Emergency Medicine Australasia (2004) 16, 91–94

Blackwell Publishing, Ltd. Letters to the Editor

February 2004161Letters to the EditorLetters to the EditorLetters to the EditorLetters to the EditorUnethical authorship practicesBennet and Taylor present an excellent overview of un-ethical authorship practices.1 This is timely, given theprogress of our college journal to the point where paperswith significant scientific merit are now more likely to befound within its pages. A related issue that was not afocus of Bennett and Taylor’s paper is that of competinginterests. A commentary by BMJ Editor Richard Smithon this topic is worth reading.2 Smith presents a cogentargument for all papers to be accompanied by a state-ment of competing interests, noting that identificationof competing interests does not preclude publication.

Contributors to our journal are increasingly likelyto have received sponsorship by pharmaceutical anddiagnostic manufacturers that can subtly influencethe objectivity of a review article or interpretation ofresearch findings. Furthermore, our current fundingclimate encourages early commercialization of intel-lectual property that can bring significant benefits toauthors of ‘successful’ research.

The issues of competing interests and the unethicalauthorship practices outlined by Bennet and Taylorare unlikely to go away, and I would argue that ourincreasingly competitive environment will make mattersworse, unless counterbalanced by reasonable attemptsto encourage openness on the part of authors — mostof whom are keen to do the right thing. Although thesteps implemented by major journals such as TheLancet and BMJ are imperfect because of human nature,they at least provide clear and useful guidelines forethical authors. Furthermore, they have a system inplace that can be used to expose authors who fail tocomply. For this reason, I would encourage the EditorialBoard of Emergency Medicine Australasia to followthe lead of major journals such as the BMJ and Lancetand include with all published articles statements ofauthor contribution and competing interests.

Conflicts of interest: None.

References1. Bennett D, Taylor DM. Unethical practices in authorship of

scientific papers. Emerg. Med. 2003; 15: 263–70.

2. Smith R. Beyond conflict of interest: Transparency is the key.BMJ 1998; 317: 291–2.

Simon Brown, MBBS, DA(UK), FACEM,PhD Scholar, Flinders University

Emergency PhysicianFremantle Hospital

Fremantle, WA, Australia

February 2004161Letter to EditorLetters to the EditorLetters to the Editor Letters to the Editor

Do differences exist in treatment and outcome for women with STEMI in Australia?

Overseas studies have reported that women havea higher mortality rate compared with men after ST-elevation myocardial infarction (STEMI ).1 Discrepanciesrelated to gender are reported for many aspects of carefor coronary artery disease, particularly for diagnosticcatheterization and invasive reperfusion procedures.1There is also evidence that women have longer door-to-needle (DTN) times for thrombolytic therapy comparedwith men after STEMI.1,2

We recently reported on a study which investigatedthe proportion of patients treated within the British HeartFoundation (BHF)3 90-minute call-to-needle (CTN) timebenchmark for thrombolysis of STEMI, and validatedthe 90-min benchmark with respect to mortality.4 ThisVictorian study included 1147 patients with STEMItransported to hospital by ambulance and eligible forimmediate thrombolysis. Sixty-one percent of patientsreceived thrombolysis within the 90-minute benchmark,and patients with CTN times greater than 90 minutes hadan increased risk of dying (RR 1.8; 95% CI, 1.3–2.7 ).

We conducted a subanalysis of the data to investigategender differences in treatment times and mortality.Data were analysed with descriptive statistics, χ2

analysis for comparison of proportions, Mann–WhitneyU-test for comparison of continuous variables andrelative risk for mortality using Analysis-IT™ software.Multiple logistic regression was performed usingSPSS. Table 1 compares age, ‘onset to call for ambulance’times, DTN and CTN times, and in-hospital mortalityfor the gender groups.

There were more men in the study (797; 69.5%).Women were older (P < 0.0001) and had longer delaysbefore calling for an ambulance (75 min vs 50 min; P =

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0.0061). Women had longer DTN times (40 min vs 36 mins)and CTN times (87 min vs 82 min), which althoughstatistically significant, is unlikely to be of clinical signi-ficance. They were also less likely to have DTN within30 min (31% vs 41%). Women were more than twice aslikely to die during the index hospital admission (14.3%vs 6%; RR 2.4 [95% CI 1.629–3.453] ), and this remainedstatistically significant after controlling for age (P =0.020) and onset to call time (P < 0.0001).

Our study has shown that women are less likely toreceive thrombolysis within recognized benchmarks3,5

and they are less likely to survive after STEMI. Thereis clear evidence that effectiveness of thrombolysisis related to the time delay between onset of symptomsand administration of therapy, and that treatment effectdeclines as time delay increases. Women had longerdelays before seeking help, which may be the majorfactor impacting on survival rates. The findings ofour study have been observed elsewhere.1,2

These observations highlight that importantdifferences exist in demographic, treatment and outcomeof patients after STEMI related to gender, but thatthere are not clinically significant differences in DTNor CTN times. Women may benefit from targetededucation about the symptoms of heart attack andthe importance of seeking help early, preferably bycalling for an ambulance.

Conflicts of interest: None.This work was supported by a grant from the

Australian Rotary Health Research Fund.

