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JAUNDICE

Slide 001
INTRODUCTION
• The liver plays a central role in many essential
physiologic processes. It is the primary organ of
lipid synthesis, and it detoxifies endogenous and
exogenous substances such as hormones,
drugs and poisons. When the normal physiologic
process are altered, numerous hepatic and extra
hepatic manifestation of liver disease appear.
These manifestations offer the initial clue to liver
disease, regardless of the cause.

Slide 002
DEFINITION
• Jaundice or icterus, is the yellow pigmentation of the
sclerae, skin and deeper tissues caused by excessive
accumulation of bile pigments in the blood. It is a
common manifestation of a variety of liver and biliary
disease and serves as a starting point for evaluating
many of the disorders.

• Jaundice is a symptom, rather than a


disease. The bilirubin level has to be approximately three
times the normal level (2-3mg/dl) for jaundice to occur.
TYPES
The three types of jaundice are classified as:
• hemolytic
• hepatocellular
• obstructive
HEMOLYTIC JAUNDICE
• Hemolytic (pre-hepatic) jaundice is due to the
increased break down of the red blood cells
(RBCs) which produce an increased amount of
unconjugated bilirubin in the blood. The liver is
unable to handle this increased load. Causes of
hemolytic jaundice include:-
• blood transfusion reactions
• sickle cell crisis
• hemolytic anemia
HEPATOCELLULAR JAUNDICE
• Hepatocellular (hepatic) jaundice results
from the liver’s altered ability to taken up
bilirubin from the blood or to conjugate or
excrete it. Initially both unconjugated and
conjugated bilirubin serum levels are
increased. In hepatocellular disease, the
hepatocytes are damaged and leak
bilirubin.
Contd..
• In severe disease, both unconjugated and conjugated
bilirubin are elevated as a result of both the inability of
hepatocytes to conjugate bilirubin and continued cell
leaking of conjugated bilirubin and the number of
unhealthy hepatocytes increases, the ability to conjugate
bilirubin will eventually decrease because the conjugated
bilirubin is water soluble it is excreted in the urine. The
most common causes of hepatocellular jaundice are
hepatitis, cirrhosis and hepatic carcinoma.
OBSTRUCTIVE JAUNDICE
• Obstructive (post hepatic) jaundice is due to
decreased or obstructed flow of bile through the
liver or biliary duct system. The obstruction may
be intrahepatic or extrahepatic. Intrahepatic
obstruction are due to swelling or fibrosis of the
liver’s canaliculi and bile ducts. This can be
caused by damage from liver’s tumors, hepatitis
or cirrhosis.
Contd..
• Causes of extrahepatic obstruction include
cammon bile duct obstruction from a stone,
biliary structures, sclerosing cholangitis, and
carcinoma of the head of the pancreas.
Laboratory findings show an elevation of both
unconjugated and conjugated bilirubin and urine
bilirubin. Because bilirubin doesn’t enter the
intestine, there is decreased or no fecal or
urinary bilinogen. With the complete obstruction
the stools are clay coloured.
ETIOLOGY AND RISK FACTORS
• The etiology and risk factors of jaundice are:-
• blood transfusion reactions
• sickle cell crisis
• hemolytic anemia
• hepatitis
• cirrhosis
• hepatic carcinoma
• biliary tract obstructions
GILBERT’S SYNDROME
• Gilbert’s syndrome is a hereditary
condition where the liver does not process
bilirubin very well.
PATHOPHYSIOLOGY
[HEPATOCELLULAR CAUSE]
• Due to hereditary condition
• ↓
• Reduced amount of an enzyme urodine diphosphate
glucuronosyltransferase (UGT)
• ↓
• Decreased processing of bilirubin
• ↓
• Back-log of bilirubin can build up in blood stream
• ↓
• Jaundice
BILIARY ATRESIA
• Biliary atresia is a rare condition in
newborn infants in which the common bile
duct between the liver and the small
intestine is blocked or absent.
PATHOPHYSIOLOGY [POST
HEPATIC CAUSE]
• Blockage of common bile duct/hereditary cholestatic syndrome
• ↓
• Biliary tract cannot transport bile to the intestine
• ↓
• Bile retained in the liver
• ↓
• Liver cirrhosis
• ↓
• Conjugated hyperbilirubinemia
• ↓
• Jaundice
SPHEROCYTOSIS
• DEFINITION
• Hereditary spherocytosis is a
genetic disorder. Here RBC are spherical
in shape. This type of RBC are more
prone for destruction while passing
through narrow capillaries result in excess
hemolysis.
PATHOPHYSIOLOGY [PRE-
HEPATIC CAUSE]
• Due to etiological factors like genetic factor
• ↓
• The RBC will become spherical in shape
• ↓
• While passing through blood vessels
• ↓
• Hemolysis of RBC takes place
• ↓
• Bilirubin level increases
• ↓
• Jaundice.
TYPHOID
• DEFINITION
• Typhoid fever is the result of
systemic infection mainly by Salmonella
typhi found only in man. The disease is
clinically characterized by a typical
continuous fever for 3 to 4 weeks.
PATHOPHYSIOLOGY [POST
HEPATIC CASE]
• Due to the various etiological factors like ingestion of
contaminated food, microbial invasion.
• ↓
• Salmonella typhi invades intestinal wall
• ↓
• Narrowing of intestinal lumen
• ↓
• Intestinal obstruction
• ↓
• Obstructive jaundice
LIVER CIRRHOSIS
• DEFINITION
• Cirrhosis of liver is a chronic,
progressive disease characterized by
widespread fibrosis and nodule formation.
Cirrhosis occurs when the normal flow of blood,
bile and hepatic metabolites are altered by
fibrosis and changes in the hepatocytes, bile
ductules, vascular channel and reticular cells.
PATHOPHYSIOLOGY
[HEPATOCELLULAR CAUSE]
• Cirrhotic liver usually has a nodular consisting with bands of fibrosis
and small areas of generating tissue
• ↓
• Extensive destruction of hepatocytes
• ↓
• This alteration in the architecture of the liver alters flow in the
vascular and lymphatic system and bile duct channels
• ↓
• Periodic exacerbation are marked by bile stasis
• ↓
• Jaundice
LIVER CANCER
• DEFINITION
• Metastatic carcinoma of the liver is
more common than primary carcinoma. The liver
is a common site of metastatic growth because
of its high rate of blood flow and extensive
capillary network cancer cells in other parts of
the body are commonly carried to the liver via
the portal circulation.
PATHOPHYSIOLOGY
[HEPATOCELLULAR CAUSE]
• Due to tumor
• ↓
• Obstruction to the flow of bile to intestine
• ↓
• Bile packed up into the liver substance
• ↓
• Reabsorbed into the blood
• ↓
• Carried throughout the entire body
• ↓
• Staining the skin, mucus membrane and sclera
PANCREATIC CANCER
• DEFINITION
• Pancreatic cancer is the most
common neoplasm affecting the pancreas.
PATHOPHYSIOLOGY
[OBSTRUCTIVE CAUSE]
• Carcinoma of the head of the pancreas
• ↓
• Decreased or obstructed flow of bile through the liver or biliary duct
system
• ↓
• Bilirubin can’t enter into the duodenum
• ↓
• Backed up into the liver substance
• ↓
• Reabsorbed into the blood stream
• ↓

