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Ear disease in Indigenous Australians: A literature review

Introduction

The Australian Indigenous versus non-Indigenous mortality gap is worse in Australia than in any other Organisation for Economic Coopera tion and Development nation with disadvantaged Indigenous populations, including Canada, New Zealand, and the USA. [1] This gap reached a stark peak of seventeen years in 1996-2001. [2] Otitis media affects 80% of Australian children by the age of three years, being one of the most common diseases of childhood. [3]

Whilst ear diseases and their complications are now rarely a direct cause for mortality, especially since the advent of antimicrobial therapy and the subsequent reduction in extracranial and intracranial complications, [4] the statistics of ear disease nevertheless illustrate the unacceptable disparity between the health status of these two populations cohabiting a developed nation, and are an indictment of the poor living conditions in Indigenous communities. [5] Moreover, the high prevalence of ear disease among Aboriginal and Torres Strait Islanders is associated with secondary complications that represent significant morbidity within this population, most notably conductive hearing loss, which affects up to 67% of school-age Australian Indigenous children. [6]

This article aims to illustrate the urgent need for the development of appropriate strategies and programs, which are founded on evidencebased research and also integrate cultural consideration for, and design input from, the Indigenous communities, in order to reduce the medical and social burden of ear disease among Indigenous Australians.

Methodology

This review covered recent literature concerning studies of ear disease in the Australian Indigenous population. Medical and social science databases were searched for recent publications from 2000-2011. Articles were retrieved from The Cochrane Library, PubMed, Google Scholar and BMJ Journals Online. Search terms aimed to capture a broad range of relevant studies. Medical textbooks available at the medical libraries of Notre Dame University (Western Australia) and The University of Western Australia were also used. A comprehensive search was also made of internet resources; these sources included the websites of The Australian Department of Health and Ageing, the World Health Organisation, and websites of specific initiatives targeting ear disease in the Indigenous Australian population.

Peer reviewed scientific papers were excluded from this review if ear disease pertaining to Indigenous Australians was not a major focus of the paper. Studies referred to in this review vary widely in type by virtue of the multi-faceted topic addressed and include both qualitative and quantitative studies. For the qualitative studies, those that contributed new information or covered areas that had not been fully explored in quantitative studies were included. Quantitative studies with weaknesses arising from small sample size, few factors measured or weak data analysis were included only when they provided insights not available from more rigorous studies.

Overview and epidemiology

The percentage of Australian Indigenous children suff ering otitis media and its complications is disproportionately high; up to 73% by the age of twelve months. [7] In the Australian primary healthcare settng, Aboriginal and Torres Strait Islander children are five times more likely to be diagnosed with severe otitis media than non-Indigenous children. [8]

Chronic suppurative otitis media (CSOM) is uncommon in developed societies and is generally perceived as being a disease of poverty. The World Health Organisation (WHO) states that a prevalence of CSOM greater than or equal to 4% indicates a massive public health problem of CSOM warranting urgent attention in targeted populations. [9] CSOM affects Indigenous Australian children up to ten times this proportion, [5] and fifteen times the proportion of non-Indigenous Australian children, [8] thus reflecting an unacceptably great dichotomy of the prevalence and severity of ear disease and its complications between Indigenous and non-Indigenous Australians.

Comparisons of the burden of mortality and the loss of disabilityadjusted life years (DALYs) have been attempted between otitis media (all types grouped together) and illnesses of importance in developing countries. These comparisons show that the burden of otitis media is substantially greater than that of trachoma, and comparable with that of polio, [9] with permanent hearing loss accounting for a large proportion of this DALY burden.

Whilst there are some general indications that the health of Indigenous Australian children has improved over the past 30 years, such as increased birth weight and lower infant mortality, there is evidence to suggest that morbidities associated with infections such as respiratory infections and otitis media have not changed. [10-12]

Middle Ear disease: Pathophysiology and host risk factors

The disease process of otitis media is a complex and dynamic continuum. [10] Hence there is inconsistency throughout the medical community regarding defi nitions and diagnostic criteria for this disease, and controversy regarding what constitutes “gold standard” treatment. [7,13] In order to form a discussion about the high prevalence of middle ear diseases in Indigenous Australians, one must first establish an understanding of their aetiology and pathogenicity. Host-related risk factors for otitis media include young age, high rates of nasopharyngeal colonisation with potentially pathogenic bacteria, eustachian tube dysfunction and palato-facial abnormalities, lack of passive immunity and acquisition of respiratory tract infections in the early stages of life. [7,9,10,14,15]

Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis are the recognised major pathogens of otitis media. However, this disease has a complex, polymicrobial aetiology, with at least fifteen other genera having been identified in middle ear eff usions. [11] The organisms involved in CSOM are predominantly opportunistic organisms, especially Pseudomonas aeruginosa, which is associated with approximately 20-50% of CSOM in both Aboriginal, Torres Strait Islander and non-Indigenous children. [10]

Relatively new findings in otitis media pathogenicity have included the identification of Alloiococcus otitidis and human metapneumovirus. [13] A. otitidis in particular, a slow-growing aerobic gram positive bacterium, has been identified in as many as 20-30% of middle ear eff usions in children with CSOM. [13,16,17] The importance of interaction between viruses and bacteria (with the major identified viruses being adenovirus, rhinovirus, polyomavirus and more recently human metapneumovirus) is well recognised in the pathogenicity of otitis media. [13,18,19] High identification rates of viral-bacterial co-infection found in asymptomatic children with otitis media (42% Indigenous and 32% non-Indigenous children) underscore the potential value in preventative strategies targeted at specific pathogens. [19] The role of biofi lms in otitis media pathogenesis has been of great interest since a fluorescence in-situ hydridisation study detected biofi lms in 92% of middle ear mucosal biopsies from 26 children with recurrent otitis media or otitis media with eff usion. [20] This suggested an explanation for the persistence and recalcitrance of otitis media, as bacteria growing in biofi lm are more resistant to antibiotics than planktonic cells. [20]

However, translating all this knowledge into better health outcomes – by means of individual clinical treatment and community preventative strategies – is not straightforward. A more thorough understanding of the polymicrobial pathogenesis is needed if more effective therapies for otitis media are to be achieved.

Some research has been involved in the possibility of a genetic predisposition to otitis media, based on its high prevalence observed across several Indigenous populations around the world, including the Indigenous Australian, Inuit, Maori and Native American peoples. [10] However, whilst the suggestion that genetic factors may play a role in otitis media susceptibility is a worthwhile area of further research, its emphasis should not overlook the significance of poverty, which generally exists throughout colonised Indigenous populations worldwide and is a major public health risk factor. It should be remembered that socioeconomic status is a major determinant of disparities in Indigenous health, irrespective of genetics or ethnicity.

Environmental risk factors

The environmental risk factors for otitis media are well recognised and extensively documented. They include season, inadequate housing, overcrowding, poor hygiene, lack of breastfeeding, pacifier use, poor nutrition, exposure to cigarette or wood-burning smoke, poverty and inadequate or unavailable health care. [5,7,9,10,21]

Several recent studies have examined the impact of overcrowding and poor housing conditions on the health of Indigenous children, with a particular focus on upper respiratory tract infections and ear disease. [22-24] The results of these studies reinforced the belief that elements of the household and community environment are important underlying determinants of the occurrence of common childhood conditions, which impair child growth and development, contribute to the risk of chronic disease and to the seventeen year gap in life expectancy between Aboriginal and Torres Strait Islander people and non-Indigenous Australians. [22, 23] Interestingly, one study’s findings identified the potential need for interventions which could target factors that negatively impact the psychosocial status of carers and which could also target health-related behaviour, including maintenance of household and personal hygiene. [22]

Raised levels of stress and poor mental health associated with the psycho-spatial elements of overcrowded living (that is, increased interpersonal contact, lack of privacy, loss of control, high demand, noise, lack of sleep) may therefore be considered as having a negative impact on the health of dwellers, especially those whose health largely depends on care from others, such as the elderly and young children, who are more susceptible to disease. Urgent attention is needed to improve housing and access to clean running water, nutrition and quality of care, and to give communities greater control over these improvements.

Exposure to environmental smoke is another significant, yet potentially preventable, risk factor for respiratory infections and otitis media in Indigenous children. [25,26] Of all the environmental risk factors for otitis media mentioned above, environmental smoke exposure is arguably the most readily amenable to modification. A recent randomised controlled trial tested the efficacy of a family-centred tobacco control program, aimed at reducing the incidence of respiratory disease among Indigenous children in Australia and New Zealand. It was found that interventions aimed at encouraging smoking cessation as well as reducing exposure of Indigenous children to environmental smoke had the potential for significant benefit, especially when the intervention designs included culturally sound, intensive family-centred programs that emphasised capacitybuilding of the Indigenous community. [25] Such studies testify to the potentially high levels of interest, cooperativeness, pro-activeness and compliance demonstrated by Indigenous communities regarding public health interventions, given the study design is culturally appropriate and accepts that Indigenous people need to be meaningfully engaged in preventative health efforts.

Preventative strategies

The advent of the 7-valent pneumococcal conjugate vaccine has seen a substantial decrease in invasive pneumococcal disease. However, changing patterns of antibiotic resistance and pneumococcal serotype replacement have been documented since the introduction of the vaccine, and large randomised controlled trials have shown its reduction of risk of acute otitis media and tympanic membrane perforation to be minimal. [13,27] One retrospective cohort study’s data suggested that the pneumococcal immunisation program may be unexpectedly increasing the risk of acute lower respiratory infection (ALRI) requiring hospitalisation among vaccinated children, especially after administration of the 23vPPV booster at eighteen months of age. [28] These findings warrant re-evaluation of the pneumococcal immunisation program and further research into alternative medical prevention strategies.

Swimming pools in remote communities have been associated with reduced prevalence of tympanic membrane perforations (as well as pyoderma), indicating the long term benefits associated with reduction in chronic disease burden and improved educational and social outcomes. [6] No outbreaks of infectious diseases have occurred in the swimming pool programmes to date and water quality is regularly monitored according to government regulations. On the condition that adequate funding continues to maintain high safety and environmental standards of community swimming pools, their net effect on community health will remain positive and worthwhile.

Treatment: Current guidelines and practices, potential future treatments

Over the last ten years there has been a general tendency to reduce immediate antibiotic treatment for otitis media for children aged over two years, with the “watchful waiting” approach having become more customary among primary care practitioners. [7] The current therapeutic guidelines note that antibiotic therapy provides only modest benefit for otitis media, with sixteen children requiring treatment at first presentation to prevent one child experiencing pain at two to seven days. [29] Routine antibiotics are recommended only for infants less than six months and for all Aboriginal and Torres Strait Islander children at the initial presentation of acute otitis media. [8] Current guidelines acknowledge that suppurative complications of otitis media are common among Indigenous Australians; hence specific therapeutic guidelines apply to these patients. [30] For those patients in whom antibiotics are indicated, a twice-daily regimen, five day course of amoxicillin is the antibiotic agent of choice. Combined therapy with a seven day course of higher-dose amoxicillin and clavulanate is recommended for poor response to amoxicillin or patients in high-risk populations for amoxicillin-resistant Streptococcus pneumoniae. For CSOM, topical ciprofl oxacin drops are now approved for use in Aboriginal and Torres Strait Islander children, since a study in 2003 contributed to their credibility in the treatment of CSOM. [31,32]

Treatment failure with antibiotics has been observed in some Aboriginal and Torres Strait Islander communities due to poor adherence to the twice-daily regimen of five and seven day courses of amoxicillin. [33] The reasons for non-adherence remain unclear. They may relate to language barriers (misinterpretation or non-comprehension of instructions regarding antibiotic use), storage (lacking a home fridge in which to keep the antibiotics), shared care of the child patient (rather than one guardian) or remoteness (reduced access to healthcare facility and reduced likelihood of follow-up). Treatment failure with antibiotics has also been noted in cases of optimal compliance in Indigenous communities, indicating that poor clinical outcomes may also be due to organism resistance and/or pathogenic mechanisms. [11]

A recent study compared the clinical effectiveness of a single-dose azithromycin treatment with the recommended seven day course of amoxicillin among Indigenous children with acute otitis media in rural and remote communities in the Northern Territory. [33] Whilst azithromycin was found to be more effective at eradicating otitis media pathogens than amoxicillin, azithromycin treatment was associated with an increase in carriage of azithromycin-resistant Streptococcus pneumoniae. Another recent study investigated the antimicrobial susceptibility of Moraxella catarrhalis isolated from a cohort of children with otitis media in the Kalgoorlie-Boulder region of Western Australia. [34] It was found that a large proporstion of strains were resistant to ampicillin and/or co-trimoxazole. Findings from studies such as these indicate that the current therapeutic guidelines, which recommend amoxicillin as the antibiotic of choice for treatment of otitis media, may require revision.

Overall, further research is needed to determine which antibiotics best eradicate otitis media pathogens and reduce bacterial load in the nasopharynx in order to achieve better clinical outcomes. Recent studies indicate that currently recommended antibiotics may need to be reviewed in light of increasing rates of resistant organisms and emerging evidence of new organisms.

