Epidemiology: The number of cases of hepatitis A declined steadily from 12.0 cases per 100,000 population in 1995 to 1.0 case per 100,000 population in 2007.1,2 Western states have historically shown a higher incidence of hepatitis A, which in 1999 led to routine vaccinations of children from these areas. The greater decline in incidence of hepatitis A among children has resulted in a relative increase in the proportion of cases among adults.³ The number of reported cases of hepatitis B declined by more than 80% in the interval between 1990 and 2005, again with the greatest decline occurring among children younger than 15 years.³ The number of new cases of hepatitis C declined by approximately 80% during this period.² The reduced rates of hepatitis A and B most likely reflect today’s broad use of effective vaccines.⁴ Since the late 1980s, the incidence of acute hepatitis C has declined as a consequence of improved blood product screening. A majority of cases occur among adults, with injection drug use recognized as the most common risk factor.³

Hepatitis A virus (HAV), the causative agent of hepatitis A, is an RNA enteroviral picornavirus. It is spread by the fecal-oral route either directly or through contaminated water or foodstuffs. Transmission by blood is a theoretic possibility but is exceedingly rare. HAV can occur sporadically but is notorious for its association with epidemics generally linked to common-source outbreaks. HAV infection is common worldwide; serologic evidence of previous infection exists in nearly 100% of the adult population in some regions. In the United States, close to one half of all urban-dwelling adults are seropositive for antibody for HAV.⁵ High rates of seropositivity in association with the relatively small number of reported episodes support the notion that many cases may be asymptomatic. Occult disease appears to be more common in children, and 70% of those infected may be asymptomatic.⁵ The incidence of hepatitis A infection varies among ethnic groups. In the United States, the incidence among different geographic areas and ethnic groups has changed notably since endemic areas have been targeted for routine vaccination of children. In 2005, recommendations on immunization were expanded to include routine vaccination of children in all 50 states.⁵ The declines have shifted the pattern of reported risk factors, showing an increasing proportion of cases among adults—specifically, men who have sex with men (MSM), illicit intravenous drug users (IVDUs), and non–injection drug users. The most common risk factor for hepatitis A in persons older than 15 years of age is travel outside of the United States.^1,2,5

The typical incubation period for hepatitis A is 30 days, with a range of 15 to 45 days. Viremia is of relatively short duration and is most prominent before the onset of symptoms. Fecal shedding and maximum infectivity occur before the onset of symptomatic disease and generally have waned by the time jaundice appears (Fig. 90-1). HAV is not associated with a chronic carrier state.

Hepatitis B virus (HBV) is contained in a 42-nm structure called the Dane particle. Within this enveloped virion are the viral DNA, DNA polymerase, hepatitis B surface antigen (HBsAg), and hepatitis B core antigen (HBcAg). Hepatitis B e antigen (HBeAg) is an immunologically distinct antigen not incorporated into virions and instead secreted from cells into the serum of infected patients. In contrast to HAV, for which there is only a single antigenic variety, several genotypes of HBV, as defined by surface antigen, are recognized. HBV is transmitted principally by parenteral exposure but also can be transmitted through intimate contact. The highest rates of infection are among IVDUs and homosexual men. Transmission by blood transfusion, previously a common source of infection, has been eliminated because of modern blood bank screening techniques.

HBsAg has been detected in a variety of bodily secretions, including saliva, semen, stool, tears, urine, and vaginal secretions. Although the presence of HBsAg is not synonymous with infectivity, HBV DNA has been identified in several of these fluids and is likely to be infectious. The typical interval between exposure and onset of clinical illness is 60 to 90 days; however, serologic markers of infection generally appear within 1 to 3 weeks (Fig. 90-2). Approximately 10% of adults and 90% of infected neonates with immature immune systems will become asymptomatic chronic carriers of HBsAg.⁶ Health care workers who routinely come in contact with blood have a prevalence of HBsAg of 1 to 2%, and 15 to 30% show serologic evidence of previous infection. Among emergency physicians, seropositivity rates of 12% and 15% have been reported.⁷ The likelihood of becoming chronically infected with HBV varies inversely with the age at which infection occurs. HBV transmitted from HBsAg-positive mothers to their newborns results in HBV carriage in up to 90% of infants, whereas only 6 to 10% of acutely infected adults become carriers.⁶ In general, less than 5% of hepatitis B infections in healthy immunocompetent adults will progress to chronic hepatitis.⁸ Chronic hepatitis is most commonly defined as the presence of HBsAg in serum for longer than 6 months, serum HBV DNA greater than 20,000 IU/mL (105 copies/mL) (lower values are often seen in HBeAg-negative chronic hepatitis B), persistent or intermittent elevation in ALT/AST levels, and a liver biopsy showing chronic hepatitis with moderate or severe necroinflammation.⁹

