Primary care research has been described as a “lost cause”, and, although this claim has been strongly refuted, general practitioners publish less research than their colleagues in surgery, medicine and public health. Despite a fivefold increase in Australian general practice research papers from the 1980s to the 1990s, fewer than half of these focused on clinical topics. Trying to establish a global figure for expenditure on general practice and primary care research is difficult, but data show that public expenditure for primary care research is minimal in Australia, New Zealand, the Netherlands and the United Kingdom — fewer than $1.50 per capita in 2002–2003. Compared with hospital- and laboratory-based research, primary care receives significantly fewer resources, ranging from 3.2% of total public expenditure on health and medical research in the Netherlands to 6.8% in New Zealand. Government-led investment in interventions such as strengthening primary care departments and colleges and supporting primary care academics, establishing practice-based networks, fostering international initiatives for cross-national efforts, and engaging individual primary care practitioners in research projects, are all required to build research capacity in primary care.

Brian R McAvoy MD, FRACGP, FRCP

A dengue fever epidemic was recognised in the Torres Strait Islands of Queensland in late 2003. Two fatal cases of dengue haemorrhagic fever occurred in early 2004. This severe manifestation is more common when a patient is infected a second time, with a different virus serotype to the first infection. These are the first fatalities related to dengue fever in Australia in over a century. Clinical recordsPatient 1A 40-year-old woman from Thursday Island in the Torres Strait, north Queensland (Box 1), presented to a local hospital in February 2004 with a 6-day history of feeling generally unwell, plus generalised body aches and fevers, and 3 days of vomiting and diarrhoea. She had type 2 diabetes and was taking metformin. She had been seen at a primary health care clinic on Days 2 and 5 of the illness and was diagnosed clinically with dengue fever based on the typical symptoms, as this infection was epidemic at the location. Blood samples were taken on both occasions. On admission to hospital, she was delirious and restless, with a pulse rate of 120 beats/min and blood pressure of 100 mmHg systolic by palpation only. Petechiae were noted around the right elbow. She was given 2 L of intravenous fluid. Six hours after admission, she became more agitated and restless, with blood pressure of 123/55 mmHg and pulse rate of 150 beats/min. She was given a small dose of morphine. Thirty minutes later, her blood pressure became unrecordable. Despite 5 L of intravenous fluids over the next 7 hours, together with adrenaline and metaraminol, the blood pressure remained very low. A single dose of ceftriaxone (2 g) was given, and evacuation to a referral hospital was arranged. The retrieval team noted that the patient’s skin was cold and clammy and recorded a blood pressure of 90/55 mmHg. The pulse rate fell, and blood pressure became unrecordable before arrival at the referral hospital, and she could not be resuscitated. An autopsy was not performed. Between Days 2 and 6 of the illness, the patient’s haematocrit rose from 0.42 to 0.55 (reference range [RR], 0.36–0.52), and her platelet count fell from 144 × 109/L to 4 × 109/L (RR, 150–400 × 109/L). There was a moderate increase in hepatic enzyme levels: aspartate aminotransferase (AST), 1270 U/L; and alanine aminotransferase (ALT), 310 U/L (RR, < 40 U/L for both). Dengue virus type 2 was detected by both reverse transcriptase polymerase chain reaction (RT-PCR) testing and viral culture. Previous tests for dengue antibody, in 1998, were positive for IgG. The pattern of antibody response during the current illness was that of secondary infection. Culture of blood taken at the time of admission to the local hospital grew Escherichia coli. A diagnosis of dengue haemorrhagic fever was made, based on World Health Organization criteria1 (Box 2). Patient 2In March 2004, a 70-year-old man from an island north of Thursday Island had a 1-day history of dyspnoea, cough and a low-grade fever. He had type 2 diabetes, raised cholesterol level and hypertension. His wife called the local medical clinic during the night as he was agitated and semiconscious. His blood sugar level was noted to be low. Glucagon was administered on the advice of medical staff on Thursday Island, and his mental state improved slightly. His blood pressure