Author: Uday Jain, MD, PhD
ASA Monitor 11 2015, Vol.79, 16-18.
Uday Jain, M.D., Ph.D. is Staff Anesthesiologist, Alameda Health System, Oakland, California.
Classification: Perioperative acute kidney injury (AKI) was previously known as “acute renal failure.” To facilitate its management, standardized classification of severity of AKI is utilized. Two sets of criteria are popular for classification of AKI by serum creatinine (Scr) and urine output. The RIFLE classification includes graded severity of injury: (R)isk, (I)njury, (F)ailure; and adverse outcome-(L)oss, (E)nd-stage renal disease. Classes 1, 2 and 3 of the AKIN (Acute Kidney Injury Network) classification are similar to RIF: Scr increase by 50 percent, 100 percent and 200 percent.
Incidence: AKI is more common and morbid than often appreciated. Its reported incidence during cardiac surgery is 30 percent.1 After major non-cardiac surgery, the incidence is reported to be 6.3 percent.2 In another study, during non-cardiac, non-vascular surgery, the incidence of AKI was 6.7 percent.3 Incidence of AKI during abdominal surgery is reported to be 1.1 percent.4 It was 3.5 percent in exploratory laparotomy patients, who had greater acuity.4 The incidence of AKI is high in septic patients, critically ill patients and major trauma patients.
Morbidity and Mortality: AKI is a major cause of perioperative morbidity and mortality. Patients with AKI had more cardiovascular (33.3 percent versus 11.3 percent, P<.001) complications and a higher in-hospital mortality (6.1 percent versus 0.9 percent, P=0.003).3 Mortality increases with the severity of AKI5 and the duration of AKI.
Diagnosis of AKI: Despite its high incidence and morbidity, perioperative AKI is often underdiagnosed and inadequately managed. One reason for this is that AKI is not associated with specific signs or symptoms. Additionally, kidney function is commonly evaluated utilizing Scr, glomerular filtration rate (GFR) and urine output. They are markers of global kidney function rather than focal or generalized injury. They may not be elevated for up to 48 hours after surgery. Utilizing them during non-cardiac surgery, most cases were reportedly diagnosed on postoperative days one through three and diminishing numbers for over a month.4 This fact impedes crucial early detection and intervention. To increase speed and sensitivity of detection of AKI, novel biomarkers of AKI in plasma and urine are being utilized.
Urine neutrophil gelatinase-associated lipocalin (NGAL) is elevated two hours after injury. Other urinary markers include kidney injury molecule-1 (KIM-1), liver-type fatty acid-binding protein (L-FABP) and N-acetyl-beta-D-glucosaminidase (NAG). Plasma markers include cystatin C, interleukin-6 and interleukin -18. No single marker is ideal, and they may be utilized in combination. Currently, these markers are not widely utilized in clinical practice.
Prevention of AKI: AKI progresses gradually over hours to days. Although no specific treatment is available, AKI can be prevented or impeded by appropriate management. The causes of AKI to be avoided include hypotension and anemia. Intravascular myoglobin, hemoglobin, uric acid, cholesterol, thrombi and atheroemboli are also detrimental. Sodium bicarbonate alleviates AKI due to myoglobin and hemoglobin.
Hemodynamics: During elective non-cardiac surgery, mean arterial pressure (MAP) less than 60 mmHg is associated with AKI.2 Even a few minutes of MAP less than 55 mmHg is associated with AKI and cardiac injury.6
Preoperatively to early postoperatively, optimization of MAP, preload and cardiac output with appropriate fluids, inotropes and vasoactive medications was reported to lead to a reduction in AKI by two-thirds and mortality by one-half.7 Goal-directed therapy does not increase the amount of fluid administered yet may reduce AKI when utilized with inotropes.
Hemoglobin: There is a graded increase in AKI for preoperative hemoglobin (Hgb) less than 12 gm/dL or perioperative decrease in Hgb of greater than 1 gm/dL.8 Preoperative anemia, perioperative transfusion and re-exploration after surgery are associated with AKI. Utilization of older RBCs increases the risk of AKI. Erythropoietin does not protect kidney during cardiac surgery.
During cardiopulmonary bypass (CPB), avoid hematocrit (Hct) less than 20 percent, flow rate less than 2 L/min, MAP less than 50 mmHg and temperature less than 27 degrees Celsius. Off-pump CABG is associated with reduced AKI but not reduced need for renal replacement therapy or mortality.
Comorbidities: Predictors of dialysis include male gender, chronic obstructive pulmonary disease, insulin-dependent diabetes mellitus (IDDM), congestive heart failure (CHF), need for intra-aortic balloon pump, left ventricular ejection fraction <35 percent, elevated Scr, emergency surgery, type of surgery and prior cardiac surgery. During cardiac and vascular surgery, a low preoperative GFR is associated with supra-linear increase in mortality.9 Perioperative optimization of comorbidities such as DM, cardiovascular disease, CHF, chronic kidney disease, liver abnormalities and anemia is protective. Preoperative dialysis is beneficial for renal failure patients not yet on dialysis.
Medications: Avoid nephrotoxic medications, including angiotensin converting enzyme inhibitors, angiotensin receptor blockers, non-steroidal anti-inflammatory drugs, aminoglycoside and other antibiotics, intravenous contrast and aprotinin. On the other hand, atrial and brain natriuretic peptide and urodilatin are protective. Not protective are dopamine, fenoldopam, calcium channel blockers, N-acetylcysteine and anti-inflammatory agents. Statins may reduce AKI. Third-generation hydroxyethyl starch 130/0.40 is not associated with AKI.10 However, older hydroxyethyl starches (6 percent hetastarch) may cause AKI.11 Compared to low chloride lactated ringers and plasmalyte, normal saline doubles the incidence of AKI and the rate of renal replacement therapy.12 Sodium bicarbonate does not reduce AKI but may reduce severe AKI and rate of renal replacement therapy.
Morbidity: AKI can lead to hepatorenal syndrome and cardiorenal syndrome. AKI also predisposes to injury to other parts of the body, including lungs, intestines and brain. This is mediated via inflammation due to neutrophil migration, cytokine expression and increased oxidative stress, which contribute to increased mortality.
In patients requiring renal replacement therapy, mortality approximates 50 percent. Continuous renal replacement therapy is preferred in hospitalized patients, especially if they are receiving vasopressors. Intermittent hemodialysis is preferred in an outpatient setting.
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