Acute Renal Failure and Hemodialysis

Acute Renal Failure

Acute renal failure is defined as the sudden inability of the kidneys to vary urine volume and content appropriately in response to homeostatic needs. Synonymous terms are acute tubular necrosis and lower nephron nephrosis. The three major types of acute renal failure when classified according to their predominant etiologic antecedents are prerenal (caused by acute circulatory problems that impair renal perfusion), renal (caused by primary or secondary renal disease, toxins, and pigments), and postrenal (caused by obstruction of the urinary tract). ^[110] Common prerenal, renal, and postrenal causes of perioperative oliguria are listed in Table 54-9 . Prerenal failure is usually reversible if the circulatory status is promptly improved; postrenal failure is reversible when the obstruction is removed. Acute renal failure secondary to primary renal disease is the most serious of the three types and most often requires hemodialysis.

Renal failure is also classified according to urine flow rates, so the terms oliguric, nonoliguric, and polyuric renal failure are often encountered. The diagnosis of acute oliguric renal failure is made when creatinine and BUN concentrations progressively increase while urine flow remains below 20 mL/hr in an adequately hydrated patient who has stable blood pressure and a patent urinary outflow tract. Urine and blood chemistry values are as indicated in Table 54-10 . In some cases, patients with acute renal failure may have normal or high (>2.5 L/day) urine flow rates, but they have biochemical abnormalities that are similar to those occurring in patients with low urine output.^[111] Their management is less complex than that of oliguric patients because adequate drug therapy

TABLE 54-9 -- Perioperative causes of oliguria

Prerenal

Hypovolemia

Dehydration

Low cardiac output states

Aortic/renal artery clamping

Thromboembolic phenomena

Hemorrhage

Transfusion reaction

Renal

Ischemic injury from shock (cardiogenic, septic, hemorrhagic)

Nephrotoxins

Antibiotics

Chemotherapeutic agents

Radiocontrast dyes

Free hemoglobin and myoglobin

Cellular debris

Acute interstitial nephritis

Hypersensitivity reactions

Acute glomerulonephritis

Postrenal

Calculi

Tumors

Clot retention

Surgical ligation

Edema

From Patafio O: Acute renal failure and perioperative oliguria. In Malhotra V (ed): Anesthesia for Renal and Genitourinary Surgery. New York, McGraw-Hill, 1996. p 38.

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The major problem arising from acute renal failure is an inability to maintain dynamic balance between dietary intake of essential substances and production of waste products. This imbalance results in a progressive rise in serum urea, creatinine, uric acid, magnesium, sulfate, phosphate, some amino and organic acids, and polypeptides; a daily rise in serum potassium of 0.3 to 3 mEq/L except when there is concomitant potassium loss from diarrhea or vomiting (greater increases may occur in traumatized or postsurgical patients); a decrease in serum sodium and calcium; a decrease in serum proteins, particularly albumin; a consistent increase in total reducing substance in serum, frequently occurring with true hyperglycemia, which may be either sensitive or resistant to insulin; elevation of total lipids, cholesterol, phosphorus, and neutral fats; and metabolic acidosis.^{[110] [111] [112]} The kidney functions both as an endocrine and as an excretory organ. Thus, disorders of renin-angiotensin and aldosterone secretion occur and contribute to the hypertension that develops in patients with severe renal disease. Reduced erythropoietin production leads to anemia. Heart failure and abnormalities in liver function and blood coagulation may also occur in patients with renal shutdown. Infection is common and difficult to treat because the altered excretion of antibiotics leads to the rapid development of toxic levels of these drugs.

Once established, oliguria is usually present for 10 to 18 days but may persist for as long as 30 to 45 days. During this period, hemodialysis is required every 2 to 4 days. When diuresis occurs, the beginning of the recovery phase is signaled. During the diuretic phase, urine volume gradually increases until as much as 5 to 6 L of urine is produced daily. Management of the patient is directed at maintaining fluid and electrolyte balance in the face of these large losses. Finally, concentrating ability gradually returns toward normal. Complete return of all measurable parameters of renal function occurs in approximately two thirds of patients who survive. However, 50% to 60% of patients with acute renal failure do not survive long enough for recovery or the development of CRF.^[113] Arrhythmias, bleeding, and infection are the most frequent causes of death. Outcome analysis indicates that the overall mortality rate from acute renal failure has not been significantly reduced in recent years despite earlier and more frequent dialysis. In fact, it is likely that there has been an increase in the survival rate of some categories of patients without any change in the overall rate because of an increase in the proportion of seriously ill patients who are now treated in dialysis units. This conclusion is suggested by the steady improvement in mortality data of obstetric patients with renal failure. The low (15%) mortality rate for this group emphasizes that the most significant feature determining survival is the physical status of the patient before the onset of renal failure.