Social ramifications associated with ear disease

There is substantial evidence to demonstrate that ear disease has a significant negative impact on the developmental future of Aboriginal and Torres Strait Islander children. [35] Children who are found to have early-onset otitis media (under twelve months) are at high risk of developing long-term speech and language problems secondary to conductive hearing loss, with the specific areas of cognition thought to be affected being auditory processing, attention, behaviour, speech and language. [36] Between 10% and 67% of Indigenous Australian school age children have perforated tympanic membranes, and 14% to 67% have some degree of hearing loss. [37]

Sub-optimal hearing can be a serious handicap for Indigenous children who begin school with delayed oral skills, especially if English is not their first language. Learning the phonetics and grammar of a second language with the unrecognised disability of impaired hearing renders the classroom experience a difficult and unpleasant one for the student, resulting in reduced concentration and increased distractibility, boredom and non-attendance. Truancy predisposes to anti-social behaviour, especially among adolescents, who by this age tend to no longer have infective ear disease but do have established permanent hearing loss. [38] Poor engagement in education and employment, alcohol-fuelled interpersonal violence, domestic violence, and communication difficulties with police and in court have all been linked to the disadvantage of hearing loss and the eventuation of becoming involved in the criminal justice system. [39]

In the Northern Territory, where the Indigenous population accounts for only 30% of the general population, 82% of the 1100 inmates in Northern Territory correctional facilities in the year 2010 were found to be Aboriginal or Torres Strait Islander. [40] Two recent studies conducted within the past two years investigated the prevalence of hearing loss among inmates in Northern Territory correctional facilities. They found that more than 90% of Australian Indigenous inmates had a significant hearing loss of >25dB. [39] A third study in a youth detention centre in the Northern Territory demonstrated that as many as 90% of Australian Indigenous youth in detention may have hearing loss, [41] whilst yet another study found that almost half the female Indigenous inmates at a Western Australian prison had significant hearing loss, almost ten-fold that of the non-Indigenous inmates. [37]

The fact that the Northern Territory study of adult inmates showed a comparatively low prevalence of hearing loss among Indigenous persons who weren’t imprisoned (33% not imprisoned compared with 94% imprisoned) [39] demonstrates a strong correlation between the high prevalence of hearing loss and the over-representation of Indigenous people in Australian correctional facilities. Although this area warrants further research, the data from these studies demonstrate that the higher prevalence of hearing loss among Indigenous inmates suggests that ear disease and hearing loss may have played a role in many Aboriginal and Torres Strait Islander people becoming inmates.

Changes and developments for the future

As we have discussed throughout this article, the unacceptably high burden of ear disease among Indigenous Australians is due to a myriad of medical, biological, socio-cultural, pedagogical, environmental, logistical and political factors. All of these contributing factors must be addressed if a reduction in the morbidity and social ramifications associated with ear disease among Indigenous Australians is to be achieved. The great dichotomy in health service provision could eventually be eradicated if there is the political will and sufficient, specific funding.

Addressing these factors will require the integration of multi- disciplinary efforts from medical researchers, health care practitioners, educational professionals, correctional facilities, politicians, and most importantly the members of Indigenous communities. The latter’s active involvement in, and responsibility for, community education, prevention and medical management of ear disease are imperative to achievement of these goals.

The Government’s response to a recent federal Senate inquiry into Indigenous ear health included $47.7 million over four years to support changes to the Australian Government’s Hearing Services Program (HSP). This was in addition to other existing funds available to eligible members of the hearing-impaired, such as the More Support for Students with Disabilities Initiative and the Better Start for Children With a Disability intervention. [42] Whilst this addition to the federal budget may be seen as a positive step in the Government’s agenda to ameliorate the burden of ear health among the Indigenous Australian population, it will not serve any utility if the funding is not sustainably invested and effectively implemented along the appropriate avenues, which should:

1. Specifically target and reduce identified risk factors of otitis media.

2. Support the implementation of effective, evidence-based, public health prevention strategies, and encourage community control over improvements to education, employment opportunities, housing infrastructure and primary healthcare services.

3. Support constructive and practical multidisciplinary research into the areas of pathogenicity, diagnosis, treatment, vaccines, risk factors and prevention strategies of otitis media.

4. Support and encourage training and employment for healthcare and educational professionals in regional and remote areas. These professionals include doctors, audiologists, speech pathologists, and teachers, and all of these professions should off er programs that increase the number of practising Aboriginal and Torres Strait Islander clinicians and teachers.

5. Adequately fund ear disease prevention and medical treatment programs, including screening programs, so that they may expand, increase in their number and their efficacy. Such services should concentrate on prevention education, accurate diagnosis, antibiotic treatment, surgical intervention (where applicable) and scheduled follow-up of affected children. An exemplary program is Queensland’s “Deadly Ears” program. [43]

6. Support the needs of students and inmates with established hearing loss in the educational and correctional environments, for example, through provision of multidisciplinary healthcare services and the use of sound field systems with wireless infrared technology.

7. Support community and family education regarding the effects of hearing loss on speech, language and education.

All of these objectives should be fulfi lled by cost-effective, sustainable, culturally-sensitive means. It is of paramount importance that these objectives should be well-received by, and include substantial input from, Indigenous members of the community. Successful implementation of these objectives reaching the grass-roots level (thus avoiding the so-called “trickle-down” effect) will not only require substantially increased resources, but also the involvement of Indigenous community members in intervention design and deliverance.

Conclusion

Whilst there remains a continuous need for valuable research in the area of ear disease, it appears that failure to apply existing knowledge is currently more of a problem than a dearth of knowledge. The design, funding and implementation of prevention strategies, community education, medical services and programs, and modifications to educational and correctional settings should be the current priorities in the national agenda addressing the burden of ear disease among Aboriginal and Torres Strait Islander people.

Acknowledgements

Thank you to Dr Matthew Timmins and Dr Greg Hill for providing

feedback on this review.

Conflicts of interest

None declared.

Correspondence

S Hill: shillyrat@hotmail.com

 

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Review Articles Articles

Suxamethonium versus rocuronium in rapid sequence induction: Dispelling the common myths

Rapid sequence induction (RSI) is a technique used to facilitate endotracheal intubation in patients at high risk of aspiration and for those who require rapid securing of the airway. In Australia, RSI protocols in emergency departments usually dictate a predetermined dose of an induction agent and a neuromuscular blocker given in rapid succession. Suxamethonium, also known as succinylcholine, is a depolarising neuromuscular blocker (NMB) and is commonly used in RSI. Although it has a long history of use and is known for producing good intubating conditions in minimal time, suxamethonium possesses certain serious side effects and contraindications (that are beyond the scope of this article).

If there existed no alternative NMB, then the contraindications associated with suxamethonium would be irrelevant – yet there exists a suitable alternative. Rocuronium, a non-depolarising NMB introduced into Australia in 1996, has no known serious side effects or contraindications (excluding anaphylaxis). Unfortunately, many myths surrounding the properties of rocuronium have propagated through the anaesthesia and emergency medicine communities, and have resulted in some clinicians remaining hesitant to embrace this drug as a suitable alternative to suxamethonium for RSI. This essay aims to dispel a number of these myths through presenting the evidence currently available and thus allowing physicians to make informed clinical decisions that have the potential to significantly alter patient outcomes. It is not intended to provide a clear answer to the choice of NMB in RSI, but rather to encourage further debate and discussion on this controversial topic under the guidance of evidence-based medicine.

One of the more noteworthy differences between these two pharmacological agents is their duration of action. The paralysis induced by suxamethonium lasts for five to ten minutes, while rocuronium has a duration of action of 30-90 minutes, depending on the dose used. The significantly shorter duration of action of suxamethonium is often quoted by clinicians as being of great significance in their decision to utilise this drug. In fact, some clinicians are of the opinion that by using suxamethonium, they insert a certain ‘safety margin’ into the RSI protocol under the belief that the NMB will ‘wear off ’ in time for the patient to begin spontaneously breathing again in the case of a failed intubation. Benumof et al. (1997) [1] explored this concept by methodically analysing the extent of haemoglobin desaturation (SpO2) following administration of suxamethonium 1.0mg/kg in patients with a non-patent airway. This study found that critical haemoglobin desaturation will occur prior to functional recovery (that is, return of spontaneous breathing).

In 2001, a study by Heier et al. [2] was conducted, involving twelve healthy volunteers aged 18 to 45 years who were all pre-oxygenated to an end-tidal oxygen concentration >90% (after breathing a FiO2 of 1.0 for three minutes). Following the administration of thiopental and suxamethonium 1.0mg/kg, no assisted ventilation was provided and the oxygen saturation levels were closely monitored. The results demonstrated that one third of the patients included in the study desaturated to SpO2 <80% (at which point they received assisted ventilation during the trial). As the authors clearly stated, the study participants were all young, healthy and slim individuals who received optimal pre-oxygenation, yet still a significant proportion suff ered critical haemoglobin desaturation before spontaneous ventilationresumed. In a real-life scenario, particularly in the patient population who require RSI, an even higher number of patients would be expected to display significant desaturation due to their failing health and the limited time available to provide pre-oxygenation. Although one may be inclined to argue that the results would be altered by reducing the dose of suxamethonium, Naguib et al. [3] affirmed that, while reducing the dose from 1.0mg/kg to 0.6mg/kg did slightly reduce the incidence of SpO2 <90% (from 85% to 65%), it did not shorten the time to spontaneous diaphragmatic movements. Therefore, the notion that the short duration of action of suxamethonium can be relied upon to improve safety in RSI is not supported and should not be trusted as a reliable means to rescue a “cannot intubate, cannot ventilate” situation.

Having demonstrated that differences in the duration of action should not sway one in the false belief of improving safety in RSI, let us compare the effect of the two drugs on oxygen saturation levels if apnoea was to occur following their administration. As suxamethonium is a depolarising agent, it has the side effect of muscle fasciculations following administration, whereas rocuronium, a non-depolarising agent, does not. It has long been questioned whether or not the existence of fasciculations associated with the use of suxamethonium alters the time to onset of haemoglobin desaturation if the airway was unable to be secure in a timely fashion and thus prolonged apnoea occurred.

This concept was explored by Taha et al. [4] who divided enrolled participants in the study into three groups: lidocaine/fentanyl/ rocuronium, lidocaine/fentanyl/suxamethonium and propofol/ suxamethonium. Upon measuring the time to onset of haemoglobin desaturation (deemed to be SpO2 <95%), it was discovered that both groups receiving suxamethonium developed significantly faster desaturation than the group receiving rocuronium. By analysing the differences between the two groups receiving suxamethonium, one discovers a considerable difference in results, with the lidocaine/ fentanyl group having a longer onset to desaturation than the propofol group. Since lidocaine and fentanyl are recognised to decrease (but not completely attenuate) the intensity of suxamethonium-induced fasciculations, these results suggested that the fasciculations associated with suxamethonium do result in a quicker onset to desaturation compared to rocuronium.

Another recent study by Tang et al. [5] provides further clarification on this topic. Overweight patients with a BMI of 25-30 who were undergoing elective surgery requiring RSI were enrolled in the study. Patients were given either 1.5mg/kg suxamethonium or 0.9mg/ kg rocuronium and no assisted ventilation was provided following induction until SpO2 <92% (designated as the ‘Safe Apnoea Time’). The time taken for this to occur was measured in conjunction with the time required to return the patient to SpO2 >97% following introduction of assisted ventilation with FiO2 of 1.0. The authors concluded that suxamethonium not only made the ‘Safe Apnoea Time’ shorter but also prolonged the recovery time to SpO2 >97% compared to rocuronium. In summary, current evidence suggests that the use of suxamethonium results in a faster onset of haemoglobin desaturation than rocuronium, most likely due to the increased oxygen requirements associated with muscle fasciculations.

Since RSI is typically used in situations where the patient is at high risk of aspiration, the underlying goal is to secure the airway in the minimal amount of time possible. Thus, the time required for the NMB to provide adequate intubating conditions is of great importance, with a shorter time translating into better patient outcomes, assuming all other factors are equal. Suxamethonium has long been regarded as the ‘gold-standard’ in this regard, yet recent evidence suggests that the poor reputation of rocuronium in regards to the time required is primarily due to inadequate dosing. Recommended doses for suxamethonium tend to be reliably stated as 1.0-1.5mg/kg, [6] whereas rocuronium dosages have often been quoted as 0.6mg/kg, which, as will be established below, is inadequate for use in RSI.

A prospective, randomised trial study published by Sluga et al. [7] in 2005 concluded that, upon comparing intubating conditions following administration of either 1.0mg/kg suxamethonium or 0.6mg/kg rocuronium, there was a significant improvement in conditions with suxamethonium at 60 seconds post-administration. Another study [8] examined the frequency of good and excellent intubating conditions with rocuronium (0.6mg/kg and 1.0mg/kg) or suxamethonium (1.0mg/kg). Upon comparison of the groups receiving rocuronium, the 1.0mg/kg group had a consistently greater frequency of both good and excellent intubating conditions at 50 seconds. While the rocuronium 1.0mg/kg and suxamethonium 1.0mg/kg groups had a similar frequency of acceptable intubating conditions, there was a higher incidence of excellent conditions in the suxamethonium group. A subsequent study [9] confirmed this finding, with the intubating physician reporting a higher degree of overall satisfaction with the paralysis provided with suxamethonium 1.7mg/kg when compared to rocuronium 1.0mg/kg. In other words, it appears that the higher dose of 1.0mg/kg of rocuronium produces better intubating conditions than 0.6mg/kg, yet it does not do so to the same extent as suxamethonium.

