Oliguria
Emilio B. Lobato
Robert R. Kirby
CASE SUMMARY
A 48-year-old, 90-kg man with a 24-hour period of severe vomiting and abdominal pain undergoes emergency surgery for a small bowel obstruction. His baseline serum electrolytes include Na+ 145 mEq per L, Cl-90 mEq per L, K+ 3.1 mEq per L. Before surgery, he receives 3.5 L of 5% dextrose in 0.45% saline. During the 4-hour operative procedure for exploratory laparotomy, lysis of adhesions, and a 1-ft segmental small bowel resection for vascular compromise, the anesthesiologist administers 4.2 L of lactated Ringer’s solution. Total urine output during surgery is 200 mL. Postoperatively, over the first 18 hours, he receives 4.5 L of 5% dextrose in 0.45% saline. His urine output is 425 mL, but for the last 5 hours averages <30 mL per hour. Serum electrolytes are measured and reveal Na+ 119 mEq per L, Cl− 87 mEq per L, and K+ 2.9 mEq per L. He is irritable and lethargic and follows commands only sporadically. His blood pressure is 90/65 mmHg, and his pulse rate is 120 bpm. The surgeon orders furosemide, 40 mg intravenously, but over the next 2 hours he only urinates 45 mL. A nephrologist is consulted because of the oliguria and apparent alteration in renal function. After examining the patient and reviewing the chart, he recommends fluid restriction and the administration of 500 mL of 3% saline over the subsequent 5-hour period. The patient’s mental status gradually improves, and his urine output increases to 50 to 60 mL per hour, with a rise in serum Na+ to 130 mEq per L. Five days later, he was discharged after an otherwise uneventful recovery.
What Should We Know About Oliguria?
“All we really know for certain about the kidney is that it produces urine.”1 This statement was made by the eminent twentieth century renal physiologist and philosopher, Homer Smith, who thus characterized the complexity of urine formation. Normal urine production reflects the delicate balance between renal and extrarenal factors. This balance is often disrupted in multitrauma patients or those undergoing major surgery. The result is decreased urine output, or oliguria.
Historically, and often in present times, oliguria is viewed as a reflection of dysfunctional kidneys, or even renal failure. Therapy commonly is directed to restoration of a normal urinary output. Frequently overlooked is the fact that oliguria may represent an adaptive mechanism by the kidneys to restore homeostasis.2,3 However, renal compensatory mechanisms are limited, and overt renal insufficiency may occur over a short period of time (minutes to hours). As a result, the window for therapeutic intervention is limited.4,5
▪ GLOMERULAR FILTRATION
Evaluation and treatment of oliguria requires an understanding of the mechanisms involved in urine production, the risk factors that lead to oliguria, the pathophysiologic entities responsible for decreased urine output, and the
goals of therapy. Prevention of acute renal failure, as opposed to renal dysfunction, is essential to prevent the poor associated prognosis.6,7
goals of therapy. Prevention of acute renal failure, as opposed to renal dysfunction, is essential to prevent the poor associated prognosis.6,7
One hundred and sixty to 180 L of water, each containing approximately 300 mOsm of solute, are filtered daily through the glomeruli of a normal adult in a 24-hour period. Oliguria in an adult with normally functioning kidneys is usually defined by a urine output <400 mL per day (the amount of maximally concentrated urine required to excrete the normal daily nitrogenous waste).8 However, patients who receive osmotic diuretics or have severe hyperglycemia may be oliguric despite a high urinary output. Individuals with preexisting renal dysfunction may be unable to concentrate the urine effectively and therefore require a higher urinary output to maintain homeostasis.
Abnormalities in extracellular fluid volume, or osmolality, elicit increases or decreases in urine output. Marked reduction or cessation of urinary output in a trauma patient during or after surgery can occur suddenly or over a period of several hours to days. It may be the harbinger of acute renal failure. Correct diagnosis and treatment are paramount to prevent significant morbidity and mortality.