As noted earlier, many patients with acute renal failure have normal or high urinary flow rates. In these patients, the antecedent cause of renal failure may be the same as that in patients with classic oliguric renal failure, but an oliguric or anuric phase is not identifiable. Patients are unable to alter urinary volume and content appropriately, with an average daily output often in excess of 2.5 L/day. The higher incidence of nonoliguric and polyuric renal failure in recent years as compared with the 1940s and 1950s is thought to be due in part to more vigorous early treatment of patients with incipient oliguric renal failure.

Hemodialysis

The steady improvement in hemodialysis techniques (see Chapter 56 ) from the first artificial kidney developed in 1944 by Kolf and Berk ^[114] to the current practice of home dialysis has resulted in additional years of productive life for patients with CRF. That, coupled with the 1976 federal legislation extending Medicare coverage to renal failure patients, has resulted in a large increase in the number of hemodialysis patients. Dialysis improves most of the signs and symptoms of uremia (e.g., volume overload, acid-base and electrolyte imbalance, abnormal mental function, peripheral neuropathy, muscle weakness, and defective coagulation). Hypertension is improved except in patients with high renin levels. Some patients have been hemodialyzed for more than 10 years. The 3-year survival rate for U.S. patients 20 to 25 years of age treated by hemodialysis is 85%; for those aged 60 to 65 years it is 60%.

Presently, two basic dialysis techniques are used: peritoneal dialysis and hemodialysis. Peritoneal dialysis can be either chronic intermittent or continuous ambulatory, both performed at home dialysis centers. In most circumstances, hemodialysis is used, and it is generally the method of choice. However, peritoneal dialysis is preferred for patients who have had (1) recent cerebral surgery or a cerebral vascular accident or trauma because

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The dialysis principle involves equilibration of waste products in the patient's blood across a semipermeable membrane to the dialysis bath. Peritoneal dialysis relies on the patient's peritoneum as the exchange membrane, thereby avoiding the need for vascular cannulas and expensive equipment. Exchange volume rates during peritoneal dialysis are 1 to 3 L/hr. Clearance of small molecules is less than with hemodialysis (e.g., urea, 25 versus 150 mL/min), but clearance of large molecules is greater. The ionic content of the dialysate may be altered to suit the patient's needs, and the fluid may be made hypertonic or hypotonic to plasma to remove or add fluid to the patient's extracellular fluid volume, respectively. Peritoneal dialysis is less efficient than hemodialysis, so dialysis times are longer. In addition, peritonitis is a danger, and pain during dialysis may be severe.

Hemodialysis is by far the most commonly used dialysis technique today. Originally, Teflon shunts were inserted between the radial artery and a forearm vein with a connector between them to allow access to the circulation. Today, vascular access is usually obtained by the creation of an end-to-side arteriovenous fistula in the forearm or by insertion of a prosthetic arteriovenous graft when the vessels are inadequate. During hemodialysis, which is performed two or three times weekly, both the patient and the external circuit are heparinized to prevent clotting. Flow rates are usually 500 mL/min, so the patient's blood is exposed to 120 L of fluid during a standard 4-hour dialysis. Variation in ionic content and osmolarity of the dialysate permit correction of abnormalities in fluid and electrolyte balance. However, if fluid and electrolyte shifts are too rapid, dialysis disequilibrium may occur. This syndrome is characterized by weakness, nausea, vomiting, and occasionally, convulsions and coma. In the interval between treatments, clotting does not occur because the shunted circuit is short and blood flow is rapid (150 to 300 mL/min).

Local infiltration, axillary block, and general anesthesia have been used successfully for creation of arteriovenous fistulas (see Chapter 43 and Chapter 44 ). Several anesthetic precautions are appropriate. Uremic patients may be debilitated, in which case smaller doses of all drugs, including local anesthetics, should be administered. Hyperkalemia, acidosis, and overhydration can combine to cause myocardial irritability; therefore, local anesthetic solutions that contain epinephrine should be used with caution. If epinephrine is used, concentrations greater than 1:200,000 are not necessary, and solutions as dilute as 1:400,000 are probably adequate. Brachial plexus block may greatly facilitate the introduction of cannulas by producing analgesia combined with peripheral vasodilation. Of interest, Bromage and Gertel^[115] reported that brachial plexus block had a 38% shorter duration in renal failure patients than in those with normal renal function. However, this finding could not be confirmed in a subsequent study of renal failure patients.^[116]