48
Liver, Biliary Tract, and
Pancreas Problems
Mary C. Olson and Christine M. Cervini
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Health Promotion Nutrition
Infection Pain
Inflammation
LEARNING OUTCOMES
1. Distinguish among the types of viral hepatitis. 6. Explain the clinical manifestations and interprofessional
2. Describe the interprofessional and nursing management of and nursing management of the patient with pancreatic
the patient with viral hepatitis. cancer.
3. Explain the pathophysiology, clinical manifestations, 7. Describe the pathophysiology, clinical manifestations, and
complications, and interprofessional and nursing interprofessional care of gallbladder disorders.
management of the patient with cirrhosis. 8. Describe the nursing management of the patient
4. Describe the clinical manifestations and management of undergoing surgical treatment of cholecystitis and
liver cancer. cholelithiasis.
5. Distinguish between acute and chronic pancreatitis related
to pathophysiology, clinical manifestations, complications,
and interprofessional and nursing management.
KEY TERMS
acute liver failure gastric varices
acute pancreatitis hepatic encephalopathy
ascites hepatitis
asterixis hepatorenal syndrome
cholecystitis jaundice
cholelithiasis nonalcoholic fatty liver disease (NAFLD)
chronic pancreatitis nonalcoholic steatohepatitis (NASH)
cirrhosis portal hypertension
esophageal varices
This chapter focuses on the management of patients with a focuses on reducing risk through immunizations and avoiding
wide range of liver, pancreatic, and gallbladder problems. substance use.
These organs are closely positioned together anatomically
and highly associated with their digestive functions. Liver and
pancreas problems can lead to altered nutrient absorption and LIVER PROBLEMS
use, causing malnutrition and impaired elimination. Inflam-
mation may be present, with the patient having pain, nausea,
HEPATITIS
and vomiting. Nursing care focuses on helping the patient and Hepatitis is inflammation of the liver. The most common cause is
caregiver manage symptoms and develop ways to cope with viral. Other causes include substances (e.g., alcohol, medications,
the diagnosis and, sometimes, prognosis. Health promotion chemicals), autoimmune diseases, and metabolic problems.
1135
,1136 SECTION 9 Problems of Ingestion, Digestion, Absorption, and Elimination
TABLE 48.1 Characteristics of Hepatitis Viruses
Incubation Period and Mode of
Transmission Sources of Infection Infectivity
Hepatitis A Virus (HAV)
Incubation: 15–50 days (average 28) • Contaminated food, milk, water, shellfish • Most infectious during 2 weeks before
Fecal-oral (primarily fecal contamination and • Crowded conditions (e.g., day care, nursing home) onset of symptoms
oral ingestion) • Persons with subclinical infections, infected food handlers, • Infectious until 1–2 weeks after the start of
sexual contact, IV drug users symptoms
• Poor personal hygiene
• Poor sanitation
Hepatitis B Virus (HBV)
Incubation: 115–180 days (average 56–96) • Contaminated needles, syringes, and blood products • Before and after symptoms appear
Percutaneous (parenteral) or mucosal exposure • HBV-infected mother (perinatal transmission) • Infectious for months
to blood or blood products • Sexual activity with infected partners. Asymptomatic carriers • Carriers continue to be infectious for life
Sexual contact • Tattoos or body piercing with contaminated needles
Perinatal transmission
Hepatitis C Virus (HCV)
Incubation: 14–180 days (average 56) • Blood and blood products • 1–2 weeks before symptoms appear
Percutaneous (parenteral) or mucosal exposure • Needles and syringes • Continues during clinical course
to blood or blood products • Sexual activity with infected partners, low risk • 75%–85% go on to develop chronic HCV
High-risk sexual contact and remain infectious
Perinatal contact
Hepatitis D Virus (HDV)
Incubation: 2–26 weeks • Same as HBV • Blood infectious at all stages of HDV
HBV must precede HDV • Can cause infection only when HBV is present infection
Chronic carriers of HBV always at risk
Hepatitis E Virus (HEV)
Incubation: 15–64 days (average 26–42 days) • Contaminated water, poor sanitation • Not known
Fecal-oral route • Found in Asia, Africa, and Mexico • May be similar to HAV
• Not common in United States but is increasing in some areas
Viral Hepatitis
There are several types of viral hepatitis. We designate each
type by a letter (A, B, C, D, E). The different types have similar
manifestations. Their modes of transmission and disease course
vary (Table 48.1). Some can lead to chronic liver disease. Other
less common viruses can also cause liver disease. These include
cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpesvi-
rus, coxsackievirus, and rubella virus.
