Renal system
A Acute renal failure
Definition
Acute renal failure (acute tubular necrosis, vasomotor neuropathy, lower nephron necrosis) is defined as the sudden inability of the kidneys to vary urine volume and content appropriately in response to homeostatic needs.
Pathophysiology
Acute renal failure is classified according to its predominant cause or on the basis of urine flow rates. The cause of acute renal failure has prerenal, renal, or postrenal origins. Prerenal failure results from hemodynamic or endocrine factors that impair renal perfusion, renal failure results from tissue damage, and postrenal failure results from urinary tract obstruction. Prerenal or postrenal failure is reversed with attention to hemodynamics or relief of obstruction. Acute renal failure caused by parenchymal disease or damage is more serious and often requires hemodialysis. Common causes are listed below.
Primary renal disease
Failure classified according to urine flow rates is known as oliguric, nonoliguric, or polyuric failure. Oliguria is defined as a urinary flow rate less than 0.5 mL/kg/hr in a patient subjected to acute stress. This rate is higher than that seen in unstressed patients because acutely stressed patients cannot maximally concentrate urine. Polyuric failure is associated with elevations of blood urea, nitrogen, and serum creatinine levels and is characterized by urine flow rates that exceed 2.5 L/day.
Conditions that lead to prerenal oliguria include acute reductions in glomerular filtration rate (GFR), excessive reabsorption of salt or water, or both. Increases in circulating levels of catecholamines, antidiuretic hormone (ADH), or aldosterone are physiologic factors that can decrease urinary output. Hypotension may or may not be present in the initiation of acute renal failure. If not reversed, prerenal oliguria may progress to parenchymal damage and tubular necrosis.
Acute tubular necrosis
Acute tubular necrosis may be produced by a variety of factors that interfere with glomerular filtration or tubular reabsorption. The pathogenesis of acute tubular necrosis may be divided into an initiation period, a maintenance period, and a recovery period. Renal hypoperfusion or a nephrotoxic insult may initiate renal failure. Surgical patients with external and internal fluid losses or sepsis may have renal hypoperfusion. The initiating insult culminates in the development of one or more maintenance factors, such as decreased tubular function, tubular obstruction, and sustained reductions in renal blood flow and glomerular filtration. Urine flow and solute excretion are reduced. When the maintenance period has begun, pharmacologic interventions to improve renal blood flow do not reverse the failure.
Prerenal oliguria
Prerenal oliguria is associated with physiologic mechanisms that conserve salt and water. In this case, urine has low sodium levels and high osmolality. Urine sodium levels are high, and osmolality is low. Renal damage is also associated with a progressive rise in serum urea, creatinine, uric acid, and polypeptide levels. Serum potassium levels may increase by 0.3 to 3 mEq/L/day, and a decrease occurs in the serum levels of sodium, calcium, and proteins such as albumin. The creatinine clearance remains the single most helpful test in defining renal status and predicting the prognosis in cases of severe renal dysfunction.
A number of conditions may place patients at high risk for acute renal failure and are listed in the following section. Renal reserve decreases progressively with age. For each year after 50 years of age, creatinine clearance decreases by 1.5 mL and renal plasma flow by 8 mL. Older patients are less able to cope with fluid and electrolyte imbalance and are more prone to renal damage. Overall mortality rates associated with acute renal failure increase from 50% for those younger than age 40 years to 80% for those older than age 60 years.
Prevention and management
Prevention of renal failure can be based on the following generalizations:
• The most common cause of failure is prolonged renal hypoperfusion.
• Prophylaxis reduces mortality more effectively than dialytic therapy.
• The duration and magnitude of the initiating renal insult are critical in determining the severity of failure.
A key strategy in reducing the incidence of renal failure is limiting the magnitude and duration of renal ischemia. Although a number of preventive strategies have been described, none apart from maintenance of normovolemia appears to be effective.
Anesthetic considerations
In the preoperative preparation of surgical patients, high-risk patients and procedures should be identified. Reversible renal dysfunction should be sought, and fluid losses and hypovolemia should be corrected by intravenous fluids. Perioperative ADH and renin–angiotensin–aldosterone secretion can be minimized with adequate hydration before anesthetic induction. Administration of saline rather than solutions low in sodium is helpful in prevention of aldosterone secretion, hyponatremia, and oliguria.
Oliguria often signals inadequate systemic perfusion, and prevention of acute renal failure requires its rapid recognition through adequate monitoring. In addition to standard monitors and a urinary catheter, monitors for patients with questionable cardiac and pulmonary function should include a direct arterial line for blood pressure monitoring and a central venous pressure (CVP) or Swan-Ganz catheter, when appropriate, for assessment of cardiac function and volume status.
Perioperative
Use of a urinary catheter is the only means of monitoring renal function in the operating room. A fluid challenge is necessary if hourly urinary output decreases to below acceptable levels.
The use of diuretics in the face of inadequate urinary output must be carefully evaluated. Although diuretics may not be effective during the initiation of failure, large doses of furosemide may convert oliguric renal failure into nonoliguric failure, which is easier to manage. In the maintenance phase, doses of furosemide in excess of 1 g may be required to convert oliguric failure to nonoliguric failure. Diuretic therapy must be associated with aggressive monitoring and intravascular volume expansion.
Although the mechanism is unknown, prophylactic administration of mannitol in well-hydrated patients protects renal function. Loop diuretics may also prevent acute renal failure. Mechanisms for protection include the inhibition of sodium reabsorption and the prevention of tubular obstruction through the maintenance of high flow and pressure within the tubules and the reversal of intrinsic renal vasoconstriction. Prophylactic use of diuretics may be of benefit in the case of jaundice in surgical patients, excessive exposure to contrast media, hyperuricemia, or the presence of pigment in the urine. Fenoldopam, a dopamine receptor agonist, also may be helpful.
Fenoldopam mesylate (Corlopam) is a selective DA1 receptor agonist. It causes both systemic and renal arteriolar vasodilation and has no impact on DA2, α-adrenergic, or β-adrenergic receptors. Unlike dopamine, which causes renal vasoconstriction at higher doses, fenoldopam at high dose produces even greater renal vasodilation. Fenoldopam is more than six times as potent as dopamine in increasing renal blood flow.
Management of acute renal failure
If acute renal failure develops, it progresses through four distinct phases: onset, the oliguric phase, the diuretic phase, and the recovery phase. Onset, or the initiation phase, precedes actual necrotic injury and correlates with a major alteration in renal hemodynamics. The oliguric phase reflects four pathophysiologic processes:
1. Obstruction of tubules by cellular debris, tubular casts, or tissue swelling
2. Total reabsorption or backleak of urine filtrate through damaged tubular epithelium and into the circulation
3. Tubular cell damage with leakage of adenosine triphosphate (ATP) and potassium and edema
