Jaundice

Compiled BY: Mr. Ashish Roy

1. JAUNDICE COMPILED BY : MR. ASHISH H. ROY (NURSING TUTOR)

2. INTRODUCTION B ilirubin is produced when haemoglobin is broken down as part of the normal process of recycling old or damaged rbc . bilirubin is carried in the blood stream to the liver, where it binds with bile. bilirubin is then moved throuigh the bile ducts into the digestive tract; so that it can be eliminated from the body. most of bilirubin is eliminated in stool, but a small smount is eliminated in urine if bilirubin cannot be moved through the liver and bile ducts quickly enough. it builds up in the blood and is deposited in the skin that results jaundice .

3. DEFINITION JAUNDICE IS A YELLOW DISCOLOURATION OF BODY OR SKIN DUE TO ALTERATION OF BILIRUBIN METABOLISM. BILIRUBIN LEVEL EXCEEDS UPTO 3 TIMES THAN NORMAL. NORMAL VALUE IS 0.4-12 mg/dl.

4. Types HEMOLYTIC (PREHEPATIC) JAUNDICE : IT IS DUE TO BREAKDOWN OF RBCs THAT LEADS TO INCREASE UNCONJUGATED BILIRUBIN LEVEL IN BLOOD . LIVER FUNCTIONS ARE NORMAL. HEPATOCELLULAR JAUNDICE : IT IS DUE TO DISFUNCTIONING OF LIVER CELLS. OBSTRUCTION JAUNDICE : IT IS DUE TO OBSTRUCTION IN BILE DUCT THAT LEADS TO ALTERED SECRETION OF BILE. IT IS TWO TYPES : EXTRA HEPATIC OBSTRUCTION : DUE TO BLOCKAGE IN BILE DUCT, E.G., GALL STONE, TUMOR. INTRA HEPATIC CHOLESTATIS: IT OCCURS DUE TO BLOCKAGE OR SWELLING IN INTRA HEPATIC DUCT.

5. CAUSES / ETIOLOGICAL FACTORS BLOOD TRANSUSION REACTION. HAEMOLYTIC ANAEMIA. GALLBLADDER STONES. SICKLE CELL CRISIS. INFECTION - HEPATITIS VIRUS DRUG OR CHEMICAL TOXICITY. GALLSTONES, TUMOR INTRA HEPATIC DUCT

6. CLINICAL MANIFESTATIONS YELLOWISH SKIN AND SCLERA YELLOWISH SKIN AND SCLERA LIGHT GRAY OR CLAY COLORED (ALCOHOLIC ) STOOL ITCHY SKIN LACK OF APPETITE NAUSEA TEA COLOURED URUNE LOSS OF SRENGHTH PROTHROMBIN TIME INCREASED

7. DIAGNOSTIC EVALUATIONS INCREASED LEVEL OF SERUM BILIRUBIN (>0.4mg/100ml) conjugated. INCREASED INDIRECT (unconjugated) SERUM BILIRUBIN VALUES (> 0.8mg/100ml) ABSENCE OF BILIRUBIN IN URINE. REDUCED FETAL UROBILINOGEN (< 40mg/24HRS) BECAUSE IT DOES NOT REACH IN INTESTINE. PROLONGED PROTHROMBIN TIME (> 40 SECONDS)

8. Medical management /pharmacological management ONLY TREATMENT OF CAUSES IS NECESSARY OR SUPPORTIVE TREATMENT. 1. ANTIHISTAMINES DRUGS E.g., LEVOCITRIZINE - 5mg , PHERENAMINE MELEATE (AVIL) – 25mg 2.SEDATIVES FOR RESTLESSNESS AND IRRITABILITY E.g., lorenzapam , Diazepam 3. VIATMIN K AND B- COMPLEX. 4. PURGATIVE EMEMA IF CONSTIPATED 5. BROAD SPECTRUM ANTIBIOTICS 6. ANTIPYRETICS IN CASE FEVER OCCURS 7. ANALGESICS FOR PAIN MANGEMENT e.g., PCM 8. ANTIEMETICS IF VOMITING OCCURS e.g., ondestrone

9. DIETARY MANAGEMENT ADVICE THE PATIENT FOR RESTRICT FAT INTAKE. PROVIDE HIGH PROTEIN DIET. HIGH CARBOHDRATE DIET. PROVIDE PLENTY OF FLUIDS. GIVE GLUCOSE WATER.

10. NURSING DIAGNOSIS SKIN INTEGRITY IMPAIRED RELATED TO PRURITIS. RISK FOR HAEMORRHAGE RELATED TO DISTURB PROTHROMBIN FACTOR. CONSTIPATION RELATED TO DISEASE. ABDOMEN PAIN RELATED TO DISEASE. ANXIETY RELATED TO THE DISEASE CONDITION. ALTERED NUTRITION LESS THAN BODY REQUIREMENT RELATED TO CONSTIPATION AND ABDOMINAL PAIN AND DISCOMFORT.

11. NURSING MANAGEMENT PROVIDE COMFORT TO THE PATIENT. AVOID BED SORES BY CHANGING POSITION OF THE BED RIDDEN PATIENTS. MAINTAIN FLUID AND ELECTROLYTE BALANCE TO PATIENT MAINTAIIN INPUT-OUTPUT CHARTING. GIVE HEALTH EDUCATION PROVIDE PSYCOLOGICAL SUPPORT TO PATIENT.

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