INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2004 264 Indian J. Anaesth.

2004; 48 (4) : 264-275

1. M.D., Asso. Prof.
Department of Anaesthesia,
L.T.M. Medical College and L.T.M.G. Hospital,
Sion, Mumbai 400 022.
Correspond to :
Dr. Anila D. Malde
3 / Nagjibhai Mansion, Manubhai P Vaidya Marg
Ghatkopar (E), Mumbai-400 077.
E-mail : dradmalde@yahoo.com
(Accepted for publication on 25-05-2004)
VIRAL HEPATITIS AND ANAESTHESIOLOGIST
Dr. Anila D. Malde
SUMMARY
Hepatitis can occur due to infections, alcoholism, drugs and metabolic disorders. Infectious hepatitis especially viral is not only
common, but also has most serious implications. Symptoms, signs, serological markers, prophylaxis, therapy and sequelae of viral
hepatitis A to G are briefed. Anaesthesiologist may have to evaluate, prepare and anaesthetize patient of hepatitis for various surgeries
on elective, semi elective or emergency basis. These procedures may or may not be related to hepatitis. Anaesthetic recommendations
for the same are discussed. The write up also includes important perioperative considerations for the emergency procedures.
Precautions for personal and staff protection are reviewed. The article highlights the guidelines for Pre and post exposure prophylaxis
as well as rules of practice.
Keywords : Disease: Hepatitis, Anaesthesia for hepatitis, Anaesthetic implications; Hepatitis, Vaccines: Hepatitis A,
Hepatitis B, Injuries; needle-stick, Infection; transmission; hepatitis.
Hepatitis and anaesthesiologist
Hepatitis, either as acute disease, or as its sequelae
like chronic active hepatitis (CAH), cirrhosis and primary
liver cancer affect millions of people. (Figure 1)
1
Anaesthetic concerns
1. Management of patient with hepatitis
a. Pre operative evaluation of symptomatic or
asymptomatic patients.
b. Pre operative preparation
c. Anaesthetic for sequelae of hepatitis
Elective e.g. umbilical hernia
Semi elective e.g. Ligation of oesophageal varices
Emergency liver transplantation
d. Anaesthesia for unrelated procedure e.g. for LSCS
in a c/o hepatitis
e. Emergencies because of hepatitis in Emergency
Medical Service department and Intensive Care
Areas.
2. Personnel and staff protection from infection.
Viral hepatitis (VH)
Acute VH can be caused by at least six different
viral agents. Clinical symptoms are quite similar. Further
differentiation requires serology.
Symptoms and signs of acute hepatitis
Symptoms of acute viral hepatitis may begin suddenly
or develop gradually.
1,2
They may be so mild that patients
mistake the disease for the flu. Nearly all patients experience
some fatigue and often have mild fever. Gastrointestinal
problems are very common, including nausea and vomiting
and a general feeling of discomfort in the abdomen or a
sharper pain that may occur in the right hypochondrium. GI
problems can lead to loss of appetite, weight loss, and
dehydration. After about two weeks, dark urine and jaundice
develops in some, but not in all patients. About half of all
hepatitis patients have light colored stools, muscle pain,

Acute hepatitis Persistent infection
Asymptomatic
carrier
Chronic
hepatitis
Fulminant
hepatitis
95%
Recovery Death
Cirrhosis
Carcinoma
Death
Aetiology:
1
Infectious Viral hepatitis - Hepatitis virus A to G
Epstein-Barr virus
Cytomegalovirus
Herpes simplex
Alcoholic
Drugs INH, methyldopa,
diclofenac, dantrolene, etc.
Metabolic diseases
Fig. 1 : Sequelae
1
Phone: 022 25165245
REVIEW ARTICLE
264
Reprinted with permission from: Rabin L. Hepatitis. In: Mandell GM, editor in Chief, Atlas of Infectious
Diseases, volume VII, Philadelphia: Churchill Livingstone, 1996, 2.01-2.54.
MALDE : VIRAL HEPATITIS AND ANAESTHESIOLOGISTS 265
drowsiness, irritability, and itching, usually mild. Diarrhea
and joint aches occur in about a quarter of patients. The
liver may be tender and enlarged and most people have
mild anemia. In about 10% of patients, the spleen is
enlarged.
Laboratory tests reveal mild anemia and
lymphocytosis, rise in aminotransferases (AST and ALT),
7 to 14 days before the onset of jaundice. It begins to
decrease shortly after the appearance of jaundice. The
rise does not correlate with severity.
2
Plasma bilirubin
increases for 10-14 days and then decreases over 2-4 weeks.
Rise in g globulin suggest chronic hepatitis, in severe
acute VH - hypoalbuminemia and prolonged prothrombin
time (PT)
Clinical course
In most cases of acute viral hepatitis, recovery is
complete and the liver returns to normal within two to
eight weeks. In very rare cases, within two months of onset
of acute hepatitis, fulminant hepatitis develops.
3
Symptoms
may include ascities and flapping tremors. These may
be followed by gastrointestinal bleeding and mental
confusion, stupor, or coma i.e. encephalopathy. Without
liver transplantation, death occurs in up to 80% of these
cases. Pregnant women with acute hepatitis B, C, or E are
at higher risk for these complications.
In a small number of cases of hepatitis B or C, the
condition can be prolonged and recovery may not occur
for a year. About 5% to 10% of these patients will experience
a flare up of symptoms in a milder form before full recovery.
A few of these patients may go on to develop chronic
hepatitis. Clinical and epidemiological features of different
types of hepatitis are shown in table1.
1
Hepatitis A (HAV)
It has very high prevalence in India.
1
People at risk
include staff and residents of mental homes, children in day
care centers, active male homosexuals, narcotic drug
abusers, sewerage workers, health care workers (HCWs),
military personnel and people of low socioeconomic groups.
An outbreak has been reported in an ICU in Queensland.
4
The virus is shed in feces for 14-21 days before the
onset of jaundice. Patients are unlikely to be infective
for more than 21 days after the illness has begun.
5
IgM
antibody to HAV is detectable at the onset of clinical
illness and usually disappears within 60-120 days. IgG
antibody reaches a high titer during convalescence, persists
indefinitely and confers immunity. (Figure 2)
1
Table - 1 : Clinical and epidemiologic features of viral
hepatitis.
1
A B C D E G
35-37nm,
RNA, hybrid
Virus 27 nm, 42nm, 30-60nm, particles with 32-34nm RNA
RNA DNA RNA HbsAg coat RNA
+ HDV core
Incubation 15-45, 30-150, 15-120, 15-150, 15-16,
(days) mean 25 mean 75 mean 50 mean 30 mean 30
Onset Acute Insidious Insidious Insidious Acute
or acute or acute
Age Children Young adults Any age Any age, Young Young
preference or (sexual and but more similar to adults, adults
young percutaneous) common HBV 20-40
adults Babies and in adults years
Toddlers
Transmission
Fecal oral + + + - - - + + +
Percutaneous Unusual + + + + + + + + + - +
Perinatal - + + + ? + -
Sexual + + ? + + -
Clinical Mild Occasionally Moderate Occasionally Mild Generally
Severity severe severe mild
Fulminant 0.1% 0.1% - 1% 0.1% 5-20% 1-2% Reported
Chronicity 0% 5% 85% 5-70% 0% Yes
Carrier None 0.1-30% 0.5-1% Variable None
Cancer None +(neonatal + None Undeter-
infection) mined
Mortality 0.2% 0.5-2% 0.2% 2-20% 0.2% Reported
Prophylaxis Immunog- HBIg, None HBV Unknown
lobulin vaccines vaccine
Vaccines (none for
(HAVRIX HBV carrier)
and
VAQTA)
Therapy None Interferon Interferon Unknown None
40% effective 50%
effective
Reprinted with permission from : Rabin L. Hepatitis. In: Mandell GM, editor in Chief, Atlas of Infectious
Diseases, volume VII, Philadelphia: Churchill Livingstone, 1996, 2.01-2.54.
The primary indication for use of immunoglobulin
(IG) for pre exposure prophylaxis is for travelers to high
HAV endemic regions. Postexposure prophylaxis with IG
is effective if administered within 14 days of exposure.
5
The primary indication for postexposure prophylaxis is
for household or other intimate contacts of persons with
hepatitis A. In addition, postexposure prophylaxis may be
indicated when hepatitis A cases occur in some institutional
settings (e.g., child day care centers), and for some common-
source exposures (e.g., eating food prepared by an infected
food handler).
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2004 266
0 0.25 0.5 1 1.5 1.75 2 2.25 3 4 5 6 12
Months after exposure
ALT
IgM anti HAV
IgG anti HAV
Serum HAV
Stool HAV
Jaundice
Symptoms
Parenteral drugs users.
Homosexual men.
Heterosexuals with multiple partners or with STDs.
Household contacts of HbsAg positive individuals.
Newborn infants of HbsAg positive mothers. An Indian
study
11
had shown an overall transmission risk of 18.6%
from HbsAg carrier mothers versus 3% risk in HbsAg
negative mothers.
Serological course

