Download occupational exposure to hiv

31st October 2014
No. 26
Occupational Exposure to HIV and
Post Exposure Prophylaxis
NSY Padayachee
Moderator: CS Alphonsus
Discipline of Anaesthesiology and Critical Care
CONTENTS
INTRODUCTION ................................................................................................... 3
OCCUPATIONAL EXPOSURE TO HIV ................................................................ 4
RISK OF OCCUPATIONAL TRANSMISSION TO HIV ......................................... 4
POST EXPOSURE PROPHYLAXIS AND ITS RATIONALE ................................ 7
PEP CONSIDERED ON BASIS OF HIV PATHOGENESIS .................................. 8
PEP EFFICACY IN ANIMAL STUDIES ................................................................ 9
PEP EFFICACY IN HUMAN STUDIES ............................................................... 10
PEP TREATMENT FAILURE .............................................................................. 10
PEP DRUG REGIMENS ..................................................................................... 12
PEP TIMING AND DURATION ........................................................................... 13
ADVERSE EFFECTS, TOXICITY, AND DRUG INTERACTIONS ....................... 14
LEGAL FRAMEWORK OF PEP ......................................................................... 16
PREVENTATIVE STRATEGIES ......................................................................... 16
STEP WISE APPROACH TO AN OCCUPATIONAL EXPOSURE ..................... 18
GENERAL MEASURES ..................................................................................... 18
EVALUATION OF EXPOSURE .......................................................................... 18
TESTING OF THE SOURCE PATIENT .............................................................. 19
REPORTING OF THE EXPOSURE .................................................................... 19
COUNSELLING SUPPORT ................................................................................ 19
ASSESSMENT OF THE HEALTH CARE WORKER .......................................... 20
CONCLUSION .................................................................................................... 21
REFERENCES.................................................................................................... 22
Page 2 of 24
OCCUPATIONAL EXPOSURE TO HIV AND POST EXPOSURE PROPHYLAXIS
INTRODUCTION
Exposure to the human immunodeficiency virus(HIV) in an occupational setting,
creates a small but possible risk of infection(1) . Health care workers(HCW’s) are at
increased risk of contracting HIV. This is due to exposure to potentially
contaminated bodily fluids in association with inadequate safety precautions(1) .
According to the World Health Organisation(WHO), there are 1000 new HIV
infections per annum due to occupational exposure which are estimated from 3
million percutaneous injuries among 35 million HCW’s worldwide.
More than 90 % of these exposures occur in the resource constrained countries of
the developing world(2). The highest incidence of exposure being in sub-Saharan
Africa and Asia - 9 exposures/health worker/year(3.4).
The actual risk of occupational transmission of HIV is greater than usually
reported for the following reasons:
(a) suboptimal monitoring and surveillance of occupational exposures in the
developing world;
(b) higher prevalence of HIV; and
(c) inadequate safety precautions and risk reduction strategies(5).
In light of the growing HIV and AIDS epidemic, protecting health care workers in
developing countries where basic medical care is inadequate, proves to be a
formidable challenge. Human resources are depleted due to occupational
exposure to HIV. This is not only as a direct result of transmission and related
morbidity but also the psychological stressors and anxiety regarding safety and
lack of support in preventing the risk(6).
Primary preventative strategies should form the mainstay of prevention against
occupational exposure to HIV. Health care workers who sustain a significant
exposure to bodily fluids that are known or likely to be contaminated should
receive post exposure prophylaxis(6).
Page 3 of 24
OCCUPATIONAL EXPOSURE TO HIV
An occupational exposure can be defined as a percutaneous injury ( cut with a
sharp instrument or needle stick) , exposure of mucosal surfaces or broken skin (
chapped skin , abraded skin , dermatitis ) or intact skin ( when contact is
prolonged or involves extensive areas of skin ) with potentially infectious blood,
tissues or bodily fluids (7) .
These fluids include:
(a) bodily fluids visibly contaminated with blood, semen, vaginal secretions and
breast milk - these substances are associated with HIV transmission;
(b) cerebrospinal fluid, pleural fluid, pericardial fluid, synovial fluid, perito
neal
fluid and amniotic fluid - these fluids carry an undetermined risk of HIV
transmission; and
(c) HIV containing lab specimens (unfixed organs and tissues, organ cultures and
blood, concentrated virus) (7)
Other bodily fluids such as urine, saliva, tears, sputum, nasal secretions, sweat,
faeces and gastric content are non-infectious unless visibly blood stained (7).
