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VII

Chapter 19

Acute Kidney Injury

Reena Julka and Ashok Reddy

Acute kidney injury (AKI) remains a signi fi cant concern in the periop-erative period. The incidence of postoperative AKI has been found to be approximately 1 % in noncardiac surgical patients [ 1, 2 ] . In those admitted to the ICU after noncardiac surgery, the AKI rate has been shown to be 7.5 % [ 3 ] . Some studies indicate higher rates [ 3, 4 ] , and reports may vary according to the de fi nition of AKI which has evolved over recent years. AKI is associated with signi fi cant morbidity and mortality in hospitalized patients. It has further been associated with increased 30-day, 60-day, and 1-year all-cause mortality [ 1 ] .

PREOPERATIVE EVALUATION Patients should undergo risk assessment to include assessment of baseline renal function, and identi fi cation of those patients with chronic kidney disease (see Chap. 18 ).

RISK PREDICTORS A large retrospective study identi fi ed seven independent preop- ■

erative predictors of postoperative renal dysfunction (de fi ned as a Cr Cl <50 ml/min) [ 1 ] . They were age, emergent surgery, liver disease, body mass index, high-risk surgery, peripheral vascular occlusive disease, and chronic obstructive pulmonary disease necessitating chronic bronchodilator therapy. Several intraoperative management variables were independent predic-tors of acute renal failure: total vasopressor dose administered, use of a vasopressor infusion, and diuretic administration. In evaluating patients with postoperative acute kidney injury ■

(AKI) admitted to the ICU, similar risk factors were found, but ischemic and congestive heart disease, an elevated Revised

C.J. Wong and N.P. Hamlin (eds.), The Perioperative Medicine Consult Handbook, DOI 10.1007/978-1-4614-3220-3_19, © Springer Science+Business Media New York 2013

128 THE PERIOPERATIVE MEDICINE CONSULT HANDBOOK

Cardiac Risk Index score, and American Society for Anesthesiologists (ASA) physical status were identi fi ed as additional predictors [ 3 ] . A speci fi c risk index for AKI after general surgery has subse- ■

quently been developed. The signi fi cant independent risk fac-tors that were identi fi ed were age 56 or older, male gender, active congestive heart failure, ascites, hypertension, emer-gency surgery, intraperitoneal surgery, mild or moderate renal insuf fi ciency (de fi ned as preoperative creatinine between 1.2 and 1.9 or >2), and diabetes on oral or insulin therapy. Compared with 0–2 risk factors, having 3, 4, 5, 6, or more risk factors conferred a hazard ratio of AKI by 3.1, 8.5, 15.4, and 46.2, respectively [ 2 ] .

POSTOPERATIVE MANAGEMENT As with all patients, efforts should be made to minimize the risk of developing AKI.

DE FI NITION The Risk-Injury-Failure-Loss-End (RIFLE)-stage kidney dis- ■

ease and Acute Kidney Injury Network (AKIN) classi fi cations were developed to provide a consensus de fi nition and to aid in early detection and grading of severity of AKI. Early severity kidney injury is de fi ned as urine output <0.5 ml/ ■

kg/h for >6 h. Further, the RIFLE criteria include a GFR decrease >25 % or a 50 % increase in serum creatinine above baseline within a 7-day window. Meanwhile, the AKIN criteria additionally specify an increase in creatinine of 0.3 mg/dl within 48 h to re fl ect that small changes within the “normal range” can actually be signi fi cant [ 4, 5 ] .

APPROACH TO POST-OP AKI Consider the following differential diagnoses:

Prerenal Causes Most patients having procedures third space considerable ■

quantities of fl uid at their surgical site. As a result they are typi-cally intravascularly volume depleted. Signi fi cant output from NG tubes or diarrhea may also exacerbate the situation. When a patient appears to be acutely volume de fi cient a check of the

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hematocrit is reasonable as bleeding is also a common cause of acute hypovolemia and one that deserves acute attention. Acute renovascular compromise or atherosclerotic emboli can ■

occur, particularly with aortic surgery and some nephrecto-mies, but this should be obvious by the history, discussion with the team, and/or operative note. Pre-renal azotemia can occur with severe congestive heart failure (due to poor forward fl ow from the heart to the kidneys), but these patients are usually obvious by history, exam, or laboratory fi ndings. In the appro-priate patient population one should also consider pancreatitis, sepsis, abdominal compartment syndrome, and cirrhosis as pre-renal causes of AKI.

