Hepatitis and its prophylaxis

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CONTENTS

Introduction

Functions of liver

Hepatitis A,B,C,D,E

Chronic hepatitis

Drug induced liver disease

Cirrhosis

Alcoholic liver disease

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INTRODUCTION

Hepatitis is inflammation of the liver that may result from infectious or other causes.

Hepatitis is a worldwide heath problem with more than 5 million new cases occuring annually and more than 300 million persons across the globe carrying the viruses.

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Bile formation

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Functions of liver

Metabolic

Storage- glycogen, amino acids, iron, folic acid, vit A, B12, D

Synthetic- produces glucose, synthesis of plasma proteins, clotting factors, hormone binding proteins

Secretion of bile

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Excretory – excretion of cholesterol, bile pigments, heavy metals, toxins, bacteria, virus

Hemopoietic- stores vit B12 necessary for erythropoiesis and iron , thrombopoietin

Hemolytic –destruction of senile RBCs

Inactivation of hormones and drugs-catabolizes hormones

Defense and detoxification

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Causes of liver disease Congenital hyperbilirubinaemia-

Rhesus incompatibilityprematuritybiliary atresiaGilbert’s syndromeCrigler-Najjar syndrome

Dental aspects- disorders associated with an early rise in serum levels of conjugated bilirubincan cause dental hypoplasia and a greenish discoloration of the teeth

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Parenchymal liver disease (hepatocellular)

Viral hepatitis

Chronic hepatitis

Cirrhosis

Primary biliary cirrhosis

Drug induced hepatitis

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Extrahepatic biliary obstruction-

Gallstones

Ca of pancreas

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Parenchymal liver disease

Acute viral hepatitis-

5 distinct types-A,B,C,D,E

Other viruses- EBV,CMV, herpes simplex

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Hepatitis A

Infectious hepatitis

Endemic throughout the world but seen particularly where socioeconomic level is poor

Transmission- feco-oral

Can also be transmitted sexually and in body fluids including saliva

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C/f-

Incubation period is 2-6 wks

Fatigue, nausea, vomiting, abdominal pain and discomfort, loss of apetite, low grade fever, jaundice, itching

No evidence of carrier state or progression to chronic liver disease

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General management

Diagnosis is confirmed by serum antibodies to the virus- antiHAV

Can be prevented by administration of HAV immune globulin 0.02 mg/kg prophylactically or within 2 wks of exposure

Vaccine is available for prophylaxis in travellers to high risk endemic areas-Havrix, vaqta and twinrix

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Hepatitis B

HBV

Can cause lifelong infection, cirrhosis of liver, liver cancer, liver failure and death

Transmission- parenteral- via unscreened blood or blood products, IV drug abuse, sharing of needles, sexually, tattoing/body piercing, vertical transmission

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High risk groups Pts who have received unscreened blood products

or multiple plasma or blood transfusion Haemodialysis for end stage renal disease Immunosuppressed (eg. HIV) Residents and staff of long stay institutions,

particularly prisons Occupations that expose to human blood

especially surgeons IV drug abusers Travellers to endemic areas Chronic liver disease Newborns whose mothers are infected with HBV

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Clinical features

Incubation period is 2-6 months

Effects range from subclinical infections without jaundice, to fulminating hepatitis, acute hepatic failure and death

Prodromal symptoms(1-2 wks)- anorexia, malaise and nausea

Jaundice- pale stools and dark urine

Enlarged and tender liver

Muscle pain, arthralgia and rashes

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Complications

Carrier state- HBV persists within the body for more than 6 months(develops in 5-10%)

More frequent in anicteric infections

Carriage may persist for up to 20 yrs and may be asymptomatic.

Pts who have received blood products, those infected with HDV and those with immune defects are predisposed to carrier state.

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Serum enzyme estimations – AST, ALT are raised in proportion to the severity of illness

Alkaline phosphatase and serum bilirubin are also raised

Serologic markers- EM shows 3 types of particles in serum Dane particle-intact hepatitis virus (inner core of

DNA and core antigen HBcAg and outer envelope of HBsAg.

