Management of patient with hepatic disorder in dental office (hepatitis, alcoholic liver disorder)


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describes about how to manage a patient with hepatic disorder like hepatitis n alcoholic liver disorder in dental office also in general as well

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Management of patient with hepatic disorder in dental office (hepatitis, alcoholic liver disorder)

  3. 3. Introduction: • Liver dysfunction may be attributed to a number of causes, including lifestyle habits and other acquired infections and conditions. • The patient with liver disease presents a significant management challenge for the dentist because the liver plays a vital role in metabolic functions, including secretion of bile needed for fat absorption, conversion of sugar to glycogen, and excretion of bilirubin, a waste product of hemoglobin metabolism. • Impairment of liver function can lead to abnormalities in the metabolism of amino acids, ammonia, protein, carbohydrates, and lipids (triglycerides and cholesterol).
  4. 4. Introduction: • Many biochemical functions performed by the liver, such as synthesis of coagulation factors and drug metabolism, may be adversely affected in the dental patient with acute or chronic liver disease. So, along with impaired drug metabolism, significant bleeding may be a dental problem. • Viral hepatitis and alcoholic liver disease are two of the more common liver disorders. • In many cases, the liver dysfunction continues to progress over time. Therefore, patients with liver disorders are of significant interest to the dentist, as is their proper management.
  6. 6. Hepatitis: DEFINITION: Hepatitis is inflammation of the liver that may result from infectious or other causes. • Examples of hepatitis with infectious causes are viral hepatitis, infectious mononucleosis, secondary syphilis, and tuberculosis. • Noninfectious hepatitis can result from excessive or prolonged use of toxic substances (e.g., drugs [acetaminophen, alcohol, halothane, ketoconazole, methyldopa, methotrexate]; more commonly, alcohol)
  7. 7. Hepatitis: ETIOLOGY • Acute viral hepatitis is the most common form of infectious hepatitis. • Five distinct viruses—types A, B, C, D, and E—are associated with this disease • Diagnostic markers of viral hepatitis include elevation of  aspartate aminotransferase,  alanine aminotransferase,  gammaglutamyl transferase,  white blood cell count, and  prothrombin time.
  8. 8. Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E OLD TERMINOLOGY Infectious hepatitis Serum hepatitis Posttransfusion hepatitis non-A non-B Delta hepatitis Hepatitis non- A non-D FAMILY AND TYPES Picornavirus 1 serotype, 7 genotypes Hepadnavirus Flavivirus 6 major genotypes (40 related subtypes) Satellite 3 genotypes Calicivirus 3 genotypes VIRION STRUCTURE 28-nm RNA nonenveloped virus 42-nm DNA enveloped virus, enveloped Dane particles, spherical and tubular particles 30- to 80-nm ss +RNA enveloped virus 35- to 40-nm defective RNA Nonenveloped virus (uses HBsAg for viral envelope) 32- to 34-nm Nonenveloped RNA virus INCUBATION 15-50 days 45-180 days 14-180 days15-150 days 15-150 days 15-60 days MAIN ROUTE OF TRANSMISSION Fecal/oral route Parenteral, sexual contact Parenteral, sexual contact (low risk) Parenteral, sexual contact Fecal/oral route DIAGNOSIS Anti-HAV IgG HBsAg (infectious) Anti-BsAg (recovery) Anti-HBc (acute, Persistently infected, or previously infected nonprotective) HBeAg (infectious) Anti-HBeAg (clearing/cleared infection) Anti-HCV (previous infection) HCV RNA (infectivity) Anti-HDV HDAg Anti-HEV CHRONIC CARRIER STATE No Yes, 90% risk of becoming carrier if infected as neonate; 25%-50% risk of becoming carrier if infected as infant; 5%-10% risk of becoming carrier if infected as adult Yes, risk of becoming carrier is 80%-90% Yes, carrier state in 20%- 70% No COMPLICATIONS OF THE LIVER Rare Yes, increased risk of liver cirrhosis and hepatocellular carcinoma (HCC) after 25-30 years of infection Yes, 10-fold increased risk of liver cirrhosis within 20 years; 1%-5% of carriers develop HCC by 20 years; risk of HCC with chronic HCV exceeds risk with chronic HBV Yes Rare morbidity and mortality except in pregnant women
  9. 9. Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E ASSOCIATED CLINICAL SYNDROMES Yes Yes IMMUNIZATION Immune globulin Hepatitis B immune globulin (HBIG) (0.06 mg/kg) Not available Not available Not available PASSIVE IG (0.02 mg/kg) ACTIVE Harivax, Vaqta, and Twinrix Recombivax, Engerix, [‖] and Twinrix None (difficult development because of the many genotypes) Yes; protected with Recombivax, Engerix, [‖] and Twinrix Genentech has applied for vaccine patent
  10. 10. Hepatitis: PATHOPHYSIOLOGY AND COMPLICATIONS • Hepatitis viruses replicate in hepatocytes and ultimately damage the host cell. • HBV infection produces high serum titers that may reach 10 8 to 10 11 virions/mL. • In contrast, HAV produces a viremia that may reach 10 5 virions/mL in blood but 10 6 to 10 10 genomes/g in stool. • No single histopathologic lesion is characteristic of viral hepatitis, but the appearances of types A, B, C, D, and E hepatitides are similar and are described together. • Commonly, acute viral hepatitis is characterized by ballooning degeneration and necrosis of liver cells (hepatocytes). The entire liver lobule becomes inflamed and consists of lymphocytes and mononuclear phagocytes.
