NACCHO Aboriginal Health @TheMJA : The burden of invasive infections in critically ill #Indigenous children

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Children of Aboriginal and Torres Strait Islander background were three times more likely to be admitted to an ICU for severe infections than non-Indigenous children during 2002–2013, and the population-based mortality attributable to infections in Indigenous children was more than twice that for non-Indigenous children.

Our study highlights an important area of inequality in health care for Indigenous children that requires urgent attention

Remoteness and difficulties in access to health care may also significantly increase the incidence of invasive infections in indigenous children that require treatment in ICUs, as delays in initiating appropriate treatment allow disease progression

 Further research is needed to define risk factors and to develop and assess appropriately targeted interventions.

As published MJA Journal

Image above Box 2 – Age-standardised admission rate of Indigenous children to intensive care units for all invasive infections

This is the largest study to have examined life-threatening infections in Indigenous Australian children, exploring an important area of health inequity in a high income country.

Our population-based study of more than 3000 Indigenous children admitted to ICUs found a disproportionately high burden of disease associated with invasive infections in Aboriginal and Torres Strait Islander children, causing significant excess childhood mortality.

In contrast to previous studies that focused on mild to moderate infections, our study examined severe, life-threatening infections.

During 2002–2013, the ICU admission rate for invasive infections was three times as high for Indigenous as for non-Indigenous children (47.6 v 15.9 per 100 000 children per year); the estimated population-based ICU mortality attributable to invasive infections was more than double that for non-Indigenous children.

Our findings parallel reports of disproportionate infectious disease burdens in other indigenous populations.6,8,1820 High rates of infectious diseases, including ear and respiratory tract infections, have consistently been reported for Canadian First Nations, Inuit and Métis peoples, Native Americans, Alaskan and Hawaiian Natives, and New Zealand Pacific and Māori peoples. Children in these populations experience poorer overall health outcomes than non-indigenous children, including higher infant and childhood mortality.6 Risk factors that contribute to the high incidence of infectious diseases among indigenous children include lower socio-economic status, overcrowding, poor access to sanitation, clean water and health facilities, and differences in hygiene and health-seeking behaviour.21 These key social and economic factors, recognised as major causes of poor health in low income countries, must also receive attention in high income countries if we are to improve national and global health outcomes for disadvantaged groups.22

Remoteness and difficulties in access to health care may also significantly increase the incidence of invasive infections in indigenous children that require treatment in ICUs, as delays in initiating appropriate treatment allow disease progression.23

This is consistent with our finding that Indigenous Australian children admitted to ICUs with invasive infections had higher median illness severity scores (PIM2) than non-Indigenous children during 2008–2013. This finding also suggests that a lower admission threshold for Indigenous children is unlikely to have contributed to their higher admission rate in our study. Further investigations in which outcomes are stratified according to the length of time to medical care may clarify the impact of remoteness on outcomes for children with infectious diseases.

The incidence of pneumococcal, group A streptococcal, and meningococcal disease in Indigenous Australian children has been reported to be 2–10 times that for non-Indigenous children residing in the same geographical area, despite 7-valent pneumococcal and meningococcal C vaccinations.20,24,25 We measured a significant decrease in meningococcal sepsis among Indigenous children that coincided with the introduction of the conjugate meningococcal vaccine. While expanding targeted vaccination may lead to further reductions in bacterial sepsis rates, vaccine-based interventions are unlikely to be available soon for S. aureus, identified in 40% of Indigenous patients from whom bacteria were isolated in our study. In the overall Australian and New Zealand paediatric sepsis ICU study,4 only 10% of sepsis cases were attributable to S. aureus, comparable with other cohorts.26 Prospective studies that assess the continuing impact of vaccinations on severe infection rates among Indigenous children in Australia are needed to further define this important area of public health.

Very high rates of invasive staphylococcal infection have been reported in adult and paediatric Indigenous populations in Australia.11 Excess rates of S. aureus infection have also been documented among Māori, Pacific Islanders and Samoans in New Zealand, Canadian Aboriginals, Alaskan Natives, Pacific Islanders in Hawaii, and Native Americans. Miles and colleagues27 found that 81% of patients admitted to paediatric ICUs in New Zealand for invasive S. aureus infections were Pacific Island and Māori children, although these ethnic groups comprise only 22% of the population. It is possible that genetic susceptibility may contribute to differences in biological susceptibility to sepsis,21 but further research is needed to clarify this question.

A number of limitations of our study need to be considered. It was based on a prospective paediatric ICU registry that does not capture infectious disease outcomes for newborns in neonatal nurseries or for children who die before they can be admitted to an ICU. The ANZPIC Registry captures 92–94% of paediatric patients admitted to ICUs in Australia, and the number of general ICUs contributing data to the registry increased during the study period. Admissions to general ICUs represented 17.1% of non-elective admissions recorded by this registry during 2008–2013, and 9.4% of admissions during 2002–2007. We therefore cannot exclude the possibility that we underestimated the true population-based incidence of severe infections.

Our primary outcome measure was ICU mortality. We did not detect major changes over time in mortality for Indigenous children admitted to ICUs with severe infections, but our study was not powered for subgroup mortality analyses. It is noteworthy that using mortality as an endpoint does not capture the impact of ICU admission on quality of life and health after discharge; clinically significant short and long term effects in former paediatric ICU patients have been documented.27,28 Finally, Indigenous children in Australia live in diverse environments, ranging from cities to remote Indigenous communities. Our study did not stratify outcomes according to these potentially important differences, nor did we have access to data on socio-economic status.

