Acute kidney injury

Definition and epidemiology of AKI: Acute renal failure, or acute kidney injury (AKI), occurs in approximately 1% of surgical patients, although this number is substantially higher in high-risk populations.^[1] The mortality rate for perioperative AKI may be as high as 50%,^[2] making its diagnosis and treatment important for anyone involved in care of surgical patients in the Post-Anesthesia Care Unit (PACU). The definition of AKI is not uniform throughout the literature; however, the Acute Kidney Injury Network in 2007 defined AKI as an abrupt (within 48 hours) absolute increase in serum creatinine of greater than or equal to 0.3 mg/dl, a 50% or greater increase in serum creatinine, or oliguria of less than 0.5 ml/kg for more than 6 hours.^[3] In the PACU environment, patients are typically discharged after a few hours at most, so the 6-hour definition may not apply in this specific patient population. Patients who are oliguric in the PACU for several hours, particularly those who have risk factors or those who underwent high-risk surgery, should be managed aggressively in an attempt to prevent worsening of their renal function.

Risk factors for perioperative AKI: Although there is not a consensus of what constitutes the risk factors for perioperative AKI, several have been suggested. One review of the literature found that preoperative increased serum creatinine, blood urea nitrogen (BUN), or renal dysfunction predicted postoperative renal failure the best of any factors studied, while advanced age, pre-existing congestive heart failure (CHF), bacterial endocarditis, decreased serum albumin, malignancy, gout, vascular disease, elevated serum bilirubin, and prior cardiac surgery were weakly associated with postoperative AKI.^[4] The type of surgery also influences the risk, with cardiac, vascular (especially abdominal aortic aneurysm repair), and liver transplantation having the highest incidence of postoperative AKI.^[2]

Classification of AKI: AKI is traditionally divided into prerenal, intrinsic renal, and postrenal causes. In the PACU setting, postrenal causes usually involve obstruction of the ureters, bladder, or urethra, either mechanically or pharmacologically via decreased bladder tone. Certain surgical procedures, such as urological or gynecological, would obviously make a postrenal etiology more likely. Surgical injury to the genitourinary tract, renal stones, and benign prostatic hypertrophy are common mechanical causes, while bladder dysfunction can result from medications such as cholinergic antagonists or opioids. A bladder scan, which is a non-invasive method of detecting bladder volume, can suggest bladder dysfunction as the cause of postrenal failure. Alternatively, a Foley catheter or straight catheter may be placed (if it is not already in place) to look for the presence of retained urine. In patients with a Foley catheter already in place, the catheter should be checked for patency and flushed, if necessary, to ensure proper position. Postrenal causes can frequently be detected by one of these simple maneuvers, and in most cases a postrenal source of oliguria should be ruled out first because it is quick and easy to do so.

Prerenal causes, namely renal hypoperfusion, may represent 90% of perioperative AKI,^[1] although it is not clear at what point prolonged hypoperfusion causes acute tubular necrosis (ATN), which may be the underlying pathology in many cases of perioperative AKI.^[2] Prerenal AKI is due to decreased renal perfusion, usually through hypotension, hypovolemia, decreased cardiac output, renal artery stenosis, or sepsis. Oliguric patients in the PACU who experienced prolonged intraoperative hypotension or significant surgical blood loss should be aggressively managed with crystalloids, red blood cells, and, if needed, inotropes and vasopressors to maintain adequate renal perfusion and prevent the development of permanent kidney damage. Indeed, optimization of hemodynamics, especially blood pressure, in the perioperative period has been found to decrease both postoperative AKI and mortality.^[5] Patients in the PACU commonly develop oliguria, and a simple initial therapy involves the administration of a fluid challenge. Unless an obvious source of renal insult exists (a large dose of a nephrotoxin or a urethral obstruction, for example), the practitioner is left with an uncertain etiology, and a fluid challenge offers little downside in the large majority of patients. An increase in urine production following fluid administration suggests hypovolemia as the problem, while a lack of a response may prompt one to consider other causes, such as cardiac failure, sepsis, or intrinsic renal pathology. A BUN:creatinine ratio >20 suggests a prerenal cause, as does a fractional excretion of sodium (FENa) of <1%.^[6] Some patients may require multiple fluid boluses to establish urine output; however, be wary of the patient who does not respond after significant fluid administration as another cause may be likely.