  11. 11. Hepatitis: PATHOPHYSIOLOGY AND COMPLICATIONS • Icterus (jaundice) is associated with hepatitis in • approximately 70% of cases of HAV, • approximately 30% of cases of HBV infection, and • approximately 25% of cases of HCV and HEV. • This is caused by an accumulation of bilirubin in the plasma, epithelium, and urine. • Jaundice usually becomes clinically apparent when the plasma level of bilirubin approaches 2.5 mg/100 mL (normal is less than 1 mg/100 mL). If plasma bilirubin does not reach this level, the patient is anicteric(without jaundice), thus explaining nonicteric hepatitis.
  12. 12. Hepatitis: PATHOPHYSIOLOGY AND COMPLICATIONS • Most cases of viral hepatitis, especially types A and E, resolve with no complications. • HBV, HCV, and HDV may persist and can replicate in the liver when the virus is not completely cleared from the organ. • The consequences of hepatitis include • recovery, • persistent infection (or carrier state), • dual infection, chronic active hepatitis, • fulminant hepatitis, • cirrhosis, • hepatocellular carcinoma, and • death.
  13. 13. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • Patients classically exhibit three phases of acute illness. • The prodromal (preicteric) phase,  which usually precedes the onset of jaundice by 1 or 2 weeks,  consists of — abdominal pain, — anorexia, — intermittent nausea, — vomiting, — fatigue, — myalgia, — malaise, and — fever.  With hepatitis B, 5% to 10% of patients demonstrate serum sickness–like manifestations, including arthralgia or arthritis, rash, and angioedema.
  14. 14. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • The icteric phase  onset of clinical jaundice,  Many nonspecific prodromal symptoms may subside, but gastrointestinal symptoms (e.g., anorexia, nausea, vomiting, right upper quadrant pain) may increase, especially early in the phase.  Hepatomegaly and splenomegaly frequently are seen.  This phase lasts 2 to 8 weeks and is experienced by at least • 70% of patients infected with HAV, • 30% of those acutely infected with HBV, and • 25% to 30% of patients acutely infected with HCV.
  15. 15. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • During the convalescent or recovery (posticteric) phase,  symptoms disappear, but hepatomegaly and abnormal liver function values may persist for a variable period.  This phase can last for weeks or months, and recovery time for hepatitis B and C is generally longer.  HBV infrequently is associated with clinical syndromes, including polyarteritis nodosa, glomerulonephritis, and leukocytoclastic vasculitis. • Coagulopathy, encephalopathy, cerebral edema, and fulminant hepatitis are rare. • Nonspecific symptoms of chronic hepatitis C (loss of weight, easy fatigue, sleep disorder, difficulty in concentrating, right upper quadrant pain, and liver tenderness) may not appear until hepatic fibrosis, cirrhosis, or hepatocellular carcinoma is present.
