This syndrome is a rapid deterioration in kidney function that results in retention of nitrogenous waste products (azotemia). These substances, many of which behave as toxins, are byproducts of protein and amino acid metabolism. Impaired kidney metabolic activity may contribute to widespread organ dysfunction (see Chapter 30).
Kidney failure can be classified as prerenal, renal, and postrenal, depending on its cause(s), and the initial therapeutic approach varies accordingly (see Figure 31–1 and Table 31–4). Prerenal kidney failure results from an acute decrease in renal perfusion; intrinsic kidney failure is usually due to underlying kidney disease, kidney ischemia, or nephrotoxins; and postrenal failure is the result of urinary collecting system obstruction or disruption. Both prerenal and postrenal forms of kidney failure are readily reversible in their initial stages but with time both progress to intrinsic kidney failure. Most adult patients with kidney failure first develop oliguria. Nonoliguric patients with kidney failure (urinary outputs >400 mL/d) continue to form urine that is qualitatively poor; these patients tend to have greater preservation of GFR. Although glomerular filtration and tubular function are impaired in both cases, abnormalities tend to be less severe in nonoliguric kidney failure.
TABLE 31–4Management priorities in patients with acute kidney failure.1 ||Download (.pdf) TABLE 31–4 Management priorities in patients with acute kidney failure.1
Search for and correct prerenal and postrenal causes
Review medications and patient-administered substances and stop any potential nephrotoxins
Administer medications in doses appropriate for their clearance
Optimize cardiac output and renal blood flow
Monitor fluid intake and output; measure body weight daily
Search for and treat acute complications (hyperkalemia, hyponatremia, acidosis, hyperphosphatemia, pulmonary edema)
Search for and aggressively treat infections and sepsis
Provide early nutritional support
Provide expert supportive care (management of catheter and skin care; pressure sore and deep venous thromboembolic prophylaxis; psychological support).
The course of intrinsic acute kidney failure varies widely, but the oliguria typically lasts for 2 weeks and is followed by a diuretic phase marked by a progressive increase in urinary output. This diuretic phase often results in very large urinary outputs and is usually absent in nonoliguric kidney failure. Kidney function improves over the course of several weeks but may not return to normal for up to 1 year, and subsequent chronic kidney disease is common. The course of prerenal and postrenal kidney failure is dependent upon promptness in diagnosis and correction of the causal condition. Diagnostic ultrasound, including point-of-care ultrasound, is increasingly used to rapidly and noninvasively evaluate possible obstructive uropathy.
The most common causes of chronic kidney disease (CKD) are hypertensive nephrosclerosis, diabetic nephropathy, chronic glomerulonephritis, and polycystic kidney disease. The uncorrected manifestations of this syndrome (Table 31–5) are usually seen only after GFR decreases below 25 mL/min. Patients with GFR less than 10 mL/min are dependent upon RRT for survival, in the form of hemodialysis, hemofiltration, or peritoneal dialysis.
TABLE 31–5Manifestations of chronic kidney disease. ||Download (.pdf) TABLE 31–5 Manifestations of chronic kidney disease.
Congestive heart failure
Nausea and vomiting
Delayed gastric emptying
The generalized effects of severe CKD can usually be controlled by RRT. The majority of patients with end-stage kidney disease who do not undergo renal transplantation receive RRT three times per week. There are complications directly related to RRT itself (Table 31–6). Hypotension, neutropenia, hypoxemia, and disequilibrium syndrome are generally transient, if they occur, and resolve within hours after RRT. Factors contributing to hypotension during dialysis include the vasodilating effects of acetate dialysate solutions, autonomic neuropathy, and rapid removal of fluid. The interaction of white cells with cellophane-derived dialysis membranes can result in neutropenia and leukocyte-mediated pulmonary dysfunction leading to hypoxemia. Dialysis disequilibrium syndrome (DDS) is most frequently seen following aggressive dialysis and is characterized by transient alterations in mental status and focal neurological deficits that are secondary to cerebral edema.
