Infection Control Today - 06/2004: Acute Viral Hepatitis

Acute Viral Hepatitis
A PROBLEM PATHOGEN FOR HEALTHCARE PROFESSIONALS

BY CAROLYN L. TWOMEY, RN, BSN

Think back to the early days of your medical career. Hepatitis was the scourge we heard about the days of hepatitis A, hepatitis B and non-A non-B. Today, viral hepatitis is still a major player worldwide, outdistancing HIV in prevalence and risk. Current World Health Organization (WHO) statistics show that, among the 35 million health workers worldwide, about 3 million receive percutaneous exposures to bloodborne pathogens each year; two million of those to HBV, 0.9 million to HCV and 170,000 to HIV. 1 Yet in the late 1980s, the threat of HIV made the world take a new look at healthcare professionals risks. As a result, universal precautions, and then standard precautions, became the benchmark against which all practice was evaluated.

According to Fry, acute viral hepatitis results in a short-lived, debilitating acute illness that infrequently causes death of a patient. However, certain hepatitis viruses result in chronic disease that lasts for the life of the patient. 2 The impact of this chronic state is not without consequence for healthcare practitioners and perioperative practitioners in particular. We are also finding those who have developed the carrier state of the disease while not having a great deal of impact to that individual that host certainly remains infectious to others.

Today, increased numbers of patients are presenting with cirrhosis or hepatocellular carcinoma, two altogether increasingly common sequelae of chronic hepatitis. According to experts, this augmented prevalence of chronic hepatitis is a significant occupational hazard to any healthcare practitioner who encounters blood or body fluid as a reality of their practice. It is no surprise to learn that occupationally acquired hepatitis infection is on the rise.3

Today, seven specific viruses known as hepatotropic viruses have been identified as being responsible for the disease we commonly call hepatitis.4 There are other viruses that also cause liver infections, such as Epstein-Barr, yellow fever and cytomegalovirus, but these infections are not classified as acute viral hepatitis and are considered discrete syndromes.5 Of the seven acute viruses, hepatitis F has provisional designation from some experts but remains unrecognized by such bodies as the WHO.6 Many experts believe, however, that there are additional hepatitis viruses unidentified as of yet.7-8 It is important to understand the risk of each of these viruses to the patient as well as the healthcare professional.

Hepatitis A

Hepatitis A (HAV) is a single-strand RNA virus or, more specifically, a picornavirus. HAV is a non-enveloped virus that is excreted in stable form from the infected liver to the bile and hence to the gastrointestinal (GI) tract. Investigationally, it has survived in contaminated fresh water, seawater, wastewater, soils, marine sediment, live oysters and creme-filled cookies.9 This virus is quite resistant to degradation in the environment, which fosters its preservation and spread within populations.10

Sources place the U.S. prevalence rate at approximately 200,000 annually11-12 and worldwide at 1.4 million cases annually.13 Hepatitis A infections in children, as well as some adults, are often subclinical in nature, therefore the prevalence rate may indeed be quite a bit higher.

Those at risk for acquiring HAV include:

  • People in household/sexual contact with infected person
  • Medical and paramedical personnel
  • International travelers to endemic countries
  • Preschool children attending day-care centers, their parents and siblings
  • Day-care center employees
  • Residents and staff of closed institutions
  • Homosexually active men
  • Injecting drug users using unsterilized needles
  • Persons with clotting factor disorders
  • Persons with chronic liver disease
  • Food service establishments/food handlers
  • Persons who consume raw oysters or clams14

The viral antigen is found in serum, stool and liver during acute infection.15 Transmission of the virus occurs principally through the fecal-oral route and rarely via parenteral introduction. In order for the transmission to occur parenterally, a blood donor would have to be in the prodromal phase at the time of blood donation. The course of the disease can be characterized in four stages:

The incubation phase, when high concentrations of the virus are shed carrying the greatest probability of transmission, occurs within two to eight weeks (or about 10-50 days) after exposure.16-17 During this time the patient remains asymptomatic.