(Figure 3)
3
The first marker, HbsAg (Australian antigen) appears
during the incubation period, rapidly rises in the titer and
range between 1 to 50 mgml
-1
, by the onset of the symptoms.
In most cases it persists throughout the icteric phase. It is
a convenient marker for the diagnosis. However occasionally,
it clears early and at times it persists, as in carriers and
in chronic hepatitis. Therefore, IgM anti-HbC, a better
marker is often used to document acute hepatitis B.
Concurrently, HbeAg and HBV DNA become detectable
and rapidly increase in concentration. HBV DNA usually
reaches 10
5
to 10
8
genome equivalents per ml by the onset
of symptoms, and then decrease, becoming undetectable in
few weeks. They are the markers for viral replication and
hence infectivity. The polymerase chain reaction (PCR) for
the detection of DNA can detect even 100 viral genomes
per ml.
First antibody to appear is anti - HbC. Initially most
of the anti - HbC is IgM, which persists only for a few
months. It is a valuable marker for the diagnosis of acute
hepatitis B. IgG anti - HbC generally persists for life.
Anti - Hbs, a marker of recovery appears during
convalescence, after clearance of HbsAg. After natural
infection, anti - Hbs persists for decades in slowly declining
titers and reinfections are extraordinarily rare. Hepatitis B
virus serological markers in different stages of infection
and convalescence are shown in table 2.
12
Long term protection from hepatitis A virus (HAV)
infection can be achieved through active, pre exposure
vaccination with hepatitis A vaccine.
6
Inactivated hepatitis A
vaccines licensed for use are HAVRIX

, VAQTA

and
Twinrix

, a combined hepatitis A and hepatitis B vaccine.

7
The dose and schedule of administration for HAVRIX
varies according to age. For adults (>18 years of age),
1440 ELISA units (EL.U.) per dose are given in a two-dose
schedule 6-12 months apart. For children and adolescents
(2 to 18 years of age), 360 EL.U. per dose are given in a
three-dose schedule at 0, 1, and 6-12 months. The vaccine
should be given by intramuscular injection into the deltoid
muscle. Protective levels of antibody to HAV (anti-HAV)
develop among 94%-100% of vaccinated persons within
1 month after administration of the first dose. A second
dose results in protective levels of antibody among all
persons vaccinated, and is considered necessary for long
term protection. Estimates of antibody persistence suggest
protective levels of anti-HAV persist for >20 years.
Hepatitis B (HBV)
Most authorities believe that India falls in the
intermediate zone of HBV prevalence i.e., prevalence
between 2% and 7%.
8
Aproximately 5-10% of patients with
HBV infection become HbsAg carriers.
Groups with increased risk for HBV infection are
1
Medical, dental, laboratory workers with exposure to
human blood.
Past history of multiple blood transfusions. Infection
can occur with transfusion of blood or blood products,
though the risk of transmission has been reduced
significantly because of introduction of compulsory
HbsAg screening in blood banks. After screening of
blood donors for HbsAg is done, the risk of HBV
infection is about 2.8 cases per 1000 units transfused.
9
Hemophiliacs, nearly one third of the hemophilic
patients have serologic evidence of hepatitis B infection
as a result of exposure to repeated blood transfusions.
10
Fig. 2 : Hepatitis A serology
1
Reprinted with permission from : Rabin L. Hapatitis. In: Mandell GM, editor in Chief, Atlas of Infectious
Diseases volume VII, Philadelphia : Churchill Livingstone, 1996, 2.01-2.54.
Reprinted with permission from: Kawai H, Feinstone SM. Acute viral Hepatitis. In Mandell GL, Bennett JE,
and Dolin R, editors, Mandell, Douglas and Bennetts Principles And Practices Of Infectious Diseases, 5
th
edition, Philadelphia: Churchill Livingstone, 2000, 1279-1297, 2000 with permission from Elsevier, Inc.
Fig. 3 : Hepatitis B Serology
3
0 1 2 3 4 5 6 12 2
Symptoms
HBeAg
HBV DNA(PCR)
HBsAg
ALT
AntiHBc
IgM AntiHBc
Anti HBe
Anti HBs
Months After Exposure
Jaundice
MALDE : VIRAL HEPATITIS AND ANAESTHESIOLOGISTS 267
Table - 2 : Hepatitis B virus serologic markers in different
stages of infection and convalescence.
12
HbsAg Anti - Hbs Anti - HbC HbeAg AntiHbe Diagnostic interpretation
IgG IgM
+ - - - + or - - Late incubation period of
Hepatitis B
+ - + + + - Acute Hepatitis B
- - + - - - HbsAg neg. acute hepatitis B
+ - + + + +or - - + Healthy HbsAg carrier
+ - + + + - or + + - Chronic hepatitis B
- + + + + +or - - + HBV infection in recent past
- + or - + or - - - - HBV infection in distant past
- + + - - - - Recent HBV vaccination
Reprinted with permission from : Robinson WS. Hepatitis B Virus and Hepatitis
D Virus. In Mandell GL, Bennett JE, and Dolin R, editors, Principles And Practices Of Infectious Diseases,
4
th
edition, New York: Churchill Livingstone, 1995, 1406-1439, 1995 with permission from Elsevier, Inc.
HbsAg is detected by enzyme immunoassay (EIA).
Recently there are kits available for rapid detection of
HbsAg and HbeAg. In a study comparing with the EIA
method, the rapid test was highly sensitive and accurate for
the detection of HbsAg although somewhat less sensitive
and specific for detection of HbeAg.
13
Prophylaxis against HBV
Plasma derived and recombinant HBV vaccines are
available. The essential immunogen in both is HbsAg. It
stimulates the production of anti - Hbs. Anti - Hbs levels
of 10 mIUml
-1
or higher are thought to be seroprotective.
6,7
Recombinant vaccines, Engerix-B

