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Changes to the Healthy Kids Check: will we get it right?

Are we at risk of over-medicalising and under-researching?

In 2011, the Australian Government announced plans to change the voluntary Healthy Kids Check (HKCheck) during 2012–2013,1 by lowering the age of screening to children aged 3 years and incorporating elements of social and emotional wellbeing. The HKCheck will be conducted by general practitioners, practice nurses and Aboriginal health workers, and will cost about $11 million over 5 years.2

The Expert Working Group developing the HKCheck has not made public what the check comprises and what screening will be involved. While the first media release focused on 3-year-olds and “social and emotional development”, the most recent release (March 2013) announced that the expanded HKCheck will be phased in initially in eight Medicare Local areas in 2013, and the target group will be children aged from 3 to 5 years.3

It is not clear from the latest media release if social and emotional development will be included, and whether the HKCheck will identify “at-risk” families (ie, those with risk factors for children with psychological, conduct and behavioural problems) or whether it will identify risk factors for childhood psychiatric disorders. One aim of a population screening program, such as the HKCheck, is to ensure support for children by identifying and referring families to an appropriate health professional for an in-depth assessment and appropriate intervention (if initial primary health screening finds children who potentially would benefit from this).

Conducting population screening raises a number of complex issues. We will discuss the potential health benefits and risks of population social–emotional screening of children 3–4 years of age, and propose options based on currently available evidence. The first 3 years of life are crucial in terms of neurodevelopment — trauma, stress and/or attachment disruption may have adverse effects on brain and psychological development.4 Early adversity is associated with a range of later difficulties in multiple domains in life, including development and psychiatric disorders;4 however, this important topic is beyond the scope of our article.

Screening for mental health in early childhood

Social and emotional wellbeing in early childhood is defined as a “young child’s capacity to experience, regulate and express emotions, form close and secure relationships, and explore the environment and learn . . . these capacities [are] best accomplished within the context of the caregiving environment that includes family, community and cultural expectations . . .”.5 This definition implies that promoting children’s social and emotional wellbeing means alleviating current distress and suffering; enhancing social and emotional competence; establishing and sustaining positive developmental trajectories; and taking a holistic approach rather than concentrating just on the child.

Population screening aims to accurately and inexpensively identify children in need of a more comprehensive social–emotional assessment. Screening instruments used for widespread detection should be brief; easy to administer, score and interpret; of acceptable reliability and validity; and able to provide information that is both developmentally appropriate and clinically useful. Recommended levels for specificity and sensitivity are greater than 80%. There is a need for a balance between identifying a sufficient proportion of “cases” to effectively improve early detection, while minimising false positives.6 Risks of screening include over-medicalising (ie, inter-preting normal and individual variation or transient disturbances as psychopathological conditions); not identifying relationship disturbances; and labelling (with the associated stigma). Finally, screening is potentially very costly.

Currently, there are a number of clinical instruments that examine social and emotional development in 3-year-olds.

  • The one-page Pediatric Symptom Checklist, for use by paediatricians, is a brief assessment from parental reporting of dysfunction in major areas of a child’s daily life. A positive score suggests the need for further evaluation by a qualified mental health worker. This instrument has a specificity of 68% and a sensitivity of 95% when compared with clinicians’ ratings of children’s psychosocial dysfunction.7

  • The Child Behavior Checklist (CBCL/1.5-5) for ages
    1–5 years has good reliability and validity, but is lengthy (99 items).8 It is not a screening instrument, but is used as part of a comprehensive assessment by experienced clinicians.

  • The 11-item Brief Infant–Toddler Social and Emotional Assessment (BITSEA) assesses social–emotional abilities, such as empathy, prosocial behaviours and compliance,
    up to age 36 months and takes about 10 minutes to complete.9 Research has shown that its internal consistency and inter-rater reliability are marginal.10

  • The Ages and Stages Questionnaire – Social Emotional (ASQ-SE) is a comprehensive tool for screening possible delays in social–emotional and developmental functioning in children. It takes 15 minutes to complete and its sensitivity has been found to be 71%–85%.11

  • Parents’ Evaluation of Developmental Status (PEDS) is a brief screening tool for developmental and behavioural screening and ongoing surveillance of children from birth through to 8 years of age. Summary psychometric figures are sensitivity 86% and specificity 74%. However, only two specific questions concern mental health issues, and its validity testing (that it measures what it purports to measure) is mainly derived from overall development and not specifically social–emotional development.12

While the BITSEA and ASQ-SE were developed as clinical screening tools, they were not designed for large-scale population screening. These instruments may be used in a number of clinical settings, although they are most easily applied where time is not an issue and by those who have in-depth knowledge of child development (eg, staff of child health clinics). The CBCL/1.5-5, the BITSEA and the ASQ-SE need to be purchased and require training to score.

In summary, none of these tools meets all requirements for a brief population screen of children’s social–emotional development.

Is it possible to characterise psycho-pathological conditions in early childhood?

The same clustering of symptoms seen in 3-year-olds also occurs in older children and adolescents, and these symptom clusters are associated with socioemotional impairment, including social problems or a negative impact on the family. Studies using available validated instruments and clinical assessment have found the most prevalent clusters to be anxiety disorders, attention deficit hyperactivity disorder (ADHD), depressive disorder and behavioural difficulties.13 Kowalenko notes a range of prevalence figures of 7%–26%, reflecting the need for caution in interpreting these data and for further research.13 Another population study reported prevalence rates of impairment of 7%–11% (Diagnostic and statistical manual of mental disorders [DSM-IV]) in children entering school.14

Some problem behaviours and symptoms in early childhood are not transient. Typically, research in this area involves measuring internalising (eg, anxiety15) and/or externalising (eg, aggression15) symptoms, or specific symptoms, including attention problems15 and post-traumatic stress disorder.16 In general, studies suggest moderate continuity of symptoms (although most studies are not continued into adolescence), and there can be a change in symptom presentation over time.17 Children who frequently engage in externalising or internalising problem behaviours are at greater risk of a range of negative long-term outcomes, including dropping out of school and incarceration.18,19 A repeated finding is that elevated aggression persists from the age of 3 years to middle childhood. Currently, there is no research showing screening results at 3 years being predictive of specific psychopathological conditions in adulthood.20

Risk factors identified for symptom clusters in 3-year-olds are similar to those in older children.21 For example, there is evidence of long-term implications of early impairment, including that caused by parental mental health problems.4 Relatively few empirical studies have quantified the long-term predictive strength of these risk factors, when measured at, or near, the age of school entry. The moderating and mediating variables (eg, family factors, socioeconomic status) associated with the persistence of difficulties are typically not included in current screening measures.

Potential benefits of screening

Waiting to screen, identify and intervene may leave children “at risk” and miss opportunities for early intervention, prevention and improved trajectories, resulting in loss of both health and future economic benefits.22 Psychosocial problems are increasingly difficult to change or correct at an older age, but a meta-analysis has demonstrated the effectiveness of intervention in early childhood.23 However, similar to older children, younger children generally do not receive interventions because the problems remain undetected.24 From a broader perspective, identifying high-risk or symptomatic young children, and providing accurate prevalence estimates, would enable appropriate funding for the health and educational services necessary to support these children and their families.

Limitations and barriers associated with screening

As well as the previously noted risks, there are challenges in terms of both GPs using screening instruments and parents attending services offered.25 While there is research highlighting some of the short-term and longer-term problems in at-risk groups, developmental psychopathology is complex and it may not be possible to design a screening tool that can accurately identify young children who will develop disorders in the future.

Emotional and behavioural symptoms in young children are a final common pathway produced by multiple possible aetiologies requiring individual treatment planning. It is currently unclear which domains a screening instrument should include.

Evidence-based early intervention programs have often involved economically disadvantaged families. While there are well researched early intervention programs, some programs were shown not to be beneficial and, until further evidence is available, some scepticism remains about the universal application of early intervention programs.5 Is it better to have a population-based approach to treatment that does not need screening, or screening that leads to more targeted interventions? Further research is needed.

Children identified as being in need of more assessment may overwhelm currently available Australian health care resources. Jureidini and Raven note that interventions must be widely and equitably available to those who screen positive and, when targeted to those with “pre-disease”, should effectively reduce the likelihood of developing disorders.26

Future options

Given current knowledge, two fundamental steps are needed. First, we need to invest in methodologically robust, longitudinal population studies, starting before birth, which include risk factors and multiple outcome parameters. This information combined with that from the Australian Early Development Index (a population tool used in the first year of school, measuring five domains of children’s development)27 would provide much needed data on norms for Australian 3-year-olds to assist service planning.

Second, rather than spending money on screening that lacks an evidence base, a logical first step would be to develop a population-based screening instrument. One possible strategy would be to modify existing instruments to make them briefer. Alternatively, we could design a new instrument following best practice, after a comprehensive review of the existing literature, and obtain expert advice to ascertain which domains to include (infant, infant–parent interaction, family interaction). Then factor analysis and psychometric testing could be used to validate a brief population-screening version. Finally, its applicability in broader contexts could be assessed, including in different cultures.