The prodromal phase, when symptoms like loss of appetite, fatigue, abdominal pain, nausea and vomiting, fever, diarrhea, dark urine and pale stools appear, followed by the icteric phase, during which jaundice develops. Clinically, none of the hepatitis viruses can be differentiated from other hepatitis viruses, and they require serology testing to determine a virus-specific diagnosis.18 It is at this stage that patients often seek medical help. The icteric phase generally begins within 10 days of the initial symptoms. Fever usually improves after the first few days.19 It must be noted that high viral shedding continues to occur until one to two weeks after the onset of jaundice, the icteric phase and may be more prolonged in children and the immunocompromised patient.20

In rare circumstances, extensive necrosis of the liver occurs during the first six to eight weeks of the disease, resulting in fulminant hepatitis. The hallmark signs of fulminant hepatitis include high fever, marked abdominal pain, vomiting and the development of hepatic encephalopathy associated with coma and seizures. The mortality rate of these patients is 70 percent to 90 percent, with a high correlation to increased age. Survival is unusual over 50 years of age. In patients with chronic hepatitis B or C or underlying liver disease, who are super-infected with HAV, the mortality rate increases dramatically.21

Finally, there is the convalescent phase, where resolution of the disease is slow, but patient recovery is uneventful and complete. Chronic sequelae with persistence of HAV infection for more than 12 months are not observed.22 Because the liver sheds the virus into the bile, complete elimination of the virus from the host typically occurs within weeks to months.23

It has been established that during ingestion of contaminated food or water, the virus binds to the epithelium of the upper GI tract where it is absorbed into the circulation. HAV is more prevalent in areas where poor sanitation, insufficient water treatment, or inadequate (or non-existent) handwashing takes place.24 This is carried over in food-preparation situations with either poor regulation of handwashing or contaminated produce as was suspected in the recent Pennsylvania outbreak of HAV in October and November 2003 related to green onion contamination.25 Experts estimate that as many as 50 percent to 75 percent of adults in the United States are positive for antibodies to HAV.26

An effective HAV vaccine has been developed and is recommended for those who travel internationally. This vaccine is also recommended for those with chronic HBV or HCV, for whom the co-infection with HAV is severe and potentially fatal. Because HAV does not have a chronic phase, there has been little focus on occupational exposure. The frequency is low and the occupational impact on healthcare workers is negligible.27 Treatment is supportive care and antivirals are not indicated in this case.

Hepatitis B

The hepatitis B virus (HBV) is a double-stranded DNA virus made up of a core surrounded by a lipoprotein coat, which contains the surface antigen HbsAg and gives rise to the term enveloped virus. 28 In the 1940s it was identified as a disease called serum hepatitis.29 Historically, clinicians found that not only were intravenous substance abusers particularly vulnerable but also those who had received blood transfusions. It was particularly concerning that the donation of blood could take place when there was no clinical manifestation of the disease. Because patients with HBV have very high viral titers, as much as 108 to 1010 viral units per milliliter, a percutaneous exposure to even minute amounts of blood is a risk for seroconversion.30 HBV is 100 times more infectious than HIV.31 This fact also explains the severity of infection of those who received HBV-contaminated blood prior to current strategies for screening of the banked blood supply, which has been established in the last 25 years.32 It is noted that the sensitivity of the screening tests have increased significantly in the last 15 to 20 years and the risk of seroconversion in the U.S. today is nominal.33 In addition, those agents that are derived from plasma, such as clotting factors, are subjected to additional procedures, which result in little or no transmission of HBV.

The prevalence of HBV is greatest in developing nations with inadequate medical care. In countries with higher standards of living such as the U.S., Canada, the U.K., and other European nations, prevalence is much lower.34 In the U.S., infection is most common in young adults. There are four recognized modes of transmission:

  • From mother to child at birth
  • By contact with an infected individual
  • By sexual contact
  • By percutaneous exposure to blood or other infected fluids

Because the enzymes within the GI tract inactivate this virus, feces are not a risk source. Although HbsAg has been found in all body fluids, only blood, vaginal and menstrual fluids, and semen have been demonstrated to be infectious. It is important to note here that HBV can survive at least seven days on environmental surfaces or in dried blood35 and inoculation can occur via such household items as: toothbrushes, baby bottles, toys, razors, eating utensils in contact with mucous membranes or openings in the skin.36

HBV risk groups include:

  • Infants born to infected mothers
  • Children in day care
  • Sexual and household contacts of infected individuals healthcare workers
  • Patients and employees in hemodialysis centers
  • Injecting drug users
  • People sharing unsterile medical or dental equipment
  • Those providing or receiving acupuncture and/or tattooing with unsterile devices
  • Individuals traveling to or living in areas where HBV is endemic
  • Sexually active heterosexuals
  • Male homosexuals37

