ACUTE HEPATITIS
PRESENTED BY: - FAISAL ALI & MASUMEENTA MAUREEN
OBJECTIVES
 Introduction
 Causes
 Clinical presentation
 Pathophysiology
 Diagnosis
 Management
 Prevention
 Complication
 Nursing Diagnosis
INTRODUCTION
Acute hepatitis is a term used to describe a wide variety of conditions characterized by acute
inflammation of the hepatic parenchyma or injury to hepatocytes resulting in elevated liver
function indices.
In general, hepatitis is classified as acute or chronic based on the duration of the inflammation
and insult to the hepatic parenchyma.
If the period of inflammation or hepatocellular injury lasts for less than six months,
characterized by normalization of the liver function tests, it is called acute hepatitis.
If the inflammation or hepatocellular injury persists beyond six months, it is termed chronic
hepatitis.
CAUSES OF ACUTE HEPATITIS
Acute hepatic inflammation can be caused by many infectious and noninfectious causes, of
which the most common causes are secondary to a viral infection or drug-induced liver injury.
1. Infectious causes: -
Hepatotropic viruses: Non-Hepatotropic viruses:
Hepatitis A Virus (HAV) Epstein-Barr virus (EBV)
Hepatitis B Virus (HBV) Cytomegalovirus (CMV)
Hepatitis C Virus (HCV) Herpes simplex virus (HSV)
Hepatitis D Virus (HDV) Coxsackievirus
Hepatitis E Virus (HEV) Adenovirus
CONT.
Bacteria, Fungi, and parasite
2. Toxin or substance-related causes include:
Alcohol-related: fatty liver disease, acute alcoholic hepatitis, or alcoholic cirrhosis
Drugs and toxins : -
Dose-dependent, e.g. acetaminophen (paracetamol)
Non-dose-dependent, e.g., idiosyncratic drug reaction most commonly related to antibiotics
and anticonvulsants but also statins, NSAIDs, herbal/nutritional supplements
Other toxins, e.g., mushroom (Amanita phalloides), herbal and dietary supplements.
CONT.
3. Immunologic or inflammatory conditions
Autoimmune hepatitis
Biliary diseases such as primary biliary cholangitis or primary sclerosing cholangitis.
4. Metabolic or hereditary
Nonalcoholic fatty liver disease
Hemochromatosis
Wilson's disease
CONT.
5. Pregnancy-related
Preeclampsia
Acute fatty liver of pregnancy
HELLP syndrome
6. Ischemic and Vascular
Cardiogenic/Distributive shock
Hypotension
Heatstroke
Viral hepatitis – Hepatitis A & E
Hepatitis A virus (HAV) is the most prevalent of the five viruses worldwide.
This virus is also responsible for most forms of acute and benign hepatitis; although fulminant
hepatic failure can occur, it is rare.
HAV is an RNA virus, a member of the picornavirus family.
HEV is an RNA virus, a member of Hepeviridae family.
HAV is highly contagious. Transmission is almost always by person-to-person contact through
the fecal-oral route. Parenteral transmission occurs rarely.
HEV transmission is fecal-oral (often water-borne) and is associated with shedding in the stool.
CONT.
The mean incubation period for HAV is 3 weeks.
The mean incubation period for HEV is ≈40 days (range of 15–60 days).
The typical duration of illness for HAV is 7–14 days.
HEV often causing a more severe episode than HAV.
HEV tends to affect older patients with a peak age between 15 and 34 yr.
HEV is a major pathogen in pregnant women, in whom it causes ALF with a high fatality
incidence.
CLINICAL MANEFSTATIONS
 Right upper quadrant abdominal pain
 Fever, weight loss, and fatigue.
 Jaundice.
 Dark urine. (due to high direct bilirubin )
 Hepatosplenomegaly.
 Anorexia, Nausea, and vomiting.
Hepatitis B & C
HBV is a member of the Hepadnaviridae family, which includes a hepatotropic group of DNA
viruses.