If oliguria is associated with renal insufficiency, a measurable decrease in renal function is present, but serum biochemical values are normal. As renal failure supervenes, the function deteriorates to such an extent that abnormal serum biochemical values result. Significant oliguria implies a state of renal failure, because a urine output of ≤400 mL per day cannot excrete the average daily solute load of 650 to 750 mOsm (normal diet) in a maximally concentrated urine (1.2 mOsm per mL). Because renal failure may also be associated with a high urine output, oliguric and polyuric states represent the extremes of a continuum. A diagnosis of renal failure must take into account the quantity and quality of urine.
▪ RENAL BLOOD FLOW
The kidneys receive approximately one fifth the blood volume of the total cardiac output; however, their oxygen consumption is rather low (approximately 10% of total body oxygen consumption).9 The primary determinants of renal blood flow are cardiac output, renal perfusion pressure, and local hemodynamic factors such as glomerular afferent and efferent arteriolar tone.
Ninety to 95% of renal blood flow is to the cortex, where most glomeruli are located. Conversely, the medulla receives only a 5% to 10% of flow.10 Medullary cells have a higher oxygen extraction than cortical cells (80% vs. 20%),11 which, in combination with a lower blood supply, places them at a higher risk for hypoxic damage, despite what would be perceived as adequate total renal blood flow.
Renal blood flow is constant over a wide range of mean arterial pressures. The same degree of hypotension associated with hypovolemia causes a greater reduction in renal blood flow than hypotension caused by impaired left ventricular (LV) function.12 This difference results from the release of atrial and brain natriuretic peptides (BNPs) from the left atrial and ventricular endocardium in response to increased filling pressures.13 These endogenous peptides are important renal vasodilators, which also increase the glomerular filtration rate (GFR) and sodium excretion.
The response to renal hypoperfusion includes afferent arteriolar dilatation combined with efferent arteriolar constriction that increases filtration fraction and activation of the renin-angiotensin aldosterone axis, followed by increased sodium reabsorption and efferent arteriolar resistance.14,15,16,17 Prostaglandins D2, I2, and E2 produced in the kidneys autoregulate local blood flow by acting as renal vasodilators. PGE2y counteracts the renal vasoconstrictive effects of angiotensin and norepinephrine to preserve renal blood flow.18 Certain nonsteroidal anti-inflammatory agents (NSAIDs) decrease the synthesis of PGE2 by inhibiting the activity of cyclooxygenase, thereby increasing the risk of renal ischemia in susceptible patients.19
How Is Oliguria Classified?
Oliguria may be prerenal (hypovolemia, inadequate renal perfusion), renal (intrinsic), and postrenal (obstruction, extravasation) (see Table 30.1).20
▪ PRERENAL
Renal Hypoperfusion
This condition may be caused by inadequate circulating blood volume, the administration of some anesthetic agents, and the extremity compartment syndrome21 following vascular or trauma surgery. Cardiac failure and, rarely, renal artery thrombosis may be responsible. With minimal or moderate depression of renal blood flow, a compensatory increase in filtration fraction results, and GFR and urine formulation remain relatively unaffected. When marked depression of renal blood flow occurs, GFR, urine formation, and electrolyte excretion are significantly reduced.
Anesthetic Agents
Potent fluorinated volatile anesthetics cause dose-related myocardial depression and peripheral vasodilation, probably by altering calcium flux within myocardial cells and the arteriolar smooth muscle. Associated renal changes include decreased renal blood flow, GFR, sodium, potassium and chloride excretion, and decreased or increased urine osmolality. Historically, proposed mechanisms for the decrease in urinary output included increase in aldosterone and 17-hydroxy corticosteroids; increased catecholamine secretion (which was known to occur during ether and cyclopropane anesthesia); and increase in antidiuretic hormone (ADH) secretion. However, the urine solute was
reduced by 80% to 85%, and the antidiuresis was not invariably associated with hyperosmotic urine. Therefore, increased ADH secretion was not likely to have been responsible.
reduced by 80% to 85%, and the antidiuresis was not invariably associated with hyperosmotic urine. Therefore, increased ADH secretion was not likely to have been responsible.