(20 mgm) and Recombivax

HB

(10 mgm) administered in 3 dose schedules at 0, 1 and

6 months utilizing deltoid site are highly immunogenic. A
combination hepatitis A and hepatitis B vaccine, Twinrix

,
is also licensed for persons aged >18 years old.
Seroprotective levels are achieved in 95% or more patients.
Post vaccination testing to determine antibody response to
vaccination is not necessary for healthy juveniles and adults.
For immunocompromised persons (e.g., hemodialysis patients
or HIV-infected) and persons with continued known exposure
to HBV infection (e.g., infants born to HbsAg-positive
mothers, sex partners of HbsAg-positive persons, or health-
care workers), testing is needed to verify response to
vaccination and the need for possible revaccination. The
duration of vaccine-induced antibody and protection from
hepatitis B virus (HBV) infection has been evaluated among
vaccinated infants, juveniles, and adults. Studies indicate
that although loss of detectable anti-HBs has ranged from
13% to 60% by 9-15 years after vaccination, immune memory
provides protection from HBV infection, and protection
remains intact for >15 years, the longest period for which
follow up data are available. Because of the long duration
of protection afforded by the three dose vaccine series,
booster doses of vaccine are not needed among vaccinated
immunocompetent juveniles or adults.
14
Adverse reactions associated with hepatitis B
vaccine include pain at the injection site (3%-29%) and a
temperature >37.7

