Guidance on the investigation and management of occupational exposure to hepatitis C

COMMUNICABLE DISEASE AND PUBLIC HEALTH 258 VOL 2 NO 4 DECEMBER 1999

* This guidance was written by Dr Mary Ramsay and endorsed by the PHLS Advisory Committee on Blood Borne Viruses on 2 February 1999 (membership

list Appendix€1)

Summary: This document updates previous PHLS guidance on the risks and management of occupational exposure to hepatitis C. In line with recent guidance from the UK Health Departments, the PHLS now recommends that all source patients, subject to appropriate consent, should be tested for evidence of hepatitis C infection. A baseline serum should be obtained from the exposed health care worker and stored for at least two years. Health care workers exposed to known infected sources should be followed up at six, 12, and 24 weeks after exposure. Serum taken at six and 12 weeks should be tested for hepatitis C virus (Hepatitis C Virus) RNA and serum taken at 12 and 24 weeks for anti-Hepatitis C Virus. Health care workers exposed to a source believed not to be infected do not require active follow up for hepatitis C unless requested or if they develop symptoms or signs of liver disease. Management of personnel exposed to a source whose hepatitis C status is unknown or a source unavailable for testing will depend upon a risk assessment by a designated doctor.

Health care workers who are found to be positive for Hepatitis C Virus RNA or antibody to hepatitis C should be referred to an appropriate consultant for consideration of early treatment.

Introduction

Guidance on the risks and management of occupational exposure to hepatitis C was last issued in 1993 by the PHLS Hepatitis Subcommittee 1 . Since then, knowledge has increased about the prevalence of hepatitis C virus (Hepatitis C Virus) infection in the United Kingdom (UK), the risks of occupational transmission, and the benefits of treatment. Guidance on the management of potential exposures to Hepatitis C Virus was issued recently in the United States (US) 2 and Canada 3 and recommendations in these documents differ from those in the previous PHLS guidance 1 . In addition, the UK Health Departments have issued recommendations on the management of significant exposures with regard to the potential risks of HIV, hepatitis B virus, and Hepatitis C Virus infection 4 . These developments provided an opportunity for the PHLS Advisory Committee on Blood Borne Virus Infections to reconsider and revise the recommendations of the PHLS group. This guidance is intended to supplement the detailed guidance on the management of blood exposure incidents produced by the UK Health Departments 4 .

The evidence base

Risks of exposure to hepatitis C Population based studies suggest that the prevalence of Hepatitis C Virus infection in western Europe and North America is below 2.5%, lower than in many other parts of the world 5 . Studies of low risk groups in the UK suggest that the prevalence of anti-Hepatitis C Virus in the general population is below 1% 6-8 . The prevalence among new blood donors is currently 0.06% 6 but a seroprevalence of 0.72% was found in UK organ donors 7 . The prevalence in the West Midlands of anti-Hepatitis C Virus among pregnant women was 0.14% 8 but in a more recent PHLS study of pregnant women the prevalence was 0.33% in Greater London and 0.22% in Yorkshire (J Parry, personal communication).

 Patients receiving health care in the UK are likely to have a higher prevalence of Hepatitis C Virus infection than the general population. Known high risk exposures for Hepatitis C Virus infection in the UK include injecting drug use, receipt of blood transfusion or blood products, tattooing, and having been born abroad 9,10 . The prevalence of Hepatitis C Virus among injecting drug users (IDUs) in studies in England and Wales was 46% in South Wales 11 , 59% in one area of rural England 12 , 59% among IDUs undergoing voluntary HIV testing in north west England (J Craske, personal communication), and 67% in IDUs attending a regional drug clinic in the north east 13 . In Scotland, studies of IDUs have found prevalences of anti-Hepatitis C Virus between 77% and 90% 14,15 . People with haemophilia who received untreated clotting factors 16-18 and patients on renal dialysis in some units 19 are also known to have a high prevalence, although the prevalence has been low in some renal units 16,20 . In some specialties and geographical locations, therefore, the risk of exposure to an Hepatitis C Virus infected source may be high. Exposure to Hepatitis C Virus positive sources in the UK is likely to be commoner than exposure to sources positive either for HIV or for hepatitis B surface antigen 21 .

