Mercury poisoning from home gold amalgam extraction

This is the first Australian report of confirmed minimal change disease with nephrotic syndrome, which occurred in a 62-year-old man who inhaled mercury vapour in his home. This case highlights the immediate and delayed effects of such poisoning on multiple organs. Prompt and sometimes prolonged treatment may prevent long-term damage.

Clinical record

A 62-year-old man first presented to his general practitioner complaining of a cough, dyspnoea and lethargy for which he was prescribed oseltamivir phosphate, as his symptoms were presumed to indicate influenza. He re-presented 2 days later with worsening dyspnoea, at which point he revealed a history of mercury exposure. He had attempted to extract gold from an amalgam containing mercury by heating the amalgam in an aluminium pan inside his home. He was exposed for 3 hours — initially, to fumes, and subsequently, through direct skin contact as he attempted to clean up some spilt liquid amalgam. The windows were open and he used a tea towel covering his nose as protection from the fumes. A chest x-ray showed extensive alveolar shadowing consistent with pneumonitis. He was admitted to a regional hospital, and was given supplemental oxygen and antibiotics. His blood mercury level was 5933 nmol/L (level of concern, > 70 nmol/L). On the advice of a toxicologist, he was transferred to a tertiary hospital for chelation therapy.

On arrival at the tertiary hospital, his oxygen saturation on room air was 92% and signs on examination and repeat chest x-ray results were consistent with severe pneumonitis. His other vital signs were stable. Findings of other clinical examinations, including neurological examination, were unremarkable. Laboratory investigations showed he had an increased white cell count of 16.3 × 109/L (reference interval [RI], 4.0–11.0 × 109/L), a platelet count of 617 × 109/L (RI, 150–400 × 109/L), a serum albumin level of 21 g/L (RI, 34–48 g/L), and mild abnormalities in liver function test results (total protein, 60 g/L [RI, 65–85 g/L]; globulin, 39 g/L [RI, 21–41 g/L]; total bilirubin, 15 µmol/L [RI, 2–24 µmol/L); γ-glutamyl transpeptidase, 274 U/L [RI, < 60 U/L]; alkaline phosphatase, 228 U/L [RI, 30–110 U/L]; alanine aminotransaminase, 92 U/L [RI, < 55 U/L]; aspartate aminotransferase, 102 U/L [RI, < 45 U/L]; and lactate dehydrogenase, 294 U/L [RI, 110–230 U/L]). In a spot urine sample, the mercury concentration was 7556 nmol/L and the mercury : creatinine ratio was 2519 nmol/mmol (level of concern, > 5.8 nmol/mmol). Pulmonary function testing was suboptimal owing to the patient’s inability to suppress coughing on inspiration, but the results suggested a restrictive deficit. Analysis of a spot urine sample showed a protein concentration of 60 mg/L (RI, < 150 mg/L) and a protein : creatinine ratio of 18 mg/mmol (RI, < 12 mg/mmol). The patient’s serum creatinine level was 82 µmol/L (RI, 50–120 µmol/L) and his estimated glomerular filtration rate was > 60 mL/min/1.73 m2.

The patient was treated with dimercaptosuccinic acid (DMSA) chelation therapy, 800 mg three times a day for 7 days, after which the dose was reduced to 800 mg twice daily for a further 14 days. He was also treated with prednisolone 50 mg daily, gradually tapering the dose to zero over 3 weeks. Box 1 shows the 24-hour urinary mercury excretion in relation to exposure to mercury vapour, serum albumin concentrations and treatment with chelation therapy.

During this initial hospital stay, the patient’s dyspnoea decreased markedly, and subsequent chest x-rays showed resolution of interstitial shadowing. His liver function test results also normalised, and his serum albumin level rose to 33 g/L. The mild vertigo he had reported, with no other neurological symptoms or deficits, resolved spontaneously.

He was discharged on DMSA 800 mg twice daily and prednisolone 15 mg daily (tapering dose), and it was planned to repeat the assessment of his mercury levels after completion of the initial 3-week course of DMSA. This reassessment showed ongoing elevated levels (blood mercury, 418 nmol/L; urinary mercury, 1019 nmol/24 h), so the patient was rechallenged with DMSA at 800 mg three times a day for 34 days, commencing on Day 66 after exposure. Improved clearance resulted, as evidenced by a subsequent increase in urinary mercury excretion (from 1762 nmol/24 h on Day 62 to a maximum of 5790 nmol/24 h on Day 67). Consequently, treatment with DMSA at 800 mg twice daily was resumed, with the intention of giving a prolonged course, and his blood mercury levels and renal mercury clearance were assessed periodically. His serum albumin level had normalised by this point, and his prednisolone course had been completed.

Approaching 1 month into this prolonged course of DMSA, he re-presented with a history of fatigue, increasing peripheral oedema, nausea and vomiting. Physical examination revealed significant peripheral oedema with intravascular volume depletion. Biochemical analysis showed a serum albumin level of 6 mg/L (nadir, 3 g/L), urinary protein level of 13.4 g/24 h (RI, < 150 mg/24 h), serum creatinine level of 133 µmol/L (peak, 220 µmol/L) and serum cholesterol level of 13 mmol/L, indicating severe nephrotic syndrome. A renal ultrasound scan was unremarkable. In a renal biopsy specimen, light microscopy showed glomeruli of normal appearance and electron microscopy showed podocyte effacement consistent with minimal change disease (Box 2). He was treated with prednisolone, regular infusions of concentrated albumin, and diuretics, and was restricted to 1.2 L of fluids daily. Treatment with an HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitor and prophylactic warfarin therapy were also commenced. His nephrotic syndrome abated and renal function gradually normalised over the course of 4 months.

The patient experienced significant nausea, which necessitated cessation of chelation therapy after a total of 7 weeks. At this point, his blood mercury level was 112 nmo/L; within 1 month it fell below the level of concern. Three months after cessation of treatment with DMSA, his urinary mercury level was also normal. When last reviewed, his serum albumin level was 35 g/L and urinary protein excretion was 0.25 g/24 h. Resolution of his respiratory injury was almost complete, without evidence of developing neurotoxicity.

Discussion

We present a case of prolonged exposure to mercury vapour with characteristic “fume fever” illness followed by pneumonitis and nephrotic syndrome, and an associated body mercury burden requiring prolonged chelation therapy.

Heating of mercury forms mercury vapour, which is actively absorbed in the lungs. About 80% of mercury vapour formed from amalgams is absorbed through inhalation.1 Once absorbed, metallic mercury is rapidly oxidised to mercurous and mercuric ions,2 and distributes in a variety of tissues including the brain, kidneys, liver, testes, thyroid gland and oral mucosa. A small amount of elemental mercury remains in the blood and can easily pass through the blood–brain barrier and the placental barrier.

The symptoms and signs of mercury inhalation vary according to the concentration of mercury to which the patient is exposed and the duration of exposure. Acute exposure to high levels primarily causes respiratory symptoms such as dyspnoea, chest pain, tightness, and dry cough, secondary to chemical pneumonitis. Absorption at the alveolar and bronchiolar levels causes capillary damage, pulmonary oedema, and desquamation and proliferation of airway lining cells, leading to the obliteration of air spaces.3 Airway obstruction and capillary leakage may cause alveolar dilatation, pneumothorax and, in severe cases, acute respiratory distress syndrome.4 Systemically, mercurous and mercuric ions can bind with sulfhydryl groups, leading to inactivation of sulfhydryl-containing enzyme systems and structural proteins and alteration of cell-membrane permeability.5

The evolution of clinical symptoms after mercury vapour inhalation may be described in three phases.6 The initial phase is typically an influenza-like illness occurring 1 to 3 days after exposure. The intermediate phase is dominated by severe pulmonary toxicity and may involve renal, hepatic, haematological, and dermatological dysfunction. Our patient had hypoalbuminaemia and a mild and transitory abnormality in liver enzyme levels, followed by a delayed onset of minimal change disease with severe nephrotic syndrome. It is possible that DMSA chelation may have contributed to the nephrotic syndrome by subjecting nephrons to a high load of chelated mercury. Both his initial hypoalbuminaemia and subsequent nephrotic syndrome appeared to respond to steroid therapy. The most commonly reported histological abnormality in the kidney associated with mercury exposure is membranous glomerulopathy;7 however, minimal change disease, with negative findings on light microscopy and confirmed by characteristic findings from immunofluorescence and electron microscopy, has been previously described.8 The late phase is characterised by gingivostomatitis, tremor and erethism, which we have not seen in our patient.