Hepatitis A Virus
Hepatitis A is a self-limiting infection. It can cause a mild flu-
like illness and jaundice. In more severe cases, it can cause acute
liver failure. Hepatitis A virus (HAV) is a ribonucleic acid (RNA) Fig. 48.1 Jaundiced person. (© Jun/iStock.com.)
virus. It is transmitted primarily through the fecal-oral route. It
often occurs in small outbreaks caused by fecal contamination sex with men (MSM), and persons traveling to developing
of food or drinking water. countries.1
Poor hygiene, improper food handling, homelessness, The greatest risk for transmission occurs before symptoms
crowded situations, and poor sanitary conditions are risk fac- appear. The virus is in feces 1 to 2 weeks before the onset of
tors. Transmission occurs between family members, institu- symptoms and at least 1 week after the onset of illness (Fig.
tionalized persons, and children in daycare centers. Foodborne 48.1). This means it can be carried and transmitted by persons
outbreaks are usually due to food contaminated by an infected who have undetectable infection. It is present only briefly in
food handler. People at increased risk for infection include blood, usually less than 3 weeks. Fecal excretion can occur in
drug users (both IV and non-injection drugs), men who have infants for months.
, CHAPTER 48 Liver, Biliary Tract, and Pancreas Problems 1137
Incubation Acute Convalescence BOX 48.1 PROMOTING HEALTH
period symptoms and recovery EQUITY
Jaundice Liver, Pancreas, and Gallbladder Problems
↑ ALT Anti-HAV IgG Hepatitis
• Hepatitis B has a higher incidence among Asian Americans and Pacific
Anti-HAV IgM Islanders
• Hepatitis C has a higher incidence among Blacks
HAV • Deaths from hepatitis C are more common in Blacks
in stools
Liver and Pancreatic Cancer
• Primary liver cancer has the highest incidence in Hispanics
• Pancreatic cancer occurs more often among Blacks
Gallbladder Disease
0 1 2 3 4 5 6 12 24 • Whites and Native Americans have the highest incidence of gallbladder
Months after exposure disease
Fig. 48.2 Course of infection with hepatitis A virus (HAV). ALT, Alanine
aminotransferase. (From McCance KL, Huether SE: Pathophysiology:
the biologic basis for disease in adults and children, ed 6, St Louis, lower HBV concentrations than blood, but the virus can be
2010, Mosby.)
transmitted via these secretions. If gastrointestinal (GI) bleed-
ing occurs, virus in the blood can contaminate feces. There is no
Antibody to HAV immunoglobulin M (IgM) (HAV IgM) evidence of fecal-oral transmission. Organ and tissue transplan-
appears during the acute phase. The presence of HAV IgM indi- tation is another potential source of infection. In some patients
cates acute hepatitis. Levels stay high for about 8 weeks. HAV with acute HBV, there is no readily identifiable risk factor.
IgG without HAV IgM indicates past infection. IgG antibody HBV is a complex structure with 3 distinct antigens: sur-
provides lifelong immunity (Fig. 48.2). HAV vaccination and face antigen (HBsAg), core antigen (HBcAg), and e antigen
thorough hand washing are the best ways to prevent outbreaks. (HBeAg). Each antigen, along with its corresponding antibody,
In the United States, the incidence of HAV is low among chil- may appear or disappear in serum depending on the phase of
dren and adolescents due to vaccination and highest among infection and immune response.