Despite good intentions, further research and planning are needed before starting large-scale, population social–emotional screening of 3-year-old children in Australia.

Screening, referral and treatment for depression in patients with coronary heart disease

In 2003, an Expert Working Group of the National Heart Foundation of Australia (NHFA) issued a position statement on the relationship between “stress” and heart disease. They concluded that depression was an important independent risk factor for first and recurrent coronary heart disease (CHD) events.1 Here, we provide an update on evidence obtained since 2003 regarding depression in patients with CHD, and include guidance for health professionals on screening and treatment for depression in these patients. Our statement refers to depression in general (mild, moderate and severe), as all grades of depression have an impact on CHD prognosis. The process for developing this consensus statement is described in Box 1. Treatment decisions should take into account the individual clinical circumstances of each patient.

Epidemiology

The prevalence of depression is high in patients with CHD. Rates of major depressive disorder of around 15% have been reported in patients after myocardial infarction (MI) or coronary artery bypass grafts.3,4 If milder forms of depression are included, a prevalence of greater than 40% has been documented.3,4 Recently, the EUROASPIRE III study investigated 8580 patients after hospitalisation for CHD.5 The proportion of patients with depression, measured by the Hospital Anxiety and Depression Scale, varied from 8.2% to 35.7% in men and 10.3% to 62.5% in women. This is consistent with Australian and New Zealand data from a 6-year study, Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID).6,7 At the end of this trial, 27% of men and 35% of women were identified as depressed, using the Beck Depression Inventory II (BDI-II) questionnaire.

A large systematic review in 2006 suggested that individuals with depression, but no current CHD, have a moderately elevated risk of 1.6 for a later index CHD event.8 This elevated risk was confirmed in the Whitehall II study of 5936 healthy individuals over a 6-year period, in which depression was associated with a hazard ratio of 1.93 for cardiovascular events.9 In the Nurses Health Study, 78 282 healthy women were assessed for depression. In the 6-year follow-up period, 4654 deaths were reported, including 979 deaths from cardiovascular disease.10 Depression was associated with increased all-cause mortality, with an age-adjusted relative risk of 1.76 (95% CI, 1.64–1.89).10 The effect of depression on CHD incidence is thought to be strongest around the time of the depressive episode, with longer-term effects mediated via recurrence of depression.11 In young people the association between depression and CHD may be stronger.12

The case–control INTERHEART Study included 11 119 patients with MI from 52 countries.13 Perceived stress and depression were shown to be important risk factors, which together accounted for 32.5% of the population attributable risk (PAR) for CHD, suggesting that together they were as important as smoking and more important than diabetes (PAR, 9.9%) and hypertension (PAR, 17.9%) as risk factors for CHD.13

For people with CHD and comorbid depression, the relative risk (RR) of death is increased (RR, 1.80 [95% CI, 1.50–2.15]), independent of standard risk factors for secondary prevention.8 Comorbid depression also leads to a higher risk of other adverse outcomes in patients with CHD, such as a lower likelihood of return to work, poorer exercise tolerance, less adherence to therapy, greater disability, poorer quality of life, cognitive decline and earlier dependency.1420 Individuals with CHD and comorbid depression often have less access to interventions for CHD, despite being in a higher-risk group.2123

Definition of depression and types of depression

The diagnosis of depression can be difficult in people with cardiovascular disease, as depressive symptoms such as fatigue and low energy are common to both CHD and heart failure, and may also be a side effect of some drugs used to treat cardiovascular disease, such as β-blockers.24 The diagnosis may be further complicated in such patients by their responses to their disease (and the associated stigma), which may include denial, avoidance, withdrawal and anxiety.

According to the Diagnostic and statistical manual of mental disorders, fourth edition (DSM-IV),25 major depression is diagnosed when there is a minimum of 2 weeks of depressed mood and/or lack of pleasure (anhedonia), accompanied by four or more other (listed) symptoms such as sleep disturbance, appetite disturbance, poor energy, psychomotor impairment or agitation, poor concentration or poor decision making, and suicidal ideas or thoughts of death. The association with CHD appears to increase with greater severity of depressive symptoms across the spectrum, with no discrete cut-off point at “major depression”. Some studies have suggested links between particular subtypes of depression, such as somatic or anhedonic depression, but these are not consistent findings.2628

Screening for depression in patients with coronary heart disease

Screening of a population group for a risk factor or disease is worthwhile when the risk factor or disease has a reasonably high prevalence, there is a robust screening test, and effective and cost-effective treatments are readily available.29,30 Depression is both a risk factor and a disease in its own right, and fulfils these criteria for population screening. Screening for depression in patients with CHD would be expected to produce a higher yield than screening for depression in the general population, owing to a much higher prevalence of depression in patients with CHD. It is important to recognise depression in patients with CHD in order to provide the best possible care. Asymptomatic patients with significant cardiovascular risk factors (eg, those with diabetes) may also be considered for screening, as they have a high risk of depression.31

Many self-reported screening tools exist with the aim of detecting possible depression. These include the Patient Health Questionnaire (PHQ-2, PHQ-9), the Cardiac Depression Scale (CDS), the BDI-I and -II, and the Hospital Anxiety and Depression Scale.32,33 The BDI appears to be the most commonly used tool in studies involving cardiac patients. The CDS was developed by a member of the Expert Working Group (D L H) specifically for patients with cardiac disease.33 The short version (short form) has only five items. There is limited but expanding information on the use of the PHQ-9 in patients with cardiac disease.34,35 It is used widely in primary care. Simple tools such as the Kessler Psychological Distress Scale (K10),36 a measure of general distress, will often overdiagnose depression. This tool is currently used in mental health plans in Australia; however, there is no evidence of its use specifically for patients with CHD.

Recognising the need for a simple screening tool for depression in cardiovascular patients, the 2008 American Heart Association (AHA) Science Advisory suggested the use of the PHQ-2.37 The PHQ-2 is an abbreviated form of the PHQ-9, with only the first two of the nine questions in the PHQ-9 (Box 2).38 There are also other versions of the PHQ-2, which may use shorter time frames. The AHA recommended the use of the PHQ-9 if depression was noted using the PHQ-2.37 The Royal Australian College of General Practitioners’ Guidelines for preventive activities in general practice (the red book) also uses a categorical (Yes/No) version of the PHQ-2.39

The PHQ-2 and the PHQ-9 screening tools are associated with reasonable sensitivity and specificity.34 Importantly, depression diagnosed with the PHQ-2 and the PHQ-9 has been shown to predict worse CHD outcomes. In the Heart and Soul Study, positive responses to either question in the PHQ-2 (Yes/No version) predicted a 55% greater risk of cardiovascular events.35 Furthermore, the validity of the PHQ-2 and the PHQ-9 has been assessed in a variety of patients with varying clinical problems, ages and ethnicities, including in Australian Aboriginal people from urban and rural areas and people from the Torres Strait Islands.4042 Adapted versions exist for use with Indigenous people.

Access to each of the tools varies. No copyright is breached by use of the PHQ-2 and the PHQ-9, and the PHQs and the CDS are free.43 However, some questionnaires such as the BDI-I and -II are subject to copyright and a royalty must be paid each time they are used.44

Implicit in the AHA Science Advisory37 is that screening and identification of patients with depression leads to appropriate treatment, or referral for treatment, by the responsible attending medical practitioner. Unfortunately, research has shown that screening may have little or no impact on the treatment of depression or on outcomes.45,46 Screening by nurses, researchers, receptionists or social workers is not sufficient without appropriate referral or treatment.

It is recommended that a simple tool, such as the PHQ-2 or the short-form CDS, is incorporated into routine screening of patients with CHD. Routine screening for depression is indicated at first presentation, and again at the next follow-up appointment. A follow-up screen should occur 2–3 months after a CHD event. Screening should then be considered on a yearly basis, as for any other major risk factor for CHD. Consideration should also be given to screening the partner or spouse of these patients for depression, as studies show that they are at an increased risk of developing depression.47 If screening is followed by comprehensive care, depression outcomes are likely to be improved.

Treatment of depression in patients with CHD

Collaborative care

Although individual treatment approaches and strategies have been studied, in practice a collaborative-care or stepped-care approach is probably optimal for managing patients with CHD and comorbid depression. The concept of collaborative care involves a group of health professionals working together in a coordinated manner, and this approach has consistently been shown to be associated with greater improvement in depression for patients with CHD compared with standard care, and to be cost-effective.4852 For example, collaborative care after coronary artery bypass grafting improved depression scores, but not physical function or re-hospitalisation rates.48 In patients with depression comorbid with poorly controlled diabetes and/or CHD, the collaborative approach resulted in improvement in depression scores, glycated haemoglobin levels, low-density lipoprotein cholesterol levels, and systolic blood pressure.50

The Coronary Psychosocial Evaluation Studies (COPES) trial52,53 used a stepped-care treatment approach in patients with acute coronary syndromes (ACS) and persistent depression. Depressive symptoms decreased substantially in the intervention (stepped-care) group. Only three (4%) of the intervention patients experienced major adverse cardiac events compared with 10 (13%) of the patients given usual care, suggesting improved cardiovascular outcomes. Moreover, this stepped-care approach was associated with a 43% lower total health cost over the 6-month trial period.54

Pharmacological therapy

The efficacies of fluoxetine,55 sertraline (Sertraline Antidepressant Heart Attack Randomized Trial [SADHART],56 Enhancing Recovery in Coronary Heart Disease Patients [ENRICHD] trial),57 citalopram (Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy trial [CREATE])58 and mirtazapine (Myocardial Infarction and Depression Intervention Trial [MIND-IT])59 have been evaluated in clinical trials involving patients with CHD.