In the occupational setting a broad range of personnel are exposed to the risk of
HIV infection. These are categorised as health care workers and non-health care
workers. Health care personnel comprise of medical doctors, nurses, traditional
healers, paramedics, dentists. Non-health care personnel comprise of bar
bouncers, educators, sex workers and firemen(8).
RISK OF OCCUPATIONAL TRANSMISSION TO HIV
The first reported case of a health care worker contracting the HIV infection was
documented in 1984 following a needle stick injury(9). According to 23 prospective
studies conducted globally the risk of HIV infection following percutaneous injury
with HIV infected blood is 0.3% and 0.09% following mucocutaneous
exposure(7,10).
The risk of HIV transmission following non-intact skin exposure has not been
quantified but is estimated to be less than the risk for mucocutaneous exposure
(11)
. Whilst the risk of transmission following exposure to fluids or tissues other
than HIV infected blood, which has not been quantified, is most likely lower than
blood exposure (12). The risk of HIV transmission varies with the type and severity
of exposure.
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It is important to note that the statistics above are calculated from data acquired
from developed countries. This is due to a lack of monitoring and reporting in the
developing world. Occupational exposures reported from North America and
Western Europe comprise 90% of cases, whilst only 4% of cases were reported
from sub-Saharan Africa where approximately 70% of the worlds HIV infected
population live(1).
The risk of occupational transmission of HIV infection depends on multiple factors
relating to the health care worker, the source patient and the circumstances of
exposure(1).
Genetic variation maybe responsible for reduced susceptibility to HIV infection.
This can be seen in high risk groups of prostitutes and homosexual men who
remain HIV free despite frequent exposure(13).This reduced susceptibility to HIV
infection is associated with a deletion in the CCR5 co-receptor which inhibits viral
entry into the cell thus creating a relative resistance to HIV infection(14).
Cardo et al. (15) has shown the risk of HIV transmission from a percutaneous injury
is enhanced under the following circumstances :
(a) a deep injury;
(b) injury with device that was visibly contaminated with blood;
(c) injuries where needle placed directly into artery or vein; and
(d) hollow bore and thick needle.
These above features are consistent with a transfer of a greater quantity of blood
from the source patient to the exposed health care worker.
Other factors associated with increased risk of transmission following occupational
exposure include :
(1) prevalence of infection in the specific population : risk of occupational
exposure is substantially increased due to high prevalence of HIV in
developing countries;
(2) frequency of activities capable of transmitting the infectious agent: unsafe
practices together with cultural influence regarding injections increase the risk
of occupational injuries in developing countries;
(3) nature and efficacy of transmission of exposure : percutaneous injury has an
increased risk of transmission compared to mucocutaneous or skin exposures;
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(4) virus present in contaminated fluid and viral load : greater number of patients
with primary HIV infection, advanced disease and high viral loads are present
in developing countries; and
(5) availability and efficacy of pre-exposure and post-exposure prophylaxis :
appropriate guidelines are still not available in some developing countries(16).
More than half a million health care workers (HCW’s) per year are documented to
be exposed to HIV in the USA, with in excess of 50% of exposures left unreported(8).
Data from Southern African countries are poor. Amongst the largest study
conducted in West African countries, 45% of HCW’s sustained at least one
accidental blood exposure, although over 60% of which went unreported(8).
In 2001, Chris Hani Baragwanath Hospital in Gauteng revealed that 69% of its
interns sustained at least one percutaneous injury. Whilst 45% of interns
sustained a mucocutaneous blood exposure(18). More than 60% of exposures
were unreported. A study conducted in 2002 revealed that 91% of needle stick
injuries were sustained amongst junior doctors at Tygerberg Hospital. The
majority of these injuries occurred “after hours “or on calls(19).
Occupational exposure to HIV was further highlighted by a study conducted in
Durban in 2000,in the department of Obstetrics and Gynaecology at King Edward
VIII Hospital. It revealed that 13% of staff reported injuries with HIV positive
patients. These injuries being percutaneous in 94% of cases. Majority of injuries
occurring during emergency surgery(65%), with the highest risk group being
registrars(60%)(5).
Page 6 of 24
Omrani S,Freedman A. Prophylaxis of HIV infection. British Medical Bulletin. 2005;73,74:93-105
POST EXPOSURE PROPHYLAXIS AND ITS RATIONALE
According to the World Health Organisation, post exposure prophylaxis refers to
the medical response instituted to prevent the transmission of blood -born
pathogens following a potential exposure to HIV(20). Post exposure prophylaxis
refers to interventions that aim to manage specific aspects of HIV exposure and
assists to prevent infection in the individual that is at risk(20). Services include first
aid, counseling including assessment of risk exposure, HIV testing, and
Page 7 of 24
dependent on outcome, a course of antiretroviral therapy with appropriate support
and follow up(20).