was 80/60 mmHg. The patient was evacuated to Thursday Island the following day. On arrival, his temperature was 37.1°C, pulse rate was 93 beats/min, and blood pressure was 120/70 mmHg. His respiratory rate was 28 breaths per minute, oxygen saturation was 93% breathing room air, and he had several episodes of diarrhoea. He was given 2 L of intravenous fluid. He continued to complain of dyspnoea, and a chest x-ray showed hyperinflated lungs. A provisional diagnosis was made of an acute exacerbation of airways disease, and treatment was begun with prednisolone (50 mg per day). His blood pressure remained low (90–100 mmHg systolic). Thrombocytopenia (11 × 109 cells/L) was noted on a blood film, and the possibility of dengue fever was raised, although the infection was not then known to have spread to the patient’s home island. Hepatic enzyme levels were mildly elevated (AST, 126 U/L; ALT, 99 U/L). The following day, the patient had a sudden large melaena and became hypotensive. This was followed by bradycardia and cardiac arrest. He was resuscitated, intubated and ventilated, and then evacuated to a referral hospital. He received a blood transfusion but had further melaena, and was dependent on inotropic support in the intensive care unit. Blood was noted in his stomach after insertion of a nasogastric tube. Despite receiving antibiotics for presumed sepsis, he died later the same day. An autopsy was not performed. A retrospective diagnosis was made of probable dengue haemorrhagic fever. Dengue virus type 2 was cultured from blood taken on Day 4 of the illness. Dengue IgG, but not IgM, antibodies were detected in serum taken on Day 2, consistent with a secondary dengue infection. There was a fall in haematocrit from 0.48 to 0.39 between Days 4 and 5 of the illness. A chest x-ray done in the intensive care unit showed a right upper lobe infiltrate, but no evidence of pleural effusions. DiscussionThese two cases are, to my knowledge, the first fatalities related to dengue fever in Australia in over a century. Previous fatalities were described during a large epidemic of dengue fever in Charters Towers (north Queensland) in 1897.2 Dengue fever is caused by infection with one of four serotypes of dengue virus and is transmitted from human to human through the bite of the mosquito vector Aedes aegypti. Clinically, the infection is characterised by a febrile illness associated with generalised body aches, and occasional minor bleeding manifestations. A more severe form of the disease, dengue haemorrhagic fever, has become an increasing cause of morbidity and mortality throughout the tropical world. There are an estimated 50–100 million cases of dengue infection each year, including about half a million cases of dengue haemorrhagic fever. The number of cases of both dengue fever and dengue haemorrhagic fever has increased dramatically over the past few decades, and the geographical range has extended to involve most tropical countries.3 The frequency of dengue haemorrhagic fever is much greater during secondary dengue infections than during primary infection. As immunity to infection with the same dengue serotype is probably lifelong, secondary infections are usually caused by a different virus serotype. Antibodies raised in the initial dengue infection may cause an immune enhancement in a subsequent infection with a different dengue serotype.4 Epidemics of dengue haemorrhagic fever can occur when a particular population is subject to sequential epidemics caused by different serotypes.5 Cases of dengue haemorrhagic fever, including some fatal cases, were first described in Australia during the 1897 epidemic in Charters Towers.2 This followed another large epidemic in the town in 1894–1895. As individuals were described with symptoms during both epidemics, they were probably caused by different serotypes. A large epidemic of dengue fever in Townsville and Charters Towers in 1992–1993 raised the possibility of the re-emergence of dengue haemorrhagic fever in Australia.6 These fears have been repeated with each subsequent epidemic.7 Diagnosis of dengue haemorrhagic fever is based on clinical and laboratory findings (Box 2), and severity is graded 1 to 4.1 Grade 3 is defined as circulatory failure manifested by rapid and weak pulse, and narrowing of pulse pressure (20 mmHg or less) or hypotension, with the presence of cold clammy skin and restlessness. Grade 4 is defined as profound shock with undetectable blood pressure and pulse. Grades 3 and 4 dengue haemorrhagic fever are termed dengue shock syndrome.1 Both Patient 1 and Patient 2 were