The manifestation of HBV infection varies considerably depending on the patients age, immune status and the stage of disease progression when the infection is identified. Some report that only 25 percent of infected patients present with a clinical syndrome. Seventy-five percent present with nonspecific viral symptoms or no clinical presentation manifestation at all.38 The clinical phases of the infection are:

1. The incubation period varies between 45 and 120 days, depending on the level of the inoculum, mode of transmission, and host immunity. The average is 60 to 90 days. The onset of symptoms is insidious, initiating with tiredness, anorexia, abdominal discomfort, nausea and vomiting, mild fever if at all, and sometimes a rash. The larger the inoculum, the shorter the incubation period, with the largest inoculum occurring through blood transfusion.

2. The icteric phase usually occurs within 10 days of the onset of initial symptoms, beginning with dark urine and clay-colored stools. Initial jaundice appears in the mucous membranes, conjunctiva, sclera, and then skin. It becomes clinically apparent when total bilirubin exceeds 20 to 40 mg/l. This rise in bilirubin is accompanied by hepatomegaly and splenomegaly.

3. The recovery phase follows in about four to 12 weeks, with the resolution of jaundice and the development of protective antibodies in nearly 95 percent of adults.39 As little as 1 percent may progress to fulminant hepatitis.40

4. The chronic phase of HBV occurs in 5 percent to 10 percent of those who acquire acute HBV as adults as the virus continues to survive in the body. In children, this percentage can be considerably higher, but they instead become chronic carriers. Chronic hepatitis can result in serious destructive liver disease, including cirrhosis (in as much as 20 percent) and hepatocellular carcinoma. World-wide HBV is attributed with causing 60 percent to 80 percent of liver cancers.41 HBV is a serious world-wide pathogen for which there is an effective vaccine.

Many experts believe that global control of HBV is possible through vaccination. According to the WHO, 85 percent to 90 percent of HBV-associated deaths are vaccine-preventable.42 There are those who have been vaccinated and report no subsequent titer. The recommended subsequent step is to repeat the series at double the dose.43 If one is a clinical practitioner, Fry believes a prudent choice would be to leave a practice arena that has a risk for blood-borne pathogen exposure. Finally, treatment is focused primarily on management of symptoms.

Other treatment strategies may include:

  • Antivirals, which help support the patients immune system
  • Immune modulators, which help the patients immune system base a defense
  • Interferon , used in the case of chronic HBV, which results in a sustained remission for about 35 percent of chronic HBV patients

Treatment of the sequelae of end-stage chronic hepatitis B, such as peritoneovenous shunts, sclerotherapy, resection of hepatocellular carcinoma and liver transplantation are among the surgical intervention options. These patients represent a significant occupational risk for any perioperative practitioner.

A single hollow-needle percutaneous exposure has the risk of 30 percent probability of transmission insusceptible hosts. Occupationally acquired HBV is common among surgeons; it has been identified as having occurred in 25 to 30 percent of operating surgeons who have been in the practice of surgery for more than 10 years. Lastly, it is estimated that 250 HCWs, primarily nurses and surgeons, die annually as a result of occupationally acquired HBV. The HBV vaccine can prevent occupationally acquired HBV.44

One particularly thorny issue is that of whether a chronically infected professional should continue to participate in surgery. Transmission rates (practitioner to patient) of as much as 13 percent in surgical cases have been reported.45 An expert panel, which has been very recently convened, is currently studying this very issue.

Some sources consider hepatitis C (HCV) to be the virus of greatest significance in the U.S. 46-47 While this may be true, it is important to review some of the material contained within the NIH Consensus Statement of Management of Hepatitis C: 2002. The state-of-the-science conference was convened to review current well-substantiated clinical data and to establish a consensus report (June 2002). The report states that the incidence of newly diagnosed HCV has declined in the US. Although the exact reasons are ambiguous, it is acknowledged that there has been a decrease in cases among injecting drug users, as well as a decrease in cases directly attributable to the implementation of blood donor screening.48 Current estimates place new HCV infections in the U.S. at 35,000 per year.49