The third type of renal failure seen in the PACU is that involving intrinsic renal injury. Common sources of such injury include medications (aminoglycosides, angiotensin-converting enzyme [ACE] inhibitors, vancomycin, non-steroidal anti-inflammatory drugs [NSAIDs], intravenous contrast dye), endotoxin, myoglobin, and prolonged ischemia.^[1] AKI due to prerenal causes, such as hypotension, can progress to ATN if not corrected. If one suspects an intrinsic renal problem, consultation with a nephrologist is recommended, as prompt treatment is mandatory.

Chronic renal failure

Patients with chronic renal failure (CRF) frequently undergo surgical procedures, and as a result those involved in PACU care are faced with the challenge of caring for them. The following discussion will focus on patients with end stage renal disease (ESRD) on dialysis. Overall, the increase in mortality in patients with ESRD who undergo general surgery is greater than 4%, significantly higher than that of patients with normal renal function.^[7,8] During the handoff from the intraoperative to the postoperative period, the timing of the last dialysis session and the frequency of dialysis should be mentioned. A CRF patient who was dialyzed several days ago can present very differently from one who received dialysis several hours prior to surgery. The patient’s current weight and dry weight (if known) should be discussed, as this is often a good indicator of his or her fluid status. A plan for fluid management in the PACU should be made and the choice of fluid should also be determined, although the commonly held belief that lactated Ringer’s solution (which contains a small amount of potassium) should be replaced with normal saline in ESRD patients is unfounded.^[9]

Electrolyte abnormalities: Patients with ESRD exhibit multiple electrolyte abnormalities, the most important of which for the practitioner in the PACU is hyperkalemia. Patients with CRF are at greater risk for hyperkalemia due to both decreased excretion and increases from multiple sources, such as blood products, medications, and a shift of potassium from the intra- to the extracellular compartment that follows acidosis.^[7] It is the most frequent cause of perioperative morbidity in patients with ESRD.^[7] Of primary concern to those providing care in the PACU are possible electrocardiogram (ECG) changes that can occur with hyperkalemia. At potassium levels of 5.5 to 7.0 mmol/l, tall, peaked, narrow T waves are observed, along with fascicular block.^[10] This can progress to ST segment depression and eventually sinus arrest. Any ESRD patient with these changes observed on the PACU monitor should have a 12-lead ECG performed and a serum.

The chronicity of the patient’s hyperkalemia and his or her baseline potassium level can also play a role in guiding the decision to treat or not. A patient with baseline potassium of 5.0 mmol/l, for example, may tolerate the increase to 6.0 mmol/l better than a patient with baseline potassium of 4.0 mmol/l. Treatment of acute hyperkalemia in the PACU involves administering calcium carbonate or calcium gluconate to stabilize cardiac membranes and prevent lethal arrhythmias, followed by insulin with glucose to shift potassium from the extracellular compartment to the intracellular compartment. A recent review concluded that insulin, at a dose of 10 to 20 units, effectively decreases serum potassium levels 0.5 to 1.0 mmol/l faster than albuterol for a period of about 2 hours.^[11] It must be given with glucose to prevent hypoglycemia.

Nebulized albuterol and other β₂ agonists are another effective treatment of hyperkalemia. However, they may take up to 30 minutes to take effect, making them less desirable in the PACU setting.^[11]

Sodium bicarbonate, advocated by some for hyperkalemia treatment, has not been shown to be as effective as insulin and β₂ agonists for the acute setting.^[11]

Postoperative bleeding and anemia: For multiple reasons, patients with CRF are more likely to bleed postoperatively than patients with normal renal function. First, CRF patients have a qualitative platelet dysfunction that impairs the platelet–platelet and platelet–vessel wall interactions, creating a propensity to bleed.^[12] The dysfunction is not typically severe enough to cause spontaneous bleeding but with the insult of surgery can certainly make existing bleeding more significant. Second, CRF patients often have co-morbidities, such as atrial fibrillation, coronary artery disease, and valvular disorders, that require anticoagulation. A large, prospective cohort study found that the incidence of atrial fibrillation in patients with mild to moderate renal failure was 20%, which is three times the incidence in the general population, and 25% in those patients age 70 or greater.^[13] Consequently, many CRF patients take warfarin, or various other medications that affect coagulation. One needs a high index of suspicion for bleeding in the PACU as a possible cause of postoperative hypotension in a patient with ESRD, especially in abdominal, thoracic, or orthopedic surgery where the bleeding may not be obvious.

ESRD patients on dialysis are frequently anemic because of the inability of the failing kidney to effectively produce erythropoietin. This decreases aerobic capacity and quality of life and could worsen myocardial dysfunction in certain patients.^[14] As a result, surgical blood loss that would ordinarily not be problematic in normal patients can compromise oxygen delivery to the tissues or necessitate blood transfusion.