  16. 16. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • Hepatic damage is caused by the cytopathic effects of the virus and inflammatory changes related to immune activation. • Extrahepatic immunologic disorders associated with chronic HCV infection result from the production of autoantibodies and include  immune complex–mediated disease (vasculitis, polyarteritis nodosa),  autoimmune disorders (rheumatoid arthritis,  glomerulonephritis,  thrombocytopenic purpura,  thyroiditis, pulmonary fibrosis), and  two immunologic disorders: lichen planus and Sjögren's-like syndrome (lymphocytic sialadenitis). • If these diseases or signs of advanced liver disease (bleeding esophageal varices, ascites, jaundice, spider angioma, dark urine) are noted, testing for chronic hepatitis is recommended.
  17. 17. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • HDV infection often results in severe acute hepatitis or rapidly progressive chronic liver disease. • Coinfection usually leads to transient and self-limiting disease, whereas superinfection more often results in severe clinical disease, indicated by sudden exacerbation in a chronic carrier of HBV.
  18. 18. Hepatitis: MEDICAL MANAGEMENT
  19. 19. Hepatitis: TREATMENT • As with many viral diseases, basic therapy is palliative and supportive. • Bed rest and fluids may be prescribed, especially during the acute phase. • A nutritious, high-calorie diet is advised. • Alcohol and drugs metabolized by the liver are not to be ingested. • Viral antigen and ALT levels should be monitored for 6 months • Standard therapy for patients with chronic hepatitis is interferon (IFN) alfa-2b (3 to 10 million units) administered three times weekly for 6 months to 1 year. • Newer modalities have used the pegylated form of IFN with better sustained virologic response. • IFN therapy normalizes ALT levels in up to 17% of patients infected with HDV, 30% of those infected with HCV, and 40% of those infected with HBV and reduces the risk for development of hepatocellular carcinoma. • Adverse effects (e.g., fatigue, flulike symptoms, bone marrow suppression) are common. The addition of lamivudine (a nucleoside analog active against HBV) or ribavirin (a guanosine analog active against HCV) results in a virologic response in an additional 15% to 25%. • Corticosteroids are usually reserved for fulminant hepatitis. • Liver transplantation is a last resort for patients who develop cirrhosis
  20. 20. Hepatitis: DENTAL MANAGEMENT Medical Considerations • Identification of potential or actual carriers of HBV, HCV, and HDV is problematic because in most instances, carriers cannot be identified by history. • The inability to identify potentially infectious patients extends to HIV infection and other sexually transmitted diseases. • Therefore, all patients with a history of viral hepatitis must be managed as though they are potentially infectious. • Recommendations for infection control practices in dentistry published by the CDC and the American Dental Association have become the standard of care for preventing cross- infection in dental practice . • all dental health care workers who provide patient care should receive vaccination against hepatitis B virus
  21. 21. Hepatitis: DENTAL MANAGEMENT Medical Considerations Patients With Active Hepatitis.  No dental treatment other than urgent care (absolutely necessary work) should be rendered unless the patient is clinically and biochemically recovered.  Urgent care should be provided only in an isolated operatory with adherence to strict standard precautions.  Aerosols should be minimized and drugs metabolized in the liver should be avoided as much as possible.  If surgery is necessary, preoperative prothrombin time and bleeding time should be obtained and abnormal results discussed with the physician.  The dentist should refer the patient who has acute hepatitis for medical diagnosis and treatment.
  22. 22. Dental Drugs Metabolized Primarily by the Liver Local anesthetics (appear safe for use during liver disease when used in appropriate amounts) • Lidocaine (Xylocaine) • Mepivacaine (Carbocaine) • Prilocaine (Citanest) • Bupivacaine (Marcaine) Analgesics • Aspirin * • Acetaminophen (Tylenol, Datril) † • Codeine † • Meperidine (Demerol) † • Ibuprofen (Motrin) * • (*) Limit dose or avoid if severe liver disease (acute hepatitis and cirrhosis) or hemostatic abnormalities are present. • (†) Limit dose or avoid if severe liver disease (acute hepatitis and cirrhosis) or encephalopathy is present, or if taken with alcohol. • (‡) Avoid if severe liver disease (acute hepatitis and cirrhosis) is present. Sedatives • Diazepam (Valium) † • Barbiturates † Antibiotics • Ampicillin • Tetracycline • Metronidazole‡ • Vancomycin ‡
  23. 23. Hepatitis: DENTAL MANAGEMENT Medical Considerations Patients With a History of Hepatitis. • Most carriers of HBV, HCV, and HDV are unaware that they have had hepatitis. • For those patients who report a positive history of hepatitis, additional historical information occasionally may be of help to the clinician in determining the type of disease. • An additional consideration in patients with a history of hepatitis of unknown type is the use of the clinical laboratory to screen for the presence of HBsAg or anti-HCV. • This may be indicated even in patients who specifically indicate which type of hepatitis they had, because information of this type derived from the patient's history is unreliable 50% of the time. Patients at High Risk for HBV or HCV Infection. • Several groups are at unusually high risk for HBV and HCV infection. • Screening for HBsAg and anti-HCV is recommended for individuals who fit into one or more of these categories unless they are already known to be seropositive. • In addition, the patient might have undetected chronic active hepatitis, which could lead to bleeding complications or drug metabolism problems.
