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INTRODUCTION AND EPIDEMIOLOGY

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This chapter discusses the ED presentation, evaluation, and treatment of acute hepatitis, chronic liver disease, and fulminant liver failure. Specific entities addressed in this chapter include viral and toxic hepatitis, nonalcoholic fatty liver disease (NAFLD), and complications of cirrhosis including coagulopathy, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and hepatic encephalopathy. Cholecystitis and biliary colic are addressed in Chapter 79, “Pancreatitis and Cholecystitis.” Variceal bleeding is addressed in Chapter 75, “Upper Gastrointestinal Bleeding.”

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PATHOPHYSIOLOGY

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Acute hepatitis is caused by an infectious, toxic, or metabolic injury to hepatocytes. The initial injury leads to inflammation, cellular death, and eventual scarring in the liver. In chronic disease, liver parenchyma is replaced by fibrous tissue, which separates the functioning hepatocytes into isolated nodules. This disruption of the normal tissue structure can become severe and lead to the central characteristics of cirrhosis and liver failure: loss of metabolic and synthetic function at the cellular level, and portal hypertension, ascites formation, and portal-systemic shunting at the gross level.

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Hepatic disease impairs the liver’s synthetic functions, including production of albumin as well as coagulation and anticoagulation factors. The liver is responsible for production of the vitamin K–dependent clotting factors II, VII, IX, and X; proteins C and S; and other elements of the clotting and thrombolytic processes.1 Inadequate production of these clotting factors makes uncontrolled bleeding one of the life-threatening features of liver disease and a potentially serious complication of hepatic failure.

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Portal hypertension is the increased hydrostatic pressure in the portal vein and its feeder vessels caused by resistance to blood flow through the cirrhotic liver. It eventually causes esophageal and gastric varices and portal-systemic shunting. Increased hydrostatic pressure in the intraperitoneal veins, hypoalbuminemia, and poor renal management of sodium and water lead to ascites in the cirrhotic patient. Ascites can cause respiratory compromise when abdominal distension increases intrathoracic pressure. It can also lead to spontaneous bacterial peritonitis (SBP), which occurs when normal flora translocate across an edematous bowel wall into the peritoneal cavity. Bacteremia and infection of preexisting ascitic fluid ensue.2

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Encephalopathy is a pivotal characteristic of chronic liver disease and is a hallmark of liver failure. Ammonia is often presumed to be the cause of confusion and lethargy in encephalopathic patients but, in fact, the pathophysiology is not completely understood. In cirrhosis, portal hypertension allows ammonia formed by colonic bacteria to enter the general circulation through portal-systemic shunting. Large intestinal protein loads, such as a high-protein meal or GI bleeding, fuel this process. Although levels of ammonia do not reliably correlate with mental status, it is reasonable to think of ammonia as a contributing factor to alterations in mental status. In fulminant liver failure, cerebral edema and resulting increased intracranial pressure can develop. In this end-stage state, loss of autoregulation of cerebral blood flow, ammonia-related edema, and a systemic inflammatory response are all thought ...

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