TABLE 30.1 Oliguria | |||||||||||||||||||||||||||||||||||||||
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General anesthesia may abolish the autoregulation that normally maintains renal perfusion in the face of hypotension, thereby leading to decreased renal blood flow and GFR. Although degradation of sevoflurane to compound A that is nephrotoxic in rats has been demonstrated,22 low-flow isoflurane and sevoflurane do not appear to alter renal function in patients with preexisting stable renal disease.23 With the exception of methoxyflurane, which was associated with high output renal failure and no longer is used, anesthetic-induced changes of renal function are readily reversed when the agent is discontinued.24,25,26,27 However, the antidiuresis may persist well into the postoperative period and argues against any persistent anesthetic agent role.
Reduction of Circulating Blood Volume
Oliguria caused by blood loss, fluid sequestration into a surgical or traumatic third space, dehydration, or gastrointestinal loss is a complex problem. If hypovolemia is sufficient to cause renal ischemia, functional lesions acquire a renal morphologic component. In extreme cases, simple prerenal oliguria is transformed into oliguric renal failure.28 The anesthesia provider in such circumstances must administer sufficient blood or fluid to replete the intravascular volume and restore renal blood flow and GFR.
Drugs
Prerenal oliguria can occur from thrombosis of the glomerular afferent arterioles following chemotherapy with vinblastine, bleomycin, or cisplatin.29 Oliguria and azotemia have occurred after captopril therapy30,31 or following treatment with amphotericin B. In the latter situation, renal vasoconstriction is thought to occur concomitantly with nephrotoxicity.
Other Factors
Tubular obstruction and backflow of filtrate into damaged tubules may be causative factors.32 Most common in the pathogenesis of acute renal failure is the suppression of glomerular filtration.33 Light and electron microscopic studies of glomeruli generally failed to reveal structural abnormalities; hence, reduced glomerular filtration likely is caused by vasomotor phenomena.34
▪ RENAL
Causes
Nephrotoxic Agents
Ionic and nonionic contrast materials used in digital vascular imaging and selective renal angiography can impair renal function. NSAIDS such as phenylbutazone, ibuprofen, and indomethacin; and aminoglycoside antibiotics may lead to oliguria and renal insufficiency. The latter agents account for 5% to 10% of all hospital-acquired acute renal failure.35,36,37,38,39,40
Hemoglobin and Myoglobin
Reduction of the GFR, rather than tubular obstruction, appears to be the primary event leading to oliguric
renal failure when hemoglobin enters the glomeruli.41,42 In addition, when incompatible blood is transfused, disseminated intravascular coagulation results, with fibrin deposition in renal tubules. Red cell membranes are thought to initiate the coagulation process, ultimately leading to a decrease in platelets, fibrinogen, and factors II, V, and VII.41 Myoglobinuria following extensive, crushingtype muscle injuries also may contribute to oliguric renal failure.41,42 The mechanism is probably similar as that for hemoglobin.
renal failure when hemoglobin enters the glomeruli.41,42 In addition, when incompatible blood is transfused, disseminated intravascular coagulation results, with fibrin deposition in renal tubules. Red cell membranes are thought to initiate the coagulation process, ultimately leading to a decrease in platelets, fibrinogen, and factors II, V, and VII.41 Myoglobinuria following extensive, crushingtype muscle injuries also may contribute to oliguric renal failure.41,42 The mechanism is probably similar as that for hemoglobin.
▪ POSTRENAL
Extrinsic Obstruction
Extrinsic obstruction results from compartment syndromes,21,43,44 retroperitoneal malignancies, rapidly growing cervical carcinomas, massive uterine fibromyomata, complete bilateral ureteral obstruction from lymphomatous or leukemic involvement of the lymph nodes, giant intra-abdominal cysts,45 and inadvertent ligation of or trauma to the ureters. The latter mishaps occur in 0.1% to 0.25% of patients undergoing gynecologic surgery.46,47 Twenty percent to 25% of ureteral injuries are bilateral, resulting in immediate anuria. Fecal impaction in elderly patients can produce obstructive uropathy and oliguria.
