Royal Medical Services Provider Unit

Nursing Continuing Education and Training

Department

HEPATIC DISORDERS

Prepared by captain :
Jumana AL-Momani RN.MSN
 HEPATIC DISORDERS

• ACUTE HEPATITIS
 ACUTE HEPATITIS

• Hepatitis is an acute or chronic inflammation

of the liver.
Etiology :
• a virus, chemical or drug reaction, or other
diseases.
• Non viral causes of hepatitis include
autoimmune hepatitis, Wilson's disease, and
steatohepatitis.
 six viruses cause most cases (90%) of viral hepatitis:

• Hepatitis A virus (HAV)

• Hepatitis B virus (HBV)
• Hepatitis C virus (HCV)
• Hepatitis D virus (HDV)
• Hepatitis E virus (HEV)
• Hepatitis G virus (HGV)
 Hepatitis A
( HAV )
• is the most common form of acute viral
hepatitis in most parts of the world.
• infection affects individuals of all ages, but the
highest incidence occurs among preschool- or
school-age children younger than 15 years.
• transmitted primarily in contaminated stool
spread via the fecal-oral route .
• Incubation period approximately 3 wks.
WHO,2013
 Hepatitis B (HBV)
• HBV asymptomatic and limited to causing fatal
fulminant (rapid and severe) hepatitis.

• incubation period of HBV infection varies from

45 to 160 days.
• Worldwide, some 240 million people have
chronic hepatitis B virus with the highest rates
of infection in Africa and Asia. People with
chronic hepatitis B infection are at increased
risk of dying from cirrhosis and liver cancer.
(WHO,2013)
 Transmission
(1) individuals with hemophilia and others who
have received multiple transfusions.
(2) children and adolescents involved in IV drug
abuse.
(3) institutionalized children and adolescents.
(4) preschool-age children in endemic areas.
(5) individual engaged in heterosexual or
homosexual activity with infected partners.
 Hepatitis C (HCV)
• The clinical course of HCV infection is variable.
• Incubation averages 6 to 7 weeks, with a range of 2
weeks to 6 months.
• HCV causes acute hepatitis that progresses to
chronic disease in more than 70% of affected
individuals and can cause end-stage liver disease in
10% of these patients.
• both acute and chronic HCV infection often produce
only mild nonspecific symptoms or no symptoms .
 Recommendations
• To evaluate :
• Interval regular monitor for chronic hepatitis.
• Liver biopsy.
• Monitor liver enzyme.
 Hepatitis D.(HDV)
• important cause of acute and chronic liver
disease.
• a defective RNA virus that requires the
function of HBV.
• HDV infection occurs primarily in hemophiliac
patients and IV drug abusers
• . The incubation period is 2 to 8 weeks.
• Both acute and chronic forms are more
severe than HBV infection and can lead to
cirrhosis.
• Testing for HDV infection is recommended in
children with chronic HBV infection or severe
liver disease or in children with acute
exacerbation of a previously stable liver
disease.
 Hepatitis E.(HEV)
• HEV infection is enterally transmitted. Fecal oral
route or from contaminated water.
• The incubation period is 2 to 9 weeks.
• is uncommon in children, does not cause chronic
liver disease, is not a chronic condition, and has no
carrier state.
• The mortality rate resulting from submissive hepatic
necrosis is low except in pregnant women in their
third trimester, in whom mortality reaches 20%.
 Hepatitis G(HGV)
• HGV is a blood borne virus that may also be
transmitted by organ transplantation.
• High-risk groups include transfusion recipients,
IV drug users, and individuals infected with HCV.
• Individuals with the virus are often
asymptomatic, and most infections are chronic.
• The incubation period is unknown.
 Diagnostic Evaluation
• History and physical examination.
• LFT (ALT,AST),billurbin LEVEL.
• Hepatitis Profile .
• Abdomen U/S.
• Liver biopsy.
 Patho physiology
• Pathologic changes parenchyma cells of the liver and
result in varying degrees of swelling, infiltration of liver
cells by mononuclear cells, subsequent degeneration,
necrosis, and fibrosis.
• fulminant hepatitis, which is characterized by a
severe, acute course and massive destruction of the liver,
which results in liver failure and death in 1 to 2 weeks.
• Sub acute or chronic active hepatitis is characterized by
progressive liver destruction, uncertain regeneration,
scarring, and potential cirrhosis.
 Patho physiology
• The initial anicteric (absence of jaundice) phase
usually lasts 5 to 7 days and is often mistaken for
influenza.
• Symptoms include nausea, vomiting, extreme
anorexia, malaise, easy fatigability, arthralgia, skin
rashes, slight to moderate fever, and epigastria or
upper right quadrant abdominal pain.
• Dark urine is a symptom of the icteric (jaundice)
phase. Pruritus may accompany jaundice and can
be a bothersome,
 Prognosis.
• HAV –mild illness NO carrier status.
• HBV- acute, chronic
Chronic- ¼ to 1/3 lead to liver cirrhosis.
Hepatocellular carcinoma fatal complication
for HBV.
• HCV- Chronic& cirrhosis indication for liver
transplant.
 Therapeutic Management
• HVA : Self-limited with focusing on diet and proper
isolation.
• HBV,HCV – interferon antiviral, anti proliferative,
immunomodulatory effect.
• Hospitalization is necessary if coagulopathy or
fulminant hepatitis are present.
 Nursing Considerations
• Educate family route of transmission.
• Well balanced diet.
• cautioned about administering any medication
to the child.
• Hand washing is the single most critical
measure in reducing risk of transmission.
 Prevention.
• Proper hand washing and standard isolation
precautions .
• HCV, HBV vaccination.
• Prophylactic (IG)
Cirrhosis of the Liver