HBV has a circular, partially double-stranded DNA genome
HBV antigens
I. The surface of the virus includes particles designated hepatitis B surface antigen (HBsAg)
II. The inner portion of the virion contains hepatitis B core antigen (HBcAg)
III. A nonstructural antigen called hepatitis B e antigen (HBeAg).
CONT.
CONT.
HBsAg – stimulates protective antibodies, a marker for current infection
HBcAg – localized within liver cells, identifies acute infection, anti-HBcAg persists for life and is
a marker of past infection
HBeAg – Serves as a marker of active replication and infectivity;
Replication of HBV occurs predominantly in the liver but also occurs in the lymphocytes, spleen,
kidney, and pancreas.
HBV infection can be self-limited(Acute) or chronic.
CONT.
HCV is the cause of most cases previously known as “transfusion-related non-A, non-B
hepatitis.”
HCV is a single-stranded RNA virus.
HCV infection is the most common cause of chronic liver disease in adults.
Risk factors for HBV & HCV infections in children and adolescents include: -
intravenous acquisition by drugs or blood products,
acupuncture or tattoos
sexual contact
intimate contact with carriers.
CONT.
CONT.
The incubation period of HBV ranges from 45 – 160 days. But the mean IP is 120 days.
The incubation period for HCV ranges from 14 – 160 days.
PATHOPHYSIOLOGY
Invasion of Hepatitis A virus in the body through the fecal-oral route, the virus is then absorbed
through the oropharynx and intestines and through the bloodstream reaches the hepatocytes.
The virus then replicates within the hepatocytes and the virions are secreted into bile and
excreted through feces. This continues for 11 days until the patient shows symptoms and thus
becomes infectious.
Hepatitis B & C have the same pathophysiology as A & E, as all of them will cause injury and
inflammation to the hepatocytes that will lead to spontaneous resolution of the inflammation or
the progress of inflammation into scarring and eventually into liver cirrhosis.
TRANSMISSION
Hepatitis A & E usually spread through the fecal-oral route.
Hepatitis B usually spreads through unsafe sexual practices, infected needles, vertical
transmission from mother to fetus, surgical and dental procedures, and blood transfusions.
Hepatitis C is also transmitted through blood transfusions, intravenous drug abusers, use of
unsterilized razors for shaving (barbers), nose piercing, and infected needles or instruments
during surgical procedures
Diagnosis
History and Physical examination
Laboratory test
 Increased direct bilirubin.
 Liver function test (LFT) increase 5-10 times above normal, both ALT or AST (ALT Higher )
● Increased ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST).
 Increased alkaline phosphatase
Note: The severity of the Disease is assessed by the prothrombin time (PTT), and serum
bilirubin.
Complete blood count and Liver biopsy
CONT.
Specific Diagnostic Tests.
❏ PCR: which tells the amount of active viral replication. (Disease activity of hepatitis )
❏ Serology ( antibody and antigen )
● Hepatitis A, C, D, and E: The "best initial diagnostic test" for each of these is simply an IgM
antibody for the acute infection and an IgG antibody to detect the resolution of infection.
● Hepatitis B antigens: -
CONT.
Management Of Acute Hepatitis
 Hepatitis A and E resolve spontaneously over
a few weeks and are almost always benign
conditions.
Management Of Chronic Hepatitis
Treat with antivirals if the patient has any one of these:
All persons with chronic HBV infections who have cirrhosis (whether compensated or not) based on
clinical findings and/or APRI score >2, irrespective of liver enzyme levels, HbeAg status or hepatitis B
viral load)
HIV co-infection (use a tenofovir-based combination)
Patients with no cirrhosis (APRI score <2) but persistently elevated ALT on 3 occasions within 6-12
months and viral load >20,000 IU/L (if available) regardless of HbeAg status
Contd
First line antivirals
Adults and children >12 years or >35 kg: tenofovir
300 mg once a day
Child 2-11 years (>10 kg): Entecavir 0.02 mg/kg
The following patients should NOT be treated
 Patients without evidence of cirrhosis (APRI ≤2), and with persistently normal ALT level and
HBV viral load < 2000 IU/ml (if available)
PREVENTION
I. Hygiene and sanitation
II. Immunization against hepatitis B (all children, health workers, household contacts of people
with chronic hepatitis B, sex workers, and other populations at risk).
