Perioperative Management of the Cirrhotic Patient
The management of acute surgical pathologies in patients with advanced liver disease can be challenging for even the most experienced surgeon. Appropriate surgical decision making requires an understanding of not only the surgical problem itself, but also
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Perioperative Management of the Cirrhotic Patient Maamoun A. Harmouch and Mark J. Hobeika
Etiology and Clinical Manifestations of Cirrhosis Cirrhosis is the eventual result of chronic hepatocellular injury resulting from multiple etiologies (Table 4.1) [1, 2]. During the past decade the most common etiologies of cirrhosis have been chronic hepatitis C infection, alcoholic liver disease, and non-alcoholic steatohepatitis (NASH) [3]. As a result of demographic changes, the obesity epidemic, and the recent introduction of novel treatments for hepatitis C, NASH is expected to become the most common cause of cirrhosis in the coming decades [2]. In a recent study, NASH was the most rapidly rising etiology of cirrhosis, increasing in prevalence by 4 fold between 2004 and 2012 [3]. Importantly, 69 % of patients with chronic liver disease are unaware of their disease, and thus a high index of suspicion and vigilance is required by the evaluating surgeon [1]. Clinical manifestations of cirrhosis result from both primary hepatocellular synthetic dysfunction and portal hypertension and affect multiple organ systems in the perioperative setting (Table 4.2). Chronic and repetitive injury to hepatocytes results in diffuse inflammation and fibrosis of liver parenchyma with subsequent development of regenerative nodules. As fibrosis progresses, the intrahepatic vasculature is distorted leading to portal hypertension. In addition, a significant degree of circulatory shunting occurs which deprives
M.A. Harmouch Department of Surgery, The University of Texas Health Science Center at Houston, 6431 Fannin Street, MSB 6.254, Houston, TX 77030, USA e-mail: [email protected] M.J. Hobeika (*) Department of Surgery and Internal Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, MSB 6.254, Houston, TX 77030, USA e-mail: [email protected]
hepatocytes from blood exposure, resulting in impaired hepatocyte synthetic function. The combination of portal hypertension and impaired synthetic function leads to the anatomic and metabolic derangements that make the cirrhotic patient a very challenging operative candidate. Each of these complications of liver disease may influence periand intra-operative decision making during surgical care of the cirrhotic patient.
Coagulopathy Hepatocellular synthetic dysfunction results in abnormal production of vitamin-K dependent factors II, VII, IX, and X, as well protein C and S [4–7]. This synthetic dysfunction is compounded by poor absorption of vitamin K in patients with significant cholestasis [8, 9]. As a result, conventional tests of coagulation status such as the International Normalized Ratio (INR) may be significantly abnormal in cirrhotic patients. These conventional tests must be interpreted with caution because cirrhotic patients may in fact be hypercoagulable despite an elevated INR due to imbalances in the ratio of pro-thrombotic factors and anti-thrombotic factors [5–7]. Newer tests of coagulation status such as the thromboelastography (TEG) may
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