Perioperative oliguria and ATN

ByMohamed Helmy Khafaga

Departement of anesthesia and surgical intensive care

Some important definitions:

1.Definition Of Oliguria :The diagnosis of acute oliguric renal failure is made

when creatinine and BUN concentrations progressively increase while urine flow remains less than 20 mL/hr in an adequately hydrated patient who has stable blood pressure and a patent urinary outflow tract.

2. Definition of ATN(acute tubular necrosis) :The intrinsic renal disorders encountered in the ICU usually

fall into two categories: acute tubular necrosis (ATN), or acute interstitial nephritis (AIN).

ATN is characterized by (oxidative) injury to the renal tubular epithelial cells with sloughing of the cells into the lumen of the renal tubules . The sloughed cells create an obstruction that increases the pressure in the proximal tubules. This decreases the net filtration pressure across the glomerular capillaries and reduces the glomerular filtration rate (GFR). This process is called tubulo-glomerular feedback.

3.Definition of Acute Renal Failure :Acute renal failure (ARF) 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 ARF 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).

. Prerenal failure is usually reversible if the circulatory status is promptly improved; postrenal failure is reversible when the obstruction is removed. ARF secondary to primary renal disease is the most serious of the three types and most often requires hemodialysis.

• Renal failure also is classified according to urine flow rates, so the terms oliguric, nonoliguric, and polyuric renal failure are often encountered.

Glomerular Filtration Rate

The GFR is the best measure of glomerular function. Normal GFR is approximately 125 mL/min. Manifestations of reduced GFR are not seen, however, until the GFR has decreased to 50% of normal. When GFR decreases to 30% of normal, a stage of moderate renal insufficiency sets in. When the GFR is 5% to 10% of normal, it is called end-stage renal disease (ESRD), and continued survival without renal replacement therapy becomes impossible.

Blood Urea Nitrogen

The blood urea nitrogen (BUN) concentration is not a direct correlate of reduced GFR. BUN is influenced by nonrenal variables, such as exercise, bleeding, steroids, and massive tissue breakdown. The more important factor is that BUN is not elevated in kidney disease until the GFR is reduced to almost 75% of normal.

Creatinine and Creatinine Clearance

Creatinine in serum results from turnover of muscle tissue and depends on daily dietary intake of protein. Normal values are 0.5 to 1.5 mg/100 mL; values of 0.5 to 1 mg/100 mL are present during pregnancy.

and creatinine clearance is a specific measure of GFR. Creatinine clearance can be calculated by the following formula derived by Cockcroft-Gault that accounts for age-related decreases in GFR, body weight, and sex: This value should be multiplied by 0.85 for women because a lower fraction of body weight is composed of muscle.

Creatinine and Creatinine Clearance =(140-age) × body weight (kg)Plasma creatinine × 72

Conditions Affecting Blood Urea Nitrogen (BUN) Independently of Glomerular Filtration Rate

Increased BUN • Reduced effective circulating blood volume (prerenal azotemia)• • Catabolic states (gastrointestinal bleeding, corticosteroid use)• • High-protein diets• • Tetracycline•

Decreased BUN • • Liver disease• • Malnutrition• • Sickle cell anemia• • SIADH

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

Urinary composition of OliguriaPrerenal failure

ATN

Urinary sodium <25 mEq/L >35 mEq/L

Urinary specific gravity

>1.015 1.010-1.015

Urinary/plasma urea

>20 : 1 3 : 1, rarely >10 : 1

Urinary/plasma creatinine

>30 : 1, rarely <10 : 1 <10 : 1

Fractional sodium excretion

>1 >0.5

Prevention of perio-perative ATN. Preservation of good hydration status of the patient and maintaining

a good circulating blood volume and adequate hemodynamics..Dopamine has been used for decades to prevent or ameliorate renal

insufficiency. Use of dopamine is criticized because of the lack of prospective, large, randomized clinical trials

. Mannitol has been described to have a protective renal effect if administrated in the setting of a preischemic renal insult therapy This benefit is postulated to occur by renal vasodilation via prostaglandin effect, from free radical scavenging to reduce the effects of hydroxyl-type free radical injury, and by maintaining or improving urine production as an osmotic diuretic to diminish tubular obstruction

.

. Loop diuretics continue to be administered in the clinical setting without reproducible evidence of a renoprotective perioperative benefit.

