CHAPTER 47 Surgical Risk of Transmittable Diseases
The first reports of transmission of blood-borne pathogens from patients to surgeons occurred more than 50 years ago.1,2 These early reports of “serum hepatitis” were generally viewed with a detached attitude by surgeons as something that occasionally happened, and these events did not arouse concern about occupational risks. With the recognition of hepatitis A virus (HAV) and hepatitis B virus (HBV) as distinct viral pathogens and the development of specific antibody detection methods, the scope of HBV infection in patients and surgeons was appreciated. Surgeons had a disproportionately higher prevalence of HBV positivity than did the population in general, and it was rapidly appreciated that transmission of the infection from patients to surgeons (and other health care workers [HCWs]) was a far more common event than had been appreciated. Moreover, a nonserotyped hepatitis was identified, and this indicated that yet another form of transmissible hepatitis existed after blood transfusion and other forms of percutaneous blood exposure.3 This nonserotyped hepatitis was labeled non-A, non-B hepatitis (NANBH).4 During the 1970s, evidence was mounting that surgeons and other HCWs worked in an environment with multiple potential hepatitis viruses, but an attitude of indifference persisted with respect to these risks.
In 1981, acquired immunodeficiency syndrome (AIDS) was first identified,5 and subsequent investigations then characterized human immunodeficiency virus (HIV) as the putative agent. HIV infection was associated with blood transfusion and other mechanisms of percutaneous exposure to contaminated blood. During the 1980s, it became apparent that nearly 1 million individuals in the United States had HIV infection and that clinical AIDS was a uniformly fatal disease.6 Furthermore, it became apparent that HIV infection was a latent disease that otherwise healthy-appearing individuals carried for a number of years before AIDS was evident clinically.7 Events surrounding the recognition of AIDS led to great concern and anxiety in the surgical profession about the occupational risks for both AIDS and hepatitis infection.
More than 25 years has passed since the first AIDS cases were reported, and many events have temporized the great fears that surfaced about the occupational risks of this infection in the 1990s. The risk of occupational transmission has been proved to be very uncommon. The development of highly active antiretroviral therapy (HAART) has not eradicated HIV infection but has provided long-term quality life for many of these patients,8 and by virtue of reduced circulating viral loads in these patients receiving treatment, HAART has further reduced the risks of transmission. On the hepatitis front, a highly effective HBV vaccine has been developed from recombinant technology that has dramatically reduced the risk of occupational HBV infection for surgeons. Unfortunately, these developments have created an environment of lassitude and indifference once again about occupational infection in the operating room.
Hepatitis
The past 20 years have yielded a dramatic expansion in our understanding of the world of hepatitis infection. Currently, six distinct hepatitis viruses have been identified (Table 47-1). There remains a probability that at least one additional virus remains to be characterized. At present, only HBV and hepatitis C virus (HCV) appear to be of great occupational concern to surgeons. The majority of the following discussion is limited to HBV and HCV infection.
HAV is transmitted by the fecal-oral route and is usually acquired after the ingestion of contaminated water or food products.9 It is an RNA virus that causes an acute and frequently severe hepatitis syndrome. Infected individuals with the hepatitis syndrome (jaundice, malaise, and so on) are acutely ill, but seldom is the outcome of the infection lethal. Importantly, once HAV clinical infection has resolved, there is no state of chronic infection in the aftermath of the acute infection. The absence of a chronic state of infection and the infrequently identified transmission of HAV from blood or blood products do not make this a virus of occupational concern in health care.
Hepatitis E virus is identified primarily in Southeast Asia and is infrequently seen in the United States.10 It too is transmitted by the fecal-oral route, and like HAV, there is no chronic infection after resolution of the acute infection. It is mentioned only for completeness.
Hepatitis D virus, also known as the delta agent, is an incomplete RNA virus that cannot cause infection or replicate without the coexistence of concurrent acute or chronic HBV infection.11 It is seen principally in the intravenous drug abuse population. Infection with hepatitis D virus amplifies the severity of the underlying HBV infection. It is a blood-borne pathogen and theoretically could be an occupational infection for HCWs if preexistent HBV infection were present. Effective vaccination against HBV infection eliminates this risk.
Hepatitis G virus is the most recently identified agent (hepatitis F was putatively identified but has not been validated).12 It is considered the same as the GB virus, where the “GB” initials came from the index infected surgeon who was the source of the virus used in early studies. It is blood borne and found commonly with HBV and HCV infection, and it has genetic homology to HCV. Hepatitis G virus is infrequently found as the sole agent in clinical hepatitis. It is present in as many as 1.4% of blood donors and persists in a chronic state for many years.13 The full scope of its clinical relevance and its risk for occupational transmission continue to be debated.
