Medical Management of Acute Kidney Injury

Chapter 191

Medical Management of Acute Kidney Injury

The term acute kidney injury (AKI) has replaced the historical term acute renal failure because it is believed to better describe the pathophysiologic changes and duration of the different phases of injury. It is defined as the rapid loss of nephron function (over hours to several days) resulting in azotemia; fluid, electrolyte, and acid-base abnormalities; and uremia. Many causes of AKI have been identified in dogs and cats. Although supportive therapy is similar in all cases, the prognosis and clinical outcome have been shown to vary depending on the cause (Vaden et al, 1997).

AKI can be divided into four pathophysiologic stages. The first, initiation, occurs during and immediately following the renal insult when pathologic damage to the kidneys is occurring. The second stage is extension during which ischemia, hypoxia, inflammation, and cellular injury continue, leading to cellular apoptosis or necrosis. The initiation and extension stages usually last less than 48 hours, and clinical and laboratory abnormalities may not be apparent during this time. The third stage, maintenance, is characterized by azotemia, uremia, or both and may last for days to weeks. Oliguria (<1 ml of urine per kilogram of body weight per hour) or anuria (no urine production) may occur during the maintenance stage. Urine production can be highly variable. The fourth stage is recovery, during which azotemia improves and renal tubules undergo repair. Marked polyuria may occur during this stage as a result of partial restoration of renal tubular function and osmotic diuresis of accumulated solutes. Renal function may return to normal, or the animal may be left with residual renal dysfunction. This stage also may last for weeks to months. Nonazotemic renal failure can occur and is characterized by abnormalities similar to those seen during the polyuric recovery stage of AKI. Treatment of AKI consists of treatment specific for the cause and supportive therapy based on the stage of AKI and the animal’s fluid, electrolyte, and acid-base status. It is important to remember that the doses of drugs excreted primarily by the kidneys should be reduced or the dosing interval extended in proportion to the degree of azotemia.

Supportive Therapy

Fluid Therapy

Intravenous fluid therapy remains the mainstay of treatment for AKI. Frequent monitoring of the animal’s hydration status, renal function, acid-base status, and electrolyte levels is necessary to determine appropriate intravenous fluid types and amounts. Placement of a catheter in the jugular vein allows monitoring of central venous pressure and more precise assessment of intravascular volume status. However, if hemodialysis is a treatment option, the jugular veins should not be used for intravenous catheters or even for venipuncture to obtain blood samples; rather, they should be preserved for placement of a central catheter for hemodialysis or other renal replacement therapy (see Chapter 192).

The initial volume of fluid to be administered should be calculated based on the animal’s body weight and degree of hydration. Water deficits should be corrected within 4 to 6 hours to restore renal blood flow to normal as soon as possible. Maintenance fluid requirements (44 to 66 ml/kg/day) must be met and estimated fluid losses from vomiting or diarrhea replaced. Urine production should be monitored during the first few hours of fluid therapy. Placement of an indwelling urinary catheter is the most accurate method for such monitoring. However, the benefits of an indwelling catheter must be weighed against the risk of ascending infection and the need for sedation or anesthesia to place the catheter. The risk of infection can be reduced by scrupulous attention to sterile placement of the catheter, maintenance of a closed collection system, and daily cleansing of the visible portions of the catheter with disinfectant. Changing the urinary catheter every 2 to 3 days is recommended because the incidence of catheter-induced infections increases rapidly after 3 days when the same catheter is left in (Barsanti, 2010).

An isotonic, polyionic fluid such as lactated Ringer’s solution or Plasma-Lyte A may be administered initially. If hyperkalemia is present or suspected because of oliguria or anuria, use of a potassium-free fluid such as 0.9% sodium chloride is indicated. Following rehydration, the type of fluid should be adjusted based on the animal’s fluid and electrolyte status. Polyionic fluids may contain too much sodium for maintenance, and half-strength lactated Ringer’s solution or 0.45% sodium chloride in 2.5% dextrose may be used for long-term therapy.