Risk of transmission to health care workers

Health care workers may be at greater risk of hepatitis C than the general UK population 9,10 , but the prevalence of anti-Hepatitis C Virus in such staff is lower than among health care workers in the US 22 , and western Europe 22,24 . In the UK, the overall prevalence of infection was estimated to be 0.23% among all health care workers and 0.28% in those at risk of occupational contact with blood and body fluids 25,26 .

In the US, a review of published studies in health care workers who received a needlestick injury from an anti-Hepatitis C Virus positive source estimated the risk of transmission to be 1.8% (range 0%-7%) 2 . In a recent meta-analysis, the risk of transmission was shown to be greater if the source patient was known to be positive for Hepatitis C Virus RNA; no transmission occurred from Hepatitis C Virus RNA negative sources 27 .

 Risk of transmission from health care workers

Only two episodes of transmission from an Hepatitis C Virus infected surgeon to patients have been described to date 28,29 . In the UK, transmission from an Hepatitis C Virus infected surgeon was implicated in a single case of acute hepatitis C detected after cardiothoracic surgery 28 . In the lookback investigation that followed, 277 patients were tested but no other infected individuals were identified 30 . This suggests that the risk of transmission from health care worker to patient is much lower than the risk of transmission from surgeons positive for hepatitis B e antigen 30 .

Based on this evidence, health care workers with Hepatitis C Virus infection in the UK are not restricted from performing exposure prone procedures unless they have been shown to transmit hepatitis C to a patient 28 . Nevertheless, health care workers with Hepatitis C Virus infection should be seen in occupational health departments to be advised on scrupulous adherence to the optimal precautions for control of bloodborne virus infections in order to reduce the potential risk of transmission during exposure prone procedures 4 . In addition, infected health care workers should be advised about the local arrangements for the reporting, assessment, and management of any incidents in which patients appear to have been exposed to a health care worker™s blood. Patients who sustain a significant exposure to blood (box 1) should be managed in the same way as exposed health care staff.

Management of hepatitis C infection

The UK Health Departments have concluded that there is no effective post exposure prophylaxis for hepatitis C 4 . The use of immunoglobulin has been suggested, but a US review in 1998 concluded that it did not prevent Hepatitis C Virus infection 31 . Prophylaxis with alpha-interferon did not prevent transmission of hepatitis C after a needlestick injury in Japan 32 . No formal assessments of antiviral agents for post exposure prophylaxis have been performed, but their use has not been recommended in the US 2 .

Alpha-interferon is now commonly used to treat chronic hepatitis C infection 33,34 . Better response rates are likely to be seen with combination therapies that include ribavirin 35-37 . A recent European consensus statement recommended that combination therapy should be offered to all previously untreated infected individuals without contraindications 38 . Evidence based guidance on the management of patients with hepatitis C currently being developed by professional groups in the UK may involve the selection of patients on the basis of abnormal liver function, Hepatitis C Virus RNA positivity, and grade of abnormality on a liver biopsy 33 . A decision about whether to continue treatment may depend upon demonstration of a virological response as assessed by genome detection.

Evidence on the optimal timing of treatment for acute and chronic hepatitis C infection is unclear. The use of interferon for acute hepatitis in a small number of patients suggested that early treatment might prevent chronic carriage 32 . A subsequent meta- analysis of the use of alpha- and beta-interferon in acute hepatitis C infection concluded that short term early treatment produced better response rates than treatment of chronic infections 39 . Control data on untreated infections were limited, however, so the difference in response could reflect the natural clearing of acute infection. More recently, workers in Italy reported the results of a randomised controlled trial of beta-interferon in acute hepatitis C, in which the rates of chronic infection in treated (15/20) and untreated groups (16/20) were similar 40 .