HCV is a RNA virus, which is bloodborne and is therefore communicable in much the same routes as HBV through contact with blood and bloody fluids. And much like HBV, some place those who demonstrate the clinical syndrome (once infected) at about 15 percent to 30 percent, while those who are infected and not identified at as much as 70 percent to 85 percent. 50-52 Because of this lack of identification, experts anticipate a fourfold increase in the number of adults diagnosed with chronic HCV from 1990-2015. 53 Experts now concede that the majority of HCV infections become chronic and estimate that about 4 million Americans have been infected and 2.7 of them are chronically infected.54 The Consensus statement did point out that the National Health and Nutrition Examination Survey (NHANES) is a survey of households. It does not take into account those individuals who are incarcerated, homeless or institutionalized, all of which are acknowledged high-risk groups.

HCV is not related to the other hepatitis viruses, as a member of the flavivirus. It is instead related to viruses that cause yellow fever and dengue fever.55 Interestingly enough, there are now six major genotypes of HCV. While all six types occur throughout the world, the most common genotype in the U.S. is genotype 1 (a and b) and it accounts for 70 percent to 80 percent of what is seen in the US.

Experts believe that the many varieties of HCV play a role in the survival of the virus. It makes creating a vaccine exceedingly difficult with todays technology, and it contributes to the difficulty the hosts immune system has in destroying the virus or creating antibodies. HCV can also mutate its amino acid pattern in an infected individual over a period of time, contributing to the difficulty in making a successful vaccine.56-57 In addition, this ability to mutate explains why some patients respond to interferon and others do not.

Those patients with HCV types 2 or 3 are more likely to respond to interferon while those with types 1 or 4 do not.58-59 Recent studies have shown that combined therapy with interferon and ribavirin is more successful than monotherapy alone and is becoming the treatment of choice.60-62

  • Those at risk for HCV include:
  • Intravenous drug users (accounts for 60 percent of new cases)
  • Recipients of blood transfusions before 1992
  • Transplant recipients of solid organ transplants
  • Those acquiring tattoos, ear piercings or body piercings
  • Those who practice substance abuse, such as snorting of cocaine63-66

The clinical phases of HCV are:

  • The incubation period, which may occur from 15-150 days
  • The icteric phase, when the acutely infected patient may exhibit fatigue and jaundice
  • The recovery phase
  • The chronic phase, where the majority of patients who are acutely infected progress

In those chronically infected, cirrhosis occurs in as much as 20 percent with hepatocellular carcinoma occurring in as much as 2 percent to 4 percent per year during the first five years after diagnosis.67-68 Although we tend to view HCV as a less severe disease, one study reports a cumulative rate of hepatocellular carcinoma at 75 percent after 15 years in patients with cirrhosis.69

As to HCW risk, estimates place the risk of infection at a rate of as much as 10 percent after percutaneous exposure with a contaminated hollow needle. There have also been two reports of transmission through splash to the eyes. To date, there is no solid information of transmission via solid needles although surgical acquisition of HCV has been documented.70 Experts consider this virus a significant occupational risk.

Diagnosis today has changed because of the availability of RT-PCR studies. This study is positive within two to three weeks of infection, long before the antibody test is positive. Because of HCW concern regarding transmission today, most proceed with the RT-PCR rather than the recombinant immunoblot assay (RIBA). There is no vaccine and no studies show any benefit from using interferon as a post-exposure treatment.71 The only strategy for prevention is avoidance of exposure to blood and body fluids.

Hepatitis D

Hepatitis D, or delta, is an RNA virus, which is bloodborne. In and of itself, it cannot cause infection of the liver but it is synergistic with HBV because it can only replicate in the presence of HBV. It is seen primarily among injecting drug users. Diagnosis is suspected when the course of HBV is remarkably severe, more than 50 percent of those cases resulting in fulminant HBV being attributed to HDV coinfection. Infection is established using the RT-PCR assay. There are reports of some benefit from interferon . However, many of these patients will progress to endstage liver disease and become candidates for transplantation.72-72

Prevalence rates are as yet unknown. It is considered of minimal risk to HCWs as an occupational infection. It is important to remember that effective HBV vaccination thwarts the infection risk of HDV as well.74-77

Hepatitis E

Hepatitis E is a RNA virus, which causes sporadic and epidemic hepatitis. It is endemic in developing countries with poor sanitation. HEV is seen most commonly in ages 15 to 40. If it is present in children, they are almost always asymptomatic and anicteric.