  24. 24. Hepatitis: DENTAL MANAGEMENT Medical Considerations Patients Who Are Hepatitis Carriers. • If a patient is found to be a hepatitis B carrier (HBsAg positive) or to have a history of hepatitis C, standard precautions (see Appendix B ) are to be followed to prevent transmission of infection. • In addition, some hepatitis carriers may have chronic active hepatitis, leading to compromised liver function and interference with hemostasis and drug metabolism. • Physician consultation and laboratory screening of liver function are advised for determination of current status and future risks. Patients With Signs or Symptoms of Hepatitis. • Any patient who has signs or symptoms suggestive of hepatitis should not be given elective dental treatment but instead should be referred immediately to a physician. • Necessary emergency dental care should be provided with the use of an isolated operatory and minimal aerosol production.
  25. 25. Hepatitis: DENTAL MANAGEMENT Medical Considerations CDC Guidelines for Exposure to Blood. • To reduce the risk of transmission of hepatitis viruses, the CDC has published postexposure protocols for percutaneous or permucosal exposure to blood. Implementation of these protocols is dependent on the virus present in the source person and the vaccinated state of the exposed person . • Briefly, a vaccinated individual who sustains a needlestick or puncture wound contaminated with blood from a patient known to be HBsAg positive should be tested for an adequate titer of anti-HBs if those levels are unknown. • If levels are inadequate, the individual immediately should receive an injection of HBIG and a vaccine booster dose • If the antibody titer is adequate, nothing further is required. • If an unvaccinated individual sustains an inadvertent percutaneous or permucosal exposure to hepatitis B, immediate administration of HBIG and initiation of the vaccine are recommended.
  26. 26. Hepatitis: DENTAL MANAGEMENT Medical Considerations CDC Guidelines for Exposure to Blood. • Although no postexposure protocol or vaccine is available at this time for HCV infection, current CDC guidelines recommend that 1. the source person should receive baseline testing for anti-HCV 2. exposed persons should receive baseline and follow-up testing at 6 months for anti-HCV and liver enzyme activity, 3. anti-HCV enzyme immunoassay positive results should be confirmed by recombinant immunoblot assay (RIBA), 4. postexposure prophylaxis should be avoided with immunoglobulin or antiviral agents, 5. health care workers should be educated regarding the risks and prevention of bloodborne infection.
  27. 27. Hepatitis: DENTAL MANAGEMENT Medical Considerations Exposure Control Plan. • With respect to hepatitis viruses, the U.S. Occupational Safety and Health Administration mandates that all employers must maintain an exposure control plan and must protect employees from the hazards of bloodborne pathogens by applying standard precautions and by providing the following as a minimum:  Hepatitis B vaccinations to employees  Postexposure evaluation and follow-up  Recordkeeping of exposures  Generic bloodborne pathogen training  Personal protective equipment at no cost to employees
  28. 28. Hepatitis: DENTAL MANAGEMENT Drug Administration • No special drug considerations are required for a patient who has completely recovered from viral hepatitis. • However, if a patient has chronic active hepatitis or is a carrier of HBsAg or HCV and has impaired liver function, the dosage of drugs metabolized by the liver should be decreased, or these drugs should be avoided, if possible as advised by the physician. • As a guideline, drugs metabolized in the liver should be considered for diminished dosage when one or more of the following are present:  Aminotransferase levels elevated to greater than 4 times normal values  Serum bilirubin elevated to above 35 μM/L or 2 mg/dL  Serum albumin levels lower than 35 mg/L  Signs of ascites and encephalopathy, and prolonged bleeding time • A quantity of three cartridges of 2% lidocaine (120 mg) is considered a relatively limited amount of drug.