What was historically referred to as non-A, non-B hepatitis is caused by at least two distinct RNA viruses: hepatitis C virus (HCV) and hepatitis E virus. Before the advent of widespread screening of the blood supply in 1992, hepatitis C was commonly transmitted through blood transfusions and organ transplants in the United States. With the screening of donor blood for surrogate markers (aminotransferases), antibody to hepatitis C, and nucleic acid amplification testing, the hepatitis C transmission risk from blood transfusion has been reduced to approximately 1 in 2 million blood units.¹⁰ The strongest risk factors for HCV infection are a history of intravenous drug use, having had 20 or more lifetime sex partners, and having undergone blood transfusions before 1992.¹¹ Among patients infected with human immunodeficiency virus (HIV), the incidence of coinfection with hepatitis C is 15 to 30%. This rate approaches 50 to 90% in those who acquired HIV through intravenous drug use.¹² Patients coinfected with HIV and HCV generally have a more aggressive course of both infections. In 40 to 57% of cases of hepatitis C, no source of infection is identified. The incubation period for hepatitis C is 30 to 90 days, with a mean of 50 days. Approximately 90% of HCV infections progress to chronic hepatitis. Long-term follow-up studies indicate that clinical liver disease develops in only 10 to 20% of those infected, during a period of approximately 20 years after transfusion.¹² In the United States, it is estimated that 4.1 million persons are infected with HCV, and 3.2 million persons have chronic hepatitis C infection.¹² Hepatitis E, which is associated with fecal-oral transmission, is encountered most often in Asia, Africa, and Russia. Hepatitis E has an incubation period of 15 to 60 days.

Hepatitis delta virus (HDV) was discovered in 1977 in liver specimens from patients with chronic HBV infection. It is a defective RNA virus that can infect only patients who are actively producing HBsAg, which is required for its viral coating. In the United States the incidence of HDV antibody is 4 to 30% of patients with chronic HBV infection.¹³ As a consequence of the routine association with chronic HBV infection, it is likely that many cases of HDV infection are misdiagnosed as acute or reactivated hepatitis B. HDV infection is spread in a manner similar to that for hepatitis B, being most common among IVDUs, promiscuous homosexual men, and patients with hemophilia. Infection with HDV can occur either concomitantly with HBV (coinfection) or subsequent to earlier HBV infection (superinfection), because HDV cannot replicate in the absence of HBV. In cases of superinfection the presentation may range from acute self-limited disease to fulminant hepatitis or chronic infection. Severe or fulminant hepatitis is more often observed with HBV-HDV coinfection than with HBV monoinfection.¹³

Hepatitis G virus (HGV), also referred to as hepatitis GB virus type C, is the most recently identified virus associated with hepatitis. It is an RNA virus in the Flaviviridae family. Transmission of HGV seems to occur through blood transfusion and parenteral exposure to blood or blood products, and possibly during intimate sexual contact. The virus has been identified in patients with acute and chronic hepatitis. However, it generally is believed to be an “innocent bystander,” with disease manifestations attributable to coinfection with another hepatitis virus.¹⁴

Principles of Disease: The pathophysiology of viral hepatitis is not completely understood. In the most common varieties of hepatitis, liver injury appears to be related to the development of the immunologic response to infection rather than to the cytopathologic effect of the virus. HDV appears to be an exception, having significant direct cytotoxic potential.

