Hepatic disorder

SEMINAR ON
HEPATIC DISORDER
PATEL NEEPA A
2nd year M.sc Nursing student
CHILD HEALTH NURSING

Introduction
 The liver is the largest gland in the body .It is situated in the
upper part of the abdominal cavity occupying the greater part
of the right hypochondriac region .
 Liver supports almost every organ in the body and is vital for
survival. Because of its strategic location and
multidimensional functions, the liver is also prone to many
diseases.

 Hepatic cirrhosis
 Hepatitis
 Fulminant Hepatic Failure(FHF)
 Budd–Chiari syndrome

 Cirrhosis is a condition in which
the liver does not function properly
due to long-term damage. Typically,
the disease comes on slowly over
years.
INTRODUCTION

CAUSES
 Alcoholic liver disease
 Non alcoholic liver disease
 Choric hepatitis C and B
 Hepatotoxic drugs or toxins
 Cystic fibrosis
 Primary biliary cirrhosis
 Primary sclerosing cholangitis
 Autoimmune hepatitis
 Wilson’s disease
 Galactosemia
 Glycogen storage disease type IV

commonly causes
 Cirrhosis is most commonly caused
by
alcohol,
hepatitis B,
hepatitis C,
 Non-alcoholic fatty liver disease.
Typically, more than two or three
drinks per day over a number of
years is required for cirrhosis to
occur.

 Non-alcoholic fatty liver
disease is due to a number of
reasons, including
being overweight, diabetes,
high blood fats, and high
blood pressure

SIGNS AND SYMPTOMS
 Cirrhosis has many possible manifestations. These signs
and symptoms may be either as a direct result of the
failure of liver cells or secondary to the resultant ;
 Cirrhosis of the liver is slow and gradual in its development.
 Weakness and loss of weight may be early symptom

Sign and symptoms have classified :
 Liver dysfunction
 Portal hypertension
 Unestablished causes
 Advanced disease

Liver dysfunction
spider angioma
Palmar erytherma
Gynecomastia
Hypogonadism
Ascites
Liver size can be enalrged
Fetro hepaticus
Jaundice

spider angioma
Palmar
erytherma
Gynecomastia Ascites

PORTAL HYPERTENSION
 Splenomegaly
 Caput medusa
 Esophageal varices
UNESTABLISHES CAUSE
 NAIL CHANGE
 Muehrcke’s line
 Terry’s nail
 Clubbing
 Hypertrophic Osteoarthropathy
 Duputren’s Contracture

 Esophageal varices
Splenomegaly
Esophageal varices
Caput medusa

Muehrcke’s line
Terry’s nail
Clubbing

Hypertrophic Osteoarthropathy Duputren’s Contracture

ADVANCED DISEASE
 Bruising and bleeding
 Hepatic encephalopathy
 Acute kidney injury

Bruising and bleeding Hepatic encephalopathy

 The liver plays a vital role in synthesis of proteins (for
example, albumin, clotting factors andcomplement),
detoxification, and storage (for example, vitamin A).
 In addition, it participates in the metabolism
of lipids and carbohydrates.
 Cirrhosis is often preceded by hepatitis and fatty liver
independent of the cause.

 The pathological hallmark of cirrhosis is the development of
scar tissue that replaces normal parenchyma
.
 This scar tissue blocks the portal flow of blood through the
organ therefore disturbing normal function.
 Recent research shows the pivotal role of the Hepatic
stellate cell, a cell type that normally stores vitamin A, in the
development of cirrhosis.

 In addition, it secretes TGF-β1, which leads to a fibrotic response
and proliferation of connective tissue.
 Furthermore, it secretes TIMP 1 and 2, naturally occurring
inhibitors of matrix metallo proteinases, which prevents them
from breaking down fibrotic material in the extracellular matrix
 The fibrous tissue bands (septa) separate hepatocyte nodules,
which eventually replace the entire liver , leading to decreased
blood flow throughout.
 The spleen becomes congested, which leads to hypersplenism and
increased sequestration of platelets. Portal hypertension is
responsible for most severe complications of cirrhosis

Liver biopsy
Endosocopy
Lab finding
 PT
 Thrombocytopenia
 Aminotranseferases
 Billirubin
 Albumin
DIAGNOSIS

Imaging
utrasound is routinely used in the evaluation of
cirrhosis.
Pathology

Complication
 Ascites
 Esophageal variceal bleeding
 Hepatic encephalopathy
 Hepatorenal syndrome
 Infection
 Hepatocellular carcinoma

MANGEMENT
Generally, liver damage from cirrhosis cannot be reversed,
but treatment could stop or delay further progression and
reduce complications.
Antibiotics are prescribed for infections, and various
medications can help with itching.
 Laxatives, such as lactulose, decrease risk of constipation;
their role in preventing encephalopathy is limited.