adults due to low vaccination rates.2 In most people who acquire HBV infection as an adult, the
infection completely resolves without any long-term complica-
Hepatitis B Virus tions. In those who develop chronic HBV infections, there is
Hepatitis B virus (HBV) is a blood-borne pathogen that can an association with liver cancer and severe liver inflammation
cause either acute or chronic hepatitis. The global prevalence and scarring (fibrosis). Those who become chronically infected
of HBV is 3.5% to 3.9%. The disease burden is largely in Sub- have an increase in comorbidities. These include cardiovascu-
Saharan Africa, Western Pacific Regions, and Southeast Asia lar disease, hypertension, hyperlipidemia, renal disease, and
(Box 48.1). The United States has policies to prevent HBV trans- osteoporosis.3
mission through immunizations of newborns, children, and Screening for HBV includes identifying those at high risk
high-risk populations.3 for infection and testing the blood for the presence of hepati-
HBV is a deoxyribonucleic acid (DNA) virus. It can be trans- tis B surface antigen (HBsAg), hepatitis B antibody (anti-HBs),
mitted in several ways: (1) perinatally from mothers infected and hepatitis B core antibody (anti-HBc). The presence of anti-
with HBV to their infants; (2) percutaneously (e.g., IV drug HBs in the blood indicates immunity from the HBV vaccine
use, accidental needle-stick punctures); or (3) via small cuts or from past HBV infection (Fig. 48.3). HBsAg in the serum
on mucosal surfaces and exposure to infectious blood, blood for 6 months or longer after infection indicates chronic HBV
products, or other body fluids (e.g., semen, vaginal secretions, infection.
saliva).
Sexual transmission is a common mode of HBV transmis- Hepatitis C Virus
sion. MSM (especially those practicing unprotected anal inter- Hepatitis C virus (HCV) causes a type of hepatitis that can
course) are at an increased risk for HBV infection. Most believe result in both acute illness and chronic infection. Acute HCV
that casual encounters, like hugging, kissing, and sharing uten- can be hard to detect unless a diagnosis is made with laboratory
sils do not transmit the disease. testing. The most common causes of acute HCV outbreaks are
Other at-risk persons include those who live with chron- among IV drug users and MSM with HIV infection.
ically HBV-infected persons, patients on hemodialysis, health HCV is a blood-borne RNA virus that is primarily transmit-
care personnel, public safety workers, blood product recipients, ted percutaneously. The most common mode of HCV trans-
prisoners, Veterans, and homelessness. mission is the sharing of contaminated needles and equipment
HBV has been detected in almost every body fluid. Infected among IV drug users. High-risk sexual behavior especially
semen, cervicovaginal secretions, and saliva contain much among MSM is associated with increased risk.
, 1138 SECTION 9 Problems of Ingestion, Digestion, Absorption, and Elimination
is through contaminated water. HEV infection epidemics occur
Incubation Acute
period symptoms Convalescence Recovery in the tropics, but it is widely circulating in the west. It is gener-
Jaundice
ally acute and self-resolving. Chronicity in immunosuppressed
persons, such as liver transplant recipients and HIV positive
↑ ALT Anti-HBs IgG
persons, can occur. Pregnant women may be affected severely.
An IgM antibody test is available to test for acute hepatitis E.7
Anti-HBc IgM
HBeAg Anti-HBc IgG
HBV-DNA
HBsAg
Pathophysiology
Anti-HBe
Liver
In viral hepatitis, hepatocytes become targets of the virus in 1 of
2 ways: through direct action of the virus (as in HCV infection)
or through a cell-mediated immune response to the virus (as in
HBV and HCV infection).
0 1 2 3 4 5 6 12 24 Months
During acute viral hepatitis, large numbers of infected
Fig. 48.3 Course of infection with hepatitis B virus (HBV). ALT, Alanine
hepatocytes are destroyed. Hepatocyte destruction leads to a
aminotransferase; anti-HBc, antibody to hepatitis B core antigen; anti-
HBe, antibody to HBeAg; anti-HBs, antibody to HBsAg; HBeAg, hepati- wide range of liver-related dysfunction. Bile production, coag-
tis B e antigen; HBsAg, hepatitis B surface antigen. (From McCance KL, ulation, blood glucose, and protein metabolism can be affected.
