Prevention of acute kidney injury and protection of renal function in the intensive care unit

Acute renal failure on the intensive care unit is associated with significant mortality and morbidity. To determine recommendations for the prevention of acute kidney injury (AKI), focusing on the role of potential preventative maneuvers including volume expansion, diuretics, use of inotropes, vasopressors/vasodilators, hormonal interventions, nutrition, and extracorporeal techniques. A systematic search of the literature was performed for studies using these potential protective agents in adult patients at risk for acute renal failure/kidney injury between 1966 and 2009. The following clinical conditions were considered: major surgery, critical illness, sepsis, shock, and use of potentially nephrotoxic drugs and radiocontrast media. Where possible the following endpoints were extracted: creatinine clearance, glomerular filtration rate, increase in serum creatinine, urine output, and markers of tubular injury. Clinical endpoints included the need for renal replacement therapy, length of stay, and mortality. Studies are graded according to the international Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) group system Several measures are recommended, though none carries grade 1A. We recommend prompt resuscitation of the circulation with special attention to providing adequate hydration whilst avoiding high-molecular-weight hydroxy-ethyl starch (HES) preparations, maintaining adequate blood pressure using vasopressors in vasodilatory shock. We suggest using vasopressors in vasodilatory hypotension, specific vasodilators under strict hemodynamic control, sodium bicarbonate for emergency procedures administering contrast media, and periprocedural hemofiltration in severe chronic renal insufficiency undergoing coronary intervention

Remifentanil in the intensive care unit: tolerance and acute withdrawal syndrome after prolonged

SEDATION in the intensive care unit should be minimized to reduce the duration of mechanical ventilation and its related complications.1 The drug regimen would ideally allow rapid awakening, to perform neurologic and respiratory evaluation on a daily basis.2,3 In this context, remifentanil, with its unique pharmacokinetic profile, should be considered an agent of choice.4,5 However, acute tolerance and even hyperalgesic response have been observed after opioid administration.6-8 In addition, withdrawal syndrome after cessation of opioid-based sedation has been seen in the intensive care unit setting.9-11 We report three cases of severe and fast-onset withdrawal syndrome, with signs of acute tolerance, after remifentanil-based sedation of between 2 and 30 days' duration, requiring reintroduction of remifentanil and then tapering over 24-48

Open surgical repair of ruptured juxtarenal aortic aneurysms with and without renal cooling: Observations regarding morbidity and mortality

ObjectivesLittle is known about the outcome of ruptured juxtarenal aortic aneurysm (RJAA) repair. Surgical treatment of RJAAs requires suprarenal aortic cross-clamping, which causes additional renal ischemia-reperfusion injury on top of the pre-existing hypovolemic shock syndrome. As endovascular alternatives rarely exist in this situation, open repair continues to be the gold standard. We analyzed our results of open RJAA repair during an 11-year period.DesignRetrospective observational study.Materials and methodsBetween July 1997 and December 2008, all consecutive patients with RJAAs were included in the study. Part of these patients received cold perfusion of the kidneys during suprarenal aortic cross-clamping. Perioperative variables, morbidity, and 30-day or in-hospital mortality were assessed. Renal insufficiency was defined as an acute rise of ≥0.5 mg/dL in serum creatinine level. Multiple organ failure (MOF) was scored using the sequential organ failure assessment score (SOFA score).ResultsA total of 29 consecutive patients with an RJAA, confirmed by computed tomography-scanning, presented to our hospital. In eight patients, the operation was aborted before the start of aortic repair, because no blood pressure could be regained in spite of maximal resuscitation measures. They were excluded from further analysis. Of the remaining 21 patients, 10 died during hospital stay. Renal insufficiency occurred in 11 out of 21 of the patients. Eleven out of 21 patients developed MOF postoperatively. In a subgroup of patients who received renal cooling during suprarenal aortic clamping, the 30-day or in-hospital mortality was two of 10 vs eight of 11 in patients who did not receive renal cooling (P = .03); renal insufficiency occurred in one out of 10 patients in the subgroup with renal cooling vs 10 out of 11 without renal cooling (P < .001) and MOF in two of 10 vs nine of 11, respectively (P = .009).ConclusionsOpen surgical repair of RJAAs is still associated with high mortality and morbidity. To our knowledge, this is the first report of cold perfusion of the kidneys during RJAA repair. Although numbers are small, a beneficial effect of renal cooling on the outcome of RJAA repair is suggested, warranting further research with this technique

Short-term effects of terlipressin bolus infusion on sublingual microcirculatory blood flow during septic shock

Terlipressin bolus infusion may contribute to overshooting increases in systemic vascular resistance with concomitant reductions in systemic blood flow and oxygen delivery. Whether these effects negatively impact on microcirculatory perfusion is still not known. The objective of the present study was, therefore, to elucidate the effects of a single terlipressin bolus dose of 0.5 mg on microcirculatory perfusion in patients with catecholamine-dependent septic shock. This prospective clinical cohort study was performed in a multidisciplinary intensive care unit at a university hospital. We enrolled 20 patients suffering from catecholamine-dependent septic shock. After restoring normovolaemia, norepinephrine (NE) was titrated to maintain mean arterial pressure (MAP) between 65 and 75 mmHg. Thereafter, all patients received a bolus infusion of 0.5 mg terlipressin, and NE was adjusted to maintain MAP between the threshold values. Sublingual microcirculatory blood flow of small vessels was assessed by sidestream dark-field imaging. All measurements, including data from right heart catheterization and NE requirements, were obtained at baseline and 6 h after terlipressin administration. Terlipressin stabilized haemodynamics and, at the same time, decreased NE requirements (0.42 +/- 0.67 vs. 0.74 +/- 0.73 mu g/kg per minute, p < 0.05). Whereas the pH and arterial lactate concentrations remained unchanged, microcirculatory flow index of small vessels had increased at the end of the 6-h study period (2.6 +/- 0.6 vs. 2.0 +/- 0.5 units, p < 0.05). In fluid-resuscitated patients with septic shock (with a MAP between 65 and 75 mmHg), a bolus infusion of 0.5 mg terlipressin was effective in reducing NE requirements without worsening microcirculatory blood flow. Randomized clinical trials are now warranted to verify these preliminary results