Alcoholic cirrhosis caused by alcohol abuse is treated by
abstaining from alcohol.
Treatment for hepatitis-related cirrhosis involves medications
used to treat the different types of hepatitis,
such as interferon for viral hepatitis and corticosteroids
for autoimmune hepatitis.
Cirrhosis caused by Wilson's disease, in which copper builds up
in organs, is treated with chelation therapy
(for example, penicillamine) to remove the copper.

Preventing further liver damage
 Vaccination of susceptible patients should be considered
for Hepatitis A and Hepatitis B.
Transplantation
 Main article: Liver transplantation
Palliative care

HEPATITIS DISORDER
 Hepatitis is a acute or chronic inflammation of the liver
and can be caused by a variety of different viruses,
chemical or drug reaction, or other disease.
 Non – viral causes of hepatitis include autoimmune
hepatitis, Wilson disease, alpha1 – antitrypsin deficiency,
and steatohepatitis.

The following six viruses cause 90% of cases of viral
hepatitis.
Hepatitis A virus
Hepatitis B virus
Hepatitis C virus
Hepatitis D virus
Hepatitis E virus.
Hepatitis G virus.

 Hepatitis A and E are responsible for most of the water –
borne (community acquired).
 Hepatitis while B, C and D are responsible for post –
transfusion hepatitis.
 Since a considerable number of cases of both post –
transfusion and community – acquired hepatitis are not
identified as being caused by hepatitis A – E, investigators
have sought to identify.

 Other potentially hepatotropic viral agents, including
hepatitis G virus, TT virus and SEN virus.
 Although each type of hepatitis is unique, assessment
findings and treatment have many similarities.

 Hepatitis A is caused by infection with the hepatitis A
virus (HAV), a non enveloped RNA virus, first identified by
electron microscopy in 1973.
It is classified within the genus hepatovirus of the
picornavirus family. In humans, a single serotype of HAV
exists. HAV infection induces lifelong protection against
reinfection.

 HAV is extremely resistant to degradation by
environmental conditions, a property that allows its
maintenance and spread within populations.
 In developing countries with poor environmental
hygienic conditions, nearly all children are infected with
HAV before 9 – years of age.

 It is spread via the fecal oral route through
contaminated food and water, and person – to – person
spread under poor sanitary conditions.
 Infections occur early in life in area where HAV is
highly endemic.

INCUBATION PERIOD:
 15 – 50 days (average 25 – 30 days) most contagious
1 – 2wk before symptoms onset at 28 – 30days.
TYPE/ETIOLOGY:
 Hepatitis A virus (HAV) previously called infectious
hepatitis.
PERIOD OF COMMUNICABILITY:
 Believed to be later half of incubation period to the
first week after the onset of clinical illness.

MODE OF TRANSMISSION:
 Principal route – fecal – oral.
 Rarely – parenteral.

CLINICAL FEATURES
 If you have this infection, you have inflammation in
your liver that's caused by a virus. You don't always get
symptoms, but when you do, you might have:
Jaundice (yellow eyes and skin, dark urine)
Pain in your belly
Loss of appetite
Nausea
Fever
Diarrhea
Fatigue

:
DIAGNOSIS
 The diagnosis is based on the history (especially
regarding possible exposure to a hepatitis virus); physical
examination; and serologic markers (antibodies and
antigens).
 The specific diagnosis of acute hepatitis A is made by
finding anti – HAV IgM in the serum of patients.

As IgG anti – HAV persists lifelong after acute infection,
detection of IgG anti – HAV alone indicates past infection
Laboratory evaluation of liver function includes
estimation of total and direct
 Bilirubin,
 transaminases,
 alkaline phosphatises Prothrombin time,
 total protein and albumin

PREVENTION OF SPREAD:
 Hand washing
 Gloves
 Identifying infected food handlers
IMMUNE PROPHYLAXIS:
The administration of immunoglobin can reduce the
incidence of hepatitis A up to 90%, and it is most effective
if given before exposure.