Huether SE: Pathophysiology: the biologic basis for disease in adults Detoxification and processing of drugs, hormones, and metabo-
and children, ed 6, St Louis, 2010, Mosby.) lites (e.g., ammonia from protein catabolism) may be disrupted.
After acute infection resolves, liver cells can regenerate. If no
Many people infected with HCV develop chronic infection. complications occur, the liver can resume its normal appearance
However, because signs and symptoms of HCV infection are gen- and function. In some patients, the acute hepatitis can become
erally mild, most people are unaware of their infection. We think so severe and irreversible that they develop liver failure or die.
that greater than 50% of people in the United States infected with Chronic viral hepatitis can be insidious and silent, causing
HCV are undiagnosed. About 20% develop cirrhosis and eventu- persistent and continual destruction of infected hepatocytes.
ally liver failure and/or liver cancer if left untreated. HCV hepatitis Over time scar tissue can develop, which leads to fibrosis, cir-
is a common reason for liver transplantation in the United States.4 rhosis, and compromised liver function. Fibrosis can lead to
Persons at risk for HCV infection are also at risk for HBV and cirrhosis and liver failure. Cirrhosis is a generally irreversible
HIV infections. About 30% to 40% of HIV-infected patients also condition that can increase one’s risk for liver dysfunction, por-
have HCV. This high rate of co-infection is primarily related to tal hypertension, and primary liver cancer.
IV drug use. Co-infection with HIV and HCV places the patient
at greater risk for progression to cirrhosis if HCV is untreated. Systemic Effects
A positive antibody test for HCV (anti-HCV) is followed by a In the early phases of hepatitis infection, antigen-antibody com-
positive viral load test to confirm active infection because an plexes between the virus and its corresponding antibody may
anti-HCV can also indicate a past infection. form circulating immune complexes. The circulating immune
With the use of direct-acting antiviral (DAA) medications, it complexes activate the complement system (see Chapter 12).
is possible to cure HCV in almost all cases. There is no vaccine The manifestations of this activation are rash, angioedema,
for HCV. However, with DAA regimens and the ability to cure arthritis, fever, and malaise. Cryoglobulinemia (abnormal pro-
HCV, the focus in chronic HCV is now on efforts to prevent teins found in the blood), glomerulonephritis, vasculitis, and
transmission, screening, and provide needed health care.5 involvement of other organs can occur from immune complex
activation.
Hepatitis D Virus
Hepatitis D virus (HDV), also called delta virus, is uncom- Clinical Manifestations and Complications
mon in the United States. HDV is a defective single-stranded We classify the manifestations of the different viral hepatitis
RNA virus that cannot survive on its own. It requires HBV sur- infections into acute hepatitis and chronic hepatitis (Table 48.2).
face Ag to serve as its outer shell and to infect the hepatocyte.
So, only those who with HBV infection can be infected with Acute Hepatitis
HDV. It can be acquired at the same time as HBV or a person Many patients with acute hepatitis have no symptoms. They may
with HBV can be infected with HDV later. HDV is transmit- not even know they are infected. Others may have anorexia,
ted like HBV. It causes more rapid progression of liver disease lethargy, nausea, vomiting, skin rashes, diarrhea or constipa-
and mortality than HBV infection alone. There is no vaccine tion, malaise, fatigue, muscle pain, joint pain, other flu-like
for HDV. However, HBV vaccination reduces the risk for HDV symptoms, and right upper quadrant (RUQ) tenderness (caused
co-infection.6 by liver inflammation).
Although the acute phase of viral hepatitis varies depend-
Hepatitis E Virus ing on the type of hepatitis, it usually lasts from 1 to 6 months.