C (1%-6%), although these effects are

reported no more frequently among vaccine recipients than
among placebo recipients in controlled trials. Anaphylaxis
has been reported in 1/600,000 vaccine recipients; however,
no deaths have been attributed to vaccination. A number of
case reports and case series have claimed an association
between hepatitis B vaccination and serious adverse health
events (e.g., multiple sclerosis); however, these have not
been proven by other epidemiologic studies.
7
Each year, approximately 600,000 HBV related
deaths occur worldwide.
15
An estimated 93% of these
deaths result from the chronic sequelae of HBV infection
i.e. cirrhosis and hepatocellular carcinoma (HCC).
Approximately 21% of HBV related deaths result from
infection acquired in the perinatal period and 48% from
infection acquired in early childhood (age <5 years).
Therefore, vaccination of infants and children is the
highest priority for hepatitis B vaccination programs.
Three doses of hepatitis B vaccine are 90%-95%
efficacious in preventing HBV infection and its chronic
sequelae. To prevent perinatal HBV transmission, the first
dose of vaccine should be administered within the first
24 hours after birth.
15
In 1992, the World Health Organization (WHO)
set a goal for all countries to integrate hepatitis B
vaccination into their universal childhood vaccination
programs by 1997. Goals for global hepatitis B vaccination
are for the vaccine to be introduced in all countries by
2007 and for coverage with the 3 dose hepatitis B vaccination
series to reach 90% by 2010.
15
To characterize the
epidemiology of acute hepatitis B in the United States,
CDC analyzed data for 1990-2002. The incidence of
acute hepatitis B declined 67%, from 8.5 to 2.8 per
100,000 population. This decline was greatest among
children and adolescents, indicating the effect of routine
childhood vaccination.
16
After implementation of universal
infant hepatitis B vaccination in Taiwan, the incidence
of HCC among children declined from 0.7 to 0.36 per
100,000.
17
As of May 2003, a total of 151 (79%) of 192
WHO member states had adopted universal childhood
hepatitis B vaccination policies, including six that have
policies for vaccinating adolescents. Of the 137 member
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2004 268
states that have adopted universal childhood hepatitis
B vaccination and for which data are available, 76 (55%)
have a policy for administering the first dose of vaccine
soon after birth.
15
Hepatitis B immunoglobulin (HBIG): HBIG is
prepared from human plasma known to contain a high titer
of antibody to HbsAg (anti-HBs). The plasma from which
HBIG is prepared is screened for HbsAg and antibodies to
HIV and HCV. The process used to prepare HBIG
inactivates and eliminates HIV from the final product. Since
1996, the final product has been free of HCV RNA as
determined by the polymerase chain reaction (PCR). No
evidence exists that HBV, HCV, or HIV has ever been
transmitted by HBIG commercially available in the United
States. It provides passive immunity to those with acute
exposure to HbsAg positive blood. After use there is
detectable level of circulating anti - Hbs, which persist for
three months.
18,19
Dosage in adults 1000-2000 IU IM,
children 32-48 IUkg
-1
within 7 days (preferably within
48 hours of exposure) and in neonates initial dose is 100-
200 IU. The first dose should be administered within 5 days
of birth. The booster dose should be 32-48 IUkg
-1
2-3 months
after the initial dose.
Infants born to HbsAg positive mothers should receive
HBV vaccine and HBIG (0.5 ml), both within 12 hours of
birth. Protective efficacy exceeds 95%.
Prophylaxis for HBV During Pregnancy:
19
No
apparent risk exists for adverse effects to developing fetuses
when hepatitis B vaccine is administered to pregnant women.
HBIG is not contraindicated for pregnant or lactating women.
Short term therapy with lamivudine may prevent perinatal
transmission in pregnant women with high HBV DNA
levels.
20
Chronic hepatitis : Japanese researchers studied the
long-term impact of acute hepatitis B on the liver and found
that occult HBV infection persists in the liver and is
accompanied by abnormal liver histology for a decade after
complete clinical recovery from acute hepatitis B.
21
Persistent carriage of hepatitis B is defined as the presence
of HbsAg in serum for >6 months.
22
Chronic hepatitis
B virus (HBV) infection affects an estimated 350 million
persons globally.
23
The rate of progression from acute to
chronic HBV is ~90% for perinatal infection, but <5%
for adult infection.
24
There are over 45 million carriers of
HBV in India and 80 % of the cases progress towards liver
cancer.
25
Progression to cirrhosis and liver cancer occurs in
patients with chronic HBV who have active viral replication
characterized by presence in the serum HBV DNA. In
chronic HBV patients with raised ALT level, the presence
of HbeAg should be considered a surrogate marker of HBV
DNA.
26
Liver biopsy assesses degree of inflammation and
fibrosis. In the future, universal HBV vaccination is likely
to decrease the burden of cirrhosis and liver cancer from
this disease.
Therapy of chronic hepatitis B : The aim of
treatment is to suppress viral replication and eliminate the
virus. Endpoints of treatment are normalization of ALT
levels and elimination of HbeAg and HBV DNA from the
blood.
22
The goal of interferon (IFN) therapy is suppression
of viral replication or elimination of infection. It is successful
in 25% to 40% of cases.
24
Response to IFN therapy results
in a prolonged clinical remission with an increased rate of
HbsAg seroconversion and improved liver histology.
27
It
increases survival and reduces the risk of developing HCC.
27
Disadvantages are that it needs prolonged therapy,
contraindications and side effects are many, and treatment
is costly.
Lamivudine a nucleoside analogue inhibiting viral
replication is effective in patients who respond poorly to
IFN. Several studies have demonstrated the efficacy of
lamivudine in patients with chronic hepatitis B with
seroconversion rates of 18%, 29% and 40% after one, two
and three years respectively.
22
Most responses are durable.
It is well tolerated; however, it is associated with a high
incidence of resistance and mutations in the virus. There is
little data to support combination of interferon and
lamivudine at this time.
Adefovir, famciclovir, emtricitabine, entecavir, and
thymosin are antiviral agents that have been shown to have
activity against HBV and are at various phases of clinical
efficacy evaluation and can result in significant improvement.
Adefovir has been demonstrated to be effective in patients
with chronic hepatitis B who have experienced resistance
to lamivudine.
22
Additional morbidity from other hepatic insults
can be reduced through hepatitis A vaccination, alcohol
reduction counseling, and risk reduction education.
Hepatitis C virus (HCV)
It is responsible for most of the cases of post
transfusion hepatitis, the half of who develop chronic liver
disease. Anti - HCV, a marker of HCV infection is present
in 0.5% of blood donors with normal aminotransferases
and in 44% with increased levels. Anti - HCV is used to
screen blood donors, although the test is not sensitive, and
seroconversion may be delayed for three months or longer.
28
MALDE : VIRAL HEPATITIS AND ANAESTHESIOLOGISTS 269
In a community based study in West Bengal, India
prevalence of HCV infection (HCV antibody positive) was
found to be 0.87%.
29
The predominant risk factors for HCV
are IV drug use, tattoos, exposure to blood products and
occupational risk. Nosocomial transmission of HCV is well
documented, especially in haemodialysis patients (24% in
one study).
30
Most of the cases are anicteric. Following acute
HCV infection, a lag period of 2-3 months occurs before
anti HCV is detectable in serum. ELISA for anti - HCV
detect the immune response to the virus and hence is less
sensitive, compared to methods like PCR, which detect the
viral genome directly. Usually infected patients are detected
following the finding of raised AST/ALT during a medical
check up or following manifestations of chronic hepatitis
or hepatocellular carcinoma.
28
Short term (4 weeks) IFN
treatment of patients with acute hepatitis C may be
associated with satisfactory results, if initiated at an early
stage of the disease.
31
No pre exposure or post exposure prophylaxis is
available. Anti - HCV positive persons should not donate
blood, body organs, other tissue, or semen or share personal
articles such as toothbrushes and razors that could be
contaminated with blood. The risk of perinatal transmission
appears to be low (<10%). At the present time, there is
no evidence to support advising against pregnancy or
breastfeeding based on anti-HCV status alone, or to advice
any special treatments or precautions for pregnant women
or their offspring.
32
Therapy of chronic HCV: Persons with hepatitis C
should be counseled to avoid alcohol, because its use
(>10 gday
-1
for women and >20 gday
-1
for men) has been
associated with more rapid progression to cirrhosis, which
puts patients at higher risk for HCC. HCV positive persons
benefit from evaluation for the presence and severity of
chronic liver disease. The role of IFN treatment in acute
HCV infection is under study. Antiviral therapy (ribavirin)
is recommended for persons with persistently elevated
ALT levels, detectable HCV RNA, and a liver biopsy that
indicates either portal or bridging fibrosis or moderate
degrees of inflammation and necrosis. No clear consensus
exists on whether to treat patients with persistently normal
serum transaminases.
32
Liver transplantation is indicated in
patients with end stage liver disease.
Hepatitis D (HDV or delta infection)
HDV is an incomplete virus, which requires the
helper function of hepatitis B virus. Patients who develop
delta infection are HbsAg positive.
Two types of infection persists
1. Co infection along with HBV : Acute delta infection
is self limiting, because it cannot outlive HBs
antigenemia. However, the attack may be fulminant.
2. Super infection : An individual chronically infected
with HBV may become super infected with HDV.
This can accelerate the course of chronic disease or
render previously asymptomatic disease apparent.
HDV prevalence is low in India.
1
HDV is diagnosed
by the presence of delta antigen or IgM antibody to
delta in the serum. Successful vaccination against HBV
will prevent HDV.
Hepatitis E (HEV)
It shares several key features with HAV. But unlike
HAV it can cause fatal fulminant hepatitis in pregnancy
(20% of cases occur in last trimester).
Arankalle et al
33
have performed a retrospective
seroepidemiologic study of 17 epidemics of water borne
hepatitis in India. They have confirmed that 16 of the
17 epidemics were caused at least in part by serologically
closely related hepatitis E viruses.
Hepatitis G (HGV): It causes persistent infection
with slow progression to chronic hepatitis. Coinfection with
HCV or HBV is possible. HGV infection may explain the
occurrence of non-A, non-B, and non-C post transfusion
hepatitis.
1
Anaesthetic considerations
Following emphasizes importance of proper
preoperative evaluation
1. In a Mayo clinic review,
34
following laparotomy in
unsuspected cases of viral hepatitis 9.5% mortality
and 11.9% significant morbidity i.e. nonlethal major
complications were noted.
2. Kings college, Londons review
35
seven patients of
acute hepatitis (viral or alcoholic) died following
laparotomy. Three of them died within four days of
surgery.
3. Liver function in patients with mild alcoholic hepatitis
after enflurane, nitrous oxide narcotic and spinal
anaesthesia were not altered when patients underwent
peripheral or superficial surgery.
36
However the same
may not be expected for upper abdominal or thoracic
surgery.
Misdiagnosis results from insufficient attention to
the history and physical findings and omission or
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2004 270
misinterpretation of LFTs.
37
If possible, elective surgery
should be postponed in patients with acute hepatitis because
of increase risk of morbidity and mortality. Both general
and regional anaesthetic, reduce hepatic blood flow by
30-50%. Total hepatic necrosis may be precipitated by
relative hypoperfusion in an already diseased liver.
In patients with chronic hepatitis, surgical risk
appears to correlate with the clinical, biochemical, and
histological severity of disease. Elective surgery has been
reported to be safe in patients with asymptomatic mild
chronic hepatitis (formerly chronic persistent hepatitis),
38
whereas patients with symptomatic and histologically severe
chronic hepatitis have an increased surgical risk, particularly
if hepatic synthetic or excretory function is impaired, portal
hypertension is present, or bridging or multilobular necrosis
is seen on liver biopsy specimens.
39,40
Moreover, patients
with severe histological activity have been reported to have
a higher rate of tumor recurrence after resection of
hepatocellular carcinoma compared with patients with mild
inflammation.
41
Following points to be remembered during
preoperative evaluation
The degree of rise of aminotransferases dictates the
management (figure 4).
42
Fig. 4: Algorithm for workup of unexpected abnormality in transaminase levels
42
Complete abstinence of alcohol is to be advised and
repeat LFT after a week. If repeat LFT is abnormal, then
do full workup i.e. CBC, platelet count, viral serologies,
autoantibodies, ceruboplasmin and iron studies. A right upper
quadrant USG is indicated in cases of persistent abnormality.
Alcoholic hepatitis patient can have other systemic
effects. Do blood sugar, BUN, Serum creatinine, X-ray
chest, ECG, coagulation studies, serum electrolytes.
In acute hepatic injury, prothrombin time and,