ACTIVE IMMUNIZATION:
 Inactivated HAV vaccines are available that are safe, highly
immunogenic and provide long – term protection from
infection.
 The vaccine is highly effective and provides seroconversion
rates of more than 99% when given as a single primary
immunization, followed by a booster dose 6 months later.
 Given as two injections at age 2 yr and 6 – 18 month later.
Only recommended for children with chronic liver disease or
haemophilia

POSTEXPOSURE PROPHYLAXIS:
Within 2 wk, give hepatitis A
Immune globin (HAIG), 0.02 ml/kg IM.

TREATMENT
 As no specific treatment exists, prevention is the most
effective approach against the disease
 Therapy is supportive and is aimed at maintaining
adequate nutrition. There is no evidence to suggest that
restriction of fats has any beneficial effects on the course
of the disease.
 Eggs, milk and butter may actually help provide a correct
caloric intake.

Antiviral agents have no role because the hepatic
injury appears to be immunopathologically mediated.
Referral to a liver transplant centre is appropriate for
patients with fulminant hepatitis A.
Temporary auxiliary liver transplantation for sub acute
liver failure may be a way to promote native liver
regeneration

Hepatitis B virus is a 3.2kb, circular, partially double
stranded DNA virus.
 HBV contains four open reading frames, which encode
major structural and non-structural proteins for HBV.
HBV infection can occur as an acute or chronic infection
and may range from being asymptomatic and limited to
causing fatal fulminant (rapid and severe) hepatitis.

 HBV varies greatly throughout the world.
High prevalence areas have been identified in Africa and
Asia; the United States is considered a low – prevalence
area.
INCUBATION PERIOD/PATHOGENESIS AND
NATURAL COURSE:
 30 - 180days (average 50 - 90days).
 Following a primary HBV infection, the host may run an
acute, fulminant or chronic course

TYPE/ETIOLOGY:
 Hepatitis B virus (HBV) previously called serum
hepatitis.
 Variable, virus in blood or other body fluids during
late incubation period and acute stage of disease; may
persist in carrier state for years to lifetime.

 Principal route – parental
 Less frequent route – oral, sexual, any body fluid
Perinatal transfer – transplacental blood (last trimester), at
delivery, or during breastfeeding, especially if mother has
cracked nipples.

CLINICAL FEATURES:
 Onset – more insidious
 Fever – less frequent
 Anorexia – mild to moderate
 Nausea and vomiting – sometimes presents
 Rash – common
 Arthralgia – common
 Pruritus – sometimes presents
 Jaundice – present

DIAGNOSIS:
 History
Physical examination;
 Serologic markers (antibodies and antigens) indicating
the presence of active infection with hepatitis A, B, or C
or previous infection. (Because the liver has a large
functional reserve abnormal laboratory tests may be the
only indication of hepatitis)
serum aspirate and alanine Aminotransferases

 Serum Bilirubin levels
 HAV immunoglobulin
(immunoglobin M [IgM]) antibody in
the serum.
 The diagnosis of HCV is based on the
detection of anti – HCV antibodies
and confirmation by polymerase chain
reaction for hepatitis C RNA
 An abdominal ultrasound
 Liver biopsy

why should be done the HBV diagnosis test ?
 HBV diagnosis depends on the presence of hepatitis B surface
antigen (HBsAg) or anti – HBV core (anti – HBc) IgM antibody,
chronic HBV infection is associated with the persistence of
HBsAg and HBV DNA markers.

 Sterilization of needles
 Blood precautions
 Gloves

 Vaccine 80% - 90% effective
 Three injection at 0, 1 and 6 months
 Recommended for all infants, children, and adolescents.

 For neonates of infected mothers, give HB immune
globulin (HBIG) within 12 hr of birth followed by
vaccines
 HBIG, 0.06 ml/kg, within 24hr of any Percutaneous
exposure

INTRODUCTION
Hepatitis C virus (HCV) was recognized in 1989 as a
major cause of non – A, non – B hepatitis.
HCV is an envelope, single – stranded, positive – sense
ribonucleic acid (RNA) virus, classified as an independent
genus (hepacivirus) within the flavivirus family.

INCUBATION PERIOD:
2 weeks – 6 months, average 6 – 7 weeks. The mean
incubation period of post – transfusion acute HCV infection
is 7 to 8 weeks, with range of 2 to 26 weeks.
TYPE/ETIOLOGY:
 Hepatitis C virus (HCV) is non – A, non – B hepatitis.
 Begins before onset of symptoms, may persist in carrier
state for years

Principal route – parenteral
Non parenteral spread possible.