Aggressive supportive care including continuous cardiac monitoring and pulse oximetry, supplemental oxygen therapy and mechanical ventilation4 remains the cornerstone of therapy after acute inhalational mercury poisoning. Several chelating agents bind mercury, increasing its water solubility and augmenting its renal elimination. Historically, dimercaprol, D-penicillamine and N-acetyl-penicillamine have been used.5 Recently, DMSA has proven to be more effective and less toxic. It is unclear to what extent chelation therapy reduces mercury tissue burden or prevents long-term neurological injury.9 Awareness among clinicians of the immediate and the delayed consequences of mercury poisoning, with prompt treatment, may help to avoid long-term organ damage.

1 Twenty-four-hour urinary mercury excretion in relation to exposure to mercury vapour, serum albumin concentrations and treatment with chelation therapy

DMSA = dimercaptosuccinic acid; shading indicates periods of therapy.

2 Micrographs of the patient’s renal biopsy specimen, showing features consistent with minimal change disease

A: Light micrograph showing glomeruli of normal appearance (haematoxylin and eosin stain; original magnification, × 200). B: Electron micrograph showing flattening of podocyte foot processes (arrows).

The approach to patients with possible cardiac chest pain

Chest pain is a confronting symptom for patients and clinicians alike. Some patients presenting with chest pain will have serious acute illness with a high short-term risk of mortality, but this will be excluded in most patients. Chest pain is one of the most common causes of attendance at hospital emergency departments (EDs) and a frequent cause of presentations to general practice.1 Missed diagnosis, with associated adverse outcomes, can occur when chest pain assessment is based on clinical features alone.2

Regardless of the clinical setting, a stepwise approach should be applied to patients with chest pain (Box 1). In the absence of trauma, the primary focus should be exclusion of four potentially fatal conditions: acute coronary syndrome (ACS; encompassing acute myocardial infarction and unstable angina), pulmonary embolism, aortic dissection and spontaneous pneumothorax. ACS is by far the most common of these. All these conditions may present without immediately obvious physical signs, but the latter three may be accurately excluded by rapid diagnostic testing (predominantly medical imaging). However, ACS is more challenging as it cannot be readily excluded with an acceptable level of accuracy on initial clinical evaluation or with a single investigation. After excluding these conditions, attention should be turned to chronic but serious conditions that may require additional evaluation, such as stable coronary artery disease or aortic stenosis. Next, non-life threatening conditions that may benefit from specific therapy (eg, herpes zoster, gastro-oesophageal reflux) should be considered. If the clinician is confident that all these causes have been excluded, the patient can be reassured that the chest pain is due to an insignificant cause.

Here, we focus on several evolving areas relating to the assessment of patients with possible cardiac chest pain, including risk stratification, cardiac biomarkers and the role of non-invasive testing for myocardial ischaemia and coronary artery disease. This article is aimed at all clinicians who assess patients with acute, undifferentiated chest pain. It is not a systematic review, but we have directed the reader towards these where appropriate.

The aim of chest pain assessment

There is a dichotomy in the assessment of patients with possible ACS. First, early and accurate identification of patients with ST-segment-elevation myocardial infarction (STEMI) enables provision of emergency reperfusion therapy, which has a major impact on outcome, while accurate identification of patients with other types of ACS (non-ST-segment elevation myocardial infarction [NSTEMI] or unstable angina) allows for early initiation of targeted treatment known to improve outcomes in these groups. Second, accurate exclusion of myocardial ischaemia in patients with chest pain is essential to minimise the morbidity and mortality associated with missed diagnoses, while avoiding unnecessary overinvestigation in those without the disease. However, assessment is complex because of the diversity of clinical presentations of ACS and the lack of a single diagnostic test for the entire spectrum of disease.

Despite recognition that clinical systems are imperfect, a high degree of safety in chest pain assessment processes is demanded. A recent large survey of emergency physicians suggests that the target rate of unexpected adverse outcomes in patients with a negative chest pain assessment should be < 1% at 30 days;3 this target is likely to be equally stringent in primary care. Achieving this level of safety in a timely and cost-effective fashion in an era of increasing demand on acute services presents challenges. This must be considered when the potential value and safety of new developments are assessed.

Clinical approach and risk stratification

Most current diagnostic strategies for acute chest pain focus on the identification of ACS and are based on the premise that other obvious diagnoses have been excluded with accurate clinical assessment.

Systematic reviews of the diagnostic value of clinical features in the assessment of chest pain have largely been carried out in hospital settings,4 where the prevalence of serious disease is higher than in general practice. It is widely understood that no single clinical feature or combination of features can be used to exclude ACS with sufficient sensitivity to obviate the need for further investigation. Thus, a strategic approach based on clinical risk stratification, a period of observation, electrocardiography and serial biomarker evaluation has emerged. In all settings, a 12-lead electrocardiogram (ECG) should be performed immediately in patients presenting acutely with chest pain to exclude ST-segment-elevation.

In general practice, the aim should be to differentiate patients who require urgent hospital-based assessment for possible ACS from those with more stable symptoms who may be investigated on an outpatient basis. Limited access to investigations encourages the use of clinical judgement or clinically based decision rules to triage patients who can continue to be managed safely in primary care. Several such decision rules exist, but with limited validation for use in primary care. Despite the lower prevalence of coronary disease in patients presenting with chest pain in primary care, the same limitations found in hospital-based cohorts apply to the value of clinical assessment. A recent well conducted Swedish study concluded that the accuracy of clinical assessment of chest pain by general practitioners was high, but insufficient to safely rule out coronary artery disease.5 Clinicians in general practice should refer patients promptly to hospital for assessment when features suggesting a diagnosis of ACS are present (Box 2).

The value of further investigation in general practice of patients with an acute onset or ongoing symptoms is limited, given that a normal ECG cannot exclude a significant short-term risk of an adverse outcome, and serial biomarker testing is required to exclude myocardial infarction. Nevertheless, in all settings, the resting ECG has a critical role in identifying patients with ST-segment elevation who require emergency reperfusion therapy. Patients with suspected ACS and ongoing pain, pain within the past 12 hours that has resolved but with an abnormal ECG, or other high-risk features (Box 3) should be referred to hospital as an emergency. Given the release kinetics of troponin, a single troponin test may have value in assessing patients with a normal ECG and no high-risk features who present more than 12 hours after resolution of symptoms suggestive of ACS. In such cases, appropriate mechanisms must be in place for prompt review of results and referral to hospital where necessary. If these facilities are unavailable, patients should be referred to the ED for same-day chest pain assessment.

Demographic and cardiovascular risk factors, such as age and sex, influence population risk of disease but should not unduly influence the assessment of individual patients. In the absence of a clear alternative diagnosis, most patients will require additional investigation to exclude coronary artery disease, and the critical decision is usually not whether, but with what urgency, this should be undertaken. In some countries, rapid-access chest pain assessment clinics offering early assessment of patients (usually within 14 days) have become an integral part of strategies for chest pain assessment as an alternative to ED-based assessment.6 However, these have not been widely implemented in Australia, and all acute care facilities with an ED should have an evidence-based strategic approach to assessing patients with chest pain.

Patients should be stratified as being at low, intermediate or high risk of short-term adverse outcomes in the context of possible ACS, in line with the joint guidelines of the National Heart Foundation and Cardiac Society of Australia and New Zealand (NHF/CSANZ) stratifying patients with ACS (Box 3).6 This model has performed well in the ED setting, with 30-day risks of adverse cardiac outcome of 0, 7% and 26% in these risk strata, respectively, when the criteria were strictly applied in one cohort.7 Risk stratification models may have greater utility in the ED, where the prevalence of ACS is about 10% (compared with primary care, where rates are lower) and where facilities to further assess patients at increased risk are readily available. The main limitation of this risk stratification model is that few patients qualify as low risk when the criteria are strictly applied. Alternative approaches include the Thrombolysis in Myocardial Infarction (TIMI) score, the Global Registry of Acute Coronary Events (GRACE) score and the GRACE Freedom-from-Event score.8,9 These models, derived from higher-risk populations, were not designed to identify low-risk patients who do not require detailed assessment for exclusion of ACS. Consequently, none can be relied on to identify patients who can be safely discharged from the ED without some period of observation and additional investigation. Nevertheless, risk stratification is essential to guide the appropriate use of resources based on pretest probability of ACS.

