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Corticosteroids are commonly used in the peri-operative setting for patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). The inflammatory response to CPB is associated with organ dysfunction and increased mortality. Corticosteroids reduce biochemical inflammatory markers associated with CPB, however the impact on clinical outcomes is mixed. The purpose of this article is to evaluate the evidence of changes in clinical outcomes associated with the peri-operative administration of corticosteroids in patients undergoing cardiac surgery with CPB. Randomized, placebo-controlled trials and meta-analyses were reviewed for evidence evaluating the impact of corticosteroids on clinical outcomes including mortality, myocardial infarction, atrial fibrillation (AF), duration of intubation, length of intensive care unit (ICU) or hospital stay, hyperglycemia, and gastrointestinal complications. Most of the relevant studies are underpowered to assess major clinical outcomes. Although corticosteroids likely reduce the risk of AF, this needs to be evaluated when used in addition to or in lieu of other anti-arrhythmic agents. Evidence does not equivocally support the use of corticosteroids to improve clinical outcomes in cardiac surgery patients.

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STUDY OBJECTIVE: Because alkalinization of the renal tubules can theoretically protect against the mechanisms of acute kidney injury, we sought to determine whether a sodium bicarbonate infusion can prevent acute kidney injury after cardiac surgery. DESIGN: Prospective, randomized, double-blind, controlled trial. SETTING: Cardiac surgery service in a community hospital. PATIENTS: Ninety-two patients with stage 3 or higher chronic kidney disease who underwent cardiac surgery using cardiopulmonary bypass. INTERVENTION: Forty-eight patients received a perioperative intravenous infusion of 0.9% sodium chloride 154 mEq/L, and 44 patients received an infusion of sodium bicarbonate infusion 150 mEq/L in 5% dextrose solution; the infusions were started 1 hour preoperatively and continued for 6 hours after cardiopulmonary bypass. MEASUREMENTS AND MAIN RESULTS: The primary outcome was the development of any stage of acute kidney injury within 5 days after surgery as defined by the Acute Kidney Injury Network criteria. No statistically significant difference in the primary outcome was noted between the two groups: 32% in the bicarbonate group versus 42% in the sodium chloride group (p=0.12). Likewise, no significant differences in the 30-day hospital mortality rate or other adverse outcomes were noted between the two groups. CONCLUSION: A perioperative infusion of sodium bicarbonate did not reduce the rate of acute kidney injury or adverse outcomes in patients with chronic kidney disease who underwent cardiac surgery.

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PURPOSE: The efficacy and safety of dexmedetomidine when used longer than the manufacturer-recommended 24 hours were evaluated. SUMMARY: Dexmedetomidine is the newest agent available for use in the critical care setting to induce and maintain sedation and analgesia. However, concerns over efficacy and safety during prolonged administration are a limiting factor for use in this patient population. A literature review was conducted to assess the clinical evidence regarding the efficacy and safety of dexmedetomidine for longer than 24 hours. A total of 11 studies were identified. Of these trials, 6 included adult patients and 5 included pediatric patients. Of the 6 adult trials, 3 comparative trials demonstrated a similar efficacy with benzodiazepines (i.e., midazolam and lorazepam) or propofol, with a reduction in the incidence of delirium and coma associated with dexmedetomidine. In noncomparative trials, dexmedetomidine was efficacious in achieving sedation goals with only mild adverse effects. In the 5 pediatric trials evaluated, efficacy to achieve a target sedation scale score could not be assessed, as most studies did not use validated sedation scales to measure goal sedation. Alternatively, the safety of dexmedetomidine has been demonstrated throughout an extended duration of use. In all of the studies evaluated, dexmedetomidine was associated with bradycardia; however, there were no reports of withdrawal effects, including rebound tachycardia and hypertension, upon discontinuation of dexmedetomidine infusion. CONCLUSION: Dexmedetomidine is an alternative to traditional sedatives and analgesics in critically ill patients. The safety and efficacy of dexmedetomidine in adults likely persist beyond 24 hours, without the emergence of rebound effects after discontinuation.

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Aprotinin is a serine protease inhibitor with antithrombotic, antifibrinolytic, and antiinflammatory effects. It is effective in reducing bleeding and the need for blood transfusions after cardiac surgery with cardiopulmonary bypass. Additional benefits, such as cerebral protection, are hypothesized but not yet thoroughly substantiated. The safety of aprotinin has been questioned based on a phase IV analysis of large data sets, including patients undergoing cardiac surgery. Potential risks including increased occurrences of stroke, myocardial infarction, renal failure, and death are implied by these analyses; however, adequate study group matching is lacking from these nonrandomized, retrospective studies. In October 2007, a large randomized controlled trial comparing antifibrinolytics in patients undergoing cardiac surgery was stopped after a preliminary analysis suggested a trend toward an increase in all-cause 30-day mortality associated with aprotinin. Subsequently, the manufacturer of aprotinin temporarily suspended marketing and halted all shipment of aprotinin on a worldwide basis. Pending a complete analysis of this study, the use of aprotinin could be considered as one component of a blood conservation strategy. After contemplating the benefits and risks of this controversial drug, clinicians should reserve its use for patients at high risk for postoperative blood loss.

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STUDY OBJECTIVES: To determine if aprotinin is safe and effective in patients at low risk for requiring blood transfusion after cardiac surgery by evaluating whether there is any significant difference in blood product use or other significant clinical outcomes between patients who received aprotinin versus those who did not. DESIGN: Retrospective review. SETTING: Inpatient community nonteaching hospital. PATIENTS: Three hundred thirty-five patients who underwent primary cardiac surgery involving cardiopulmonary bypass between November 1, 2003, and December 31, 2005, and were considered at low risk for requiring postoperative blood transfusion; 162 patients received aprotinin and 173 patients received aminocaproic acid (control). MEASUREMENTS AND MAIN RESULTS: Comparison of patients in the aprotinin group versus those in the aminocaproic acid group revealed no difference in total donor exposures to blood products (1.86 vs 1.16 units/patient, p=0.07), total packed red blood cells (PRBCs) received (1.25 vs 0.86 units/patient, p=0.09), postoperative donor exposures to blood products (0.91 vs 0.48 unit/patient, p=0.13), or postoperative PRBCs received (0.61 vs 0.40 unit/patient, p=0.23). No difference was noted in any other clinical outcome in the aprotinin group versus the aminocaproic acid group, including postoperative azotemia (13.0% vs 10.4%, p=0.46), new onset of atrial fibrillation (14.8% vs 15.0%, p=0.95), myocardial infarction, stroke, or death. Mean +/- SD total hospital length of stay was similar in the aprotinin group versus the aminocaproic acid group (8.1 +/- 3.8 vs 7.4 +/- 2.8 days, p=0.08), but length of stay from surgery to discharge was longer in the aprotinin group than in the aminocaproic acid group (5.9 +/- 0.17 vs 5.4 +/- 0.12 days, p=0.032). CONCLUSION: Although aprotinin appeared to be safe in this low-risk patient population, it was not more effective than aminocaproic acid in reducing blood product use after cardiac surgery. More robust evidence is needed from a controlled randomized trial to demonstrate the safety, efficacy, and pharmacoeconomic benefit of aprotinin.

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The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

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