TABLE 31–6Complications of renal replacement therapy. ||Download (.pdf) TABLE 31–6 Complications of renal replacement therapy.
Dialysis disequilibrium syndrome
Intravascular volume depletion
Large protein losses
Manifestations of Kidney Failure
Multiple metabolic abnormalities, including hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, hyperuricemia, and hypoalbuminemia, typically develop in patients with kidney failure. Water and sodium retention can result in worsening hyponatremia and extracellular fluid overload, respectively. Failure to excrete nonvolatile acids produces an increased anion gap metabolic acidosis (see Chapter 50). Hypernatremia and hypokalemia are uncommon complications.
Hyperkalemia is a potentially lethal consequence of kidney failure (see Chapter 49). It usually occurs in patients with creatinine clearances of less than 5 mL/min, but it can also develop rapidly in patients with higher clearances in the setting of large potassium loads (eg, trauma, hemolysis, infections, or potassium administration).
Hypermagnesemia is generally mild unless magnesium intake is increased (commonly from magnesium-containing antacids). Hypocalcemia is secondary to resistance to parathyroid hormone, decreased intestinal calcium absorption secondary to decreased kidney synthesis of 1,25-dihydroxycholecalciferol, and hyperphosphatemia-associated calcium deposition into bone. Symptoms of hypocalcemia rarely develop unless patients are also alkalotic.
Patients with kidney failure also rapidly lose tissue protein and readily develop hypoalbuminemia. Anorexia, protein restriction, and dialysis are contributory.
Anemia is nearly always present when the creatinine clearance is below 30 mL/min. Hemoglobin concentrations are generally 6 to 8 g/dL due to decreased erythropoietin production, red cell production, and red cell survival. Additional factors may include gastrointestinal blood loss, hemodilution, bone marrow suppression from recurrent infections, and blood loss for laboratory testing. Even with transfusions, it is often difficult to maintain hemoglobin concentrations greater than 9 g/dL. Erythropoietin administration may partially correct the anemia. Increased levels of 2,3-diphosphoglycerate (2,3-DPG), which facilitates the unloading of oxygen from hemoglobin (see Chapter 23), develop in response to the decrease in blood oxygen-carrying capacity. The metabolic acidosis associated with CKD also favors a rightward shift in the hemoglobin–oxygen dissociation curve. In the absence of symptomatic heart disease, most CKD patients tolerate anemia well.
Both platelet and white cell function are impaired in patients with kidney failure. Clinically, this is manifested as a prolonged bleeding time and increased susceptibility to infections, respectively. Most patients have decreased platelet factor III activity as well as decreased platelet adhesiveness and aggregation. Patients who have recently undergone hemodialysis may also have residual anticoagulant effects from heparin.
Cardiac output increases in kidney failure to maintain oxygen delivery due to decreased blood oxygen-carrying capacity. Sodium retention and abnormalities in the renin–angiotensin system result in systemic arterial hypertension. Left ventricular hypertrophy is a common finding in CKD. Extracellular fluid overload from sodium retention, in association with increased cardiac demand imposed by anemia and hypertension, makes CKD patients prone to congestive heart failure and pulmonary edema. Increased permeability of the alveolar–capillary membrane may also be a predisposing factor for pulmonary edema associated with CKD (see later discussion). Arrhythmias, including conduction blocks, are common, and may be related to metabolic abnormalities and to deposition of calcium in the conduction system. Uremic pericarditis may develop in some patients, who may be asymptomatic, may present with chest pain, or may present with cardiac tamponade. Patients with CKD also characteristically develop accelerated peripheral vascular and coronary artery atherosclerotic disease.
Intravascular volume depletion may occur in high-output acute kidney failure if fluid replacement is inadequate. Hypovolemia may occur secondary to excessive fluid removal during dialysis.