Renal Causes The most common renal cause for postoperative AKI is acute ■

tubular necrosis (ATN). Patients with intra- or postoperative hypotension are at the highest risk and a review of the anesthe-sia record and postoperative vital signs can be very helpful in these circumstances. As with other forms of trauma, creatinine kinase levels will rise ■

after surgery; speci fi cally, obese patients and those with long procedures are at risk for rhabdomyolysis. A check of serum CK or urine myoglobin is reasonable. Acute interstitial nephri-tis (AIN) can occur, with one potential cause being periopera-tive medications such as antibiotics. Urine sediment may show white blood cells, red blood cells, white cell casts, and eosino-philuria. Intravenous contrast administered during radiology procedures may exacerbate renal insuf fi ciency.

Postrenal Causes When patients with acute renal insuf fi ciency are post-op from ■

abdominal procedures it is reasonable to check an ultrasound to assess that they do not have unilateral or bilateral hydro-nephrosis due to some unexpected consequence of their surgery. Kidney stones may also form acutely, and these can also be ■

identi fi ed (or at least the obstruction noted) by ultrasound. If bladder outlet obstruction is suspected, a bladder scan (or ■

single I/O cath) can help eliminate this concern immediately (although it should be noted that bladder scans are dif fi cult to interpret in patients with ascites). For patients with an indwell-ing catheter and an indeterminate bladder scan, consider fl ush-ing the catheter once to assure that it is not obstructed.

130 THE PERIOPERATIVE MEDICINE CONSULT HANDBOOK

EVALUATION Patients need a thorough review of their records with attention ■

to vital signs, input/output, weights, medications, and recent studies. Findings on physical exam of tachycardia, a low JVP, poor skin turgor, dry mucous membranes, and minimal amounts of concentrated urine suggest volume depletion. In dif fi cult cases when patients are not responding as expected to fl uid challenges, measurement of central venous pressure with a central venous catheter can be helpful. A marked increase in clear output from pelvic or abdominal ■

drains should raise concerns for urinary leaks or fi stula forma-tions. A spot fl uid creatinine performed on the drain output will settle the question quickly. Drain output usually has a crea-tinine value that is near serum levels. When a drain is contami-nated by urine the creatinine in the fl uid is usually markedly elevated (10- to 100-fold). Placement of a Foley catheter may be appropriate in some cir- ■

cumstances to monitor urine output closely and to assess for distal obstruction. Renal ultrasound may be used when indi-cated to assess for proximal urinary tract obstruction and extra-vesicular fl uid collections. Laboratory studies should include a basic metabolic panel, ■

complete blood count, and full urinalysis with examination of sediment, along with a urinary Na, creatinine, and osmolality. High urinary speci fi c gravity/osmolarity, a low urinary sodium, and <1 % fractional excretion of sodium (FENa) support the diagnosis of prerenal azotemia (see below). The changes of ATN are typi fi ed by muddy brown granular and epithelial cell casts. The presence of signi fi cant number of red cells may indi-cate a stone or a ureteral trauma. Excessive number of eosino-phils can indicate interstitial nephritis. Urine myoglobin and/or blood without RBCs in urinalysis can suggest rhabdomyoly-sis (Table 19.1 ).