classified with grade 4 dengue haemorrhagic fever. Patient 1 had skin petechiae, haemoconcentration, thrombocytopenia, and fever. The presence of E. coli in the blood may have contributed to her death, but the pattern of illness was otherwise typical of dengue haemorrhagic fever. She was treated with an antibiotic with activity against E. coli. Concurrent bacterial infection may occur in dengue haemorrhagic fever and is more common in older patients.8 The death generated considerable publicity and has heightened awareness of the condition among clinical staff in the Torres Strait Islands. Patient 2 had a fall in haematocrit of about 20% between Days 4 and 5 of the illness, but evaluation of the degree of haemoconcentration was complicated by haemorrhage and transfusion. Although a chest x-ray did not demonstrate pleural effusion (which would have provided evidence of vascular permeability), the clinical endpoint of vascular permeability — hypotension and shock — was certainly evident. Both patients had evidence of recent infection with dengue virus type 2. A dengue 2 epidemic was recognised in the Torres Strait Islands in late 2003, following the admission of two patients (aged 32 and 42 years, respectively) to the intensive care unit at Cairns Base Hospital with severe hepatitis. Both these patients fulfilled the clinical criteria for dengue haemorrhagic fever and had serological evidence of secondary dengue infection. From November 2003 to April 2004, there were 176 laboratory-confirmed cases of dengue fever in the Torres Strait, mostly on Yam Island and Thursday Island (Alyssa Pyke, Queensland Health Scientific Services, personal communication). Smaller epidemics, also caused by dengue virus type 2, occurred concurrently in Cairns and Townsville. Previous epidemics of dengue fever in the Torres Strait Islands occurred in 1996 (dengue 2) and 1981 (dengue 1).9 The latter was the only non-dengue 2 epidemic that has been well documented in the Torres Strait Islands.10 The most plausible scenario in the four cases of dengue haemorrhagic fever in 2003–2004 is that primary infection occurred in 1981. This implies that secondary infection more than 20 years after primary infection may still produce severe manifestations. The same observation was made after an epidemic of dengue 2 in Cuba, 20 years after a dengue 1 epidemic.11 The patients with dengue haemorrhagic fever described here were aged 32 to 70 years. In contrast, in south-east Asia, dengue haemorrhagic fever is predominantly a paediatric condition. A possible explanation for the older age of the Queensland patients is that the interval between the dengue 1 and dengue 2 epidemics meant that only older people had dengue 1 antibodies. Epidemics of dengue fever appear to have become more frequent in north Queensland, with five major epidemics (three affecting the Torres Strait) and many smaller epidemics between 1992 and 2004. Control measures instituted by public health authorities may have averted more frequent larger epidemics.12 In contrast, the previous five major epidemics occurred over a period of 90 years. Increasing international travel into north Queensland and global increase in dengue activity will inevitably lead to further introductions of the virus into north Queensland. Indeed, another outbreak — of dengue type 4 — was declared in the Torres Strait in March of this year.13 Aggressive case-finding and mosquito control are our major defences against further epidemics and the attendant risk of dengue haemorrhagic fever. The major clinical feature of dengue haemorrhagic fever is intravascular fluid loss. Expert clinical management of dengue haemorrhagic fever with aggressive intravenous fluid replacement has reduced the mortality rate to less than 1% in centres experienced in fluid resuscitation.14 This compares with mortality rates up to 30% in some series.3 Medical staff in high-risk areas are now alert to the possible future occurrence of this syndrome. 1 Location of the Torres Strait Islands The Torres Strait Islands lie between mainland Papua New Guinea and the tip of Cape York in Australia. The two major foci of the dengue epidemic were Yam Island and Thursday Island. 2 Diagnostic criteria for dengue haemorrhagic fever (World Health Organization)1 Clinical findings Fever lasting 2–7 days; and Haemorrhagic manifestations, ranging in severity from a positive tourniquet test through to clinically obvious bleeding. Laboratory findings Platelet count < 100 × 109 cells/L; and Haemoconcentration, as evidenced by a 20% rise in haematocrit (or a 20% fall after rehydration).