Cardiac biomarkers

Cardiac troponin levels have a central role in the diagnosis of acute myocardial infarction.10 After exclusion of ST-segment elevation and dynamic ST-segment electrocardiographic changes, serial biomarker testing identifies the remaining patients with acute myocardial infarction. Protocols for the use of serial troponin measurements have largely been based on release kinetics in experimental conditions and have tended to require waiting 6–8 hours (or longer) after presentation for the second test. Recent advances in high-sensitivity assays that allow a much shorter interval of 2 hours before the second test and incorporation of serial biomarker levels into overall risk stratification models (Box 4) have demonstrated safe accelerated processes with robust clinical outcome data.11,12 These approaches have yet to be incorporated into clinical guidelines, but almost certainly will be in the foreseeable future.

Troponin levels are considered abnormal when they exceed the 99th percentile of a healthy reference population using an assay with sufficient accuracy at this level (< 10% coefficient of variation). In practice, few available assays have possessed sufficient accuracy at this level.13 The recent development of high-sensitivity assays with this level of accuracy and lower levels of detection allows measurable troponin levels to be recorded in most of the healthy population. These assays offer the promise of being able to rule out acute myocardial infarction earlier than was possible with less sensitive assays, as well as further acceleration of risk stratification models, but with the probable cost of diminished specificity.14 This will require clinicians to have a better understanding of the causes of elevated troponin levels and the kinetics of troponin release at these new lower levels of detection, possibly by incorporating values expressing change or “delta” troponin.15 The use of delta troponin values has been incorporated into the 2011 addendum to the NHF/CSANZ guidelines, but the evidence for the best approach is still emerging.16 It is imperative that clinicians have a clear understanding of the characteristics of the local troponin assay used, as reference intervals are not transferable between different troponin assays.

Investigations for myocardial ischaemia and coronary artery disease

In two groups of patients — those who present with symptoms of ACS and in whom myocardial infarction has been excluded, and those with a stable pattern of chest pain symptoms in whom angina cannot be excluded — additional testing is required to identify those who have prognostically important coronary artery disease or unstable angina. This is an area where well established diagnostic tests exist alongside more recent developments, such as computed tomography coronary angiography (CTCA). The anatomical and pathophysiological bases for these tests are not interchangeable, with some depending on the detection of abnormal coronary blood flow (myocardial perfusion scanning) or myocardial ischaemia (stress electrocardiography and stress echocardiography), while invasive angiography and CTCA demonstrate the anatomical basis of coronary artery disease. Each investigation has different limitations depending on patient factors and the need for contrast media and ionising radiation, and the availability of each may depend on access, cost and local expertise (Box 5).

Non-invasive testing for myocardial ischaemia or coronary artery disease is of most value to patients with intermediate pretest probability of an ACS. In patients with very low risk of coronary artery disease who have symptoms of non-ischaemic pain, other causes of chest pain should be actively excluded before investigations for myocardial ischaemia or coronary atheroma are considered. Similarly, it may be futile to embark on non-invasive testing (with an attendant risk of a false negative result) in a patient with typical symptoms and a very high risk of coronary artery disease. In such cases, prompt specialist referral for consideration of an early invasive strategy should be the first step.

Investigations may identify the presence or effects of coronary artery stenosis but, where this cannot be achieved, a broader aim is to further refine risk stratification to identify patients at low risk of an adverse outcome after discharge from the hospital or ED. Exercise stress electrocardiography has become largely obsolete as a means of diagnosing reversible myocardial ischaemia, due to insufficient diagnostic accuracy, but it retains a well established role in identifying patients with chest pain who can safely be discharged from the ED.17,18 Exercise stress electrocardiography may be limited by patients’ inability to exercise at an adequate level, non-specific electrocardiographic changes (particularly in the setting of an abnormal resting ECG), and false positive results, but it remains attractive by virtue of its low cost and widespread availability.

The combination of cardiac imaging with exercise or pharmacological stress testing can increase accuracy beyond electrocardiography alone (Box 6).19–21 In the United States and Europe, cardiac magnetic resonance imaging has emerged as a safe, non-ionising and more accurate alternative to nuclear perfusion scanning, but it remains predominantly a research tool in Australia.23

CTCA is the most rapidly evolving test for assessing patients with chest pain and is the most sensitive non-invasive test for identifying coronary artery disease.22 Recent studies have shown that this technique allows patients to be safely discharged from the ED.24 A CTCA-based strategy may also be faster than other strategies, particularly when these rely on hospital admission for myocardial perfusion scanning.24,25 However, this finding is of limited value in Australia, where myocardial perfusion scanning has not been the principal investigation for chest pain assessment.

It is important to recognise some limitations of CTCA. Elevated heart rate, coronary calcium and obesity all impair image quality. The use of iodinated contrast media is risky in patients with renal impairment or in those taking metformin. In the widely cited Coronary Computed Tomographic Angiography for Systematic Triage of Acute Chest Pain Patients to Treatment (CT-STAT) trial, only 11% of the patients screened met the study’s inclusion criteria.25 Early studies suggested that CTCA should not be performed until after a second troponin measurement, as myocardial infarctions caused by moderate, rather than severe, coronary stenoses could potentially be missed.26 This emphasises that the strength of CTCA lies in excluding coronary atheroma. Furthermore, in the presence of known coronary artery disease, functional testing for ischaemia may be a more appropriate choice of investigation.27

Some centres perform CTCA with a total radiation dose of < 1 mSv, but in most centres, using general CT scanners without modern dose-reduction equipment, the total dose is likely to be significantly higher. Patients presenting to the ED, where there is an imperative to achieve a diagnostic study regardless of heart rate, may receive 10 mSv, although this is still lower than in most myocardial perfusion scans.28 There is now strong evidence that CT radiation can induce cancer.29 As CTCA could potentially be applied to more than 60% of patients presenting with chest pain in Australia, it is appropriate to remember that other tests are available and that CTCA has not yet demonstrated superiority in this setting. Nevertheless, CTCA is likely to become an increasingly important tool for ruling out significant coronary artery disease in patients with chest pain. Ongoing large clinical trials, such as the Prospective Multicenter Imaging Study for Evaluation of Chest Pain (PROMISE),30 should provide more definitive evidence in this area. Currently, Medicare regulations limit rebates to specialist referral for CTCA, and a robust system of credentialling has been introduced as a quality control measure.

Complex tests need to be appropriately incorporated into an overall strategy of risk-based chest pain assessment, integrating safe, accessible and cost-effective techniques that can accommodate the broadest range of patient presentations and comorbidities.

Conclusion

Chest pain is a common presenting symptom with many diagnostic challenges and pitfalls. Medicopolitical imperatives such as the National Emergency Access Target render the situation more complicated still. Both technology and the evidence base guiding the approach to the problem have developed considerably since the NHF/CSANZ first commissioned guidelines in this area in 2000. Clinicians can now benefit from a better understanding of risk stratification and enhanced diagnostic tools that make excluding avoidable short-term adverse events with a high degree of accuracy a realistic proposition. The challenge remains to implement these advances as widely as possible in an environment of constrained resources and increasing demand. This will be best achieved by an approach that integrates the technology and evidence into a comprehensive but straightforward and accessible strategy.

1 A pragmatic differential diagnosis of non-traumatic chest pain*

Life-threatening diagnoses that should not be missed:

Acute coronary syndrome

Acute myocardial infarction
Unstable angina pectoris

Acute pulmonary embolism
Aortic dissection
Spontaneous pneumothorax

Chronic conditions with an adverse prognosis that require further evaluation:

Angina pectoris due to stable coronary artery disease
Aortic stenosis
Aortic aneurysm
Lung cancer

Other acute conditions that may benefit from specific treatment:

Acute pericarditis
Pneumonia or pleurisy
Herpes zoster
Peptic ulcer disease
Gastro-oesophageal reflux
Acute cholecystitis

Other diagnoses:

Neuromusculoskeletal causes
Psychological causes

* This differential diagnosis is not intended to be exhaustive.