Post exposure prophylaxis is considered a medical emergency. Anti-retroviral
drugs must be available in all health care settings and at all times for
administration to employees following accidental exposure to HIV(21).
PEP is based on the following factors : (16)
(1) HIV infection pathogenesis, especially early in the course of infection;
(2) anti-retrovirals can prevent transmission of HIV based on biological plausibility;
(3) the risk benefit ratio of post exposure prophylaxis to exposed health care
workers; and
(4) proof of effectiveness of particular agents used for prophylaxis which may be
direct or indirect
HIV transmission has been shown to be significantly reduced by the post
exposure administration of anti-retroviral agents as seen in several clinical
studies. Although trials concerning efficacy of PEP were not randomised nor
placebo controlled, data obtained concerning benefit of its use are extrapolated
from animal, case control and PMTCT studies.(15,16,22).
PEP CONSIDERED ON BASIS OF HIV PATHOGENESIS
After the initial exposure there is a delay to systemic infection. Thus creating a
“window period “during which the initiation of post exposure anti-retroviral therapy
may inhibit or suppress viral entry into host cells and viral replication (16).
Experimental models of HIV infection have shown that local viral replication
occurs within 24 hours at the site of inoculation in tissue macrophages and
dendritic cells. This stimulates host cytotoxic T cells to kill infected target cells.
Failure to arrest viral replication at this stage, results in proliferation in regional
lymph nodes in the following 2 - 3 days followed by systemic dissemination
resulting in a viraemia in the next 3 - 5 days(23).
Owing to the rapid infection of target cells following viral inoculation of the host,
recommended antiretrovirals for PEP must have a rapid onset of action, a
multimodal mechanism of action and high potency to be effective(23).
A small study amongst HCW’s suggests evidence that host defences influence the
risk of HIV infection. Following percutaneous exposure to HIV there was no
Page 8 of 24
seroconversion indicating that limited viral replication can occur without infection.
HIV specific T cell proliferative response was seen in majority of subjects,as this
response is a major histocompatilibilty complex (MHC) class 1 specific its
associated with limited viral replication within tissue macrophages(23).This
indicates that host immune responses may prevent HIV infection.
In a study involving 20 HCW’s with occupational HIV exposure, one group
received zidovudine as PEP and the control did not. Results in the zidovudine
group revealed a blunted HIV specific CTL response and that early HIV replication
maybe inhibited by PEP(24). Timely initiation of anti-retrovirals post exposure to
HIV may prevent or inhibit systemic infection by limiting viral replication in the
target cells or regional lymph nodes(23).
PEP EFFICACY IN ANIMAL STUDIES
PEP has proven to be successful in animal studies in preventing the infection of
primates with simian immunodeficiency virus (SIV) . Following intravenous, oral
and rectal inoculation of SIV, the anti-retrovirals administered prevented
infection(25,26).
It is important to note that these outcomes cannot be directly extrapolated to
humans. This is due to the following differences: (23)
(a) infective strains ( SIV vs HIV );
(b) variance in host susceptibility to infection;
(c) variance in drug metabolism;
(d) inoculums route and volume; and
(e) drug regimen
However subsequent studies served to refine methodology and sought to provide
better evidence for the efficacy of PEP(27,28). These studies revealed that delays in
initiation of the first dose, decreased duration of treatment and suboptimal dosing
of PEP together with larger viral inoculums on exposure is associated with
decreased efficacy of ARV’s for PEP(27,28).
Page 9 of 24
PEP EFFICACY IN HUMAN STUDIES
The efficacy of occupational PEP in humans has not been validated in large
randomised controlled trials. A retrospective study amongst HCW’s following
percutaneous exposure to HIV revealed that zidovudine chemoprophylaxis
reduced the risk of HIV transmission by 81% in those that took a 28 day course.
However due to limitations in numbers, study design and reporting, bias could not
be excluded(14). PEP has a definitive role in preventing perinatal transmission of
HIV. Antepartum and intrapartum administration of zidovudine to the mother, with
zidovudine administration to the neonate at 6 weeks postpartum, has proved to
decrease the risk of vertical transmission by 67%(29).
The therapeutic effect of zidovudine extends beyond the maternal reduction of
HIV RNA in preventing vertical transmission. It also seems to offer direct
protective effects to the HIV exposed but uninfected neonate born to HIV infected
mothers who received no antiretroviral treatment or prophylaxis during pregnancy,
labour or delivery(30). The limitations imposed by animal and human studies must
be considered as well as the routes of exposure following perinatal transmission
versus that of occupational transmission of HIV when evaluating the efficacy of
PEP(23).