SADHART studied depression after ACS over 6 months. Depression scores in patients taking sertraline improved significantly more than in those receiving placebo. Most patients were also prescribed aspirin, statins and β-blockers. Life-threatening cardiovascular events occurred less frequently in the sertraline group; however, this result was not statistically significant.56

ENRICHD was a large trial that evaluated the effect of cognitive behaviour therapy (CBT) on depression or low social support in patients with a recent MI. Depression was diagnosed in 74% of participants. CBT improved depression but failed to reduce the number of CHD events. Patients whose depression did not respond to CBT were referred for treatment with antidepressant drugs. Selective serotonin reuptake inhibitors (SSRIs) (mainly sertraline) significantly improved depression in those patients. In the SSRI-treated group, there was a 43% (P < 0.005) reduction in deaths or recurrent MIs.57 However, this was a subset analysis, and therefore is hypothesis generating only.

In the Canadian CREATE trial58 and the MIND-IT trial,59 there were too few CHD events reported to enable analysis of cardiovascular outcomes.

Tricyclic antidepressants may worsen CHD outcomes and should be avoided in patients with CHD. Importantly, tricyclic antidepressants have been associated with increased mortality in patients with CHD.6062 In contrast, a recent meta-analysis of trials involving SSRIs in patients with CHD concluded that this class of drugs was well tolerated, with the risk of adverse events being similar to that for placebo.63

Psychological therapy

Of the various psychological therapies, CBT and integrative therapies (eg, interpersonal psychotherapy) have the best documented efficacy for treatment of major depressive disorder.64,65 CBT was used in the ENRICHD trial,57 interpersonal psychotherapy in the CREATE trial,58 and problem-solving therapy in the COPES trial.52,53 These therapies were all beneficial for depression but did not affect CHD outcomes. The efficacy of psychological therapy as a treatment for major or minor depression was evaluated in patients who underwent coronary artery bypass surgery.66 Significantly more patients in the CBT group (71%) and the stress management group (57%) had low depressive symptom levels, compared with those having usual care (33%), and these results were maintained at 6 months.66

A Cochrane review of psychological interventions for patients with CHD found evidence of small-to-moderate improvements in depression and anxiety symptoms with such interventions, but no strong evidence that the interventions reduced total deaths, risk of revascularisation, or non-fatal infarction.67 The interventions that were less effective were those that aimed to educate patients about cardiac risk factors; those that included client-led discussion and emotional support; or those that included family members in the treatment process.67 Uncertainty remains regarding the subgroups of patients who would benefit most from psychological treatments and the characteristics of successful interventions.

Exercise

Many patients with mild depression respond well to regular exercise and cardiac rehabilitation (exercise-based). A recent Cochrane review of exercise as a treatment for depression concluded that exercise improves depression with a similar efficacy to CBT.68 The benefit of exercise appears to have a dose–response relationship, needing at least 30 minutes of moderate aerobic activity on 5 days per week.69,70 This is consistent with usual public health recommendations.

The benefit of exercise in patients with CHD and depression has been demonstrated in the recent UPBEAT (Understanding the Prognostic Benefits of Exercise and Antidepressant Therapy) trial.71 Patients with CHD with at least a mildly elevated score for depressive symptoms (BDI score > 7) were allocated at random to treatment with SSRIs, exercise or neither. Exercise was equivalent to SSRI treatment in improving depression scores, with patients in both groups showing greater improvement than the control group.71 In a large randomised controlled trial (RCT) of 2322 patients with heart failure (of whom 28% were depressed), exercise, in addition to reducing mortality and hospitalisation (P = 0.03), significantly reduced depression (P = 0.002).72

Complementary and alternative therapies

Up to 50% of patients with depression have been shown to use complementary and alternative medicines without disclosing this to their treating clinician.73 Therapies that may be effective in depression are supplemental marine n-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]), S-adenosylmethionine (SAMe) and St John’s wort.74 Specific trials in patients with CHD and depression have not been performed with the latter two therapies.

Marine n-3 fatty acids (at a dose of 1 g per day of combined EPA–DHA) are recommended by the NHFA and the AHA for all patients with CHD.75 This dose also may improve mild depression. However, the addition of 2 g/day of combined EPA and DHA to sertraline 50 mg daily for depressive symptoms appears to provide no added benefit over sertraline alone.76 Some trials comparing St John’s wort and SAMe to antidepressant medications suggest a similar effectiveness in improving depression to antidepressant medications.7779 However, most commercial brands of St John’s wort have not undergone randomised trials.78,79

Adherence

Depression is a major predictor of poor adherence in patients with CHD, be it to drug therapy or lifestyle measures.80,81 Patients with depression are three times more likely to be non-compliant with medical treatment than patients without depression.82 Greater severity and chronicity of depression have been associated with poorer adherence to aspirin therapy after MI.83 Adherence to aspirin therapy after ACS has been shown to be significantly lower in persistently depressed patients (76.1%) than in those whose depression improved (87.4%), or who were not depressed (89.5%).83 Patients who are persistently depressed are also less likely to undertake behaviours that reduce risk; for example, quitting smoking, taking medications, exercising and attending cardiac rehabilitation.81 The SADHART trial showed adherence to medication increased after remission of depression in 68.4% of participants taking the trial medication.84

A recent RCT of a collaborative-care depression treatment program in 134 patients with depression after ACS demonstrated improved adherence to medications and secondary prevention behaviours and was independently associated with improvement in depression.85 However, in another RCT of 157 patients undergoing treatment for depression after ACS, there were no improvements in adherence to risk-reducing behaviours in spite of a significant reduction in depression.86

Referral

Once depression is identified through screening, treatment may be initiated immediately, or referral to psychological or psychiatric services may also be considered appropriate. Most patients with depression in Australia are managed by general practitioners.87

Members of the Cardiac Society of Australia and New Zealand, the majority of whom are clinical cardiologists, were surveyed regarding assessment of depression. Most respondents screened for depression occasionally, with only 3% using a formal tool. Lack of confidence in identifying depression was the strongest predictor of a low screening frequency. Cardiologists rarely initiated treatment for depression, and 43% did not feel they were responsible for treating depression.88

There can be a reluctance to treat depression in patients with CHD because of a belief that depression is normal after an acute cardiovascular event. Mild depression may resolve spontaneously; however, for most individuals with CHD, depression remains long term.89

Conclusion

A summary of the key evidence-based points is provided in Box 3 and Box 4, and the Appendix gives the National Health and Medical Research Council grades of recommendations and evidence hierarchy.

High-quality care for treatment of depression is achievable and affordable. The benefits of treating depression in people with CHD include improved quality of life, improved adherence to other therapies and potentially improved CHD outcomes.90 Effective treatment of depression may decrease CHD events but this is not proven, as no adequately powered trials have been completed, nor are there any ongoing.

1 Process used to develop this National Heart Foundation of Australia consensus statement

The Expert Working Group members performed relevant literature searches using key search phrases including, but not limited to, “stress”, ”depression”, “anxiety”, “treatment of depression”, “acute coronary syndromes”, “adherence and depression” and “screening for depression”. This was complemented by reference lists compiled from reviews and personal collections of the Expert Writing Group members.

Searches were limited to evidence available for human subjects with coronary heart disease published in English up to December 2012. The recommendations made in this consensus statement have been graded according to the National Health and Medical Research Council guidelines (see Appendix).2 The Cardiac Society of Australia and New Zealand, beyondblue: the national depression initiative and the Royal Australian and New Zealand College of Psychiatrists were consulted during the development of this document and have endorsed its content.

2 Patient Health Questionnaire (PHQ-2) Yes/No version35

  • During the past month, have you often been bothered by feeling down, depressed or hopeless?

  • During the past month, have you often been bothered by little interest or pleasure in doing things?

3 National Heart Foundation of Australia grades of recommendation and levels of evidence for screening, referral and treatment for depression in patients with coronary heart disease (CHD)2

Recommendation


Grade2

Level2


1

For patients with CHD, it is reasonable to screen for depression

A

I

2

Treatment of depression in patients with CHD is effective in decreasing depression

A

I

3

Treatment of depression in patients with CHD improves CHD outcomes

D

II

4

Treatment of depression in patients with CHD changes behavioural risk factors/adherence

B

III-2

5

Exercise is an effective treatment of depression in patients with CHD

A

I

6

Exercise improves CHD outcomes in patients with CHD

B

II

7

Psychological interventions improve depression in patients with CHD

B

II

8

Psychological interventions improve CHD outcomes in patients with CHD and depression

D

II

9

SSRIs improve depression in patients with CHD

A

I

10

SSRIs improve CHD outcomes in patients with CHD and depression

D

III-1

11

Collaborative-care approach improves depression in patients with CHD

B

II

12

Collaborative-care approach improves CHD outcomes in patients with CHD and depression

D

II


SSRIs = selective serotonin reuptake inhibitors.