Contd..
• ↓
• Carried through out the entire body
• ↓
• Staining the skin, mucous membrane and
sclera
• ↓
• Obstructive jaundice
CHOLELITHIASIS
• DEFINITION
• Cholelithiasis is the presence
of calculi in the gall bladder.
PATHOPHYSIOLOGY
[OBSTRUCTIVE JAUNDICE]
• Occlusion of the bile duct by a gall stone
• ↓
• Bile cannot flow normally into the duodenum but is
backed up into the liver substance
• ↓
• Bile is reabsorbed into the blood
• ↓
• Yellow colour of skin and mucous membrane
• ↓
• Obstructive jaundice
INTESTINAL OBSTRUCTION
• DEFINITION
• Partial or complete
impairment of the forward flow of intestinal
contents is known as an intestinal
obstruction.
PATHOPHYSIOLOGY
• Due to various etiological factors like microbial invasion, diseases
like typhoid fever etc.
• ↓
• Obstruction in intestine
• ↓
• Block the excretion of conjugated bilirubin
• ↓
• Absorption of bilirubin back to blood stream
• ↓
• Increased conjugated bilirubin in the serum
• ↓
• ↓
• Obstructive jaundice
• ↓
• Clinical features like clay coloured stool,
dark colored urine
SEPSIS
• DEFINITION
Blood products can become
infected from improper handling and
storage. Bacterial contamination of blood
products can result in bacteriemia or
sepsis.
PATHOPYSIOLOGY
• Due to infection of the body by pus
forming- bacteria

