Symptoms of Alcoholic Liver Disease

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Ascites: Ascites in alcoholic cirrhotics is due both to obstruction of hepatic lymphatic flow and to avid renal retention of sodium. Sodium retention arises because of marked peripheral vasodilation with a hyperdynamic circulation, high cardiac output, and low peripheral vascular resistance; this situation leads to contraction of the central plasma volume.10 Spider angiomata and palmar erythema are probably manifestations of the peripheral arterial vasodilation. Reduced renal blood flow stimulates renin and aldosterone production, and despite total body sodium overload, very little sodium is excreted. Because renal cortical blood flow is maintained by prostaglandins, nonsteroidal anti-inflammatory drugs (such as ibuprofen), which inhibit cyclo-oxygenase, can lead to functional renal failure (the so-called hepatorenal syndrome) and exacerbation of sodium retention, and thus cause or worsen ascites.

Evaluation of ascites by paracentesis is very important in alcoholic cirrhotics in order to rule out spontaneous bacterial (or secondary) peritonitis and to differentiate cirrhotic ascites from malignant ascites.11'12 In alcoholic cirrhosis, levels of protein and albumin in the fluid are very low. With spontaneous bacterial peritonitis, the absolute PMN count is, >250 cells/mL. Antibiotic treatment of the infection is imperative.

Treatment of ascites decreases the likelihood of spontaneous bacterial peritonitis, improves patient comfort and respiration, and permits percutaneous liver biopsy if the procedure is needed. More than 90% of compliant patients will respond to dietary sodium restriction and K+-sparing diuretics such as spironolactone. However, diuretics take several weeks to eliminate ascites, and large-volume paracentesis (6-8 L/d until "dry") with intravenous administration of 40-50 g of albumin is now routine prior to starting a diuretic regimen. In patients with refractory ascites, placement of transjugular intrahepatic portosystemic shunt (TIPS) is significantly better than paracentesis for control of the ascites. Although it increases encephalopathy, it also is associated with a trend toward improved survival.13

Esophageal Varices: Increased portal pressures with a gradient of > 12 mm Hg between the portal and hepatic venous systems lead to varices in the stomach and lower esophagus. These varices may bleed massively. Despite various approaches to prevention of variceal bleeding (prophylactic propranolol, portosystemic shunts of various types) and different ways to staunch bleeding (endoscopic banding, sclerotherapy, Sengstaken-Blakemore tubes, shunts, administration of octreotide or nitrates), patients with bleeding varices have a very poor prognosis. When an alcoholic patient presents with hematemesis or melena, orthostasis, and a falling hematocrit, variceal rupture should not be immediately assumed. Endoscopy should be routinely performed to rule out other causes such as ulcers or portal hypertensive gastropathy. If bleeding varices are found, endoscopic banding is the usual treatment.

Hypersplenism: With portal hypertension, the spleen enlarges and sequesters both platelets and leukocytes. Peripheral thrombocytopenia contributes to coagulopathy, and leukopenia to susceptibility to infection.

Anemia: Causes of anemia in ALD are complex; they include ethanol or acetaldehyde suppression of bone marrow function, vitamin deficiencies (e.g., folate), inflammation causing an "anemia of chronic disease," and acute and chronic blood loss leading eventually to iron deficiency. In most cases, the anemia that appears is macrocytic.

Liver Function Tests in ALD: Causes of jaundice in adults are numerous, among them, viral hepatitis, drug-induced hepatitis or cholestasis, biliary obstruction, or hemoly-tic anemia. With problems unrelated to the hepatobiliary systems, serum bilirubin is rarely >7 mg/dL (>120 mmol/L), and determination of conjugated (direct) bilirubin is unnecessary. Alcoholics presenting with jaundice should be promptly examined with ultrasonography of the right upper quadrant; if biliary obstruction is present, aggressive therapy to decompress the biliary tract is necessary.

In alcoholic hepatitis, AST and ALT are mildly elevated, and AST more so than ALT. Because these enzyme assays evaluate hepatocellular necrosis, levels may actually be normal in quiescent cirrhosis. Alkaline phosphatase (ALP) and g-glutamyltransferase (GGT) are synthesized in excess by biliary ductular cells reacting to irritation or inflammation of the intra- or extrahepatic biliary system; levels are commonly increased in many liver and biliary diseases, including ALD, biliary obstruction, and metastatic tumor. GGT is also present in microsomes and thus is especially sensitive to alcohol-induced liver disease and may be increased when ALP is still normal. On the other hand, increased ALP with normal GGT is reason to look for a nonhepatobiliary cause for ALP elevation, e.g., bone disease.

Coagulation Tests: There are several reasons for disturbances of coagulation in ALD. Thrombocytopenia and prolonged prothrombin and partial thromboplastin times (PT and PTT) are the most commonly seen. Hypersplenism causes most cases of throm-bocytopenia, but platelet consumption in a diffuse intravascular coagulopathy (DIC-like) syndrome can also occur. PT and PTT are prolonged owing to impaired hepatic production of factors II, VII, IX, X, protein C, and protein S, all of which require vitamin K for g-carboxylation and activity. Liver failure alone may account for abnormal PT and PTT, but inadequate nutritional intake of vitamin K is also a possibility. A good test for residual reserve liver function in ALD patients is to see whether PT is corrected by administration of parenteral vitamin K (10 mg subcutaneously each day for three days).

Hypoalbuminemia: Low albumin contributes to ascites and edema in ALD patients. Liver failure, poor nutrition, inflammatory conditions and infections, and protein loss from the gut or kidneys are all factors that can cause or intensify hypoalbuminemia.

Encephalopathy: The encephalopathy of liver failure has been termed portosystemic encephalopathy (PSE). Current theories explain PSE as an inability of the compromised liver to convert ammonia into urea, coupled with accumulation in plasma of aromatic amino acids (AAA) and depletion of branched-chain amino acids (BCAA). BCAA depletion is the result of their preferential utilization instead of AAA by muscle. The postulate is that the combination of increased plasma ammonia and an altered ratio of BCAA to AAA leads to generation of false neurotransmitters responsible for encephalo-pathy. The measurement of plasma ammonia (collected on ice and assayed immediately) has often been used to determine whether a patient has PSE. However, plasma ammonia concentrations are often unreliable, and it is not recommended that such measurements be used to follow a patient's course. To treat PSE, the removal of ammonia with oral lactulose therapy is usually effective. Lactulose is a nonabsorbable sugar that is fermented by colonic bacteria. This process acidifies the colon and sequesters the ammonia in the colon lumen as NH4+. The use of dietary supplements or parenteral infusions of BCAA have not been shown to be beneficial.14 In general, restriction of protein intake is contraindicated for patients with ALD since it may enhance existing nutritional deficiency. It may, however, be invoked should sensitivity to protein loads develop.

Drug Sensitivity and Feminization in Men: Patients with cirrhosis often have decreased activity of hepatic cytochromes P-450 and can be very sensitive to medications that require hepatic metabolism. This is especially true for certain sedatives, hypnotics, and psychoactive drugs. A good principle to follow is to avoid medication whenever possible; when medication cannot be avoided, use discretion in choosing the drugs and dosages. Male alcoholics often manifest feminization because estrogenic steroids, normally cleared by hepatic oxidative systems, accumulate. In addition, acute alcohol ingestion suppresses testosterone formation by the gonads, and this mechanism can be more important than estrogen accumulation in causing feminization.

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