III. Safe transfusion practices.
IV. Infection control in health facilities.
V. Screening of pregnant women.
VI. Safe sexual practices (condom use).
ACUTE HEPATITIS (causes and Clinical Features)
CONT.
NURSING DIAGNOSIS
NURSING DIAGNOSIS INTERVENTIONS
Fatigue related to tissue insufficiency and metabolic
disturbances secondary to inadequate food intake, evidenced
by the patient being generally weak.
I. Assess the patient’s level of fatigue regularly using
standardized fatigue assessment tools.
II. Encourage the patient to balance rest and activity,
avoiding excessive physical exertion.
III. Collaborate with the healthcare team to manage
symptoms, such as anemia or malnutrition, which can
contribute to fatigue.
Risk for Infection related to compromised immune function. I. Implement standard precautions and follow appropriate
infection control measures.
II. Educate the patient and family members about the
modes of hepatitis transmission and preventive
measures, such as hand hygiene, safe sex practices, and
vaccination for hepatitis A and B.
III. Monitor for signs of infection, such as fever or changes in
laboratory values, and promptly report any concerns to
the healthcare team.
Impaired Nutrition: Less than Body Requirements related to
anorexia, nausea, and altered metabolism.
I. Assess the patient’s nutritional status, dietary intake, and
weight regularly.
II. Provide small, frequent meals that are high in calories,
protein, and nutrients to meet increased metabolic
demands and promote adequate nutrition.
III. Collaborate with a registered dietitian to develop a
customized meal plan based on the patient’s preferences
and dietary restrictions.
IV. Offer antiemetic medications or alternative therapies to
manage nausea and promote better food intake.
Deficient Knowledge regarding hepatitis, transmission,
prevention, and self-care strategies.
I. Assess the patient’s understanding of hepatitis, including
its etiology, transmission, and preventive measures.
II. Provide education on the specific type of hepatitis and its
management, including medication adherence and the
importance of follow-up appointments.
ACUTE HEPATITIS (causes and Clinical Features)

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ACUTE HEPATITIS (causes and Clinical Features)

  • 1. ACUTE HEPATITIS PRESENTED BY: - FAISAL ALI & MASUMEENTA MAUREEN
  • 2. OBJECTIVES  Introduction  Causes  Clinical presentation  Pathophysiology  Diagnosis  Management  Prevention  Complication  Nursing Diagnosis
  • 3. INTRODUCTION Acute hepatitis is a term used to describe a wide variety of conditions characterized by acute inflammation of the hepatic parenchyma or injury to hepatocytes resulting in elevated liver function indices. In general, hepatitis is classified as acute or chronic based on the duration of the inflammation and insult to the hepatic parenchyma. If the period of inflammation or hepatocellular injury lasts for less than six months, characterized by normalization of the liver function tests, it is called acute hepatitis. If the inflammation or hepatocellular injury persists beyond six months, it is termed chronic hepatitis.
  • 4. CAUSES OF ACUTE HEPATITIS Acute hepatic inflammation can be caused by many infectious and noninfectious causes, of which the most common causes are secondary to a viral infection or drug-induced liver injury. 1. Infectious causes: - Hepatotropic viruses: Non-Hepatotropic viruses: Hepatitis A Virus (HAV) Epstein-Barr virus (EBV) Hepatitis B Virus (HBV) Cytomegalovirus (CMV) Hepatitis C Virus (HCV) Herpes simplex virus (HSV) Hepatitis D Virus (HDV) Coxsackievirus Hepatitis E Virus (HEV) Adenovirus
  • 5. CONT. Bacteria, Fungi, and parasite 2. Toxin or substance-related causes include: Alcohol-related: fatty liver disease, acute alcoholic hepatitis, or alcoholic cirrhosis Drugs and toxins : - Dose-dependent, e.g. acetaminophen (paracetamol) Non-dose-dependent, e.g., idiosyncratic drug reaction most commonly related to antibiotics and anticonvulsants but also statins, NSAIDs, herbal/nutritional supplements Other toxins, e.g., mushroom (Amanita phalloides), herbal and dietary supplements.