William J H McBride FRACP, FRCPA, PhD

What we need to knowWhat we need to do

Christine R Jenkins MD, FRACP · Philip J Thompson MD, FRACP · Peter G Gibson PhD, FRACP · Richard Wood-Baker PhD, FRACP

What we need to knowWhat we need to do

Julie E Byles PhD

What we need to knowWhat we need to do

Amanda Barnard BA, FRACGP · C Dimity Pond PhD, FRACGP · Timothy P Usherwood MD, FRACGP, FRCP

Six patients being evaluated for phaeochromocytoma had misleading investigative findings: all initially had raised urinary catecholamine levels, and five had adrenal masses on imaging studies. Adrenalectomy in these five patients revealed only one pathologically confirmed phaeochromocytoma. Tricyclic antidepressant use produced misleading elevations in urinary catecholamine levels in three patients. 24-hour urine studies should be performed at least twice, after eliminating confounding factors (stressors, medications). Clinical recordThe details of six patients treated in the period April 1999 – October 2003 by members of the Section of Endocrine Surgery of the Royal Australasian College of Surgeons are outlined in Box 1. In all patients, clinical suspicion of phaeochromocytoma was raised by the presence of hypertension, paroxysmal symptoms, or both. Twenty-four-hour urinary catecholamine levels were found to be elevated, although in Patients 1–5 these abnormalities were confined to one or two analytes only. In all except Patient 2, adrenal lesions were discovered on imaging, with large haemorrhagic masses detected in patients with an acute presentation (Patients 5 and 6). Patients with abnormalities on computed tomography (CT) underwent surgery. In Patients 1, 3, and 4, the excised tissues were found to be pathologically normal or to show mild enlargement (benign). In Patients 5 and 6, blood clot and necrotic tissue comprised the bulk of the specimens (Box 2), with a phaeochromocytoma discovered in the latter patient. Of note, Patients 1–3 were receiving tricyclic antidepressants for non-standard uses that did not include the treatment of major depression. DiscussionFalse positive biochemical test results for phaeochromocytoma are common and present particular problems because of the low prevalence of the disease. The reported incidence of phaeochromocytoma is 2–8 per million people annually, accounting for less than 0.2% of all patients with hypertension.1 Despite the fact that phaeochromocytoma is a rare cause of hypertension, the diagnosis merits consideration in a potentially large group of patients for two reasons. Firstly, although the disease is frequently fatal if unrecognised, surgical removal is highly effective, achieving cure in greater than 90% of cases.2 Secondly, because no array of clinical indicators has proven to reliably include or exclude phaeochromocytoma,3 physicians must maintain a high level of suspicion and consider biochemical testing in patients at risk. The pretest probability for phaeochromocytoma is close to 0.5% (1 in 200 patients tested) in the presence of hypertension and suggestive symptoms.4 Assuming a specificity of 85% for biochemical testing, 30 false positive results are generated for every one patient with phaeochromocytoma identified.5 Fortunately, most false positive tests can be unmasked with careful additional investigation and/or the elimination of factors known to confound biochemical tests for levels of catecholamines and their metabolites. The misleading elevations in urinary noradrenaline levels in Patients 1–3 can be ascribed to their taking tricyclic antidepressants. Medications and conditions that may result in raised levels of plasma and/or urine catecholamines and their metabolites, and result in false positive test results for phaeochromocytoma, are listed in Box 3. Among these drugs, tricyclic antidepressants and phenoxybenzamine have been the most frequently implicated, together accounting for more than 40% of medication-associated false positive results in a recent large study.6 In Patients 3 and 4, false positive biochemical findings led to the identification of small (1.5 cm) adrenal masses on CT scanning, both of which were found, on histopathological examination, to be benign. Clinically unapparent adrenal masses (“incidentalomas”) are found in 2.1% of subjects at autopsy and in 1%–4% of abdominal imaging studies. Most of these masses are benign, hormonally inactive tumours that do not require surgical management.7 Phaeochromocytomas presenting with acute haemorrhage at presentation have been reported previously,8,9 with haemorrhagic tumours often losing characteristic imaging appearances and functional markers. Tumour necrosis may initially result in massive catecholamine release, followed by failure to demonstrate excess catecholamine levels, as was seen in Patient 6. Mildly elevated urinary catecholamine levels may also be seen as a consequence of hyperadrenergia from an acute stress response at the time of haemorrhage into a non-phaeochromocytoma lesion, as occurred in Patient 5. Role of biochemical testingAlthough measurement of plasma free metanephrine levels has been recently advocated by some groups, 24-hour urinary catecholamine levels and total metanephrine level have consistently proven to be the most specific tests available for the diagnosis of phaeochromocytoma.5,10 Elevations in the level of one or more of these analytes (above the 95% reference range designated as the upper limit of normal by laboratories) are common in patients with paroxysmal symptoms or poorly controlled hypertension not due to phaeochromocytoma. Thus, we recommend that higher cut-off values, roughly two times the upper limit of normal for most laboratories, be used to identify patients suitable for further workup. Repeat biochemical