If no evidence were available comparing an even higher dose of rocuronium, the argument for utilising suxamethonium in RSI would defi nitely be strengthened by the articles presented above. However, a retrospective evaluation of RSI and intubation from an emergency department in Arizona, United States provides further compelling evidence. [10] The median doses used were suxamethonium 1.65mg/ kg (n=113) and rocuronium 1.19mg/kg (n=214) and the study authors state there was “no difference in success rate for first intubation attempt or number of attempts regardless of the type of paralytic used or the dose administered.” To add further weight to this issue, a Cochrane Review in 2008 titled “Rocuronium versus succinylcholine for rapid sequence induction intubation” combined 37 studies for analysis and concluded that “no statistical difference in intubating conditions was found when [suxamethonium] was compared to 1.2mg/kg rocuronium.” [11] Hence, there exists sufficient evidence that with adequate dosing, rocuronium (1.2mg/kg) is comparable to suxamethonium in time to onset of intubating conditions and thus this argument cannot be used to aid in selecting an appropriate neuromuscular blocker for RSI. In recent times, particularly here in Australia, there have been questions posed regarding a supposedly increased risk of anaphylaxis to rocuronium. Rose et al. [12] from Royal North Shore Hospital in Sydney addressed this query in a paper in 2001. They found that the incidence of anaphylaxis to any NMB will be determined by its market share. Since the market share (that is, number of uses) of rocuronium is increasing, the cases of anaphylaxis are also increasing – but importantly, they are only increasing “in proportion to usage.” Of note, the authors state that rocuronium should still be considered a drug of “intermediate risk” of anaphylaxis, compared to suxamethonium which is “high risk”. Although not addressed in this paper, there are additional factors that have the potential to alter the incidence of anaphylaxis, such as geographical variation that may be related to the availability of pholcodine in cough syrup. [13]

Before the focus of this paper shifts to a novel agent that has the potential to significantly alter the decision of selecting between suxamethonium versus rocuronium in RSI, there remains a pertinent issue that needs to be discussed. It appears as though one of the key properties of suxamethonium is its brief duration of only five to ten minutes and many clinicians tend to quote this as an important aspect, with the Cochrane Review itself stating that “succinylcholine was clinically superior as it has a shorter duration of action,” despite finding no statistical difference otherwise. [11]

The question that needs to be posed is whether this is truly an advantage of a NMB used in RSI. Patients who require emergency intubation often have a dire need for a secure airway to be established – simply allowing the NMB to “wear off ” and the patient to begin spontaneously breathing again does nothing to alter their situation. One must consider that, even if the clinician was aware of the evidence against relying on suxamethonium’s short duration of action to rescue them from a failed intubation scenario, the decision to initiate further measures (that is, progress to a surgical airway) would be delayed in such a scenario. If rocuronium, with its longer duration of action, was used, would clinicians then feel more compelled to ‘act’ rather than ‘wait’ in this rare scenario, knowing that the patient would remain paralysed? If rescue techniques such as a surgical airway were instigated, would the awakening of the patient (due to suxamethonium terminating its effect) be a hindrance? Although the use of rocuronium presents the risk of a patient requiring prolonged measures to maintain oxygenation and ventilation in a “cannot intubate, can ventilate” scenario, paralysis would be reliably maintained if a surgical airway was required.

No discussion on the debate of suxamethonium versus rocuronium would be complete without mentioning a new drug that appears to hold great potential in this arena – sugammadex. A γ-cyclodextrin specifically designed to encapsulate rocuronium and thus cause disassociation from the acetylcholine receptor, it acts to reverse the effects of neuromuscular blockade from rocuronium. In addition to its action on rocuronium, sugammadex also appears to have some crossover effect on vecuronium, another steroidal non-depolarising NMB. While acetylcholinesterase inhibitors are often used to reverse NMBs, they act non-specifically on both muscarinic and nicotinic synapses and cause many unwanted side effects. If they are given before there is partial recovery (>10% twitch activity) of neuromuscular blockade, they do not shorten the time to 90% recovery and thus are ineffective against profound block.

Sugammadex was first administered to human volunteers in 2005 with minimal side effects. [14] It displayed great potential in achieving quick recovery from rocuronium-induced paralysis within a few minutes. Further trials were conducted, including by de Boer et al. [15] in the Netherlands. Neuromuscular blockade was induced with rocuronium 1.2mg/kg and doses ranging from 2.0 to 16.0mg/kg of sugammadex given. With recovery of the train-of-four ratio to 0.9 designated as the primary outcome, the authors found that successive increases in the dose of sugammadex resulted in decreased time required to reverse profound blockade at five minutes following administration of rocuronium, with sugammadex 16mg/kg giving a mean recovery time of only 1.9 minutes compared to the placebo recovery time of 122.1 minutes. In a review article, Mirakhur [16] further supported the use of high-dose sugammadex (16mg/kg) in a situation requiring rapid recovery of neuromuscular blockade.

With an effective reversal agent for rocuronium presenting a possible alternative to suxamethonium in rapid sequence inductions, Lee et al. [17] closely examined the differences in time to termination of effect. They studied 110 patients randomised to either rocuronium 1.2mg/kg or suxamethonium 1mg/kg. At three minutes following administration of rocuronium, 16mg/kg sugammadex was given. The results of this study confirmed the potential of sugammadex and its possible future role in RSI, as the study group given rocuronium and sugammadex (at three minutes) recovered significantly faster than those given suxamethonium (mean recovery time to first twitch 10% = 4.4 and 7.1 minutes respectively). The evidence therefore suggested that administering sugammadex 16mg/kg at three minutes after rocuronium 1.2mg/kg resulted in a shorter time to reversal of neuromuscular blockade compared to spontaneous recovery with suxamethonium. While sugammadex has certainly shown great potential, it remains an expensive drug and there still exist uncertainties regarding repeat dosing with rocuronium following reversal with sugammadex, [18] as well as the need to suitably educate and train staff on its appropriate use, as demonstrated by Bisschops et al. [19] It is also important to note that for sugammadex to be of use in situations where reversal of neuromuscular blockade is required, the full reversal dose (16mg/kg) must be readily available. Nonetheless, it appears as if sugammadex may revolutionise the use of rocuronium not only in RSI, but also for other forms of anaesthesia in the near future.

As clinicians, we should strive to achieve the best patient outcomes possible. Without remaining abreast of the current literature, our exposure to new therapies will be limited and, ultimately, patients will not always be provided with the high level of medical care they desire and deserve. I urge all clinicians who are tasked with the difficult responsibility of establishing an emergency airway with RSI to consider rocuronium as a viable alternative to suxamethonium and to strive to understand the pros and cons associated with both agents, in order to ensure that an appropriate choice is made on the basis of solid evidence-based medicine.

Conflicts of interest

None declared.

Correspondence

S Davies: sjdav8@student.monash.edu

References

[1] Benumof JL, Dagg R, Benumof R. Critical haemoglobin desaturation will occur before return to an unparalysed state following 1 mg/kg intravenous succinylcholine. Anesthesiology. 1997; 87:979-82.

[2] Heier T, Feiner JR, Lin J, Brown R, Caldwell JE. Hemoglobin desaturation after succinylcholine-induced apnea. Anesthesiology. 2001; 94:754-9.

[3] Neguib M, Samarkandi AH, Abdullah K, Riad W, Alharby SW. Succinylcholine dosage and apnea-induced haemoglobin desaturation in patients. Anesthesiology. 2005; 102(1):35-40.

[4] Taha SK, El-Khatib MF, Baraka, AS, Haidar YA, Abdallah FW, Zbeidy RA, Siddik-Sayyid SM. Effect of suxamethonium vs rocuronium on onset of oxygen saturation during apnoea following rapid sequence induction. Anaesthesia. 2010; 65:358-361.

[5] Tang L, Li S, Huang S, Ma H, Wang Z. Desaturation following rapid sequence induction using succinylcholine vs. rocuronium in overweight patients. Acta Anaesthesiol Scand. 2011; 55:203-8.

[6] El-Orbany M, Connolly LA. Rapid Sequence Induction and Intubation: Current Controversy. Anaesth Analg. 2010; 110(5):1318-24.

[7] Sluga M, Ummenhofer W, Studer W, Siegemund M, Marsch SC. Rocuronium versus succinylcholine for rapid sequence induction of anesthesia and endotracheal intubation a prospective, randomized trial in emergent cases. Anaesth Analg. 2005; 101:1356-61.

[8] McCourt KC, Salmela L, Mirakhur RK, Carroll M, Mäkinen MT, Kansanaho M, Kerr C, Roest GJ, Olkkola KT. Comparison of rocuronium and suxamethonium for use during rapid sequence induction of anaesthesia. Anaesthesia. 1998; 53:867-71.

[9] Laurin EG, Sakles JC, Panacek EA, Rantapaa AA, Redd J. A comparison of succinylcholine and rocuronium for rapid-sequence intubation of emergency department patients. Acad Emerg Med. 2000; 7:1362-9.

[10] Patanwala AE, Stahle SA, Sakles JC, Erstad BL. Comparison of Succinylcholine and Rocuronium for First-attempt Intubation Success in the Emergency Department. Acad Emerg Med. 2011; 18:11-14.

[11] Perry JJ, Lee JS, Sillberg VAH, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev. 2008:CD002788.

[12] Rose M, Fisher M. Rocuronium: high risk for anaphylaxis? Br J Anaesth. 2001; 86(5):678-82.

[13] Florvaag E, Johansson SGO. The pholcodine story. Immunol Allergy Clinic North Am. 2009; 29:419-27.

[14] Gijsenbergh F, Ramael S, Houwing N, van Iersel T. First human exposure of Org 25969, a novel agent to reverse the action of rocuronium bromide. Anaesthesiology. 2005; 103:695- 703.

[15] De Boer HD, Driessen JJ, Marcus MA, Kerkkamp H, Heeringa M, Klimek M. Reversal of rocuronium-induced (1.2 mg/kg) profound neuromuscular block by sugammadex. Anesthesiology. 2007; 107:239-44.

[16] Mirakhur RK. Sugammadex in clinical practice. Anaesthesia. 2009; 64:45-54.

[17] Lee C, Jahr JS, CandiottKA, Warriner B, Zornow MH, Naguib M. Reversal of profound neuromuscular block by sugammadex administered three minutes after rocuronium. Anesthesiology. 2009; 110:1020-5.

[18] Cammu G, de Kam PJ, De Graeve K, van den Heuvel M, Suy K, Morias K, Foubert L, Grobara P, Peeters P. Repeat dosing of rocuronium 1.2 mg/kg after reversal of neuromuscular block by sugammadex 4.0 mg/kg in anaesthetized healthy volunteers: a modelling-based pilot study. British Journal of Anaesthesia. 2010; 105(4):487-92.

[19] Bisschops MM, Holleman C, Huitink JM. Can sugammadex save a patient in a simulated ‘cannot intubate, cannot ventilate’ situation? Anaesthesia. 2010; 65:936-41.

Categories
Review Articles Articles

Control of seasonal influenza in healthcare settings: Mandatory annual influenza vaccination of healthcare workers

Introduction: The aim of this review is to emphasise the burden and transmission of nosocomial seasonal influenza, discuss the influenza vaccine and the need for annual influenza vaccination of all healthcare workers, discuss common attitudes and misconceptions regarding the influenza vaccine among healthcare workers and means to overcome these issues, and highlight the need for mandatory annual influenza vaccination of healthcare workers. Methods: A literature review was carried out; Medline, PubMed and The Cochrane Collaboration were searched for primary studies, reviews and opinion pieces pertaining to influenza transmission, the influenza vaccine, and common attitudes and misconceptions. Key words used included “influenza”, “vaccine”, “mandatory”, “healthcare worker”, “transmission” and “prevention”. Results: Seasonal influenza is a serious disease that is associated with considerable morbidity and mortality and contributes an enormous economic burden to society. Healthcare workers may potentially act as vectors for nosocomial transmission of seasonal influenza. This risk to patients can be reduced by safe, effective annual influenza vaccination of healthcare workers and has been specifically shown to significantly reduce morbidity and mortality. However, traditional strategies to improve uptake consistently fail, with only 35 to 40% of healthcare workers vaccinated annually. Mandatory influenza vaccination programs with medical and religious exemptions have successfully increased annual influenza vaccination rates of healthcare workers to >98%. Exemption requests often reflect misconceptions about the vaccine and influenza, and reflect the importance of continuous education programs and the need for a better understanding of the reasons for compliance with influenza vaccination. Conclusion: Mandatory annual influenza vaccination of healthcare workers is ethically justified and, if implemented appropriately, will be acceptable. Traditional strategies to improve uptake are minimally effective, expensive and inadequate to protect patient safety. Therefore, low voluntary influenza vaccination rates of healthcare workers leave only one option to protect the public: mandatory annual influenza vaccination of healthcare workers.