  • 6. CONT. 3. Immunologic or inflammatory conditions Autoimmune hepatitis Biliary diseases such as primary biliary cholangitis or primary sclerosing cholangitis. 4. Metabolic or hereditary Nonalcoholic fatty liver disease Hemochromatosis Wilson's disease
  • 7. CONT. 5. Pregnancy-related Preeclampsia Acute fatty liver of pregnancy HELLP syndrome 6. Ischemic and Vascular Cardiogenic/Distributive shock Hypotension Heatstroke
  • 8. Viral hepatitis – Hepatitis A & E Hepatitis A virus (HAV) is the most prevalent of the five viruses worldwide. This virus is also responsible for most forms of acute and benign hepatitis; although fulminant hepatic failure can occur, it is rare. HAV is an RNA virus, a member of the picornavirus family. HEV is an RNA virus, a member of Hepeviridae family. HAV is highly contagious. Transmission is almost always by person-to-person contact through the fecal-oral route. Parenteral transmission occurs rarely. HEV transmission is fecal-oral (often water-borne) and is associated with shedding in the stool.
  • 9. CONT. The mean incubation period for HAV is 3 weeks. The mean incubation period for HEV is ≈40 days (range of 15–60 days). The typical duration of illness for HAV is 7–14 days. HEV often causing a more severe episode than HAV. HEV tends to affect older patients with a peak age between 15 and 34 yr. HEV is a major pathogen in pregnant women, in whom it causes ALF with a high fatality incidence.
  • 10. CLINICAL MANEFSTATIONS  Right upper quadrant abdominal pain  Fever, weight loss, and fatigue.  Jaundice.  Dark urine. (due to high direct bilirubin )  Hepatosplenomegaly.  Anorexia, Nausea, and vomiting.
  • 11. Hepatitis B & C HBV is a member of the Hepadnaviridae family, which includes a hepatotropic group of DNA viruses. HBV has a circular, partially double-stranded DNA genome HBV antigens I. The surface of the virus includes particles designated hepatitis B surface antigen (HBsAg) II. The inner portion of the virion contains hepatitis B core antigen (HBcAg) III. A nonstructural antigen called hepatitis B e antigen (HBeAg).
  • 12. CONT.
  • 13. CONT. HBsAg – stimulates protective antibodies, a marker for current infection HBcAg – localized within liver cells, identifies acute infection, anti-HBcAg persists for life and is a marker of past infection HBeAg – Serves as a marker of active replication and infectivity; Replication of HBV occurs predominantly in the liver but also occurs in the lymphocytes, spleen, kidney, and pancreas. HBV infection can be self-limited(Acute) or chronic.
  • 14. CONT. HCV is the cause of most cases previously known as “transfusion-related non-A, non-B hepatitis.” HCV is a single-stranded RNA virus. HCV infection is the most common cause of chronic liver disease in adults. Risk factors for HBV & HCV infections in children and adolescents include: - intravenous acquisition by drugs or blood products, acupuncture or tattoos sexual contact intimate contact with carriers.
  • 15. CONT.
  • 16. CONT. The incubation period of HBV ranges from 45 – 160 days. But the mean IP is 120 days. The incubation period for HCV ranges from 14 – 160 days.
  • 17. PATHOPHYSIOLOGY Invasion of Hepatitis A virus in the body through the fecal-oral route, the virus is then absorbed through the oropharynx and intestines and through the bloodstream reaches the hepatocytes. The virus then replicates within the hepatocytes and the virions are secreted into bile and excreted through feces. This continues for 11 days until the patient shows symptoms and thus becomes infectious. Hepatitis B & C have the same pathophysiology as A & E, as all of them will cause injury and inflammation to the hepatocytes that will lead to spontaneous resolution of the inflammation or the progress of inflammation into scarring and eventually into liver cirrhosis.