4 Treatment of depression in patients with coronary heart disease (CHD) — summary of treatment subgroup effects showing grade of recommendation and level of evidence

Treatment

Depression


CHD outcome


Grade2

Level2

Grade2

Level2


Non-drug

Exercise

A

I

B

II

Psychological, including CBT

B

II

D

II

St John’s wort*

D

—*

D

—*

n-3 fatty acids

D

II

D

II

SAMe*

D

—*

D

—*

Collaborative

B

II

D

II

Drug

SSRIs

A

I

D

III-1


CBT = cognitive behaviour therapy. SAMe = S-adenosylmethionine. SSRIs = selective serotonin reuptake inhibitors. * Insufficient evidence to rate or no trials have been performed. Data not available in patients with CHD.

Appendix: Definition of National Health and Medical Research Council (NHMRC) grades of recommendations and evidence hierarchy*

Definition of NHMRC grades of recommendations

Grade

Description


A

Body of evidence can be trusted to guide practice

B

Body of evidence can be trusted to guide practice in most situations

C

Body of evidence provides some support for recommendation(s) but care should be taken in its application

D

Body of evidence is weak and recommendation must be applied with caution

NHMRC evidence hierarchy: designation of levels of evidence


Level

Intervention

I

A systematic review of level II studies

II

A randomised controlled trial

III-1

A pseudorandomised controlled trial (ie, alternate allocation or some other method)

III-2

A comparative study with concurrent controls:

  • Non-randomised, experimental trial

  • Cohort study

  • Case—control study

  • Interrupted time series with a control group

III-3

A comparative study without concurrent controls:

  • Historical control study

  • Two or more single arm study

  • Interrupted time series without a parallel control group

IV

Case series with either post-test or pre-test/post-test outcomes


* From NHMRC additional levels of evidence and grades for recommendations for developers of guidelines.2

The boy who didn’t cry wolf

Someone once told me that during his life, Winston Churchill would often refer to his depression as a “black dog” — a vile, loathsome creature that would shadow every decision and thought in his mind. But to me,
it was not just a dog, but something more sinister and predatory.

The beast followed me in the same way that a lapdog would follow its master, though there was no doubt of who was in charge. Behind every thought, decision and doubt in my mind, the black dog would be not too far away, waiting for a moment of weakness. Feeding off my shame, regret and self-loathing, its hunger knew no bounds and it could smell the fear that seeped from my skin.

For most of my adolescent years, that’s what it was like living with my depression. Every day was a new trial for me to fail and a new reason to undermine my existence. No matter what I did, no matter how hard I worked, I would always come home beaten and shamed. I was constantly making mistakes and no matter how trivial they were, I always punished myself. Every transgression I made was
a constant reminder of how worthless I was.

I never felt more alone than I did during those years. While my peers enjoyed themselves by going out, playing sports or singing in musicals, I spent my breaks eating my lunch alone. I always compared myself to them, asking myself why I couldn’t be like them. Each time, the conclusion was the same; it was because they were normal and I wasn’t. I felt there was something wrong with me, something I couldn’t fix. It was a period of time in which I felt my life was spinning out of control and my sanity was slowly unravelling.

The only thing keeping me alive was my desire to do medicine. Even before I met the black dog, becoming a doctor was all I ever wanted. To work in a craft that was centred around people and their ability to care. It was my calling in life and it was something that I needed to do. But most importantly, it allowed me to push past my depression and survive. No matter how hard things got, I had the strength to continue. I wanted desperately to speak to the school counsellor and confide in her all the pain and misery I was feeling. Maybe there was a cure. I owed it to myself to try. But what would happen if people found out that I was seeing her? What if my peers thought I was insane? The disgrace and humiliation I would feel if everyone knew would be too hard for me to handle. No, I decided. It was
my burden to bear and no one else needed to find out.

It wasn’t long before I tumbled. Months passed, the days became harder for me to bear and my depression deepened. As life continued and my peers moved forward, I was left behind, forgotten. It was as if everyone was in on a big secret that I was not privy to. The cruel isolation wreaked havoc on my self-esteem, pushing me further towards the brink of insanity. As my mind unravelled, my body ached with constant agony.

And then everything became too much. I felt numb and sick at the same time. Waves of nausea, spite and humiliation washed over me as all my mistakes flashed before my eyes. My breathing became laboured and what little tenacity I had left crumbled. I had finally convinced myself that I was a complete and utter failure. I wept. While I sobbed, I wondered what it was like to feel normal and why I lived a cursed life. I pleaded with the Almighty for sweet relief, one way or another. I didn’t care anymore, I just wanted out. As the depression took hold, I reached the chasm’s edge. One step and I would be committed forever. I asked a God I didn’t believe in to give me a break.

To this day, I am thankful for what happened next. After I confessed everything to the counsellor, she helped me realise that no matter how alone I felt, I had my family, my friends and the school to stand by me. That this unbearable agony
I was feeling was common. That people do care. It was something I needed to hear. I was quickly referred to a psychologist for further treatment and I began acceptance and commitment therapy, where I learnt how to acknowledge my faults and move on with my life. Just sharing my problems with someone else and feeling as if they cared was enough to relieve my grief. The pain and doubt that used to hound my every move had less of an impact now. With each session, I could feel the dog — my dog — being pushed further away until it was out of sight.

During the course of the next few months, I was able to complete my final year and secure an interview for medicine. As the date of my interview approached, I became nervous and anxious but I strengthened my resolve. It was my only chance to rectify what had happened to me and I wasn’t going to throw it away. When the day came, I gave it my all.
I talked about why I loved medicine and how I couldn’t see myself doing anything else. I showed them the passion I
had for the profession and the drive necessary to succeed. Afterwards, I was able to rest knowing that I did everything I could. My biggest fight was over.

One month later, I received a call that I had started to believe would never come. I was offered a place to study medicine. It was as if a burden was lifted off my chest. I finally had what I so dearly coveted. It made me realise that anything was possible. That I could live again. Despite being harder than anything I had ever done, studying medicine was the best thing that ever happened to me. I was no longer held back by the expectations that others had of me and was able to become whoever I wanted to be.

That said, I still needed to control my depression. At times, I could feel it edging back into my life and I fought to keep it in check. It was the little things, like new experiences and social pressure, that I struggled with. However, the hardest part was learning about depression at university. Learning about its causes and symptoms made me relive the trauma
I went through. But I always remembered what my life was like before medicine, and how grateful I am for my life now.

Despite my terrible ordeals, I feel that my depression has made me more empathetic. As I remember my clinical experience as a patient, I find it easier to understand what the patient is going through. This recognition allows me to identify with the patient and develop rapport. I know that the dog is not gone forever and I still have bad days. But for the first time in my life, I think I can handle it. I am ready for the next step and this time I’m not alone.

The case for CBT over antidepressants

THIS BOOK is by a doctor with an abiding interest in the philosophy of medicine. Paul Biegler is an Australian Research Council Postdoctoral Fellow at the Centre for Human Bioethics, Monash University, and a recipient of the 2011 Australian Museum Eureka Prize for Research in Ethics.

The book describes the therapeutic use of antidepressant medication (ADM) versus cognitive behaviour therapy (CBT), and concludes that it is unethical to provide the former as a first option to all patients suffering from depression. This is based on the author’s view that ADMs do not promote autonomy nor change vulnerability, whereas CBT enhances resilience and changes cognitive vulnerability to depression.

However, Biegler does not sufficiently discriminate between different types of depression. He acknowledges that some types may require ADMs to allow patients to process information, but underplays this point. In these cases — such as melancholic and psychotic depression, some medical illnesses and, arguably, depression related to serious personality disorders — ADMs can improve cognition and judgement to enable sufferers to make informed choices, while ongoing ADMs and psychotherapy may be necessary to decrease vulnerability and promote autonomy. And although Biegler talks about precipitating stressors, he doesn’t acknowledge the place that environmental stressors can play in melancholic depression, often a point of confusion.

The case is meticulously built up through progressive chapters. It is a thought-provoking book, but not one to skim through or dip into. It is recommended for people with a serious interest in the area. It addresses important issues and is timely as the costs of providing CBT have become less of an issue with the advent of excellent self-help books and internet programs, and greater access to clinicians providing CBT. It will be of interest to general practitioners, psychiatrists, psychologists and people involved in health economics and health planning, albeit with the aforementioned caveats in mind.

What can and should we predict in mental health?

David Foster Wallace, in his novel Infinite jest (1996), described the impulse for a person at the point of suicide as like that of jumping from a burning high-rise building. “Their terror of falling from a great height is still just as great as it would be for you or me … [but] when the flames get close enough, falling to death becomes the slightly less terrible of two terrors.”

