Enoxaparin and bleeding complications: a review in patients with and without renal insufficiency.

STUDY OBJECTIVE: To compare the frequency of bleeding complications from enoxaparin in patients with normal renal function versus patients with renal insufficiency. DESIGN: Retrospective chart review. SETTING: University-based tertiary care center. PATIENTS: One hundred six patients who received two or more doses of enoxaparin. MEASUREMENTS AND MAIN RESULTS: Total bleeding complications occurred in 22% of patients with normal renal function and 51% with renal insufficiency (p<0.01). Major bleeds were also significantly different, 2% and 30%, respectively (p<0.001). No patients with normal renal function were given fresh-frozen plasma or packed red blood cells, whereas in those with renal insufficiency, 13% and 32%, respectively, received these products (p<0.01). CONCLUSION: Enoxaparin may have resulted in increased bleeding complications and use of blood products in patients with renal insufficiency. Prospective studies need to be conducted to define the drug's role and dosage adjustments in these patients.

Contrast medium-induced nephrotoxicity: pathophysiology and prevention.

Contrast medium-induced nephrotoxicity (CMN) is a common form of iatrogenic acute renal failure. Typically, patients experience changes in serum creatinine or creatinine clearance between 1 and 5 days after exposure to a contrast medium, but they rarely require dialysis. The mechanism for CMN is not understood, but renal insufficiency, dehydration, and congestive heart failure are risk factors. The frequency of CMN with high-osmolality versus low-osmolality media is controversial. Prophylaxis can reduce CMN. Of many different strategies, hydration with normal saline before and after exposure offers the best protection with the fewest adverse effects.

Diuretic treatment for the sodium retention of congestive heart failure.

The use of diuretics for the treatment of sodium retention in congestive heart failure was evaluated. Particular focus was given to the altered renal response to diuretics in patients with heart failure and adverse responses to diuretic therapy. Highlighted information included historical aspects of the development of diuretics, mechanisms of sodium retention, the physiologic and clinical response to diuretics, and the altered pharmacokinetics and pharmacodynamics of diuretics in congestive heart failure. Despite more than 60 years of empiric diuretic use in heart failure, the actual database regarding the long-term efficacy, adverse effects, and altered mortality outcome in heart failure is relatively small. Existent pharmacokinetic and pharmacodynamic data are typically not collected within the context of heart failure efficacy trials. In addition to altered electrolyte transport and total-body electrolyte depletion, diuretics may be associated with adverse neurohormonal activation. Thus, guidelines for acute and long-term therapy with diuretics in heart failure remain somewhat empiric. Diuretics will remain a mainstay for the treatment of edema in congestive heart failure but must be accompanied by moderate sodium restriction. However, large clinical trials of diuretics would be necessary to demonstrate that improved clinical efficacy with edema reduction is not offset by adverse effects, which include electrolyte depletion, ventricular arrhythmias, and subsequent increased mortality.

Approaches to diuretic therapy and electrolyte imbalance in congestive heart failure.

This review has summarized the current role of diuretic therapy in heart failure, emphasizing those aspects most relevant to this patient population. Recommended diuretic usage is as follows: Asymptomatic left ventricular dysfunction--establish moderate sodium intake, Mild sodium retention--thiazide-type diuretic or low-dose loop diuretic; continue moderate sodium intake; combine with an ACE inhibitor, Moderate sodium retention--loop diuretic, adjusting for renal function, if necessary; continue moderate sodium intake; combine with an ACE inhibitor, Severe sodium retention--large-dose loop diuretic combined with a thiazide-type diuretic; continue moderate sodium intake; ACE inhibitor, unless contraindicated; consider addition of a potassium-sparing diuretic Treatment measures for refractory sodium retention--intermittent intravenous loop diuretic; short-term infusion of a loop diuretic; intensified combination oral diuretic therapy; intravenous positive inotropic therapy; ultrafiltration or dialysis. In addition, the well-known adverse effect of electrolyte depletion and guidelines for electrolyte replacement have been discussed. It is evident that the diuretic class of pharmacologic therapy has not been as well assessed as both the positive inotrope and vasodilator classes. Limitations in this regard have been summarized recently. Even relatively simple parameters or instruments, such as the sodium retention score, when applied to clinical trials will yield a greater understanding of the utility and limitations of diuretic therapy for heart failure.

Occurrence of nosocomial pneumonia in mechanically ventilated trauma patients: a comparison of sucralfate and ranitidine.

OBJECTIVE: To determine if there is a difference in nosocomial pneumonia frequency rate in mechanically ventilated trauma patients treated with sucralfate vs. ranitidine for stress ulcer prophylaxis. DESIGN: Prospective, randomized trial. SETTING: A 640-bed urban teaching hospital and trauma center. PATIENTS: Ninety-two mechanically ventilated trauma patients. INTERVENTIONS: Thirty-nine patients received sucralfate and 44 patients received intravenous ranitidine for stress ulcer prophylaxis; nine patients were excluded from the study for protocol breaks. MEASUREMENTS AND MAIN RESULTS: The study population was severely injured and critically ill. The Trauma Score averaged 11.3, the Injury Severity Score averaged 27.7, and the Acute Physiology and Chronic Health Evaluation (APACHE) score averaged 18.1. There were no significant differences in demographics, mechanisms of injury, Trauma Score, Injury Severity Score, APACHE score, length of hospital stay, length of surgical intensive care unit stay, or duration of endotracheal intubation between the sucralfate and ranitidine groups. Eleven (13.2%) patients developed nosocomial pneumonia: six (15.4%) of 39 patients in the sucralfate group and five (11.4%) of 44 patients in the ranitidine group; these numbers were not significantly different (chi 2 = 0.0226, p = .8805). There were no episodes of significant upper gastrointestinal bleeding. Six patients died during hospitalization, all secondary to severe head injury and none with pneumonia. CONCLUSIONS: There was no statistically significant difference in pneumonia rate in mechanically ventilated trauma patients receiving stress ulcer prophylaxis with sucralfate vs. ranitidine.

Long-term dobutamine therapy for refractory congestive heart failure.

The proposed benefit of long-term dobutamine therapy is explained, relevant clinical trials are described, and recommendations for this treatment are discussed. Dobutamine increases cardiac contractility and causes vasodilation with little change in heart rate. It is routinely administered for short periods to relieve exacerbations of congestive heart failure (CHF) in hospitalized patients. Sustained effects have been seen with dobutamine infusions, although the known properties of the drug do not explain these effects. Long-term dobutamine therapy can lessen the symptoms of CHF and improve exercise tolerance and cardiac function. Nine published reports showed consistent improvement in 77 patients treated with multiple infusions of dobutamine. At Ohio State University, long-term dobutamine therapy (typically 5.0-7.5 micrograms/kg/min infused continuously) is used in patients with refractory CHF and those awaiting heart transplantation. Because the therapy does not prolong survival in most patients, specific endpoints of therapy should be determined for each patient. Because it may cause sudden death, patients receiving this therapy must be carefully monitored. Long-term use of dobutamine infusion lessens the symptoms of CHF but does not prolong survival.