Introduction

Each year, between 1,500 and 3,500 Australians die from seasonal influenza and its complications. [1] The World Health Organization (WHO) estimates that seasonal influenza affects five to fifteen per cent of the population worldwide annually, with an associated three to five million cases of serious illness and 250,000-500,000 deaths. [2] In Australia, it is estimated that seasonal influenza causes 18,000 hospitalisations and over 300,000 general practitioner (GP) consultations every year. [3] Nosocomial seasonal influenza is associated with considerable morbidity and mortality among the elderly, neonates, immuno-compromised and patients with chronic diseases. [4] The most effective way to reduce or prevent nosocomial transmission of seasonal influenza is annual influenza vaccination of all healthcare workers. [5,6] The Centre for Disease Control and Prevention (CDC) has recommended annual influenza vaccination of all healthcare workers since 1981, and the provision and administration of the vaccine to healthcare workers at the work site, free of charge, since 1993. [7] Despite this, only 35% to 40% of healthcare workers are vaccinated annually. [8]

 

Transmission of seasonal influenza

The influenza virus attaches and invades the epithelial cells of the upper respiratory tract. [8] Viral replication in these epithelial cells leads to pro-infl ammatory cytokines, and necrosis of epithelial cells. [8] Influenza is primarily transmitted from person to person by droplets that are generated when an infected person breathes, coughs, sneezes and speaks. [8] These droplets settle on the mucosal surfaces of the upper respiratory tract of susceptible persons; thus transmission of influenza primarily occurs in those who are near the infected person. [8]

The influenza vaccine

The influenza vaccines currently available in Australia are inactivated, split virion or subunit vaccines, produced using viral strains propagated in fertilised hens’ eggs. [9] The inactivated virus is incapable of replication inside the human body, and thus incapable of causing infection. [10] Influenza vaccines are trivalent, i.e. they protect against three different strains of influenza. [9] As influenza viruses are continually subject to antigenic change, annual adaptation of the influenza vaccine is needed to ensure the vaccine provides protection against the virus strains likely to be circulating during the influenza season. [9] The composition of the influenza vaccine in 2011 covered pandemic H1N1 2009 (swine flu), H3N2 and B strains of influenza. [11] Influenza vaccines are included in the Australian National Immunisation Program only after evaluation of their quality, safety, effectiveness and cost-effectiveness for its intended use in the Australian population. [9] The only common adverse effect of the influenza vaccine is minor injection site soreness for one to two days. [10] Influenza vaccine effectiveness depends on the age and immune status of the individual being vaccinated, and on the match between the strains included in the vaccine and those strains circulating in the community. [12] The influenza vaccine is 70 to 90% effective in preventing influenza infection in healthy individuals under 65 years of age; the majority of healthcare workers fall into this category. [12] Influenza vaccination has been shown to be 88% effective in preventing laboratory-confirmed influenza in healthcare workers. [13]

The need for annual influenza vaccination

Transmission of influenza has been reported in a variety of healthcare settings and healthcare workers may often be implicated in the outbreaks. [13] Healthcare workers are at an increased risk of acquiring seasonal influenza because of exposure to the virus in both the healthcare and community settings. [13] However, simply staying home from work during symptomatic illness is not an effective strategy to prevent nosocomial transmission of seasonal influenza. [10] The incubation period ranges from one to four days; the contagious period begins before symptoms appear, and the virus may be shed for at least one day prior to symptomatic illness. [4,10] Less than 50% of people show classic signs of influenza; asymptomatic healthcare workers may fail to recognise that they are infected, yet can shed the virus for five to ten days. [13,14] Symptomatic healthcare workers also often continue to work despite the presence of symptoms of influenza. [10,15] In one study, 23% of serum samples from healthcare workers contained specific antibody suggesting seasonal influenza infection during a single season; however, 59% of those infected could not recall influenza-like illness and 28% were asymptomatic. [13] The direct implication of this fact is that healthcare workers themselves may potentially act as vectors for nosocomial transmission of seasonal influenza to patients who are at increased risk of morbidity and mortality from seasonal influenza. [10] Many of these patients do not mount an appropriate immune response to influenza vaccination, making vaccination of healthcare workers especially important. [16] Only 50% of residents in long-term care settings develop protective influenza vaccinationinduced antibody titres. [17] Influenza vaccination of healthcare workers may reduce the risk of seasonal influenza outbreaks in all types of health care settings and has been specifically shown to significantly reduce morbidity and mortality. [12] A randomised controlled trial evaluating the effect of annual influenza vaccination of healthcare workers found that it was significantly associated with a 43% reduction in influenza-like illness and a 44% reduction in mortality among geriatric patients in long-term care settings. [12] Furthermore, an algorithm evaluating the effect of annual influenza vaccination of healthcare workers on patient outcomes predicted that if all healthcare workers in healthcare settings were vaccinated annually with the influenza vaccine, then approximately 60% of patient influenza infections could be prevented. [18]

Although a number of factors contribute to the overall burden of seasonal influenza, the economic burden to society results primarily from the loss of working time/productivity associated with influenza-related work absence and increased use of medical resources required to treat patients with influenza and its complications. [19] Typically, the indirect costs associated with loss of working time/productivity due to illness account for the greater proportion (>80%) of the economic burden of seasonal influenza. [19] One study reported those healthcare workers who received the influenza vaccine had 25% fewer episodes of respiratory illness, 43% fewer days of sickness absenteeism due to respiratory illness and 44% fewer visits to physicians’ offices for upper respiratory illness than those who received placebo. In a review of studies that confirmed seasonal influenza infection using laboratory evidence, the mean reported sickness absenteeism per episode of seasonal influenza ranged from 2.8 to 4.9 days for adults. [19] Furthermore, a retrospective cohort study investigating the association between influenza vaccination of emergency department healthcare workers and sickness absenteeism found that a significantly larger proportion took sick leave because of influenza-like illness in the vaccine non-recipient group (55% against 30.3%). [20]

Attitudes and misconceptions

Self-protection, rather than protection of patients, is often the dominant motivation for influenza vaccination. Many healthcare workers report they would be more willing to be vaccinated against pandemic influenza, which is perceived to be more dangerous than seasonal influenza. [15] One study found that the most popular reason (100% of those surveyed) for receiving the influenza vaccine among healthcare workers was self-protection against influenza. [21] Seventy percent of healthcare workers were also concerned about their colleagues, patients and community in preventing cross-infection. [21] Popular reasons mentioned for not receiving the influenza vaccine included “trust in, or the wish to challenge natural immunity”, “physician’s advice against the vaccine for medical reasons”, “severe localised effects from the vaccine” and “not believing the vaccine to have any benefit.”[21] A multivariate analysis of a separate study revealed that “older age”, “believing that most colleagues had been vaccinated” and “having cared for patients suffering from severe influenza” were significantly associated with compliance with influenza vaccination, with the main motivation being “individual protection”. [22] Lack of information as to effectiveness, recommended use, adverse effects of the vaccine and composition, again reflect the importance of continuous education programs and the need for a better understanding of the reasons for compliance with influenza vaccination. [22]

Major issues

Analysis of interviews with healthcare workers indicated that successfully adding mandatory annual influenza vaccination to the current policy directive would require four major issues to be addressed: providing and communicating a solid evidence base supporting the policy directive; addressing the concerns of staff about the influenza vaccine; ensuring staff understand the need to protect patients; and addressing the logistical challenges of enforcing an annual vaccination campaign. [23] A systematic review of influenza vaccination campaigns for healthcare workers revealed that a combination of education or promotion and improved access to the influenza vaccine yielded greater increases in coverage among healthcare workers. [24] Campaigns involving legislative or regulatory components such as mandatory declination forms achieved higher rates than other interventions. [24]

Influenza vaccination is currently viewed as a public health initiative focused on personal choice of employees. [12] However, a shift in the focus of vaccination strategy is appropriate – seasonal influenza vaccination of healthcare workers is a patient health and safety initiative. [12] In 2007, the CDC Advisory Committee on Immunisation added a recommendation that health care settings implement policies to encourage influenza vaccination of healthcare workers with informed declination. [25] A switch from influenza vaccination of healthcare workers on a voluntary basis to a mandatory policy should be considered by all public-health bodies. [4]

Mandatory annual influenza vaccination

Fifteen states in the USA now have laws requiring annual influenza vaccination of healthcare workers, although they permit informed declination; and at least five states require it of all healthcare workers. Many individual medical centres have instituted policies requiring influenza vaccination, with excellent results. [26]

A year-long study of approximately 26,000 employees at BJC HealthCare found that a mandatory influenza vaccination program successfully increased vaccination rates to >98%. [27] Influenza vaccination was made a condition of employment for all healthcare workers, with those still not vaccinated or exempted, terminated after one year. [27] Medical or religious exemption could be sought, including hypersensitivity to eggs, prior hypersensitivity reaction to influenza vaccine, and history of Guillain-Barre syndrome. [27] Exemption requests often reflected misconceptions about the vaccine and influenza. [27] Several requests cited chemotherapy or immuno-compromise as a reason not to get the influenza vaccine, even though these groups are at high risk for complications from influenza and are specifically recommended to be vaccinated. [27] Several requests cited pregnancy, although the influenza vaccine is recommended during pregnancy. [27]

Similarly, a five-year study of mandatory influenza vaccination of approximately 5,000 healthcare workers from Virginia Mason Medical Centre sustained influenza vaccination rates of more than 98% during 2005-2010. [28] Less than 0.7% of healthcare workers were granted exemption for medical or religious reasons and were required to wear a mask at work during influenza season, and less than 0.2% of healthcare workers refused vaccination and leftthe centre. [28]

Conclusion

Mandatory annual influenza vaccination of healthcare workers raises complex professional and ethical issues. However, the arguments in favour are clear. 1. Seasonal influenza is a serious and potentially fatal disease, associated with considerable morbidity and mortality among the elderly, neonates, immuno-compromised and patients with chronic diseases. [4] 2. The influenza vaccine has been evaluated for safety, quality, effectiveness and cost-effectiveness for its intended use in the Australian population. [9] 3. Healthcare workers themselves may potentially act as vectors for nosocomial transmission of seasonal influenza and this risk to patients can be reduced by safe, effective annual influenza vaccination of healthcare workers. [10] 4. The contagious period of seasonal influenza begins before symptoms appear and the virus may be shed for at least one day prior to symptomatic illness. [14] 5. Influenza vaccination of healthcare workers may reduce the risk of seasonal influenza outbreaks in all types of health care settings and has been specifically shown to significantly reduce morbidity and mortality. [12] 6. Seasonal influenza contributes an enormous economic burden to society from the loss of working time/productivity associated with influenza-related work absence and increased use of medical resources required to treat patients with influenza and its complications. [19] 7. Traditional strategies to improve uptake by healthcare workers consistently fail, with only 35% to 40% of healthcare workers vaccinated annually. [8] 8. Mandatory influenza vaccination programs with medical and religious exemptions have successfully increased annual influenza vaccination rates of healthcare workers to >98%. [27,28] 9. Exemption requests often reflected misconceptions about the vaccine and influenza, and reflect the importance of continuous education programs and the need for a better understanding of the reasons for compliance with influenza vaccination. [27, 22]

These facts suggest that mandatory annual influenza vaccination of healthcare workers is ethically justified and, if implemented appropriately, will be acceptable. [15] For this to occur, a mandatory program needs leadership by senior clinicians and administrators; consultation with healthcare workers and professional organisations; appropriate education; free, easily accessible influenza vaccine and adequate resources to deliver the program efficiently. It further requires provision for exemptions on medical and religious grounds and appropriate sanctions for those who refuse annual influenza vaccination, for example, requirement to wear a mask during influenza season, or termination of employment. [15] Healthcare workers accept a range of moral and other professional responsibilities, including a duty to protect patients in their care from unnecessary harm, to do good, to respect patient autonomy, and to treat all patients fairly. They also accept reasonable, but not unnecessary, occupational risk such as exposure to infectious diseases. [15] Vaccination is often seen as something that people have a right to accept or refuse. However, freedom to choose also depends on the extent to which that choice affects others. [15] In the healthcare settng, the autonomy of healthcare workers must be balanced against patients’ rights to protection from avoidable harm, and the moral obligation of healthcare workers not to put others at risk. [15] Mandatory annual influenza vaccination of healthcare workers is consistent with the right the public have to expect that healthcare workers will take all necessary and reasonable precautions to keep them safe and minimise harm. [15] Traditional strategies to improve uptake by healthcare workers are minimally effective, expensive, and inadequate to protect patient safety. Therefore, low voluntary influenza vaccination rates of healthcare workers leave only one option to protect the public: mandatory annual influenza vaccination of healthcare workers.

Conflicts of interest

None declared.

Correspondence

K Franks: kathryn.franks@my.jcu.edu.au

References

[1] Australian Bureau of Statistics. 3303.0 – Causes of death, Australia. 2007.

[2] World Health Organization. Fact sheet no. 211. Revised April 2009.

[3] Williams U, Finch G. Influenza specialist group – influenza fact sheet. Revised March2011.

