LIVER DISEASE AND DENTAL MANAGEMENT

This discussion will be limited to the effects of viral hepatitis and alcoholic liver disease on the provision of dental care.

General description. Acute viral hepatitis is characterized by degeneration and necrosis of liver cells with ballooning degeneration of the hepatocytes. Icterus (jaundice) is commonly associated with hepatitis and is caused by an accumulation of bilirubin in the skin.

Acute viral hepatitis is caused by at least five distinct viruses:

• Type A hepatitis (formerly called infectious hepatitis) is caused by the hepatitis A virus (HAV), which is an RNA-type virus. Serologic tests for HAV and its antibodies are readily available.
• Type B hepatitis (formerly called serum hepatitis) is caused by the hepatitis B virus (HBV), which is a DNA-type virus. Serologic tests are available for all but one (HBcAg) of its antigen-antibody systems.
• Delta hepatitis is caused by a defective RNA-type virus that requires the presence of HBV for infection. It can occur as either a coinfection or a superinfection with hepatitis B. The hepatitis delta virus (HDV) and its antibody anti-HD can be detected with serologic testing.
• Non A non-B—type C hepatitis was originally a diagnosis of exclusion in posttransfusion hepatitis when serologic markers of types A and B were not present. Serologic tests are now available for both the viral antigen and its antibody.
• Non-A-non-B--- type E hepatitis is an enterically transmitted virus, similar to type A. Serologic tests for both antigen and antibody have recently become available.

Epidemiology. Because the means of transmission overlap and the clinical expression of the various forms of hepatitis are often indistinguishable, no absolute statements can be made regarding epidemiology. However, certain recurring patterns of disease are recognized for each type.

Hepatitis A is transmitted almost exclusively by fecal contamination of food or water. Because the reservoir for infections is frequently a common food or water source, hepatitis A often occurs as an epidemic. Transmission is enhanced by poor personal hygiene, especially among school-aged children and food handlers.

Hepatitis A is a common disease, with serologic evidence of infection in about 40% of urban populations in the US.¹ Of importance is the fact that no carrier state is known to exist for it. No vaccine is currently available, and recovery usually conveys immunity against reinfection.

Hepatitis B may be transmitted in a number of ways:

• direct percutaneous inoculation of infected serum or plasma by needle or transfusion of infective blood or blood products
• indirect percutaneous introduction of infective serum or plasma absorption of infective serum or plasma (e.g., through mucosal surfaces of the mouth or eye)
• absorption of other potentially infective secretions (e.g., saliva or semen)
• transfer of infective serum or plasma via inanimate environmental surfaces

The role of saliva in HBV transmission, except by percutaneous or permucosal routes, does not appear to be significant.²

Groups at high risk for hepatitis B are:

• health care workers (including dentists and dental staff)
• hemodialysis patients
• users of illicit drugs
• homosexuals
• heterosexuals with multiple partners
• recipients of blood transfusions

The risk of infection is directly related to exposure to blood. This has resulted in a reported past prevalence rate of infection among general dentists ranging from 13 to 30 percent, and a rate among oral surgeons as high as 38 percent.^3-5 More recently, the prevalence rate for general dentists was reported to be 8.89 percent.

Hepatitis B has greater associated morbidity and mortality than hepatitis A, especially in older patients. An additional significant feature of hepatitis B is the existence of a chronic carrier state that can persist for variable periods after resolution of acute disease. While the carrier rate of dentists in the US has decreased (reflecting the effectiveness of prophylactic measures), the risk is still estimated to be three to ten times that of the general population. It is significant to note that since many cases are mild or subclinical, most carriers are unaware that they have had hepatitis B.

Delta hepatitis occurs only as a coinfection with acute hepatitis B or as a superinfection in carriers of hepatitis B and, therefore, is transmitted parenterally via infected blood or blood products. It is seen primarily in drug addicts and hemophiliacs.

NANB hepatitis—type C is similar to type B in behavior and characteristics. It is transmitted primarily parenterally and is the major etiologic agent of posttransfusion non-A non-B hepatitis. While forty percent of patients with hepatitis C have no identifiable risk factors for infection,⁷ those at high risk include:

• health care workers exposed to blood
• illicit drug users
• hemodialysis patients
• recipients of whole blood, blood cellular components, or plasma

Clinical presentation. Many of the signs and symptoms of acute viral hepatitis are common to viral diseases and may be described as flulike. This is especially true in the early stage of the disease. There are classically three phases of acute viral hepatitis, each lasting for a certain duration, and each manifesting particular symptoms.

• Prodromal (preicteric) phase. Symptoms include anorexia, nausea, vomiting, fatigue, myalgia, malaise, and fever.
• Icteric phase. Many of the nonspecific prodromal symptoms may subside, but gastrointestinal symptoms may increase. Hepatomegaly and splenomegaly are also frequently seen.
• Posticteric phase. Symptoms disappear, but hepatomegaly and abnormal liver function values may persist. This phase can last for weeks or months, with recovery time for hepatitis types B and C generally being longer.