• Impaired excretion of bilirubin from the
liver

• Conjugated hyperbilirubinemia
HEMATOMA
• DEFINITION
Extra vasation of blood of
sufficient size cause visible swelling called
hematoma.
PATHOPHYSIOLOGY
• The unconjugated bilirubin is converted to conjugated
bilirubin in the presence of glucuronic acid in liver
• ↓
• When there is any bleeding from hepatic blood vessels
• ↓
Fibrosis takes place
• ↓
• Obstruction in the flow of conjugated bilirubin
• ↓

• ↓
• Increased level of bilirubin

• Jaundice
CARDIAC CIRRHOSIS
• DEFINITION
Chronic liver disease
associated with severe right sided long-
term heart failure (fairly rare).
PATHOPHYSIOLOGY
• Due to severe right sided congestive heart failure
• ↓
• Retrograde transmission of elevated venous pressure via
inferior venacava and hepatic veins
• ↓
• Hepatic sinusoids become dilated and engorged with
blood
• ↓
• Liver swollen
• ↓
Contd..
• ↓
• Prolonged congestion

• Necrosis and ischemia
• ↓
• Impaired liver function elevated conjugated and
unconjugated bilirubin
• ↓
• Jaundice
SCLEROSING CHOLANGITIS
• DEFINITION
Sclerosing cholangitis is an
uncommon inflammatory disease of the
bile ducts that causes fibrosis and
thickening of their walls and multiple short,
concentric strictures.
PATHOPHYSIOLOGY
• Intrahepatic obstruction resulting from stasis and inspissation
• ↓
• Bile cannot flow normally into the intestine
• ↓
• Backed up into the liver substance
• ↓
• Reabsorbed into the blood and carried throughout the entire body
• ↓

