J. (2008) 49: 587-95
Methods: The authors conducted an observational study in which patients were recruited who had been been hospitalized for at least one week for decompensated heart failure and had failed to respond to IV diuretics. Exclusion criteria included infection, cardiogenic shock, SBP<80 or >140, HFpEF, or myocarditis. Patients could receive IV ionotropes so long as they were maintaining blood pressure. Prednisone (1 mg/kg/day with max dose of 60 mg) was added to therapy for nine days. Primary end-points were urine volume, patient assessed dyspnea, changes in renal function, and physician assessed clinical status.
Results:
Cohort: The authors recruited 35 patients with median age of 52.3 years and gender distribution of 48.6% male. All patients were in class IV heart failure with all patients having LVEF less than 30%. Besides IV diuretics, 74% of patients (26/35) were also receiving IV ionotropes with the majority also getting IV nitroglycerine (91.4%, 32/35) and digoxin (82.9%, 29/35).
Outcomes: After nine days of prednisone therapy, mean urine output increased from 1400 mL/day to 2400 mL/day (statistically significant). Interestingly, the main jump in urine output occurred at day 3 when urine output jumped to about 2100 ml/day. Patient assessed dyspnea improved in 80% of patients (p<0.01). All but one patient were transitioned entirely to PO medications (off IV diuretics, ionotropes, or nitroglycerin) by day nine. GFR increased from baseline of 63.4 mL/min to 74.1 mL/min (p<0.05). Average weight loss was 3.17 kg.
Safety: There were no deaths. Prednisone therapy increased fasting glucose levels in diabetic patients but did not affect fasting levels in non-diabetic patients. There were no new infections noted in the cohort.
Discussion: This study could really benefit from a control group! The patients improved remarkably with prednisone administration, but one could also argue that if you stick with diuresis long enough, you will eventually make some headway. The argument made by the authors is that the patients had received conventional therapy for the week prior without improvement in clinical status. A concurrent control group or even a historical control group in the second week of therapy for CHF would make the case more convincing. On the flip side, 34 out of 35 patients progressed from decompensated CHF dependant on IV therapy to PO therapy. The progress was quite dramatic and may suggest benefit from prednisone. So, how does this change therapy? I would still not add prednisone to usual therapy for CHF, but if a patient presents with dyspnea along with the usual CHF/COPD combination, I would be less hesitant to add on the steroids. Also, this topic is a great mini research project for a retrospective outcomes analysis for CHF patients who got steroids (likely for COPD) compared to CHF patients who did not get steroids.
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