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Chapter: Clinical Anesthesiology: Perioperative & Critical Care Medicine: Critical Care

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Reversible Azotemia Versus AKI

It is important to differentiate prerenal and postrenal azotemia from renal azotemia.

REVERSIBLE AZOTEMIA VERSUS AKI

 

It is important to differentiate prerenal and postrenal azotemia from renal azotemia. Exclusion of postre-nal azotemia requires physical diagnosis and imag-ing, whereas exclusion of prerenal azotemia depends on the response to treatments aimed at improving renal perfusion. Diagnosis and treatment may be facilitated by analysis of urine (see Table 57–8); uri-nary composition in postrenal azotemia is variable and depends on the duration and severity of obstruc-tion. In prerenal azotemia, tubular concentrating ability is preserved and reflected by a low urinary sodium concentration and high urine/serum creati-nine ratio. Calculation of the fractional excretion of filtered sodium (F ENa+) may also be extremely use-ful in the setting of oliguria:


FENa+ is less than 1% in oliguric patients with prerenal azotemia but typically exceeds 3% in patients with oliguric AKI. Values of 1–3% may be present in patients with nonoliguric AKI. The renal failure index, which is the urinary sodium concen-tration divided by the urine/plasma creatinine ratio, is a sensitive index for diagnosing kidney failure. The use of diuretics increases urinary sodium excre-tion and invalidates indices that rely on urinary sodium concentration as a measure of tubular func-tion. Moreover, intrinsic kidney diseases that pri-marily affect renal vasculature or glomeruli may not affect tubular function and therefore are associated with indices that are similar to prerenal azotemia. Measurement of a 3-h creatinine clearance can esti-mate the residual glomerular filtration rate but may underestimate the degree of renal impairment if the serum creatinine concentration is still rising.

Etiology of AKI

 

Causes of AKI are listed in Table 57–9. Up to 50% of cases follow major trauma or surgery; in the majority of instances, ischemia and nephrotoxins are responsible. AKI associated with ischemia is often termed acute tubular necrosis. Postischemic acute tubular necrosis follows certain surgical pro-cedures more frequently than others: open abdomi-nal aortic aneurysm resection, cardiac surgery with cardiopulmonary bypass, and operations to relieve obstructive jaundice. Aminoglycosides, ampho-tericin B, radiographic contrast dyes, cyclosporine, and cisplatin are the most commonly implicated exogenous nephrotoxins. Amphotericin B, con-trast dyes, and cyclosporine also appear to produce direct intrarenal vasoconstriction. Hemoglobin and myoglobin are potent nephrotoxins when they are released during intravascular hemolysis and rhabdomyolysis, respectively. Cyclooxygenase inhibitors, particularly nonsteroidal antiinflam-matory drugs, may play an important role in at least some patients. Inhibition of prostaglandin


synthesis by the latter group of agents decreases prostaglandin-mediated renal vasodilation, allow-ing unopposed renal vasoconstriction. Other fac-tors predisposing to AKI include preexisting renal impairment, advanced age, atherosclerotic vascular disease, diabetes, and dehydration.

Pathogenesis of AKI

 

The sensitivity of the kidneys to injury may be explained by their very high metabolic rate and ability to concentrate potentially toxic substances. The pathogenesis of AKI is complex and probably has both a vascular endothelial and a renal epithe-lial (tubular) basis. Inadequate oxygen deliver to the kidney is the likely triggering event, leading to afferent arteriolar constriction, decreased glo-merular permeability, increased vascular perme-ability, altered coagulation, inflammation, leukocyte activation, direct epithelial cell injury, and tubular obstruction from intraluminal debris or edema. All can decrease glomerular filtration. A backleak of filtered solutes through damaged portions of renal tubules may allow reabsorption of creatinine, urea, and other nitrogenous wastes.

Oliguric versus Nonoliguric AKI

 

AKI is often classified as oliguric (urinary volume <400 mL/d), anuric (urinary volume <100 mL/d), or nonoliguric (urinary volume >400 mL/d). Nonoli-guric AKI accounts for up to 50% of cases. Urinary sodium concentrations in patients with nonoligu-ric AKI are typically lower than those in oliguric patients. In some studies, nonoliguric patients also appear to have a lower complication rate and to require shorter hospitalizations. In another study of AKI patients who required dialysis, nonoliguric AKI patients had a delayed initiation of dialysis, a longer hospital stay, and an increased likelihood of death. It was speculated that it might be possible to convert oliguric AKI into nonoliguric AKI by administering mannitol, furosemide, “renal” doses of dopamine (1–2 mcg/kg/min), or fenoldopam. Theoretically, the resulting increase in urinary output might be therapeutic by preventing tubular obstruction. How-ever, recent studies have found increased mortality in patients with AKI who received diuretics, and a meta-analysis showed no improvement in mortality or decrease in need for dialysis; therefore diuretics should not be routinely administered in AKI.

Treatment of AKI

 

AKI accounts for approximately 15% of ICU admis-sions. Despite advances in critical care medicine, the mortality rate for AKI remains approximately 50% and management is primarily supportive. Diuret-ics continue to be useful for conventional medical indications (eg, pulmonary edema or rhabdomy-olysis). AKI due to glomerulonephritis or vasculitis may respond to glucocorticoids. Standard treatment for oliguric and anuric patients includes restric-tion of fluid, sodium, potassium, and phospho-rus. Daily weight measurements help guide fluid therapy. Sodium and potassium intake is limited to 1 mEq/kg/d. Hyponatremia can be treated with water restriction. Hyperkalemia may require admin-istration of an ion-exchange resin (sodium polysty-rene), glucose and insulin, calcium gluconate, or sodium bicarbonate. Sodium bicarbonate therapy may also be necessary for metabolic acidosis when the serum bicarbonate level decreases to less than 15 mEq/L. Hyperphosphatemia requires dietary phosphate restriction and phosphate binders such as sevelamer, aluminum hydroxide, calcium carbon-ate, calcium acetate. The dosages of renally excreted drugs should be adjusted to the estimated glomeru-lar filtration rate or measured creatinine clearance to prevent accumulation.


 

Renal replacement therapy may be employed to treat or prevent uremic complications (see Table 30–6). A double-lumen catheter placed in the internal jugular, subclavian, or femoral vein is usu-ally used. The high morbidity and mortality rates associated with AKI would seem to argue for early dialysis, but supporting studies are controversial. Dialysis does not appear to hasten recovery but C may in fact aggravate kidney injury if hypotension occurs or too much fluid is removed.

Because of concern that intermittent hemodialy-sis associated with hypotension may perpetuate renal  injury, continuous renal replacement therapy (CRRT; continuous venovenous hemofiltration or continu-ous venovenous hemodialysis, which removes fluid and solutes at a slow controlled rate) has been used in critically ill patients with uremic AKI who do not tolerate the hemodynamic effects of intermittent “standard” hemodialysis. The main problem asso-ciated with CRRT is the expense, as the membrane is prone to clot formation and, therefore, must be periodically replaced. Despite this limitation, many experts believe CRRT is the best way to manage uremic ICU patients with AKI. The indications for CRRT are being expanded from oliguria and uremia to metabolic acidosis, fluid overload, and hyperkale-mia. Nevertheless, recent clinical trials have failed to show benefit of continuous technique over intermit-tent hemodialysis in these critically ill patients.

The nutritional management of AKI with ure-mia continues to evolve, and there is now consensus among nephrologists, intensivists, and nutritionists that nutrition should be provided, and 1.0–1.5 g/kg/d of protein can be given, particularly for patients on CRRT.

 

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