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 Description

• A chronic, progressive disease of the liver

• Extensive parenchyma cell degeneration
• Destruction of parenchyma cells
• Regenerative process is disorganized,
resulting in abnormal blood vessel and bile
duct relationships from fibrosis
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 Statistics

• Approximately 10- 20% of clients with chronic

hepatitis B will develop cirrhosis.

• Approximately 20% of clients with chronic

hepatitis C will develop cirrhosis.

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 Etiology and Pathophysiology

• Cell necrosis occurs

• Destroyed liver cells are replaced by scar
tissue

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Etiology and Pathophysiology
• Four types of cirrhosis:
– Alcoholic (previously called Laënnec’s )
cirrhosis
– Post-necrotic cirrhosis
– Biliary cirrhosis
– Cardiac cirrhosis

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 Etiology and Pathophysiology
• Post-necrotic Cirrhosis
– Complication of toxic or viral hepatitis
– Accounts for 20% of the cases of cirrhosis
– Broad bands of scar tissue form within the liver

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 Etiology and Pathophysiology

• Biliary Cirrhosis
– Associated with chronic biliary obstruction and
infection
– Accounts for 15% of all cases of cirrhosis

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 Etiology and Pathophysiology

• Cardiac Cirrhosis
– Results from long-standing severe right-sided
heart failure

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Manifestations of Liver Cirrhosis

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Fig. 42-5
 Clinical Manifestations
Early Manifestations

• Onset usually insidious

• GI disturbances:
– Anorexia
– Dyspepsia
– Flatulence
– change in bowel habits

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 Clinical Manifestations
Early Manifestations

• Abdominal pain
• Fever
• Weight loss
• Enlarged liver or spleen

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 Clinical Manifestations
Late Manifestations

• Two causative mechanisms

– Hepatocellular failure
– Portal hypertension

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 Clinical Manifestations
Jaundice

• Occurs because of insufficient conjugation

of bilirubin by the liver cells, and local
obstruction of biliary ducts by scarring and
regenerating tissue

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 Clinical Manifestations
Jaundice

• Intermittent jaundice is characteristic of

biliary cirrhosis
• Late stages of cirrhosis the client will
usually be jaundiced

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 Clinical Manifestations
Skin

• Spider angiomas (telangiectasia, spider

nevi)
• Palmar erythema

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 Clinical Manifestations
Endocrine Disturbances

• Steroid hormones of the adrenal cortex

(aldosterone), testes, and ovaries are
metabolized and inactivated by the normal
liver

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 Clinical Manifestations
Endocrine Disturbances

• Alteration in hair distribution

– Decreased amount of pubic hair
– Axillary and pectoral alopecia

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 Clinical Manifestations
Hematological Disorders