testing 6 weeks after stopping drugs likely to confound the results is ideal, and tests performed during major physical or psychological stress should be interpreted with extreme caution (if performed at all). It is important to note that alterations in plasma catecholamine levels may be caused not only by medications, but also by the underlying diseases being treated (eg, major depression in the case of tricyclic antidepressants or severe heart disease in the case of β-blockers).11-13 All patients should undergo at least two 24-hour urine collections for measuring levels of catecholamines and their metabolites. Clonidine suppression testing — the measurement of plasma free normetanephrine before and after the oral administration of 0.3 mg clonidine — is highly sensitive and specific, and may be a useful adjunct in patients with more than one prior set of equivocal tests.6 Role of imagingWhether imaging studies (both anatomical and functional) play a role in diagnosing phaeochromocytoma, as opposed to only localising tumours already diagnosed biochemically, remains controversial. In the patients described above, 131I‑metaiodobenzylguanidine scanning yielded true negative results in Patients 1–3, consistent with its known high specificity.4 However, current evidence suggests that, when appropriate biochemical tests are used, little discriminatory value is to be gained from imaging,14 and our experience illustrates how incidental radiographic findings may lead to unnecessary surgery. 1 Summary of the clinical records of six patients investigated for phaeochromocytoma Patient age/sex Presentation Blood pressure (mmHg) Medications 24-h Urinary catecholamine levels (nmol/d or μmol/d)* Radiological investigation† Surgical findings/ Clinical course Pathology Patient 1 49/M Weight loss (5 kg in 3 months), paroxysmal anxiety attacks, drenching sweats, chronic right flank pain 124/80 Clomipramine, 50 mg/day (anxiety) Adrenaline, 91/84 Noradrenaline, 860/1224 CT: 3 x 6-cm mass abutting upper pole of right kidney MIBG: negative Lobulated upper pole of kidney due to right renal artery branch running within posterior cleft Normal adrenal tissue Patient 2 41/M Migraines, chronic back pain, worsening hypertension, palpitations 145/85 Amitriptyline, 150 mg/day (migraine prophylaxis); amlodipine, 5 mg/day; ramipril, 5 mg/day; indapamide, 2.5 mg/day Adrenaline, 7/12 Noradrenaline, 485/1295 CT: No abnormalities MIBG: No abnormalities Normal findings on repeat urine studies after stopping amitriptyline — Patient 3 64/M Metastatic prostate cancer, poorly controlled hypertension 180/95 Imipramine, 100 mg/day (neuropathic pain); nifedipine, 180 mg/day; ramipril, 5 mg/day; chlorothiazide, 1000 mg/day Adrenaline, 115/99 Noradrenaline, 1070/1130 VMA, 33/38 CT: 1.5-cm left adrenal mass MIBG: negative Small left adrenal mass, macroscopically consistent with an adenoma Benign adrenal adenoma Patient 4 76/F Chronic hypertension, 15-month history of paroxysmal nausea and vomiting 144/80 Captopril, 25 mg/day Adrenaline, 65/129 Noradrenaline, 371/451 Dopamine, 1.55/2.02 CT: 1.5-cm left adrenal mass Smooth lesion palpable within left adrenal gland Enlarged adrenal gland (10.2 g; reference, 4 g) with thickened cortex but normal medulla Patient 5 75/M Sudden onset of intense back and left loin pain, chronic hypertension, weight loss (22 kg in 6 months), atrial fibrillation, diabetes, polymyalgia rheumatica 150/90 Warfarin, 5 mg/day; captopril, 25 mg/day; digoxin, 0.25 mg/day; isosorbide mononitrate, 60 mg/day; verapamil, 240 mg/day; prednisone, 5 mg/day; metformin, 2 g/day; rosiglitazone, 4 mg/day; thyroxine, 0.125 mg/day Adrenaline, 250 Noradrenaline, 720 Metanephrine, 1.68 Normetanephrine, 2.49 CT: 12-cm heterogeneous left adrenal mass (Box 2) Large blood clot with associated desmoplastic reaction occupying most of left adrenal gland Myelolipoma with haemorrhagic fat necrosis Patient 6 58/M Acute abdominal pain and hypertension, otherwise healthy 210/95 — Adrenaline, 2426/51 Noradrenaline, 18 370/464 Metanephrine, 13.3/0.8 Normetanephrine, 35.5/3.6 CT: 5-cm haemorrhagic left adrenal mass MRI (2 weeks after presentation): subacute haemorrhage into area without any distinct adrenal mass 12-cm dumbbell-shaped mass 3-cm phaeochromo-cytoma, large organising blood clot and necrotic tissue * Values separated by a forward slash represent separate collections, with abnormal values in bold. Reference ranges: adrenaline, < 100 nmol/d; noradrenaline, < 680 nmol/d; metanephrine, < 2.1 μmol/d; normetanephrine, < 5.6 μmol/d; VMA (vanillylmandelic acid), < 40 nmol/d; dopamine, < 3.0 μmol/d. †CT = computed tomography; MIBG = 131I-metaiodobenzylguanidine scanning; MRI = magnetic resonance imaging. 2 Computed tomography image of the haemorrhagic left adrenal mass in Patient 5 3 Medications and conditions that may cause false positive results of biochemical tests for phaeochromocytoma Medication or condition Test(s) confounded Tricyclic antidepressants Urinary catecholamines and metanephrines, plasma free metanephrines Clozapine Urinary catecholamines and metanephrines Phenoxybenzamine Plasma free metanephrines Calcium channel blockers Plasma noradrenaline, urinary noradrenaline, urinary adrenaline β-adrenergic blockers Urinary catecholamines and metanephrines, plasma free metanephrines (minor effect) α1-adrenergic blockers Urinary noradrenaline Sympathomimetics Urinary catecholamines and metanephrines, plasma free metanephrines Buspirone Urinary metanephrines Major physical or psychological stress* Urinary catecholamines and metanephrines, plasma free metanephrines * Hypoglycaemia, hypoxia, hypovolaemia, stroke, surgery, myocardial infarction, heart failure, severe pain, depression, panic disorder, sleep apnoea.