Hepatitis B
HBV infection is the most thoroughly studied of the blood-borne hepatitis events in humans. HBV is a DNA virus that is very efficiently transmitted by exposure to blood or blood products. Before the era of effective vaccination, HBV infection was the most common and most serious of occupational infections for surgeons. A single hollow-needle percutaneous injury is associated with a 25% to 30% risk of transmission to a naïve host.14 In society, intravenous drug abuse with shared needles has been a major source of transmission of the infection. The virus is a sexually transmitted disease, which has led to a national initiative to vaccinate the pediatric and adolescent populations against HBV.15 Effective screening of the blood supply has virtually eliminated contaminated units of transfused blood as a source of new cases of HBV infection.
Access of the HBV virus to the host results in binding and internalization of the virus within hepatocytes. Viral replication occurs at varying rates after infection. In only about 25% of acute infections is there a clinically discernible hepatitis syndrome.16 The majority of cases either are characterized by a mild malaise without jaundice or have a completely indolent character. Among all acute infections, about 5% of cases result in chronic sustained infection that persists indefinitely.17 The incidence of chronic infection is not related to whether acute infection was identified, which means that many individuals with chronic disease are unaware of the disease. This chronic state of infection is associated with sustained damage to the liver, although selected cases may have a persistent viremia without evidence of continued liver damage. Hepatocellular carcinoma, portal hypertension, and end-stage liver disease from hepatic cirrhosis are the consequences of the chronic disease for many patients.18 An individual with chronic HBV infection is a reservoir of virus for the infection of others. It is currently estimated that more than 1 million individuals in the United States have chronic HBV infection,19 and the numbers in the international community are many millions more.
HBV infection in surgeons in the era before the availability of a vaccine was quite common. In a 1996 study, about a third of surgeons in practice for more than 10 years had serologic evidence of previous HBV infection.20 About a third had been vaccinated, but a third were serologically devoid of antibody and remained vulnerable to acute infection. It was estimated in the late 1980s by the Centers for Disease Control and Prevention (CDC) that 250 HCWs die annually from the consequences of occupationally acquired chronic HBV infection that had obviously been contracted many years previously.21 A more recent analysis has attributed 75 to 250 deaths to occupationally acquired HBV infection for the year 2002.22
In the 1980s, a highly effective HBV vaccine was developed by using attenuated virus from infected patients.23 Recombinant technology rapidly emerged and resulted in the development of an equally effective vaccine that was not derived from other persons. The vaccine is administered in three doses, with the second and third doses being given 1 and 6 months after the initial administration. About 95% of individuals will have an appropriate antibody response to the surface antigen of HBV. Documentation of antibody response is essential, with revaccination being necessary for those who do not seroconvert from the initial immunization effort. Revaccination after a failed initial attempt has a 30% to 50% probability of being successful.24 Vaccination of all surgeons and HCWs is necessary, and not being vaccinated is unacceptable.
Hepatitis C
HCV was identified in 1989 and has for the most part been the virus responsible for NANBH.25 HCV is an RNA virus with multiple different serotypes. It is a source of occupational infection for surgeons and HCWs, but it is less efficiently transmitted than HBV. A percutaneous needlestick from a hollow needle has about a 2% risk of transmission of the infection.26 HCV shares many of the same epidemiologic characteristics of HBV with respect to high-risk populations of patients and means of infection within society.27 Screening of the blood supply for antibody to the virus has dramatically reduced the risk for transfusion-associated infection.
The clinical sequelae after infection of the hepatocyte follow patterns similar to those of HBV. Like HBV, the majority of acute infections are clinically indolent and not associated with a clinical picture of hepatitis.28 However, unlike HBV infection, rates of chronic infection are 60% to 80%.29 The natural history of chronic disease is highly variable, with some patients progressing to end-stage liver disease or hepatocellular carcinoma and others having chronic antigenemia but not an evolving pattern of liver damage.30 Still others may have spontaneous resolution of the infection at a later time. It has an unpredictable time course. Individuals who are antigen positive are infectious to others. There are 3 to 4 million persons in the United States who have chronic HCV infection,31 and HCV has become the primary cause of disease leading to hepatic transplantation.32
There is no vaccine for HCV, although progress has been made with antiviral treatment of this infection.33 HCV infection results in a circulating antibody that is believed to ineffectively neutralize the virus. There are multiple different serotypes of the virus, and reinfection can occur with the same viral type in patients who actually cleared the initial infection. The prospects for a vaccine are challenging when even acute infection does not confer protective immunity for the host against future infection. The antibody response may be delayed for up to 6 months after acute infection, which makes HCV detection in the blood supply more difficult in donors with recent acute infection.