PEP TREATMENT FAILURE
There has been 21 cases in which PEP has failed to prevent HIV transmission in
HCW’s. In the majority of cases PEP monotherapy with zidovudine was used
versus dual therapy and triple drug therapy in others, in which HIV seroconversion
was respectively less according to the greater number of agents utilised.
Despite this evidence there has been documented cases of occupational
transmission of HIV with combination drug therapy being used(31,32,33).
Antiretroviral resistance testing in cases of PEP treatment failure have revealed
resistant strains of the source virus to all classes of antiretrovirals as well as
specific agents (23). Antiretroviral drug resistance can be suspected in source
patients who despite being on prolonged therapy, display: (33)
(a) clinical progression of disease;
(b) falling CD4 counts; and
(c) increasing viral loads
(d)
In addition to treatment failure due to resistant viral strains, other factors such
as high viral titre, large inoculums of exposure, delayed initiation, suboptimal
dosing and short duration of PEP together with decreased host immunity
contribute to cases of treatment failure(23).
Page 10 of 24
Morbidity and Mortality weekly report. Updated U.S Public Health Service Guidelines for the Management of Occupational
Exposures to HBV, HCV and HIV and Recommendations for Postexposure Prophylaxis. 2001 June/Vol.50/No.RR-11.
Page 11 of 24
PEP DRUG REGIMENS
Zidovudine is the only drug proven to show risk reduction in HIV transmission
following occupational exposure(14). No data exists to support the addition of other
ARV’s in improving the efficacy of post exposure prophylaxis.
However, combination therapy of antiretrovirals in HIV infected patients aims to
achieve superior suppression of viral replication compared to zidovudine
monotherapy(34,35). Hence combination drug therapy enhances the efficacy of post
exposure prophylaxis as a result of activity at various levels of the viral replication
cycle. This is especially important with exposures associated with an increased
risk of transmission. Combination therapy PEP also addresses the concern of
PEP treatment failure in cases of viral resistance(33,34).
However post exposure prophylaxis is poorly tolerated and associated with poor
adherence in 20 - 40 % of cases due to toxicity and side effect profile(36). It is
imperative that exposures are assessed according to the substance/body fluid
involved and the route and severity of the exposure together with details of the
source patient to guide judicious PEP therapy regimens(36).
Low risk exposures require a basic PEP regimen (2 drugs) consisting of 2
nucleoside/nucleotide
reverse
transcriptase
inhibitors(NRTI’s)
viz.
zidovudine(AZT) and lamivudine(3TC) or stavudine(D4T) and lamivudine(3TC).
High risk exposures require an expanded regimen (3 drugs) consisting of 2 NRTI’s
and a PI (lopinavir/ritonavir) or an NNRTI (efavirenz). Expanded regimens should
be reserved for increased risk of transmission or in cases of suspected viral drug
resistance(34,36).
Latest South African guidelines regarding PEP, advocate triple drug regimen for
prophylaxis and treatment of all significant exposures. Rationale for this
recommendation is based on the extremely high HIV prevalence, high patient
volume and attendant risk of high number of exposures. Although the risk of HIV
transmission following an occupational exposure in our setting has not been
quantified, the aforementioned risk factors makes these recommendations
plausible(8).
Page 12 of 24
PEP TIMING AND DURATION
PEP is a medical emergency and requires urgent initiation of antiretrovirals within
2 hours of exposure following adequate evaluation of the HCW, exposure incident
and source patient to avoid inappropriate antiretroviral therapy. If concern over
source patient or complexity of exposure exists regarding instituting a basic or
expanded regime, a basic regime should be immediately prescribed whilst
awaiting necessary details to guide further therapy.
An absolute time after which PEP has no efficacy in administration cannot be said
with certainty but animal and PMTCT studies have shown that the efficacy
decreases beyond 36 - 72 hours of exposure incident. Delayed PEP
administration beyond 72 hours maybe advocated in circumstances of delayed
presentation and increased risk of transmission (following transfusion of HIV
infected blood products) under specialist advice(37,38).
Duration of PEP for all regimens must be 28 days. Minimal efficacy is associated
with therapy of less than 2 weeks duration and no added benefit is offered with
therapy extending beyond 28 days as documented in animal and case control
studies(16).
Status of the Source
HIV Positive
Percutaneous
exposure
to
bloodor potentially infectious Triple Therapy
fluids
Mucocutaneous
splash
or
contact with open wound with Triple Therapy
blood or potentially infectious
fluids
Percutaneous
exposure,
mucocutaneous
splash
or No PEP
contact with an open wound,
with non infectious bodily fluids
Unknown
HIV Negative
Triple Therapy
No PEP
Triple Therapy
No PEP
No PEP
No PEP
Post Exposure Prophylaxis. The South African Journal of HIV Medicine-Winter 2008.