MANAGEMENT Because hypovolemia is the most common cause of postopera- ■

tive renal insuf fi ciency, treatment should generally start with a vigorous fl uid resuscitation. Classically lactated ringers or nor-mal saline are used for resuscitation. However, caution should be used with massive infusions of normal saline as it can precipitate hyperchloremic metabolic acidosis. Routine use of diuretics in the immediate postoperative period is generally contraindicated. If there is any doubt about the patient’s

131CHAPTER 19: ACUTE KIDNEY INJURY

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intravascular volume status, measurement of the central venous pressure may be helpful. If the patient’s renal function does not improve once it is deter- ■

mined that the patient is volume replete, then a search for an alternate diagnosis should be started. If the patient maintains reasonable urine output, then fl uids can be continued at a maintenance rate. If urine output falls off, some attempt at maintaining urine output with IV furosemide may be worth considering. If there is any concern for an obstructive process (e.g., recent abdominal or pelvic surgery) an ultrasound should be performed immediately. Any medications that could be adversely affecting renal function should be discontinued if possible and all other medications should be adjusted for the patient’s current level of renal function (See Chap. 18 for man-agement details). Nephrology consultation is usually advisable.

DISCUSSION Although risk factors have been identi fi ed for development of ■

post-op AKI, there has been a lack of reliable evidence behind pharmacologic strategies during surgery to prevent AKI [ 6 ] . A meta-analysis has not shown n -acetylcysteine to prevent AKI after major surgery [ 7 ] . However, recent literature suggests that

TABLE 19.1 URINE CHARACTERISTICS IN THE WORKUP OF ACUTE KIDNEY INJURY

Urine fi ndings Pre-renal Renal

Urinary sediment None or hyaline casts

Muddy brown casts, eosinophils

Speci fi c gravity >1.020 <1.010 Osmolality >500 <350 Sodium <20 >40 Fractional excretion of sodium

<1 >1

Fractional excretion of sodium: ×= ××

UNa PCrFENa, percent 100,

PNa UCr

where U = urine, P = plasma, Na = sodium, Cr = creatinine

132 THE PERIOPERATIVE MEDICINE CONSULT HANDBOOK

statin use preoperatively is associated with lower odds of AKI, acute dialysis, and mortality [ 8 ] . While some of the causes of AKI are similar to those of medical ■

patients, it is important to remember the causes of AKI that are speci fi c to surgery. Patients undergoing cardiac surgery with the use of cardiopulmonary bypass have a high occurrence of AKI, ranging around 20–30 %. The etiology is felt to be multi-factorial, including reduced renal perfusion pressure, activa-tion of proin fl ammatory agents, and possibly direct nephrotoxicity [ 5 ] . Similar etiologies have been identi fi ed for postoperative AKI in noncardiac surgery including prerenal/hemodynamic factors and a surgery-related in fl ammatory response with activation of cytokines and leukocyte in fi ltration [ 4 ] . Other possible contributors are exposure to renally toxic agents (contrast, myoglobin, anti-in fl ammatories, aminoglyco-sides), surgical trauma (e.g., cross clamping of the aorta), and surgical complications (ligation of a ureter).

REFERENCES 1. Kheterpal S, Tremper KK, Englesbe MJ, et al. Predictors of postoperative acute renal failure

after noncardiac surgery in patients with previously normal renal function. Anesthesiology. 2007;107:892–902.

2. Kheterpal S, Tremper KK, Heung M, et al. Development and validation of an acute kidney injury risk index for patients undergoing general surgery. Results from a national data set. Anesthesiology. 2009;110:505–15.

3. Abelha FJ, Botelho M, Fernandes V, Barros H. Determinants of postoperative acute kidney injury. Crit Care. 2009;13:R79.

4. Brienza N, Giglio M, Marucci M. Preventing acute kidney injury after noncardiac surgery. Curr Opin Crit Care. 2010;16(4):353–8.

5. Kumar A, Suneja M. Cardiopulmonary bypass-associated acute kidney injury. Anesthesiology. 2011;114(4):964–70.

6. Zacharias M, Conlon NP, Herbison GP, et al. Interventions for protecting renal function in the perioperative period. Cochrane Database Syst Rev. 2008;4:CD003590.

7. Ho KM, Morgan DJ. Meta-analysis of n-acetylcysteine to prevent acute renal failure after major surgery. Am J Kidney Dis. 2009;53(1):33–40.

8. Molnar AO, Coca SG, Devereaux PJ, et al. Statin use associates with a lower incidence of acute kidney injury after major elective surgery. J Am Soc Nephrol. 2011;22(5):939–46.