The US Centers for Disease Control and Prevention has concluded that there is insufficient evidence to suggest that treatment of acute hepatitis is more successful than early treatment of chronic hepatitis 2 . In Canada, however, early treatment of health care workers who seroconvert following percutaneous exposures is now recommended 3 . A recent consensus conference in Europe also stated that most experts now favour treating patients with acute hepatitis C infection 38

Recommendations

The recommendations of the committee for the management of a significant exposure (box 1) 1 are as follows:

Investigation of source patients

In most settings, most source patients are likely to be anti-Hepatitis C Virus negative. The exclusion of Hepatitis C Virus infection in the patient should reassure the exposed health care worker. Identification of a source patient who is positive for anti-Hepatitis C Virus should prompt appropriate assessment of the patient and follow up of the health care worker. The advisory committee therefore recommends that, where possible, a baseline serum from the source patient should be obtained and tested for anti-Hepatitis C Virus. Patients who are anti-Hepatitis C Virus positive should be further investigated for Hepatitis C Virus RNA (an EDTA plasma may be required by the local laboratory). In immunocompromised patients (including those on renal dialysis) 41 or in patients with features suggestive of acute hepatitis C infection, the use of genome detection should be considered even if the source patient is found to be anti-Hepatitis C Virus negative. These investigations will normally entail pre-test discussion and obtaining fully informed consent from the source patient 4 . Specimens from the source patient must be stored in a secure archive at a temperature at or below 20 o C for at least two years after the incident.

Source patients found to be anti-Hepatitis C Virus and/or Hepatitis C Virus RNA positive should be referred to an appropriate consultant with an interest in hepatitis C infection.

In the event that the source patient cannot be identified or if the patient refuses to be tested or is unavailable for testing, management should be based upon a risk assessment. This risk assessment should be conducted by one of the doctors designated to offer advice on the managment of exposures to bloodborne viruses within the health authority or NHS Trust 4 . Epidemiological and clinical information about the incident and/or the source patient should be obtained and reviewed. If the source patient is considered to be ‚high risk™ then the health care worker may be managed as if exposed to a source known to be positive. Such high risk exposures would normally be limited to sharps injuries contaminated with fresh blood from a member of a known high risk group (for example, an IDU). Because the risk of transmission of bloodborne viruses from dried blood is likely to be lower than from fresh blood, the advisory committee does not consider community needlestick injuries from discarded needles to be ‚high risk™ exposures.

Investigation of the exposed health care worker

Baseline serum should be obtained from the exposed person and stored in a secure archive at -20 o C or below for at least two years (box 2). If the source patient is not infected with Hepatitis C Virus, no further follow up with respect to Hepatitis C Virus is required unless the health care worker develops liver disease. Information, counselling, and psychological support should be available for any employee who reports an exposure and a potential risk of any bloodborne viral infection 4 . If, after the provision of information, the exposed person requests follow up, additional testing may be offered. At a minimum, this follow up should include testing for anti-Hepatitis C Virus at six months.

For health care workers exposed to a source known to be positive for anti-Hepatitis C Virus or Hepatitis C Virus RNA (or a source whose hepatitis C status is unknown but who is assessed to be at ‚high risk™), serum should be obtained from the health care worker at baseline, six weeks, 12 weeks, and 24 weeks after exposure (box 2). Serum should be tested for Hepatitis C Virus RNA at six and 12 weeks and for anti-Hepatitis C Virus at 12 weeks and 24 weeks.

Early testing of the serum of the health care worker for Hepatitis C Virus RNA will, if negative, give some reassurance at this stage. In a follow up study of individuals who sustained needlestick exposures to patients with non- A, non-B hepatitis, both of the health care workers who developed anti-Hepatitis C Virus were Hepatitis C Virus RNA positive one month after exposure 45 ; early genome detection was not performed on health care workers who did not seroconvert. The negative predictive value of genome detection at six weeks is therefore not documented, but it seems likely that this would correlate with a lower risk of transmission.