Like HAV, the hepatitis E virus (HEV) is an RNA virus trans- During this time, the patient may have a decreased sense of
mitted by the fecal-oral route. The usual mode of transmission smell and find food repugnant. Smokers may have distaste for
Liver, Biliary Tract, and
Pancreas Problems
Mary C. Olson and Christine M. Cervini
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Health Promotion Nutrition
Infection Pain
Inflammation
LEARNING OUTCOMES
1. Distinguish among the types of viral hepatitis. 6. Explain the clinical manifestations and interprofessional
2. Describe the interprofessional and nursing management of and nursing management of the patient with pancreatic
the patient with viral hepatitis. cancer.
3. Explain the pathophysiology, clinical manifestations, 7. Describe the pathophysiology, clinical manifestations, and
complications, and interprofessional and nursing interprofessional care of gallbladder disorders.
management of the patient with cirrhosis. 8. Describe the nursing management of the patient
4. Describe the clinical manifestations and management of undergoing surgical treatment of cholecystitis and
liver cancer. cholelithiasis.
5. Distinguish between acute and chronic pancreatitis related
to pathophysiology, clinical manifestations, complications,
and interprofessional and nursing management.
KEY TERMS
acute liver failure gastric varices
acute pancreatitis hepatic encephalopathy
ascites hepatitis
asterixis hepatorenal syndrome
cholecystitis jaundice
cholelithiasis nonalcoholic fatty liver disease (NAFLD)
chronic pancreatitis nonalcoholic steatohepatitis (NASH)
cirrhosis portal hypertension
esophageal varices
This chapter focuses on the management of patients with a focuses on reducing risk through immunizations and avoiding
wide range of liver, pancreatic, and gallbladder problems. substance use.
These organs are closely positioned together anatomically
and highly associated with their digestive functions. Liver and
pancreas problems can lead to altered nutrient absorption and LIVER PROBLEMS
use, causing malnutrition and impaired elimination. Inflam-
mation may be present, with the patient having pain, nausea,
HEPATITIS
and vomiting. Nursing care focuses on helping the patient and Hepatitis is inflammation of the liver. The most common cause is
caregiver manage symptoms and develop ways to cope with viral. Other causes include substances (e.g., alcohol, medications,
the diagnosis and, sometimes, prognosis. Health promotion chemicals), autoimmune diseases, and metabolic problems.
1135
,1136 SECTION 9 Problems of Ingestion, Digestion, Absorption, and Elimination
TABLE 48.1 Characteristics of Hepatitis Viruses
Incubation Period and Mode of
Transmission Sources of Infection Infectivity
Hepatitis A Virus (HAV)
Incubation: 15–50 days (average 28) • Contaminated food, milk, water, shellfish • Most infectious during 2 weeks before
Fecal-oral (primarily fecal contamination and • Crowded conditions (e.g., day care, nursing home) onset of symptoms
oral ingestion) • Persons with subclinical infections, infected food handlers, • Infectious until 1–2 weeks after the start of
sexual contact, IV drug users symptoms
• Poor personal hygiene
• Poor sanitation
Hepatitis B Virus (HBV)
Incubation: 115–180 days (average 56–96) • Contaminated needles, syringes, and blood products • Before and after symptoms appear
Percutaneous (parenteral) or mucosal exposure • HBV-infected mother (perinatal transmission) • Infectious for months
to blood or blood products • Sexual activity with infected partners. Asymptomatic carriers • Carriers continue to be infectious for life
Sexual contact • Tattoos or body piercing with contaminated needles
Perinatal transmission
Hepatitis C Virus (HCV)
Incubation: 14–180 days (average 56) • Blood and blood products • 1–2 weeks before symptoms appear
Percutaneous (parenteral) or mucosal exposure • Needles and syringes • Continues during clinical course
to blood or blood products • Sexual activity with infected partners, low risk • 75%–85% go on to develop chronic HCV
High-risk sexual contact and remain infectious
Perinatal contact
Hepatitis D Virus (HDV)
Incubation: 2–26 weeks • Same as HBV • Blood infectious at all stages of HDV
HBV must precede HDV • Can cause infection only when HBV is present infection
Chronic carriers of HBV always at risk
Hepatitis E Virus (HEV)
Incubation: 15–64 days (average 26–42 days) • Contaminated water, poor sanitation • Not known
Fecal-oral route • Found in Asia, Africa, and Mexico • May be similar to HAV
• Not common in United States but is increasing in some areas
Viral Hepatitis
There are several types of viral hepatitis. We designate each
type by a letter (A, B, C, D, E). The different types have similar
manifestations. Their modes of transmission and disease course
vary (Table 48.1). Some can lead to chronic liver disease. Other
less common viruses can also cause liver disease. These include
cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpesvi-
rus, coxsackievirus, and rubella virus.