• ↓
• Conjugated hyperbilirubinemia
• ↓
• Obstructive jaundice
LIVER ABSCESS
• DEFINITION
Two categories of liver abscess
have been identified: amebic and
pyogenic. Amebic liver abscesses are
most commonly caused by entamoeba
histolytica.
PATHOPHYSIOLOGY
• Organisms reach the liver through the biliary system, portal venous
system or hepatic arterial or lymphatic system
• ↓
• Bacterial toxins destroy the neighboring liver cells
• ↓
• Necrosis of the hepatic tissue
• ↓
• Impaired liver function depend on the amount of hepatocellular
damage
• ↓
Contd..
• ↓
• Endoplasmic reticulum responsible for protein
and glucomide conjugation which will get altered
• ↓
• Increased unconjugated bilirubin
• ↓
• Jaundice
HEMOLYTIC JAUNDICE
• BLOOD TRANSFUSION REACTION
The most dangerous and
potentially life threatening, type of transfusion
reaction occurs when the donors blood is
incompatible with that of recipient. Antibodies
already present in the recipients plasma rapidly
combine with antigens on donor RBCs and the
RBCs are hemolysed in the circulation.
PATHOPHYSIOLOGY
• Antigen-antibody reaction
• ↓
• Hemolysis of RBCs
• ↓
• Flood the plasma with bilirubin
• ↓
• Liver cannot excrete the bilirubin as quickly as it is formed
• ↓
• Unconjugated hyperbilirubinemia
• ↓
• Fecal and urine urobilinogen levels are increased
• ↓
• Hemolytic jaundice
MALARIA
• DEFINITION
• Malaria is a protozoal disease
caused by infection with parasites of the
genous plasmodium and transmitted to
man by certain species of infected female
anopheline mosquito.
PATHOPHYSIOLOGY
• Fatal falciparum malaria is characterized by
prominent involvement of brain
• ↓
• Cerebral blood vessels are full of parasitized red
cells and often occluded by microthrombe.
• ↓
• Falciparum malaria may pursue a chronic cause
but may be puncturated at any time
• ↓
• ↓
• Complication like black water fever
• ↓
• Associated with massive hemolysis
• ↓
• Jaundice
HEPATITIS
• DEFINITION
• Hepatitis is the inflammation
of the liver or viral infection of liver
associated with a broad spectrum of
clinical manifestation from asymptomatic
infection through icteric hepatitis to hepatic
necrosis.
PATHOPHYSIOLOGY
• Due to the etiological factor like viral infection
• ↓
• Hepatocytes undergo pathologic changes induced by the
body immune response to virus
• ↓
• Inflammation of liver with areas of necrosis
• ↓
• Impaired liver function depend on the amount of
hepatocellular damage
• ↓
• ↓
• Endoplasmic reticulum responsible for protein
and glucomide conjugation which will get altered
• ↓
• Increased unconjugated bilirubin
• ↓
• Jaundice
SICKLE CELL ANEMIA
• DEFINITION
• Sickle cell anemia is a severe
hemolytic anemia that results from
inheritance of sickle hemoglobin gene.
This gene causes hemoglobin molecule to
be defective. The sickle hemoglobin
acquires crystal like formation when
exposed to low oxygen tension.
PATHOPHYSIOLOGY
• RBC containing sickle hemoglobin looses its round very pliable
biconcave disc shape
• ↓
• RBC becomes deformed and sickle shaped
• ↓
• Rigid RBC adheres to the endothelium of small blood vessels
• ↓
• Sickle cells do not live as long as normal RBC
• ↓
• Therefore they are dying more rapidly than liver can filter them out
• ↓
Contd..
• ↓
• Bilirubin from those broken down cells builds up in the
system
• ↓
• Unconjugated hyperbilirubinemia
• ↓
• Pigmentation especially in the sclera
• ↓
• Jaundice
BILIARY CIRRHOSIS
• DEFINITION
Biliary cirrhosis is the condition
in which bile flow decreased with
concurrent cell damage to hepatocytes
around the bile ductules.
PATHOPHYSIOLOGY
• Functional dearrangement of liver cells
• ↓
• Compression of bile ducts by connective tissue
overgrowth
• ↓
• Obstruction in bile duct
• ↓
• Decrease ability to excrete bilirubin
• ↓
• Obstructive jaundice
CHOLECYSTITIS
• DEFINITION
• Cholecystitis refers to acute
inflammation of the gallbladder wall.
PATHOPHYSIOLOGY
• Cholecystitis caused by the obstruction of bile duct
• ↓
• Venous and lymphatic drainage is impaired, proliferation of bacteria
localized cellular irritation or infiltration or both takes place, areas of
ischemia may develop
• ↓
• Necrosis of the tissue
• ↓
• Impaired liver function depend on the amount of hepatocellular
damage
• ↓
Contd..
• ↓
• Endoplasmic reticulum responsible for protein
and glucomide conjugation which will get altered
• ↓
• Increased unconjugated bilrubin
• ↓
• Jaundice
PANCREATITIS
• DEFINITION
• Acute pancreatitis is a acute
inflammatory process of the pancreas.
PATHOPHYSIOLOGY
• Due to etiological factors like, biliary tract disease,
alcoholism etc
• ↓
• Injury to pancreatic cells
• ↓
• Autodigestive effects of pancreatic enzyme
• ↓
• Ulceration in the pancreas
• ↓
• ↓
• Impaired excretion of bilirubin
• ↓
• Unconjugated hyperbilirubinemia
• ↓
• Jaundice
CLINICAL FEATURES
• The manifestation of jaundice includes:
• yellow sclera
• yellowish orange skin
• clay coloured feces
• tea-coloured urine
• pruritis (itching)
• fatigue
• anorexia
DIAGNOSTIC STUDIES
HEMOLYTIC HEPATOCELL OBSTRUCTIVE
ULAR
Serum bilirubin increase increase Somewhat
Unconjugated increase
(indirect)
Conjugated normal Increase/decrease Moderately
(direct) increase
Urine bilirubin negative increase increase