  • 18. TRANSMISSION Hepatitis A & E usually spread through the fecal-oral route. Hepatitis B usually spreads through unsafe sexual practices, infected needles, vertical transmission from mother to fetus, surgical and dental procedures, and blood transfusions. Hepatitis C is also transmitted through blood transfusions, intravenous drug abusers, use of unsterilized razors for shaving (barbers), nose piercing, and infected needles or instruments during surgical procedures
  • 19. Diagnosis History and Physical examination Laboratory test  Increased direct bilirubin.  Liver function test (LFT) increase 5-10 times above normal, both ALT or AST (ALT Higher ) ● Increased ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST).  Increased alkaline phosphatase Note: The severity of the Disease is assessed by the prothrombin time (PTT), and serum bilirubin. Complete blood count and Liver biopsy
  • 20. CONT. Specific Diagnostic Tests. ❏ PCR: which tells the amount of active viral replication. (Disease activity of hepatitis ) ❏ Serology ( antibody and antigen ) ● Hepatitis A, C, D, and E: The "best initial diagnostic test" for each of these is simply an IgM antibody for the acute infection and an IgG antibody to detect the resolution of infection. ● Hepatitis B antigens: -
  • 21. CONT.
  • 22. Management Of Acute Hepatitis  Hepatitis A and E resolve spontaneously over a few weeks and are almost always benign conditions.
  • 23. Management Of Chronic Hepatitis Treat with antivirals if the patient has any one of these: All persons with chronic HBV infections who have cirrhosis (whether compensated or not) based on clinical findings and/or APRI score >2, irrespective of liver enzyme levels, HbeAg status or hepatitis B viral load) HIV co-infection (use a tenofovir-based combination) Patients with no cirrhosis (APRI score <2) but persistently elevated ALT on 3 occasions within 6-12 months and viral load >20,000 IU/L (if available) regardless of HbeAg status
  • 24. Contd First line antivirals Adults and children >12 years or >35 kg: tenofovir 300 mg once a day Child 2-11 years (>10 kg): Entecavir 0.02 mg/kg The following patients should NOT be treated  Patients without evidence of cirrhosis (APRI ≤2), and with persistently normal ALT level and HBV viral load < 2000 IU/ml (if available)
  • 25. PREVENTION I. Hygiene and sanitation II. Immunization against hepatitis B (all children, health workers, household contacts of people with chronic hepatitis B, sex workers, and other populations at risk). III. Safe transfusion practices. IV. Infection control in health facilities. V. Screening of pregnant women. VI. Safe sexual practices (condom use).
  • 27. CONT.
  • 28. NURSING DIAGNOSIS NURSING DIAGNOSIS INTERVENTIONS Fatigue related to tissue insufficiency and metabolic disturbances secondary to inadequate food intake, evidenced by the patient being generally weak. I. Assess the patient’s level of fatigue regularly using standardized fatigue assessment tools. II. Encourage the patient to balance rest and activity, avoiding excessive physical exertion. III. Collaborate with the healthcare team to manage symptoms, such as anemia or malnutrition, which can contribute to fatigue. Risk for Infection related to compromised immune function. I. Implement standard precautions and follow appropriate infection control measures. II. Educate the patient and family members about the modes of hepatitis transmission and preventive measures, such as hand hygiene, safe sex practices, and vaccination for hepatitis A and B. III. Monitor for signs of infection, such as fever or changes in laboratory values, and promptly report any concerns to the healthcare team.
  • 29. Impaired Nutrition: Less than Body Requirements related to anorexia, nausea, and altered metabolism. I. Assess the patient’s nutritional status, dietary intake, and weight regularly. II. Provide small, frequent meals that are high in calories, protein, and nutrients to meet increased metabolic demands and promote adequate nutrition. III. Collaborate with a registered dietitian to develop a customized meal plan based on the patient’s preferences and dietary restrictions. IV. Offer antiemetic medications or alternative therapies to manage nausea and promote better food intake. Deficient Knowledge regarding hepatitis, transmission, prevention, and self-care strategies. I. Assess the patient’s understanding of hepatitis, including its etiology, transmission, and preventive measures. II. Provide education on the specific type of hepatitis and its management, including medication adherence and the importance of follow-up appointments.