Page 13 of 24
ADVERSE EFFECTS, TOXICITY, AND DRUG INTERACTIONS
The primary objective of PEP is successful completion of 28 days of uninterrupted
prophylaxis. Side effects due to prophylactic antiretroviral therapy appears to be
more frequent and severe in HIV negative exposed HCW’s than in HIV positive
patients on antiretroviral treatment. Side effect management is critical to
completion and is often under managed. Approximately 50% of HCW’s experience
adverse side effects whilst taking PEP resulting in premature discontinuation of
prophylaxis in 35% of cases. Common side effects include: nausea , vomiting and
diarrhoea, headaches, malaise(8,16,23).
Counseling, reassurance, follow-up and prescription of anti-emetics and antidiarrhoeal agents together with modification of dosing intervals if needed serve to
improve compliance without the need to change the PEP regimen(8).
Zidovudine (AZT) and protease inhibitors (PI’s) are associated with significant side
effects. AZT is poorly tolerated in PEP settings and shows no clear advantage
over tenofovir which forms part of the preferred regimen of PEP prophylaxis in the
developed world. D4T and tenofovir are associated with successful outcomes in
PMTCT regimens, with D4T being far better tolerated than AZT(23,38).
The use of PI’s are associated with new onset diabetes, exacerbation of preexisting diabetes, hyperglycaemia, diabetic ketoacidosis, dyslipidaemia and
peripheral neuropathy. Specifically indinavir use is associated with
hyperprolactinaemia and galactorrhoea whilst use in pregnancy is associated with
hyperbilirubinaemia and nephrolithiasis, whilst cases of cholestatic jaundice have
been reported with nelfinavir. Nelfinavir and Indinavir are generally poorly
tolerated, with PI’s having several drug interactions and complicating
management of several pathologies including hypertension, diabetes, asthma,
tuberculosis, pregnancy, epilepsy, DVT/PE(8,16,23).
Abacavir (NRTI) should be avoided due to increased risk of hypersensitivity
reactions. Combination of stavudine and didanosine should be avoided due to
possibility of mitochondrial toxicity and lactic acidosis (fatal and non fatal) most
commonly seen in pregnancy(23).
With regard to NNRTI’s, efavirenz though accepted as treatment of choice for
chronic HIV infection, its use in initial PEP prophylaxis ( basic regimen) is not
recommended due to the following reasons including : (23)
(a) CNS side effects being common complicating the need for the first dose and
impairing work ability with subsequent dosing;
Page 14 of 24
(b) teratogenic to pregnant woman and should be avoided in woman of
childbearing age unless effective contraception is taken and adherence is
assured.
Nevirapine carries a high risk of hepatotoxicity and Steven Johnsons syndrome
and is associated with reverse transcriptase gene mutation, leading to cases of
NNRTI resistance, when used for PEP and as result should be avoided both in
PEP regimens and in pregnancy.
Post Exposure Prophylaxis. The South African Journal of HIV Medicine-Winter 2008
Page 15 of 24
LEGAL FRAMEWORK OF PEP (22)
Exposure to HIV and other blood borne viruses in the work place should be
prevented as per the responsibility of both the employer and the employee.
The Occupational Health and Safety Act No. 85 of 1993 ( OHSA ):
Employers are to ensure a safe and secure work place for the
employees as far as is possible. The implication of the Act regarding HIV
specifically is that the employer needs to minimise the risk of infection within the
workplace.
Compensation for Occupational Injuries and Diseases Act No. 130 of 1993:
The Act provides for compensation to be paid to an employee for illnesses or
accidents sustained during the course of his or her employment. To qualify for
compensation, an employee is required to prove that the HIV infection was
acquired as a result of occupational exposure. It’s imperative that meticulous
recording and reporting of an occupational injury is undertaken by the employee
who should also be subject to HIV testing.
PREVENTATIVE STRATEGIES
Occupational exposures to HIV are avoidable and warrant investigation with a
view to improve infection control(8).
Studies have suggested that circumstances involved in predisposing the HCW to
occupational exposure to HIV include (16,40) :
(1) the unnecessary use of needles;
(2) lack of sharps containers and needle holders;
(3) repeated resheathing of needles after use;
(4) lack of training of HCW’s;
(5) long working hours > 40 hours/week;
(6) lack of wearing gloves when tasked with needle use ; and
(7) belief amongst HCW’s that HIV seroconversion following occupational
exposure to HIV is low
Page 16 of 24
Behaviour modification in the work place forms the cornerstone of primary
preventative strategies in reducing the risk of occupational exposure to HIV.