Hepatitis A Virus
Hepatitis A is a self-limiting infection. It can cause a mild flu-
like illness and jaundice. In more severe cases, it can cause acute
liver failure. Hepatitis A virus (HAV) is a ribonucleic acid (RNA) Fig. 48.1 Jaundiced person. (© Jun/iStock.com.)
virus. It is transmitted primarily through the fecal-oral route. It
often occurs in small outbreaks caused by fecal contamination sex with men (MSM), and persons traveling to developing
of food or drinking water. countries.1
Poor hygiene, improper food handling, homelessness, The greatest risk for transmission occurs before symptoms
crowded situations, and poor sanitary conditions are risk fac- appear. The virus is in feces 1 to 2 weeks before the onset of
tors. Transmission occurs between family members, institu- symptoms and at least 1 week after the onset of illness (Fig.
tionalized persons, and children in daycare centers. Foodborne 48.1). This means it can be carried and transmitted by persons
outbreaks are usually due to food contaminated by an infected who have undetectable infection. It is present only briefly in
food handler. People at increased risk for infection include blood, usually less than 3 weeks. Fecal excretion can occur in
drug users (both IV and non-injection drugs), men who have infants for months.
, CHAPTER 48 Liver, Biliary Tract, and Pancreas Problems 1137
Incubation Acute Convalescence BOX 48.1 PROMOTING HEALTH
period symptoms and recovery EQUITY
Jaundice Liver, Pancreas, and Gallbladder Problems
↑ ALT Anti-HAV IgG Hepatitis
• Hepatitis B has a higher incidence among Asian Americans and Pacific
Anti-HAV IgM Islanders
• Hepatitis C has a higher incidence among Blacks
HAV • Deaths from hepatitis C are more common in Blacks
in stools
Liver and Pancreatic Cancer
• Primary liver cancer has the highest incidence in Hispanics
• Pancreatic cancer occurs more often among Blacks
Gallbladder Disease
0 1 2 3 4 5 6 12 24 • Whites and Native Americans have the highest incidence of gallbladder
Months after exposure disease
Fig. 48.2 Course of infection with hepatitis A virus (HAV). ALT, Alanine
aminotransferase. (From McCance KL, Huether SE: Pathophysiology:
the biologic basis for disease in adults and children, ed 6, St Louis, lower HBV concentrations than blood, but the virus can be
2010, Mosby.)
transmitted via these secretions. If gastrointestinal (GI) bleed-
ing occurs, virus in the blood can contaminate feces. There is no
Antibody to HAV immunoglobulin M (IgM) (HAV IgM) evidence of fecal-oral transmission. Organ and tissue transplan-
appears during the acute phase. The presence of HAV IgM indi- tation is another potential source of infection. In some patients
cates acute hepatitis. Levels stay high for about 8 weeks. HAV with acute HBV, there is no readily identifiable risk factor.
IgG without HAV IgM indicates past infection. IgG antibody HBV is a complex structure with 3 distinct antigens: sur-
provides lifelong immunity (Fig. 48.2). HAV vaccination and face antigen (HBsAg), core antigen (HBcAg), and e antigen
thorough hand washing are the best ways to prevent outbreaks. (HBeAg). Each antigen, along with its corresponding antibody,
In the United States, the incidence of HAV is low among chil- may appear or disappear in serum depending on the phase of
dren and adolescents due to vaccination and highest among infection and immune response.