This is one way to conceptualise the situation for at least 2273 people in Australia who committed suicide in 2011. To understand how to prevent such deaths, we need to know — following Wallace’s metaphor — the point at which an individual will choose to jump rather than face the flames. Can we predict this? And to what extent can we predict any outcomes in psychiatry?

Much effort has gone into trying to identify patients who are at particular risk of completed suicide within a year after presenting in psychological crisis or after attempting suicide. Ryan and Large (doi: 10.5694/mja13.10437) argue that predicting the short-term risk of suicide for such patients is not possible given the lack of identified risk factors that sufficiently discriminate between those who successfully suicide and those who do not. In addition, many people without the factors suggested as being associated with increased risk go on to attempt suicide. In this light, the authors recommend renewed, close clinical engagement with each patient’s situation and appropriate tailored intervention.

While prediction of suicide risk in individuals may be problematic, at a population level, suicide prevention has for some time been integral to mental health policies. Christensen and Petrie (doi: 10.5694/mja12.11793) outline six recommendations that should be part of any suicide prevention strategy. These revolve around targeting interventions, addressing risk factors, providing online resources and addressing gaps in community knowledge and discussion.

There have been recent moves to encourage more public discussion about suicide. But, as Fitzpatrick and Kerridge argue (doi: 10.5694/mja12.11540), community discussion should not simply be equated to media reporting of suicides. While there is some evidence of an association between increased media reporting and the incidence of attempted or completed suicide, they argue that this should not cloud strategies to encourage general community discussion about how suicide affects us all. There is reason to hope that talk beyond that filtered through the media prism will more effectively address the social and cultural factors that relate to suicide.

The possibility of identifying children at high risk of emotional and behavioural problems has been the basis of the expansion of the voluntary Healthy Kids Check for 3-year-olds to include social and emotional wellbeing. Will such assessment predict later problems? Daubney and colleagues (doi: 10.5694/mja12.11455) argue that although early intervention in this age group does have benefits, many children with problems go undetected, and none of the currently available assessment instruments are suited to screening. In addition, no symptom clusters are predictive of later psychopathology, and there are potential problems with overdiagnosis and overmedicalisation.

From the outsider’s perspective, there often seems to be more bad than good news in mental health, with controversy, lack of progress and confusing evidence. However, there are bright spots, even in those conditions previously thought to be intractable. Grenyer (doi: 10.5694/mja13.10470) shows that the prognosis for borderline personality disorder has significantly improved, with effective psychotherapies and support to patients and their family members offering real hope for more stable and productive lives. This should also lower sufferers’ risk of suicide, which, either attempted or completed, is a well known feature of the disorder.

Twelve years after the publication of Infinite jest, David Foster Wallace committed suicide on a background of worsening, difficult-to-treat depression. His strangely prescient metaphor of flames rising up a burning building reaches beyond literary dilettantism. Perhaps, in the context of suicide, we need to ask ourselves whether we know what causes the fire, and how much we understand the person poised in terror at the top.

Suicide risk assessment: where are we now?

A definitive way to identify patients who will suicide remains elusive

Patients who present in psychological crisis or after a suicide attempt are more than 50 times more likely than the general population to die by suicide in the following year.1,2 They require careful assessment and management. Numerous publications suggest, and some health department policies insist, that such patients should undergo a “comprehensive suicide risk assessment” in addition to a standard clinical assessment.3,4 Although most guidelines warn that suicide risk assessment does not substitute for clinical judgement, almost all also include long lists of patient characteristics that are claimed to enable identification of those patients at high risk of suicide. These lists are often fashioned into ad-hoc scales that purportedly stratify patients into categories of low, medium and high risk. However, it is simply not possible to predict suicide in an individual patient, and any attempt to subdivide patients into high-risk and low-risk categories is at best unhelpful and at worst will prevent provision of useful and needed psychiatric care. Here, we explain why this is so and outline what we believe clinicians should do instead.

Although patients presenting after suicide attempts or in crisis have a greatly increased probability of eventual suicide compared with the general community, fewer than one in 200 will actually die by suicide in the next 6 months.1 Suicide risk assessment is usually suggested as a way of determining who among these presenting patients should be offered different or more intensive treatment. However, the low base rate of completed suicide, combined with the lack of defining characteristics of people who proceed to suicide, makes this task impossible. Any useful further risk assessment would need to rely on a risk factor or a combination of risk factors that are consistently present, can be reliably assessed, and are very strongly overrepresented in the few people who do eventually suicide and yet rare or absent in those who do not. There is no evidence that such a risk factor or combination of risk factors exists. In 1983, the author of a large, well conducted prospective study of suicide lamented that “we do not possess any item of information or any combination of items that permit us to identify to a useful degree the particular persons who will commit suicide”.5 Thirty years later, nothing has changed: a similarly large and methodologically sound prospective study of psychiatric inpatients found that only 12% of suicides occurred among high-risk patients, and that fewer than one in 400 high-risk patients suicided.6,7

The list of generally accepted suicide risk factors is long and includes male sex, old age, divorce, medical illness, substance use, past suicide attempts and guilt. The most often cited risk factor for future suicide is expressed suicidal ideation.3,4 However, among psychiatric patients, expressed suicidal ideation does not discriminate between suicide completers and non-completers.8 Presumably this is because thoughts of self-destruction are very common in this group and because many people intent on suicide will not disclose that intent. Other intuitively appealing candidate characteristics include depressed mood and hopelessness. These, too, are almost universally found in the risk factors nominated in suicide risk assessment guidelines.3,4 However, not only are they very common in patients presenting with psychological problems, but most people with depressed mood will also feel hopeless, and vice versa; therefore, the combination of these risk factors offers little additional discriminative ability.

In recent decades, an enormous amount of research has gone into finding the magic combination of risk factors that acts as a sensitive and specific discriminator.5,6,9,10 Almost every study of completed suicide is retrospective, examining dozens, sometimes hundreds, of characteristics recorded in the medical records of both patients who suicided and controls, searching for factors or combinations of factors that were present more often in the patients who died.11,12 Such studies are likely to yield chance findings that appear to be significant, and they could identify some potentially reproducible associations with suicide. However, meta-analysis finds contradictory results between studies, leaving very few candidate risk factors among all the studies examined.1113 Moreover, even a combination of reproducible risk factors still fails to provide a useful way of identifying high-risk patients. We examined studies investigating risk factors for completed suicide within a year of inpatient psychiatric treatment. Even making assumptions that optimise the power of suicide risk assessment, we estimated that while some patients could be categorised as “ultra-high-risk”, as few as 3% of these would go on to suicide in the year after discharge. Meanwhile, about 60% of people who did eventually suicide during the same period would have been categorised as being at lower risk.11

In original research and in meta-analyses, no generally accepted risk factors individually or in combination provide any useful way of further categorising patients who present in crisis. We understandably want to identify those who will later kill themselves — but this is simply not possible.

Here and now, clinicians should not be conducting “comprehensive suicide risk assessments”. They should be conducting comprehensive clinical assessments of each patient’s situation and needs. Suicidal ideation, for example, is not useful as an indicator of the likelihood of future suicide, but it is an invaluable sign of a person’s inner despair. So-called risk factors like depression, hopelessness and substance misuse are far too common and non-specific to be useful indicators of suicide risk, but they can be seen as symptoms of mental illness and important pieces of a revealed inner life that, taken together, give us a better understanding of the individual person and guide us towards what needs attention and discussion.

This is not to say that we should abandon patient safety. Bolstering family or social support, restricting access to lethal methods of suicide or making a crisis plan are steps that should be taken for all patients in psychological crisis — not just those whom we imagine might be more likely to suicide than others.

We cannot prevent tragedy by trying to identify those few souls who will be consumed by it. We must instead gather a comprehensive picture of each individual patient, and use this to tailor optimal management for the patients and families needing our care.

Clinical staging for mental disorders: a new development in diagnostic practice in mental health

Matching the timing and intensity of interventions to the specific needs of patients

The release of the fifth edition of the Diagnostic and statistical manual of mental disorders (DSM-5)1 classification system, scheduled for May 2013, will create controversy due to the expanded range of problems now classed as mental disorders. However, in our view, it is unlikely to improve clinical care. The ultimate test for any system of diagnosis is its clinical utility. That is, does it assist clinicians to improve their selection or sequencing of treatments and enable them to make more accurate prognostic statements in keeping with newer concepts and knowledge? We propose that a refinement to traditional diagnostic practice — clinical staging — is more likely to improve clinical care and inform future research into the causes of mental disorders.25 Further, clinical staging draws the practice of clinical psychiatry closer to general medicine, especially with regard to chronic disease management.

