Case Scenario: Hemodynamic Management of Postoperative Acute Kidney Injury EDUCATION

A cute kidney injury (AKI) is associated with poor outcome both in critically ill patients and after major surgery. 2 Several risk factors of postoperative AKI have been identified, and may help identifying patients with the highest risk of AKI. However, recognizing contributors to AKI (e.g., systemic inflammation, systemic hemodynamics alterations, nephrotoxic agents, and others) remains a challenge for anesthesiologists and intensivists because these factors are often associated and AKI multifactorial. The early diagnosis of AKI remains another issue. Interest in the development and validation of AKI biomarkers has increased among the medical community. In this article, we analyze the risk factors of and contributors to AKI after major surgery, and specifically discuss the strategy of fluid management and potential negative outcome associated with inappropriate fluid administration, with a case scenario intended to illustrate the current knowledge of perioperative AKI. We emphasize hemodynamic management for the prevention and correction of acute renal failure. Case Report A 59-yr-old woman with a history of diabetes and hypertension underwent abdominal surgery for recurrent ovarian cancer. She had received systemic chemotherapy during the 18 months preceding the surgery, including paclitaxel, carboplatin, bevacizumab, doxorubicin, and cyclophosphamide, and had remained asymptomatic since then. The surgery included an ovarian resection and peritoneal carcinosis cytoreduction. The only preoperative medication was an angiotensin-converting enzyme inhibitor to treat arterial hypertension. The preoperative creatinine clearance was estimated at 80 ml/min (Modification of Diet in Renal Disease formula). Because she was asymptomatic (no dyspnea or recent change in her clinical status), left ventricular function was not preoperatively assessed. The known large fluid losses associated with peritoneal carcinosis cytoreduction, intraoperative oliguria, and hypotension led to the infusion of a total of 24 ml·kg −1 ·h −1 of crystalloids during the 9-h surgery (half saline and half Ringer's lactate solutions). Perioperative maintenance of mean arterial pressure at 70 mmHg was achieved by intravenous infusion of neosynephrine (0.35 μg·kg −1 ·min −1 ). In the recovery room, cold extremities and discrete knee mottles were noted, which motivated a switch to norepinephrine infusion (0.2-0.3 μg·kg −1 ·min −1 ). Because of oliguria during the surgical procedure and anuria in the immediate postoperative period, with urine output less than 0.5 ml·kg −1 ·h −1 , the patient was transferred to the postoperative intensive care unit (Icu). Blood analysis showed a metabolic acidosis, with a chloride concentration of 114 mM and bicarbonates of 12 mM, with a normal anion gap (14 mM). Serum alanine aminotransferase and alanine transaminase were increased (245 and 257 u, respectively), and serum troponin t was 0.223 μg/l. Icu-admission urine level of neutrophil gelatinase-associated lipocalin was 353 ng/mmol urine creatinine. Serum cystatine c was 1 mg/l

Short-and Long-term Prognostic Value of Postoperative Cardiac Troponin I Concentration in Patients Undergoing Coronary Artery Bypass Grafting

Background: The value of postoperative cardiac troponin I (cTnI) has been shown to indicate a higher risk of in-hospital death after cardiac surgery. The authors therefore assessed the long-term prognostic value of cTnI in patients undergoing elective coronary artery bypass grafting. Methods: Consecutive patients (n ‫؍‬ 202) were included and divided into two groups according to the postoperative value of cTnI (< or > 13 ng/ml). In-hospital mortality and nonfatal cardiac events (delayed extubation > 24 h; postoperative requirement of inotropic agent; ventricular and supraventricular arrhythmia; postoperative myocardial infarction) were recorded. Survivors were then followed up over a 2-yr period. Data are median and odds ratio (95% confidence interval). Results: Of all patients, 174 (86%) had a low cTnI (4.1 ng/ml; range, 1.1-12.6) and 28 (14%) had a high cTnI (23.8 ng/ml; range, 13.4 -174.6). In-hospital mortality was not significantly different (4 vs. 2%), whereas long-term mortality (18 vs. 3%, P ‫؍‬ 0.006) and mortality from cardiac cause (18 vs. 1%, P < 0.001) was greater in patients with a high cTnI. A high cTnI was a significant factor predicting death (odds ratio, 7.3 [2.0 - 27.1]) or death from cardiac causes (odds ratio, 37.4 [4.2-334.4]). Nonfatal cardiac events were also more frequent in the hospital (64 vs. 41%, P ‫؍‬ 0.02) and within the 2-yr follow-up period (39% vs. 16%, P ‫؍‬ 0.03) in patients with high cTnI. Conclusion: A high postoperative peak of cTnI is associated with increased risk of death, death from cardiac causes, and nonfatal cardiac events within 2 yr after coronary artery bypass grafting

EDUCATION Case Scenario: Postoperative Liver Failure after Liver Resection in a Cirrhotic Patient

H EPATIC resection for malignant liver tumors improves overall survival. However, liver surgery continues to be associated with significant morbidity and mortality. 1 A combination of careful patient selection, meticulous operative technique and specialized perioperative care is required to achieve low perioperative mortality (less than 5%) even in cases of hepatocellular carcinoma resections in cirrhotic patients. 1 Postoperative hepatic failure (POLF) is one of the most serious complications following liver surgery with a mortality that can exceed 70%. 2 The aim of this case scenario is to highlight the perioperative management of POLF after liver resection for hepatocellular carcinoma in patient with cirrhosis. Case Reports A 51-yr-old man with hepatocellular carcinoma in the setting of hepatitis B cirrhosis was scheduled for a right hepatectomy. He had been diagnosed with chronic hepatitis B 6 yr ago and had no other significant medical conditions. A rise in ␣-fetoprotein to 700 ng/ml led to the diagnosis of two hepatocellular carcinoma tumors in the right liver (60 mm in segment VII and 25 mm in segment IV and VIII) delineated on computed tomography (CT) scanning. Preoperative assessment did not show esophageal varices, portal hypertension, ascites, or evidence of portal vein thrombosis on abdominal CT-scan. Nontumor liver biopsy displayed macronodular cirrhosis. Bone scintigraphy and lung CTscan did not show any evidence of metastasis. Preoperative liver and kidney functions were normal. There was no evidence of ongoing hepatitis B viral replication. An arterial chemoembolization of the segment IV artery was performed first, followed by a right venous portal embolization to induce hypertrophy of the left liver 1 month later. 3 Four weeks after embolization, a postprocedure liver CT-scan showed a 10% increase in the volume of the left liver, suggesting that the postoperative remaining liver volume would be approximately 40% of the original liver volume. A right hepatectomy (resection of hepatic segments V, VI, VII, and VIII) was performed 6 weeks after portal embolization. Anesthesia consisted of propofol, sufentanil, atracurium, and desflurane. Perioperative hemodynamic monitoring was performed with a radial artery catheter, a right internal jugular catheter and esophageal doppler. Intermittent portal clamping lasted 34 min. There were no intraoperative complications and no red cell transfusions were required. The patient was extubated in the operating theater and then transferred to the intensive care unit as part of standard postoperative care. The patient was alert and hemodynamically stable, without respiratory or renal failure. Postoperative analgesia was provided through patient-controlled analgesia with morphine. Acetaminophen was not given. Immediate postoperative data showed metabolic acidosis with hyperlactatemia (4 mM), which normalized after 12 h. Postoperatively, bilirubinemia increased steadily and prothrombin time (PT) remained low (vitamin K had been supplemented)