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“The only thing necessary for these diseases to the triumph is for good people and governments to do nothing.”

 

    

Gastroenterology And Hepatology: Alcoholic Liver Disease, Liver Failure, and Chronic Liver Disease

 

http://www.vh.org/adult/provider/familymedicine/FPHandbook/Chapter05/19-5.html

 

University of Iowa Family Practice Handbook, Fourth Edition, Chapter 5

 

Jatinder P. S. Ahluwalia, MD, Mark A. Graber, MD, and William B. Silverman, MD
Division of Gastroenterlogy and Hepatology and Departments of Internal Medicine, Family Medicine, and Emergency Medicine
University of Iowa Hospitals and Clinics and College of Medicine

Peer Review Status: Externally Peer Reviewed by Mosby


        Alcoholic Liver Disease (ALD).

                            A.            General Background.

                                                    1.            It is caused by chronic alcohol ingestion-consumption exceeding 80 g/day (equivalent to six 12 oz cans of beer, 1 liter of wine, or 5-6 liquor drinks).

                                                    2.            It is the most prevalent form of liver disease in the developed countries and affects women and those with hepatitis C infection at a lower consumption level than men.

                                                    3.            Three histologic forms of ALD are recognized: hepatic steatosis (fatty liver), alcoholic hepatitis, and alcoholic cirrhosis.

                                                    4.            An increased prevalence of hepatitis C in patients with ALD.

                           B.            Clinical Presentation.

                                                    1.            Presenting features range from non-specific signs and symptoms to frank liver failure. Also see chronic liver disease below for signs and symptoms.

                                                    2.            Parotid gland hypertrophy may be present due to recurrent emesis.

                                                    3.            Epigastric or right-sided abdominal pain, progressive jaundice, increasing abdominal girth or lower extremity swelling may be the reasons compelling the patient to seek medical attention.

                                                    4.            Anorexia, nausea, and vomiting are also reported by these patients.

                                                    5.            Fever and tachycardia may be noted in the absence of an infection.

                                                    6.            Tender hepatomegaly may occur due to acute inflammation of the liver.

                                                    7.            Progressive jaundice, palmar erythema, Dupuytren’s contractures, cutaneous telangiectasias, feminization (gynecomastia and testicular atrophy) and complication of portal hypertension (see below) are some of the other findings.

                                                    8.            Alteration in mental status may be noted due to hepatic encephalopathy (see below) and/or alcohol withdrawal.

    

                           C.            Diagnosis and laboratory evaluation. A thorough history of alcohol use, complete liver panel, biochemical profile, CBC and PT with INR should be obtained on all patients. The CAGE questionnaire can be used to screen for alcohol abuse or dependency.

                                                    1.            Elevated GGT in most.

                                                    2.            AST:ALT ratio is typically between 2:1 to 8:1 with both usually being <300 IU/L. Unless associated with acetaminophen toxicity, transaminase values higher than seven times the upper limit of normal should make one question the diagnosis of ALD.

                                                    3.            Leucocytosis (with neutrophilia) in the absence of an infection may be present due to inflammation of the liver.

                                                    4.            Coagulopathy persisting despite replacement of vitamin K is indicative of decreased hepatic synthetic function.

                                                    5.            Prognosis. Patients with alcoholic hepatitis and discriminant function (DF) >32 have a poor prognosis with a predicted probability of mortality within 1 month of ~ 50%. DF = 4.6 (PT - normal PT) + total bilirubin (mg/dl).

                                                    6.            A liver biopsy may be necessary if the diagnosis is unclear or if there are atypical features. It aids in the selection of patients being considered for steroid therapy as up to 28% of patients with a clinical picture of alcoholic hepatitis do not have histological features consistent with alcoholic hepatitis on the biopsy.

                          D.            Treatment.

                                                    1.            Alcohol abstinence and supportive care are key to the successful treatment of ALD. Liver enzyme abnormalities persisting for 6 months after the cessation of alcohol intake should prompt workup to rule out other causes of liver disease including a liver biopsy.

                                                    2.            Symptomatic patients should be hospitalized and given thiamine 100 mg via IV fluids initially to prevent Wernicke-Korsakoff’s syndrome.

                                                    3.            Treat alcohol withdrawal

                                                    4.            Patients with ALD are usually malnourished so protein intake should not be restricted severely. At least 60 g of protein should be given daily.

                                                    5.            Steroids. If an infectious process has been ruled out, patients with severe alcoholic hepatitis (hepatic encephalopathy or DF > 32 may benefit from corticosteroids. Prednisolone 40 mg qd x 4 weeks followed by tapering over several days to weeks should be used.

                                                    6.            Patients with end-stage alcoholic liver disease should be referred for liver transplantation especially if they have been abstinent of alcohol for 6 months.