Urobilinogen increase Normal to decrease


stool increase
urine increase Normal to decrease
increase
MANAGEMENT
• MEDICAL MANAGEMENT
• DETERMINE THE CAUSE OF
JAUNDICE:
• An early goal in managing jaundice is to determine which category
of disease explains the clients jaundice. The clinical evaluation is an
important element in this determination and includes a carefully
documented health history, physical examination, basic tests of liver
function, and a complete blood count (CBC).
Contd..
• Additional tests, such as imaging studies, serological
tests and laboratory pathologic evaluation, may be
required.
• The health history should focus on specific
manifestation, including the presence and character of
pain, fever, or other manifestations of active
inflammation and changes in appetite, weight and bowel
habits. The clinical evaluation should on features of the
clients illness that point to hereditary cholestatic
syndromes, hepatocellular disease or biliary obstruction.
REDUCE PRURITIS AND
MAINTAIN SKIN INTEGRITY
• Pruritis, caused by an accumulation of bile salts in the
skin, results from obstructed biliary excretion. Some
clients experience only mild itching, other suffer such
extreme itching that they tear at their skin or scratch
during sleep It skin lesion develop and become infected
antibiotic may be ordered.
• Oral cholestyramine resin provides some relief by
binding bile salts in the intestine so that they can be
excreted. Anti histamines and phenobarbitol (Which
enhances bile flow) may also relieve itching.
SURGICAL MANAGEMENT
• To treat the underlying causes of jaundice,
based on the part affected, following
surgical treatment are done.
CHOLECYSTITIS AND
CHOLELITHIASIS
• LAPROSCOPIC CHOLECYSTECTOMY
• Laparoscopic cholecystectomy has dramatically changed the
approach to the management of cholecystities. If the common bile
duct is thought to be obstructed by a gall stone, an ERCP with
sphineterotomy may be performed to explore the duct before
laparoscopy.
• Before the procedure, the patient is informed that an open
abdominal procedure may be necessary and general anesthesia
is administered. Laparoscopic cholecystectomy is performed
through a small incision or puncture made through the abdominal
wall in the umbilicus.
Contd..
• The abdominal cavity is insufflated with carbon
dioxide to assist in inserting the laparoscope and
to aid the surgeon in visualizing the abdominal
structures. The fibre optic scope is inserted
through the small umbilical incision.
Contd..
• Several additional punctures or small incisions are made in the
abdominal wall to introduce other surgical instruments the biliary
system through the laparoscope a camera attached to the scope
permits a view of the intra abdominal field to be transmitted to a
television monitor. After the cystic duct is dissected the common bile
duct is imaged by ultrasound or cholangiography to evaluate the
anatomy and identify stones. The cystic artery is dissected free and
clipped. The gall bladder is separated away from the hepatic bed
and dissected. The gall bladder is then removed from the abdominal
cavity after bile and small stones are aspirated stone forceps also
can be used to remove or crush large stones.
CHOLECY STECTOMY
• In this procedure, the gall bladder is removed through an
abdominal incision after the cystic duct and artery are
ligated. The procedures is performed for acute and
chronic cholecystities In some patents, a drain may be
placed close to the gall bladder bed and brought out
through a puncteure wound; if there is a bile leak. The
drain type is chosen based on the physician’s
preference. A small leak should close spontaneously in a
few days with the drain preventing accumulation of bile.
• MINI CHOLECY STECTOMY
• CHOLEDOCHOSTOMY
• SURGICAL CHOLECYSTOSTOMY
• PERCUTANEOUS CHOLECYSTOSTOMY
PANCREATITICS.
• PANCREATICOJEJUNOSTOMY
DIET MANAGEMENT
• The diet management for jaundice include
the management of underlying causes.
HEPATITIS
• Adequate nutrition is important in assisting hepatocytes
to regenerate.
 During acute viral hepatitis, adequate calories are
important because the patient usually loses weight
 Fat content should be reduced because of decrease
bile production.
 Vitamin supplements, particularly B complex vitamin
and Vitamin K are frequently used .
 Fluid and electrolyte balance should be maintained.
CIRRHOSIS OF LIVER
• The diet for the patient with cirrhosis without
complication is high in calories with high carbohydrate
content and moderate to low fat levels.
 Low protein diets were routinely recommended for
patients with cirrhosis well prevent exacerbation of
hepatic encephalopathy.
 Sufficient carbohydrate intake must be provided to
maintain a minimum intake of 1500-2000 calories to
prevent hypoglycemia and catabolism.
Contd..
 Patient with alcoholic cirrhosis frequently has
protein caloric malnutrition, provided hepatic-
Acd II instant drink which contain protein from
branched chain amino acids that are
metabolized by liver .
 The patient with ascites and edema low –
sodium diet should be provided. The degree of
sodium restriction varies depending on the
patient condition.
PANCRETITIS
• The patient with acute pancreatitis is on NPO status to
reduce pancreatic secretion.
 In case of moderate to severe pancreatitis, the patient
may require enteral feeding via a jejunal feeding.
 Diet usually high in carbohydrate content because that is
the least stimulating to the exocrine portion of pancreas.
 If severs nutritional deficiencies exist parentral nutrition
may be used
CHOLELSTHIASIS
 The low fat diet reduces stimulation of gall
bladder.
 Food that are avoided include dairy
products such as whole milk, cream butter,
ice cream. Fried foods, gravies etc.
 Many patients have fewer problems if they
eat smaller more frequent meals.
NURSING MANAGEMENT
• The client should be observed closely for
development of jaundice often the first
manifestation the client notices is a change in
taste manifested as a distaste for a food or drink
the client previously liked, such as coffee,
purities is another early manifestation of incipient
jaundice check (another early mda---) the sclera
daily for the development of yellow coloration.
NURSING DIAGNOSIS
1. Impaired skin integrity related to pruritis.
• Expected outcome:-
The client itching will be controlled as
evidenced by the client’s statement of relief
decreased dryness of skin, maintainence of
skin and mucous membrane integrity, and a
decrease in scratching
Contd..
• Interventions:-
 Administer antihistamines and Phenobarbital as
prescribed to relieve the itching for clients with extreme
itching, administer oral cholestyramine resin to bind with
bile salts in the intestine so that they can be excreted.
Suggest other interventions including tepid water or
emollient baths, avoidance of alkaline soap and frequent
application of lotions. Encourage the client to wear loose,
soft clothing provide soft bed lines, and change soiled
linens as soon as possible. Keep the room cool.
2. Disturbed body image related to yellowing skin and sclerae
• Expected Outcomes