Persitance of HBsAg beyond 13 wks of clinical illness indicates carrier state is developing

HBeAg

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Anti-HBs develops after infection or vaccination and in the absence of HBsAgimplies immunity

HBeAg- active disease and high infectivityfound only in serum that is HBsAg positive.persistance beyond 4 wks of the onset of

symptoms indicates tht the patient will probably remain infectious and develop chronic liver diseaseAnti Hbe indicates complete recovery and loss of infectivity provided HBeAg is lost

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HBcAg- found in liver biopsy in acute hepatitis

Sensitive marker of viral replication and indicates current or recent infection

antiHBc associated with antiHBs indicates recovery and immunity

If antiHBs is absent it indicates carrier state or chronic hepatitis

DNA polymerase appears transiently in the serum early in the course infection. If it is demonstrable in HBsAg carriers , it indicates high infectivity

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General management Bed rest Avoid hepatotoxins like alcohol Chronic HBV infection can be treated with

lamivudine or interferon or adefovir dipivoxil Prevention- avoiding contact with HBV and having

hepatitis B vaccination Giving HBIG and vaccine within 12 hrs after birth

to infants born to HBV infected mothers Drug users should not share needles, syringes Not sharing personal care items like razors,

toothbrushes Avoiding tattoing or body piercing

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Healthcare workers should always follow universal precautions, safely handling needles and other sharps and being vaccinated

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Dental aspects Drugs should be used with caution There may be bleeding tendency if the platelet

count is low or if PT is prolonged Saliva may contain HBV Human bite can also transmit HBV Needlestick injury- 25% of these may transmit

HBV infection. HBIG should be given within 24 hours and 1st shot of hepatitis B vaccine

If adequate precautions are taken dental surgery is no longer a significant source of infection

Practitioners ill with hepatitis should stop dental practice until fully recovered.

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Hepatitis C

Previously known as non A non B hepatitis

Transmission- blood and blood products

Persons at risk- those who have received blood from a donor who later tested positive for HCV, illegal IV drug user, long term renal dialysis, health care workers exposed to blood

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C/f: 80-90% of infected persons have no signs or symptoms

25-80% of pts with HCV have abnormal liver function tests after one year and may go on to chronic liver disease(up to 85%) or liver cancer or die(<3%)

Coinfection with HGV- 15%

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General management

Serologic test (ELISA) are available to detect HCV

No vaccine available

Drug treatment with alpha interferon

Chronic HCV- combination of ribavirin plus interferon alpha

Prevention: routine barrier precautions and safely handling needles

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Dental aspects

HCV has been found in saliva

Transmitted in 10 % of needlestick injuries

Infected staff should not perform exposure prone procedures

The main salivary gland disorders associated with HCV infection are xerostomia, Sjögren’ssyndrome, lichen planus and

sialadenitis.

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Hepatitis D Incomplete virus carried within the

hepatitis B particle and will only replicate in the presence of HBsAg

Transmission- parenteral mainly by shared needles

C/f: 90% are asymptomatic

70-80% of HBV carriers with HDV superinfection develop chronic liver disease with cirrhosis

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HDV antigen indicates recent infection and delta antibody indicates chronic hepatitis or recovery

Vaccination against HBV protects indirectly against HDV

Drug treatment with alpha interferon

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Hepatitis E

Spreads via feco-oral route

In developing countries with poor sanitation

Causes a disease similar to hepatitis A

High mortality in pregnant women (more than 40%)

Not known to be transmitted in dentistry

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Hepatitis Non A -E

Cases of acute hepatitis than appear to have viral origin but that cannot attributed to any known virus

This includes unknown viruses such as hepatitis F virus, hepatitis G virus and TTV

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Chronic hepatitis Persists longer than 6 months Causes: hepatitis B or C

autoimmuneAlcoholismwilsons diseasealpha 1 antitrypsin deficiency

Drugs: aspirincytotoxic agentshalothaneisoniazidmethyldopaacetaminophen

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Clinical features Many patients are asymptomatic Malaise Anorexia Fatigue Low grade fever Upper abdominal discomfortSigns: splenomegalySpider naeviAscitesFluid retentionJaundice

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General management

Liver biopsy is essential for definitive diagnosis

Liver enzymes: Aminotransferases are raised

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Treatment includes withdrawl of causative drugs and management of complications

Chronic HBV /HCV: interferon alpha, lamivudine

Chronic HCV: ribavirine plus interferon alpha

Liver transplantation for advanced hepatitis C

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Hepatotoxic agents aspirin and paracetamol should be avoided

No common oral problems in chronic hepatits but sjogrens syndrome is relatively common and oral lichenoidlesions may develop

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Cirrhosis

Liver cell necrosis followed by fibrosis, nodular regeneration and vascular derangement