. N-acetyl cysteine and intravenous NaHCO3 therapy have been used and evaluated mainly in the setting of contrast-induced nephropathy with inconsistent conclusions .

. Several additional renal preservation therapy studies, including the use of atrial natriuretic peptide, theophylline, dopexamine (β2-agonist), calcium channel blockers, prostaglandin E1, growth factors, hemodialysis, and hemofiltration, have been published. Results from these clinical trials are often inconsistent .

Intra-operative management of Oliguria

• Should the Anesthesiologist Be Concerned?Decreases in urinary output during anesthesia are very common. Although decreases may be expected owing to the physiological effects of surgery and anesthesia (above), a urinary output of less than 20 mL/h in adults generally requires evaluation.

• What Issues Should Be Addressed?• The following questions should be

answered:• (1) Is there a problem with the urinary

catheter and drainage system?• (2) Are hemodynamic parameters compatible

with adequate renal function?• (3) Could the decrease in urinary output be

directly related to surgical manipulations?

• How Can the Urinary Catheter and Drainage System Be Evaluated Intraoperatively?

Incorrect catheter placement is not uncommon and should be suspected if there has been a total absence of urine flow since the time of catheter insertion. The catheter may be inadvertently placed and inflated in the urethra in men or the vagina in women. Catheter displacement, kinking, obstruction, or disconnection from the reservoir tubing can all present with features similar to this case, with complete or near-complete cessation of urinary flow. The diagnosis of such mechanical problems requires retracing and inspecting the path of urine (often under the surgical drapes) from the catheter to the collection reservoir. Obstruction of the catheter can be confirmed by an inability to irrigate the bladder with saline through the catheter.

• What Hemodynamic Parameters Should Be Evaluated?• Decreased urinary output during surgery is most

commonly the result of hemodynamic changes. In most instances, a decrease in intravascular volume (hypovolemia), cardiac output, or mean arterial blood pressure is responsible. Redistribution of renal blood flow from the renal cortex to the medulla may also play a role.

• Intravascular volume depletion can rapidly develop when intravenous fluid replacements do not match intraoperative blood loss, insensible fluid losses, and sequestration of fluid by traumatized tissues (third-spacing). Oliguria requires careful assessment of intravascular volume to exclude hypovolemia . An increase in urinary output following an intravenous fluid bolus is highly suggestive of hypovolemia. In contrast, oliguria in patients with a history of congestive heart failure may require inotropes, vasodilators, or diuretics. Central venous or pulmonary artery pressure monitoring is useful in patients with underlying cardiac, renal, or advanced hepatic disease, as well as in patients experiencing extensive blood loss .

• When mean arterial blood pressure drops below the lower limit of renal autoregulation (80 mm Hg), urinary flow may become blood pressure dependent. The latter may be particularly true in patients with chronic systemic hypertension, in whom renal autoregulation occurs at higher mean arterial blood pressures. Reductions in anesthetic depth, intravenous fluid boluses, or the administration of a vasopressor may increase blood pressure and urinary output in such instances.

• Occasionally, otherwise normal patients may exhibit decreased urinary output in spite of normal intravascular volume, cardiac output, and mean arterial blood pressure. A small dose of a loop diuretic (furosemide, 5–10 mg) usually restores normal urinary flow in such instances.

• How Can Surgical Manipulations Influence Urinary Output? In addition to the neuroendocrine response to surgery, mechanical factors related to the surgery itself can alter urinary output. This is particularly true during pelvic surgery, when compression of the bladder by retractors, unintentional cystotomy, and ligation or severing of one or both ureters can dramatically affect urinary output. Retractor compression combined with a head-down (Trendelenburg) position commonly impedes emptying of the bladder. Excessive pressure on the bladder will often produce hematuria. When mechanical problems with the urinary catheter drainage system and hemodynamic factors are excluded (see above), a surgical explanation should be sought. The surgeon should be notified so that the position of the retractors can be checked, the ureters identified, and their path retraced in the operative area. Intravenous methylene blue or indigo carmine—both dyes that are excreted in urine—are useful in identifying the site of an unintentional cystotomy or the end of a severed ureter. Note that the appearance of the dye in the urinary drainage reservoir does not exclude unilateral ligation of one ureter. Methylene blue and, to a much lesser extent, indigo carmine can transiently give falsely low pulse oximeter readings