2 Case vignette

A 66-year-old man calls his general practitioner for advice. He has been treated for type 2 diabetes and primary prevention of cardiovascular disease for about 5 years. He calls from the airport where he is due to board an interstate flight but is concerned because he experienced 20 minutes of “burning” central chest discomfort while walking into the airport. He has had similar self-limiting symptoms with exertion for 4 weeks. During this time, he underwent upper gastrointestinal endoscopy that was unremarkable.

Comment: Even with the limited information available from a telephone call, and despite the atypical description of the chest pain, this patient exhibits several features suggestive of intermediate risk for an acute coronary syndrome.6 As such, he should be advised to attend hospital for assessment of chest pain without delay.

The patient is reviewed in the emergency room, where he has an unremarkable electrocardiogram and a cardiac troponin I level of 0.01 μg/L on admission, and 0.02 μg/L 6 hours and 25 minutes later (99th percentile of a healthy reference population,
0.04 μg/L). After the second troponin measurement, an exercise stress echocardiogram is strongly positive at a low workload, with reproduction of the index symptoms at < 50% of the predicted workload and evidence of reversible ischaemia in the territory of the left anterior descending coronary artery. He has cardiac catheterisation the same day and is found to have a critical stenosis of the mid left anterior descending artery, which is treated with percutaneous coronary intervention and deployment of a drug-eluting stent. He makes an uneventful recovery, with normal left ventricular function.

3 Features associated with high risk, intermediate risk and low risk of adverse short-term outcomes in patients presenting with chest pain due to possible acute coronary syndrome

High risk

Presentation with clinical features consistent with acute coronary syndrome (ACS) and any of the following features:

Repetitive or prolonged (> 10 minutes) ongoing chest pain or discomfort
Elevated level of at least one cardiac biomarker (troponin recommended)
Persistent or dynamic electrocardiographic changes of ST-segment depression ≥ 0.5 mm or T-wave inversion ≥ 2 mm
Transient ST-segment elevation of ≥ 0.5 mm in more than two contiguous leads
Haemodynamic compromise
Sustained ventricular tachycardia
Syncope
Significant left ventricular (LV) dysfunction (LV ejection fraction < 40%)
Prior percutaneous coronary intervention within 6 months or prior coronary artery bypass surgery
Presence of diabetes or chronic kidney disease (estimated glomerular filtration rate < 60 mL/minute) and typical symptoms of ACS

Intermediate risk

Presentation with clinical features consistent with ACS and any of the following features, without high-risk features:

Chest pain or discomfort within the past 48 hours that occurred at rest, or was repetitive or prolonged (but currently resolved)
Age > 65 years
Known coronary artery disease
Prior aspirin use
Two or more of: hypertension, family history, current smoking, hyperlipidaemia
Presence of diabetes or chronic kidney disease and atypical symptoms of ACS

Low risk

Presentation with clinical features consistent with ACS without intermediate-risk or high-risk features. This includes onset of anginal symptoms within the past month, or worsening in severity or frequency of angina, or lowering of anginal threshold.

* Adapted from Box 8 in the National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand Guidelines for the management of acute coronary syndromes 2006.6 Copyright 2006 The Medical Journal of Australia. Used with permission.

4 A proposed algorithm, incorporating an accelerated diagnostic protocol,* for assessment of possible cardiac chest pain after exclusion of ST-segment elevation on initial ECG

NHF/CSANZ = National Heart Foundation and Cardiac Society of Australia and New Zealand. ACS = acute coronary syndrome.
ECG = electrocardiogram. TIMI = Thrombolysis in Myocardial Infarction. * Based on the ADAPT study.11 † NHF/CSANZ Guidelines for the management of acute coronary syndromes 2006.6

5 Features of non-invasive tests available for further risk stratification of patients with chest pain, after excluding acute myocardial infarction

Procedural considerations

Relative contraindications*

Condition and test

Cost†

Radiation

Iodinated
contrast media

Inability to exercise

Significant resting ECG abnormality‡

Renal
impairment

Obesity

Severe airway disease

Myocardial ischaemia or perfusion

Exercise stress electrocardiography

Yes

Yes§

Stress echocardiography

No¶

Yes

No¶

Myocardial perfusion scanning

$$$

Yes

No¶

Yes

Yes§**

Obstructive coronary artery disease

Computed tomography coronary angiography

Yes

ECG = electrocardiogram. * Relative contraindications should be discussed further for individual patients. † Relative cost indications are based on current Medicare rebates. ‡ For example, left bundle branch block. § If there is significant functional impairment. ¶ If pharmacological stress testing can be performed. ** Adenosine is contraindicated.

6 Representative performance characteristics of non-invasive tests to identify myocardial ischaemia or obstructive coronary artery disease in patients with chest pain

Test	Sensitivity	Specificity

Exercise stress electrocardiography21	68%	77%
Stress echocardiography20	83%	77%
Exercise stress myocardial perfusion scanning19	85%–90%	70%–75%
Computed tomography coronary angiography22	99%	89%

General practice patients in the emergency department

Mostly, it is more appropriate for patients to seek care in the emergency department rather than visit a general practitioner

One of the mysteries of public policy is that at times the public discourse settles on a perspective that is based on flimsy or even contradictory evidence. One such discussion relates to the factors that contribute to the congestion of hospital emergency departments (EDs) in Australia.

In Australia, 30% of people attend EDs each year and that rate is growing at 2% per annum.1,2 The reasons behind this are unclear; however, demographic factors (eg, ageing population), epidemiological factors (eg, rising rates of chronic disease), health system changes (eg, the scope and availability of primary care) and individual factors (eg, socioeconomic status) are likely contributing factors. The relative contribution of these factors is unknown. The growth in ED attendance is across all age groups, among more urgent categories and highest for trauma.3

There are more people seeking care in EDs (increased demand) and EDs continue to experience difficulty obtaining access to ongoing care for their patients (access block). Access block is a direct consequence of diminishing per capita hospital bed numbers and inefficient bed use in an environment of increasing demand for inpatient care. However, despite the clarity of the evidence, many still believe that a major contributor is the “inappropriate” use of the ED by “general practice-type” patients.

In this issue of the Journal, Nagree and colleagues4 compare four different methods of determining the proportion of general practice-type patients attending EDs; one of which is that used by the Australian Institute of Health and Welfare (AIHW). These data are often cited in the public debate. The study found that three of the methods based on diagnostic and outcome criteria arrived at similar figures (about 10%), whereas the AIHW approach relatively overestimated the proportion (about 25%).

The study highlights the dichotomy between the tone of the public debate and the evidence. The public and political discourse maintains that ED congestion is contributed to significantly by “inappropriate” attendance by general practice-type patients. Some imply that this view is a deliberate ploy by politicians and health bureaucrats to shift responsibility between tiers of government.

However, each method used by Nagree and colleagues is potentially flawed. They are all statistical methods that do not (and cannot) take into consideration the particularities of each case. Additionally, each is based on diagnosis or outcome, neither of which is predictable by the patient when deciding where to obtain urgent medical advice. Extensive international research into the concept of ED attendance by general practice-type patients demonstrates not only a variable rate ranging from 4.8% to 90%5 but also exceptional variability between clinicians.6

While it is clear that some ED patients can be treated in a general practice setting, we reject the premise on which the methods of determining general practice-type patients is based. Interviews with actual patients have shown that the vast majority genuinely perceive that they have a serious illness and need urgent advice.6–8 It is absurd to expect patients to make clinical judgements when they do not have the expertise to do so.

The authors of the article conclude that the AIHW method grossly overestimates the load of general practice-type patient attending EDs. The use of the Australasian Triage Scale categories 4 and 5 as a surrogate indicator of inappropriate attendance represents a misunderstanding of the concept of triage.9 The Australasian Triage Scale assesses urgency, which is different from complexity and severity. These three concepts are distinct, although complementary.

