Subspecialty Management |
|Chapter 54:||Anesthesia and the Hepatobiliary System|
CHRONIC PARENCHYMAL LIVER DISEASE
This pattern of liver disease may produce little alteration in standard liver tests and may be clinically and biochemically undetectable. Hepatic reserve, however, may be limited and decompensation may occur when an additional insult, often iatrogenic, is introduced. Chronic parenchymal disease can be subdivided into two major categories: chronic hepatitis (precirrhotic) and cirrhosis.
Chronic hepatitis is an hepatic inflammatory process that has persisted for at least 24 weeks and has resulted in abnormalities in hepatic function. 38 Patients have been classified as having chronic persistent or chronic active hepatitis based on liver biopsy, but the distinction is often difficult to make. Chronic persistent hepatitis is the milder hepatic lesion, characterized by inflammation in the portal tracts with minimal cell necrosis and no disruption of the normal architecture. 39 Abnormalities in liver function are trivial, with modest elevations of transaminase being the only notable feature.
Liver biopsies of patients with chronic active hepatitis reveal scar tissue and inflammatory cells, which disrupt normal hepatic structure. Not surprisingly, patients with chronic active hepatitis have higher rates of morbidity and mortality than those with chronic persistent hepatitis. The estimated 5-year survival rate is 97 percent for patients with chronic persistent hepatitis, 86 percent for chronic active hepatitis, and 55 percent for chronic active hepatitis. 40 Despite these percentages, the natural history of chronic active hepatitis in an individual patient is extremely variable. Patients with chronic active hepatitis in remission may be totally asymptomatic, but most complain of fatigue and malaise. Stigmata of chronic liver disease should be sought on clinical examination. In symptomatic cases, liver function tests are usually markedly abnormal, with evidence of hepatocellular injury (high transaminases) and diminished synthetic function (low albumin, prolonged prothrombin time).
Patients with persistence of HBsAg 6 months after exposure are considered chronic carriers of hepatitis B (Table 54–2). A chronic state develops in 5 to 10 percent of acutely infected patients. These patients do not develop the protective anti-HBs. Chronic carriers of virus have low, fluctuating, or absent titers of IgM anti-HBc. 41 Persistent high titers of IgG anti-HBc may indicate increased infectivity. The presence of hepatitis B DNA polymerase is considered a marker of active viral replication and infectivity and may be assayed in the absence of conventional hepatitis B markers. 42 A chronic carrier state follows infection with hepatitis C virus in 40 percent of cases. These patients may be infectious for prolonged periods. 43
TABLE 54–2. Serologic Markers of Hepatitis B Viral Infection
Until recently, therapeutic options for these patients with chronic viral disease were extremely limited. Corticosteroid therapy alone is not useful in patients with chronic hepatitis B. 44 Interferon therapy showed some promise when used alone, 45, 46 but a regimen of prednisone withdrawal followed by interferon shows particular promise. 47 Recent studies suggest that recombinant human a-interferon can improve the biochemical abnormalities associated with hepatitis C virus. 48 Furthermore, a combination of ribavirin together with a-2B interferon appears to be especially efficacious. 49
Several drugs are known to cause chronic liver disease that is pathologically identical to virally induced forms of hepatitis. 19 These drugs include methyldopa 50 and isoniazid. 51 In most cases, drug-induced hepatitis resolves after drug ingestion ceases.
Autoimmune hepatitis is characterized by the presence of humoral and cellular markers of immunologic disease. Patients may have smooth muscle antibody or antinuclear antibody in their serum. Selected patients may benefit from treatment with steroids or immunosuppressants, drugs that must be considered in the anesthetic plan.
Diagnosis of metabolic causes of chronic hepatocellular disease requires specific laboratory studies. For example, serum a-1 antitrypsin 52 may be assayed and phenotyped by isoelectric focusing of serum proteins, whereas the genotype can be established by PCR. Diagnosis may be confirmed by the demonstration of characteristic periodic acidSchiff positive diastase-resistant globules adjacent to liver portal tracts. Adult patients with this disorder often have emphysema. 53
Wilson disease is an inherited disorder characterized by copper accumulation, especially in the liver, kidneys, central nervous system, and eyes. 54 Copper deposits in the eyes seen under slit-lamp, Kayser-Fleischer rings, are pathognomonic for Wilson disease. Most patients with this disease have low serum ceruloplasmin levels and increased urinary copper levels. 55 The chelating agent, penicillamine, is first-line therapy. 56
Cirrhosis is a syndrome characterized by severe hepatic fibrosis and nodular regeneration. Worldwide, 50 percent of cirrhosis is linked to alcohol abuse, but in some countries the rate is as high as 90 percent. All types of alcoholic beverages cause liver disease, and their tendency to do so depends only on alcohol content. Regular daily consumption in excess of 80 g of alcohol for more than 9 years is more dangerous than intermittent sprees. 57 Women are more susceptible to liver damage from alcohol than are men. Chronic active hepatitis of any cause may progress to cirrhosis.
In addition to the types of hepatitis discussed previously, other rare causes of liver disease with a propensity to progress to cirrhosis include hemochromatosis and primary biliary cirrhosis. In patients with hemochromatosis, iron accumulates in hepatic parenchymal cells. 58 Patients with cirrhosis resulting from hemochromatosis have a high rate of liver cancer. 59 Characteristically, patients with hemochromatosis have elevated serum ferritin levels and an increase in transferrin saturation, but the diagnosis is often best made by liver biopsy. 60
Primary biliary cirrhosis, which predominantly affects women, is characterized by cholestasis progressing to hepatic fibrosis. Women with this disorder frequently have malabsorption, osteoporosis, and autoimmune diseases. 61 Serum cholesterol levels are very high, and serum is usually positive for antimitochondrial antibodies. Cryptogenic cirrhosis (no cause found) is another rare diagnosis.
The clinical presentation of cirrhosis ranges from the asymptomatic patient with normal or nearly normal liver function to the severely decompensated patient with deep jaundice and ascites. Patients with compensated cirrhosis may be completely asymptomatic or have nonspecific symptoms such as malaise, weight loss, loss of libido, and menstrual disturbances. Physical signs, if any, may include such changes as white skin spots, paper-money skin, palmar erythema, and white nails. Clubbing and cyanosis are occasionally seen.
A high-output circulatory state is a frequent feature of advanced cirrhosis, 62 associated with arteriovenous shunting, especially in the lungs. Hepatosplenomegaly may be present. Occasionally, the left lobe of the liver is prominent (particularly in alcoholics), resulting in an easily palpable and diagnostically confusing epigastric mass. Regardless of the cause, the complications of cirrhosis are similar and protean.
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