CLINICAL FEATURES
Onset – usually insidious.
Fever – less frequent
Anorexia – mild to moderate
Nausea and vomiting – mild to moderate
Rash – sometimes present
Arthralgia – rare
Pruritus – sometimes presents
Jaundice – present

DIAGNOSIS:
 History
 Physical examination;
 Serologic markers (antibodies and antigens) indicating the
presence of active infection with hepatitis A, B, or C or
previous infection. (Because the liver has a large functional
reserve abnormal laboratory tests may be the only
indication of hepatitis)
 Serum Bilirubin
The detection of anti – HCV antibodies and confirmation
by polymerase chain reaction for hepatitis C RNA.

Nucleic acid tests directly detect circulating virus
 An abdominal ultrasound provides
 A liver biopsy aids

 Standard precautions
 None
 Not currently recommended by centre for disease control
and prevention.

HBsAg
RNA
 antigen
Hepatitis D (Delta) Virus

INTRODUCTION
 Hepatitis D virus (HDV) was first detected as a new
nuclear antigen in the hepatocytes of patients infected with
hepatitis B virus (HBV) and was frequently associated
with severe acute or chronic hepatitis.
 Transmission of HDV requires either co – infection with
HBV or super infection in individuals who are HBV
carriers.

INCUBATION PERIOD:
 The incubation period is 2 to 8 weeks (21 to 90 days).
TYPE/ETIOLOGY:
 Hepatitis Delta virus (HDV), occurs only in patients
with acute or chronic HBV infection.
 Blood and blood products
 More common in Mediterranean countries and among IV
drug users and haemophiliacs.(Impair the body's ability to
control blood clotting, which is used to stop bleeding when a
blood vessel is broken.)

DIAGNOSIS:
History
Physical examination;
Serum Bilirubin levels peak 5 to 10 days

 Testing for HDV infection is recommended in children
with chronic HBV infection in severe liver disease and
in children with acute exacerbation of a previously stable
liver disease
 Although serum aspirate and alanine Aminotransferases
(AST and ALT) levels are markedly elevated in viral
hepatitis, other disease or conditions may cause their
elevation

 Sterilization of needles
 Blood precautions
 Gloves.
 Protecting from HBV will protect because HDV cannot
exist alone.

 Hepatitis B immunoglobulin (HBIG) is used in the post –
exposure prophylaxis of newborns of HBV infected
women.
 It is administered IM and may be given concurrently with
HBV vaccine, at a different site.
 The dose for infants is 0.5ml.
 Combination of HBIG and HBV vaccination in infants
born to HBsAg positive mothers prevents transmission in
approximately 95% of those at risk.

 Hepatitis E virus (HEV) was first described in
1978 after an epidemic affecting 52,000
individuals in Kashmir.
 Hepatitis E is caused by infection with the
hepatitis E virus (HEV), a single – standard RNA
virus.

 It is usually transmitted through contaminated
drinking water. Hepatitis E virus causes acute
sporadic( isolated). and epidemic viral hepatitis.
 Symptomatic HEV infection is most common in
young adult aged 15 – 40 years and is uncommon in
children since it is mostly asymptomatic and anicteric

INCUBATION PERIOD:
 The incubation period is 3 to 8 weeks (15 to 60 days)
average 40 days.
TYPE/ETIOLOGY:
 Hepatitis E virus (HEV), enteric ally transmitted
non – A, non – B hepatitis.
 Fecal – oral, more common in adults

CLINICAL FEATURES
 The clinical features of HEV are similar to HAV infection.
The severity of an HEV infection is generally greater than
the severity of an HAV infection.
 In pregnant women, the disease is particularly severe
where mortality approaches 20% with infections in the
third trimester. Premature deliveries with high infant
mortality up to 33% are observed.