Collation of information on such exposures will contribute towards the prospective estimation of transmission risks and the likely predictive value of laboratory investigations. All exposures to known anti-Hepatitis C Virus or Hepatitis C Virus RNA positive sources should therefore be reported to the PHLS national surveillance scheme for health care workers occupationally exposed to bloodborne viruses (box 3). An equivalent scheme for Scotland is coordinated by the Scottish Centre for Infection and Environmental Health. If the health care worker is found to be positive for anti-Hepatitis C Virus or Hepatitis C Virus RNA at any stage, retrospective investigation of baseline specimens from the health care worker and source patient for Hepatitis C Virus RNA, if not already available, can then be performed. Additional studies that may be useful at this stage include genotyping and viral load. Genotyping of source and health care worker will help to confirm whether transmission from patient to health care worker has occurred 43 , and specimens for genotyping can then be referred to the PHLS Hepatitis and Retrovirus Laboratory in Colindale. Estimates of viral load in the source patient may also help to inform the management of such incidents in the future.

Advice to exposed health care workers

during follow up

It is difficult to offer advice on the appropriate management of health care workers exposed to a known Hepatitis C Virus infected source during follow up. The risk of transmission is small 2 , and there is insufficient evidence to advise mandatory restriction of work practices. Occupational health departments may wish, however, to suggest additional precautions during certain procedures 4 . In line with the Blood Transfusion Service recommendations 44 , before donating blood, health care workers who have been exposed to an individual infected with hepatitis should be referred to the medical officer for assessment. We advise similar caution with respect to donations of other tissues. In studies of chronic Hepatitis C Virus infection, the transmission of infection from mother to child is believed to occur in less than 10% of cases 45 . Sexual transmission from chronically infected individuals occurs, but the risk appears to be low 46-48 . The risk of transmission to infants and sexual partners may be higher in acute than chronic infections, but the magnitude of this increased risk is unknown. Discussion of the possible benefits of adopting safer sexual practices and the avoidance of pregnancy during follow up is therefore recommended.

Health care workers found to be anti-Hepatitis C Virus and/or Hepatitis C Virus RNA positive at any stage during follow-up should be referred to an appropriate consultant with an interest in hepatitis C infection. The evidence for the effectiveness of early treatment is limited, but referral will allow early assessment and a consideration of the potential role of treatment. As treatment options are likely to change over the next few years, early detection will enable recruitment into clinical trials and the early implementation of any treatment shown to improve outcome. Health care workers found to be anti-Hepatitis C Virus and/or Hepatitis C Virus RNA positive should also be referred to occupational health for advice.

References

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2. CDC. Recommendations for follow-up of health-care workers after occupational exposure to hepatitis C virus. MMWR Morb Mortal Wkly Rep 1997; 46: 603-6.

3. Sherman M. Management of viral hepatitis: clinical and public health perspectives Πa consensus statement. CASL Hepatitis Consensus Group. Canadian Association for the Study of the Liver. Can J Gastroenterol 1997; 11: 407-16.

4. UK Health Departments. Guidance for clinical health care workers: protection against infection with bloodborne viruses. Recommendations of the Expert Advisory Group on AIDS and the Advisory Group on Hepatitis.3rd edition. London: Department of Health, 1998.

5. WHO. Hepatitis C: global prevalence. Wkly Epidemiol Rec 1997; 72: 341-8.

6. CDSC. Surveillance of viral infections in donated blood. Commun Dis Rep CDR Wkly 1997; 7: 256.

7. Wreghitt TG, Gray JJ, Allain JP, Poulain J, Garson JA, Deaville R, et al. Transmission of hepatitis C virus by organ transplantation in the United Kingdom. J Hepatol 1994; 20:768-72.

8. Boxall E, Skidmore S, Evans C, Nightingale S. The prevalence of hepatitis B and C in an antenatal population of various ethnic origins. Epidemiol Infect 1994; 113: 523-8. 

9. Goodrick MJ, Gray SF, Rouse AM, Waters AJ, Anderson NA. Hepatitis C (Hepatitis C Virus)-positive blood donors in south-west England: a case control study. Transfus Med 1994; 4: 113-9.