  29. 29. Hepatitis: DENTAL MANAGEMENT TREATMENT PLANNING MODIFICATIONS Treatment planning modifications are not required for the patient who has recovered from hepatitis. Oral Manifestations and Complications • Abnormal bleeding is associated with hepatitis and significant liver damage. • This may result from  abnormal synthesis of blood clotting factors,  abnormal polymerization of fibrin,  inadequate fibrin stabilization,  excessive fibrinolysis, or  thrombocytopenia associated with splenomegaly that accompanies chronic liver disease.
  30. 30. Hepatitis: DENTAL MANAGEMENT Oral Manifestations and Complications • Before any surgery is performed, the platelet count should be obtained, and it should be confirmed that the international normalized ratio (INR) is lower than 3.5. • If the INR is 3.5 or greater, the potential for severe postoperative bleeding exists. • In this case, extensive surgical procedures should be postponed. • If surgery is necessary, an injection of vitamin K usually corrects the problem and should be discussed with the physician. • Chronic viral hepatitis increases the risk for hepatocellular carcinoma. • This malignancy rarely metastasizes to the jaw (fewer than 30 cases in the jaw were reported as of this writing). • Oral metastases primarily present as hemorrhagic expanding masses located in the premolar and ramus regions of the mandible.
  32. 32. Alcoholic liver disease: DEFINITION Alcoholism is a chronic addiction to ethanol in which a person craves and uncontrollably consumes ethanol, becomes tolerant to its intoxicating effects, and has symptoms of alcohol withdrawal when the drinking stops. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) defines alcohol dependence as repeated alcohol-related difficulties in at least three of seven areas of functioning. These include any combination of the following: • Tolerance • Withdrawal • Ingestion of larger amounts of alcohol over longer periods than intended • Inability to control use • Giving up important activities to drink • Spending a great deal of time involved with alcohol use • Continued use of alcohol despite physical or psychological consequences
  33. 33. Alcoholic liver disease: Etiology • Alcohol consumption in large or chronic amounts contributes to disease and injury. • In contrast, moderate consumption of alcohol (2 to 6 drinks per week) is associated with decreased mortality and cardiovascular disease rates. • The quantity and duration of alcohol ingestion required to produce cirrhosis are not clear. • alcohol is hepatotoxic and its metabolite, acetylaldehyde, is fibrinogenic. • Chemokines also are implicated in the pathogenesis of alcoholic liver disease. • Alcohol-induced influx of endotoxin (lipopolysaccharides) from the gut into the portal circulation can activate Kupffer cells, which leads to enhanced chemokine release. • Chemokines, in turn, directly and indirectly damage liver hepatocytes.
  34. 34. Alcoholic liver disease: Pathophysiology and Complications • Alcohol has a deleterious effect on  neural development,  the corticotropin-releasing hormone system,  the metabolism of neurotransmitters, and  the functions of their receptors. • As a result, the acetylcholine and dopaminergic systems are affected, which causes sensory and motor disturbances (e.g., peripheral neuropathies). • Prolonged abuse of alcohol contributes to malnutrition (folic acid deficiency), anemia, and decreased immune function. • The pathologic effects of alcohol on the liver are expressed by one of three disease entities  The earliest change seen in alcoholic liver disease is a fatty infiltrate.  A second and more serious form of alcoholic liver disease is alcoholic hepatitis.  The third and most serious form of alcoholic liver disease is cirrhosis, which is generally considered an irreversible condition characterized by progressive fibrosis and abnormal regeneration of liver architecture in response to chronic injury or insult
  35. 35. Alcoholic liver disease: Pathophysiology and Complications • Cirrhosis results in progressive deterioration of the metabolic and excretory functions of the liver and ultimately leads to hepatic failure. Hepatic failure is manifested by a myriad of health problems. • Some of the more important of these are • esophagitis, • gastritis, and • pancreatitis, all of which contribute to generalized malnutrition, weight loss, protein deficiency (including coagulation factors), impairment of urea synthesis and glucose metabolism, endocrine disturbances, encephalopathy, renal failure, portal hypertension, and jaundice. • Accompanying portal hypertension is seen as the development of ascites and esophageal varices. • In addition, chronic large consumption of ethanol can result in • dementia and psychosis (Wernicke's and Korsakoff's syndromes), • cerebellar degeneration, • upper alimentary tract cancer and • Liver cancer, and hematopoietic changes.