to a
lesser extent, total bilirubin are the best indicators

of severity
of disease.
Specific tests of viral markers should

be the initial
differential tests in both acute and chronic

hepatic injury;
when positive, they are also useful for monitoring
recovery from hepatitis B and C. (Figure 5)
2
and (table 3)
1
Table - 3 : Viral hepatitis-diagnostic markers.
1
Stage of HAV HBV HCV HDV HEV
infection
Acute disease IgM anti IgM anti Anti HD Ag Anti
HAV HbC HCV HEV
Chronic disease - HbsAg Anti HCV Anti HD -
Infectivity HAV HbeAg Anti HCV Anti HD HEV RNA
RNA HbsAg HCV RNA HDV RNA
HBV DNA
Recovery None Anti Hbe None None None
Anti - Hbs
Carrier state - HbsAg None Anti HD -
HDAg
Screen for Total anti Anti - Hbs None None Anti HEV
immunity HAV Total anti-
HbC
Reprinted with permission from: Rabin L. Hepatitis. In: Mandell GM, editor in Chief, Atlas of
Infectious Diseases, volume VII, Philadelphia: Churchill Livingstone, 1996, 2.01-2.54.
Drug induced hepatitis resolves after cessation of
drug.
Autoimmune hepatitis patients may be on steroids or
immunosuppressant.
Emergency surgery- Preoperative preparation and
intraoperative considerations
In patients with acute encephalopathy, sedatives
drugs as premedication may dramatically exacerbate
encephalopathy and therefore should be avoided. Drug
disposition may be difficult to predict because of the marked
differences in liver response to high and low extraction
drugs. For e.g. half life of meperidine is considerably
prolonged.
Reprinted with permission from: Maze M and Bass NM. Anesthesia and the Hepatobiliary System.
In: Miller RD, editor. Anesthesia, 5
th
edition. Philadelphia: Churchill Livingstone,
2000: 1960-72. 2000 with permission from Elsevier Inc.
MALDE : VIRAL HEPATITIS AND ANAESTHESIOLOGISTS 271
emergency LSCS. Clotting factors were replenished
prior to surgery. GA with low dose ketamine infusion
and high inspired oxygen fraction was used.
44
3. A case of reactivation of hepatitis B and development
of fulminant hepatic failure in pregnant hepatitis B
virus carrier was reported. This patient did not survive.
The author suggested early delivery and liver
transplantation, in case of fulminant hepatic failure.
45
4. In a German study, continuous ketamine drip
anaesthesia was used in 151 patients. Authors reported
that ketamine does not impaire hepatocellular
function.
46
Hepatitis and liver transplantation
Hepatitis recurrence is almost universal without
prophylaxis, if liver transplantation is performed for
VH.
47,48
Following can be used for prevention and treatment:
1. Long term treatment with HBIG.
2. IFN a, is also used, but rapid deterioration in liver
function can occur with immunologic flare. It can be
given after transplantation.
3. Lamivudine before and after transplantation.
4. Combination therapy with IFN a and ribavirin has
shown promise for patients with recurrent HCV after
transplantation.
Fulminant Hepatic failure (FHF)
Intensivist may have to manage FHF. Most common
causes of FHF are HBV or HCV. Mortality rate is 40-85%.
The goal is to temporize until hepatic regeneration occurs
or until transplantation can be performed. Prevention, timely
recognition and management of major complications are
crucial. These include hepatic encephalopathy, respiratory
failure, infections, profound coagulopathy, bleeding, renal
failure and cerebral edema. Complete recovery occurs after
surgery in most patients who undergo transplantation with
stage III or early stage IV encephalopathy; however, major
neurological complications can occur because of cerebral
edema in patients who have prolonged stage IV hepatic
encephalopathy before transplantation.
49
Personnel and staff protection
Hepatitis A virus
Nosocomial HAV transmission is relatively
uncommon. For practical purposes adults with acute HAV
can be assumed to be non infectious one week after the
onset of symptoms. In neonates, viral shedding has been
documented by using PCR for as long as six months after
onset of infection.
5,18