Treatment. There is no specific treatment for acute viral hepatitis. Therapy is basically palliative and supportive. A nutritious and high-calorie diet is advisable.

Medical considerations. Since infectious patients cannot necessarily be identified by history, it is necessary to manage all patients as though they are potentially infectious. The Center for Disease Control and the American Dental Association have published recommendations for infection control that have become the standard of care to prevent crossinfection in dental practice. These standards should be strictly adhered to.

There are five categories of patients with a history of hepatitis that must be considered by the dentist:

• Patients with active hepatitis. No treatment other than urgent care should be rendered to these patients. If a patient is seen with acute hepatitis, the physician should be contacted immediately.
• Patients with a history of hepatitis. Since it is estimated that there are between 750,000 and 1 million carriers of hepatitis B in the US today, the only practical method of protection from infection is to adopt a strict program of clinical asepsis for all patients. In addition, inoculation of all dental personnel with hepatitis B vaccine is strongly urged.
• Patients at high risk for HBV infection. Patients who fit into one or more of the high risk categories should routinely be screened for HBsAg before dental care is provided unless laboratory evidence exists for anti-HBs. While this measure may seem redundant, it could yield information that would be of benefit in certain situations. For example, if an accidental needle stick or puncture occurs during treatment and the dentist is not vaccinated, it would be of extreme importance to know whether the patient was HBsAg positive, which would dictate the need for vaccination.
• Patients who are hepatitis carriers. If a patient is found to be a hepatitis B carrier or to have a history of NANB hepatitis, recommendations from the Center for Disease Control for avoiding transmission of infection should be closely followed. In addition, some hepatitis carriers may have chronic active hepatitis, leading to compromised liver function and interfering with hemostasis and drug metabolism. Physician consultation or laboratory screening for liver function is advised.
• Patients with signs or symptoms of hepatitis. Any patient having signs or symptoms suggesting hepatitis should be referred to a physician, and should not be treated. If emergency care becomes necessary, it should be provided as for the patient with acute disease.

Potential drug interactions. In a completely recovered patient there are no special drug considerations. However, if a patient has chronic active hepatitis or is a carrier of HBsAg and has impaired liver function, drugs metabolized by the liver should be avoided if possible. Although a number of local anesthetics, analgesics, sedatives, and antibiotics commonly used in dentistry are, in fact, metabolized principally by the liver, these drugs can be used in limited amounts in all but the most severe cases of hepatic disease.

Oral complications. The only oral complication associated with hepatitis is the potential for abnormal bleeding in cases of significant liver damage. If surgery is required, it is advisable to:

• Check the prothrombin time. If it is greater than 35, an injection of vitamin K will usually correct the problem. This should, however, be discussed with the patient's physician.
• Monitor the bleeding time to check platelet function. If it is not less than 20 minutes, the patient may require platelet replacement before surgery. This should also be discussed with the patient's physician.

PRIMARY REFERENCE

Little JW, Falace DA. Dental Management of the Medically Compromised Patient. 4th ed. St. Louis, MO: Mosby Year Book, Inc; 1993: 258-275.

ADDITIONAL REFERENCES

1. Dienstag JL, Wands JR, Isselbacher KJ. Acute hepatitis. In Wilson JD et al, eds. Harrison's Pnnciples of Internal Medicine, 12th edition. New York: McGraw-Hill; 1991.
   
   
2. Centers for Disease Control. Hepatitis: United States, 1975-1976, MMWR 1977: 26;177.
   
   
3. Bass BD, Andors L, Pierri LK et al. Quantitation of hepatitis B viral markers in a dental school population, J Am Dent Assoc 1982: 104 (5); 629-632.
   
   
4. Mosley JW, Edwards VM, Casey G et al. Hepatitis B viruses infection in dentists, N Engl J Med 1975: 293; 729-734.
   
   
5. Schiff ER, DeMedina MD, Kline SN et al. Veterans Administration cooperative study on hepatitis and dentistry, J Am Dent Assoc 1986: 113 (3); 390-396.
   
   
6. Cottone JA. Recent developments in hepatitis: new virus, vaccine, and dosage recommendations, J Am Dent Assoc 1990: 120 (5); 501 -508.
   
   
7. Centers for Disease Control: Public Health Service inter-agency guidelines for screening disorders of blood, plasma, organs, tissues, and semen for evidence of hepatitis B and hepatitis C. MMWR 1991: 40 (RR-4); 6-17.

General description. The pathologic effects of alcohol on the liver can result in three disease entities, which commonly appear in combination:^1-2

• With fatty infiltrate, the hepatocytes become engorged with fatty lobules and distended, with enlargement of the entire liver. These changes may occur after only moderate usage of alcohol for a brief time, and are completely reversible.
• Alcoholic hepatitis is a diffuse inflammatory condition of the liver characterized by destructive cellular changes. Some of these may be irreversible, thereby leading to necrosis. While this condition can be fatal if damage is widespread, it is generally reversible.
• Cirrhosis, the most serious form of alcoholic liver disease, is characterized by progressive fibrosis and abnormal regeneration of liver architecture in response to chronic injury or insult (i.e., prolonged and heavy use of ethanol). It results in the progressive deterioration of metabolic and excretory functions of the liver, and ultimately leads to hepatic failure.