Deterioration of liver function, flow of blood through the organ gets obstructed

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Causes of cirrhosis idiopathic alcoholism Hepatitis C,B,D Chronic hepatitis Primary biliary cirrhosis wilson’s disease alpha 1 antitrypsin deficiency congestive cardiac failure drugs

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C/F anorexia ,malaise, weight loss Jaundice Splenomegaly Ascites GI haemorrhage Palmer erythema Spider naevi Finger clubbing Opaque nails Pigmentation Fluid retention Bruising Gynaecomastia, testicular atrophy

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Alcoholic cirrhosis – parotid swelling

Dupuytren’s contracture

Gastric ulceration, or pancreatitis

Complications from hepatocellular damage and portal hypertension:

vomiting of blood

thrombocytopenia

bleeding tendency

anaemia

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General management

Serum bilirubin levels, immunoglobulins, transaminases and alkaline phosphatasemay be raised

Serum albumin is low

Prolonged PT

Thrombocytopenia, anaemia

Liver damage from cirrhosis cannot be reversed but treatment can stop or delay further progression

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Treatment of the cause

Treatment is directed towards prevention and treatment of complications

Liver transplantation when complications cannot be controlled

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Dental aspects

SBP is a potential problem in cirrhosis with ascites

Invasive dental or oral surgical procedures may increase the risk of SBP

Antibiotic prophylaxis should be considered

Amoxicillin orally 2-3g with metronidazole 1 h preop or intravenous imipenem are recommended

Some pts have sialosis, or tooth erosion from gastric regurgitation

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Drug induced liver disease

Dose related liver damage-alcohol, acetaminophen, tetracyclines, ketoconazole, isoniazid, methyldopa

Non dose related – erythromycin, halothane and sulfonamides , antithyroid drugs, phenytoin,nitrofurantoin

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Tetracyclines in massive doses can cause liver damage

Erythromycin estolate is potentially hepatotoxic but the effect is reversible when the drug is stopped

Halothane can cause hepatitis Halothane hepatitis causes pyrexia 1 week post op

and malaise , anorexia and jaundice may then appear

Halothane should never be given repeatedly or within a period of 3 months

Enflurane, isoflurane, desflurane and sevoflurane do not induce hepatitis in those who have had halothane hepatitis

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Aspirin: reye’s syndrome in children-liver damage with encephalopathy and abnormal accumulation of fat in the liver and other organs alone with a severe rise in intracranial pressure

Therefore it is contraindicated in children below 16 yrs

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Liver cancer

Fifth most common cancer worldwide

Cancer of the hepatocytes- hepatocellularcarcinoma or malignant hepatoma

It has been estimated that HBV and HCV are responsible for over 80% of all hepatocarcinomas.

Risk factors: old age, a positive family history, chronic HCV or HBV, cirrhosis , aflatoxin, long term oral contraceptive use

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Clinical features

Early stages- no symptoms

Later- wasting,

jaundice,

pain in the right upper abdomen,

swollen abdomen,

loss of appetite,

weakness,

nausea and vomiting ,

fever

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General management

Ultrasound, MRI scan , biopsy

High alpha fetoprotein levels

Treatment- surgical resection (partial hepatectomy)

Liver transplantation

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Extrahepatic biliaryobstruction

Causes- gall stones and Ca of pancrease

C/f-

Gall stones are often asymptomatic

Passage of the stones into the bile ducts can cause severe pain because of biliary colic, acute cholecystitis or acute pancreatitis

Jaundice, pruritus, dark urine and pale stools

Impaired absorption of fats and vitamin K

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General management

Diagnosis- ultrasound and endoscopic

Rise in serum bilirubin esters, alkaline phosphatase, 5’ nucleosidase, gamma glutamyl transpeptidase and transaminase

Treatment- lithotripsy,

Cholecystectomy

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Dental aspects Main danger in surgery is

excessive bleeding resulting from vitamin k malabsorption

Surgical intervention should be deferred whenever possible in the presence of jaundice until hemostatic function returns to normal

Obstructive jaundice in neonates may result in greenish discoloration of teeth

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Alcoholic liver disease

Earliest change- fatty infiltrate, enlargement of liver (reversible)

Alcoholic hepatitis- diffuse inflammatory condition of liver with destructive cellular changes(irreversible)

Irriversible changes can lead to necrosis

Cirrhosis- progressive fibrosis and abnormal regeneration of liver architecture

Cirrhosis leads to liver failure

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Patients with alcoholic hepatitis can present glossitis, angular cheilitis and gingivitis, particularly in combination with nutritional deficiencies

Sialadenosis

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A patient with untreated alcoholic liver disease is not a candidate for outpatient dental care and should be referred to a physician.