• Clients will cope with body image disturbances as evidenced by


clients not isolating themselves, verbalizing and demonstrating
acceptance of appearance, and initiating or re-establishing support
systems.
• Interventions:-
• Reassure the client that the discoloration is usually temporary.
Assist the client in personal hygiene as needed, and promote
activity as tolerated. Encourage clients to express their feelings
about their self image.
3. Ineffective health maintenance related to lack of
knowledge of jaundice.
• Expected Outcomes:
• The client will understand the cause of jaundice as
evidenced by the clients statements and ability to
define the illness.
• Interventions.
• Clients often wonder why they have jaundice, how
long the condition will last, and how to cope with the
problem. Encourage clients with jaundice to ask
questions about their health treatment and progress.
• Evaluation :-
• Jaundice should resovle with treatment
of the underlying condition. It usually
begins to disappear within 4 to 6 weeks
and body image improve and the prurites
subsides .
HOME CARE
• Most patients with viral hepatitis will be cared for at home, so the
nurse must assess the patients knowledge of nutrition and provide
the necessary dietary teaching rest and adequate nutrition are
especially important until liver function has returned to normal the
patient is cautioned about overcorrection and the need to follow the
health care provider’s advice about when to return to work. The
nurse must also teach the patient and family how to prevent
transmission to other family members. The patient should know
what symptoms should be reported to health care provider. The
patient should be instructed to have regular follow up for at least, 1
year after the diagnosis of hepatitis.
Contd..
• The patient with cirrhosis may be faced with a
prolonged course and the possibility of serious,
life threatening problems and complications. The
patient and the family need to understand the
importance of continuous health care and
medical supervision. They should be taught
symptoms of complications and when to seek
medical attention. Patients with cirrhosis should
avoid activities that place them at risk for
contracting viral hepatitis.
Contd..
• When the patient has conservative therapy, long-term
nursing management depends on symptoms and on
whether surgical intervention is being planned dietary
teaching is usually necessary the diet is usually low in
fat, and sometimes a weight- reduction diet is also
recommended. The patient may need to take fat soluble
vitamin supplements. The nurse should provide
instructions regarding observations that the patient
should make indicating obstruction (stool and urine
changes, jaundice, and prurites ) continued health care
is important, and its significance should be explained and
stressed.
Conclusion:-
• Liver is an important organ, essential for physiological
processes like synthetic function, detoxification etc.
There are several causes which leads to the damage of
liver. It will be either hepatocellular damage, pre-hepatic
damage or post hepatic damage. This will affect the
obstruction of bile flow or conjugation of bilirubin which
will give the clinical feature like jaundice which leads to
various signs and symptoms like yellowish sclera etc.
Inorder to manage this condition, various medical
management, surgical management and diet
management are done with various remedial home care.
BIBLOGRAPHY
• Black M joyce, “Medical Surgical Nursing”
United States: Elsevier publications, 2007:
(1319-1323p)
• Smeltzer.C. Suzanne, “Medical Surgical
Nursing” United States: Lippincott Williams
And Wilkins 2007: (1081-1082p)
• Lewis, ”Medical Surgical Nursing”, United
States : Elsevier Publications
2008:(1087-1133P)

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