adults due to low vaccination rates.2 In most people who acquire HBV infection as an adult, the
infection completely resolves without any long-term complica-
Hepatitis B Virus tions. In those who develop chronic HBV infections, there is
Hepatitis B virus (HBV) is a blood-borne pathogen that can an association with liver cancer and severe liver inflammation
cause either acute or chronic hepatitis. The global prevalence and scarring (fibrosis). Those who become chronically infected
of HBV is 3.5% to 3.9%. The disease burden is largely in Sub- have an increase in comorbidities. These include cardiovascu-
Saharan Africa, Western Pacific Regions, and Southeast Asia lar disease, hypertension, hyperlipidemia, renal disease, and
(Box 48.1). The United States has policies to prevent HBV trans- osteoporosis.3
mission through immunizations of newborns, children, and Screening for HBV includes identifying those at high risk
high-risk populations.3 for infection and testing the blood for the presence of hepati-
HBV is a deoxyribonucleic acid (DNA) virus. It can be trans- tis B surface antigen (HBsAg), hepatitis B antibody (anti-HBs),
mitted in several ways: (1) perinatally from mothers infected and hepatitis B core antibody (anti-HBc). The presence of anti-
with HBV to their infants; (2) percutaneously (e.g., IV drug HBs in the blood indicates immunity from the HBV vaccine
use, accidental needle-stick punctures); or (3) via small cuts or from past HBV infection (Fig. 48.3). HBsAg in the serum
on mucosal surfaces and exposure to infectious blood, blood for 6 months or longer after infection indicates chronic HBV
products, or other body fluids (e.g., semen, vaginal secretions, infection.
saliva).
Sexual transmission is a common mode of HBV transmis- Hepatitis C Virus
sion. MSM (especially those practicing unprotected anal inter- Hepatitis C virus (HCV) causes a type of hepatitis that can
course) are at an increased risk for HBV infection. Most believe result in both acute illness and chronic infection. Acute HCV
that casual encounters, like hugging, kissing, and sharing uten- can be hard to detect unless a diagnosis is made with laboratory
sils do not transmit the disease. testing. The most common causes of acute HCV outbreaks are
Other at-risk persons include those who live with chron- among IV drug users and MSM with HIV infection.
ically HBV-infected persons, patients on hemodialysis, health HCV is a blood-borne RNA virus that is primarily transmit-
care personnel, public safety workers, blood product recipients, ted percutaneously. The most common mode of HCV trans-
prisoners, Veterans, and homelessness. mission is the sharing of contaminated needles and equipment
HBV has been detected in almost every body fluid. Infected among IV drug users. High-risk sexual behavior especially
semen, cervicovaginal secretions, and saliva contain much among MSM is associated with increased risk.
, 1138 SECTION 9 Problems of Ingestion, Digestion, Absorption, and Elimination
is through contaminated water. HEV infection epidemics occur
Incubation Acute
period symptoms Convalescence Recovery in the tropics, but it is widely circulating in the west. It is gener-
Jaundice
ally acute and self-resolving. Chronicity in immunosuppressed
persons, such as liver transplant recipients and HIV positive
↑ ALT Anti-HBs IgG
persons, can occur. Pregnant women may be affected severely.
An IgM antibody test is available to test for acute hepatitis E.7
Anti-HBc IgM
HBeAg Anti-HBc IgG
HBV-DNA
HBsAg
Pathophysiology
Anti-HBe
Liver
In viral hepatitis, hepatocytes become targets of the virus in 1 of
2 ways: through direct action of the virus (as in HCV infection)
or through a cell-mediated immune response to the virus (as in
HBV and HCV infection).
0 1 2 3 4 5 6 12 24 Months
During acute viral hepatitis, large numbers of infected
Fig. 48.3 Course of infection with hepatitis B virus (HBV). ALT, Alanine
hepatocytes are destroyed. Hepatocyte destruction leads to a
aminotransferase; anti-HBc, antibody to hepatitis B core antigen; anti-
HBe, antibody to HBeAg; anti-HBs, antibody to HBsAg; HBeAg, hepati- wide range of liver-related dysfunction. Bile production, coag-
tis B e antigen; HBsAg, hepatitis B surface antigen. (From McCance KL, ulation, blood glucose, and protein metabolism can be affected.