• Bleeding tendencies as a result of

decreased production of hepatic clotting
factors (II, VII, IX, and X)

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 Clinical Manifestations
Hematological Disorders

• Anemia, leukopenia, and

thrombocytopenia are believed to be
result of hypersplenism

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 Clinical Manifestations
Peripheral Neuropathy

• Dietary deficiencies of thiamine, folic acid,

and vitamin B12

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 Complications

• Portal hypertension and esophageal varices

• Peripheral edema and ascites
• Hepatic encephalopathy

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 Complications
Portal Hypertension

• Characterized by:
– Increased venous pressure in portal circulation
– Splenomegaly
– Esophageal varices
– Systemic hypertension

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 Complications
Peripheral Edema and Ascites

• Ascites:
- Intraperitoneal accumulation of
watery fluid containing small amounts
of protein

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 Complications
Peripheral Edema and Ascites

• Factors involved in the pathogenesis of ascites:

- Hypoalbuminemia
-  levels of aldosterone
-  portal hypertension

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 Complications
Hepatic Encephalopathy

• Liver damage causes blood to enter

systemic circulation without liver
detoxification

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Development of Ascites

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 Diagnostic Studies

• Liver function tests

• Liver biopsy
• Liver scan
• Liver ultrasound

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 Diagnostic Studies

• Esophagogastroduodenoscopy
• Prothrombin time
• Testing of stool for occult blood

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 Collaborative Care

• Rest
• Avoidance of anticoagulants
• Management of ascites

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 Collaborative Care

• Prevention and management of

esophageal variceal bleeding
• Management of encephalopathy

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 Collaborative Care
Ascites

• High-carbohydrate, low-protein, low-Na+

diet
• Diuretics
• Paracentesis

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 Collaborative Care
Ascites

• Peritoneovenous shunt
– Provides for continuous reinfusion of ascitic
fluid from the abdomen to the vena cava

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Peritoneovenous Shunt

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Fig. 42-8
 Collaborative Care
Esophageal Varices

• If bleeding occurs, stabilize client and

manage the airway, administer vasopressin
(Pitressin)

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 Collaborative Care
Esophageal Varices

• Endoscopic sclerotherapy or ligation

• Balloon tamponade
• Surgical shunting procedures (e.g.,
portacaval shunt, TIPS)

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Sengstaken-Blakemore Tube

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Portosystemic Shunts

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Fig. 42-11
 Collaborative Care
Hepatic Encephalopathy

• Goal: reduce NH3 formation

– Protein restriction
– Sterilization of GI tract with antibiotics (e.g.,
neomycin)
– lactulose – traps NH3 in gut
– levodopa

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 Drug Therapy

• There is no specific drug therapy for cirrhosis

• Drugs are used to treat symptoms and
complications of advanced liver disease

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 Nutritional Therapy
• Diet for client without complications:
– High in calories
–  CHO
– Moderate to low fat
– Amount of protein varies with degree of liver
damage

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 Nutritional Therapy

• Client with hepatic encephalopathy

– Very low to no-protein diet
• Low sodium diet for client with ascites and
edema

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 Nursing Management
Nursing Assessment

• Past health history

• Medications
• Chronic alcoholism
• Weight loss

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 Nursing Management
Nursing Diagnoses

• Imbalanced nutrition: less than body

requirements
• Impaired skin integrity
• Ineffective breathing pattern
• Risk for injury

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 Nursing Management
Planning

• Overall goals:
– Relief of discomfort
– Minimal to no complications
– Return to as normal a lifestyle as possible

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 Nursing Management
Nursing Implementation

• Acute Intervention
– Rest
– Edema and ascites
– Paracentesis
– Skin care
– Dyspnea
– Nutrition

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 Nursing Management
Nursing Implementation

• Acute Intervention
– Bleeding problems
– Balloon tamponade
– Altered body image
– Hepatic encephalopathy

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 Nursing Management
Nursing Implementation

• Ambulatory and Home Care

– Symptoms of complications
– When to seek medical attention
– Remission maintenance
– Abstinence from alcohol

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 Nursing Management
Evaluation

• Maintenance of normal body weight

• Maintenance of skin integrity
• Effective breathing pattern
• No injury
• No signs of infection

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