Jaundice and case discussion
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Jaundice is characterized by elevated bilirubin levels in the blood and classified into pre-hepatic, hepatic, and post-hepatic types. Treatment involves addressing the underlying cause, with options including phototherapy for neonates and supportive care for adults, as illustrated in a case study of a 68-year-old woman with alcoholic liver disease. Key management strategies include fluid restriction, sodium management, and adjustment of medications to address complications such as ascites, nausea, and confusion.
Jaundice and case discussion
- 1. PATHOLOGY AND TREATMENT OF JAUNDICE Dr. S P Srinivas Nayak, PharmD, (MSc). Assistant Professor, Sultan-ul-Uloom college of Pharmacy, Hyderabad, Telangana, India.
- 2. INTRODUCTION • Jaundice is the result of elevated levels of bilirubin in the blood termed hyperbilirubinaemia. • Normal serum bilirubin concentration ranges from 0.3-1.3 mg/dl, about 80% of which is unconjugated. • Jaundice becomes clinically evident when the total serum bilirubin exceeds 2 mg/dl. • A rise of serum bilirubin between the normal and 2 mg/dl is generally not accompanied by visible jaundice and is called latent jaundice.
- 5. Metabolism of bilirubin • About 80-85% of the bilirubin is derived from the catabolism of haemoglobin, and 15-20% of the bilirubin comes partly from non-haemo globin haem-containing pigments such as myoglobin, catalase and cytochromes, and partly from ineffective erythropoiesis • Haeme converts to biliverdin by oxygen and NADPH • Unconjugated Bilirubin is formed from biliverdin by biliverdin reductase.
- 6. • Bilirubin from plasma in the form of Albumin-bound unconjugated bilirubin enters into the hepatocyte, is dissociated into bilirubin and albumin. The bilirubin gets bound to cytoplasmic protein glutathione-S-transferase (GST) • Bilirubin UDP-glucuronosyl transferase conjugates bilirubin. • Conjugated (water-soluble) bilirubin is rapidly transported directly into bile canaliculi by energydependent process and then excreted into the bile • From gall bladder transports to intestines through bile, in the intestines again converts to urobilinogen and further to stercobilinogen • Small portion of Urobilinogen reabsorbs through EHC, oxidized to urobilin and finally excretes in urine
- 7. FACTORS THAT CAUSE HYPERBILIRUBINAEMIA Based on pathophysiology, jaundice may result from one or more of the following mechanisms: • 1. Increased bilirubin production • 2. Decreased hepatic uptake • 3. Decreased hepatic conjugation • 4. Decreased excretion of bilirubin into bile. age-old classification of jaundice pre-hepatic (haemolytic), hepatic, and post-hepatic cholestatic. However, hyperbilirubinaemia due to first three mechanisms is mainly unconjugated while the last variety yields mainly conjugated hyperbilirubinaemia.
- 9. DRUGS THAT CAUSE HAEMOLYSIS • Cephalosporins (a class of antibiotics), most common cause. • Dapsone. • Levodopa. • Levofloxacin. • Methyldopa. • Nitrofurantoin. • Nonsteroidal anti-inflammatory drugs (NSAIDs) • Penicillin and its derivatives.
- 11. NEONATAL JAUNDICE • Jaundice appears in neonates when the total serum bilirubin is more than 3 mg/dl. It may be the result of unconjugated or conjugated hyperbilirubinaemia
- 12. TREATMENT • TREAT THE SPECIFIC CAUSE • In Neonates, Phototherapy • Restrict fat diet • Maintain better liver function • Blood transfusion • Removal of gall stones • Symptomatic supportive therapy
- 13. CASE STUDY • A 68-year-old woman with a long-standing history of alcoholic liver disease is admitted to hospital with a 2-week history of vomiting, confusion, increased abdominal distension and worsening jaundice On admission laboratory data are as follows: • Na 116 (133–143mmol/L) • K 3.8 (3.5–5mmol/L) • Urea 8.5 (3.3–7.7mmol/L) • Bilirubin 40 (1-2mg/dl) • Albumin 23 (35–50g/L) • ALT 23 (0–35 iu/L) • Alk P 524 (70–300 iu/L) • PT 18.6 (13s) • Drugs on admission are as follows: Spironolactone: 300mg each morning. Temazepam: 10mg at night. Lactulose: 10mL twice daily
- 14. Questions Discuss the initial treatment plan for the management of: 1. Ascites 2. Nausea and vomiting 3. Confusion
- 15. ANSWERS Answer.1 • The patient should be sodium restricted and confined to bed. Spironolactone therapy should be stopped in view of the low sodium and confusion, as overuse of diuretics can precipitate encephalopathy. Fluid restriction is necessary to reduce the ascites, but sufficient fluid is required to rehydrate the patient following vomiting. • Paracentesis should be used to manage the ascites. Every litre of ascitic fluid removed should be replaced with 6–8g of albumin. • A diagnostic ascitic tap should be taken to ensure there is no infection in the ascites.
- 16. Answer 2 • Nausea/vomiting management. • Urea is slightly raised, indicating possible dehydration as a result of vomiting. The patient should be rehydrated with dextrose 5%, not saline, as this will worsen the ascites. • The patient's nausea can be managed with a suitable antiemetic such as domperidone 10mg four times a day initially and then titrated according to the response.
- 17. Answer 3 • Confusion. • Confusion may be an early sign of encephalopathy in this patient. • Temazepam should be stopped. The patient is on an inadequate dose of lactulose for the management of encephalopathy, so this should be increased to produce 2–3 loose motions per day. • A typical dose would be 20mL three or four times daily. In view of the patient's confusion, it may be worth considering other agents in the management of the encephalopathy, such as metronidazole 400mg twice daily.