DIAGNOSIS:
 Laboratory evaluation of HEV is similar to that of
HAV
 History
 Serum Bilirubin

 IgM anti – HEV titer declines rapidly during early
convalescence, while IgG anti – HEV persist for long
duration and provides protection aganist subsequent
infection

 Standard precautions
VACCINES:
 Hepatitis E is preventable by vaccination. Studies in Nepal
and China had shown 95% efficacy of a recombinant
genotype 1 HEV vaccine in preventing infection and
clinical disease
 genotype 1 HEV vaccine in preventing infection and
clinical disease

PREVENTION:
 As with HAV good personal hygiene, high quality standards
for public water supplies and proper disposal of waste
have resulted in a low prevalence of HEV infection in
developed countries.
TREATMENT:
 As no specific therapy is capable of altering the course
of acute hepatitis E infection, prevention is the most effective
approach against the disease. (immunosuppressive therapy
Antiviral therapy )

INTRODUCTION
 GB virus C (GBV-C), formerly known as hepatitis G
virus (HGV), is a virus in the Flaviviridae family which
has not yet been assigned to a genus, is known to infect
humans, but is not known to cause human disease.
 There have been reports that HIV patients co-infected with
GBV-C can survive longer than those without GBV-C, but
the patients may be different in other ways.

 Hepatitis G virus and GB virus C (GBV-C) are RNA
viruses that were independently identified in 1995, and
were subsequently found to be two isolates of the same
virus.
 Hepatitis G virus (HGV) is a blood – born 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.

INCUBATION PERIOD
 The incubation period is unknown
TYPE/ETIOLOGY
 Hepatitis E virus (HEV), enteric ally transmitted
non – A, non – B hepatitis.
MODE OF TRANSMISSION
 Parenteral, sexual and vertical transmission of GBV-C has
all been documented, and because of shared modes of
transmission, individuals infected with HIV are commonly
co-infected with GBV-C.
 Among people with HIV infection, the prevalence of
GBV-C viraemia ranges from 14 to 43%

 Laboratory evaluation of HEV is similar to that of
HAV
 History
 Serum Bilirubin

 An abdominal ultrasound.
 Finally, a liver biopsy aids in assessing the severity of
the disease.

PATHOPHYSIOLOGY
FOR HEPATITIS
A, B, C, D, E AND G

THERAPEUTIC
MANAGEMENT
FOR
HEPATITIS A, B, C, D,
E AND G:

Treatment options for viral hepatitis are limited.
The goals of management include early detection,
recognition of chronic liver disease, support and
monitoring, and prevention of spread of the disease.
HBV and HCV treatment is directed at managing the viral
load to prevent further with interferon’s, naturally
occurring proteins that exert antiviral, antiproliferative,
and immunomodilatory effects.

Lamivudine and adefovir are two other interferon analogs
that suppress the replication of HBV.
A combination of alpha – interferon and ribavirin has
resulted in a sustained response in only 50% of patients
with HBV and HCV
Another important aspect of the therapeutic management
of hepatitis involves hospitalization
Hospitalization is necessary if coagulopathy or fulminant
hepatitis is present.

 A recent interferon formulation, pegylated interferon, can
be administered once a week and has been found to
sustain plasma levels and enhance viral suppression
 HAV infection is an acute disease that resolves with
support and management of symptoms.

PREVENTION FOR
HEPATITIS A, B, C, D, E AND G:

 Proper hand washing and standard isolation precautions can
prevent the spread of hepatitis.
 Prophylactic use of standard immune globulin (Ig) is
effective in preventing HAV infection in situations of pre
exposure (e.g., anticipated travel to areas where HAV is
prevalent) or in situations of post exposure during the early
part of the incubation period.
 Hepatitis B immune globulin (HBIg) is effective in
preventing HBV infection after exposure.

 Ig and HBIg must be administered less than 2 weeks after
exposure.
 Vaccines have been developed to prevent HAV and HBV
infection.
 HBV vaccination is recommended for all newborns and
for high – risk groups.
 HAV is also recommended for high – risk groups.
 Active immunizations are not available against HCV.
 It is possible to prevent HDV infection by preventing
HBV infection

NURSING CARE MANAGEMENT FOR
HEPATITIS A, B, C, D, E AND G

 If further assistance is needed for parents to comply
with therapy, a public health nursing referral may
necessary.
 A well – balanced diet and a realistic schedule of rest
and activity adjusted to the child’s condition are
encouraged.
 HAV is not infectious within a week after the onset of
jaundice, and children may feel well enough to
resume school.

 Hand washing is the single most critical measure in
reducing risk of transmission.
 The nurse should explain to parents and children the ways
in which HAV (oral – fecal route) and HBV (parenteral
route) are spread.
 Nursing caring for young people with HBV infection and
a known or suspected history of illicit drug use should
help these teens realize the dangers of drug abuse.