Human Immunodeficiency Virus
HIV infection is transmitted by sexual contact and by intravenous drug abuse. Vertical transmission from infected mothers to newborns has been dramatically reduced in frequency in the United States by the use of antepartum antiretroviral therapy.34 Transmission secondary to blood transfusion has essentially been eliminated with effective screening procedures in the United States and western Europe. HIV infection remains an international pandemic, especially in the African continent, where preventive strategies have been ineffective and treatment of established infection has been unavailable. At present, about 750,000 people are living with HIV infection in the United States, and nearly 600,000 have died since recognition of the disease.35
Considerable effort has been extended in the evaluation and prevention of occupational HIV infection in HCWs. A serologic survey of more than 3000 orthopedic surgeons at a national meeting identified only 2 cases of HIV infection, both of which occurred in individuals with nonoccupational risks for infection.36 Prospective evaluation of mucous membrane and percutaneous exposure events in HCWs has documented 57 cases of occupational infection (Table 47-2).37 The rate of transmission to HCWs from percutaneous exposure is thought to be 0.3%.38 Epidemiologic evaluation of HCWs in whom HIV infection has developed but who do not have nonoccupational risk factors for the disease has resulted in the identification of 139 cases of probable occupational transmission (Table 47-3).
TABLE 47-2 Number of Patients with Documented Seroconversion to HIV after a Specific Exposure Incident*
| OCCUPATION | NO. DOCUMENTED OCCUPATIONAL HIV INFECTIONS |
|---|---|
| Nurses | 24 |
| Clinical laboratory workers | 16 |
| Physicians, nonsurgical | 6 |
| Nonclinical laboratory workers | 3 |
| Housekeeping/maintenance workers | 2 |
| Surgical technician | 2 |
| Embalmer/morgue technician | 1 |
| Health aide/attendant | 1 |
| Respiratory therapist | 1 |
| Dialysis technician | 1 |
| Total | 57 |
* All patients had negative serology at the time of the exposure event and then seroconverted to a positive HIV status after the event.
TABLE 47-3 Number of Health Care Personnel Who Are Thought to Represent Possible Seroconversions for Occupational HIV Infection*
| OCCUPATION | NO. POSSIBLE OCCUPATIONAL HIV INFECTIONS |
|---|---|
| Nurses | 35 |
| Clinical laboratory workers | 17 |
| Health aide/attendants | 15 |
| Housekeeping/maintenance workers | 13 |
| Nonsurgical physicians | 12 |
| Emergency medical technicians | 12 |
| Other technicians/therapists | 9 |
| Surgical physicians | 6 |
| Dental workers/dentists | 6 |
| Dialysis technicians | 3 |
| Surgical technicians | 2 |
| Embalmers/morgue technicians | 2 |
| Respiratory therapists | 2 |
| Others | 5 |
| Total | 139 |
* These cases were identified from the epidemiologic evaluation of health care workers reported to the Centers for Disease Control and Prevention with HIV infection but who were determined after case evaluation not to have nonoccupational risk factors for the infection.
Prevention of Occupational Infection
Personal Protective Barriers
Much has been made of the value of using eye shields and double gloving to prevent contact of blood with the skin or mucous membranes of the surgeon. Every surgeon has had the experience of an arterial or irrigation spray in the face during an operation. Protective eyewear and face shields are available in every operating room and are mandated by the Occupational and Safety Health Administration (OSHA).39 Observations in many operating rooms today will give testimony to the lassitude about occupational infection when one sees inadequate or no eye protection during operations where eye exposure is a real risk.
Double gloving has been shown in many studies to prevent blood contact by the hands of surgeons.40–42 If surgeons wash their hands with isopropyl alcohol after a lengthy craniotomy or a major spine procedure, all of the stinging about the cuticles and elsewhere will be validation that nonintact skin is present. Sustained blood contact by hands with nonintact skin means that occupational infection is a potential risk. Double gloving will prevent blood contact, and the use of indicator systems permits prompt recognition when the glove barrier has been breeched.43
In a previous study, 90% of blood contact with the skin of the operating room team occurred on the hands and forearms (Table 47-4).44