10. Neal KR, Jones DA, Killey D, James V. Risk factors for hepatitis C virus infection. A case-control study of blood donors in the Trent region (UK). Epidemiol Infect 1994; 112: 595-601. 

11. McBride AJ, Ali IM, Clee W. Hepatitis C and injecting drug use in prisons. BMJ 1994; 309: 876.

12. Majid A, Holmes R, Desselberger U, Simmonds P, McKee TA. Molecular epidemiology of hepatitis C virus infection amongst intravenous drug users in rural communities. J Med Virol 1995; 46: 48-51.

13. Serfaty MA, Lawrie A, Smith B, Brind AM, Watson JP, Gilvarry E, et al. Risk factors and medical follow-up of drug users tested for hepatitis C Πcan the risk of transmission be reduced? Drug and Alcohol Review 1997; 16: 339-47.

14. McCruden EA, Hillan KJ, McKay IC, Cassidy MT, Clark JC. Hepatitis virus infection and liver disease in injecting drug users who died suddenly. J Clin Pathol 1996; 49: 552-5.

15. Goldberg D, Cameron S, McMenamin J. Hepatitis C virus antibody prevalence among injecting drug users in Glasgow has fallen but remains high. Commun Dis Public Health 1998; 1: 95-7.

16. Jacyna MR, O™Neil K, Brown J, Drobner R, Karayiannis P, Thomas HC. Hepatitis C virus antibodies in subjects with and without liver disease in the United Kingdom. Q J Med 1990; 77: 1009-12.

17. Brettler DB, Alter HJ, Dienstag JL, Forsberg AD, Levine PH. Prevalence of hepatitis C virus antibody in a cohort of hemophilia patients. Blood 1990; 76: 254-6.

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19. Conway M, Catterall AP, Brown EA, Tibbs C, Gower PE, Curtis JR, et al. Prevalence of antibodies to hepatitis C in dialysis patients and transplant recipients with possible routes of transmission. Nephrol Dial Transplant 1992; 7: 1226-9.

20. Brind AM, Codd AA, Cohen BJ, Gabriel FG, Collins JD, James OF, et al. Low prevalence of antibody to hepatitis C virus in North East England. J Med Virol 1990; 32: 243-8.

21. Cummins AJ, Tedder RS. Inadequate information on needlestick accidents. Lancet 1992; 339: 1178-9.

22. Miller-Tereskerz P, Petrosillo N, Puro V, Jagger J. Hepatitis C virus in health care workers. Advances in Exposure Prevention 1995; 2: 1,7-9.

23. Jochen AB. Occupationally acquired hepatitis C virus infection. Lancet 1992; 339: 304.

24. Struve J, Aronsson B, Frenning B, Forsgren M, Weiland O. Prevalence of antibodies against hepatitis C virus infection among health care workers in Stockholm. Scand J Gastroenterol 1994; 29: 360-2.

25. Zuckerman J, Clewley G, Griffiths P, Cockcroft A. Prevalence of hepatitis C antibodies in clinical health-care workers. Lancet 1994; 343: 1618-20.

26. Neal KR, Dornan J, Irving WL. Prevalence of hepatitis C antibodies among health care workers of two teaching hospitals. Who is at risk? BMJ 1997; 314: 179-80.

27. Dore GJ, Kaldor JM, McCaughan GW. Systematic review of role of polymerase chain reaction in defining infectiousness among people infected with hepatitis C virus. BMJ 1997; 315: 333-7.

28. CDSC. Hepatitis C virus transmission from health care worker to patient. Commun Dis Rep CDR Wkly 1995; 5: 121.

29. Esteban JI, Gomez J, Martell M, Cabot B, Quer J, Camps J, et al. Transmission of hepatitis C virus by a cardiac surgeon. N Engl J Med 1996; 334: 555-60.

30. Duckworth GJ, Heptonstall J, Aitken C, for the Incident Control Team and others. Transmission of hepatitis C from a surgeon to a patient. Commun Dis Public Health 1999; 2: 188-92.