 Nurses should stress the parenteral mode of transmission
of hepatitis and encourage them to seek counselling
through a drug program..
 Many communities have multidisciplinary clinics
dedicated to the management of these diseases.

NURSING CARE FOR
HEPATITIS A, B, C, D, E AND G:

Assessment:
 The nursing history may identify a source of infection.
 In children, flu – like symptoms of fever, anorexia,
fatigue, and nausea may be the only symptoms of viral
hepatitis.
 Abdominal assessment may disclose right upper quadrant
tenderness and hepatomegaly.
 Stools will be pale and clay – colored, and urine may be
dark and frothy.

 Jaundice, if present, is best assessed in sclera, nail beds,
and mucous membranes and usually follows a
cephalocaudal progression.
 In HBV infection, arthralgia may be the presenting
complaint.
 Fulminant hepatitis will likely manifest as acute hepatic
failure with associated encephalopathy, bleeding, fluid
retention, ascites, and an icteric appearance.

Nursing Diagnosis and Planning
 The following nursing diagnosis and expected
outcomes may be appropriate after assessing the child
with viral hepatitis and the child’s family:
 Imbalanced nutrition: less than body requirements
related to anorexia
 Expected outcomes: the child will tolerate an age
appropriate diet without weight loss, vomiting, or
abdominal pain and will return to a normal activity level.
 Risk for infection related to exposure of family members
to infectious agents.

Expected outcomes: the child will return to pre – illness
weight and activity level.
Deficient knowledge related to incomplete information
about home care and long – term prognosis
Expected outcomes: the parents will verbalize a basic
understanding of hepatitis and the importance of treatment
and prevention.

 Expected outcomes: the family will practice good
hand washing and other necessary isolation procedures
and will remain free from infection.
 Risk for injury related to fulminant hepatitis

Interventions
 Unless fulminant hepatitis develops, children are usually
treated at home, so parental education is crucial.
 Teaching parents the importance of a nutritious, low – fat
diet as tolerated by the child, rest, and general supportive
care are important.
 The child with hepatitis is often anorexia.
 Several small meals and snacks throughout the day are
better tolerated than regular portions at mealtime.

 Fatigue and malaise can last for several weeks.
 Adequate rest and sleep are important for recovery,
because HAV is not infectious within 1 week after the
onset of jaundice, the child may return to school at that
time if well enough.

Child and Parent Teaching
 Teach the parents the danger that could indicate a
worsening of the child’s condition – specifically, changes
in neurologic status, bleeding, and fluid retention.
 Jaundice may worsen before it resolves, and parents
should be prepared for this possibility.
 Also, teach parents not to give their child any over – the –
counter medications, because impaired liver function may
result in inadequate metabolism and excretion of the
medication.

 Caution adolescents not to drink alcohol during the illness
or recovery period.
 Preventing the spread of infection is an essential
intervention for HAV.
 Prevention should include the use of contact precaution
for at least 1 week after the onset of jaundice and excellent
hand washing.
 Hand washing is the most important preventive measure.
 Teach family members to institute appropriate precautions
and to clean exposed household surface with bleach.

 Diapers should not be changed on or near surfaces used
for preparing or serving food.
 Explain to family members the ways in which HAV (fecal
– oral route) and HBV (parenteral route) are spread to
others.
 Provide education about the recommendations concerning
hepatitis A and hepatitis B vaccination
 If the child has HBV infection, especially neonatal HBV,
prepare the parentns for the possibility of a chronic carrier
state and the development of cirrhosis and hepatocellular
cancer in later years.

Home care:
 Children with hepatitis are almost always managed at home
.
 Nursing interventions include teaching parents hand – washing
skills, the use of gloves, and disinfection of contaminated surfaces
and articles.
 Parents should be taught to monitor for complications, provide a
well balanced, low – fat diet, and monitor other family members for
infection.
 All children in the family should be immunized against hepatitis.

Definition –
 Fulminant hepatic failure (FHF)
or acute liver failure (ALF) is
defined as the rapid development of
acute liver injury with severe
impairment of the synthetic
function
and hepatic encephalopathy in a
patient without previous liver
disease.