[4] Maltezou H. Nosocomial influenza: new concepts and practice. Curr Opin Infect Dis.2008;21:337-43.

[5] Weber D, Rutala W, Schaff ner W. Lessons learned: protection of healthcare workers from infectious disease risks. Crit Care Med. 2010;38(8):306-14.

[6] Ling D, Menzies D. Occupation-related respiratory infections revisited. Infect Dis Clin North Am. 2010;24:655-80.

[7] Centre for Disease Control and Prevention. Influenza vaccination of healthcare personnel: recommendations of the healthcare infection control practices advisory committee and the advisory committee on immunization practices. MMWR Morb Mortal Wkly Rep. 2006;55:1-41.

[8] Beigel J. Influenza. Crit Care Med. 2008;36(9):2660-6.

[9] Horvath J. Review of the management of adverse effects associated with Panvax and Fluvax: fi nal report. In: Ageing DoHa, editor. 2011. p.1-58.

[10] McLennan S, Gillert G, Celi L. Healer, heal thyself: health care workers and the influenza vaccination. AJIC. 2008;36(1):1-4.

[11] Bishop J. Seasonal influenza vaccination 2011. In: Ageing DoHa, editor. Canberra 2011.

[12] Schaff ner W, Cox N, Lundstrom T, Nichol K, Novick L, Siegel J. Improving influenza vaccination rates in health care workers: strategies to increase protection for workers and patients. In: NFID, editors. 2004. p.1-19.

[13] Goins W, Talbot H, Talbot T. Health care-acquired viral respiratory diseases. Infect Dis Clin North Am. 2011;25(1):227-44.

[14] Maroyka E, Andrawis M. Health care workers and influenza vaccination. AJHP. 2010;67(1):25.

[15] Gilbert GL, Kerridge I, Cheung P. Mandatory influenza immunisation of health-care workers. Laninf. 2010;10:3-4.

[16] Carlson A, Budd A, Perl T. Control of influenza in healthcare settings: early lessons from the 2009 pandemic. Curr Opin Infect Dis. 2010;23:293-9.

[17] Lee P. Prevention and control of influenza. Southern Medical Journal. 2003;96(8):751-7.

[18] Ottenburg A, Wu J, Poland G, Jacobson R, Koenig B, Tilburt J. Vaccinating health care workers against influenza: the ethical and legal rationale for a mandate. AJPH. 2011;101(2).

[19] Keech M, Beardsworth P. The impact of influenza on working days lost: a review of the literature. TPJ. 2008;26(1):911-24.

[20] Chan SS-W. Does vaccinating ED health care workers against influenza reduce sickness absenteeism? AJEM. 2007;25:808-11.

[21] Osman A. Reasons for and barriers to influenza vaccination among healthcare workers in an Australian emergency department. AJAN. 2010;27(3):38-43.

[22] Takayanagi I, Cardoso M, Costa S, Araya M, Machado C. Attitudes of health care workers to influenza vaccination: why are they not vaccinated? AJIC. 2007;35(1):56-61.

[23] Leask J, Helms C, Chow M, Robbins SC, McIntyre P. Making influenza vaccination mandatory for health care workers: the views of NSW Health administrators and clinical leaders. New South Wales Public Health Bulletin. 2010;21(10):243-7.

[24] Lam P-P, Chambers L, MacDougall DP, McCarthy A. Seasonal influenza vaccination campaigns for health care personnel: systematic review. CMAJ. 2010;182(12):542-8.

[25] Centre for Disease Control and Prevention. Prevention and control of influenza, recommendation of the Advisory Committee on Immunization Practices (ACIP). MRR- 6MWR Recomm Rep. 2007;56(RR-6):1-54.

[26] Tucker S, Poland G, Jacobson R. Requiring influenza vaccination for health care workers: the case for mandatory vaccination with informed declination. AJN. 2008;108(2):32-4.

[27] Babcock H, Gemeinhart N, Jones M, Dunagan WC, Woeltje K. Mandatory influenza vaccination of health care workers: translating policy to practice. CID. 2010;50:259-64.

[28] Rakita R, Hagar B, Crome P, Lammert J. Mandatory influenza vaccination of healthcare workers: a 5-year study. ICHE. 2010;31(9):881-8.

Categories
Review Articles Articles

Is cancer a death sentence for Indigenous Australians? The impact of culture on cancer outcomes

Aim: Indigenous Australian cancer patients have poorer outcomes than non-Indigenous cancer patients after adjusting for age, stage at diagnosis and cancer type. This is not exclusive to the Indigenous population of Australia. The aim of this review is to explore the reasons why Indigenous Australians face a higher cancer mortality rate when compared to their non-Indigenous counterparts. Methods: A literature search was conducted using PubMed and Medline to identify articles with quantitative research on the differing survival rates and cancer epidemiology, and qualitative data on postulated reasons for this discrepancy. Qualitative studies, non-systematic topic reviews, quality improvement projects and opinion pieces were also reviewed in this process, with the belief that they may hold key sources of Indigenous perspectives, but are undervalued in the scientific literature. Results: Although allcause cancer incidence is lower within Indigenous Australians, the probability of death was approximately 1.9 times higher than in non-Indigenous patients. Occurrence of cancer types differ slightly among the Indigenous population, with a higher incidence of smoking-related cancers such as oropharyngeal and lung cancers, and cancer amenable to screening such as cervical cancer. Indigenous patients generally have a later stage at diagnosis, and are less likely to receive curative treatment. This discrepancy has been attributed to health service delivery issues, low uptake of screening, preventative behaviours, communication barriers, socioeconomic status and non-biomedical beliefs about cancer. Conclusion: The implication of these findings on the future of Indigenous cancer care indicates the fundamental social, cultural and serviced-based change required for long-term sustainable improvement in reducing Indigenous mortality rates. To ‘close the gap’ we need to make further collaborative system changes based on Indigenous cultural preferences.

Introduction

Indigenous Australian cancer patients have much poorer outcomes than non-Indigenous cancer patients after adjusting for age, stage at diagnosis and cancer type. [1] Statistics from 2005 show that cancer was the third highest cause of death in Indigenous people, as for all Australians, causing 17% and 30% of all deaths respectively. [1,3] However after adjusting for age and sex, Indigenous people had a 50% higher cancer death rate. [4] Indigenous Australians have a higher incidence of rapidly-fatal cancers that are amenable to screening or are preventable, particularly lung and other smoking related cancers. [2] One of the major contributors to increased mortality is the advanced stage at cancer diagnosis. In addition to this, Indigenous people are less likely to receive adequate treatment. The aim of this review is to explore the reasons why Indigenous Australians face a higher cancer mortality rate when compared to their non-Indigenous counterparts. This review will display the epidemiology of cancer types and discuss the grounds for this discrepancy, including a focus on the causes for advanced stage at diagnosis, geographical distribution of the population, socioeconomic status, service delivery and cultural beliefs about cancer.

A literature search was conducted using PubMed and Medline to identify articles with quantitative research on the differing survival rates and cancer epidemiology, and qualitative data on postulated reasons for this discrepancy. Qualitative studies, non-systematic topic reviews, quality improvement projects and opinion pieces were also reviewed in this process, with the belief that they may hold key sources of Indigenous perspectives, but are undervalued in the scientific literature. Combinations of key words such as ‘Indigenous’, ‘cancer’, ‘incidence’, ‘mortality’, ‘non-Indigenous’, and ‘cultural beliefs’ were used, in addition to criteria limiting articles to those published after 2000 and within Australia, although some key international references were included.

Generally, Indigenous Australians have a life expectancy seventeen years younger than their non-Indigenous counterparts, and a burden of chronic disease 2.5 times higher. [5] This is not exclusive to the Indigenous population of Australia; similar findings have been shown for Indigenous people of Canada, New Zealand and the United States. [6,7,8] The Aboriginal and Torres Strait Islander people of Australia, who account for 2.4% of the total population, will be referred to as Indigenous people for the purpose of this review, [9] although their separate cultural entities are recognised.

Epidemiology

Indigenous people in the Northern Territory diagnosed with cancer between 1991 and 2000 were 1.9 times more likely to die than other Australians, after adjusting for cancer site, age and sex (Figure 1). [10] The prevalence of cancer types differed among the Indigenous population, with a higher incidence of, and mortality from, smokingrelated cancers such as oropharyngeal and lung cancers, and cancers amenable to screening, such as cervical and bowel cancer. [10,11] In addition, studies from New South Wales, the Northern Territory and Queensland have found that Indigenous people are more likely to have advanced disease at diagnosis for all cancers combined. [2,12,13] Notably, lung cancer is diagnosed earlier in Indigenous people; this is thought to be due to the high prevalence of lung conditions such as tuberculosis and chronic lung disease among the Indigenous population. [2] Statistics show that only 11% of Indigenous bowel cancer patients in the Northern Territory, compared to 32% of non- Indigenous patients, had an early diagnosis. This has potential for improvement through the use of faecal occult blood programs as a cost effective screening tool. [6] In addition to the late stage at diagnosis, the low rate of cancer survival in Indigenous patients can be, in part, attributed to the prevalence of high fatality cancers, treatmentlimi ting comorbidities and high uptake of palliative or non-aggressive treatment options. [2]

Studies from across a number of states in Australia have shown that Indigenous patients are less likely to undergo treatment. In a study reported by Hall et al. in Western Australia, 26 (9.5%) of 274 Indigenous lung cancer patients underwent surgery, as compared to 1693 (12.9%) of 13,103 non-Indigenous lung cancer patients, from 1982 to 2001. [16] In the same time period, one (1.5%) of 64 Indigenous prostate cancer patients, versus 1,787 (12.7%) of 12,123 non-Indigenous prostate cancer patients underwent surgery. The study concluded that the Indigenous population with prostate or lung cancer were less likely to undergo surgery than their non-Indigenous counterparts. [14] A Queensland study by Valery et al. also reported that Indigenous cancer patients were less likely to undergo surgical treatment. [9] This may partly be explained by advanced stage at diagnosis; however, the results are statistically significant, demonstrating under-treatment after this adjustment. Treatment choice and barriers to care were identified as important contributors to this discrepancy. [14]

Longitudinal trends from 1995 to 2005 in the Northern Territory reported a downward trend in all cancer incidence among the non- Indigenous people, as opposed to an increase in Indigenous people. The all-cancer mortality declined significantly within non-Indigenous people, while there was little change in the death rate of Indigenous people. [10] Nation-wide trends between 1982 and 2007 show that the incidence of all cancers combined increased from 383 cases per 100,000 to 485 per 100,000. [15]

Rural and Remote Locations

Lower survival rates were observed in Queensland, Western Australia and the Northern Territory in Indigenous cancer patients from remote communities. [4,16] Indigenous people are ten times more likely to live in remote areas of Australia than non-Indigenous people. [17] This has implications for service delivery of screening, diagnosis and treatment, as well as access to preventative health education. In rural and remote Australia there is a shortage of healthcare providers and adequate primary health care facilities to cater for the vast geographical distances. There is a difficulty in ensuring transport links between major centres for patients requiring referral. These factors probably contribute to the outcomes.

Socioeconomic Status

Like other Indigenous populations, Indigenous Australians are overrepresented in the low socioeconomic strata. [1,2] Since the colonisation of Australia by the non-Indigenous population, the Indigenous people have progressively lost their cultural expression and practices, resulting in disempowerment. [8] Subsequent ‘welfare dependency’ with continuing loss of skills, unemployment and hopelessness have been suggested as contributory factors. [12] There are a multitude of reasons as to why disempowerment has manifest in poor levels of education, employment and health outcomes, which is beyond the scope of this discussion. In addition, Indigenous Australians are more likely, in varying degrees, to be exposed to poor environmental health such as disadvantaged living conditions. This includes overcrowding, poor nutrition and obesity, tobacco, excessive alcohol consumption and other drugs, and higher rates of human papillomavirus (HPV) infection, which are linked to the aetiology of cervical and head and neck cancers. [1,11,17] Behavioural risk factors linked to low socioeconomic status may contribute to higher levels of comorbidities.

Culture

Cultural isolation, power imbalances and differing health beliefs of cancer causation are patient factors that also contribute to poorer prognosis. Indigenous people are sensitive to power imbalances in their interaction with healthcare providers. [12] Psychological stress, common to many vulnerable populations, has been consistently associated with sub-optimal health outcomes for Indigenous people and an important obstacle in accessing healthcare. Peiris et al. believes that ‘cultural safety’ within healthcare facilities is paramount in addressing this problem. [12] Creating open-door policies, welcoming waiting rooms and reception staff who know the community are means of reorientating the health services and preventing the cultural disconnect. [12] However, there is a lack of community-controlled health services in many areas, and a relative lack of skilled Indigenous people in the workforce. Improving these factors would greatly enhance the cultural safety and community-specific delivery of health. [4,12] Studies comparing the Maori and Pacific Islander people in New Zealand have extrapolated on similar causes of ethnic inequalities in access to culturally acceptable health services. [6,7,8]

Language

In 2002, 66% of Indigenous Australians in the Northern Territory reported speaking a language other than English at home; in Western Australia, South Australia and Queensland the number of Indigenous language speakers was eleven to fourteen percent. [18] A study by Condon et al. reported that cancer survival was strongly associated with the patient’s first language. [2] After adjusting for treatment, cancer stage and site, it was shown that the risk of death for Indigenous native language speakers was almost double that of Indigenous English speaking and non-Indigenous patients. [2] It is postulated that communication difficulties, social and cultural ‘disconnect’ from mainstream health services and poor health literacy may be linked to native first language. [9] This valuable finding reinforces the importance of using Aboriginal Health Workers and translators in clinical practice.