Suspicion of acute viral hepatitis based on: History, physical
examination, epidemiological situation
Elevated ALT/AST
Obtain viral serologies:
Anti-HAV IgM
HBsAg and Anti HBc IgM
Anti-HCV (EIA or RIBA)
Anti-HAV
IgM +
Anti-HBcIgM
+ HBsAg
Anti HCV Negative
serologies
- Acute
Hepatitis A
Acute
Hepatitis B
Acute HCV infection or
exacerbation of chronic
HCV infection
Suspicion of HDV
coinfection based on: Risk
factors (e.g. IVDA)
clinical s/o severe hepatitis
check anti HDV
Check HBsAg and
ALT/AST in
6-9 months
Consider non-viral etiologies
e.g. ischemia, toxins or other
infections etiologies
(e.g. CMV, EBV)
Anti HDV + HBsAg +
Abnormal ALT/AST
Consider HEV infection
of recent foreign travel
- HBV/HDV
coinfection
-chronic HBV
infection
Recheck anti HCV
in 3-6 months
Fig. 5 : Algorithm for further workup of suspected hepatitis case
2
Reprinted with permission from: Hsu H, Feinstone SM, Hoofnagle JH. Acute Viral Hepatitis. In Mandell
GL, Bennett JE, and Dolin R, editors, Principles And Practices Of Infectious Diseases, 4
th
edition, New
York: Churchill Livingstone, 1995, pp - 1136-1153, 1995 with permission from Elsevier, Inc.
Frequent blood glucose monitoring is needed to avoid
hypoglycemia. Acid base disturbance particularly respiratory
alkalosis may be profound. Electrolyte imbalance may
contribute to encephalopathy and appropriate therapy should
be initiated before the surgical procedure. Hypoxemia is a
frequent finding despite hyperventilation. Renal insufficiency
is common. If coagulopathy is present, surgical bleeding
may be severe. Correction with Vitamin K and FFP may
be indicated. Appropriately timed platelet transfusion may
aid to surgeon. They are prone to bacterial infection. So
proper asepsis is needed. The main goal is to maintain
hepatic blood flow at near normal levels. Isoflurane is the
inhalational agent of choice, as it has no deleterious effect
on hepatic circulation.
42
PaCO
2
should be maintained between
35-40 mmHg.
Few Reports on anaesthetic management for acute VH
Very few reports are available as only really emergent
surgeries are performed.
1. Propofol was used for induction and maintenance of
anaesthesia in a 4 year old girl with hepatitis A and
haematmesis. The anaesthetic was uneventful with no
post operative sequelae.
43
2. An elderly primigravida with severe acute VH,
complicated by GI bleeding, hypofibronogenemia,
thrombocytopenia and prolonged PT and PTTK required
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2004 272
Outbreak of HAV transmission has been reported in
ICUs.
4
Risk factors are because of practices that contribute
to fecal contamination of hands and practices that increase
hand to mouth contact (eating, drinking in ICU).
Routine use of vaccination for HCW is not
recommended. Immunoglobulin (0.02 mlkg
-1
) is only
recommended during outbreaks.
HCWs who become infected with HAV are advised
not to provide care to patients until seven days after the
onset of jaundice, which is the usual time, when viral
shedding and infectivity (in adults) decline to minimal levels.
Hepatitis B virus
Overt parenteral transmission
HBV is the most infectious out of HBV, HCV and
HIV. Infectious blood contains 10
6
infectious units per ml.
Even 0.04 ml blood may be enough to infect an
anaesthesiologist.
30
Infectivity to HbeAg positive blood may
be over 30% following needle stick injuries; whereas, for
HCV figure is 2-10%; For HIV, it is 0.36%. Hollow needles
are more dangerous than solid needles.
Inapparent parenteral transmission
It can be because of : Percutaneous inoculation
without overt needle puncture; Contamination of mucosal
surfaces with infective serum or plasma or secretions like
saliva, urine; Transfer of infective material to skin lesions
or mucous membranes via inanimate environmental surfaces
or contaminated medical devices.
5
Surfaces not visibly
contaminated with blood may also yield HbsAg. In blood,
HBV remains viable for more than a week after desiccation
at room temperature. Very high dilutions of HBV containing
blood can transmit HBV.
30
About 1 in 500 of the adult population is a carrier
of HBV; some of them will be asymptomatic and their
carrier state will therefore not be realized.
18
Four outbreaks
of HBV and HCV infections occurred in outpatient health-
care settings.
50
The investigation of each outbreak suggested
that unsafe injection practices, primarily reuse of syringes
and needles or contamination of multiple dose medication
vials, led to patient to patient transmission. So for all patients,
universal precautions must be applied. i.e. wearing gloves;
use of plastic apron, mask, eye protection etc, when significant
spillage of blood may occur, avoidance of resheathing of
needles, disposal of needles in tough disposable bin, covering
of all cuts, abrasions with waterproof dressing, use of
disposable items, sterilization of nondisposable items,
cleaning of contaminated floor and surfaces with solution of
hypochlorite containing 10000 ppm available chlorine.
Protection of breathing system by filter is also recommended.
51
Agents to kill hepatitis virus include ethylene oxide,
steam, sodium hypochlorite 0.1% to 1% (bleach), activated
glutaraldehyde 2%, iodophores (0.05% free iodine) and
formaldehyde 10%.
30
Vaccination
Any person who performs tasks involving contact
with blood, blood contaminated body fluids, other body
fluids, or sharps should be vaccinated against hepatitis B.
Pre vaccination serologic screening for previous infection
is not indicated for persons being vaccinated because of
occupational risk, unless the health care organization
considers screening cost effective.
52
Various studies
53,54
have shown that 15-31% of
anaesthesiologists have serological evidence of prior exposure
to HBV. In fact, Fyman et al,
55
using more sensitive
serological markers found 49% anaesthesiologists positive
for HBV exposure. So vaccination by using three injections
of either Engirix-B (20 mgm), or Recombivax-HB (10 mgm)
at 0, 1 and 6 months are recommended. Post vaccination
screening for anti - Hbs should be done with in 1 to 6
months after third dose of vaccine. There are very few
genuine non responders. They also respond to booster doses.
Non responder can also continue to practice.
6,18, 30
Rules of practice : HbeAg is associated with high
concentration of virus. These individuals with HbeAg are
highly infectious and hence are not allowed to perform
exposure prone procedure.
5
Postexposure prophylaxis (PEP) should be considered
for any percutaneous, ocular, or mucous membrane exposure
to blood in the workplace and is determined by the HbsAg
status of the source and the vaccination and vaccine response
status of the exposed person.
56
Post exposure prophylaxis
for needle stick injury is given in table 4.
57
Hepatitis C virus
The risk of HCV transmission after a needle stick
contaminated with blood from an antiHCV positive source
is estimated to be ~10% based on PCR technique.
5
So use
of barrier precautions and personal protective devices is
must.
The role of the environment in the transmission of
HCV is unimportant because, compared with HBV, HCV
is relatively fragile and rapidly degraded in serum at room
temperature.
5
Anti HCV test has limitation in detecting HCV
infection, because sensitivity is low and there may be delay