HCW’s should be:
(1)
educated about the risks in the workplace;
(2)
aware of the magnitude of these risks;
(3)
trained in decreasing exposure by appropriate risk reduction strategies
(standard precautions )
- All patients to be treated as potential carriers of HIV
- Use of appropriate personal protective equipment viz.
Mask, gown, gloves, visors etc during procedures that carry a high risk
of contamination with blood or bodily fluids
- Meticulous handling of sharps and avoidance of injury
- Proper disposal of sharps and infectious waste;
(4)
Training provided to modify procedures that carry an increased risk; and
(5)
Adequate provision of instruments and devices that reduce risk of exposure
by advanced manufacturing technique
Institutional policy is an important aspect of management in health care settings
for post exposure management of HCW’s to potentially infectious bodily fluids.
Page 17 of 24
STEP WISE APPROACH TO AN OCCUPATIONAL EXPOSURE
The following are recommendations
contaminated blood or bodily fluids:
following
exposure
to
potentially
GENERAL MEASURES
Immediate treatment of the exposure site follows washing area with soap and
water. Mucous membranes that have been exposed should be irrigated with water
or normal saline. Although the use of antiseptics have been encouraged by some
authors, others have discouraged its use as it may impair local host defense
mechanisms and has not been proven to decrease the risk of HIV transmission.
Squeezing the wound has also been advised against due to the promotion of
hyperaemia and inflammation at the wound site, potentially increasing systemic
exposure to HIV(16,40).
EVALUATION OF EXPOSURE
The route and severity of exposure determines the risk of potential HIV
transmission.
Whilst awaiting for the source patient to be tested for HIV, PEP should be
indicated in the following circumstances: (22)
- breach of the skin by a sharp object that has blood, bloody fluid, or other
infectious material or that has been in the source patients blood vessel
- patient with blood exposed in the mouth that bites and causes bleeding in the
the HCW
- mucocutaneous exposure (mouth, nose, eyes ) to blood, bloody fluid or other
potentially infectious material
- non-intact skin exposure to blood, bloody fluid, or potentially infectious material
Page 18 of 24
TESTING OF THE SOURCE PATIENT
The HIV status of the source patient should be determined as soon as possible,
this can be done via documented sources of the patient’s status or if unknown
informed consent can be obtained prior to HIV testing. If the source patient is
incapable of providing informed consent, a surrogate will be able to do so.
If consent for HIV testing is refused by the source patient, the HCW should
assume the patient to be HIV +ve.
If the patient is HIV -ve, it is assumed there is no risk of HIV unless reasonable
suspicion exists that the patient is in the “ window period “, which will necessitate
continuation of PEP until lab tests ( HIV DNA PCR ) exclude the window period.
REPORTING OF THE EXPOSURE
The incident requires to be reported to the supervisor as soon as possible, the
occupational clinic within 1-2 hours (if during working hours) and the institutional
manager within 24 hours.
Trained medical personnel should document the following information in the
HCW’s medical record:
-
demographic details of the source patient
chronology of the exposure
type of exposure
body area involved and duration of exposure
HIV status of the source patient if known
a descriptive report of percutaneous wounds if present
circumstance of the exposure
previous testing and serostatus of the exposed HCW
COUNSELLING SUPPORT
Supportive counselling must be available to the exposed HCW and services
should include:
-
appropriate pre and post test counselling
information on the risk of transmission of HIV
information on the reduction in risk of HIV transmission with PEP
information on side effects of ARV’s and methods to address it
emphasis on importance of PEP adherence
Page 19 of 24
The HCW should also be advised of the following:
- barrier method of contraception for 6 months to avoid possible infection of
sexual partners during the “ window period “
- avoid pregnancy until seroconversion has been excluded
- pregnancy does not preclude the use of PEP
- not to donate blood and organs for 3 months
ASSESSMENT OF THE HEALTH CARE WORKER
The HCW must be tested to qualify for PEP and possible compensation. Testing
is based on informed consent.
If the HCW refused baseline HIV testing, they do not qualify for PEP in terms of
government (DOH) policy in Kwazulu-Natal and they must be informed that such
refusal negates the right to any future claim for compensation in respect of that
particular exposure and therefore must indemnify the Department of Health in
writing.
Blood must be taken confidentially from the HCW, and the details on the lab
request form must document the specimen is from a HCW who sustained an
occupational exposure and the contact details of the attending doctor or
professional nurse must be reflected to facilitate the results being issued.