   II.            Liver Failure and Chronic Liver Disease

                            A.            Fulminant hepatic failure (FHF).

                                                    1.            FHF develops within 2 weeks and subfulminant hepatic failure develops within 2-8 weeks of the onset of jaundice. It occurs due to acute onset of massive hepatocellular necrosis resulting in sudden and severe impairment of liver function. Encephalopathy is usually present.

                                                    2.            Causes include acetaminophen toxicitiy, viral hepatitis, drug reaction, toxins (mushroom poisoning), ishemic hepatitis, Wilson’s disease, autoimmune chronic active hepatitis, fatty liver of pregnancy and Reye’s syndrome.

                                                    3.            FHF needs intensive monitoring and emergent evaluation for orthotopic liver transplant.

                           B.            Cirrhosis.

                                                    1.            Cirrhosis of the liver is a diffuse process characterized by the formation of islands of regenerated liver surrounded by dense fibrosis (abnormal nodules) that occurs after a protracted insult (such as alcohol, chronic active hepatitis, etc.).

                                                    2.            Most complications of cirrhosis occur as a result of development of portal hypertension or decreased synthetic function of the liver.

                           C.            Signs and symptoms of liver failure.

                                                    1.            FHF. One of the earliest signs of FHF is a change is personality. Uncooperative and violent behavior is not uncommon. Jaundice does not correlate with neuropsychiatric changes in the early stages and is deep in the late stage. Fetor hepaticus, flapping tremor and hyperreflexia may be present. Spontaneous bleeding from mucosal surfaces may occur due to coagulopathy. In later stages, decerebrate rigidity with spasticity can be noted. In contrast to chronic liver disease, the liver is non-nodular and splenomegaly and vascular telan-giectasias are not present.

                                                    2.            Chronic liver disease (CLD). Weight loss, malnutrition, fatigue, easy bruising (caused by reduced levels of factors II, VII, IX, and X), jaundice, pruritus, edema, ascites and encephalopathy with asterixis. The patient may also have GI bleeding from esophageal varices (caused by portal hypertension) or coma. GI bleeding is a common precipitant of hepatic encephalopathy and coma in liver failure patients because of the large gastrointestinal protein load.

    

                          D.            Laboratory Evaluation and Monitoring.

                                                    1.            FHF. Obtain routine biochemical profile and complete liver panel. Serum albumin is usually normal initially. Hypoglycemia is found in a large percentage of patients with FHF. Lactic acidosis develops in approximately half the patients with grade 3 coma. Hyponatremia and hypokalemia are found especially in the later stages. Coagulopathy develops due to decreased hepatic synthesis of coagulation factors. The prothrombin (PT) time is also a good prognostic indicator. Cerebral edema can also lead to respiratory depression and respiratory acidosis. Hence, neurologic status and PT/INR should be followed closely in patients with FHF.

                                                    2.            CLD. Laboratory evaluation may show normal liver enzymes in end-stage disease because of the small amount of residual hepatic tissue. These patients will usually have low serum albumin. Anemia and thrombocytopenia may also be present. Blood ammonia levels may be elevated. Electrolyte abnormalities include hyponatremia, hypokalemia, and free water overload. There may also be concomitant acidosis or alkalosis.

                           E.            Management.

                                                    1.            Acute treatment.

                                                                            a.            For patients in FHF, a referral to a specialist should be obtained promptly.

                                                                            b.            Since cerebral edema is an important cause of death in patients with fulminant hepatic failure, intracranial pressure (ICP) monitoring is used in specialized units.

                                                                             c.            Hypoglycemia is corrected with 50% glucose. If patient is to be moved to an another medical center, patient is started on 20% glucose infusion during transport.

                                                                            d.            Coagulopathy is managed by parenteral vitamin K 5-10 mg SQ QD x 2-3 days and by transfusion with blood, platelets, and fresh frozen plasma.

                                                                             e.            Hepatic encephalopathy is treated as described below.

                                                                               f.            Hypokalemia and other electrolyte abnormalities are corrected with appropriate replacement.

                                                                            g.            Infections are sought after early and the patient should be pancultured.

                                                                            h.            Charcoal hemoperfusion for removal of toxic metabolites is also being tried in some centers.

                                                    2.            Chronic treatment.

                                                                            a.            A nonselective beta-blocker, such as propanolol or nadolol, reduces the risk of initial bleeding from esophageal varices. Propanolol can be started at a dose of 10 mg BID and titrated (to 60 mg QD) to effect a 25% reduction in the base-line heart rate. Nonselective beta-blockers are also the treatment of choice for bleeding from portal hypertensive gastropathy. Isosorbide may have an additive effect to the beta-blocker. New studies show that endoscopic band ligation of esophageal varices is more effective than propanolol for the primary prevention of variceal bleeding. Endoscopic ligation can be repeated every 4-6 weeks until the esophageal varices have all been obliterated.

                                                                            b.            Management of other complication of chronic liver disease is as described below under individual sections.