Clinical Features: The clinical presentation of viral hepatitis is highly variable. A significant number of cases, possibly a majority, are asymptomatic. The protean nature of symptoms and the common occurrence of anicteric disease can result in misdiagnosis. The most common symptoms and signs are malaise, fever, and anorexia, followed by nausea, vomiting, abdominal discomfort, and diarrhea. The first symptom leading to physician consultation typically is jaundice. A small number of patients with hepatitis B may experience a prodromal illness characterized by arthralgia or arthritis and dermatitis. The joint involvement typically is polyarticular; the small joints of the hands and the wrists are most commonly affected. Joint fluid usually is noninflammatory, but cell counts for aspirated fluid can be as high as 90,000/mm³. The characteristic dermatitis is urticarial but may be macular, papular, or petechial.

Fulminant hepatitis is characterized by acute onset and progresses to hepatic failure and encephalopathy over a period of days. Although most often encountered with HBV and HDV coinfection, fulminant hepatitis can occur in association with all of the causative viruses. The overall incidence of fulminant hepatitis is 1 to 2% of all cases. The hallmarks of fulminant disease are altered mentation and spontaneous mucosal bleeding.

Physical findings include elevated temperature, scleral or cutaneous icterus, and abdominal tenderness. If significant vomiting has occurred, tachycardia and supine or orthostatic hypotension may be noted. Hepatomegaly may be detected and generally is characterized by a smooth, homogeneous, and tender liver surface. Even if liver enlargement is not appreciated, the patient often exhibits tenderness to percussion over the lower right ribs. Scleral icterus is generally noticeable earlier than cutaneous discoloration, particularly in people of pigmented races. Muddy sclera, commonly found among African-American patients, may obscure or confuse this finding. An alternative in this setting is examination of sublingual or subungual surfaces. Scleral icterus usually is not clinically apparent until serum bilirubin is above 2.5 mg/dL. Spider angiomata and splenomegaly, although more commonly associated with cirrhosis, may be features in acute presentations. Gray or acholic stools are distinctly uncommon.

Diagnostic Strategies: Laboratory tests are critically important in diagnosing hepatitis and determining the specific cause. The most useful tests are measurements of the hepatic aminotransferases and bilirubin. Typically, hepatitis is associated with elevations (tenfold to 100-fold) of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT), with ALT generally elevated in excess of AST. Bilirubin may be moderately increased (5-10 mg/dL) and occasionally is markedly elevated (15-25 mg/dL). Hyperbilirubinemia typically emerges several days to a week or more after the onset of clinical symptoms. Both direct and indirect bilirubin levels are elevated in close to equal proportions. Alkaline phosphatase and lactate dehydrogenase may be elevated but rarely are more than two to three times normal. Prothrombin time (PT) or international normalized ratio (INR) is useful in assessing the degree of hepatic synthetic dysfunction. Elevation of the PT or INR may be the first clue to a complicated course. The white blood cell (WBC) count generally is not useful in the diagnosis because values range from low overall counts with a lymphocytic predominance to marked polymorphonuclear leukocytosis.

Although determination of the precise cause of hepatitis can rarely be achieved in the ED, this evaluation should be initiated as soon as possible. Identification of the causative agent has significant impact on prognosis and public health issues. In this regard, it is important to be able to interpret the significance of certain serologic tests (Table 90-1).

Acute hepatitis A is diagnosed by the presence of immunoglobulin M (IgM) HAV antibody, whereas previous infection is determined by detection of an immunoglobulin G (IgG) antibody. Acute hepatitis B is characterized by the presence of HBsAg and IgM antibody to HBcAg. HBsAg alone does not establish the diagnosis of acute hepatitis B because it can be either absent late in the course of acute disease or present chronically unrelated to the cause of the current episode. Anti-HBcAg antibody generally is the best indicator of previous HBV infection, whereas anti-HBsAg antibody is the best marker for immunity to HBV.

Currently, the diagnosis of hepatitis C is based on the exposure history and the elimination of other causes. The serologic assay for an antibody to this virus facilitates a definitive diagnosis, but there can be a delay between the onset of symptoms and the development of assayable antibody. Furthermore, the HCV test does not distinguish acute from chronic infection.