Traditionally, intravenous fluids have been administered at as high a rate as the animal will tolerate without adverse signs, with the goal of maximizing glomerular filtration rate and renal blood flow and increasing elimination of metabolic waste products. However, an increase in fluid administration does not necessarily equate to increased urinary excretion of such substances. Recent studies in people have concluded that fluid overload is associated with adverse consequences and decreased survival; mortality decreased when fluid overload was corrected by dialysis (Bouchard et al, 2009). Although similar studies in clinical veterinary patients have not been reported, it would seem reasonable that avoiding fluid overload would be similarly beneficial, especially because dialysis is not readily available to many practices. One of the reasons for fluid overload is failure to adjust the fluid administration rate in the face of decreased urine production (see Chapter 186).

Management of Oliguria or Anuria

Once the animal has been hydrated, urine flow should increase rapidly to 2 to 5 ml/kg/hr, depending on the rate of intravenous fluid administration. If urine production is not sufficient, the clinician first should reassess the animal’s circulating blood volume. Such assessment may include physical examination of hydration status, visual estimation of jugular venous pressure, measurement of packed cell volume and total solids, thoracic radiography to evaluate cardiac size and pulmonary vascular markings, and ultrasonographic imaging of the cardiac chambers and hepatic veins. Failure to restore circulating volume to normal is a common reason for decreased urine volume. If circulating blood volume is normal or increased, the rate of fluid administration should be slowed to prevent fluid overload. An indwelling urinary catheter should be placed if not already present. Calculation of inputs and outputs then can be used to provide appropriate quantities of intravenous fluids to match urine output. The maintenance fluid requirement (estimated at 22 ml/kg/day for insensible losses) is calculated for a short interval of time, typically 4 hours. The volume of urine produced during the previous time interval is added to the maintenance amount to obtain the volume of intravenous fluids to be administered over the next 4-hour period. This protocol helps maintain hydration while minimizing the risk of fluid overload.

Specific therapy to increase urine flow, consisting of administration of one or more diuretics, should be instituted next (Table 191-1). Furosemide can be administered as a bolus of 2 mg/kg IV, with escalation of doses to 4 to 6 mg/kg at hourly intervals if the initial dose fails to increase urine production. However, constant-rate infusion (CRI) has been shown to be more effective in producing diuresis than intermittent bolus doses (Adin et al, 2003). A loading dose of 1.0 mg/kg followed by a CRI at 1.0 mg/kg/hr is recommended. If furosemide administration fails to increase urine flow, osmotic diuresis can be attempted. Twenty percent mannitol can be given as a bolus dose of 0.5 to 1 g/kg of body weight over 15 to 20 minutes. If it is effective, urine flow will increase within 1 hour. Repeat bolus doses then can be administered every 4 to 6 hours, or mannitol can be administered as a CRI at 1 to 2 mg/kg/min. Mannitol may have additional beneficial effects in addition to its action as a diuretic. It inhibits renin release because of its hyperosmolar effect on tubular luminal filtrate. Mannitol also acts as a free-radical scavenger, blunting damaging increases in intramitochondrial calcium, and may result in a beneficial release of atrial natriuretic peptide. In actuality, mannitol is used infrequently because administration of a hypertonic solution is contraindicated in oliguric animals that are volume overloaded, and oliguria often is not recognized until overload already is present. Dopamine infusion traditionally has been recommended for oliguric or anuric animals. However, it is no longer considered to have a role in the prevention or treatment of AKI in people, based on several metaanalyses that failed to show a clinical benefit with regard to survival or need for dialysis (Friedrich et al, 2005; Kellum and Decker, 2001). There is little or no documentation of the efficacy of dopamine in dogs and cats with AKI, and its routine use to increase urine production in oliguric or anuric AKI cannot be justified.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Medical Management of Acute Kidney Injury

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