HIV testing should be conducting at baseline, 6 weeks, 12 weeks and 24 weeks,
whilst baseline FBC, U&E, LFT should be done to monitor for possible toxicity and
should be repeated in the 2nd and 4th week. Pregnancy testing should also be
done at baseline for woman of child bearing age.
Page 20 of 24
CONCLUSION
Developing countries are afflicted by the greatest burden of HIV/AIDS where
access to antiretrovirals is limited. Health care workers are scarce but highly
valued, and need to be protected from occupational hazards that pose an
increased risk of acquiring HIV.
Primary preventative strategies should form the mainstay of management in terms
of prevention of occupational HIV exposure but in resource constrained countries
this is not always possible to achieve. Post exposure prophylaxis if initiated
timeously in the appropriate setting with the appropriate regimen for the
appropriate duration can prevent occupational HIV infection.
It is imperative to provide on-going support and counseling to the exposed HCW
whose psychological burden of exposure and risk of contracting a fatal illness
together with the adverse effects of antiretroviral therapy associated with PEP,
may result in the loss of hospital staff resources.
Page 21 of 24
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Sagoe-Moses C, Pearson RD, Perry J. Risks to healthcare workers in
developing countries. New England Journal of Medicine. 2001;345(7):538541.
Pruss-Ustun A, Rapiti E, Hutin Y. Estimation of the global burden of disease
attributable to contaminated sharps injuries among healthcare workers.
American Journal of Industrial Medicine. 2005;48(6):482-490.
Gumodoka B, Favot I, Berege ZA, Dolmans WM. Occupational exposure to
the risk of HIV infection among healthcare workers in Mwanza Region,
United Republic of Tanzania. 1997;75(2):133-140.
Gupta A, et al. High risk for occupational exposure to HIV and utilisation of
post-exposure prophylaxis in a teaching hospital in Pune, India. BMC
Infectious Diseases. 2008;8(142):1-10.
Gounden YP, Moodley J. Exposure to human immunodeficiency virus
among healthcare workers in South Africa. Int J Gynaecol Obstet.
2000;69:265-270.
Aitken JO,Kemp J. HIV/AIDS, equity and health personnel in Southern
Africa. EQUINET Discussion Paper. 2003;12.
Bell DM. Occupational risk of human immunodeficiency virus infection in
healthcare workers: an overview. Am J Med. 1997;102:9-15
Post Exposure Prophylaxis. The South African Journal of HIV MedicineWinter 2008.
Anonymous. Needle stick transmission of HTLV-3 from a patient infected
in Africa. Lancet. 1984;ii:1376-1377.
Ippolitio G, Puro V, De Carli G. The italian study on occupational risk of HIV
infection.The risk of occupational HIV infection in health care workers. Arch
Intern Med. 1993;153:1451.
Fahey BJ, Koziol DE, Banks SM, Hendersen DK. Frequency of
nonparenteral occupational exposures to blood and bodily fluids before and
after universal precautions training. Am J Med. 1991;90:145-153.
Hendersen DK, Fahey BJ, Willy M, et al. Risk for occupational transmission
of human immunodeficiency virus type 1 (HIV-1) associated with clinical
exposures: a prospective evaluation. Ann Intern Med. 1990;113:740-746.
Paxton WA, Martin SR, Tse D, et al. Relative resistance to HIV-1 infection of
CD4 lymphocytes from persons who remain uninfected despite multiple high
risk sexual exposure. Nat Med. 1996;2:412-417.
Liu R, Paxton WA, Choe S, et al. Homozygous defect in HIV-1 coreceptor
accounts for resistance of some multiply-exposed individuals to HIV-1
infection. 1996;86:367-377.
Page 22 of 24
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
Cardo DM, Culver DH, Ciesielski CA, et al. A case control study of HIV
seroconversion in healthcare workers after percutaneous exposure. N Eng J
Med. 1997;337:1485-1490.
Varghese GM, Abraham DC, Mathai D. Post exposure prophylaxis for blood
born viral infections in health care workers. Postgrad Med J. 2003;79:324328.
Tarontolaa A, Koumare’b A, Rachlinea A, et al, the Groupe d’Etude des
Risques d’ Exposition des soignants aux agents infectieux (GERES). J Hosp
Infect 2005;60:276-282.
Kartaedt AS, Pantanowitz L. Occupational exposure of interns to blood in an
area of high HIV seroprevalence. S Afr Med J. 2001;91:57-61.
Marais BJ, Cotton M. Occupational exposure to HIV in paediatricians-a
previously undescribed high risk group. XIV International AIDS Conference,
Barcelona Spain. 2002 July;Abstract no. Molec 3515.