in appearance of anti HCV. Confirm all anti - HCV results
reported positive by enzyme immunoassay using supplemental
anti - HCV testing (e.g., recombinant immunoblot assay)
MALDE : VIRAL HEPATITIS AND ANAESTHESIOLOGISTS 273
Table - 4 : Prophylaxis after parenteral exposure to HBV
57
Status of exposed Treatment Comment
person
Unvaccinated One dose of HBV A substantial proportion of HCW
at high risk for exposure to blood
hyperimmunoglobulin; (10-40% insome studies) may be
Vaccine (primary series) immune or may be chronic
carriers of HBV as a consequence
of natural infection. Screening for
antibody to hepatitis B core
antigens will identify these persons.
If the test result is available within
24-72 hours after exposure,
unnecessary treatment can be
avoided.
Known response
to previous
vaccination.
Serum anti - HbsAg
titre >10 mIUml
-1
No treatment
Serum anti - HbsAg 1 booster dose of
titre <10 mIUml
-1
vaccine
Serum anti - HbsAg 1 booster dose of
titre unknown vaccine
No response to 2 doses of HBV If reimmunization with a further
previous hyperimmunoglobulin one or more doses of vaccine has
vaccination 1 mo apart not been attempted, HBV vaccine
(upto 3 doses) should be provided.
Previous vaccinated
but response
unknown
Serum anti - HbsAg
titre 10mIUml
-1
No treatment Consider giving a second dose of
Serum anti - HbsAg HBV hyperimmunoglobulin in 1
titre <10 mIUml
-1
1 dose of HBV month if risk factors for a lack of
hyperimmunoglobulin, response are present.
1 booster dose of vaccine.
Serum anti - HbsAg 1 booster dose of vaccine Consider giving HBV
titre unknown hyperimmunoglobulin if risk
factors for a lack of response
are present.
Reprinted with permission from: Geberding JL: Management of Occupational
Exposure to Blood Borne Viruses. New England Journal of Medicine 1995; 332, 444.
Immunoglobulin is not effective for prevention for
HCV.
The following are recommendations for follow up
of occupational HCV exposures: a) Perform anti - HCV
testing for the source, b) Baseline and 6 months follow - up
testing of the exposed person for anti - HCV and ALT
activity.
Ig and antiviral agents are not recommended for
PEP after exposure to HCV positive blood. In addition, no
guidelines exist for administration of therapy during the
acute phase of HCV infection. However, limited data indicate
that antiviral therapy might be beneficial when started early
in the course of HCV infection.
To date, the CDC and other advisory groups have
not made recommendations regarding restrictions of HCWs
who are anti - HCV positive and instead suggest full aseptic
precautions by HCWs while performing invasive
procedures.
5
To provide optimum care to a patient with hepatitis,
anaesthesiologist must understand epidemiology as well
as acute and chronic effects of the disease. One should also
become familiar with and follow the recommended
precautions for self and public protection, while caring for
the patient with hepatitis.
References
1. Rabin L. Hepatitis. In: Mandell GM, editor in Chief, Atlas
of Infectious Diseases, volume VII, Philadelphia: Churchill
Livingstone 1996; 2.01-2.54.
2. Hsu H, Feinstone SM, Hoofnagle JH. Acute viral Hepatitis.
In Mandell GL, Bennett JE, and Dolin R, editors, Principles
And Practices Of Infectious Diseases, 4
th
edition, New York:
Churchill Livingstone, 1995; 1136-1153.
3. Kawai H, Feinstone SM. Acute viral hepatitis. In: Mandell
GL, Bennett JE, Dolin R editors. Principles and Practice of
Infectious Diseases. 5
th
edition, Philadelphia: Churchill
Livingstone, 2000; 1280-282.
4. Hanna JN, Loewenthal MR, Negel P, Wencke DJ. An Outbreak
of Hepatitis A in an Intensive Care Unit. Anaesth Intens Care
1996; 24: 440-44.
5. Tablan OC, Bolyaed EA, Shapiro CN, Williams WW. Personnel
Health Services. In Benett JV and Brachmann PS, editors
Hospital Infections 4
th
edition, Philadelphia: Lipincott Raven,
1998; 33-37.
6. Koff R. Hepatitis Vaccines. In: Schiff ER, Sorrell MF, Maddrey
WC, editors. Schiffs Diseases of the Liver, 8
th
edition,
Philadelphia: Lippincott-Raven 1999; 897-905.
7. Centers for Disease Control. Hepatitis A and B Vaccines.
MMWR 2003; 52(RR01): 34-36.
8. Lodha R, Jain Y, Anand K, Kabra SK, Pandav CS. Hepatitis
B in India: A Review of Disease Epidemiology. Indian
Pediatrics 2001; 38: 349-371.
9. Hollinger FB, Mosley JW, Szmuness W. Non-A, Non-B
hepatitis following blood transfusion, risk factors associated
with donor characteristics. In: Szmuness W, Alter HJ, Maynard
JE, eds. Viral hepatitis1981 International Symposium.
Philadelphia: Franklin Institute Press; 1982: 361-76.
10. Troisi CL, Hollinger FB, Hoots WK, Contant C, Gill J, Ragni
M. et al. A multicenter study of viral hepatitis in a United
States hemophilic population. Blood 1993; 81: 412-18.
11. Nayak NC, Panda SK, Zuckerman AJ, Bhan MK, Guha DK.
Dynamics and impact of perinatal transmission of Hepatitis B
virus in North. India J Med Virol 1987; 21: 137-45.
12. Robinson WS. Hepatitis B virus and Hepatitis D virus. In:
Mandell GL, Bennett JE and Dolin R, editors. Principles and
INDIAN JOURNAL OF ANAESTHESIA, AUGUST 2004 274
Practices of Infectious Diseases. Fourth edition. New York:
Churchill Livingstone, 1995: 1406-39.
13. DT Lau and others. A rapid immunochromatographic assay
for hepatitis B virus screening. Journal of Viral Hepatitis
2003; 10(4): 331-34.
14. Banatvala JE and van Damme P. Hepatitis B vaccine -
do we need boosters? Journal of Viral Hepatitis 2003; 10(1):
1-6.
15. Centers for Disease Control. Global Progress Toward Universal
Childhood Hepatitis B Vaccination, 2003. MMWR 12, 2003;
52(36): 868-70.
16. Centers for Disease Control. Incidence of Acute Hepatitis B
United States, 1990-2002. MMWR 2004; 52(51): 1252-4.
17. Chang MH, Chen CJ, Lai MS. et al. Universal hepatitis B
vaccination in Taiwan and the incidence of hepatocellular
carcinoma in children. N Engl J Med 1997; 336: 1855-9.
18. Valenti WM. Selected viruses of Nosocomial Importance. In:
Benett JV and Brachman PS, editors. Hospital Infections 4
th
edition, Philadelphia: Lippincott Raven 1998; pp 647-51.
19. Centers for Disease Control. Updated U.S. Public Health Service
Guidelines for the Management of Occupational Exposures to
HBV, HCV, and HIV and Recommendations for Postexposure
Prophylaxis: MMWR 29, 2001; 50(RR-11): 1-42.
20. Van Zonneveld M et al. Lamivudine treatment during pregnancy
to prevent perinatal transmission of hepatitis B virus infection.
Journal of Viral Hepatitis 2003; 10(4): 294-98.
21. Yuki N, Nagaoka T, Yamashiro M et al. Long term histologic
and virologic outcomes of acute self limited hepatitis B.
Hepatology 2003; 37(5): 1172-9.
22. Davis GL. Update on the Management of Chronic Hepatitis
B. Reviews In Gastroenterological Disorders 2002; 2(3): 115.
23. Lavanchy D. Hepatitis B virus epidemiology, disease burden,
treatment, and current and emerging prevention and control
measures. Journal of Viral Hepatitis 2004; 11(2): 97-107.
24. Raj V. Treatment of Hepatitis B. Clinical Cornerstone 2001;
3(6): 24-36.
25. Correspondent. Government to extend Hepatitis B vaccination
programme. Indian Express 1998 December 5, Saturday.
26. Hussain AB et al. Correlation of HBV DNA PCR and HbeAg
in hepatitis carriers. Journal of the College of Physicians and
Surgeons Pakistan 2004; 14(1).
27. Van Zonneveld