Jane L Harding MB BS · Michael W Yeh MD · Leigh W Delbridge MD, FRACS · Stan B Sidhu MB BS, FRACS · Bruce G Robinson MD, FRACP

Patients with chronic obstructive pulmonary disease and a stable daytime Pao2 of ≤ 55 mmHg (7.3kPa) live longer and have a better quality of life if provided with long-term continuous oxygen therapy. It is reasonable to offer continuous oxygen therapy also to patients with other lung diseases that cause chronic hypoxaemia. Indications for supplemental oxygen therapy during exercise (ambulatory oxygen therapy) and sleep (nocturnal oxygen therapy) are less clear.

Christine F McDonald PhD, FRACP · Alan J Crockett PSM, MPH · Iven H Young BSc, MB BS, PhD, FRACP

Trials online Last September, the International Committee of Medical Journal Editors (ICMJE) announced their intention to publish only “registered” clinical trials. Far from being another layer of red tape, well-conducted trials registers will ensure that the public has free access to information about all the drugs, interventions and devices that are currently being tested in clinical trials. As outlined by the ICMJE members in “Is this clinical trial fully registered?”, the new policy applies to trials that start enrolling patients after 1 July 2005. An Australian registry is on its way. For details see <http://www.nhmrc.gov.au/research/general/clincreg.htm>. An unkind cut Imagine that you are about to undergo surgery in a public hospital. After a long waiting time, you have finally been admitted and are waiting nervously in a ward, no doubt pondering the events of the day to come. Expecting to hear the rattle of a theatre trolley, you are surprised to get a visitor of a different kind, bearing bad news. Should surgical cancellations really come down to the wire like this? Schofield et al have studied the rates of and reasons for day-of-surgery cancellations in one Australian hospital. In response, Cregan discusses how we can make these cancellations rare events. Backstreet boys Anyone who cycles, runs or walks to work in the city learns to love the smell of exhaust fumes in the morning. Yet the components of these emissions can promote heart and lung disease, and even cancer. What should we tell urban exercisers? Sharman has some advice. (→ Clinicians prescribing exercise: is air pollution a hazard?) Tailor made A small but increasing number of drugs that target the specific genetic characteristics of patients or their tumours are now available in Australia. This area is exciting and promising, but, according to Hall et al, the steep learning curve associated with developing and using these drugs will be matched by the challenges of funding them. (→ Tailoring access to high cost, genetically targeted drugs) Notable anorexia complication It is not uncommon for patients with severe anorexia nervosa to develop electrolyte imbalance and abnormal renal function. The two women described by Roberts et al, however, had renal impairment from a pathological process not previously associated with the disease. (→ Severe renal failure and nephrocalcinosis in anorexia nervosa) Little bones . . . In the last issue, Young et al embarked on an update of the treatment of minor injuries in children. In the second half of their contribution to the Practice Essentials – Paediatrics series the same authors present a practical overview of the treatment of common fractures . . . and some sound advice on head injuries. (→11. Fractures and minor head injuries: minor injuries in children II) Old black dog Elderly people may experience depression somewhat differently to younger people, and the course of their illness and their management may be complicated by various co-existing medical problems. Commensurate with the complexity of the problem, many different treatment strategies have been recommended. In “Effectiveness of treatments for depression in older people”, Frazer et al have assembled a systematic review of the evidence for the usual (and unusual) therapies. Eye-opener In a subsistence society like the Solomon Islands, visual impairment is particularly disabling, but the country still lacks the ophthalmic surgery capacity to deal with the treatable causes. Participation in a visiting Australian eye team provided Baker with some valuable insights. (→ Sight-seeing in the Solomon Islands) Who