Diagnosing HDV infection requires an aggressive search because the disease can easily be mistaken for acute or chronic HBV infection. A serologic test for the antibody to HDV (anti-HDV) is available. The presence of this antibody in conjunction with IgM antibody to HBcAg suggests coinfection with HDV and HBV. Anti-HDV in association with IgG antibody to HBcAg supports the diagnosis of superinfection.

The temporal relationships among infection, clinical symptoms, and serologic responses for the two most common causes of viral hepatitis—HAV and HBV—are delineated in Figures 90-1 and 90-2.

Differential Considerations: The protean nature of the symptoms and signs associated with viral hepatitis makes the differential diagnosis of this disorder quite broad in scope. Beyond a variety of nonhepatic viral illnesses, all of the infectious, chemical, and immunologic causes of hepatic inflammation in addition to biliary tract disease must be considered. A viral cause often is suggested by a history of exposure and a suggestive medical history, but serologic tests are required for confirmation. Alcoholic hepatitis usually is associated with a history of chronic or excessive alcohol consumption, less marked elevation of hepatic transaminases, and AST levels elevated above those of ALT. Extrahepatic obstruction, cholecystitis, and cholelithiasis are excluded by their lack of association with significant elevation of aminotransferases; however, abdominal ultrasound imaging may be required to eliminate these other diseases.

Management: Treatment of viral hepatitis is primarily symptomatic. It often is necessary to correct fluid and electrolyte imbalances secondary to poor oral intake or excessive diarrhea or vomiting. Antiemetics may allow resumption of adequate oral intake, thereby avoiding the need for hospital admission. In the anorexic or nauseated patient, fluid intake should be encouraged, with avoidance of solids until they are palatable. Medications requiring primarily hepatic metabolism generally do not need to be discontinued nor the dosage modified unless there is significant hepatic dysfunction. Nonessential drugs with hepatotoxic potential should be avoided. Alcohol consumption should be completely discontinued until signs of liver injury have disappeared. Although various active interventions (e.g., corticosteroid administration) have been suggested, no reliable data suggest that such therapies offer clear benefit; they may even be harmful.

Complications of acute hepatitis are most commonly related to fluid or electrolyte imbalance as a result of inadequate oral intake or refractory emesis. Severe vomiting can result in upper gastrointestinal (GI) bleeding from an esophageal tear. The most severe complication of acute disease is the development of liver failure, heralded by the emergence of hepatic encephalopathy. Most patients with viral hepatitis have self-limited disease, with symptomatic and histologic resolution in 2 to 4 weeks. Chronic disease will develop in approximately 10% of patients with hepatitis B and in as many as 50 to 84% of those with hepatitis C.¹⁵ Clinical liver disease develops in only 10 to 20% of chronically infected patients within approximately 20 years after becoming infected. Many of these patients will eventually die of cirrhosis secondary to their disease.¹⁵

Disposition: Hospital admission is rarely required for management of viral hepatitis and generally is reserved for the patient with significant fluid and electrolyte imbalance or refractory vomiting. Patients with less severe illness may require hospitalization for concomitant medical problems or if suitable living arrangements are not available. Altered sensorium, prolongation of the PT beyond 5 seconds, or increase in the INR above 1.5 may suggest fulminant disease or an increased likelihood of a complicated course, necessitating hospitalization for observation. The emergence of fulminant disease should lead to consideration of transfer to a facility that can offer liver transplantation.

Treatment with interferon alfa-2b has resulted in a 35 to 45% remission rate after a 4-month course of treatment in selected patients with active immune responses in the symptomatic stage 2 period of hepatitis B infection. Early treatment of acute hepatitis C infection with interferon alfa-2b alone prevents the development of chronic HCV infection in most patients.¹⁵ Hepatitis C treatment recommendations suggest that duration of treatment with interferon and ribavirin should be based on the HCV genotype and pretreatment viral load. Polyethylene glycol added to interferon alfa (peginterferon alfa) extends the half-life and duration of the therapeutic activity of the interferon. Corresponding clinical benefits include both a higher rate of response than with conventional daily interferon monotherapy and feasibility of once-weekly administration. Referral to a hepatic disease specialist is recommended.

Anxiety about disease communicability may affect the ease of disposition. Patients with possible HAV infection should be advised to practice meticulous personal hygiene, not to share toiletries, and to ensure cleaning of utensils and kitchenware between uses. In patients with suspected HBV or HDV infection, the relatively low risk of transmission by means of intimate personal contact or parenteral exposure should be emphasized.