Beliefs about Cancer

Attitudes to cancer and medical services strongly influence the use of diagnostic or curative care. Shahid et al. interviewed Indigenous people from various geographical areas in Western Australia about their beliefs and attitudes towards cancer. [3] The findings were surprising. Many Indigenous people believe cancer is contagious, and attributed cancer to spiritual curses, bad spirits or as punishment from a past misdeed. It was found that blaming others or one’s own wrongdoing as a cause of cancer or illness is widespread within Aboriginal communities, where spiritual beliefs about one’s wellbeing predominate. [3] Shahid et al. claimed that attribution of cancer to spiritual origins lead to acceptance of disease without seeking healthcare. [3] In addition, the Indigenous cancer sufferer may feel ashamed of their ‘wrongdoings’ and hide their symptoms, delaying diagnosis. [3]

Fatalistic attitudes towards cancer diagnosis in the general Australian population has changed in recent times, with the dissemination of information regarding curative cancer treatments, and the shifting focus toward understanding the biological basis of cancer and educating the public about screening and preventative behaviours such as the bowel cancer screening and the HPV vaccination. However, the low socioeconomic status and poor educational background of many Indigenous Australians has limited their access to such information. [3] In many Indigenous communities the fatalistic expectations of a cancer diagnosis remain. Such fatalistic beliefs are associated with delays in cervical cancer screening, late presentation of cancer symptoms, and patients who are lost to follow-up, contributed to by the aforementioned beliefs. For example, some Indigenous women with cervical cancer in Queensland blamed cancer on the loss of a traditional lifestyle. [19] Other beliefs about cancer are that screening protects from cancer and that cancer is contagious. Studies from New Zealand, Canada and the US have shown similar themes concerning non-biomedical Indigenous beliefs about cancer. [6]

In addition to the view that “cancer means death” were views of overreliance or mistrust in doctors. Often personal stories of an individual’s unmet expectations of the medical system spread within the community and influenced other’s attitudes; examples include patients who had fi nished treatment, thought they had been cured of cancer, and were then lost to follow-up, or the idea that screening prevents cancer. [20] Traditional healing still has a role in many Indigenous communities for health and wellbeing, as well as the importance during palliation of the cancer patients, often as a link to their connection with their country and ancestral roots. [3]

Recommendations

Culturally-appropriate service delivery

Diagnosing cancers earlier in the Indigenous population would increase the chance for curative treatment and reduction in overall mortality. Increasing primary health care services and their culturally appropriate delivery would address this need. However, improving the access to and use of relevant services for Indigenous people currently remains a challenge. For women’s issues, there may be stigma, shame and embarrassment associated with sexually transmitted infections and cervical cancer, as well as the cultural factors associated with denial of symptoms and gender roles of healthcare workers. [20] Service delivery failures are related to inadequate or inappropriate recallsystems, privacy during screening, especially in small communities, sex of the healthcare provider, timing and location of screening, discontinuity of care, difficulty maintaining cold chain and promoting vaccinations such as GardasilTM. [17] National data for breast and cervical cancer screening reveals that Indigenous women participate at about two-thirds of the national rate. However, the implementation of the culturally acceptable “Well Women’s Screening Program” in the Northern Territory, substantially improved Indigenous participation in PAP test screening from 33.9% in 1998 to 44% in 2000. [19] Similar initiatives have also been successfully implemented in Queensland. [22] This highlights the efficacy of culturally appropriate services tailored to the population.

Education

Programs to decrease tobacco use and to improve other behavioural risk factors need to be designed appropriately for use in the settng of communication difficulty and poor health literacy, and they need to address the cultural role of smoking in Indigenous people. [1] In addition, health service delivery improvements such as health education, promotion, screening programs and cultural safety, such as those demonstrated in the successful “Well Women’s Screening Program”, [19] will also contribute to a successful intervention.

Conclusion

Australian national ‘Closing The Gap’ targets include “to halve the life expectancy gap [between Indigenous and non-Indigenous Australians] within a generation.” [5] Language, cultural barriers, geographical distance, low socioeconomic status, high-risk health behaviours and traditional and non-biomedical beliefs about cancer are all reasons why Indigenous Australians have worse cancer outcomes than non- Indigenous Australians. The implication of these findings on the future of Indigenous cancer care and on meeting the national targets signifies the fundamental social, cultural and service-based changes required for long-term sustainable improvement in reducing the Indigenous mortality rates. The underlying cultural beliefs and individual perceptions about cancer must be specifically addressed to develop effective screening and treatment approaches. Educational material must be designed to better engage Indigenous people. In addition, Aboriginal cancer support services and opportunities for Aboriginal cancer survivors to be advocates within their communities may increase Indigenous peoples’ willingness to accept modern oncology treatments. Through these improvements, a tailored approach to Indigenous cancer patients can meet the spiritual, cultural and physical needs that are imperative for a holistic approach in their management.

Conflicts of interest

None declared.

Correspondence

S Koefler: sophia.koefler@gmail.com

References

[1] Cunningham J, Rumbold A, Zhang X, Condon J. Incidence, aetiology and outcomes of cancer in Indigenous people of Australia. Lancet Oncology. 2008;8:585-95.

[2] Condon J, Barnes T, Armstrong B, Selva-Nayagam S, Elwood M. Stage at diagnosis and cancer survival for Indigenous Australians in the Northern Territory. Med J Aust. 2004;182(6):277-80.

[3] Shahid S, Finn L, Bessarab D, Thompson S. Understanding, beliefs and perspectives of Aboriginal people in Western Australia about cancer and its impact on access to cancer services. BMC Health Services Research. 2009;9:132-41.

[4] Roder D, Currow D. Cancer in Aboriginal and Torres Strait Islander people of Australia. Asian Pacific J Cancer Prev. 2008;9(10):729-33.

[5] Anderson I. Closing the indigenous health gap. Aust Fam Physician. 2008;37(12):982.

[6] Shahid S, Thompson S. An overview of cancer and beliefs about the disease in Indigenous people of Australia, New Zealand and the US. Aust NZ J Public Health. 2009;33:109-18.

[7] Paradies Y, Cunningham J. Placing Aboriginal and Torres Strait Islander mortality in an international context. Aust NZ J Public Health. 2002;26(1):11-6.

[8] Jeff reys M, Stevanovic V, Tobias M, Lewis C, Ellison-Loschmann L, Pearce N et al. Ethnic inequalities in cancer survival in New Zealand: linkage study. Am J Public Health. 2005;95(5):834-7.

[9] Valery P, Coory M, Stirling J, Green A. Cancer diagnosis, treatment, and survival in Indigenous and non-Indigenous Australians: a matched cohort study. The Lancet. 2006;367:1842-8.

[10] Zhang X, Condon J, Dempsey K, Garling L. Cancer incidence and mortality in Northern Territory, 1991-2005. Department of Health and Families; Darwin 2006:1-65.

[11] Condon J, Barnes T, Cunningham J, Armstrong B. Long-term trends in cancer mortality for Indigenous Australians in the Northern Territory. Med J Aust. 2004;180:504-407.

[12] Peiris D, Brown A, Cass A. Addressing inequities in access to quality health care for indigenous people. Canadian Med Ass J. 2008;179(10): 985-6.

[13] Supramaniam R, Grindley H, Pulver LJ. Cancer mortality in Aboriginal people in New South Wales, Australia, 1994-2001. Aust NZ J Public Health. 2006;30(5):453-6.

[14] Hall S, Bulsara C, Bulsara M, Leahy T, Culbong M, Hendrie D et al. Treatment patterns for cancer in Western Australia, does being Indigenous make a difference? Med J Aust. 2004; 181(4): 191-4.

[15] Australian Institute of Health and Welfare & Australasian Association of Cancer Registries 2010. Cancer in Australia: an overview. AIHW. 2010;60(10):14-5.

[16] Hall S, Holman C, Sheiner H. The influence of socio-economic and locational disadvantage on patterns of surgical care for lung cancer in Western Australia 1982-2001. Aust Health Rev. 2004;27(2):68-79.

[17] Jong K, Smith D, Yu X, O’Connell D, Goldstein D, Armstrong B. Remoteness of residence and survival from cancer in New South Wales. Med J Aust. 2004;180:618-21.

[18] Condon J, Cunningham J, Barnes T, Armstrong B, Selva-Nayagam S. Cancer diagnosis

and treatment in the Northern Territory: assessing health service performance for

Indigenous Australians. Intern Med J. 2006;36:498-505.

[19] Binns P, Condon J. Participation in cervical screening by Indigenous women in the Northern Territory: a longitudinal study. Med J Aust. 2006;185(9):490-4.

[20] Lykins E, Graue L, Brechting E, Roach A, CochettC, Andrykowski M. Beliefs about cancer causation and prevention as a function of personal and family history of cancer: a national, population-based study. Psycho-oncology. 2008;17:967-74.

[21] Henry B, Houston S, Mooney G. Institutional racism in Australian healthcare: a plea for decency. Med J Aust. 2004;180:517-9.

[22] Augus S. Queensland Aboriginal and Torres Strait Islander women’s cervical screening strategy. Population Health Branch Queensland Health 2010. 10-27.

Categories
Review Articles Articles

The influence of vitamin D on cardiovascular disease

Background: Vitamin D is essential for many biological functions in the body. Populations that are deficient in vitamin D have increased cardiovascular morbidity and mortality. Current research is controversial, and the evidence base is still developing. This review looks at the interaction between vitamin D levels and cardiovascular disease, including the major cardiovascular risk factors – diabetes, obesity, hyperlipidaemia and hypertension. Methods: A literature review was undertaken through MEDLINE / PubMED / Ovid / Springerlink / Web of Science databases. The terms, “vitamin D”, “vitamin D deficiency”, “cardiovascular risk”, “cardiovascular disease”, “structure”, “function”, “ergocalciferol”, “cholecalciferol”, “calcitriol”, “vitamin D receptors”, “1α-hydroxylase”, “diabetes”, “obesity”, “hypercholesterolaemia”, “hyperlipidaemia” and “hypertension” were used. Sixty-eight articles were selected and analysed, with preference given to studies published in English and published within recent years. Results: There is a correlation between adequate vitamin D levels and type two diabetes mellitus, but limited research to support this. Obesity, physical inactivity and elevated circulating lipids are more common in vitamin D deficiency. These relationships have not been shown to be causal. Some studies have shown an inverse correlation between hypertension and vitamin D levels, while others have shown no relationship. Conclusion: The studies analysed show there is limited evidence to suggest that cardiovascular disease may be prevented by adequate vitamin D levels. There are few well-designed studies that demonstrate the relationship between the cardiovascular risk factors – diabetes, obesity, hyperlipidaemia, hypertension, and vitamin D. Further research is needed to clarify the infl uence of vitamin D on cardiovascular disease.

What is vitamin D, and how do you get it?

Vitamin D is a group of secosteroids, derived from steroid precursors by the opening of the steroid B-ring between carbons nine and ten. Vitamin D has a cis-triene structure which is susceptible to oxidation, ultraviolet (UV) light-induced conformational changes, heat-induced conformational changes and attack by free radicals. [1,2]

Cholecalciferol, also known as vitamin D3, is a 27-carbon molecule derived from cholesterol. [2] It is available through diet and through synthesis in the skin. [1] 7-dehydrocholesterol found in skin is converted to previtamin D3 following exposure to ultraviolet B (UVB) light. Previtamin D3 is unstable and breaks down to vitamin D3. This binds to vitamin D binding protein (VDP) and is delivered to the liver and other sites of action via the circulatory system. [3,4] Vitamin D levels are regulated in the body in a number of ways. While exposure to UVB radiation causes vitamin D3 production in the skin, excessive exposure to sunlight degrades it into inactive photoproducts. [5]

Ergocalciferol, also known as vitamin D2, is a 28-carbon molecule produced by irradiation of ergosterol found in plant and fungi, which is available through diet. [2,4] Vitamin D2 and D3 (available via diet) are absorbed with fat in the gastrointestinal system into chylomicrons, which are delivered to the liver or storage sites outside the liver, such as adipose tissue. [1]

The liver converts vitamin D3 to biologically inactive 25-hydroxyvitamin D3 (calcidiol). This is converted to biologically active 1,25-dihydroxyvitamin D3 (calcitriol) under the infl uence of renal 1α-hydroxylase predominantly in the kidney. [5,6] 1α-hydroxylase is under the control of parathyroid hormone (PTH). Calcitriol is regulated by negative feedback on itself, by increasing production of 25-hydroxyvitamin D-24 hydroxylase. This enzyme catabolises calcitriol to its biologically inactive form, calcitroic acid, which is excreted in the bile and urine. Other factors such as serum phosphorus, calcium and fibroblast growth factor 23 (FGF-23) can increase or decrease production of calcitriol. Increased serum calcium levels reduce PTH, causing down-regulation of 1α-hydroxylase, reducing calcitriol, and therefore calcium levels. [5,6] A simplified diagram of the biological function of vitamin D is outlined in Figure 1.