In the past century, a major challenge for psychiatry was a lack of international consensus on diagnostic categories. For many decades, DSM and other international systems strived to enhance the reliability of psychiatric diagnoses. Recent field trials for DSM-5 indicate that acceptable reliability remains elusive.6 However, even diagnostic categories with modest reliability have limited validity. A major weakness is that the diagnoses refer to “categorical phenotypes” that fail to address critical differences in clinical presentations associated with age of onset or stage or course of illness.25 Most criteria reinforce categories derived from observations of middle-aged people with long-established stable illnesses, who have often been treated extensively by specialised mental health services. Inevitably, these map poorly onto earlier, less specific clinical presentations seen in general outpatient, primary care or community settings. They also presuppose that independent causal pathways exist for each clinical phenotype — an assumption that is not supported by contemporary family, genetic, neurobiological or risk factor research.2,3

What are the alternatives? Twenty-first century health care places an increasing premium on personalised or stratified medicine, with the goal of delivering more tailored treatments. Consequently, there is increasing international support for applying the concepts of clinical staging, particularly for adolescents and young adults with significant mood or psychotic disorders.4,7 Given that 50% of major mental disorders begin between 15 and 25 years of age, a focus on enhanced care and novel clinical research during this critical developmental phase is a timely test of this framework.5,8,9

At its core, the clinical staging model recognises the full spectrum of illness experience. For example, for ischaemic heart disease, the staging model identifies individuals at risk (because of genetics, lifestyle or other risk factors), those with symptoms or related syndromes that suggest illness progression (eg, hypertension, metabolic syndrome) and those with overt evidence of cardiac disease (eg, angina). Further, treatments differ at each point on the illness continuum, with interventions with lower risk–benefit ratios being provided at earlier stages (ie, dietary change or increased exercise for the at-risk stage, and more complex medical treatments for later stages). In psychiatry, this approach also differentiates at-risk individuals (stage 0; eg, family history of severe mental disorders) from those with early subthreshold or attenuated syndromes (stage 1; eg, brief episodes of psychotic or hypomanic symptoms) from those meeting threshold diagnostic criteria (stage 2) or with established or persisting illness (stage 3). Importantly, staging suggests that disorders emerge via a limited set of overlapping and fluctuating symptom clusters (microphenotypes), some of which resolve, while others progress and stabilise into clinical presentations (macrophenotypes) that ultimately resemble more traditional diagnoses.25 The clinical staging model is compatible with clinical reality and can be tested for reliability, predictive validity and patterns of association with developmental epidemiology and neurobiological markers.7,10

For mental health, the critical challenge is to help all patients entering care by reducing symptoms, promoting recovery and quality of life, and preventing progression to premature death or further disability.8 The means for achieving these outcomes may be better assisted by clinical staging rather than by prematurely assigning categorical diagnoses to an evolving clinical profile. Also, rather than encouraging early use of medical interventions, the specific intent of staging models is to mimic the disease-management principles now widely applied in general medicine, which enable clinicians to target stage-appropriate interventions from early in the course of illness. Thus, for most young people entering care before the development of full-blown mood or psychotic disorders, the emphasis is on providing relevant information and psychological strategies (including e-mental health), reducing known risk factors (notably alcohol and/or substance misuse), minimising self-harm, promoting resilience, encouraging self-monitoring and reviewing longitudinal course.8 In future, low-risk, evidence-based neuroprotective strategies (which are behaviourally, psychologically or medically based) may also become available.

Clinical staging revolutionised general medical practice, focusing attention on the benefits of intervening earlier in the course of life-threatening illnesses. For clinical psychiatry, it could enable appropriate matching of the timing and intensity of interventions to the specific needs of help-seeking individuals. Also, staging sheds light on the evolution of symptom networks and syndromes,5 and enhances our chances of validating specific pathophysiological pathways and of introducing more objective measures of illness risk, onset and progression.2 In medicine, the successor of clinical staging was clinicopathological staging. In the future, we hope that clinical psychiatry will also be based on the combination of objective markers of illness course and enhanced clinical care.

The role of depression in the primary prevention of cardiovascular disease

To the Editor: We would like to add a cautionary note to O’Neil’s support for the inclusion of “depression and other psychosocial factors” in the updated National Vascular Disease Prevention
Alliance guidelines for assessing cardiovascular disease (CVD) risk. Her statement “it is now clear that depression is also an important risk factor for CVD” is premature.1 Different authors have challenged the suggested relationship and, given divergent findings and opinions, it is misleading to claim that the matter is now “clear”.25 We do not deny a possible link between depression and coronary heart disease (CHD) but suggest that the extent and nature of the relationship has yet to be clarified. Premature acceptance and promotion of the idea that depression is a risk factor for CHD might contribute to overdiagnosis and overtreatment of depression as well as undue worry about the risk of CHD by individuals diagnosed with depression.

The role of depression in the primary prevention of cardiovascular disease

In reply: I thank Stampfer, Hince and Dimmitt for their response.
While I acknowledge that there are aspects of the relationship between cardiovascular disease (CVD)
and depression that remain undetermined, recent evidence clearly supports the role of depression as an independent risk factor for CVD and is indeed convincing.13 This is especially true in studies that assess depression using diagnostic criteria.4 We know that the risk of developing coronary heart disease (CHD) for individuals with depression is twofold, and these individuals have a similar risk of CVD-related death.2 We also know that the independent contribution of depression to CVD is at least comparable to that of more traditional risk factors including diabetes, hypercholesterolaemia, smoking or obesity.5 A decade has now passed since the National Heart Foundation’s seminal position paper concluded that: “there is strong
and consistent evidence of an independent causal association between depression, social isolation and lack of quality social support and the causes and prognosis of CHD”.5 Despite this, depression remains underestimated as a meaningful contributor to CVD.

Long-term health and wellbeing of people affected by the 2002 Bali bombing

The 2002 Bali bombing resulted in the deaths of over 200 people, including 88 Australians and 35 Indonesians, making it the single worst act of terrorism to have affected either country.1 A further 209 people were injured, including 66 Australians who suffered severe burns and complex shrapnel wounds.2,3

Terrorism exposure may have significant long-term effects on the mental health and wellbeing of survivors. Post-traumatic stress disorder (PTSD) is the most common psychological condition observed in the aftermath of such events, but it often coexists with depression, functional impairment or substance misuse.4,5 Few studies have examined the long-term effects on terrorism survivors, although one large study found increases in PTSD between 3 and 5 years after the September 11 attacks.6,7 Risk factors included direct exposure (proximity, injury, witnessing horror), incident-related bereavement and low social support.

Bereavement that occurs in traumatic circumstances may have a considerable long-term impact on psychological distress and appears to slow the rate of recovery.8 Deaths involving deliberate violence are associated with higher prevalence of trauma conditions, depression and prolonged or “complicated” grief.8,9 Complicated grief is characterised by continuing separation distress and bereavement-related traumatic distress. While frequently comorbid with depression or PTSD, it is increasingly recognised as a distinct condition that is associated with persistent functional impairments and negative health outcomes, particularly among those bereaved through terrorism.9,10

The health and psychosocial effects of terrorism exposure have rarely been investigated beyond 3–4 years after such incidents.4,11 No studies have examined these effects among Australian survivors. Our aim was to examine the physical and mental health status of individuals directly affected by the 2002 Bali bombing, 8 years after the incident, and to determine demographic, exposure and loss-related correlates of these health outcomes.

Methods

Participants constituted a cross-sectional convenience sample of individuals who had experienced personal exposure and/or loss related to the 2002 Bali bombing and had current contact details listed with a New South Wales Ministry of Health therapeutic support program (Bali Recovery Program), where they had attended at least one consultation. Those who registered interest in response to a written invitation were contacted, given a description of the study, and asked for verbal consent. Professional interviewers from the NSW Health Survey Program completed computer-assisted telephone interviews between 9 July and 22 November 2010, excluding a period around the bombing anniversary (1–23 October). The validity of telephone-based interviews to assess stress and anxiety conditions has been demonstrated.12

Measures

We examined demographic and exposure factors to determine their relationship with physical and mental health outcomes. Exposure variables were: lifetime traumatic incident exposure,13 presence in Bali during/after the bombing, involvement in the search for missing friends/relatives (first 48 hours), and bereavement circumstance (eg, multiple loss, family). Perceived social support from family and friends was assessed with two items from the Perceived Social Support Scale,14 as well as single items regarding neighbourhood social connectedness15 and overall support since the bombing.

Current bereavement experience (“experiential” grief) was measured using six items from the Inventory of Complicated Grief-Revised (ICG-R): separation distress (longing/yearning) and cognitive, affective or behavioural items (anger, acceptance, detachment, emptiness/meaninglessness, difficulty moving on). High factor loadings related to the single underlying complicated grief factor and elapsed time since bereavement guided item selection.16

Self-rated physical health in the previous month was measured with a single validated item from the NSW Population Health Survey.15 We used the short form of the Connor-Davidson Resilience Scale (CD-RISC2) to measure current perceived personal adaptability and ability to continue to function effectively in stressful circumstances.17 A score of 7–8 indicates high personal resilience.

