symptom analysis of jaundice

JAUNDICE

INTRODUCTIONThe 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.

DEFINITIONJaundice 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.

TYPESThe three types of jaundice are classified as hemolytic, hepatocellular and

obstructive.

HEMOLYTIC JAUNDICEHemolytic (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 JAUNDICEHepatocellular (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. 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 JAUNDICEObstructive (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. 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 FACTORSThe etiology and risk factors of jaundice are:-

- Blood transfusion reactions - Sickle cell crisis- Hemolytic anemia- Hepatitis- Cirrhosis- Hepatic carcinoma- Biliary Tract Obstructions

GILBERT’S SYNDROMEGilbert’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 buitd up in blood stream

↓Jaundice.

BILIARY ATRESIABiliary 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

DEFINITIONHereditary 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

DEFINITIONTyphoid 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

DEFINITIONCirrhosis 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

DEFINITIONMetastatic 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

DEFINITIONPancreatic 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↓

Carried through out the entire body↓

Staining the skin, mucous membrane and sclera↓


CHOLELITHIASIS

DEFINITIONCholelithiasis 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↓


INTESTINAL OBSTRUCTION

DEFINITIONPartial or complete impairment of the forward flow of intestinal contents is known

as an intestinal obstruction.

PATHOPHYSIOLOGYDue 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 dryed stool, dark colored urine

SEPSIS

DEFINITIONBlood products can become infected from improper handling and storage.

Bacterial contamination of blood products can result in bacteriemia or sepsis.

PATHOPYSIOLOGYDue to infection of the body by pus forming- bacteria

↓Impaired excretion of bilirubin from the liver


HEMATOMA

DEFINITIONExtra vasation of blood of sufficient size cause visible swelling called hematoma.

PATHOPHYSIOLOGYThe unconjugated bilirubin is converted to conjugated bilirubin in the presence of

glucosonce 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

DEFINITIONChronic liver disease associated with severe right sided long-term heart failure

(fairly rare).

PATHOPHYSIOLOGYDue 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↓

Prolonged congestion↓

Necrosis and ischemia↓

Impaired liver function elevated conjugated and unconjugated bilirubin↓

Jaundice

SCLEROSING CHOLANGITIS

DEFINITIONSclerosing cholangitis is an uncommon inflammatory disease of the bile ducts that

causes fibrosis and thickening of their walls and multiple short, concentric strictures.

PATHOPHYSIOLOGYIntrahepatic 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



LIVER ABSCESS

DEFINITIONTwo categories of liver abscess have been identified: amebic and pyogenic.

Amebic liver abscesses are most commonly caused by entamoeba histolytica.

PATHOPHYSIOLOGYOrganisms 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↓

Endoplasmic reticulum responsible for protein and glucomide conjugation which will get altered

↓Increased unconjugated bilirubin

↓Jaundice

HEMOLYTIC JAUNDICE

BLOOD TRANSFUSION REACTIONThe most dangerous and potentially life threatening, type of transfusions 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.

PATHOPHYSIOLOGYAntigen-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.

PATHOPHYSIOLOGYFatal falciforam malaria is characterized by prominent involvement of brain

↓Cerebal 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

DEFINITIONHepatitis 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.

PATHOPHYSIOLOGYDue 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.

PATHOPHYSIOLOGYRBC 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

↓Bilirubin from those broken down cells builds up in the system


↓Pigmentation especially in the sclera

↓Jaundice

BILIARY CIRRHOSIS

DEFINITIONBiliary cirrhosis is the condition in which bile flow decreased with concurrent cell

damage to hepatocytes around the bile ductules.

PATHOPHYSIOLOGYFunctional dearangement of liver cells

↓Compression of bile ducts by connective tissue overgrowth

↓Obstruction in bile duct

↓Decrease ability to excrete bilirubin


CHOLECYSTITIS

DEFINITIONCholecystitis refers to acute inflammation of the gallbladder wall.

PATHOPHYSIOLOGYCholecystitis 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↓

Endoplasmic reticulum responsible for protein and glucomide conjugation which will get altered

↓Increased unconjugation bilrubin

↓Jaundice

PANCREATITIS

DEFINITIONAcute pancreatitis is a acute inflammatory process of the pancreas.

PATHOPHYSIOLOGYDue 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


↓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 HEPATOCELLULAR OBSTRUCTIVESerum BilirubinUnconjugated (Indirect)

Increase Increase Somewhat Increase

Conjugated (Direct) Normal Increase/Decrease Moderately Increase

Urine Bilirubin Negative Increase IncreaseUrobilinogenStool

Increase Normal To Increase Decrease

Urine Increase Normal To Increase Decrease

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). 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 INTEGRITYPruritis, 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 MANAGEMENTTo treat the underlying causes of jaundice, based on the part affected, following

surgical treatment are done.

1) CHOLECYSTITIS AND CHOLELITHIASIS a) 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. 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. 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.

b) CHOLECYSTECTOMYIn 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.

c) MINI CHOLECY STECTOMYd) CHOLEDOCHOSTOMYe) SURGICAL CHOLECYSTOSTOMYf) PERCUTANEOUS CHOLECYSTOSTOMY PANCREATITIS.g) PANCREATICOJEJUNOSTOMY

DIET MANAGEMENTThe diet management for jaundice include the management of underlying causes.

HEPATITISAdequate 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.

à Low protein diets were routinely recommended for patients with cirrhosis well prevent exacerbation of hepatic encephalopathy.à Sufficient carbohydrate intake must be provided to maintain a minimum intake of 1500-2000 calories to prevent hypoglycemia and catabolism.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 .à 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.

à In case of moderate to severe pancreatitis, the patient may require enteral feeding via a jejunal feeding.à Diet usually high in carbohydrate content because that is the least stimulating to the exocrine portion of pancreas.à If severs nutritional deficiencies exist parentral nutrition may be used.

CHOLELSTHIASIS.

à The low fat diet reduces stimulation of gall bladder.à Food that are avoided include dairy products such as whole milk, cream butter, ice cream. Fried foods, gravies etc.à 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 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

Interventions:-à 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 OutcomesClients 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.

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.

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.

BIBLOGRAPHY1. Black M Joyce, “Medical Surgical Nursing” United States: Elsevier publications,

2007:(1319-1323p)2. Smeltzer. C. Suzanne, “Medical Surgical Nursing” United States: Lippincott

Williams And Wilkins 2007: (1081-1082p)3. Lewis, ”Medical Surgical Nursing”, United States : Elsevier Publications 2008:

(1087-1133P)

symptom analysis of jaundice

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