1α-hydroxylase is the rate-limiting step in production of calcitriol. Although calcidiol is the most abundant form of vitamin D in the blood, it has minimal capacity to bind to vitamin D receptors (VDRs). 1α hydroxylation of calcidiol to calcitriol causes vitamin D to gain affinity for VDRs. [7] In recent years, 1α-hydroxylase has been found to exist at many extra-renal sites. The role of extra-renal vitamin D activation remains controversial, but may play a role in the hypothesised actions of vitamin D. [8]

VDRs are found in almost every cell in the body. Calcitriol actions occur through intracellular receptors and interaction with DNA via the classic steroid pathway. These receptors were originally thought to regulate genes responsible for regulation of serum calcium and phosphate. [1] More recently, they have been found to regulate transcription in many tissues and cells, including immune cells, bone marrow, skin, muscle and intestine. [1,9]

How does vitamin D affect cardiovascular disease?

Vitamin D deficiency has been associated with high blood pressure, risk for cardiovascular-related deaths, symptoms of depression, cognitive deficits and mortality. [10] Calcitriol inhibits renin synthesis, increases insulin production and increases myocardial contractility. [11-13] Vitamin D deficiency reduces serum calcium levels, causing an increase in PTH, which promotes atherosclerosis and cardiovascular risk. [14,15]

The majority of evidence for the role of vitamin D in cardiovascular disease (CVD) has arisen from studies involving patients with end stage renal disease. Cardiovascular mortality is ten to twenty times higher in patients undergoing dialysis. [16] In patients using dialysis, the risk of death from CVD can be reduced with vitamin D replacement. [17,18]

As kidney function deteriorates, calcitriol levels decline. [19] Reduced calcitriol production can lead to hypocalcemia, and in turn, compensatory elevated PTH. Overstimulation of the parathyroid gland eventually leads to secondary hyperparathyroidism (SHPT). [20] Patients with ESRD are thought to suffer from reduced cardiac inotropy, increased heart weight, increased myocardial collagen content, and increased vascular smooth muscle cell proliferation as a result of the vitamin D depletion. PTH excess may impair intracellular calcium metabolism of the cardiomyocyte and promotes chronic atherosclerosis. Elevated PTH may increase cardiac contractility, insulin resistance, calcium and phosphate deposition in vessel walls, chronic myocardial calcification, and chronic heart valve calcification. [14,15] In patients with SHPT, treatment advice usually consists of correction of calcitriol deficiency using calcitriol or vitamin D analogues. [6]

Mechanisms for cardiovascular risk reduction with vitamin D supplementation include the inhibition of smooth muscle proliferation, the suppression of vascular calcification, the down-regulation of inflammatory cytokines, the up-regulation of anti-inflammatory cytokines, and the negative regulation of the renin-angiotensin-aldosterone system (RAAS). [21-26] Inappropriate stimulation of the RAAS is associated with hypertension, myocardial infarction and stroke. [14] Calcitriol treatment has been shown to reduce blood pressure, renin activity and angiotensin II levels. [27] The effects of vitamin D deficiency on the cardiovascular system are outlined in Figure 2.

A systematic review and meta-analysis looked at the relationship between the naturally occurring level of vitamin D and cardiometabolic disorders including CVD, diabetes and metabolic syndrome. [28] Twenty-eight studies were selected, including nineteen crosssectional studies, three case-control studies and six cohort studies, analysing 99,745 patients. [28] High vitamin D levels were associated with a 43% reduction in cardiometabolic disorders. [28] There was a significant association between high levels of vitamin D and risk of having cardiovascular disease (33% reduction), type two diabetes (55% reduction) and metabolic syndrome (51% reduction). [28] Vitamin D supplementation has been shown to have a protective effect in limited studies of CVD, but further research is needed. [29]

Diabetes

The research surrounding the interaction between vitamin D supplementation and type two diabetes mellitus is controversial. To date, there have been no adequate, large and prospective, randomised controlled trials to test the efficacy of vitamin D supplementation for the prevention and treatment of type two diabetes mellitus. The current available data allows a recommendation that further research be conducted to determine whether adequate vitamin D levels may prevent the onset of type two diabetes. Type one diabetes mellitus will not be discussed in this review.

Insulin resistance has been associated with low serum vitamin D, which improved after treatment with vitamin D. [30-36] One study demonstrated a positive relationship between calcitriol and insulin sensitivity, and a negative effect of vitamin D deficiency on beta cell function. [12] These studies are limited by small sample size, subject selection and lack of randomisation. However, there was a clinical correlation and it is worthwhile investigating further the possibility of improvement in insulin sensitivity with vitamin D supplementation. Serum blood sugar levels and prevalence of type two diabetes mellitus increases with age, and vitamin D levels tend to fall with age. [37,38] Type two diabetes is associated with systemic inflammation, which may induce beta-cell dysfunction and death. [39] Several studies show that vitamin D could directly affect beta-cell growth and differentiation via modulation of systemic inflammation and the immune response. [39-42] One of these was a double-blinded 39-week follow-up study of interleukin-1 blockade with anakinra. [40] Although being limited by small sample size and limitations in subject selection, the study showed improvement in markers of systemic inflammation 39 weeks after treatment withdrawal. [40]

Several studies indicate that calcitriol regulates beta-cell function by regulating intracellular calcium levels. This is thought to influence insulin secretion, increase beta-cell resistance to apoptosis and increase beta-cell replication. Calcitriol is thought to bind to nuclear VDRs in the beta-cell to increase preproinsulin mRNA level. Research to support this hypothesis is limited, due to being conducted in rats. [39,43-45]

Obesity and hyperlipidaemia

Studies have shown that high body mass index (BMI) is associated with low serum vitamin D levels. [46] Vitamin D is fat soluble and readily stored in adipose tissue. [1,47] Sequestration of cholecalciferol in adipose tissue reduces bioavailability in obese individuals. [1,48,49] The distribution of fat may be associated with vitamin D status, but this relationship may be dependent on metabolic factors. [49]

Vigorous physical activity is a strong and modifiable contributor to vitamin D status. This may be due to sun exposure correlated with physical activity, however, a number of studies have shown the positive effect on vitamin D status may be independent of sun exposure. [50-54] Further research is needed to clarify this.

A large, prospective study of the modifiable predictors of vitamin D status was conducted using 2,621 healthy individuals aged 55-74 in the USA. [46] Predictors of low vitamin D status were found to be low dietary vitamin D intake, BMI > 30kg/m2, physical inactivity and low milk and calcium supplement intake. [46] There is an inverse relationship between apolipoprotein A-I and high density lipoprotein cholesterol with vitamin D levels in a survey of 358 Belgian people. [55] This relationship was not shown to be causal, but further research is warranted to see if vitamin D provides this cardioprotective link.

Vitamin D deficiency may increase insulin resistance and thereby increase circulating lipids, but supplementation has not been shown to improve circulating lipid levels. [56,57] Statin therapy increases the circulating levels of 7-dehydrocholesterol, leading to an increase in conversion to vitamin D (in the presence of UVB radiation), and therefore vitamin D levels. [58-61]

Hypertension

To date, there are few good quality randomised controlled trials looking at the relationship between vitamin D levels and blood pressure. There is weak evidence to suggest that there may be a relationship between the two, however, further research is needed to draw any conclusions that may change the management of blood pressure.

Vitamin D may regulate blood pressure via an interaction with the RAAS, which is often activated in hypertension. Calcitriol is a known negative regulator of the RAAS. [11,21] The effects of vitamin D on the suppression of renin activity may be due to increased intracellular calcium levels. [62] It is hypothesised that vitamin D regulation of renin is independent of calcium metabolism, by regulating renin mRNA production with VDRs. [11] This study was completed using a line of cells derived from transgenic mice kidney tumours. [11]

There are some studies which show an inverse correlation between vitamin D levels and blood pressure. [63-66] A meta-analysis which included eleven randomised controlled trials (small, variable methodological quality) found weak evidence to support a small effect of vitamin D on blood pressure in studies of hypertensive patients. [67] There was a small statistically significant reduction in diastolic blood pressure, and no significant reduction in systolic blood pressure in hypertensive subjects supplemented with vitamin D or UV radiation. [67]

Several studies have shown differing results when trying to establish a relationship between vitamin D intake and hypertension. [10] There are two cross-sectional studies that have been completed using the Third National Health and Nutrition Examination Survey data. One study demonstrated a significant difference in systolic blood pressure and pulse pressure between the highest and lowest quintile groups divided by vitamin D level. [10,63] Participants with hypertension were excluded from analysis. [63] Another study revealed increased systolic blood pressure with reducing levels of vitamin D, and a twenty percent reduction in systolic blood pressure in those with vitamin D levels greater than 80 nmol/L compared with those with less than 50 nmol/L. [64] Both of these studies had a good sample size, but were limited by the methods of the study. [10] A cross-sectional study using a different data set with low prevalence of vitamin D deficiency showed no association between systolic blood pressure and vitamin D level. [10,65] A different study did not show any significant relationship between vitamin D levels and blood pressure after adjusting for confounding variables, however, this may have been due to low estimated vitamin D intake. [10,68]

Conclusion

Vitamin D is an important molecule to consider in the pathogenesis of cardiovascular disease. Current research shows that vitamin D deficiency contributes to cardiovascular morbidity and mortality. The mechanisms proposed for this include direct actions on the heart and vasculature, as well as by increasing the risk of cardiovascular risk factors such as diabetes, obesity, hyperlipidaemia and hypertension. Further research is needed to clarify the influence of vitamin D on cardiovascular disease and its risk factors, and whether vitamin D is an efficient, cost-effective and safe intervention to prevent cardiovascular morbidity and mortality.

Acknowledgements

Dr Ruan Lakemond, for his kind assistance in proof-reading this article and technical support. Prof Rick Jackson, for his generous support and help finding a suitable topic.

Confl icts of interest

None declared.

Correspondence

R Lakemond: rachel.lakemond@gmail.com

Categories
Review Articles Articles

Australia’s experience of Bordetella pertussis and a proposed national preventive strategy into the future

Elimination of Bordetella pertussis, an exclusively human pathogen, has proven to be elusive in Australia despite universal vaccination. Australia has witnessed a resurgence of pertussus particularly in infants less than 6 months old, and adults over 20 years old. This resurgence has resulted in high notification rates, morbidity and mortality in the two age groups. This may be due to the largely asymptomatic presentation in young infants and adults, as well as sub-optimal immunity due to lack of development, or waning immunity in adults. Various levels of prevention need to be identified so that a national preventative strategy may be sought to reduce the impact of pertussis infection amongst Australians in the future.

 
Introduction
Pertussis is an acute illness caused by Bordetella pertussis, a Gram-negative coccobacillus with exclusive affinity for the mucosal layers of the human respiratory tract. Pertussis is highly contagious and spread by air borne respiratory droplets when an infected person coughs or sneezes, or via direct contact with secretions from the nose or throat. [1] Following an incubation period of 9-10 days, patients usually present with an irritating cough that gradually becomes paroxysmal and lasts for 1-2 months. [2] However, in adults and older children, the diagnosis of pertussis is often subclinical and delayed due to an absence of classical symptoms, resulting in potential transmission of infection for several weeks. [3] In Australia, the preferred methods for laboratory diagnosis of pertussis are culture and polymerase chain reaction (PCR), and it is recommended in most cases that both tests be performed. However, there is a trend to move towards PCR, which provides rapid results, and is more sensitive in previously immunised individuals, and more likely to be positive in patients who have received antimicrobial treatment than culture. [1-4]
 
Since the 1950s, effective pertussis immunisation programs have reduced hospitalisations and deaths in Australia dramatically. [4] Currently, the acellular pertussis vaccine (DTPa) is safer and more effective than whole cell pertussis vaccine (DTPw), which is no longer used in Australia. [1] DTPa vaccines are associated with lower incidence of fever and local reactions than DTPw, and serious side effects are rare. [1,6] DTPa is free for Australian children at 2, 4 and 6 months of age, with a booster available at 4 years and during adolescence. [5] Despite the availability of vaccines in Australia, it remains a challenging disease to control among two age groups: under the age of 6 months who suffer the most severe infections and highest mortality, and those older than 20 years. [1,6] Adolescents and adults are an important reservoir for infection as they are capable of transmitting pertussis to infants who were too young to have received two or more DTPa vaccines required for optimum protection. [1]
 