needs home oxygen? While the current funding arrangements for domiciliary oxygen therapy generally require the involvement of a respiratory physician or cardiologist, any doctor can order home oxygen therapy at the patient’s expense. Who should benefit? In a position statement in “Adult domiciliary oxygen therapy. Position statement of the Thoracic Society of Australia and New Zealand”, the Thoracic Society of Australia and New Zealand provides clear guidance on when and how this useful adjunct should and should not be used. URTIs given notice To reduce unnecessary antibiotic use along the South Australian coast, Dollman et al conducted an information campaign in the community, on the place (and risks) of taking antibiotics for URTIs; they also visited GPs to discuss antibiotic guidelines and scoring systems for deciding whether to prescribe antibiotics. Read their success story in “A community-based intervention to reduce antibiotic use for upper respiratory tract infections in regional South Australia”. Confounded phaeo Six patients with poorly controlled hypertension or paroxysmal symptoms that make you think “phaeochromocytoma”. All have elevated 24-hour urinary catecholamine levels, but only one has the condition. What were the diagnostic confounders here? Find out in this issue’s Diagnostic Dilemmas by Harding et al. (→ Potential pitfalls in the diagnosis of phaeochromocytoma) Another time ... another place Operating Theatre information systems vary across sites, and there is, as yet, no strategy to rationalise these . . . the wide variety of operating theatre systems in use is a significant constraint and mitigates against detection of patterns of regular cancellation of elective surgery, and identification of best practice. New South Wales Auditor General, September 2003

Ray Kernutt was born on 2 September 1926 in the small town of Wagin, south of Perth. At the age of 10, he won a scholarship to attend a prestigious school in Perth, but went instead to a public school at Albany, where his sister at boarding school was able to look after him. After matriculation, he studied science at Perth University before winning a scholarship to study medicine at the University of Melbourne. He graduated with honours in 1949. Over the next few years, Ray gained his Master of Surgery and Fellowship of the Royal Australasian College of Surgeons while working as a Hospital Medical Officer at the Royal Melbourne Hospital. He gained his Fellowship of the Royal College of Surgeons in London in 1955, but cut short his postgraduate position as Surgical Registrar to return to Australia. In 1956, he was appointed founding Senior Surgeon at the new surgical unit at Box Hill Hospital, Melbourne, a position he held until retirement. Ray was no stranger to rural surgery. Having attained a commercial pilots licence in 1963, he offered a surgical service to doctors in Apollo Bay and Tocumwal. He was also absorbed in breeding cattle on his 200 acre farming property at Whittlesea. On retirement from public hospital surgery and a busy private practice, Ray became bored with a life of relaxing and playing golf and was drawn to the prospect of rural general practice. He joined a practice in the small town of Cohuna, and, although by then in his 70s, diligently revived his medical skills to become knowledgeable about diabetes, hypertension and respiratory medicine. His undiminished skill, judgement and speed in surgery were also much valued by his colleagues. Ray also came out of retirement on several occasions to provide lengthy locums at other locations where there was an acute shortage of doctors (eg, Christmas Island, Nauru and Castlemaine). It was fitting that he served his last active service in Cohuna before reluctantly retiring due to ill health and failing eyesight. Ray was set apart from his colleagues, not only because of his superb technique and speed — a “surgeon’s surgeon” — but also as a dedicated rural GP. In 2002, he was presented with the first Honorary Fellowship of the Australian College of Rural and Remote Medicine. His last illness was short and unexpected, following complications of vascular investigations. He died on 27 September 2004, and is survived by his second wife, Jillian, and children Graeme, David, Gillian, Paul and Jonathon. Peter W Graham