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32. Nakano Y, Kiyosawa K, Sodeyama T, Tanaka E, Matsumoto A, Ichijo T, et al. Acute hepatitis C transmitted by needlestick accident despite short duration interferon treatment. J Gastroenterol Hepatol 1995; 10: 609-11

33. Foster GR, Goldin RD, Main J, Murray-Lyon I, Hargreaves S, Thomas HC. Management of chronic hepatitis C: clinical audit of biopsy based management algorithm. BMJ 1997; 315: 453-8.

34. Poynard T, Leroy V, Cohard M, Thevenot T, Mathurin P, Opolon P, et al. Meta-analysis of interferon randomized trials in the treatment of viral hepatitis C: effects of dose and duration. Hepatology 1996; 24: 778-89.

35. McHutchinson JG, Poynard T. Combination therapy with interferon plus ribavirin for the initial treatment of chronic hepatitis C. Semin Liver Dis 1999; 19: suppl-65.

36. Poynard T, Marcellin P, Lee SS, Niederau C, Minuk GS, Ideo G, et al. Randomised trial of interferon alpha2b plus ribavirin for 48 weeks or for 24 weeks versus interferon alpha2b plus placebo for 48 weeks for treatment of chronic infection with hepatitis C virus. Lancet 1999; 352: 1426-32.

37. Davis GL, Esteban-Mur R, Rustgi V, Hoefs J, Gordon SC, Trepo C, et al. Interferon alfa-2b alone or in combination with ribavirin for the treatment of relapse of chronic hepatitis C. N Engl J Med 1998; 339: 1493-9.

38. Anon. EASL International Consensus Conference on Hepatitis C. Paris, 26-28 February 1999. Consensus statement. J Hepatol 1999; 30: 956-61.

39. Quin JW. Interferon therapy for acute hepatitis C viral infection Πa review by meta-analysis. Aust NZ J Med 1997; 27: 611-7.

40. Calleri G, Colombatto P, Gozzelino M, Chieppa F, Romano P, Delmastro B, et al. Natural beta-interferon in acute type- C hepatitis patients: a randomized controlled trial. Ital J Gastroenterol Hepatol 1998; 30: 181-4.

41. Bukh J, Wantzin P, Krogsgaard K, Knudsen F, Purcell RH, Miller RH. High prevalence of hepatitis C virus (HVC) RNA in dialysis patients: failure of commercially available antibody tests to identify a significant number of patients with Hepatitis C Virus infection. J Infect Dis 1993; 168: 1343-8.

42. Sodeyama T, Kiyosawa K, Urushihara A, Matsumoto A, Tanaka E, Furuta S, et al. Detection of hepatitis C virus markers and hepatitis C virus genomic-RNA after needlestick accidents. Arch Intern Med 1993; 153: 1565-72.

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BOX 1

Definitions of occupational exposure 1

Percutaneous exposure: the skin of the health care worker is cut or penetrated by a needle or other sharp object (for example, scalpel blade, trochar, bone fragment, or tooth), which is contaminated with blood or other body fluid

Mucocutaneous exposure: the eye(s), the inside of the nose or mouth, or an area of non-intact skin of the health care worker is contaminated by blood or other body fluid

Significant exposure: includes all percutaneous exposures and any mucocutaneous exposure to blood or bloody body fluids (but not mucocutaneous exposure to other body fluids).

BOX 2

Summary of investigation and follow up of healthcare workers

Known Hepatitis C Virus infected source

1.         Obtain baseline serum for storage from health care worker

2.         Obtain serum/EDTA for genome detection at six and 12 weeks

3.                   Obtain serum for anti-Hepatitis C Virus at 12 and 24 weeks

Source known not to be infected with Hepatitis C Virus

      1.         Obtain baseline serum for storage from health care worker

2.                   Obtain follow up serum if symptoms or signs of liver disease develop

Hepatitis C Virus status of source unknown

1.         obtain baseline serum for storage from health care worker

2.         designated doctor to perform risk assessment

High risk

Manage as known infected source

Low risk

                        Obtain serum for anti-Hepatitis C Virus at 24 weeks