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In this issue of the Journal, Hanna et al highlight
the serious problem of acute hepatitis A in Indigenous children in far
north Queensland communities.1 This should come as no
surprise, as these communities are plagued by poverty, educational
disadvantage and poor living conditions -- the very circumstances in
which this infection occurs. Indeed, Indigenous children in rural
and remote Australia generally have an extraordinarily high burden
of infectious disease, with attack rates for conditions such as
invasive pneumococcal disease as high as any in the world.2 The incidence of
hepatitis A virus (HAV) infection in north Queensland in 1996-1997
was up to six times higher among Aboriginal and Torres Strait Islander
people than among non-Indigenous people.3 Indigenous people
accounted for 29% of all HAV infections but only 8.1% of the
population, and contracted HAV infection at a mean age of 12 years
compared with 30 years for the general population. The most common
risk factor for HAV infection was living in or visiting a rural
Aboriginal or Torres Islander community.
An effective hepatitis A control program requires effective
vaccines as well as generic programs for improving Indigenous
health. An effective vaccine for HAV infection exists,4 but it has been
suggested that HAV vaccination is not necessary in Aboriginal and
Torres Strait Islander communities, as HAV infection is endemic (eg,
a 1994 study found that 98.5% of people over the age of 10 years had had
HAV infection5). However, young children
(aged three to five years) are both very vulnerable to severe
infection and significant transmitters of infection, and could be
targeted by community-wide HAV vaccination programs.3
The patients reported by Hanna et al highlight a severe complication
of HAV infection -- fulminant hepatic failure. As the case fatality
rate for HAV infection in Australia is thought to be 0.2%,6 cases of
fulminant hepatic failure are not unexpected in communities with a
high prevalence of HAV infection. Generally, outcomes of fulminant
hepatic failure are better if it is secondary to HAV infection than to
other causes, such as drugs, hepatitis B or hepatitis "X" (caused by
unidentified viruses).7 However, children aged
under 10 years and adults aged over 40 years do worse, irrespective of
cause.7 The children reported by
Hanna et al were all under 10 years, had severe hepatitis and were
transferred to tertiary care centres relatively late in the course of
their illness. All three died of cerebral oedema, raising the
important issue of fluid management in patients with fulminant
hepatic failure: aggressive fluid replacement is not part of the
management of acute liver failure and may even be detrimental by
precipitating cerebral oedema. In the children reported by Hanna et
al, delayed diagnosis and late referral were probably contributing
factors to cerebral oedema. Early indicators of fulminant hepatitis
include a serum bilirubin level of > 300 µmol/L,
prolongation of clotting time and hypoglycaemia.7
These cases also raise the issue of organ transplantation in
Aboriginal and Torres Strait Islander populations. Aboriginal
people from remote regions have worse outcomes than non-Aboriginal
people after renal transplantation, probably because of their
higher rates of comorbidity, especially "syndrome X" disorders
(insulin resistance, associated obesity and
hyperlipidaemia).8 Obviously, this would be
much less of a problem for liver transplantation in Aboriginal
children with fulminant hepatic failure.8 There is no reason that
Aboriginal and Torres Strait Islander people would have inherently
poorer outcomes after liver transplantation than other people,
although issues related to primary health care and long term
follow-up must be addressed. Indeed, the high prevalence of
hepatitis B in the adult Aboriginal community makes the issue of liver
transplantation even more relevant. Liver transplantation should
clearly be considered a therapeutic option for severe liver disease
in the Aboriginal population. The Australian National Liver
Transplant Unit has performed liver transplants on two Aboriginal
adults with good medium-term outcomes.
However, none of the above issues can be addressed in isolation from
general issues of Aboriginal health. Prevention and detection of
disease and treatment of severe infection are possible only if the
basic requirements for improving Aboriginal health are in place.
These include improved environmental and living conditions and
comprehensive and competent primary healthcare delivery systems.
There is now considerable evidence that poor living conditions in
Aboriginal communities can be improved by focusing on delivery and
maintenance of "health hardware" (such as waste removal and supply of
cold and hot water and the means to clean living areas).9 Furthermore,
effective vaccination programs and appropriate primary care
management of sick children can occur only in the setting of
sustainable, primary healthcare systems. This requires a range of
initiatives, in particular supply of a competent rural health
workforce.
Appropriate protocols for referring sick children are also needed,
as well as access to rapid and appropriate evacuation to large
regional hospitals. We believe that the recommendations of Hanna et
al on when to refer are far too conservative. Surely, any young child
with clinical or biochemical hepatitis needs to be referred at least
to a large base hospital, where immediate investigation and
assessment is possible.
The patients reported by Hanna et al raise many issues about
healthcare in Aboriginal and Torres Strait Islander communities,
including the need to:
- provide and maintain
functioning "health hardware";
- establish sustainable primary healthcare systems;
- deliver effective vaccines for common infectious diseases;
- develop protocols for patient referral;
- provide rapid access and evacuation to large regional hospitals;
and
- demystify organ transplantation as an effective therapeutic
procedure for fulminant hepatic failure.
These are all achievable!
Geoffrey W McCaughan
A W Morrow Professor of Gastroenterology
and Hepatology A W Morrow
Gastroenterology and Liver
Centre Australian National Liver
Transplant Unit
Royal Prince Alfred Hospital
and University of
Sydney, Sydney, NSW
Paul J Torzillo
Medical Director, Nganampa Health Council, Umuwa, SA
Clinical Associate Professor of Medicine
Department of
Respiratory Medicine
Royal Prince Alfred Hospital
and University
of Sydney, Sydney, NSW
- Hanna JN, Warnock TH, Shepherd RW, Selvey LA. Fulminant hepatitis A
in Indigenous children in north Queensland. Med J Aust 2000;
172: 19-21.
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Torzillo PJ, Hanna JN, Morey F, et al. Invasive pneumococcal
disease in central Australia. Med J Aust 1995; 162:
182-186.
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Merritt A, Symons A, Griffiths M. The epidemiology of acute
hepatitis A in North Queensland 1996-1997. Commun Dis Intell
1999; 23: 120-124.
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Bader TF. Hepatitis A vaccine. Am J Gastroenterol 1996; 91:
217-222.
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Bowden SJ, Currie BJ, Miller NC, et al. Should Aboriginals in the
"Top End" of the Northern Territory be vaccinated against hepatitis
A. Med J Aust 1994; 161: 372-373.
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Amin J, Heath T, Morrell S. Hepatitis A in Australia in the 1990s:
future directions in surveillance and control. Commun Dis
Intell 1999; 23: 113-120.
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O'Grady JG, Alexander GHM, Haylor KM, Williams R. Early
indications of prognosis in fulminant hepatic failure.
Gastroenterology 1989; 97: 439-445.
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Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal
failure amongst Aboriginal Australians. Med J Aust 1998;
168: 537-541.
-
Pholeros P, Rainow S, Torzillo PJ. Housing for health -- towards a
healthier living environment for Aborigines. Sydney:
Healthabitat, 1994.
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