Epidemiology. It is estimated³ that:

• Up to ninety percent of people drink alcohol.
• Forty to fifty percent of men have temporary alcohol-induced problems.
• Ten percent of men and three to five percent of women develop pervasive and persistent alcoholism.

Alcohol abuse and dependence are not limited to any particular group. All ages and races, both sexes, and all socioeconomic levels are affected.

Clinical presentation.

• Fatty liver. There are no clinical manifestations of a fatty liver, and the diagnosis is usually made incidentally in conjunction with another illness.
• Alcoholic hepatitis. Signs and symptoms of alcoholic hepatitis are often nonspecific and may include nausea, vomiting, anorexia, malaise, weight loss, and fever. More specific findings include hepatomegaly, splenomegaly, jaundice, ascites, ankle edema, and spider angiomas. With advancing disease, encephalopathy and hepatic coma may ensue, ending in death.
• Cirrhosis. Cirrhosis may remain asymptomatic for many years. Hemorrhage from esophageal varices is frequently the initial sign, but ascites, spider angiomas, ankle edema, or jaundice may also be among the early signs. The hemorrhagic episode may progress to hepatic encephalopathy, coma, and death.

Treatment. The cornerstone of treatment for alcoholic liver disease is abstinence from alcohol. Other measures include:

• strict dietary modification (high-protein, high calorie, low-sodium diet)
• fluid restriction
• vitamin supplementation

Anemia is corrected by iron replacement and folic acid supplementation.

Medical considerations. The two major treatment considerations in an alcoholic patient are:

• bleeding tendencies
• unpredictable metabolism of certain drugs

Dental management must, therefore, begin with detection by history and/or by clinical examination. When there is a high index of suspicion, a number of laboratory tests should be ordered for screening purposes:

• CBC with differential
• AST, ALT
• bleeding time
• thrombin time
• prothrombin time

If a patient has a history of alcoholic liver disease or alcohol abuse, the physician should be consulted to verify:

• the patient's current status
• medications
• laboratory values
• contraindications for medications, surgery, and other treatment

A patient with untreated alcoholic liver disease is not a candidate for elective, outpatient dental care and should be referred to a physician. Once the patient is managed medically, dental care may be provided after consultation with the physician. Bleeding diatheses (as reflected on laboratory tests) should be managed in consultation with the physician.

Metabolic concerns. Concern about the unpredictable metabolism of drugs is twofold:

• In mild to moderate alcoholic liver disease, significant enzyme induction is likely to have occurred, leading to an increased tolerance of sedative drugs, hypnotic drugs, and general anesthesia. Larger than normal doses of these medications are thus required to obtain the desired effects.
• With more advanced liver destruction, drug metabolism may be markedly diminished and can lead to an increased or unexpected effect. Drugs metabolized primarily by the liver (i.e., certain anesthetics, analgesics, sedatives, and antibiotics) should be used with caution, and avoided if possible. When used, doses should be adjusted.

Oral complications. Poor oral hygiene and neglect are common findings in chronic alcoholics. Other abnormalities that may be found are:^4-5

• glossitis
• angular or labial cheilosis
• candidiasis
• gingival bleeding
• oral cancer
• petechiae
• ecchymoses
• jaundiced mucosa
• parotid gland enlargement
• alcohol breath odor
• impaired healing
• bruxism
• dental attrition
• xerostomia

Since alcohol abuse (and tobacco use) are also strong risk factors for the development of oral cancer, practitioners should be aggressive in detecting suspicious soft-tissue lesions.

PRIMARY REFERENCE

Little JW, Falace DA. Dental Management of the Medically Compromised Patient. 4th ed. St. Louis, MO: Mosby Year Book, Inc; 1993: 258-275.

ADDITIONAL REFERENCES

1. Golden A, Powell DE, Jennings CD. Pathology: Understanding Human Disease. Baltimore: Williams & Wilkins; 1985.
   
   
2. Podolsky DK, Isselbacher KJ. Cirrhosis of the liver. In Wilson JD et al, eds. Harrison's Principles of Intemal Medicine, 12th ed. New York: McGraw Hill; 1991.
   
   
3. Schuckit JA. Alcohol and alcoholism. In Wilson JD et al, eds. Harrison's Principles of Intemal Medicine, 12th ed. New York: McGraw-Hill; 1991.
   
   
4. Friedlander AH, Mills MJ, Gorelick DA. Alcoholism and dental management. Oral Surg 1987: 62; 42-46.
   
   
5. Leonard RH. Alcohol, alcoholism and dental treatment. Compendium 1991: 12; 274-283.