The problem is complicated further by the definition of a general practitioner and therefore of a general practice-type patient. Reasonable patients may well seek attention from GPs if those services are available when the illness occurs and the GP has the requisite skills and facilities to meet the patient’s needs. Further, the nature of community care means that investigations require further appointments and travel. It actually represents a sound and sophisticated choice for many to seek care in an ED for purely practical reasons of timely access to all of the services required at a single location (one-stop shop), even when they could otherwise be treated in general practice.

It is also important to emphasise that notwithstanding the difficulty in defining general practice-type patients, these patients are not a significant contributor to ED congestion or burden. They account for less than 5% of ED length of stay1,10 and a very small proportion of ED costs.11

We appeal for a more rational basis to this discussion and thank the authors for their contribution.

First, we contend that there are not general practice patients or ED patients; there are just patients, who need medical care. The onus is on our health system to understand those needs and to provide accessible, affordable and quality services that meet those needs. Patients should not be blamed for our failure to do so.

Second, we need to understand that demand for acute health care is growing among those who need it. We should understand that need, and attend to the capacity constraints that are the real cause of the current system-wide congestion.

Finally, we need to better compile the evidence to inform the public debate and identify ways in which that evidence can be made accessible to those responsible for policymaking.

Why can’t we get permanent general practitioners for our country town?

To the Editor: A rural general practitioner’s workload is significantly larger than that of his or her urban colleagues, and this is attributable
to work activities in rural public hospitals.1 A GP who provides
after-hours on-call service to the community through the local hospital or emergency department is not only valued, but also more likely to be retained in the rural workforce.2 However, on-call commitments and the unrelenting nature of after-hours care can negatively affect professional and personal wellbeing, family life and opportunities to enjoy the rural location.3

I currently work in the city, but did much of my training in rural and regional areas. Doing GP locums allows me to stay in touch with rural and regional practice. However, working as a locum has highlighted to me how arduous on-call commitments can be. When you are working as the solo town doctor, or one of two, there is not much opportunity to share the on-call roster as recommended by the Rural Doctors Association of Australia.4

In my experience, some hospitals have restrictive service contracts, which further contribute to the GP’s burden. For example, the doctor is mandated to be within 10–15 minutes away from the hospital at all times while on-call, and must attend, when requested, within the times specified in the contract. These times are the same as those expected in large urban hospitals.

In large urban tertiary teaching hospitals with on-site doctors, the median time taken for a doctor to attend patients whose condition has deteriorated unexpectedly is 13 minutes. One in five episodes had a recorded response time longer than 30 minutes.5 By requiring on-call GPs to meet or better the expected response times of urban tertiary hospitals, “on-call” in effect becomes “on duty”.

An on-call weekend results in being confined to home from 8 am Friday to 8 am Monday. I empathise with GPs working permanently in a country town and having to cope with such restrictions.

Given what we know about the negative impact of onerous on-call and after-hours commitments on doctors, including GPs, and the subsequent negative effect on workforce retention in rural and remote Australia,2 why are we still setting ourselves up for continuing failure?

Quantifying the proportion of general practice and low-acuity patients in the emergency department

Between June 2005 and October 2009, attendances to emergency departments (EDs) across Australia increased by 21.2%. This represents an annual increase of 4.9%, which significantly exceeds the rate of population growth.1 Reasons postulated include an ageing population, the rising incidence of chronic illness and decreased availability of general practitioners, especially for after-hours and urgent visits. The latter issue has led to suggestions that overcrowding in EDs is due to patients with general practice-type conditions attending inappropriately and is driven to some extent by poorly validated definitions of “inappropriate” attendances.2

In Australia, methods to determine the number of general practice-type patients attending EDs often use the Australasian Triage Scale (ATS). The ATS is a method used to prioritise care within EDs, with all patients allocated a category from 1 to 5 on arrival. Category 1 patients are regarded as the highest priority, while category 5 patients are the least urgent.3 It has been postulated that general practice-type patients are associated with ATS categories 4 and 5, but this is not well founded.1,3–5

The ATS is an urgency scale, not a complexity scale. A patient can have a low triage category but need complex care. An example is an elderly patient living independently who falls and fractures her forearm. She is low in urgency but high in complexity, requiring extended allied health support to ensure safe discharge. Such a patient cannot be easily managed in most GP settings. Conversely, some high-urgency patients are low complexity. A young patient with fever and a rash should be seen rapidly to assess for serious illnesses such as meningitis. However, once serious illness is excluded, the patient can usually be discharged. This patient might be equally well managed in a primary care environment by experienced GPs.

Estimating the proportion of ED attendees suitable for general practice is complex, with experienced researchers devising a number of approaches to quantify such patients. There is no agreed standard definition for identifying patients as appropriate or inappropriate to attend an ED. A recent extensive literature review4 found that the calculated rate of non-urgent ED attendances varied between 4.8% and 90%, confirming that there is no standard methodology for determining the true proportion of general practice-type patients in EDs.

A number of methods are currently used in Australasia to estimate the number of general practice-type patients presenting to EDs.1,5,6 Only one of these has been validated in the literature.6 We aimed to compare this validated method with other Australasian methods using data from three major tertiary hospitals in Perth, Western Australia.

Methods

Data were extracted from the Emergency Department Information Systems (EDIS version 9.46, iSoft) for the calendar years 2009, 2010 and 2011 at three tertiary hospitals (two adult-only, one mixed) in Perth. Average annual census was 55 000, with admission rates between 35% and 55%.

Four methods were used to estimate the number of general practice-type patients:

The Australian Institute of Health and Welfare (AIHW) method, which considers a general practice-type patient to be any patient allocated an ATS category 4 or 5, who does not arrive by ambulance, police or correctional vehicle, and is not admitted to hospital, is not referred to another hospital and does not die.1
The method developed by Sprivulis,6 which examines the difference between the discharge rates of self-referred patients and GP-referred patients, with calculations based on the self-referred, non-admitted, ATS category 3, 4 and 5 patients.
The Australasian College for Emergency Medicine (ACEM) method, which considers that any self-referred, non-ambulance patient with a medical consultation time under 1 hour may have been suitable for a GP.5 Patients who did not wait or had an invalid consultation time are excluded as their consultation time cannot be calculated.
The diagnosis method, which uses a list of diagnoses of conditions possibly suitable for GP management. Self-referred, non-admitted, ATS category 4 and 5 patients arriving by private transport and meeting one of these diagnoses were considered to be potential GP cases. Patients without a diagnosis were excluded as a diagnosis is required to determine if they were general practice-type. This method was originally developed by Kevin Ratcliffe at the Tasmanian Department of Health and Human Services.

Two of the hospitals have co-located after-hours GP practices, and patients presenting to the ED for a referral to these practices were excluded. These comprised less than 700 (0.2%) patients over the 3 years of the study.

The WA South Metropolitan Health Service Human Research Ethics Committee considered this to be an audit activity and approval was given by the Clinical Governance Unit of Fremantle Hospital. As the data was de-identified, permission was sought and granted by the Head of ED at each hospital as per the WA Guidelines for the release of data (August 2012) and the Information access and disclosure policy (February 2012). Permission to use the diagnosis list was granted by the Tasmanian Department of Health and Human Services.

As it has been postulated by Australian governments7 that the number of general practice-type cases is greater in the evening and overnight due to lack of after-hours GPs, presentation times were grouped as overnight (00:00–08:00), weekends (Saturday and Sunday, 08:00–00:00), weekday daytime (Monday–Friday, 08:00–17:00) and weekday evening (Monday–Friday, 17:00–00:00).

Results

From 2009 to 2011, there were 532 129 ED presentations (Box 1). There was a slight predominance of males, and 36.0% of attendances occurred during the weekday daytime.

Incomplete data resulted in the exclusion of 10 582 (2.0%) records from the ACEM method, 7587 (1.4%) from the diagnosis method, four from the AIHW method and 10 from the Sprivulis method.

The ACEM, diagnosis and Sprivulis methods estimated that 10%–12% of patients were general practice-type, whereas the AIHW method estimated > 25% (Box 2). The confidence intervals showed some differences between the non-AIHW methods, but all ranged between 8.7% and 11.6%, whereas those for the AIHW method ranged between 24.8% and 26.7%.