Peter W Graham

Quid pro quo Australian researchers have suggested that any extra life gained by healthy, elderly people using low-dose aspirin is just as likely to be lost through related adverse events. Nelson and colleagues used epidemiological modelling to simulate the broad implications of routine low-dose (75–150 mg) aspirin use in a hypothetical Victorian population of 10 000 men and 10 000 women, aged 70 years or older, all without overt cardiovascular disease. Calculating health outcomes by applying available evidence, they found that the prevention of 721 myocardial infarctions and 54 ischaemic strokes would be offset by excess episodes of serious bleeding — 1071 gastrointestinal and 130 intracranial. However, they acknowledged that due to statistical uncertainty, this balance could, in reality, tip either way — towards harm or benefit. A randomised controlled trial in elderly people could help settle the matter. BMJ Online First 20 May 2005 (www.bmj.com) Dementia linked to obesity Mid-life overweight and obesity increase the risk for dementia in later life, according to US researchers. They followed a large multi-ethnic cohort of 5564 women and 4712 men aged 40-45 years who underwent detailed health evaluations at the start of the study. At the conclusion of follow up — an average of 27 years later — dementia had been diagnosed in 713 participants. Compared with people of normal weight in mid-life, people who were obese in mid-life were 75% more likely to have dementia; and overweight people were 35% more like to have dementia. This increase in risk was most marked in women, and could not be explained by the presence of common co-morbidities, such as diabetes and hypertension. BMJ Online First 16 May 2005 (www.bmj.com) Death by breastfeeding? Sudden infant death is a potential, albeit extremely rare, complication of breastfeeding, say US authors. They reported two cases of male infants, aged 5 and 6 weeks, who died while their mothers were breastfeeding them. Both mothers were distracted at the time of infant death — one was shopping, and the other was watching a movie in a cinema. Given that pre-mortem evaluation and post-mortem examination revealed no abnormality in the infants, the authors concluded their deaths were caused by oronasal obstruction associated with breastfeeding. J Paediatr Child Health 2005; 41: 215-217 No more Misters? With the rise of non-medically qualified surgical care practitioners in the UK, the president of the Royal College of Surgeons of England, Mr Hugh Phillips, has suggested that there may be a good case for surgeons to use the title of "doctor" — principally so that patients will know whether the person treating them is a doctor, or not.1 The tradition of addressing a surgeon as Mr (or Miss) is thought to have its origin in the days of the unqualified barber surgeons, becoming a symbol of status when the Royal College of Surgeons of London was set up in 1745.2 1. Ann R Coll Surg Engl (Suppl) 2005; 87: 153 2. BMJ 2005; 330: 1103 Asleep on the job? Australian editorialists, Grunstein and Rogers, say that there is evidence of a harsher legal climate for doctors who continue to work despite sleep loss — just as society and the law is tiring of dangerous drivers escaping punishment due to "fall asleep" defences. Falling asleep behind the wheel, in most cases, is now recognised as being foreseeable, avoidable and an act of recklessness. In fact, since 2003, a US state law known as "Maggie’s Law" has held that causing the death of another person in a motor vehicle accident after driving without any sleep in the previous 24 hours is a criminal offence. Grunstein and Rogers believe that unless senior medical staff review their own work hours and those of their on-call registrars, it will be only a matter of time before there will be a Maggie’s Law for doctoring. Intern Med J 2005; 35: 269-271 Predicting sudden death A man’s heart-rate profile during exercise and recovery could help predict his risk of sudden death, according to French researchers. They conducted exercise testing in a cohort of 5713 asymptomatic men, enrolled in the Paris Prospective Study I, aged 42-53 years. Over a 23-year follow-up period, 81 subjects died suddenly. The risk of sudden death was increased in subjects with a higher resting heart rate (> 75 beats per minute), a smaller increase in heart rate during the exercise, and a smaller drop in heart rate after stopping the exercise test. The researchers say their findings are consistent with the idea than an underlying autonomic nervous system imbalance predisposes such subjects to life-threatening cardiac arrhythmias. They suggest that regular exercise training may help to prevent sudden death in those at risk, by shifting autonomic balance through an increase in vagal activity. N Engl J Med 2005; 352: 1951-1958 Dr Ann Gregory, MJA

Ann Gregory