Chapter 80: Hepatic Disorders

INTRODUCTION AND EPIDEMIOLOGY

This chapter discusses the ED presentation, evaluation, and treatment of acute and chronic liver disease as well as fulminant liver failure. Specific entities addressed in this chapter include viral and toxic hepatitis, nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), 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."

Liver disease is associated with many ED complaints: abdominal pain, vomiting, shortness of breath, altered mental status, GI bleeding, and even nonspecific malaise can all be attributed to malfunction of the liver. Globally, hepatitis A, B, C, D, and E are major public health problems. About two billion people are infected with hepatitis B and 150 million with hepatitis C, and cancer and cirrhosis resulting from these infections account for about 3% of deaths worldwide.¹ Cirrhosis is the 12th leading cause of death in the United States, and hepatitis C is the leading cause of cirrhosis in the United States, followed by alcoholic liver disease.² Acute, or fulminant, liver failure is uncommon and is caused primarily by acetaminophen poisoning (46%), with hepatitis B being the most common infectious cause.³

PATHOPHYSIOLOGY

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 liver failure: loss of metabolic and synthetic function at the cellular level, progressive development of portal hypertension, ascites formation, and portal-systemic shunting at the gross level.

The liver's synthetic functions include the production of 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.⁴ Inadequate production of these clotting factors makes uncontrolled bleeding one of the life-threatening features of liver disease and a potentially dramatic complication of hepatic failure.

Portal hypertension is 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. The 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 and lead to spontaneous bacterial peritonitis (SBP), which occurs when normal flora translocate across an edematous bowel wall into the peritoneum. Bacteremia and infection of preexisting ascitic fluid ensue.⁵

Encephalopathy is a pivotal characteristic of chronic liver disease ...