| ID | 54 |
|---|---|
| Name | CIRRHOSIS OF LIVER |
| Cause | Causes of cirrhosis: Common causes: 1. Viral hepatitis B & C ± D 2. Alcoholic hepatitis (common cause mostly in the west) Other causes: 3. Primary biliary cirrhosis 4. Secondary biliary cirrhosis (stones, strictures) 5. Primary sclerosing cholangitis 6. al-antitrypsin deficiency 7. Haemochromatosis (hereditary or secondary) 8. Autoimmune hepatitis 9. Budd-Chiari syndrome 10. Wilson’s disease (Hepatolenticular degeneration) 11. Cystic fibrosis 12. Galactosaemia 13. Glycogen storage disease 14. Chronic severe heart failure (leading to hepatic venous congestion) 15. Drugs- such as INH, methyldopa, Methotrexate etc. 16. Idiopathic (cryptogenic) cirrhosis. |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: 1. Liver function tests-modest elevation of AST & serum alkaline phosphatase & progressive elevation of bilirubin: Serum albumin is low; gammaglobulin is high. Prothrombin time may be prolonged. 2. Plain radiological examination may reveal hepatic or splenic enlargement. 3. Ba-swallow and enema may reveal the presence of varices. 4. Ultrasonogram is helpful for assessing liver size & detecting ascites or hepatic nodules or any malignancy. 5. Hepatic scanning and peritoneoscopy may be helpful. 6. Liver biopsy- confirms the diagnosis. |
| Management | |
| Introduction | Cirrhosis is an irreversible chronic disorder of liver characterised by hepatic cellular damage, diffuse fibrosis and formation of regenerative nodules with distortion of hepatic architecture. These derangements lead to the development of impaired liver cell function, portal hypertension and abnormal portosystemic shunt (arteriovenous shunt). Cirrhosis can occur at any age group causing a prolonged morbidity with very poor prognosis |
| History | |
| Etiology | |
| Clinical Features | Clinical features: Symptoms: 1. The disease may remain dormant for a long period with some minor complaints, such as- anorexia, nausea, vomiting, flatulence etc. 2. Gradual weakness, fatiguability and weight loss. 3. Gradual swelling of the abdomen and lower limbs. 4. Haematemesis and melaena from ruptured oesophageal varices due to portal hypertension. 5. Bleeding from haemorrhoids^’ 6. Diarrhoea or constipation. 7. Amenorrhoea in females. 8. Loss of libido, impotence and painful enlargement of breast in male. Signs: 1. Facies- hepatic facies is present. 2. Anemia may be present. 3. Jaundice may be present if there is cholestasis. 4. Spider naevi, palmer erythema, white nail may be present. 5. Oedema is present and pitting in type. 6. Ascites- presence of fluid thrill and shifting dullness. 7. Abdomen is bloated; flanks are more bulged and umbilicus everted; presence of caput medusae. 8. Gynaecomastia may be present in male. 9. Absence of axillary and pubic hair. 10. There may be rise of temperature. 11. Digital clubbing & pigmentation. 12. Spleen is palpable (in portal hypertension). 13. Liver may be palpable in the early stage, but shrinks later. 14. Haemorrhagic tendency: epistaxis, menorrhagia, purpura, bruises. 15. Occasionally Dupuytren’s contracture (hyper-plasia of the palmar fascia & related structures, with nodule formation & contracture of the palmar fascia). |
| Preventions | |
| Treatment | Treatment: A. In cirrhosis with little symptoms patient is advised to -a Reduce activity. b. Take high protein (75-100gm/day) and carbohydrate diet, c. Clear bowel regularly, d. Take vitamin supplement, e. Avoid alcohol. f. Take only phenobarbitone or diazepam in smaller doses for sedation, if needed only. B. Complicated cirrhosis with 1. Ascites, 2. Hepatic precoma, 3. Portal hypertension, 4. Spontaneous bacterial peritonitis & other complications- 1. For ascites & oedema: a. Bed rest. b. Salt restriction- initially diatary sodium is 800mg/day can be given, but it should be reduced to 400mg/day in more severe ascites. NSA1D should not be given as it retains sodium. c. Fluid restriction- fluid intake should be restricted to 800-1000ml/day for patients with hyponatraemia (serum sodium <125meq/L). d. Diuretics- single or in combination. i. Initially single drug e.g spironolactone 100-400mg daily (drug of choice) ii. If failed then give spironolactone + frusemide with potassium supplement e. Paracentesis: removing ascitic fluid directly by paracentesis- in patients with massive ascites and respiratory compromise, ascites refractory to diuretics or intolerable diuretic side effects, large-volume paracentesis (4-61) is effective; when it is done, it is safest to give i.v albumin concomitantly at a dosage of l0gm/1 of ascites fluid removed to protect the intravascular volume. Large-volume paracentesis can be repeated daily until ascites is largely resolved. f. Peritoneovenous shunts- have been advocated for use in patients with refactory ascites; but these shunts may carry a consitdrable complications e.g DIG (in 65% of patients), infections (4-8%), CCF (2-4% patients). g. Transjugular intrahepatic portosystemic shunts (TIPS)- is an effective alternative to surgical portosystemic shunting in selected cases of variceal bleeding refractory to standard therapy (e.g, endoscopic band ligation or sclerotherapy) & has shown benefit in the treatment of severe refractory ascites. 