Using the ACEM and AIHW methods, there were slightly more males in the general practice-type population compared with the total population, but the diagnosis and Sprivulis methods showed similar numbers (Box 3). Proportionally more general practice-type patients presented during the weekday daytime (Box 4). The total ED time of general practice-type patients was 3%–5% for the ACEM, Sprivulis and diagnosis methods and 10%–11% for the AIHW method (Box 5).

Discussion

Our data demonstrate that 10%–12% of patients attending tertiary EDs in Perth between 2009 and 2011 may have been suitable for general practice. These patients contributed 3%–5% of overall ED length of stay, and probably a lesser proportion of resource, staffing and cubicle usage. These data are based on consistent estimates using the Sprivulis method, which is validated in the literature, the ACEM method, which is used by the peak body for emergency medicine in Australasia, and the diagnosis method.

A recent review in the United States concluded that 7%–10% of patients attending EDs may have been suitable for general practice.8 The US study used yet another method based on presenting symptom and diagnoses. However, its results were similar to those of all the Australasian methods except that of the AIHW.

We found that the AIHW method consistently overestimated the proportion of general practice-type patients in EDs. We believe that this was due to its use of the ATS (an urgency rather than a complexity scale); it therefore fails to take into account the nature of the presenting condition(s), diagnostic requirements or treatment pathways. Additionally, the AIHW method includes as general practice-type, patients who have actually been referred to the ED by a GP. Admission as a proxy for complexity is becoming less relevant with admission-avoidance strategies such as home nursing.9 Complex patients can often be discharged, limiting the use of admission as a marker for complexity.

The diagnosis method might appear to be more robust as it relies on a diagnosis classification. However, using diagnoses to determine whether a specific patient needed to use an ED may be inaccurate, because triaging clinicians do not have the full clinical picture until after a full physician assessment. For example, a 70-year-old man may be discharged with a diagnosis of non-specific abdominal pain but, to reach that diagnosis, will have required an extensive workup including pathology, imaging and/or surgical consultation. A more robust method might use presenting problems, as these drive the ED resource use.

The Sprivulis method is a relatively complex analytical approach that produces results consistent with those of the ACEM and diagnosis methods and the recent US study.8

The ACEM method has the advantage of being simple to calculate and intuitive. However, by assuming that a patient may be suitable for a GP if the consultation time in the ED is less than 1 hour, it may overestimate the number of general practice-type patients in the ED, as most GP consultations last about 15 minutes. Although medical consultation times in teaching hospitals can be longer than those in non-tertiary hospitals, it may be more appropriate to assume a consultation time nearer to that of general practice when extending the analysis to non-tertiary hospitals.

Reasons for patients attending the ED instead of a general practice include financial constraints and availability of access.10 Patients may also believe that their condition is an emergency.11,12 This is supported by a study that found that self-referred patients had significantly higher acuity profiles than GP-referred or healthdirect-referred patients.13 However, the reasons for general practice-type patients attending EDs are difficult to interpret because the capability of general practices can differ widely, even within a city. General practice models can range from solo practitioners with no allied health support, to practices operating in a financial environment that requires high throughput, and to “super clinics” with onsite x-ray, multidisciplinary teams and practice nurses.

Australia’s dual health system funding model may provide incentives for state governments to support overestimations of the proportion of general practice-type patients attending EDs.7

After-hours GP clinics, super clinics and polyclinics may fill gaps in medical services but have minimal effects on ED attendances.9,14–19 The impact on the ED from diverting general practice-type patients is low, and inaccurate reporting of the true proportion of these patients results in policy and program initiatives that do not address the real cause of ED overcrowding, which is the lack of available inpatient beds.20

Evidence consistently demonstrates that overcrowding leads to increased patient mortality, morbidity and prolonged hospital stays.14,21–23 Much work has been directed into trying to reduce emergency demand as a solution to reducing overcrowding; however, very few of the strategies have produced results.24

While general practice-type patients may add to waiting room numbers, they do not cause ED overcrowding or ambulance diversion and have little effect on ED workload or waiting times.6,14,16,17,22

It is also unlikely general practice-type patients will ever be completely removed from the patient cohort presenting to EDs. Small numbers of general practice-type patients will continue to present overnight, as alternative facilities do not exist and the ED provides a cost-effective model for overnight acute care as the marginal cost is minimal.

It is commonly held that the number of general practice-type cases is greater outside working hours due to a lack of after-hours GPs. However, Box 4 suggests that this is not the case. Although the weekday daytime only accounts for 27% of the week, 36% of general practice-type patients attended during this time.

It is essential to estimate accurately the proportion of general practice-type patients in the ED, as incorrect data lead to poor policy and planning. This results in misdirected and costly interventions, which inevitably fail to resolve ED overcrowding or its underlying causes.15,25

Our study was limited to three tertiary hospitals in Perth. It is likely that these results are generalisable; however, detailed analysis of the Perth population and Perth GP availability compared with the rest of Australia was beyond the scope of the study.

The proportion of general practice-type patients in outer metropolitan and regional centres may be higher; however, it is likely that overestimation by the AIHW methodology for these EDs would be of a similar magnitude. Further work is underway to extend the analysis to all WA hospitals.

The methods used here are statistical methods and will fail to capture individual patient decisions as a qualitative study might. A qualitative study is resource-intensive and impractical to conduct beyond small numbers.

The ACEM method was the easiest to use and has clinician validity for calculating the small proportion of possible general practice-type patients to EDs in Australasia, although it may require minor modifications for use outside tertiary hospitals. The AIHW methodology overestimated general practice-type patient workload in EDs and should no longer be used to guide policy decisions.

1 Attendances at the emergency departments in three major hospitals in Perth, by sex and time of presentation

Year	Total male and female	Male	Weekday daytime*	Weekday evening†	Overnight‡	Weekend§

2009	164 352	88 777 (54.0%)	58 595 (35.7%)	38 203 (23.2%)	28 726 (17.5%)	38 828 (23.6%)
2010	175 721	94 910 (54.0%)	63 366 (36.1%)	40 844 (23.2%)	30 192 (17.2%)	41 319 (23.5%)
2011	192 056	103 320 (53.8%)	69 719 (36.3%)	45 085 (23.5%)	31 844 (16.6%)	45 408 (23.6%)

* Mon–Fri, 08:00–17:00. † Mon–Fri, 17:00–00:00. ‡ Mon–Sun, 00:00–08:00. § Sat–Sun, 08:00–00:00.

2 Number of general practice-type patients presenting to emergency departments, calculated by four commonly used methods

ACEM

Sprivulis6

Diagnosis*

AIHW

Year

Total

No.

95% CI

No.

95% CI

No.

95% CI

No.

95% CI

2009

164 352†

16 905 (10.6%)

10.3%–10.6%

15 984 (9.7%)

9.5%–10.0%

17 888 (11.1%)

10.9%–11.2%

43 452 (26.4%)

26.2%–26.7%

2010

175 721‡

19 140 (11.1%)

10.9%–11.3%

15 741 (9.0%)

8.7%–9.2%

19 127 (11.0%)

10.8%–11.3%

44 495 (25.3%)

25.1%–25.6%

2011

192 056§

21 877 (11.6%)

11.3%–11.8%

18 151 (9.5%)

9.2%–9.7%

21 242 (11.2%)

11.0%–11.4%

48 041 (25.0%)

24.8%–25.2%

ACEM = Australasian College of Emergency Medicine. AIHW = Australian Institute of Health and Welfare. * Method developed by the Tasmanian Department of Health and Human Services. † Data missing in 2009 for 4673 patients for the ACEM method, four patients for the Sprivulis method, 3192 patients for the diagnosis method, and two patients for the AIHW method.‡ Data missing in 2010 for 3181 patients for the ACEM method, three patients for the Sprivulis method, 2161 patients for the diagnosis method, and one patient for the AIHW method.§ Data missing in 2011 for 2728 patients for the ACEM method, three patients for the Sprivulis method, 2234 patients for the diagnosis method, and one patient for the AIHW method.

