Vasoactive drugs and acute kidney injury.
ABSTRACT The use of norepinephrine, and probably vasopressor therapy in general, in intensive care patients with hypotensive vasodilatation despite fluid resuscitation and evidence of acute kidney injury remains the subject of much debate and controversy. Although there is concern about the use of these drugs, these concerns are unfounded. At this time, the experimental and human data strongly suggest that, in these patients, vasopressor therapy is safe and probably beneficial from a renal, and probably general, point of view. On the basis of currently available evidence, in hypotensive vasodilated patients with acute kidney injury, restoration of blood pressure within autoregulatory values should occur promptly with noradrenaline and be sustained until such vasodilatation dissipates. The additional role of other vasopressors in these situations remains unclear. The addition of vasopressin may be helpful in individual patients, but widespread use is not supported by evidence. Alpha-dose dopamine has no advantages over noradrenaline and is not as reliably effective in restoring blood pressure and urine output. Its widespread use cannot be supported in patients with vasodilatation and acute kidney injury. Other vasopressor drugs such as epinephrine and phenylephrine may be similar in efficacy to noradrenaline. However, experience and available data with their use is vastly less than with noradrenaline. Adrenaline, in addition, is associated with hyperglycemia, hyperlactatemia, acidosis, and hypokalemia. Terlipressin appears useful in patients with acute kidney injury secondary to hepatorenal syndrome. Whether it is superior to noradrenaline in this setting remains uncertain, and more studies are needed before recommendations can be made.
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ABSTRACT: Acute kidney injury is commonly encountered in critically ill patients, and is associated with worse outcomes. Fluid therapy is a key component in the management of these patients, often leading to fluid overload, especially in the setting of septic acute kidney injury. Emerging data overwhelmingly suggest that fluid overload in these patients may be associated with adverse outcomes. Management of such patients should include a strategy of early guided resuscitation, followed by careful assessment of fluid status, and early initiation of renal replacement therapy as soon as it is deemed safe, aiming for a neutral or negative fluid balance. This review will focus on the pathophysiological link between fluid overload and acute kidney injury, mechanisms of organ dysfunction in fluid overload, and strategies for management.Hemodialysis International 10/2010; 14(4):348-54. · 1.44 Impact Factor
Article: [Acute kidney injury].[Show abstract] [Hide abstract]
ABSTRACT: Acute kidney injury (AKI) is defined as an abrupt decline in the glomerular filtration rate with accumulation of nitrogenous waste products and the inability to maintain fluid and electrolyte homeostasis. Occurring in 7% of all hospitalized patients and 28% to 35% of those in intensive care units, AKI increases hospital mortality. Early evaluation should include differentiating prerenal and postrenal components from intrinsic renal disease. Biological markers can give early warning of AKI and assist with differential diagnosis and assessment of prognosis. The most effective preventive measure is to maintain adequate circulation and cardiac output, avoiding ischemia- or nephrotoxin-induced injury. To that end, patients and situations of risk must be identified, hemodynamics and diuresis monitored, hypovolemia reversed, and nephrotoxins avoided. Protective agents such as sodium bicarbonate, mannitol, prostagiandins, calcium channel blockers, N-acetyl-L-cysteine, sodium deoxycholate, allopurinol, and pentoxifylline should be used. Treatment includes the elimination of prerenal and postrenal causes of AKI; adjustment of doses according to renal function; avoidance of both overhydration and low arterial pressure; maintenance of electrolytic balance, avoiding hyperkalemia and correcting hyperglycemia; and nutritional support, assuring adequate protein intake. For severe AKI, several modalities of renal replacement therapy, differentiated by mechanism and duration, are available. Timing--neither the best moment to start dialysis nor the optimal duration--has been not established. Early detection of AKI is necessary for preventing progression and starting renal replacement therapy at adjusted doses that reflect metabolic requirements.Revista espanola de anestesiologia y reanimacion 01/2011; 58(6):365-74.
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ABSTRACT: Volume substitution represents an essential component of intensive care medicine. The amount of fluid administered, the composition and the timing of volume replacement seem to affect the morbidity and mortality of critically ill patients. Although restrictive volume strategies bear the risk of tissue hypoperfusion and tissue hypoxia in hemodynamically unstable patients liberal strategies favour the development of avoidable hypervolemia with edema and resultant organ dysfunction. However, neither strategy has shown a consistent benefit. In order to account for the heavily varying oxygen demand of critically ill patients, a goal-directed, demand-adapted volume strategy is proposed. Using this strategy, volume replacement should be aligned to the need to restore tissue perfusion and the evidence of volume responsiveness. As the efficiency of volume resuscitation for correction of tissue hypoxia is time-dependent, preload optimization should be completed in the very first hours. Whether colloids or crystalloids are more suitable for this purpose is still controversially discussed. Nevertheless, a temporally limited use of colloids during the initial stage of tissue hypoperfusion appears to represent a strategy which uses the greater volume effect during hypovolemia while minimizing the risks for adverse reactions.Der Anaesthesist 02/2011; 60(5):457-64, 466-73. · 0.85 Impact Factor