Without RRT or bicarbonate therapy, CKD patients may be dependent on increased minute ventilation as compensation for metabolic acidosis (see Chapter 50). Pulmonary extravascular water is often increased in the form of interstitial edema, resulting in a widening of the alveolar to arterial oxygen gradient and predisposing to hypoxemia. Increased permeability of the alveolar–capillary membrane in some patients can result in pulmonary edema even with normal pulmonary capillary pressures.
Abnormal glucose tolerance is common in CKD, usually resulting from peripheral insulin resistance (type 2 diabetes mellitus is one of the most common causes of CKD). Secondary hyperparathyroidism in patients with chronic kidney failure can produce metabolic bone disease, predisposing to fractures. Abnormalities in lipid metabolism frequently lead to hypertriglyceridemia and contribute to accelerated atherosclerosis. Increased circulating levels of proteins and polypeptides normally degraded by the kidneys are often present, including parathyroid hormone, insulin, glucagon, growth hormone, luteinizing hormone, and prolactin.
Anorexia, nausea, vomiting, and ileus are commonly associated with uremia. Hypersecretion of gastric acid increases the incidence of peptic ulceration and gastrointestinal hemorrhage, which occurs in 10% to 30% of patients. Delayed gastric emptying secondary to kidney disease–associated autonomic neuropathy may predispose patients to perioperative aspiration. Patients with CKD also have an increased incidence of hepatitis B and C, often with associated hepatic dysfunction.
Asterixis, lethargy, confusion, seizures, and coma are manifestations of uremic encephalopathy, and symptoms usually correlate with the degree of azotemia. Autonomic and peripheral neuropathies are common in patients with CKD. Peripheral neuropathies are typically sensory and involve the distal lower extremities.
Most perioperative patients with acute kidney failure are critically ill, and their kidney failure is frequently associated with trauma or perioperative medical or surgical complications. They are typically in a state of metabolic catabolism. Optimal perioperative management is dependent upon RRT. Hemodialysis is more effective than peritoneal dialysis and can be readily accomplished via a temporary internal jugular, subclavian, or femoral dialysis catheter. Continuous renal replacement therapy (CRRT) is often used when patients are too hemodynamically unstable to tolerate intermittent hemodialysis. Indications for RRT are listed in Table 31–7.
TABLE 31–7Indications for renal replacement therapy. ||Download (.pdf) TABLE 31–7 Indications for renal replacement therapy.
Refractory gastrointestinal symptoms
Patients with chronic kidney failure commonly present to the operating room for creation or revision of an arteriovenous dialysis fistula under local or regional anesthesia. Preoperative dialysis on the day of surgery or on the previous day is typical. However, regardless of the intended procedure or the anesthetic employed, one must be certain that the patient is in optimal medical condition; potentially reversible manifestations of uremia (see Table 31–5) should be addressed.
The history and physical examination should address both cardiac and respiratory function. Signs of fluid overload or hypovolemia should be sought. Patients are often relatively hypovolemic immediately following dialysis. A comparison of the patient’s current weight with previous predialysis and postdialysis weights may be helpful. Hemodynamic data and a chest radiograph, if available, are useful in confirming clinical suspicion of volume overload. Arterial blood gas analysis is useful in evaluating oxygenation, ventilation, hemoglobin level, and acid–base status in patients with dyspnea or tachypnea. The electrocardiogram should be examined for signs of hyperkalemia or hypocalcemia (see Chapter 49) as well as ischemia, conduction block, and ventricular hypertrophy. Echocardiography can assess cardiac function, ventricular hypertrophy, wall motion abnormalities, and pericardial fluid. A friction rub may not be audible on auscultation of patients with a pericardial effusion.
Preoperative red blood cell transfusions are usually administered only for severe anemia as guided by the patient’s clinical status. Bleeding time and coagulation studies (or perhaps a thromboelastogram) may be advisable, particularly if neuraxial anesthesia is being considered. Serum electrolyte, BUN, and creatinine measurements can assess the adequacy of dialysis. Glucose measurements guide the potential need for perioperative insulin therapy.
Drugs with significant renal elimination should be avoided if possible (Table 31–8). Dosage adjustments and measurements of blood levels (when available) are necessary to minimize the risk of drug toxicity.
