Management of Acute Renal Failure

IN RESPONSE:

We coined the term pseudo ARDS to focus on a very common, clinically important situation in intensive care units. A parallel could be made between prolonged prerenal azotemia eventually leading to ischemic ATN. Prolonged pseudo or preadult ARDS may lead to ARDS in association with evidence of pulmonary capillary damage and stiff lungs, as diagnosed clinically by a decrease in pulmonary compliance. We use the term pseudo ARDS or pre-ARDS to describe a clinical syndrome of noncardiogenic pulmonary edema in the absence of evidence of decreased pulmonary compliance. We realize that many clinicians group these clinical entities together, independent of pulmonary compliance, as ARDS; we believe, however, that from a pathophysiologic, prognostic, and therapeutic viewpoint, these clinical entities may be substantially different.

Both pseudo ARDS and ARDS are frequently associated with sepsis. Studies in animals have shown that vasodilation with an arterial vasodilator, such as minoxidil, is associated with increases in albumin distribution space and a failure of interstitial hydrostatic pressure to rise during saline administration (1). These changes in interstitial Starling forces thus favor an increase in interstitial fluid volume during saline infusion. We frequently consult on ventilated patients with acute renal failure in the intensive care unit who have a 20-L positive fluid balance that has not been quantitatively recognized because the pulmonary capillary wedge pressures are not considered elevated (<18 mm Hg). Excess saline fluid has been administered to resuscitate the patient and has led to pulmonary edema, hypoxia, and ventilatory support. In the early stage, most of these patients do not have decreased pulmonary compliance, that is, stiff lungs. However, the mortality rate among them will ultimately be as high as 80%. It has been reported that patient mortality rates begin increasing after the patient has spent 48 hours on a respirator. The potential barotrauma, oxygen toxicity, and pulmonary infections that may occur with prolonged ventilatory support frequently lead to stiff lungs and what virtually all authorities would consider bona fide ARDS.

We believe that not distinguishing clinically between pseudo ARDS and ARDS may be detrimental to patients in the intensive care unit. Marked improvement in the pulmonary edema of pseudo ARDS after diuresis or ultrafiltration may allow much earlier extubation and removal of ventilatory support before ARDS develops. With ARDS and prolonged ventilatory support, mortality rates are very high, particularly in the presence of renal and multiorgan failure.

Randomized studies should be performed in septic patients to determine whether early resuscitation with limited volume expansion (for example, 2 to 3 L of saline), albumin, and vasopressin (which constricts vasodilated areas associated with sepsis, including skin, muscle, and splanchnic circulation), compared with large volumes of saline, can reduce the need for ventilatory support and the development of ARDS with decreased pulmonary compliance, and thereby improve survival.

Regarding Dr. Finucane's comments, it is important to emphasize that the urinary chemistry values in our table are generally applicable to both oliguric and nonoliguric ATN. Large daily volumes of glucose and water administered to burn patients with nonoliguric ATN were originally reported with low urinary sodium concentration of less than 10 mmol/L. However, in other settings, urinary sodium levels in nonoliguric patients with ATN generally exceed 30 mmol/L. Urinary sodium level and fractional excretion of sodium are usually somewhat lower in patients with nonoliguric ATN than in those with oliguric ATN but are generally well above those seen with prerenal azotemia (2).

• Copyright ©2004 by the American College of Physicians