3 Number of males presenting to emergency departments with general practice-type conditions, calculated by four commonly used methods

	ACEM		Sprivulis6		Diagnosis*		AIHW
Year	Total male and female	Male	Total male and female	Male	Total male and female	Male	Total male and female	Male

2009	16 905	10 231 (60.5%)	15 984	8923 (55.8%)	17 888	9488 (53.0%)	43 452	25 329 (58.3%)
2010	19 140	11 438 (59.8%)	15 741	8776 (55.8%)	19 127	10 109 (52.9%)	44 495	25 787 (58.0%)
2011	21 877	13 108 (59.9%)	18 151	10 164 (56.0%)	21 242	11 164 (52.6%)	48 041	27 855 (58.0%)

ACEM = Australasian College of Emergency Medicine. AIHW = Australian Institute of Health and Welfare. * Method developed by the Tasmanian Department of Health and Human Services.

4 Number of patients presenting with general practice-type conditions to emergency departments, calculated by four commonly used methods, by time of presentation

		General practice-type patients
Time of presentation	All patients (n = 532 129)	ACEM (n = 57 922)	Sprivulis6 (n = 49 399)	Diagnosis* (n = 58 257)	AIHW (n = 135 988)

Weekday daytime: Mon–Fri, 08:00–17:00	191 680 (36.0%)	21 135 (36.5%)	17 399 (35.2%)	21 961 (37.7%)	52 500 (38.6%)
Weekday evening: Mon–Fri, 17:00–00:00	124 132 (23.3%)	12 526 (21.6%)	11 026 (22.3%)	11 497 (19.7%)	28 268 (20.8%)
Overnight: Mon–Sun, 00:00–08:00	90 762 (17.1%)	8520 (14.7%)	7862 (15.9%)	9434 (16.2%)	19 560 (14.4%)
Weekend: Sat–Sun, 08:00-00:00	125 555 (23.6%)	15 741 (27.2%)	13 112 (26.5%)	15 365 (26.4%)	35 660 (26.2%)

ACEM = Australasian College of Emergency Medicine. AIHW = Australian Institute of Health and Welfare. * Method developed by the Tasmanian Department of Health and Human Services.

5 Length of stay of general practice-type patients in emergency departments, as a proportion of total emergency department length of stay, calculated by four commonly used methods

Year	ACEM	Sprivulis6	Diagnosis*	AIHW

2009	3.1%	5.0%	5.3%	11.8%
2010	2.8%	3.8%	4.5%	10.1%
2011	3.3%	4.3%	4.9%	10.5%

ACEM = Australasian College of Emergency Medicine. AIHW = Australian Institute of Health and Welfare. * Method developed by the Tasmanian Department of Health and Human Services.

Take a deep breath . . . and talk

To the Editor: We congratulate Nowak on her discussion surrounding communication in the emergency department (ED).1 This is certainly an issue that has an impact on both patient safety and satisfaction, and is an area in which all medical personnel can improve. The challenges in ED are manifold, and time-based targets tend to militate against effective communication.2 A strategy that we have employed in our department is to involve the patient and their family in discussions that are relevant to them — in particular, the ward round. The first step in the round is to introduce the participating doctors, nurses and students to the patient, explain why it is being done, and let the patient listen to the presentation, which, after all, is about them and should not be a secret.

Once the presentation is finished, the patient is invited to add to or challenge anything that has been said. This is listened to and responded to in the same manner as any of the participants’ contributions to the process.

We have found that not only are patients, doctors and nurses more satisfied with this process, but we often find out extra information, particularly pertaining to the patient’s history and their stage in the journey through the ED.

This small change, which usually adds less than a minute to each patient encounter on the round, is well worth considering not only in the ED but also in other ward-based environments.

The effectiveness of helmets in reducing head injuries and hospital treatment costs: a multicentre study

To the Editor: Debate continues regarding the health benefits and consequences of helmet use in pedal cyclists.1 Australia is one of few countries in the world with mandatory helmet laws for both pedal cyclists and motorcyclists. To place the protective effect of helmets in pedal cyclists into perspective, we report on the relationship between helmet use and head injury severity in a retrospective cohort of both pedal cyclists and motorcyclists.

Trauma registry data on such patients admitted to seven tertiary level hospitals in Sydney, New South Wales (Liverpool, St George, Royal Prince Alfred, Westmead, Royal North Shore, St Vincent’s and Prince of Wales hospitals) between July 2008 and June 2009 were obtained. Patients were included if they were aged 15 years or over with an incident occurring on a public road. The Abbreviated Injury Scale and Injury Severity Score were used to classify body regions and severity of injury, respectively. Helmet use, incident and other injury details were routinely collected by trained data and case managers from standard ambulance and trauma clinical case notes. Inhospital costs were calculated using standardised cost weights (NSW Program and Product Data Collection, 2008–09). Primary outcomes were any head injury and severe head injury (Abbreviated Injury Scale severity score ≥ 3), including significant intracranial haemorrhages, and diffuse axonal injury. Logistic regression was used to determine odds ratios for head injury and severe head injury, adjusting for age (as a continuous variable) and location of incident (based on incident postcode) as a-priori confounders based on previous work.2

There were 398 cases identified. Of these, 50 patients (13%) had missing helmet information, leaving 348 cases analysed. Baseline characteristics stratified by helmet use are shown in the Box. For any head injury associated with helmet non-use, the adjusted odds ratio was 5.6 (95% CI, 2.1–14.9; P < 0.001) for pedal cyclists and 2.2 (95% CI, 0.9–5.0; P = 0.06) for motorcyclists, compared with helmeted patients in each group. For severe head injury associated with helmet non-use, the adjusted odds ratio was 5.5 (95% CI, 1.5–20.6; P = 0.01) for pedal cyclists and 3.5 (95% CI, 1.3–8.9; P = 0.01) for motorcyclists, compared with helmeted patients in each group. For the 50 patients with severe head injury, inhospital costs (AUD) were around three times higher in non-helmeted patients (median, $72 000; interquartile range, $33 000–$140 000) compared with helmeted patients (median, $24 000; interquartile range, $15 000–$60 000) (P = 0.02).

The protective effect of helmet use with respect to head injury prevention therefore appears to be greater in pedal cyclists compared with motorcyclists. There was no association observed between helmet use and diffuse axonal injury. Limitations to our study include the small number of patients with severe head injury, and the inability to control for other incident factors such as speed, collision details and intoxication. The use of hospital data biases observations towards patients with more severe injuries. Nevertheless, the results add to the growing weight of observational data supporting the use of helmets, 3–5 which should therefore be considered at least as protective for pedal cyclists as they are for motorcyclists.

Characteristics of cyclists and motorcyclists with head injuries, by helmet use

	Cyclist (n = 110)			Motorcyclist (n = 238)
Characteristic	Helmet (n = 70)	Non-helmet (n = 40)	P	Helmet (n = 206)	Non-helmet (n = 32)	P

Demographic
Median age (IQR), years	41 (29–53)	35 (23–44)	0.02	31 (24–43)	25 (21–38)	0.06
Male	64 (91%)	35 (88%)	0.51	194 (94%)	31 (97%)	0.53
Incident details
After hours*	25 (36%)	14 (35%)	0.94	65 (32%)	14 (44%)	0.17
Location†
Inner Sydney	21 (30%)	11 (28%)		40 (19%)	13 (41%)
Suburban Sydney	26 (37%)	20 (50%)		76 (37%)	11 (34%)
Regional/rural	23 (33%)	9 (23%)	0.37	91 (44%)	8 (25%)	0.02
Injury severity
Median ISS (IQR)	9 (5–14)	9 (5–21)	1.0	9 (5–17)	15 (5–25)	0.15
Multiregion injury (%)	46 (66%)	29 (73%)	0.46	153 (74%)	21 (66%)	0.32
ICU	11 (16%)	7 (18%)	0.81	47 (23%)	12 (38%)	0.07
Outcomes
Head injury	27 (39%)	30 (75%)	< 0.001	68 (33%)	14 (44%)	0.23
Severe head injury	6 (9%)	9 (23%)	0.04	26 (13%)	9 (28%)	0.02
Diffuse axonal injury	0	0	na	5 (2%)	3 (9%)	0.08
Rehabilitation‡	3 (4%)	6 (15%)	0.07	35 (17%)	4 (13%)	0.53
Median cost (IQR), AU$1000	6.5 (2.8–10.7)	5.6 (2.5–15.2)	0.91	7.7 (3.0–20.7)	11.4 (4.4–41.0)	0.05

ICU = intensive care unit admission required. IQR = interquartile range. ISS = Injury Severity Score. na = not applicable. * Recorded incident times between 19:00 and 07:00 hours. † Postcode of location of incident was used to classify incident locations in the inner Sydney (within 10 km of central business district), suburban Sydney (bounded by Hornsby to the north, Royal National Park to the south and Penrith to the west), and regional and rural regions of New South Wales. ‡ Discharge from hospital to a rehabilitation facility.