TABLE 31–8Drugs with a potential for significant accumulation in patients with renal impairment. ||Download (.pdf) TABLE 31–8 Drugs with a potential for significant accumulation in patients with renal impairment.
Alert patients who are stable can be given reduced doses of a benzodiazepine, if needed. Chemoprophylaxis for patients at risk for aspiration is reviewed in Chapter 17. Preoperative medications—particularly antihypertensive agents—should be continued until the time of surgery (see Chapter 21). The management of diabetic patients is discussed in Chapter 35.
Patients with kidney disease and failure are at increased risk for perioperative complications, and their general medical condition and the planned operative procedure dictate monitoring requirements. Because of the risk of thrombosis, blood pressure should not be measured by a cuff on an arm with an arteriovenous fistula. Continuous invasive or noninvasive blood pressure monitoring may be indicated in patients with poorly controlled hypertension.
Patients with nausea, vomiting, or gastrointestinal bleeding should undergo rapid-sequence induction. The dose of the induction agent should be reduced for debilitated or critically ill patients, or for patients who have recently undergone hemodialysis and who remain relative hypovolemic. Propofol, 1 to 2 mg/kg, or etomidate, 0.2 to 0.4 mg/kg, is often used. An opioid, β-blocker (esmolol), or lidocaine may be used to blunt the hypertensive response to airway instrumentation and intubation. Succinylcholine, 1.5 mg/kg, can be used to facilitate endotracheal intubation in the absence of hyperkalemia. Rocuronium (1 mg/kg), vecuronium (0.1 mg/kg), cisatracurium (0.15 mg/kg), or propofol–lidocaine induction without a relaxant may be considered for intubation in patients with hyperkalemia.
The ideal anesthetic maintenance technique should control hypertension with minimal deleterious effect on cardiac output, because increased cardiac output is the principal compensatory mechanism for tissue oxygen delivery in anemia. Volatile anesthetics, propofol, fentanyl, sufentanil, alfentanil, and remifentanil are satisfactory maintenance agents. Meperidine should be avoided because of accumulation of its metabolite normeperidine. Morphine may be used, but prolongation of its effects may occur.
Controlled ventilation should be considered for patients with kidney failure under general anesthesia. Inadequate spontaneous ventilation with progressive hypercarbia under anesthesia can result in respiratory acidosis that may exacerbate preexisting acidemia, lead to potentially severe circulatory depression, and dangerously increase serum potassium concentration (see Chapter 50). On the other hand, respiratory alkalosis may also be detrimental because it shifts the hemoglobin dissociation curve to the left, can exacerbate preexisting hypocalcemia, and may reduce cerebral blood flow.
Superficial procedures involving minimal physiological trespass require replacement of insensible fluid losses only. In situations requiring significant fluid volume for maintenance or resuscitation, isotonic crystalloids, colloids, or both may be used (see Chapter 51). Current evidence suggests balanced crystalloids such as Plasma-Lyte or lactated Ringer’s solution are preferable in such circumstances to chloride-rich crystalloids such as 0.9% saline because of the deleterious effects of hyperchloremia on kidney function. However, 0.9% saline is preferable to balanced crystalloids in patients with alkalosis and hypochloremia. Lactated Ringer’s solution should be avoided in hyperkalemic patients when large fluid volumes are required, because it contains potassium 4 mEq/L. Glucose-free solutions should generally be used because of the glucose intolerance associated with uremia. Blood that is lost should generally be replaced with colloid or packed red blood cells as clinically indicated. Allogeneic blood transfusion may decrease the likelihood of kidney rejection following transplantation because of associated immunosuppression. Hydroxyethyl starch has been associated with increased risk of AKI and death when administered to critically ill patients or those with preexisting impaired kidney function, or when used for volume resuscitation. Its use in other circumstances is controversial at this time and the subject of many investigations. Intraoperative fluid therapy can be guided by noninvasive measurements of stroke volume and cardiac output.