People who are at risk of contracting HEV include:

  • Persons residing in endemic areas International travelers to endemic areas
  • Refugees in temporary overcrowded camps following catastrophes78

The incubation period is from three to eight weeks with an average of 40 days. The clinical presentation is analogous to HAV although the severity is generally greater than HAV. Typically HEV is self-limiting, although it can result in a fulminant form in rare circumstances. At present, there has not been any documentation of a carrier state or associated cirrhosis or hepatocellular carcinoma.79

Hepatitis G/GBV-C was identified in 1995-1996 when studying the frozen sera of a surgeon (with the initials GB) who had presented with non-A non-B hepatitis more than 20 years previously.80 There were three viral serotypes identified, which were named GBV-A, GBV-B and GBV-C. GBV-C or HGV, as well as the other two, are similar in sequencing to HCV and other flavivirus organisms. This may indicate that HCV and HGV could be the first in a series of related viruses that had previously escaped identification.81-82

HGV is a bloodborne pathogen with routes of transmission similar to HBV and HCV. While the disease is still to be defined, to date the acute phase appears to be occult and the frequency of chronic infection is unresolved. There has been little documentation of progression to cirrhosis when it is the only infecting pathogen. There is also substantiation that HGV is synergistic with HBV and HCV yielding a much more rapid course to cirrhosis in these cases. RT-PCR is the only way to identify this virus. It is interesting to note that in large numbers of banked blood units, HGV has been identified with at least the same prevalence of HCV as in the general population.83 To date, there is no screening test of blood products for HGV as the long-term sequelae are yet defined. Although the risk of HGV hasnt been determined, remember that the original virus was isolated from a surgeon.84

Occupational Risk

The No. 1 indication for liver transplantation today are patients with endstage renal disease and portal hypertension secondary to viral hepatitis.85 Because of this need and the occult nature of so many of these hepatitis viruses, hepatitis, particularly B, C, and G, have become a significant risk to HCWs. Occupational exposure to HCV via hollow needlestick and subsequent seroconversion is estimated at 1.8 percent and HBV at 30 percent.86 For susceptible surgeons who have been in practice for more than 10 years, 25 percent to 30 percent have occupationally-acquired HBV. There have been reports of transmission of HBV and HCV from splash to the eyes. There is no data available on solid needle transmission in the surgical environment. Experts warn that because there is no vaccine or immunoglobin therapy in the case of HCV or HGV, the only preventive measure is prudent selection of barrier protection.87

While all of the science and research is interesting, the final conclusions determined throughout the studies and papers are:

  • Get your Hepatitis B vaccine, no excuses.
  • Check your Hepatitis B titer and repeat vaccine at double the dose if titers are inadequate
  • If your HBV titer continues to reflect lack of vaccination, consider your risk of exposure in your chosen profession
  • Assure your best barrier protection. Optimally, in the perioperative environment, this means eye protection, double gloving, perhaps double gowning or sleeving when cases demand it
  • Maintain a keen awareness of sharps in your working environment and consider employing changes in your practice, such as no-touch passing of instruments or the use of blunt needles
  • Use a surgical scrub with the best persistence you can achieve in order to give you your best barrier protection under your glove88-91

One final note about your selection of barrier protection. Consider this question. The last time you removed your gloves after a case in the OR and found blood on your hands, did you know you had a barrier breech? Would the benefit of knowing at the time of the barrier breech have been of benefit?

I would guess that most answered yes to this question. Of course, we want to know, but how do we go about doing just that? There are two methods on the market today either electronic monitoring devices or a proprietary color puncture indicator glove system.92 Electronic monitoring systems, which include a pad for the practitioners to stand on and a freestanding monitor, are both equipment-intensive and costly. The colored puncture indication system, which includes a colored under-glove used with a translucent outer glove, significantly increases the immediate awareness of perforation in the presence of fluid.93-94 Think of it as a good, better, best scenario: a high-quality single glove barrier is good; a double-gloving barrier is better; and a color puncture indicator glove system that tells you immediately that there is a breach in your first line of defense is the best. Numerous experts and practitioners call it fundamental and vital... you call it visible protection.

Carolyn L. Twomey, RN, BSN, is a clinical nurse consultant for Regent Medical.

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