  36. 36. Alcoholic liver disease: Pathophysiology and Complications • Bleeding tendencies are a significant feature in advanced liver disease. • The basis for the diathesis is in part a deficiency of coagulation factors, especially the prothrombin group (factors II, VII, IX, and X). • These all rely on vitamin K as a precursor for production. • Anemia and leukopenia also may be noted because of the toxic effects of alcohol on the bone marrow and nutritional deficiencies. • Accelerated fibrinolysis also may be seen. • The combination of hemorrhagic tendencies and severe portal hypertension sets the stage for episodes of  gastrointestinal bleeding,  epistaxis,  ecchymosis, or  ruptured esophageal varix. • Ethanol abuse predisposes the individual to infection by several mechanisms • Alcohol-induced impairment of Kupffer cell function and T-cell responses result in increased risk of infection.
  37. 37. Alcoholic liver disease: CLINICAL PRESENTATION Signs and Symptoms • The behavioral and physiologic effects of alcohol vary. • Chronic heavy alcohol intake can result in clinically significant cognitive impairment (even when the person is sober) or distress. • If the condition is allowed to progress untreated, many individuals develop other psychiatric problems (e.g., anxiety, antisocial behavior, affective disorders), whereas some develop alcohol amnestic disorder • Clinically, with the possible exception of enlargement, no visible manifestations of fatty liver are present, • The clinical presentation of alcoholic hepatitis often is nonspecific and may include features such as  nausea,  vomiting,  anorexia,  malaise,  weight loss, and  fever.
  38. 38. Alcoholic liver disease: CLINICAL PRESENTATION Signs and Symptoms • More specific findings include  hepatomegaly,  splenomegaly,  jaundice,  ascites,  ankle edema, and  spider angiomas. • With advancing disease, encephalopathy and hepatic coma may ensue, resulting in death. • Other less specific signs of alcoholic liver disease include  anemia,  purpura,  ecchymoses,  gingival bleeding,  palmar erythema,  nail changes, and  parotid gland enlargement (known as sialadenosis)
  39. 39. Alcoholic liver disease: Laboratory Findings. • Liver abnormalities cause elevations in  bilirubin,  alkaline phosphatase,  AST,  ALT,  gamma-glutamyl transpeptidase,  amylase,  uric acid,  prothrombin time  triglycerides, and  cholesterol. Leukopenia (or leukocytosis) or anemia often is present. • Elevated blood levels of gamma-glutamyl transpeptidase and mean corpuscular volume are highly suggestive of alcoholism • Thrombocytopenia may be caused by hepatosplenomegaly, resulting in decreased platelet count and increased bleeding time. • Increased fibrinolytic activity
  40. 40. Alcoholic liver disease: MEDICAL MANAGEMENT • Treatment of patients with alcoholism consists of three basic steps. • The first is identification and intervention.  A thorough physical examination is performed to evaluate organ systems that could be impaired.  This includes a search for evidence of  liver failure,  gastrointestinal bleeding,  cardiac arrhythmia and  glucose or electrolyte imbalance.  Hemorrhage from esophageal varices and hepatic encephalopathy require immediate treatment.  Ascites mandates measures to control fluids and electrolytes,  alcoholic hepatitis is often treated with glucocorticoids,  infection or sepsis is managed with antimicrobial agents.
  41. 41. Alcoholic liver disease: MEDICAL MANAGEMENT • The second step is withdrawal from alcohol or, in cases of severe dependence, reduction in alcohol consumption.  Abrupt alcohol withdrawal results in  loss of appetite,  tachycardia,  anxiety,  insomnia, and  delirium tremens (DT), characterized by hallucinations, disorientation, impaired attention and memory, and extreme agitation.  Physical findings include severe sweating, elevated blood pressure, and tachycardia.  Strict dietary modifications, including a  high-protein,  high-calorie,  low-sodium diet and  possibly fluid restriction, are required.