 Altered mental status with
coagulopathy in setting of acute
liver disease.
Hepatic encephalopathy
occurring within 8 weeks of
onset of illness defines FHF

Viral hepatitis
 Hepatitis A - rarely
 Hepatitis B - appx 1% of hep B
 Hep C -- probably not, but ??
 Hep D -- delta agent coinfects with Hep B
 Hep E
 CMV, HSV

Toxins
 Carbon tetrachloride
 Phosphorus
 Amanita phalloides (antidote penicillin and silybin)
 Industrial cleaning solvents

Drugs
 Acetaminophen
 Acetaminophen in Tx doses with alcohol
 Idiosyncratic reaction -- halothane, sulfonamides,
phenytoin, and others.
Vascular
 Heart failure -- centrolobular necrosis
 Sinusoidal obstruction secondary to metastatic dz
 Budd Chiari
 Veno-occlusive disease

Clinical Presentation
 Typically -- nonspecific symptoms, nausea, jaundice,
altered mental status, coma -- all over a few days.
The altered mental status occasionally precedes clinical
jaundice.
Mental status changes often start with agitation, delusions,
irritability before progressing to lethargy, stupor, and
coma.

Treatment
 Prevent hypotension
 Lactulose -- although not shown to work well in FHF
and felt to be less effective than in chronic liver disease.
 Branch chain amino acids -- theoretically appealing but
studies are mixed results -- most authors feel they are not
helpful.
 Mannitol -- shown to be effective in improving outcome

 Hyperventilation -- probably useful for acute spikes in
ICP. Has not been shown to be effective in hepatic failure.
Concerns about effect on cerebral perfusion warrant
consideration.
 Elevation of head -- ?? What is effect on CPP? Keep
head midline, perhaps 20 - 30 degrees of elevation.
 Pentobarbital coma, hypothermia -- unproven,
occasionally may be indicated.
 Steroids -- no good, may worsen outcome

Management
 Avoid bleeding
 GI prophylaxis
 Avoid nasal intubation
 Beware with surgical procedures, line placement, etc.
 FFP -- Not shown to be effective in changing bleeding risk (?).
Most authors discourage routine attempts at normalizing PT.
Use for active bleeding and procedures.
 Antifibrinolytics (Amicar) may be considered if bleeding and
primary fibrinolysis is occurring. Caution with DIC.
 Maintain platelet count >50K, or 100K if bleeding

PICO
Lipid profile and cardiovascular risk factors in pediatric liver transplant recipients.
Abstract
 Cardiovascular diseases induce long-term morbidity and mortality of adult LT recipients. The
aim of this retrospective study was to assess CVRF, lipid abnormalities, and atherosclerosis
(appraised by c-IMT), more than 10 yr after pediatric LT. Thirty-one children who underwent
LT between December 1990 and December 2000 were included. Median age at LT was 14
months (range 4-64), and median follow-up after LT was 11.9 yr (range 9.0-17.3). In our
cohort, obesity (9.7%) and treated hypertension (9.7%) were rare. None of the patients was
smoker or diabetic. High TC and TG were both observed in 6.5% of the patients. The mean c-
IMT for male patients was 1.22 ± 1.55 and 1.58 ± 1.23 mm in female patients. Seven patients
(22%) had a mean c-IMT above +2 s.d. Values below the 5th percentile were noted for LDL-
cholesterol (58.1%), HDL-cholesterol (25.8%), apolipoprotein B (40%), and apolipoprotein A1
(20%). LDL-cholesterol and apolipoprotein B levels were significantly lower in patients
treated by tacrolimus in comparison with CsA (p < 0.05). In conclusion, our results suggest
that pediatric LT patients do not present significant CVRF; moreover, instead of
hyperlipidemia, hypocholesterolemia (LDL-C) is frequent and immunosuppressive therapy is
probably the cause.

P I C O
Cardiovascular dise
ases retrospective study
- pediatric LT
patients do not
present significant
CVRF; moreover,
instead of
hyperlipidemia,
hypocholesterolemi
a (LDL-C) is
frequent and
immunosuppressive
therapy is probably
the cause

BIBLIOGRAPHY:
 Dutta Parul. Pediatric nursing. 2nd ed. New Delhi: Jaypee
brother medical publishers.
 Marlow.R Dorothy, Redding.A Barbara. Text book of pediatric
nursing. 6th ed. Philadelphia, Pennsylynia : Elsevier
publication; 2009.
WEB SITE
 https://en.wikipedia.org/wiki/Cirrhosis
 http://www.stlouischildrens.org/diseases-conditions/liver-
disease
 http://www.ncbi.nlm.nih.gov/pubmed/26750745

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