Viral hepatitis is a reportable disease requiring notification of the local health department. Immunoprophylaxis should be provided to the patient’s family members and close personal contacts. Although the nature of prophylaxis depends on the specific viral cause, it is wise to offer gamma globulin to household contacts immediately unless they are known to have been previously immunized, pending serologic determination. Table 90-2 outlines the guidelines for immunoprophylaxis. Patients with HAV infection who process or handle food must not return to work while potentially infectious. Although infectivity is greatly diminished by the time jaundice emerges, it is best to delay return to work until after jaundice has cleared.

Perspective: In the United States, an estimated 15 to 20 million people are chronic alcoholics. Alcohol and its metabolites are toxic to most organ systems and contribute to disease or death from many different causes. The liver is the most common site of injury from chronic ethanol ingestion. Alcoholic liver disease is the third leading preventable cause of death in the United States. Alcohol-associated mortality is disproportionately high among young people, resulting in approximately 30 years of life lost because of alcohol-associated death.¹⁹

Principles of Disease: Alcohol is largely eliminated by metabolic degradation in the liver. Approximately 2 to 15% of alcohol is excreted unchanged in the urine or expired air.²⁰ The precise pathogenesis of alcoholic liver disease is unknown and probably is multifactorial. Coexistent malnutrition, accumulation of toxic metabolites (e.g., acetaldehyde), excessive production of nicotinamide adenine dinucleotide (NADH), induction of microsomal enzymes as a result of the metabolism of alcohol, and alteration of immune function all may play a role.²⁰

Regardless of the precise mechanism of injury, genetic heterogeneity in susceptibility to liver damage is likely. Women and possibly Native Americans appear to have an increased propensity for injury relative to white men. Although susceptibility to alcohol varies, a rough correlation is recognized between the amount of ethanol ingested and the risk of developing liver disease. The risk of liver injury increases as daily consumption exceeds 80 g of ethanol daily in men and 20 g in women. For men, this is equivalent to a six-pack of beer, four to six glasses of wine, or three to four mixed drinks daily.

The most common variety of alcohol-induced liver disease is steatosis. Fatty infiltration of the liver is most likely a consequence of altered fatty acid metabolism resulting from a diminished NAD⁺/NADH ratio, which favors triglyceride production. Fatty infiltration appears to depend on the duration and amount of alcohol consumed and, in general, is reversible when the patient stops drinking. Beyond enlargement of the liver, which usually is painless, this tends to be a benign process.

Clinical Features: Alcoholic hepatitis is a potentially severe form of alcohol-induced liver disease. Most cases probably are subclinical, but the spectrum of presentation can range from nausea, vomiting, and abdominal pain to acute liver failure. Physical findings include tachycardia, fever, and supine or orthostatic hypotension. Abdominal tenderness usually can be elicited, especially in the right upper quadrant. Coexistent fatty infiltration may produce palpable hepatomegaly; cirrhosis from chronic disease may result in a small, nonpalpable liver. The characteristic physical signs of cirrhosis (gynecomastia, spider angiomata, muscle wasting, ascites, and palmar erythema) may be present. Jaundice can be noted in patients with a bilirubin level of at least 2.5 mg/dL.

Diagnostic Strategies: Laboratory tests reveal moderate elevations of AST and ALT. Values in excess of 10 times normal are unusual, even in severe cases associated with eventual liver failure. Compared with viral hepatitis, a relative predominance of AST to ALT is expected. Bilirubin is commonly elevated. The WBC count often is high, with a polymorphonuclear leukocytosis in the range of 10,000 to 20,000/mm³. The PT and the INR provide a rough assessment of hepatic dysfunction. An acutely prolonged PT or elevated INR in a patient not suspected to have chronic cirrhotic disease suggests a complicated course. Electrolyte or acid-base disturbances may develop as a consequence of excessive vomiting or alcoholic ketoacidosis.