Anxiety, depression, agitation, psychological fatigue and associated functional impairment (ie, full days unable to manage day-to-day activities due to symptom effects) in the past month were measured using the Kessler Psychological Distress Scale (K10+). Individual scores range from 10 to 50, indicating low (10–15), moderate (16–21), high (22–29) and very high (30–50) psychological distress. The latter is indicative of a significant mental health condition.18

We used the Primary Care PTSD Screen (PC-PTSD) to measure past-month traumatic stress-related symptoms (TSRS) specific to Bali-related experiences. Single items relate to one underlying characteristic specific to PTSD: re-experiencing, numbing, avoidance and hyper-arousal. The endorsement of 3–4 symptoms indicates “probable” PTSD and the need for specialist assessment.19

Statistical analysis

The dataset was weighted by age and sex to reflect registered participants in the Bali Recovery Program (n = 115). Current physical and mental health were analysed as outcome measures, with demographic, traumatic incident exposure, perceived support and bereavement factors used as independent variables.

Responses to the support and bereavement questions were expressed as dichotomous variables, with a value of 1 assigned to responses “agree” or “strongly agree”, and 0 to “disagree”, “strongly disagree” and “don’t know”. The outcome variables of physical health, personal resilience and functional loss were dichotomised into high and low (or good and poor) outcomes. Three outcome categories based on established clinical cut-offs were adopted for psychological distress (low–moderate, high and very high) and TSRS (low, moderate and high).18,19

Analyses were performed using Stata statistical software, version 12.0 (StataCorp), with “Svy” commands to allow for adjustments for sampling weight. We used the Taylor series linearisation method to determine prevalence estimates, and χ2 tests to test for significant differences in the prevalence of physical and mental health outcomes. Due to the relatively small sample size, an α significance level (P < 0.15) was adopted, as it is a commonly used threshold for entry into multiple logistic regression analyses,20 and could provide indicative findings in the context of this exploratory study. Multiple testing using the Bonferroni correction was also carried out by dividing the target α level by the number of tests being performed. The significant adjusted P values are reported.

Ethics approval

All study protocols were approved by the ethics committees of the Northern Sydney Local Health District and the University of Western Sydney (H7143).

Results

Of 81 individuals contacted, 55 agreed to participate (68% of eligible respondents). The mean interval between the 2002 bombing and the interview was 7 years and 11 months (range, 7 y 9 m – 8 y 1 m). There were no significant differences between the respondents and the total Bali Recovery Program population in terms of mean age (P = 0.38) or male sex (P = 0.39).

Respondent characteristics

Demographic, exposure and bereavement characteristics of the respondents are shown in Box 1. Of the 55 respondents, 21 were present in Bali during or shortly after the bombing. Almost three-quarters (39/54) experienced at least one family bereavement due to the bombing. The loss of children (of adult age) was predominant (21/54). Fifteen respondents experienced multiple losses of exclusively non-family members (average of seven friends and acquaintances killed).

Physical health and personal resilience

Physical and mental health prevalence estimates for the weighted sample are presented in Box 2 and Box 3. Good physical health in the past month and high personal resilience were reported by 45 and 30 of the 55 respondents, respectively. Respondents had an aggregate resilience score on the CD-RISC2 of 6.45. Poor self-rated health showed a significant relationship with current yearning for the deceased (P = 0.04) and perceived current difficulties moving on with life after the loss (P = 0.02). Experiential bereavement factors were the only variables associated with low personal resilience: current yearning (P = 0.02); perceived detachment from others (P = 0.04); life feeling empty without the deceased (P = 0.02); and perceived difficulty moving on (P = 0.003).

Psychological distress and daily functioning

Current high and very high psychological distress was reported by seven and five respondents, respectively. High distress was significantly associated with difficulty accepting the loss (P = 0.03); feeling detached (P = 0.001); and anger (P = 0.04). Very high distress was associated with bombing-related injury (P = 0.005); current yearning (P = 0.004); difficulty moving on (P = 0.003); and life feeling empty (P < 0.001). Very high distress also showed significant inverse relationships with current marital or de facto relationship (P = 0.02); perceived family support (P = 0.03); and better neighbourhood connectedness (P = 0.02). Loss of at least one full day of functioning in the past month was reported by nine respondents (range, 0–16 days; mean, 0.74). Significantly greater functional loss was associated with bombing-related injury (P = 0.04) and not being in a current marital or de facto relationship (P = 0.04).

Traumatic stress-related symptoms

Moderate TSRS (two symptoms) and high TSRS (three or more symptoms) in the past month were reported by 11 and 15 respondents, respectively. High TSRS was positively associated with all assessed features of bereavement but no other outcome variables: current yearning (P = 0.007); difficulty accepting the loss (P = 0.005); feeling detached (P = 0.01); anger (P = 0.002); life feeling empty (P = 0.02); and difficulty moving on (P < 0.001).

Comparisons with the NSW
general population

Compared with NSW population estimates, the respondents reported greater rates of high (12.7% v 8.2%) and very high (9.1% v 2.9%) psychological distress (Box 4) and functional impairment (mean, 0.74 v 0.60 days lost in the past month).15 Respondents were significantly less likely to report low levels of psychological distress (P < 0.05). Good self-reported health was slightly higher among respondents than the population mean (81.8% v 80.4%).

Discussion

Eight years after the first Bali bombing, a substantial proportion of this directly affected group were experiencing high levels of psychological distress and TSRS. These individuals, who had sought help, were also experiencing near-normal physical health, and their aggregate resilience score fell within a “high resilience” range observed in United States population estimates.17 Although a specific comparison group is not available, access to modern treatment methods and support may have promoted these positive long-term outcomes. Notably, experiential features of grief (eg, emptiness, difficulty moving on) were the only factors associated with reduced resilience, suggesting that early intervention with a specific focus on these factors may be indicated for such groups.10

Direct exposure to disasters is considered to have a dose–response effect. Factors such as proximity, injury and perceived threat to life are consistently associated with adverse mental health effects, but they are rarely examined beyond 3–4 years after terrorism incidents because of difficulty accessing affected cohorts.11 Eight years after the Bali bombing, a significant association was observed between incident-related physical injury and both psychological distress and functional impairment. These findings extend the current literature, showing that some of the most direct forms of exposure (proximity and injury) remain substantial risk factors at this extended time point.

Social support has a positive role in mental health and may foster recovery from trauma over time.21 We found that being in a marital or de facto relationship was the only demographic factor associated with distress in the respondent group, showing an inverse relationship with high psychological distress. Inverse relationships were also observed with the broader social support factors of high perceived family support and neighbourhood social connectedness.

The strength of our findings in relation to complicated grief variables appears to highlight important aspects of grief, as it relates to terrorism violence and loss. The ability to “make sense” of a loved one’s death is considered a central process of grieving.8 However, the irrational or meaningless nature of violent death, particularly through terrorism, has been found to interfere with this cognitive process for many survivors.22 Moreover, it is associated with more severe complicated grief, higher psychological distress and poorer physical health.23 While such mediating variables cannot be inferred in relation to our data, it is notable that complicated grief symptoms in this study were also associated with distress and poor physical health, as well as TSRS. Similarly, grief symptoms were also the only factors associated with significantly lower personal resilience. This suggests that among bereaved survivors of terrorism, grief maladaptation may represent a more significant long-term risk factor for health outcomes than incident exposure or post-event variables.

Our findings have implications for the support of people directly affected by terrorism. Complicated grief factors emerged as the strongest correlates of adverse physical and mental health status. Longer-term monitoring of survivor groups is indicated, including screening programs that incorporate grief-specific items. Previous short-term screening has effectively linked survivors with evidence-based care.10,24 However, case-finding from primary care pathways was poor, suggesting that outreach is required for longer-term initiatives.24 Significantly, 7 years after the September 11 attacks, registered individuals who had escaped the World Trade Center reported difficulty accessing physical and mental health care and often failed to connect long-term symptoms with their September 11 exposures.25

Our study has some notable strengths and several limitations. The sample ostensibly constitutes a traumatically bereaved population, with varying levels of direct incident exposure and use of clinical services. Respondents may represent a more seriously affected, but possibly better supported cohort than those who did not seek services from the program. This may limit generalisability of these findings to other survivor groups. This cross-sectional study can only determine significant associations at a single time point. No conclusions can be drawn regarding longitudinal health effects or their causes.

The response rate had the potential to introduce responder bias, although no significant differences in sex or age were found between the respondent sample and the total program population. Items from the complicated grief measure (ICG-R) examined a subset of symptoms only and cannot be considered to indicate syndrome-level complicated grief.

Importantly, this analysis presents the largest study sample to date of Australians directly affected by a single terrorist incident. In completing a quantitative analysis of their health status 8 years after a major bombing, it also represents, to our knowledge, the longest follow-up period of a terrorism-affected population reported in the literature.