Conclusion

Children of Aboriginal and Torres Strait Islander background were three times more likely to be admitted to an ICU for severe infections than non-Indigenous children during 2002–2013, and the population-based mortality attributable to infections in Indigenous children was more than twice that for non-Indigenous children. Our study highlights an important area of inequality in health care for Indigenous children that requires urgent attention. Further research is needed to define risk factors and to develop and assess appropriately targeted interventions.

Box 1 – Baseline characteristics and severity of disease at admission for Indigenous children admitted to an intensive care unit (ICU) with an invasive infection

Invasive infection without sepsis/septic shock

Invasive infection with sepsis/septic shock


Number of children

423

303

Age of child

Median (IQR), years

1.6 (0.4–5.5)

1.9 (0.4–8.5)

Neonates (< 28 days old)

8 (1.9%)

19 (6.3%)

Infants (28–364 days old)

162 (38.3%)

95 (31.4%)

1–4 years old

138 (32.6%)

88 (29.0%)

5–9 years old

59 (14.0%)

43 (14.2%)

10–15 years old

56 (13.2%)

58 (19.1%)

Sex

Boys

235 (55.6%)

170 (56.1%)

Admission category

Direct paediatric ICU admission*

284 (67.1%)

219 (72.3%)

Inter-hospital transport

180 (42.6%)

140 (46.2%)

Risk category

Any comorbidity

148 (35.0%)

140 (46.2%)

Immunodeficiency or immunosuppression

Oncology

6 (1.4%)

19 (6.3%)

Bone marrow transplantation

4 (0.9%)

2 (0.6%)

Transplantation

0

1 (0.3%)

Chronic neurological disease

42 (9.9%)

18 (5.9%)

Chronic respiratory disease

38 (9.0%)

14 (4.6%)

Congenital heart disease

13 (3.1%)

17 (5.6%)

Premature birth

27 (6.4%)

30 (9.9%)

Burns

6 (1.4%)

10 (3.3%)

Chronic renal failure

4 (0.9%)

1 (0.3%)

Severity

Mean ICU length of stay (SD), days

5.2 (9.6)

6.8 (8.3)

Mechanical ventilation in the first hour

222 (52.5%)

161 (53.1%)

Intubation and ventilation

256 (60.5%)

215 (71.0%)

Mean PIM2 score (range)

5.0% (0.2–95.6%)

8.4% (0.2–99.5%)

Extracorporeal membrane oxygenation

1 (0.2%)

7 (2.3%)

Acute respiratory distress syndrome

7 (1.7%)

14 (4.6%)

Renal replacement therapy

4 (0.9%)

11 (3.6%)


PIM2 = Paediatric Index of Mortality 2 (mean probability of death). * Other admissions were to mixed ICUs. † Including primary immunodeficiency and secondary immunodeficiency (oncology, bone marrow transplantation, other transplantation, other immunosuppression). ‡ Excluding bone marrow transplantation.

Box 3 – Identified pathogens in Indigenous children admitted to an intensive care unit with sepsis or septic shock

Year of admission


2002–2007

2008–2013

P*

2002–2013


Number of patients

108

195

303

Bacterial

Staphylococcus aureus (methicillin-sensitive or -resistant)

21 (19%)

46 (24%)

0.40

67 (22%)

Neisseria meningitidis

17 (16%)

16 (8%)

0.044

33 (11%)

Streptococcus pneumoniae

2 (2%)

9 (5%)

0.22

11 (4%)

Coagulase-negative Staphylococcus

0

2 (1%)

0.29

2 (1%)

Group A Streptococcus, Streptococcus viridans

6 (6%)

11 (6%)

0.98

17 (6%)

Group B Streptococcus

0

1 (1%)

0.46

1 (< 1%)

Escherichia coli

4 (4%)

4 (2%)

0.39

8 (3%)

Pseudomonas aeruginosa

4 (4%)

4 (2%)

0.39

8 (3%)

Klebsiella spp.

1 (1%)

6 (3%)

0.23

7 (2%)

Haemophilus influenzae type B

2 (2%)

0

0.057

2 (1%)

Other bacteria

8 (7%)

25 (13%)

0.15

33 (11%)

Any bacteria

56 (52%)

108 (55%)

0.55

164 (54%)

Fungal

Candida, Aspergillus spp., other fungus

5 (5%)

13 (7%)

0.47

18 (6%)

Viral co-infection

Influenza

2 (2%)

2 (1%)

0.55

4 (1%)

Parainfluenza

0

2 (1%)

0.29

2 (1%)

Respiratory syncytial virus

2 (2%)

7 (4%)

0.39

9 (3%)

Adenovirus

1 (1%)

7 (4%)

0.17

8 (3%)

Cytomegalovirus, Epstein–Barr, herpes simplex, varicella zoster viruses

1 (1%)

5 (3%)

0.33

6 (2%)

Enterovirus

0

2 (1%)

0.29

2 (1%)

Other viruses

1 (1%)

3 (2%)

0.66

4 (1%)

Any viral co-infection

7 (6%)

26 (13%)

0.067

33 (11%)

No bacterial, fungal or viral organism identified

47 (44%)

67 (34%)

0.12

114 (38%)


* 2002–2007 v 2008–2013.

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