M, Honkoop

P et al. Long-term follow-up of
alpha-interferon treatment of patients with chronic hepatitis
B. Hepatology 2004; 39: 804-10.
28. Liddle C. Hepatitis C. Anaesthesia and Intensive Care 1996;
24: 180-83.
29. Chowdhury A, Santra A, Chaudhuri Susmista et al. Hepatitis
C Virus Infection in the General Population: A Community-Based
Study in West Bengal, India. Hepatology 2003; 37: 802-09.
30. Favero MS, Alter MJ, Tokars JI, Arduino MJ. Dialysis
Associated Infections and their Control. In: Benett JV and
Brachman PS, editors. Hospital Infections, 4
th
edition,
Philadelphia: Lippincott-Raven, 1998; 370-7.
31. Nomura

H, Sou

S, Tanimoto

H et al. Short-term interferon-
alfa therapy for acute hepatitis C: A randomized controlled
trial. Hepatology 2004; 39: 1213-19.
32. Centers for Disease Control. Prevention and Control of
Infections with Hepatitis Viruses in Correctional Settings.
MMWR 2003; 52(RR01): 1-33.
33. Arankalle VA, Chadha MS, Tsarev SA et al. Seroepidemiology
of Water-Borne Hepatitis in India and Evidence for a Third
Enterically Transmitted Hepatitis Agent. Proceedings of the
National Academy of Sciences 1994; 91: 3428-32.
34. Harville DD, Summerskill WHJ. Surgery in Acute Hepatitis.
Causes and effects. JAMA 1963; 184: 257-61.
35. Powell Jackson P, Greenway B, Williams R. Adverse Effects
of exploratory laparotomy in patients with unsuspected liver
disease. Br J Surg 1982; 69: 449-51.
36. Zinn SE, Failey B, Glenn JD. Liver function in Patients
with Mild Alcoholic Hepatitis, after Enflurane, Nitrous Oxide
Narcotic, and Spinal Anesthesia. Anesth Analg 1985; 64: 487-
90.
37. Marx G, Nagayoshi M, Shoukas JA, Wollman SB. Unsuspected
Infectious Hepatitis in Surgical Patients. JAMA 1968; 205:
793-95.
38. Runyon BA. Surgical procedures are well tolerated by patients
with asymptomatic chronic hepatitis. J Clin Gastroenterol
1986; 8: 542-44.
39. Hargrove MD. Chronic active hepatitis: possible adverse
effect of exploratory laparotomy. Surgery 1970; 68: 771-73.
40. Higashi H, Matsumata T, Adachi E, Taketomi A, Kashiwagi
S, Sugimachi K. Influence of viral hepatitis status on
operative morbidity and mortality in patients with primary
hepatocellular carcinoma. Br J Surg 1994; 81: 1342-45.
41. Ko S, Nakajima Y, Kanehiro H, Hisanaga M, Aomatsu Y, Kin
T, Yagura K et al. Significant influence of accompanying
chronic hepatitis status on recurrence of hepatocellular
carcinoma after hepatectomy: result of multivariate analysis.
Ann Surg 1996; 224: 591-95.
42. Maze M, Bass NM. Anesthesia and the Hepatobiliary System.
In: Miller RD, editor. Anesthesia 5
th
edition. Philadelphia:
Churchill Livingstone 2000; 1960-72.
43. Shaw A. The use of propofol in a child with hepatitis A.
Anaesthesia 1993; 48: 591-92.
44. Schaer HM, Marx GF. Anaesthesia for cesarean section in a
patient with acute viral hepatitis. Anaesthesist 1978; 27: 553-6.
45. Sato T, Hashiguchi A, Mitsuse T. Anesthesia for Cesarean
Delivery in a Pregnant Woman with Acute Hepatic Failure.
Anesth Analg 2000; 91: 1441-42.
46. Schaps D, Hauenschild E. The use of ketamine in patients
with liver damage. Anaesthesist 1977; 26(4): 172-75.
47. Shaw Stiffel TA. Chronic Hepatitis. In: Mandell GL, Bennett
JE, Dolin R editors. Principles and Practice of Infectious
Diseases. 5
th
edition, Philadelphia: Churchill-Livingstone,
2000; 1305-16.
MALDE : VIRAL HEPATITIS AND ANAESTHESIOLOGISTS 275
48. Rubin RH, Fishman JA. Infection in Transplant Recipient. In:
Benett JV and Brachman PS, eds. Hospital Infections, 4
th
edition, Philadelphia: Lippincott-Raven 1998; 734-5.
49. Mc Donald M, Ralph DD, Carithers RL Jr. Severe Liver
Disease. In: Shoemaker, Ayres, Grenvik, Holbrook, editors.
Textbook of critical care, 3
rd
edition, Philadelphia: W. B.
Saunders Company, 1995; 991-1002.
50. Centers for Disease Control. Transmission of Hepatitis B
and C Viruses in Outpatient Settings New York, Oklahoma,
and Nebraska, 2000-2002. MMWR 2003; 52(38): 901-06.
51. Knoblanche GK. Revision of the Anaesthetic Aspects of an
Infection Control Policy Following Reporting of Hepatitis C
Nosocomial Infection. Anaesth Intens Care 1996; 24: 169-72.
52. Centers for Disease Control. Immunization of Health Care
Workers. MMWR 1997; 46 (RR-18): 22-23.
53. Denes AE, Smith JL, Maynard JE et al. Hepatitis B infections
in physicians: Results of a nationwide seroepidemologic
survey. JAMA 1978; 239: 210-12.
54. Janzen J, Tripatzis I, Wagner U et al. Epidemiology of hepatitis
B surface antigen (HBs Ag) and antibody to HBs Ag in hospital
personnel. Journal of Infectious Diseases 1978; 137: 261-65.
55. Fyman PN, Hartung J, Weinbers S et al. Prevalence of hepatitis
B viral markers in the anesthesia staff of a large inner city
hospital. Anesthesia and Analgesia 1984; 63: 433-6.
56. Centers for Disease Control. Updated U.S. Public Health
Service Guidelines for the Management of Occupational
Exposures to HBV, HCV, and HIV and Recommendations
for Postexposure Prophylaxis: MMWR June 29, 2001;
50(RR-11): 1-42.
57. Geberding JL. Management of Occupational Exposure to
Blood Borne Viruses. New Eng J Med 1995; 332: 444.
RESPIRATORY RATE (F)
Description
The respiratory rate or frequency of breathing
(f), is the number of breaths per unit of time, usually
per minute.
Technique
The respiratory rate may be determined by
counting the chest movements or the excursions of a
spirometer. Counting the rate for several minutes and
taking an average produces a more accurate value than
shorter measurements.
Significance
The normal respiratory rate ranges from 10 to
20 breaths per minute. Increased demand for ventilation,
such as during exercise, usually results in increases in
the rate and depth of breathing, so that respiratory
frequency is often a good indicator of the stimulus to
ventilate.
Increases or decreases in the respiratory rate
are indication of a change in the ventilatory status.
Breathing frequency, when evaluated with the tidal
volume, may be used as an index of ventilation. Hypoxia,
hypercapnia, metabolic acidosis, conditions that cause
decreased lung compliance, and exercise all result in
increases in respiratory rate, in the presence of a normal
respiratory drive. Decreased breathing frequency is
common in central nervous system depression and in
CO
2
narcosis. Measurements of both tidal volume and
respiratory rate may be artifactually elevated in subjects
breathing through mouthpieces and other unfamiliar
breathing circuits, and/or using a nose clip.
It is quite essential for the anaesthesiologist to
differentiate between tachypenea and hyperventilation.
Tachypenea: Means an increase in the rate of
respiration without an increase in the depth of
respiration.The work of breathing is minimal.There is
also an mild increase in the pulmonary ventilation
(25%)
Hyperventilation:Means an increase in
ventilation out of propotion to carbondioxide
production.Seen in metabolic acidosis either due to
diabetic coma or renal failure.The work of breathing
is maximal.There is marked increase in the pulmonary
ventilation (75%).
Prof. Dr. M. Chandrasekhar
Prof. and HOD, Dept. of Physiology
Sri Jayendra Swamigal Institute of
Medical Sciences and Research,
Sri Kanchi Kamakoti Snakara Hosptial,
Cheran Nagar, Perumbakkam, CHENNAI 601 302
APPLIED PHYSIOLOGY