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Chapter 37 - Renal Function Monitoring


Solomon Aronson


Renal dysfunction remains a serious complication during the perioperative period in critically ill patients undergoing major surgery.[1] [2] [3] [4] [5] [6] [7] The onset of acute perioperative renal failure portends a poor prognosis from the loss of renal function with consequent volume and solute overload and from associated life-threatening complications, including sepsis, respiratory failure, gastrointestinal hemorrhage, and central nervous system dysfunction. Acute renal failure (ARF) requiring dialysis develops in 1% to 7% of patients after cardiac or major vascular surgery and is strongly associated with morbidity and mortality[8] [9] [10] [11] (see Chapter 50 and Chapter 52 ). The mortality rate of ARF was 91% during World War II, 68% in Korea, and 67% in Vietnam. Today, depending on associated comorbidities, postoperative renal failure is responsible for up to 60% mortality in the postoperative period. ARF in the presence of no other comorbidities has about a 10% to 40% mortality rate, whereas ARF in the intensive care unit setting carries a 50% to 80% mortality rate. [12] Perioperative renal failure accounts for one half of all patients requiring acute dialysis.[12] Perhaps one reason for the persistently frequent incidence of perioperative renal failure is a shift in medical populations to older and more critically ill patients undergoing increasingly higher-risk procedures. The persistently frequent incidence of perioperative renal failure observed may also result from our inability to adequately monitor renal function changes and to predict the onset of ARF in the operative and critical care setting.

An understanding of how to interpret information derived from monitoring presumes an understanding of terms used to describe the observations made. In the case of renal function monitoring, these assumptions may not always be warranted. Perioperative renal failure, for example, has been defined clinically as the need for postoperative dialysis or, in some cases, as a postoperative serum creatinine level exceeding a predetermined preoperative value (e.g., an increase of 0.5 mg/dL or of 50% or more). In one review,[13] no two studies of 26 defined ARF the same way. The overall reported frequency of ARF among all patients admitted to the hospital is 1%[14] and may increase to 2% to 5%[4] [15] during hospitalization; however, there is no universally accepted standard for detecting renal insufficiency or failure. Reporting on the cause, incidence, and management of renal dysfunction also varies greatly because of wide variations in the definition of terms used to describe degrees of renal dysfunction in the literature. It is not surprising therefore that an estimated 5% of the general population has renal disease (however defined) that is severe enough to adversely affect surgical outcome. [16]

Several mechanisms involving a renal tubule, a tubulointerstitial process, and a reduction in filtering capacity of the glomerulus have been implicated in renal dysfunction. Prerenal causes are responsible for most cases of perioperative ARF. Since World War II, it has become clear that ARF can result from decreased renal blood flow from myriad causes ( Table 37-1 ). Prerenal azotemia accounts for 70% of general community-acquired ARF[14] [15] and for


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TABLE 37-1 -- Causes of renal hypoperfusion associated with acute renal failure
Intravascular Volume Depletion
Major trauma, burns, crush syndrome
Fever
Hemorrhage
Diuretic use
Pancreatitis, vomiting, diarrhea, peritonitis, dehydration, NPO status, bowel preparations
Decreased Cardiac Output
Congestive heart failure or low output syndrome
Pulmonary hypertension, massive pulmonary embolism
Positive pressure mechanical ventilation
Increased Renal/Systemic Vascular Resistance Ratio
Renal vasoconstriction
  α-Adrenergic agonists
  Hypercalcemia, amphotericin
  Cyclosporine
System vasodilation
  Afterload reduction
  Antihypertensive medications
  Anaphylactic shock
  Anesthesia sepsis
Renovascular Obstruction
Renal artery: atherosclerosis, embolism, thrombosis, dissecting aneurysm, vasculitis
Renal vein: thrombosis, compression
Glomerular and Small-Vessel Obstruction
Glomerulonephritis
Vasculitis
Toxemia of pregnancy
Hemolytic uremic syndrome
Disseminated intravascular coagulation
Malignant hypertension
Radiation injury
Increased Blood Viscosity
Macroglobulinemia
Polycythemia
Interference with Renal Autoregulation
Prostaglandin inhibitors in presence of congestive heart failure (CHF), nephritic syndrome, cirrhosis, hypovolemia
Angiotensin-converting enzyme inhibition in presence of renal artery stenosis or CHF

more than 90% of perioperative ARF.[13] [17] Typically, an early compensatory phase of normal renal adaptation (e.g., pre-prerenal failure) progresses to become decompensatory as prerenal failure ensues.[18] ARF may be characterized as an abrupt decline in renal function at this transitional stage. Depending on preexisting reserve capacity, this stage may persist for hours to days. At this point, the key decline in renal function is sufficient to result in retention of nitrogenous end products of metabolism and cessation of fluid and electrolyte homeostasis. These events are not reversible by modifying nonrenal factors and are difficult to predict. Prerenal azotemia and tubular ischemic injury represent extreme examples of the same problem (i.e., insufficient renal blood flow). When describing prerenal azotemia progressing to renal failure, the terms acute tubular necrosis, vasomotor nephropathy, and ischemic tubular injury are often used interchangeably in the literature.

Although most causes of ischemic renal failure are reversible, after a critical point of prolonged severe ischemia, necrosis may be irreversible. [19] In patients with inadequate renal blood flow, this irreversible injury is commonly caused by the added risk of drugs that alter the intrarenal distribution of blood flow by abnormal hemodynamics or by preexisting disease[20] (see Chapter 52 , Chapter 54 , and Chapter 56 ). These predisposing variables, as well as the onset and pathogenesis of perioperative renal failure, are often difficult to determine because direct assessment of renal hemodynamics and renal tubular function is typically not possible. Renal function must often be indirectly assessed. An understanding of normal renal physiology and of the pathophysiology of ARF is critical. Because perioperative treatment strategies depend on differentiating normal from abnormal renal function, understanding the limitations of commonly used renal function monitoring techniques is also important.

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