Epidemiology
In Australia, pertussis cases are notifiable under each state and territory Public Health Act. [4] There were 34,490 pertussis notifications received by the National Notifiable Diseases Surveillance System (NNDS) in 2010, the highest recorded since 1991 (Figure 1). A general increase in endemic peaks have occurred every 4-5 years since national notifications became available in 1991, occurring in 1997 (12,232 notifications), 2001 (9,530 notifications), 2005 (11,168 notifications) and 2010 (34,490 notifications). A clear seasonal pattern exists, with the highest number of notifications in the spring and summer months (between August and February) each year between 1993 and 2010. [2] In terms of age specifi c pertussis incidence rates, children less than 1 year old had the highest annual notification rate in all of the analysed years, and high rates were also observed in 5-9 years olds, with a peak notification rate in 1997 of 194 cases / 100,000. [4] Adults aged 20-59 years accounted for 56% of notifications, with elderly patients aged 60 years and over accounting for 15% of notifications in 2005 (Figure 2). Recently, there has been a rise in notification rates in the 20-59 year old age group, and in those over the age of 60, increasing by 57% and 17% respectively in 2010. This is in contrast to the relatively steady annual rates previously seen in these age groups between 1993-2003.
Hospitalisations, which refer to a period of time when a patient is confined to a hospital, followed a similar pattern to notifications (Figure 1) with a total of 1,478 separations recorded during 1998-2008 (Figure 3). Of these separations, they were most prominent in the 0-4 age categories, with 967 separations (Table 1). Peak separations occurred in the period of 2001-2002 (258 separations), 2004-2005 (222 separations) and 2007-2008 (250 separations).
There were 9,338 hospital bed days recorded for all ages during 1998-2008, with the highest number of hospital bed days toward the 0-4 year old group. Total hospital bed stays peaked during 2001-2002 (1,628 days) and 2004-2005 (1,640 days). Over the two years 2003-2004, two deaths were recorded where pertussis was the underlying cause, with both occurring in 2004; one case was 1 month of age and the other a 95 year old patient. [2] During 1993-2002, there was a total of 16 deaths attributed to pertussis, of which 15 (94%) occurred in infants less than 6 months of age. [6]
The latest study by Australian Department of Health and Ageing showed that between 2003-2005, only 37% of infants less than 6 months were fully vaccinated, and 12% partially vaccinated. [2,4] There are proposed explanations for increasing pertussis rates seen amongst infants in the less than 6 months of age group. Two or more doses of a pertussis-containing vaccine appear to be needed for protection, and infants less than 6 months of age are likely to be too young under Australian immunisation schedules to have reliably received two or more doses. [3] It is also likely that adults, particularly parents, are a significant source of infection to infants. Regarding individuals aged 20 and over, it is likely that increased notifications are related to greater use of serology as a diagnostic tool, and an ageing population. [4,8]
Also, waning immunity following infant vaccination and reduced opportunities for boosting immunity due to reduced circulation of pertussis may also contribute to increased susceptibility to pertussis infection and disease in the 20 years and over population. [3,8]
 
Risk factors
Understanding the risk factors for pertussis infection is essential to target areas of concern, and to provide a skeleton for drafting a national preventative strategy. They include:

  • Infants and children who are not immunised yet. In infants, the first dose of vaccine is immunogenic only from the age of 6 weeks, thus infants less than 6 weeks are at the highest risk of pertussis infection, often from the parents. [1-6]
  • Infants under 12 months old. Infants are particularly prone to infection prior to receiving the first two doses of DTPa. Adolescents and adults are an important reservoir for infection as they are capable of transmitting pertussis to infants. [1] In addition to increased susceptibility of acquiring infection, infants are also most at risk of developing severe complications, such as apnoea, bacterial pneumonia, pulmonary hypertension and cor-pulmonale. [5,10]
  • Adolescents aged between 12-17 years. Immunity, whether from immunisation or past history of Bordatella pertussis infection, decreases after approximately 6-10 years, resulting in renewed susceptibility to infection. Thus for most adolescents, if they do not receive a booster shot during adolescence, they are at risk, as their last dose of DTPa would have been at 4 years of age in Australia. [1-3,7,9]
  • Living in the same house or working in close contact with someone infected with Bordatella pertussis. Studies have demonstrated that households with members who have culture-positive Bordatella pertussis were more likely to have greater secondary spread. Hence, proximity is an important predictor of household and community-aquired infection, with adolescents being at higher risk compared with other age groups. [13] Additionally, adults working with young children, especially childcare workers and healthcare workers in contact with infected infants are at a higher risk of contracting Bordetella pertussis infection. [1]
  • Persons with immunodeficiency and other underlying medical conditions. These include patients who have congenital or acquired immunodefi ciency, cystic fibrosis, chronic heart failure, diabetes and chronic lung disease.
  • Indigenous Australian Infants. One study demonstrated that 52% of pertussis hospitalisations in Indigenous infants occurred at 0-2 months of age, and rates in these indigenous infants were signifi cantly higher in remote areas. Also, indigenous infants had higher hospitalisation rates and were more frequently delayed of vaccination than age matched non-indigenous infants. [14]

Prevention activities
When thinking about prevention in population health, there is consideration towards four types of prevention:

  • Primordial Prevention: Avoid the emergence and establishment of ‘upstream’ factors such as social, cultural and economic factors that contribute to increased disease incidence.
  • Primary Prevention: Preventing disease from occurring in the first place; to reduce the incidence of disease. [15]
  • Secondary Prevention: Reducing morbidity and mortality by improving the outcome of disease (such as early diagnosis and treatment) that has already developed. [15]
  • Tertiary Prevention: Reducing the progress or complications of disease and implying better rehabilitation or quality of life in the longer term. [15]

Table 2 outlines how these different types of prevention could be implemented in Australia in the future.
 
A national preventative strategy
A national preventative health strategy requires effective health promotion programmes. Health promotion is the process of strengthening the capability of individuals to take action and the capacity of communities to act collectively to exert control over the determinants of their health. [19]
 
Program Planning
Target Populations: Epidemiological and demographic information suggests that infants aged less than 6 months are at the highest risk of severe pertussis disease due to partial immunisation. Also, there is an increasing number of notification s in adults aged 20 years and over. [1] These two age groups could be extensively targeted as they are both a community need and are perceived as priority for intervention.
Vaccination Timing: There is evidence to suggest inadequacy of vaccination programs which provide doses at 2, 4, and 6 months, 4 years and in adolescence. There may be a role for earlier vaccination in order to protect those under 6 months of age. Furthermore, there may also be a role for the inclusion of those over the age of 20 in the national immunisation programme, as well as health care and childcare workers. Moreover, investment in screening, surveillance and patient education should be recommended.
Resource allocation: There is a need to mobilise resources. There may be a role for lobbying national and state governments to devote a greater proportion of the national budget to health care and disease prevention. Furthermore, there may be a role for the private sector (e.g. pharmaceutical companies) to also invest further in this disease in the form of vaccines, treatments, educational materials and awareness strategies. Human resources must also match financial resources, with appropriate medical staff providing increased vaccination and health promotion on this issue. Finally, building sustainable relationships between different bodies is key to the long-term success of health promotion, e.g. between Medicare Australia, the Australian Medical Association, public hospitals, pharmaceutical companies, state and federal health ministries.
 
Programme Implementation
Establishing an evidence base: This could be done by randomised controlled trial of vaccinating infants at the onset of labour, and another booster shot before the current regimen at 2 months to assess clinical outcomes. A randomised trial could also be done for adults over 20 years in limited geographical areas to assess efficacy, human resources and costs. A trial of up-skilling healthcare workers to be competent for routine pertussis screening in hospitals may be implemented and tried. Additionally, production of pamphlets and utilising media to promote health awareness of pertussis could be trialled to assess coverage, efficacy, cost and human resources.
Health promotion actions: Traditionally, health promotion activities have focused on public information, education or communication as the main method for improving knowledge and changing behaviours and thus, this should be emphasised in a pertussis preventative strategy. Dissemination of information through mass media by advertising, radio, posters and pamphlets around healthcare centres could be implemented in a cost effective way.
Organisations could also work together with pharmaceutical companies supplying vaccination. Furthermore, identified cases of pertussis should be reported early to a public health authority by private and public hospitals. Finally, prior to registration of doctors with the medical board, they could be required to undergo pertussis training.
 
Monitoring and recording of programme implementation and quality control
Increased attention must be given to the development of performance indicators which can be used to assist in assessing good management of people and resources, and assessment of success or failure. [19]
Cost-benefit analysis may be assessed for each class of preventative strategy, the availability of staff for an increasingly elderly population, assessment of penetration and impact of mass media and pamphlets for patient education could be accounted by production of surveys, and public notification s, mortality and morbidity data may constantly be monitored to assess efficacy of increased DTPa.
 
Program evaluation
Health literacy may be evaluated using measures such as assessing pertussis-related knowledge, attitudes, motivation, behavioural intentions, personal skills and self efficacy of the public. [19]
Outcomes regarding internal governmental policy developmental process, and lobbying leading to legislative change could be reviewed using measures such as policy statements, resource allocation and organisational practices. Finally, data of social outcomes (such as quality of life, equity) and health outcomes (national data on reduced morbidity, disability, avoidable mortality) may be evaluated to assess whether the preventative strategy was successful, or, if there are any program failures, may be traced to re-examine potential solutions.
 
Conclusion
Despite the largely successful history of immunisation in dramatically decreasing the incidence of pertussis, especially in terms of the number of hospitalisations and deaths, a number of changes to the immunisation strategy may be overdue. Control of the disease still remains a challenge in 21st century Australia, with increased notification rates documented in those under the age of 6 months and over the age of 20. GPs, often the fi rst point of contact, should familiarise themselves with the epidemiology those at greatest risk of pertussis, and off er vaccination accordingly. Moreover, individuals, health professionals, health organisations and governments must work synergistically to develop novel preventative strategies against modifi able risk factors, such as by increasing the number of booster vaccines, increasing surveillance, and greater dissemination of information to the population, to minimise burden of the disease for a sustainable future.
 
Acknowledgements
I would like to acknowledge Prof. Gabrielle Bammer, Director, National Centre for Epidemiology and Population Health and A/Prof. David Harley, Associate Dean of Population Health Teaching and Learning for awarding the ANU Medical School Population Health Prize towards this article.
Conflicts of interest
None Declared.
Correspondence
J Choi: josephchoi7@gmail.com
  
References
[1] Australia. Pertussis Vaccines for Australians: Information for Immunization Providers. National Centre for Immunisation Research and Surveillance fact sheet. November; 2009.
[2] Australia. Vaccine Preventable Diseases and Vaccination Coverage in Australia 2003-2005. Australian Government Department of Health and Ageing. November; 2007.
[3] Wood N, McIntyre P. Pertussis: Review of epidemiology, diagnosis, management and prevention. Paediatr Respir Rev. 2008;9:201-12.
[4] Quinn H, McIntyre. Pertussis epidemiology in Australia over the decade 1995-2005: Trends by region and age group. Commun Dis Intell. 2007;31:205-15.
[5] Paterson J, Sheppeard V. Nosocomial pertussis infection of infants: Still a risk in 2009. Commun Dis Intell. 2010;34:440-3.
[6] Senanayake S. Pertussis in Australia today: A disease of adolescents and adults that can kill infants. Aust Fam Physician. 2007;36:51-5.
[7] Australian Institute of Health and Welfare Interactive National Hospital Data [Internet]. 2010 [Cited 2011 May 14] Available from: http://aihw.gov.au/hospitas/datacubes/index.cfm.
[8] Cherry J. The epidemiology of pertussis: A comparison of the epidemiology of the disease pertussis with the epidemiology of Bordetella pertussis infection. Paediatrics. 2003;115:1422-7.
[9] Weekly epidemiological record: Pertussis Vaccines WHO position paper, 2010. World Health Organization. 2010;85:385-400.
[10] Long, S. Age Specifi c Presentation and Burden of Pertussis. Adv Stud Med. 2005;5:S444-9.
[11] Yeh S, Mink C, Edwards M, Torchia M. Clinical Features and Diagnosis of Bordetella pertussis infection in infants and children. Waltham, MA, USA: Up to Date; 2010.
[12] Wright S and Tenn N. Pertussis Infection in Adults. South Med J. 1998;91:702-9.
[13] Biellik R, Patriarca P, Mullen J, Rovira E, Brink E, Mitchell P, et al. Risk factors for community and household acquired Pertussis during a large scale outbreak in central Wisconsin. J Infect Dis. 1988;157:1134-40.
[14] Kolos V, Menzies R, McIntyre P. Higher pertussis hospitalization rates in indigenous Australian infants, and delayed vaccination. Vaccine. 2006;25(4):588-90.
[15] Webb P, Bain C and Pirozzo S (2005) Essential Epidemiology. New York, USA:Cambridge University Press; 2005.
[16] Yeh S, Edwards M, Torchia M. Treatment and prevention of Bordetella pertussis infection in infants and children. Waltham, MA, USA: Up to Date; 2010.
[17] Forsyth K, Konig C, Tan T, Caro J, Plotkin S. Prevention of pertussis: Recommendations derived from the second Global Pertussis Initiative roundtable meeting. Vaccine. 2007;25:2634-42.
[18] Mills S. Now wash your Steth. Medical Student Journal of Australia. 2011;2:42-3.
[19] Pencheon D, Guest C, Melzer D, Gray J. Oxford Handbook of Public Health. Oxford, United Kingdom: Oxford University Press; 2001.

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