Intrinsic Obstruction
Intrinsic obstruction results from blood clots, calculi, prostatic obstruction, neoplasms, fungus balls, bilharziasis, amyloidosis, and benign prostatic enlargement in older patients following operations around the groin or rectum.48,49,50,51,52,53,54 Intermittent anuria or oliguria may occur in patients with bladder stones if the calculus acts as a ball valve. Kidney transplant recipients also may develop obstructive uropathy with oliguria.53
Urine Extravasation
Extravasation of urine outside the bladder following pelvic trauma may be associated with oliguria. Pelvic fractures are associated with a 9% to 15% incidence of a ruptured bladder.55 The ureters are rarely injured, except from direct trauma during surgery.
What Are the Components Of the Differential Diagnosis?
▪ INTRAVASCULAR VOLUME ASSESSMENT
Oliguria in surgical and trauma patients signifies renal hypoperfusion until proven otherwise. No true monitor of renal perfusion exists, although esophageal Doppler ultrasound has been used to evaluate intrarenal blood flow.56 Surrogates of renal blood flow include measurement of arterial blood pressure, LV preload, and cardiac output.
Arterial Blood Pressure
Mean arterial blood pressure provides an estimate of renal perfusion pressure, whereas the variation in systolic blood pressure (SBP) during positive-pressure ventilation may provide information on effective circulating volume.57
Left Ventricular Preload
Clinicians must depend on measurements of cardiac filling pressures or left ventricular (LV) size to estimate effective circulating volume. With normal left heart function, central venous pressure (CVP) correlates reasonably well with left atrial pressure. This relationship is lost when there is significant left ventricular dysfunction, mitral valve disease, or pulmonary hypertension. Pulmonary artery occlusion pressure (PAOP) provides reasonable estimates of left ventricular preload, whereas cardiac output can be measured intermittently or continuously to determine the response to treatment. However, a poor correlation between PAOP and direct measurement of LV diastolic volume58,59,60 is found in critically ill patients, and a great deal of controversy surrounds this monitoring.
Echocardiograph
Echocardiography provides visual estimates of ventricular preload and global and regional function. Transthoracic echocardiography (TTE) in the perioperative period is confined to the intensive care unit (ICU), where its usefulness is limited.61,62 Transesophageal echocardiography (TEE), is the technique of choice for intubated patients and is widely used in the operating room. Evaluation of ventricular function can be performed rapidly and expeditiously. Additionally, Doppler technology allows measurement of cardiac output and estimates of filling pressures.63,64
Cardiac Output
Thermodilution cardiac output obtained through a pulmonary artery catheter is an invasive technique associated with complications. Less invasive methods utilize CO2 rebreathing, esophageal Doppler, or arterial thermodilution. These techniques compare favorably with pulmonary arterial thermodilution and may be considered a viable alternative in certain patient populations.65,66,67,68,69,70,71
▪ BLOOD CHEMISTRIES
An inverse relation between GFR and blood urea nitrogen (BUN) exists. Oliguria, hypercatabolism, and blood in the gut may increase the BUN, independent of a decrease in GFR.
TABLE 30.2 Relation Between Serum Creatinine and Glomerular Filtration Rate | ||||||||||||
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Serum creatinine (SCr) also is inversely proportional to GFR. Creatinine production and release are related to muscle mass. It is freely filtered by the glomeruli with very little secretion or reabsorbtion by the tubules. Serum creatinine × GFR is a constant in steady state conditions. If GFR is halved, SCr doubles (see Table 30.2). If GFR ceases, the SCr rises approximately 0.5 to 1.0 mg/dL/day. The increase is much greater following severe trauma with resultant muscle damage, or in rhabdomyolysis. Loss of muscle tissue with renal failure may result in a deceptively low SCr. In this setting, BUN and SCr values do not accurately reflect acute changes in GFR. Conditions associated with acute elevations in BUN and creatinine are summarized in Table 30.3.
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