Injuries to the head and face sustained while surfboard riding

To the Editor: Surfboard riding is an iconic pastime in Australia. Injuries to the head and face constitute a considerable proportion of surfing injuries;1–5 26% of acute surfing injuries are to the head and face, and these make up 42% of emergency department presentations by surfers.3

We conducted a retrospective review at our tertiary referral hospital of patients who underwent medical imaging for injuries sustained to the head and face while surfboard riding from January 2008 to January 2012. We searched the hospital radiology databases for patient records containing the terms “surfboard”, “surfer” or “surfing”. Patients were included if they were injured while surfboard riding and were excluded if they were injured during other water-based activities (eg, bodyboarding, kitesurfing, bodysurfing, paddleboarding). Twenty-nine patients were identified: 23 males and six females (mean age, 34 years; range, 10–73 years). Of the 26 who had acute injuries, 17 had imaging of the head only, seven had imaging of the head and cervical spine and two underwent a trauma protocol (computed tomography scans of the head, spine, chest and abdomen). Fifteen patients had been struck in the head by their own board, nine had other mechanisms of injury (primarily involving contact with the sea floor and associated neck pain), one collapsed while surfing and one was retrieved from the surf unconscious (mechanism of injury was unknown). The most common significant injuries were facial fractures (five of 26 patients, all of whom had been struck by their own board). One patient ruptured their left globe after being struck by their own board. No intracranial trauma (eg, intracranial haemorrhage, contusion) was identified.

Surfboard design and surfing accessories have evolved significantly over the past 20 years. Lighter, shorter boards are now commonly used and provide greater manoeuvrability in the water. Leg ropes are universally used to ensure that surfer and board do not become separated (Box). However, lighter boards and leg ropes might increase the risk of being struck and injured by one’s own board during a “wipe-out”. The pointed nose and fins on the undersurface of the board are also potentially injurious (Box).

Understanding injury mechanisms can drive surfboard and surfing accessory design to reduce the risk of injury and death. Protective devices — such as helmets, protective eyewear and nose guards that cover the tip of the surfboard — have been marketed, but there is no evidence of their effectiveness in injury reduction.

Innovations in surfboard design that are potentially injurious to the surfer

A: Leg rope. B: Pointed nose at the front of the board. C: Fins on the undersurface of the board (a three-fin design is the most common configuration on a modern shortboard).

Better prepared next time: considering nutrition in an emergency response

To the Editor: Cyclones, floods and bushfires are experienced in Australia every year, and Australia’s management of natural disasters centres on prevention, preparedness, response and recovery.1 Although access to safe food is a basic human need, during the 2010–2011 Queensland floods there was minimal information available to guide household food preparedness and food supply to communities.2 To ensure that Queensland is better prepared for future natural disasters, the Queensland Floods Commission of Inquiry recommended the development of consistent community education programs.2 Following the floods, a local food security resource kit3 was developed; however, there were no statewide resources. In 2011, we were members of a multidisciplinary working group — the Food Requirements in Disasters Working Group — that was established by Queensland Health to provide advice on food requirements in disasters for households and community organisations.

There is little international literature on food recommendations in disasters that is specific to high-income countries. Existing Australian resources did not consider nutritional requirements for infants, children and adults, did not provide sufficient advice for appropriate food purchasing in the event of no access to power or water and/or were no longer publicly available.4,5 Twenty-six principles and nutritional criteria (Box) — covering food safety, practical considerations and nutrient requirements — guided the development of recommendations on food requirements during disasters for infants, children and adults.

Five online fact sheets (available at http://www.health.qld.gov.au/disaster/html/prepare-event.asp) outlining the food and equipment required to sustain two people for 7 days (Emergency pantry list for Queensland households) and to support both breastfed and formula-fed infants for 3 days (including Food for infants in emergencies and Preparing ready-to-use infant formula in an emergency) were developed. The recommended types and quantities of foods align with the Australian dietary guidelines and Infant feeding guidelines (available at http://www.eatforhealth.gov.au). To facilitate purchasing choices, tips and examples of product sizes based on items available in major supermarkets are included.

Credible, easily accessible information is essential to ensure households have the capacity to prepare for and respond to disaster situations, to prevent panic buying and food shortages, and to minimise any negative impact on the health and wellbeing of individuals affected by disaster. Queenslanders now have access to a suite of resources to help them stay safe and healthy during natural disasters and severe weather conditions.

Principles and nutritional criteria used to guide recommendations on food requirements during disasters
for infants, children and adults

Principles

Nutrient requirements need to be balanced against practicality
Provision of adequate energy (kilojoules) and water are key priorities
Dietary recommendations set at population level — no individual dietary requirements
Requirements per person — should be scalable
Food products should be non-perishable
No refrigeration required
Minimal preparation required
No reheating or cooking involved
Number of days — should be scalable and informed by practical experience
Include generic products rather than specific brands
Total weight should be kept to a minimum
Foods should be safe
Packaging should be robust
Packaging should be waterproof and non-porous
Packaging should be vermin proof
Presume there are no facilities available for food storage — provide appropriate containers and serving sizes
Provide other equipment needed for preparation and consumption of food, including hand sanitiser, plastic cutlery
and plates
Wastage should be minimised
Costs should be reasonable (no luxury items)
Foods should be palatable and acceptable
Foods should be readily available, familiar and culturally appropriate
Foods should be adaptable to personal tastes

Nutritional criteria

Provide mean food and nutrient requirements for adults and children
Provide mean food and nutrient requirements for infants
(≤ 12 months)
Provide 100% of requirements (presume that households and isolated people have no other food available)
Particularly note upper limit for sodium

Injury trends and mortality in adult patients with major trauma in New South Wales

To the Editor: It is pleasing to see Curtis and colleagues report injury trends and mortality across New South Wales,1 but the data are old and precede major changes to the NSW trauma system. We are concerned that the conclusions of this study will be misapplied by policymakers, leading to unnecessary out-of-area transport of injured patients.

The authors concluded that there is a survival benefit when definitive care occurs at a “level 1” major trauma centre (MTC) rather than at a regional trauma centre (RTC).1 Unfortunately, the definitions they used for trauma centre designation are not those used by NSW Health for service planning.2 According to the NSW Health definition, there were nine MTCs and two RTCs during the study period, in contrast to eight level 1 and three level 3 hospitals defined in the study. Adding to the ambiguity, NSW Health designated two hospitals as RTCs in 20013 and three in 2004,4 with no documented dates for any of these changes. Further, the authors did not mention that Wollongong Hospital did not enter data into the NSW Trauma Registry until 2004.5 These points contradict the statement that “there were no changes in trauma centre designation or data collection resources during the study period”1 and place significant limitations on interpreting the results.

The conclusion that mortality is decreasing is not supported by the data. If 2003 is excluded, the mortality has been static in the years 2004–2007, and was the same as Victoria with two MTCs,6 and similar to outcomes in the United States.7 This negates any argument to force patients to be transported considerable distances to access trauma care, especially given that the Ambulance Service of NSW “Protocol T1” for prehospital management of major trauma performs poorly, with sensitivity for serious injury of 63% and an overtriage rate of 77%.8 The incidence of severe neurotrauma has a major impact on overall outcomes, and no casemix data were provided to confirm comparability between centres.

Finally, data did not include patients with an injury severity score < 15 — the bulk of trauma patients. However, it is essential to examine treatment and outcomes for all trauma patients — owing to the lack of specificity of the ambulance bypass tool as well as the impact of trauma bypass on the ambulance service’s ability to respond to non-trauma patients needing time-critical care. Much better, region-specific data are needed to determine what services trauma patients need and where best to provide them to optimise patient outcomes.