2. For portal hypertension & gastrointestinal bleeding: For detail management- see below under portal hypertension. 3. For hepatic precoma (hepatic encephalopathy): a. Restrict all dietary proteins (only give 60gm/day). Introduce Ryle’s tube and give plenty of glucose and liquid diet through it. If not possible then give infusion to maintain fluid and electrolyte balance. 1 b. Ensure daily movement of bowel by lactulose 15-30ml 3 times daily. If the patient is unable to take lactulose orally, rectal use is indicated. 300ml of lactulose in 700ml of saline can be used rectally as a retention enema for 30-60 minutes. It can be repeated every 4-6 hours, c. To control ammonia-producing intestinal flora, a course of gut sterilizing antibiotic may be given in addition to lactulose-Oral neomycin sulphate 0.5-lgm can be given 6 hourly by nasogastric tube for 7 days. Alternatively, metronidazole 200mg 4 times daily also can be used effectively (in case of neomycin toxicity). d. Inj. vitamin-B complex 2ml i.m daily, e. Zinc deficiency should be corrected (if any), 600mg daily orally in divided doses, f. If the patient is very restless or agitated- Oxazepam 10-30mg (as it is not metabolized or excreted by the liver) may be given carefully by mouth or nasogastric tube. Injection promethazine 50mg may be given i.m alternatively. g. Avoid all the sedatives, narcotics and tranquillizers, which are metabolized and/or excreted by the liver, h. Diuretics and paracentesis- should be avoided, then give Inj. 1 Promethazine ampoule i.m. stat. i. proper nursing care: - Care of eye. - Care of oral hygiene. - Change posture every 2 hourly. - Catheterize if necessary. - Maintain intake-output chart. - Blood electrolyte should be done, if necessary. 4. Spontaneous bacterial peritonitis: This can be assumed when there is abdominal pain, fever with increasing ascites &/or progressive encephalopathy. Culture of ascitic fluid may give a positive bacteriological result. Common organisms are E. coli & pneumococci; others are rare. •Antibiotic therapy- should be initiated with i.v Cefotaxime 2gm every 8-12 hourly for minimum 5 days. If the patient survives, the risk of recurrent peritonitis can be reduced by giving long-term Norfloxacin 400mg orally daily. In high-risk cirrhotic patient, first episode of peritonitis may also be prevented by giving prophylactic Norfloxacin or Co-trimoxazole (960mg tablet 5 times a week) or Ciprofloxacin (750mg per week). 5. Correction of anemia- if iron deficiency anemia, iron and folic acid preparation may be given orally daily. Transfusion of packed red blood cells may be necessary to replace blood loss. 6. Haemorrhagic tendency- in cirrhosis, hypoprothrombinaemia leads to bleeding tendency. In early stage of cirrhosis (when liver is able to produce coagulation factors), this can be treated with vitamin K 5-10mg orally or parenterally. But, in case of severe hepatic disease, large volume of fresh frozen plasma may be given. But, as its effect is transient, it is usually not given unless there is active bleeding. Bad prognostic signs: 1. Increasing plasma bilirubin. 2. Falling plasma albumin. 3. Marked hypoalbuminaemia (below 25gm/l). 4. Marked hyponatraemia (below 120mmol/l) not due to diuretic therapy. 5. Prolonged prothrombin time. |
| Complications | Complications of Hepatic cirrhosis: 1. Portal hypertension & gastrointestinal bleeding. 2. Severe ascites. 3. Hepatic encephalopathy. 4. Hepatorenal syndrome. 5. Infection (spontaneous bacterial peritonitis). 6.Haemorrhagic disorder (due to hypoprothrombin-aemia). 7. Hepatopulmonary syndrome. 8. Hepatocellular carcinoma |
| Prognosis | |
| Types | |
| Classification | Clinically hepatic cirrhosis has no division, but histologically can be classified as- 1. Micronodular cirrhosis- in this nodules are not larger than the size of the original lobules (i.e approx. 1mm in diameter or less); presence of regular connective tissue septa and almost all lobules are involved. 2. Macronodular cirrhosis- in this variety nodules are large in size and connective tissue septa vary in thickness; larger nodules may contain histologically normal lobules and central vein, 3. Mixed cirrhosis- in which presence of micro- and macronodules, and hence variable features of cirrhosis. In an alcoholic, fatty micronodular cirrhosis strongly suggests chronic alcoholism. On the other hand, in macronodular cirrhosis there is increased chance of hepatocellular carcinoma. The above classification and terms are descriptive rather than separate disease entity, and each form may be seen in the same patient at different stages of the disease. |
| Observation | |
| Pathology |
© Pakistan Drug Directory. All Rights Reserved.
Designed By: Pakistan Drug Directory Team