  42. 42. Alcoholic liver disease: MEDICAL MANAGEMENT  Patients should receive  adequate nutrition and rest,  oral multiple B vitamins, including 50 to 100 mg of thiamine daily for at least 1 to 2 weeks, and  iron replacement and folic acid supplementation as needed to correct any anemia present. • The third step is to manage central nervous system depression caused by the rapid removal of ethanol. • Administration of a benzodiazepine, such as diazepam or chlordiazepoxide, gradually decreases drug levels over a 3- to 5-day period and alleviates alcohol withdrawal symptoms. • Beta blockers, clonidine, and carbamazepine have been recently added to the pharmacotherapeutic management options for withdrawal. • Once the treatment of withdrawal has been completed, the patient with alcoholism is educated about alcoholism.
  43. 43. Alcoholic liver disease: MEDICAL MANAGEMENT • The drug disulfiram has been used for some patients during alcohol rehabilitation. • Disulfiram inhibits aldehyde dehydrogenase, causing accumulation of acetaldehyde blood levels and thus, sweating, nausea, vomiting, and diarrhea, when taken with ethanol. • Naltrexone (an opioid antagonist) and acamprosate (an inhibitor of the γ-aminobutyric acid system) may be used to decrease the amount of alcohol consumed or to shorten the period during which alcohol is used in cases of relapse. • Untreated disease that progresses to cirrhosis requires alcohol withdrawal and management of the complications that are present. • End-stage cirrhosis cannot be reversed and is remedied only by liver transplantation
  44. 44. Alcoholic liver disease: Dental Management of the Patient With Alcoholic Liver Disease 1. Detection by such methods as i. History ii. Clinical examination iii. Alcohol odor on breath iv. Information from family members or friends 2. Referral or consultation with physician to ascertain the following: i. Verify history ii. Check current status iii. Check medications iv. Check laboratory values v. Discuss suggestions for management
  45. 45. Alcoholic liver disease: Dental Management of the Patient With Alcoholic Liver Disease 3. Laboratory screening (if not available from physician) to record the following: i. Complete blood count (CBC) with differential ii. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) iii. Bleeding time iv. Thrombin time v. Prothrombin time 4. Assessment of risk of adverse outcomes associated with invasive procedurer infection with prognostic formula (i.e., Modified Child-Pugh Classification found in table below) 5. Minimizing of drugs metabolized by liver 6. If screening tests are abnormal, for surgical procedures, consideration is given to thrombin, gelfoam, antifibrinolytic agents, fresh frozen plasma, vitamin K, platelets—with the help of a physician or PharmD
  46. 46. Alcoholic liver disease: Modified Child-Pugh Classification
  47. 47. Alcoholic liver disease: DENTAL MANAGEMENT Medical Considerations • The dentist has an excellent opportunity to assist patients who are at risk for, or who have, alcohol abuse problems. • Areas of assistance include the following: • Screening for alcohol risks and abuse • Providing alcohol prevention information • Directing patients with abuse problems to health care providers for assessment or treatment • Supporting dependent patients during the recovery period • Minimizing relapse in recovering patients • Screening  During the medical history, the dentist should obtain information from all adolescent and adult patients about the type, quantity, frequency, pattern, and consequences of alcohol use, along with a family history of alcoholism.  Questioning should be done in a nonjudgmental manner, aided by a standardized questionnaire such as the four question CAGE questionnaire, CUGE questionnaire
  48. 48. Alcoholic liver disease: DENTAL MANAGEMENT Medical Considerations
  49. 49. Alcoholic liver disease: DENTAL MANAGEMENT Medical Considerations • Providing Preventive Information. • If the dentist suspects that a patient is abusing alcohol, a spouse or significant other can be interviewed to gather additional diagnostic information. • If suspicions are confirmed, preventive information should be provided to the patient in a nonthreatening manner. • Treatment success depends on motivating the patient to enter treatment and breaking down denial. • Guiding the Patient for Assessment or Treatment and Supportive Care. • The dentist can point out destructive patterns of alcohol use and can discuss future problems that may be anticipated if alcohol use continues. • Minimizing Relapse. • To minimize relapse, the dentist should avoid the use of psychoactive drugs, narcotics, sedatives, and alcohol-containing medications in patients who are recovering from
  50. 50. Alcoholic liver disease: DENTAL MANAGEMENT Treatment Considerations. • In addition to the considerations mentioned earlier, three major dental treatment considerations apply for a patient with alcoholism: 1. Bleeding tendencies 2. Unpredictable metabolism of certain drugs 3. Risk or spread of infection • A CBC with differential, AST and ALT, bleeding time, thrombin time, and prothrombin time are sufficient in screening for potential problems. • Abnormal laboratory values, accompanied by abnormal clinical examination or a positive history, provide the basis for referral to a physician for positive diagnosis and 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 has been managed medically, dental care may be provided after consultation with the physician
  51. 51. Alcoholic liver disease: DENTAL MANAGEMENT Treatment Considerations. • In cases where the patient has not been seen by a physician within the past several months, screening laboratory tests, including CBC with differential, AST and ALT, platelet count, thrombin time, and prothrombin time, should be ordered before invasive procedures are performed • Precautionary measures, including an INR test (prothrombin time) that is particularly sensitive to deficiency of factor VII, should be taken to minimize the risk for bleeding • this may entail the use of  local hemostatic agents,  fresh frozen plasma,  vitamin K,  platelets, and  antifibrinolytic agents. • Hemostatic measures are particularly important when major invasive or traumatic procedures are performed in a patient who has been assigned an American Society of Anesthesiologists (ASA) category of III or greater; who has signs of jaundice, ascites, and clubbing of fingers; or who has been classified as a Child-Pugh class B or C.