Differential Considerations: The differential diagnosis of alcoholic hepatitis is quite broad in scope and includes a variety of other alcohol-related GI maladies (e.g., gastritis, pancreatitis). Patients often have several ethanol-induced diseases simultaneously. Initially, all of the potential etiologic disorders must be considered; however, the clinical history and aminotransferase profile should facilitate accurate diagnosis. Mild aminotransferase elevation and marked bilirubin elevation are consistent with alcoholic hepatitis; ultrasonography will differentiate this from common duct obstruction. Serum should be sent for testing for anti-HAV IgM and hepatitis B core antibody (HBcAb) IgM, but results usually are not available to establish these diagnoses in the ED.

Management: Management of alcoholic hepatitis is principally supportive. Fluid and electrolyte imbalance must be corrected, usually requiring parenteral fluid replacement; antiemetics may mitigate the need for intravenous treatment. Alcohol may suppress gluconeogenesis, thereby causing hypoglycemia. Blood glucose should be measured and supplemented as indicated. Many alcoholics are malnourished, and if thiamine deficiency is suspected, thiamine should be given at a dose of 100 mg intravenously (IV) before glucose administration to avoid induction of acute Wernicke’s encephalopathy. Ethanol-induced magnesium wasting may not be apparent on serum magnesium measurement, and replacement should be given empirically unless the patient has a contraindication such as renal failure or known hypermagnesemia. Magnesium can be given as the sulfate salt in a dose of 1 g IV or IM or as an oxide, chloride salt, or amino acid conjugate for oral replacement therapy at a daily dose of 200 to 1000 mg.

The overall nutritional status of the patient should be addressed with the administration of a high-calorie, vitamin-supplemented diet. Protein content may require restriction if evidence of cirrhosis and incipient encephalopathy exists. Coexisting gastritis should be treated with histamine H₂ antagonists, proton pump inhibitors, or antacids. The patient should be evaluated for GI bleeding and treated appropriately. Corticosteroids, propylthiouracil, insulin-glucagon infusions, pentoxifylline, and anti–tumor necrosis factor alpha (TNF-α) therapy have been investigated for treatment of alcoholic hepatitis and look promising in severe cases, but none of these agents have gained acceptance as part of routine management.20,21

Disposition: Disposition is determined by the patient’s clinical state: the degree of fluid and electrolyte abnormality, the ability to retain oral intake, any coexistent illnesses or complications, and the patient’s socioeconomic circumstances. Admission to the hospital generally is not required. All patients should be advised to abstain from further alcohol ingestion and should be provided referral for detoxification or alcohol dependency treatment.

Principles of Disease: Cirrhosis is a generic term for an end stage of chronic liver disease characterized by destruction of hepatocytes and replacement of normal hepatic architecture with fibrotic tissue and regenerative nodules. Laennec’s cirrhosis is a diffuse process that involves the entire lobule and most often is related to chronic alcohol ingestion. From 10 to 20% of chronic alcoholics develop this type of cirrhosis. Amount and duration of alcohol ingestion, heredity, and underlying nutritional status all seem to play some role in the development of this disorder. Postnecrotic cirrhosis usually is nonhomogeneous, characterized by regions of fibrosis and hepatocyte loss alternating with normal areas. It most often is a consequence of chronic hepatitis of various causes: infectious (viral, bacterial, fungal), drug induced, or metabolic. Biliary cirrhosis is much less common and is a consequence of chronic extrahepatic biliary obstruction or a primary disorder of autoimmune-mediated intrahepatic duct inflammation and scarring. Nonalcoholic fatty liver disease has become an increasingly recognized cause of cryptogenic cirrhosis. This still poorly understood disease, with features similar to those of Laennec’s cirrhosis, is more common in obese patients and those with type 2 diabetes mellitus.²²

Clinical Features: The clinical manifestations of cirrhosis are related to loss of hepatocytes, leading to metabolic and synthetic dysfunction, or to fibrosis and altered hepatic architecture, resulting in impaired portal vein blood flow and portal hypertension. Typically the patient with cirrhosis complains of chronic fatigue and poor appetite. With the exception of those with biliary cirrhosis, many patients with cirrhosis can be asymptomatic until some dramatic complication develops, such as GI bleeding, ascites, or hepatic encephalopathy. Patients with biliary cirrhosis generally complain of pruritus or exhibit obvious jaundice before end-stage cirrhosis or complications develop. Primary biliary cirrhosis may be associated with other immune-mediated disorders; these patients may have signs and symptoms characteristic of scleroderma or the CREST syndrome (i.e., calcinosis cutis, Raynaud’s phenomenon, esophageal motility disorder, sclerodactyly, and telangiectasia).