World Health Organization. Post Exposure Prophylaxis to prevent HIV
infection Guidelines. 2007.
Department of Health Kwazulu-Natal Guidelines. Accidental occupational
exposure to potentially infective tissues.
Morbidity and Mortality weekly report. Updated U.S Public Health Service
Guidelines for the Management of Occupational Exposures to HBV, HCV
and HIV and Recommendations for Postexposure Prophylaxis. 2001
June/Vol.50/No.RR-11.
Centres for Disease Control and Prevention. Case-control study of HIV
seroconversion in healthcare workers after percutaneous exposure to HIV
infected blood-France, United Kingdom and United States,January 1988August 1994. MMWR Morb Mortal Wkly Rep.1995;44:929-933.
D’Amico R, Pinto LA, Meyer P, et al. HIV specific cytotoxic T cells in HIV
exposed but unaffected Gambian women. Nat Med. 1995;1:59-64.
Tsai CC, Follis KE, Sabo A,et al. Prevention of SIV infection in macaques by
(R1-9-(2-phosphonylmethoxypropyl)adenine. Science. 1995;270:1197-1199.
Tsai CC, Emau P, Follis KE, et al. Effectiveness of postinoculation (R1-9-(2phosphonylmethoxypropyl)adenine treatment for prevention of persistent
simian immunodeficiency virus siumne infection depends critically timing of
initiation and duration of treatment. J Virol. 1998;72:4265-4273.
Bottiger D, Johansson NG,Samuelsson B, et al. Prevention of simian
immunodefiency virus, SIV,or HIV-2 infection in cynomolgus monkeys by
pre-and postexposure administration of BEA-005. AIDS.1997;11:157-162.
Otten RA, Smith DK, Adams DR, et al. Efficacy of postexposure prophylaxis
after intravaginal exposure of pig-tailed macaques to a human-derived
Page 23 of 24
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
retrovirus (human immunodeficiency virus type 2). J Virol. 2000;74:97719775.
Conner,et al. Reduction of mother-infant transmission of human
immunodeficiency virus type 1 with zidovudine treatment. Paediatric AIDS
Clinical Trials Group Protocol 076 Study Group. N England J Med.
1994;331:1173-1180.
Wade NA, Birkhead GS, Warren BL et al. Abbreviated regimens of
zidovudine
prophylaxis
and
perinatal transmission
of
human
immunodeficiency virus. N Eng J Med.1998;335:1621-1629.
Weisbard G, Biglione J, Arbulu MM, Terazzino JC, Pesiri A. HIV
seroconversion after a workplace accident and treated with zidovudine [
Abstract Pub.C.1141 ] In: Vancouver, British Colombia, Canada. 1996;460.
Perdue B, Wolderfael D, Mellors J, Quinn T, Mergolick J. HIV-1 transmission
by a needlestick injury despite rapid initiation of four drug post-exposure
prophylaxis [ Abstract 2010 ] In: Program and Abstracts of the 6th
conference on Retroviruses and opportunistic Infections. Chicago, IL:
Foundation for Retrovirology and Human Health in scientific collaboration
with the National Institute of Allergy and Infectious Diseases andCDC.
1999;107.
Beltromi EM, Luo C-C, Dela Torre N, Cardo DM. HIV transmission after an
occupational exposure despite post exposure prophylaxis with a
combination drug regimen [Abstract P-S2-62]. In:Conference on Nosocomial
and Healthcare-Associated Infection in conjunction with the 10th Annual
Meeting of SHEA. Atlanta. GA:CDC. 2000:125-126.
Manion DJ, Hirsch MS. Combination Chemotherapy for HIV-1. Am J Med.
1997;102(5B):76-80.
Lafeuilldae A, Poggi C, Tamalet C, et al. Effects of a combination of
zidovudine, didanosine and lamivudine on primary HIV type-1 infection. J
Infect Dis. 1997;175:105
Lee LM, Henderson DK. Tolerability of post exposure antireroviral
prophylaxis for occupational exposures to HIV. Drug Saf. 2001;24:587-597.
Centres for Disease Control and Prevention. Updated U.S Public Health
Service Guidelines for the Management of Occupational Exposures to HBV,
HCV and HIV and Recommendations for Postexposure Prophylaxis. MMWR
Recomm Rep. 2000;50:1-52.
Expert Advisory Group on AIDS. HIV Post-exposure Prophylaxis-Guidance
from the UK Chief Medical Officers, London: UK Department of Health.
2004.
Omrani S,Freedman A. Prophylaxis of HIV infection. British Medical
Bulletin. 2005;73,74:93-105
Page 24 of 24