Hepatitis and

its prophylaxis

1
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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
occurring 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 incompatibility
prematurity
biliary atresia
Gilbert’s syndrome
Crigler-Najjar syndrome
Dental aspects- disorders associated with an
early rise in serum levels of conjugated bilirubin
can 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 HBsAg
implies immunity
 HBeAg- active disease and high infectivity
found 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 disease
Anti 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’s
syndrome, 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
autoimmune
Alcoholism
wilsons disease
alpha 1 antitrypsin deficiency
Drugs: aspirin
cytotoxic agents
halothane
isoniazid
methyldopa
acetaminophen
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Clinical features
 Many patients are asymptomatic
 Malaise
 Anorexia
 Fatigue
 Low grade fever
 Upper abdominal discomfort
Signs: splenomegaly
Spider naevi
Ascites
Fluid retention
Jaundice
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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 lichenoid
lesions 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 phosphatase
may 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- hepatocellular
carcinoma 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 biliary
obstruction
 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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:
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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) foetor
hepaticus (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 !