1 Demographic, exposure and bereavement-related variables of the respondents

Variable

Unweighted
(n = 55)

Weighted
(n = 115)


Mean age (range)

50 (20–73)

50 (42–53)

Male

23 (41.8%)

48 (41.8%)

Education

University degree

15 (27.2%)

31 (27.3%)

TAFE certificate or diploma

17 (30.9%)

36 (30.9%)

Higher school certificate

11 (20.0%)

23 (20.0%)

School certificate

9 (16.4%)

19 (16.4%)

Other

3 (5.5%)

6 (5.5%)

Marital status

Married or de facto

40 (72.7%)

84 (72.7%)

Widowed

3 (5.5%)

6 (5.5%)

Separated or divorced

4 (7.3%)

8 (7.3%)

Never married

8 (14.5%)

17 (14.5%)

Location during/after bombing

Bali, in club*

6 (10.9%)

13 (10.9%)

Bali, near club*

3 (5.5%)

6 (5.5%)

Bali, not nearby

3 (5.5%)

6 (5.5%)

Bali, arrived after bombing

9 (16.4%)

19 (16.4%)

Not in Bali

34 (61.8%)

71 (61.8%)

Injured during bombing

No

48 (87.3%)

100 (87.3%)

Yes

7 (12.7%)

15 (12.7%)

Involved in search (first 48 hours)

No

39 (70.9%)

84 (72.7%)

Yes

16 (29.1%)

31 (27.3%)

Primary bereavement type

Child

21 (38.2%)

44 (38.9%)

Sibling

11 (20.0%)

23 (20.4%)

Spouse

3 (5.5%)

7 (5.6%)

Other family member

4 (7.3%)

9 (7.4%)

Non-family member(s)

15 (27.3%)

32 (27.8%)

Loss

Single family member

29 (52.7%)

61 (53.7%)

Multiple family members

4 (7.3%)

9 (7.4%)

Multiple family and non-family

6 (10.9%)

13 (11.1%)

Multiple non-family

15 (27.3%)

32 (27.8%)


TAFE = technical and further education. * Bomb site.
Bereaved respondents (n = 54).

2 Prevalence estimates of individual health and wellbeing indicators in the weighted sample, by sociodemographic and perceived support factors

Covariate

Good self-rated health

High
resilience*

Functional loss

High
distress

Very high distress

Moderate TSRS§

High
TSRS§


Sex

Male

78.3%

60.9%

17.4%

8.7%

4.3%

13.0%

21.7%

Female

84.4%

53.1%

15.6%

15.6%

12.5%

25.0%

34.4%

Age

18–40 years

73.3%

57.9%

26.3%

10.5%

10.5%

26.3%

26.3%

> 40 years

86.1%

55.6%

11.1%

13.9%

8.3%

16.7%

30.6%

Education

University

86.7%

66.7%

20.0%

13.3%

6.7%

20.0%

26.7%

High school/other

80.0%

52.5%

15.0%

12.5%

10.0%

20.0%

30.0%

Employed

No

75.0%

41.7%

25.0%

16.7%

8.3%

8.3%

50.0%

Yes

83.7%

60.5%

14.0%

11.6%

9.3%

23.3%

23.3%

Household income

≤ $60 000 

77.8%

44.4%

27.8%

22.2%

11.1%

16.7%

22.2%

> $60 000 

82.9%

62.9%

11.4%

8.6%

5.7%

20.0%

31.4%

Marital status

Married or partnered

85.0%

52.5%

10.0%

12.5%

2.5%

17.5%

30.0%

Not married or partnered

73.3%

66.7%

33.0%**

13.3%

26.7%**

26.7%

26.7%

Have children

No

75.0%

58.3%

16.7%

8.3%

16.7%

33.3%

33.3%

Yes

83.7%

55.8%

16.3%

14.0%

7.0%

16.3%

27.9%

Perceived support, family

Low

80.0%

60.0%

20.0%

20.0%

40.0%

40.0%

20.0%

High

82.0%

56.0%

16.0%

12.0%

6.0%**

18.0%

30.4%

Perceived support, friends

Low

85.7%

42.9%

14.3%

14.3%

14.3%

0.0%

42.9%

High

81.3%

58.3%

16.7%

12.5%

8.3%

22.9%

27.1%

Social connections, neighbourhood

Low

88.9%

66.7%

33.3%

11.1%

33.3%

33.3%

22.2%

High

80.4%

54.3%

13.0%

13.0%

4.3%**

17.4%

30.0%

Long-term support, all sources

Low

75.0%

75.0%

0.0%

25.0%

12.5%

0.0%

37.5%

High

83.0%

53.2%

19.1%

10.6%

8.5%

23.4%

27.7%

Total
respondent group (95% CI)

81.8%
(68.9%–
90.1%)

56.4% (42.7%–69.1%)

16.4% (8.6%–29.0%)

12.7% (6.0%–24.8%)

9.1% (3.7%–20.5%)

20.0% (11.2%–33.1%)

29.1% (18.4%–42.8%)


TSRS = traumatic stress-related symptoms. * Score of 7–8 on the short form of the Connor-Davidson Resilience Scale. Unable to complete usual activities on 1 or more days in previous month. Score of 22–29 on the Kessler Psychological Distress Scale indicates high psychological distress; 30–50 indicates very high distress. § Two symptoms on Primary Care PTSD Screen indicates moderate TSRS; 3–4 symptoms indicates high TSRS. P < 0.15. ** P < 0.05.

3 Prevalence estimates of individual health and wellbeing indicators in the weighted sample, by incident exposure and bereavement factors

Covariate

Good
self-rated health

High
resilience*

Functional loss

High
distress

Very high
distress

Moderate TSRS§

High
TSRS§


Lifetime exposure

Low

84.0%

60.0%

16.0%

16.0%

4.0%

32.0%

32.0%

High

80.0%

53.3%

16.7%

10.0%

13.3%

10.0%

26.7%

In Bali during or after bombing

No

88.2%

55.9%

11.8%

11.8%

2.9%

20.6%

20.6%

Yes

71.4%

57.1%

23.8%

14.3%

19.0%

19.0%

42.9%

Injured during bombing

No

83.3%

58.3%

12.5%

12.5%

4.2%

18.8%

27.1%

Yes

71.4%

42.9%

42.9%§§

14.3%

42.9%§§

28.6%

42.9%

Involved in search (first 48 hours)

No

87.5%

60.0%

12.5%

12.5%

5.0%

22.5%

22.5%

Yes

66.7%

46.7%

26.7%

13.3%

20.0%

13.3%

46.7%

Bereavement**

Non-family member(s)

80.0%

46.7%

20.0%

13.3%

13.3%

20.0%

40.0%

Family member(s)

84.6%

61.5%

12.8%

10.3%

7.7%

20.5%

23.1%

Bereavement involved child**

No

81.8%

57.6%

15.2%

9.1%

9.1%

21.2%

30.3%

Yes

85.7%

57.1%

14.3%

14.3%

9.5%

19.0%

23.8%

Current yearning for loved one(s)**

No

93.1%

72.4%

10.3%

3.4%

0.0%

20.7%

10.3%

Yes

72.0%§§

40.0%§§

20.0%

20.0%

20.0%§§

20.0%

48.0%§§

Difficulty accepting loss**

No

90.6%

62.5%

15.6%

3.1%

6.3%

18.8%

12.5%

Yes

71.4%

47.6%

14.3%

23.8%§§

14.3%

19.0%

52.4%§§

Feel detached from others**

No

84.3%

60.8%

15.7%

7.8%

7.8%

21.6%

23.5%

Yes

66.7%

0.0%§§

0.0%

66.7%§§

33.3%

0.0%

100.0%§§

Feel angry about loss**

No

92.0%

60.0%

16.0%

0.0%

8.0%

24.0%

4.0%

Yes

75.9%

55.2%

13.8%

20.7%§§

10.3%

17.2%

48.3%§§

Life feels empty without loved one(s)**

No

86.4%

65.9%

11.4%

6.8%

2.3%

22.7%

20.5%

Yes

66.7%

22.2%§§

22.2%

33.3%

33.3%

11.1%

66.7%§§

Moving on remains difficult**

No

87.5%

64.6%

12.5%

8.3%

6.2%

22.9%

18.8%

Yes

50.0%§§

0.0%§§

21.4%

33.3%

33.3%§§

0.0%

100.0%

Total
respondent group
(95% CI)

81.8% (68.9%–90.1%)

56.4% (42.7%–69.1%)

16.4% (8.6%–29.0%)

12.7% (6.0%–24.8%)

9.1%
(3.7%–20.5%)

20.0% (11.2%–33.1%)

29.1% (18.4%–42.8%)


TSRS = traumatic stress-related symptoms. * Score of 7–8 on the short form of the Connor-Davidson Resilience Scale. Unable to complete usual activities on 1 or more days in previous month. Score of 22–29 on the Kessler Psychological Distress Scale indicates high psychological distress; 30–50 indicates very high distress. § Two symptoms on Primary Care PTSD Screen indicates moderate TSRS; 3–4 symptoms indicates high TSRS. Lifetime exposure to potentially traumatising events: low = 1–2 events; high ≥ 3 events (excluding Bali exposure). ** Bereaved respondents (n = 54). Non-dependent child. P < 0.15. §§ P < 0.05. P < 0.001 (Bonferroni adjusted).

4 Population comparison of prevalence estimates* of psychological distress in the past month

* Bali Recovery Program 2010 weighted sample and New South Wales population weighted prevalence estimates (2010).15 Measured using the Kessler Psychological Distress Scale. P < 0.05.