Screening lab tests, including CBC, AST,ALT,PT should be ordered before the invasive procedures are performed

Use drugs with caution as metabolism may be impaired. Eg. Half the dose if cirrhosis or alcoholic hepatitis is present

There is risk of infection or spread of infection. Antibiotics should be prescribed when infection develops.

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Dental considerations of hepatitis

Dentists who are hepatits virus carriers:

The CDC suggests that health care professionals who perform invasive procedures should know their infectivity status

And if found positive for a blood transmissible virus, should not perform exposure prone procedures

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All patients with a history of viral hepatitis must be managed as though they are potentially infectious

All dental healthcare workers who provide patient care should receive vaccination against hepatitis B and should implement universal precautions

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Patients with active hepatitis: no dental treatment other than urgent care

Strict adherence to standard precautions

Aerosols should be minimized and drugs metabolized in the liver should be avoided.

If surgery is necessary, preop PT and BT should be obtained.

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Patients with history of hepatitis:

Most carriers of HBV,HCV and HDV are unaware that they have had hepatitis

Thus these pts are not identified with medical history and lab screening of all the pts is impractical

The only practical method of protection from these pts is to adopt a strict program of clinical asepsis for all patients

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Patients at high risk for HBV or HCV infection:

Screening for HBsAg and antiHAV

If a patient is found to be carrier, the patient may have undetected chronic active hepatitis, which could lead to bleeding complications and drug metabolism problems.

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Drug administration

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 value

Serum bilirubin elevated to above 2mg/dL

Serum albumin levels lower than 35mg/L

Signs of ascites and encephalopathy and prolonged BT

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Oral manifestations

The oral cavity can reflect liver dysfunction in the form of mucosal membrane jaundice, bleeding disorders, petechiae,

increased vulnerability to bruising, gingivitis, gingival bleeding (even in response to minimum trauma) foetorhepaticus (a characteristic odor of advanced liver disease), cheilitis, smooth and atrophic tongue, xerostomia, bruxism and crusted perioral rash

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Before any surgery is performed, the PT should be obtained

INR should be lower than 3.5

If it is more than 3.5, extensive surgical procedure should be postponed

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The most frequent problems associated with liver disease in clinical practice refer to the risk of viral contagion on the part of the dental professionals and rest of patients (cross-infection),

the risk of bleeding in patients with serious liver disease,

alterations in the metabolism of certain drugs which increases the risk of toxicity.

HCV has been detected on different surfaces within the dental clinic after treating patients with hepatitis C, and the virus is able to remain stable at room temperature for over 5 days

Strict sterilization measures are therefore required The universal protective measures are applicable

in order to prevent cross-infection, i.e., the use of barrier methods, with correct sterilization and disinfection measures

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The measures in the case of accidental perforation of the skin with instruments or needles comprise careful washing of the wound (without rubbing, as this may inoculate the virus into deeper tissues) for several minutes with iodine solution.

pressure should be applied beneath the level of the wound in order to induce bleeding and thus help evacuate any possible infectious material. If exposure through some mucosal membrane has occurred, abundant irrigation with sterile saline solution or sterile water is advised, for several minutes. The rationale behind these measures is to reduce the number of viral units to below the threshold count needed to cause infection (i.e., the infectious dose).

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In many cases, discrimination and stigma, or fear and past experience can prevent people with hepatitis B or C from accessing dental and other healthcare services.

Therefore, we should have a welcoming and nonjudgmental approach to treating all patients to ensure the provision of effective healthcare and follow-up.

Prevention is an important aspect in controlling the spread of this viral infection as an epidemic. Knowing facts, having proper awareness, and proper behavior and attitude toward clinical aspects of the infection and toward the patients are critical to prevent the spread of these infections.

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Setia, et al. : Hepatitis B and C infection in dentistry and its management, Eur J Gen Dent 2013;2:13-9

Medical problems in dentistry, 5th edition, Crispian Scully, Roderick Cawson

Robbins basic pathology, 9th edition

Little,J.W, dental management of medically compromised patients

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Thank you !

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