  52. 52. Alcoholic liver disease: DENTAL MANAGEMENT Treatment Considerations. • A second area of concern in patients with alcoholic liver disease is the unpredictable metabolism of drugs. • In mild to moderate alcoholic liver disease, significant enzyme induction is likely to have occurred, leading to increased tolerance of 1. local anesthetics, 2. sedative and hypnotic drugs, and 3. general anesthesia. Thus, larger than normal doses of these medications may be required to attain the desired effects. • with advanced liver destruction, drug metabolism may be markedly diminished, which may lead to an increased or unexpected effect • The dentist should use the drugs primarily metabolized in liver with caution when treating patients with chronic alcoholism and should consider adjusting doses or avoiding their use, as advised by the patient's physician.
  53. 53. Alcoholic liver disease: DENTAL MANAGEMENT Treatment Considerations. • Once again, the occurrence of more than one of the following findings—  aminotransferase levels elevated to greater than 4 times normal,  serum bilirubin level elevated to above 3.5 μM/L (2 mg/dL),  serum albumin level lower than 35 g/L, and  signs of ascites, encephalopathy, or malnutrition suggests that drug metabolism may be impaired. • A third area of concern involves the risk of infection or spread of infection in the patient with alcoholic liver disease. • Risk increases with surgical procedures or trauma because oral microorganisms can be introduced into the blood circulation and may not be efficiently eliminated by the reticuloendothelial system. • Antibiotic prophylaxis is not needed if oral infection is absent. • A greater concern is the risk of spread of an ongoing infection because bacterial infections are more serious and are sometimes fatal in patients with liver disease.
  54. 54. Alcoholic liver disease: DENTAL MANAGEMENT Treatment Planning Modifications • Patients with cirrhosis tend to have more plaque, calculus, and gingival inflammation than those without the condition. • The dentist should not provide extensive care until the patient demonstrates an interest in, and an ability to care for, his or her dentition. • Liver enzyme induction and central nervous system effects of alcohol in patients with alcoholism may require increased amounts of local anesthetic or the use of additional anxiolytic procedures.
  55. 55. Alcoholic liver disease: DENTAL MANAGEMENT Oral Complications and Manifestations • Poor hygiene and neglect (caries) are prominent oral findings in patients with chronic alcoholism. • Patients with cirrhosis have been reported to have impaired gustatory function and are malnourished. • Nutritional deficiencies can result in  glossitis and loss of tongue papillae,  along with angular or labial cheilitis, which is complicated by concomitant candidal infection. • Vitamin K deficiency, disordered hemostasis, portal hypertension, and splenomegaly (causing thrombocytopenia) can produce spontaneous gingival bleeding, mucosal ecchymoses, and petechiae. • In some instances, unexplained gingival bleeding has been the initial complaint of alcoholic patients. A sweet, musty odor to the breath is associated with liver failure, as is jaundiced mucosal tissue • Bilateral, painless hypertrophy of the parotid glands (sialadenosis) is a frequent finding in patients with
  56. 56. Conclusion: Management of patient with hepatitis and alcoholic liver disease became a challenge to a dentist if (s)he does not have good knowledge of such disorder. Proper knowledge and proper application of prevention protocol minimizes the risk of spreading the infection also minimizes the further complication of the condition thus reducing the mortality.