Pre- and postoperative renal failure.

Abstract

The acute onset of oliguria and azotemia in the postoperative setting may be caused by pre-renal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history as noted above for clues regarding fluid balance, treatment with nephrotoxins, etc. The typical patient with prerenal azotemia will present with evidence of the recent onset of worsening of pre-existing cardiac disease, renal or gastrointestinal fluid loss, or the accumulation of acites, edema, or retroperitoneal fluid. In the absence of very recent diuretic therapy, he will be excreting a scant amount of concentrated (greater than 400 mOsm per L) sodium free (less than 10 to 20 mEq per L) urine. The serumBUN/Cr ratio is often greater than 15 to 20:1, and their urinary sediment will be bland. In an occasional patient in whom these studies give equivocal results, additional help may be obtained with measurements of central venous pressure (CVP) or pulmonary wedge pressure (PWP) and by noting their response to intravenous fluid loading. A rising CVP or PWP in the face of salt loading is, of course, evidence against prerenal azotemia. Patients with obstructive uropathies may be oligoanuric or polyuric-occasionally a characteristic alternating polyuria and oliguria is found (due to displacement of a stone or relief of edema). When oliguric their urine typically contains substantial amounts of sodium (greater than 20 mEq per L), is isotonic, and their OsmU:OsmP is les s than or equal to 1.2. Their urinary sediment will reflect the cause of their obstruction as noted above. A renal scan, ultrasound study, or infusion IVP are mandatory to rule out the possibility of obstructive uropathy. If these nonivasive studies are equivocal, one must consider doing a unilateral retrograde. The development of ATN usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients with be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per L of sodium. Their CrU:CrP is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. Those patients with nonoliguric ATN have urine outputs which may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful in this setting. Many such patients do have low (less than 20 mEg per L) urine sodium concentration and excrete isotonic urine.