Physical examination may reveal muscle wasting, thinning of the skin with patchy ecchymosis, spider angiomata, palmar erythema, Dupuytren’s contracture, and in men, gynecomastia or testicular atrophy. Jaundice generally is absent in mild cases or in early disease. The liver may not be palpable if it is extensively scarred, but a large regenerative nodule, tumor, or fatty infiltration can result in hepatomegaly. Ascites is common, particularly in advanced disease, and may be present in association with a characteristic pattern of abdominal wall vein distention known as caput medusae.

Diagnostic Strategies: Laboratory tests are not specific. Aminotransferase levels are rarely more than minimally elevated. Bilirubin may be increased but usually not until cirrhosis is far advanced. Elevation of alkaline phosphatase out of proportion to other liver enzymes is suggestive of biliary cirrhosis. Coagulation studies commonly show abnormalities, and the serum albumin level is low as a result of impaired hepatic synthetic function. Mild to moderate anemia and thrombocytopenia often are present in Laennec’s cirrhosis. Elevated blood urea nitrogen (BUN) or creatinine suggests dehydration or hepatorenal syndrome.

Ancillary tests are rarely of use in the ED setting. Ultrasonography is highly sensitive for the detection of ascites, but a carefully performed physical examination generally can yield equivalent results. In patients with ascites and fever or abdominal pain, paracentesis should be considered to rule out spontaneous bacterial peritonitis (SBP). Nuclear scintigraphy or computed tomography (CT) imaging may reveal a hepatic or splenic appearance characteristic of cirrhosis and portal hypertension, but in general these tests should be deferred to an elective setting.

Management: Treatment of cirrhosis in the ED is limited. Fluid and electrolyte imbalances should be corrected, and vitamin and nutritional supplements should be provided. Most patients can be discharged with referral to a general internist for further evaluation and treatment. Ascites associated with respiratory compromise or significant discomfort can be treated with paracentesis and removal of 2 L of fluid or more. Removal of very large quantities of ascitic fluid can result in body fluid and electrolyte abnormalities and hemodynamic instability. If SBP is a consideration, diagnostic paracentesis should be done.

A low-sodium diet, in conjunction with an aldosterone antagonist, may be of use in the chronic management of ascites. A low-dose regimen of a thiazide or loop diuretic may accelerate resolution of ascites and probably is safe if the patient has coexistent peripheral edema and normal renal function. Coagulopathy noted before a planned invasive procedure or in conjunction with active bleeding should be corrected with fresh frozen plasma. With uncomplicated prolongation of PT or INR, treatment with vitamin K supplementation can be given but often is ineffective. GI bleeding requires aggressive treatment. Early consultation with a gastroenterologist for endoscopy often will permit identification of a bleeding site and initiation of appropriate adjunctive treatment. An elevated creatinine level may herald the onset of hepatorenal syndrome and necessitates hospitalization of the patient for optimal fluid and electrolyte management.

Complications of cirrhosis include GI bleeding, ascites with or without infection, encephalopathy, and hepatorenal syndrome. Although GI bleeding often is related to esophageal or gastric varices, more than one half of the cases result from some other source (e.g., gastritis or a duodenal ulcer). Ascites occurs as a consequence of portal hypertension, impaired hepatic lymph flow, hypoalbuminemia, or renal salt retention. Ascites generally causes few signs and symptoms beyond abdominal distention and discomfort. However, massive ascites can lead to respiratory compromise. SBP is an important and often subtle complication. Encephalopathy occurs as a result of impaired hepatic metabolic function and portal hypertension (see later). Hepatorenal syndrome is defined as renal failure occurring in the setting of cirrhosis without obvious renal pathology. The mechanism of this almost universally fatal complication is not understood. An otherwise unexplained elevation of creatinine or BUN suggests an emerging hepatorenal state.

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