Jaundice

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 HEPATOCELLULAR

OBSTRUCTIVE

Serum bilirubin

Unconjugated (indirect)

increase increase Somewhat increase

Conjugated (direct)

normal Increase/decrease Moderately increase

Urine bilirubin negative increase increase

Urobilinogen

stool

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).

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)