Huether SE: Pathophysiology: the biologic basis for disease in adults Detoxification and processing of drugs, hormones, and metabo-
and children, ed 6, St Louis, 2010, Mosby.) lites (e.g., ammonia from protein catabolism) may be disrupted.
After acute infection resolves, liver cells can regenerate. If no
Many people infected with HCV develop chronic infection. complications occur, the liver can resume its normal appearance
However, because signs and symptoms of HCV infection are gen- and function. In some patients, the acute hepatitis can become
erally mild, most people are unaware of their infection. We think so severe and irreversible that they develop liver failure or die.
that greater than 50% of people in the United States infected with Chronic viral hepatitis can be insidious and silent, causing
HCV are undiagnosed. About 20% develop cirrhosis and eventu- persistent and continual destruction of infected hepatocytes.
ally liver failure and/or liver cancer if left untreated. HCV hepatitis Over time scar tissue can develop, which leads to fibrosis, cir-
is a common reason for liver transplantation in the United States.4 rhosis, and compromised liver function. Fibrosis can lead to
Persons at risk for HCV infection are also at risk for HBV and cirrhosis and liver failure. Cirrhosis is a generally irreversible
HIV infections. About 30% to 40% of HIV-infected patients also condition that can increase one’s risk for liver dysfunction, por-
have HCV. This high rate of co-infection is primarily related to tal hypertension, and primary liver cancer.
IV drug use. Co-infection with HIV and HCV places the patient
at greater risk for progression to cirrhosis if HCV is untreated. Systemic Effects
A positive antibody test for HCV (anti-HCV) is followed by a In the early phases of hepatitis infection, antigen-antibody com-
positive viral load test to confirm active infection because an plexes between the virus and its corresponding antibody may
anti-HCV can also indicate a past infection. form circulating immune complexes. The circulating immune
With the use of direct-acting antiviral (DAA) medications, it complexes activate the complement system (see Chapter 12).
is possible to cure HCV in almost all cases. There is no vaccine The manifestations of this activation are rash, angioedema,
for HCV. However, with DAA regimens and the ability to cure arthritis, fever, and malaise. Cryoglobulinemia (abnormal pro-
HCV, the focus in chronic HCV is now on efforts to prevent teins found in the blood), glomerulonephritis, vasculitis, and
transmission, screening, and provide needed health care.5 involvement of other organs can occur from immune complex
activation.
Hepatitis D Virus
Hepatitis D virus (HDV), also called delta virus, is uncom- Clinical Manifestations and Complications
mon in the United States. HDV is a defective single-stranded We classify the manifestations of the different viral hepatitis
RNA virus that cannot survive on its own. It requires HBV sur- infections into acute hepatitis and chronic hepatitis (Table 48.2).
face Ag to serve as its outer shell and to infect the hepatocyte.
So, only those who with HBV infection can be infected with Acute Hepatitis
HDV. It can be acquired at the same time as HBV or a person Many patients with acute hepatitis have no symptoms. They may
with HBV can be infected with HDV later. HDV is transmit- not even know they are infected. Others may have anorexia,
ted like HBV. It causes more rapid progression of liver disease lethargy, nausea, vomiting, skin rashes, diarrhea or constipa-
and mortality than HBV infection alone. There is no vaccine tion, malaise, fatigue, muscle pain, joint pain, other flu-like
for HDV. However, HBV vaccination reduces the risk for HDV symptoms, and right upper quadrant (RUQ) tenderness (caused
co-infection.6 by liver inflammation).
Although the acute phase of viral hepatitis varies depend-
Hepatitis E Virus ing on the type of hepatitis, it usually lasts from 1 to 6 months.
Like HAV, the hepatitis E virus (HEV) is an RNA virus trans- During this time, the patient may have a decreased sense of
mitted by the fecal-oral route. The usual mode of transmission smell and find food repugnant. Smokers may have distaste for
