Managing acute kidney failure (Proceedings)


Managing acute kidney failure (Proceedings)

Nov 01, 2009

Treatment of acute kidney injury involves therapy for azotemia, extra renal manifestations, supportive care, and in some cases, therapy specific for the underlying disease process. Frequent monitoring of the patient is also necessary for a good outcome.

Fluid therapy

Fluid therapy is the mainstay of treatment for both acute and chronic kidney disease. Dehydration should be replaced with a balanced polyionic solution like LRS or Plasmalyte, but a solution with less sodium such as half-strength LRS is prudent for maintenance fluid needs. Sodium derangements should be reversed at the same rate at which they developed. Colloidal support (Hetastarch, Dextran, or plasma) may also be indicated depending on the clinical status of the patient.

Determining the amount of fluid to use in AKI is a challenge that requires frequent reassessment of the patient's status. Calculate an amount to rehydrate the patient (usually over 8 to 24 hours). If the patient appears hydrated, give 5% of body weight to account for undetectable dehydration. However, if the patient is anuric or oliguric, continued IV diuresis is not helpful and can be dangerous. For the oliguric or anuric patient, fluid administration may need to be guided by volume of urine output, or "Ins and Outs." The volume lost by a patient equals the insensible loss (respiration, stool) plus urine output plus ongoing losses (vomiting, fluid exudation into wounds, nasogastric suctioning, etc.). Insensible loss is 10 ml/lb/day (22 ml/kg/day). To measure urine output, use a urinary catheter and record volume produced at least every 4 to 6 hours, and replace this volume over the next 4 to 6 hours. Ongoing losses, like vomiting, diarrhea, gastric suction, etc. can be measured but are usually estimated.

If the patient is anuric, he will get only insensible loss. If he is overhydrated, withhold the insensible loss. Overhydration in an anuric patient or inability to start diuresis an oliguric or anuric patient is a clear indication for dialysis, which is the only other effective therapeutic option.

Converting oliguria to non-oliguria

There are a variety of methods to attempt to increase urine output. Before determining that oliguria is pathologic, ensure that the patient is adequately hydrated and has sufficient blood pressure to adequately perfuse the kidneys. The mean arterial pressure should be maintained above 60-80 mmHg, or the systolic pressure above 80-100 mmHg when measured by Doppler technology. Osmotic diuretics like mannitol are freely filtered at glomerulus but not reabsorbed by tubules. Increased osmolality of filtrate draws in water, increasing flow through the tubules without increasing GFR. The mannitol dose is 0.5 gm/kg over 5-10 minutes IV, up to a maximum of 2 gm/kg per 24 hours. Do not use mannitol in dehydrated or overhydrated animals; it can exacerbate pulmonary edema if the patient is overhydrated. Mannitol can also be used as constant rate infusion (CRI) of 1 mg/kg/min to decrease BUN in animals that are producing urine.

Chemical diuretics work by inhibiting Na+ carrier systems in tubules. Since different segments of tubules have different transport molecules, different drugs affect corresponding segment. Loop diuretics are most potent, since 25% of filtered sodium is resorbed in the loop of Henle. Thiazide diuretics work on the distal convoluted tubule, where 3-5 % of filtered sodium is resorbed. Spironolactone and other collecting duct diuretics are least potent, since only 1% of filtered sodium is available. Loop diuretics are the only ones helpful in converting oliguria or anuria. A starting dose for Furosemide (Lasix), a loop diuretic, is 2 mg/kg IV. If there is no urine production in 20-30 minutes, double the dose to 4 mg/kg. If there is still no urine in 20-30 minutes, increase the dose again (6-8 mg/kg). If still no response, add a second diuretic. High doses of furosemide (10 mg/kg) can cause ototoxicity. If the loading dose of furosemide induces urine production, it can be continued as a intermittent bolus (2 mg/kg q 6 hours) or a constant infusion (0.1 to 1 mg/kg/hr). Dehydration and electrolyte imbalances can be severe with higher doses of furosemide, if the patient is making urine. This increased urine flow does not increase GFR. In people, regardless of an effect on urine output, furosemide did not improve the outcome. IV diltiazem has been used to increase urine output.

Once a diuresis has been established, polyuria can be quite profound, and aggressive fluid support may be necessary to prevent additional prerenal insult from dehydration. Once the azotemia has resolved or reached a baseline, the fluid dose can be decreased by 10-20% per day. If the urine output diminishes by a corresponding degree and the azotemia does not return, continue tapering slowly. If the urine output does not diminish, the kidneys are unable to regulate fluid balance and further reduction in the fluid administered will lead to a dehydrated patient. It can take weeks for the kidneys to regain the ability to control fluid volume, but a rule of thumb used by some is to taper fluids over the same amount of time it took to diuresis them.