References

1. Chandra NC, Ziegelstein RC, Rogers WJ et al. Observations ofthe treatment of women in the United States with myocardialinfarction: a report from the National Registry of MyocardialInfarction-I. Arch. Intern. Med. 1998; 158: 981–8.

2. Barakat K, Wilkinson P, Suliman A et al. Acute myocardial

infarction in women: contribution of treatment variables toadverse outcome. Am. Heart J. 2000; 140: 740–6.

3. Weston CF, Penny WJ, Julian DG. Guidelines for the earlymanagement of patients with myocardial infarction.British Heart Foundation Working Group. BMJ 1994; 308:767–71.

4. Kelly AM, Kerr D, Patrick I et al. Call-to-needle times forthrombolysis in acute myocardial infarction in Victoria. Med.J. Aust. 2003; 178: 381–5.

5. Heart Foundation Australia. Guidelines for Reperfusion Therapyfor Acute Myocardial Infarction December 2002. Availablefrom URL: http://www.heartfoundation.com.au/downloads/reperfusion_guidelines/

Debra C Kerr, RN, BN, MBLResearch Program Manager

Joseph Epstein Centre for Emergency Medicine Research Department of Emergency Medicine

Western Hospital

Anne-Maree Kelly, MD, FACEMDirector

Joseph Epstein Centre for Emergency Medicine Research Department of Emergency Medicine

Western Hospital The University of Melbourne,

Melbourne, Vic., Australia

February 2004161Letters to the EditorLetters to the EditorLetters to the EditorLetters to the Editor

Don’t forget the A in eclampsia

Lew and Klonis have written a comprehensive reviewof the acute management of eclampsia and severepre-eclampsia. However we wish to raise two issuesrelated to this article.

First, we are concerned by the remarks regarding theuse of pulmonary artery catheters. The implication fromthe article is that the use of an epidural in the setting ofsevere pre-eclampsia requires the consideration of a pul-monary artery catheter. This is attributed to a relatively

Table 1. Comparison of DTN, CTN, and mortality by gender

Variables Male Female P RR (95% CI )

Age (median, range) 64 (21–93) 73 (31–93) < 0.0001Onset to call (median, range) 50 (0–6552) 75 (0–2902) 0.0061DTN within 30 min 329 (41%) 108 (31%) 0.0010 1.3 (1.120–1.597)CTN within 90 min 495 (62%) 202 (58%) 0.181 1.1 (0.969–1.195)DTN time (median [mins] ) 36 40 0.0034CTN time (median [mins] ) 82 87 0.0295Deaths 48 (6%) 50 (14.3%) < 0.0001 2.4 (1.629–3.453)

DTN, door-to-needle; CTN, call-to-needle.

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dated American reference by Clark and Cotton.1 Patientswith severe pre-eclampsia routinely have epiduralsinserted in the delivery suite without the need for apulmonary artery catheter. In fact most cases can bemanaged without a central venous catheter. Standardanaesthesia practice now is to use low concentrations oflocal anaesthetic and higher opiate doses to produce aless dense block, the so-called ‘walking epidural’. Thisavoids the precipitous fall in blood pressure seen witholder style regimens. The need for invasive monitoringdepends on the patient’s underlying cardiorespiratorycompromise and not on the ‘requirement for epiduralanaesthesia’. If invasive monitoring is required in thecritically ill parturient then it should be performed inconsultation with obstetric and anaesthesia colleagues.

Second, in a review article on the emergencymanagement of eclampsia and severe pre-eclampsia wewere surprised that there was no mention of the issuessurrounding airway management. In an eclampticpatient respiratory compromise may occur for manyreasons, these include seizures, pulmonary oedemaand as part of multiple organ dysfunction.2 As a result,establishing and maintaining an airway is an essentialpart of management in the emergency department.The obstetric airway presents both anatomical andphysiological challenges and is difficult in its own right.In the setting of pre-eclampsia these risks are furthercompounded by problems such as airway oedema,bleeding tendencies and an exaggerated hypertensiveresponse to intubation.2 As a consequence, intubationis fraught with danger for both the mother and fetus.It should not be undertaken lightly and an anaesthetistshould be involved where possible.

Conflicts of interest: None.

References1. Clark SL, Cotton DB. Clinical indications for pulmonary artery

catheterization in the patient with severe pre-eclampsia. Am. J.Obstet. Gynaecol. 1988; 158: 453–8.

2. Mushambi MC, Halligan AW, Williamson K. Recent developmentsin the pathophysiology and management of pre-eclampsia. Br.J. Anaesth. 1996; 76: 133–48.

Christopher John Reid, MBBS, FANZCASenior Anaesthetic Registrar

Andrzej Con, MBBS, FRCA Obstetric Anaesthetist

Royal London Hospital London

February 2004161Letters to the EditorLetters to the EditorLetters to the EditorLetters to the EditorReply

Thank you to Drs Reid and Con for their letter.It was not our intention to imply that patients with

severe pre-eclampsia undergoing epidural analgesiarequire invasive haemodynamic monitoring. SummaryTable 6 states that ‘Invasive haemodynamic monitor-ing should not be used routinely.’ Clark and Cotton’srelatively dated, but significant, article suggestsconsideration of the pulmonary artery (PA) catheter incritically ill patients who may be at risk of hypotensionsecondary to anaesthesia (be it epidural or generalanaesthetic related).1 The bottom line is that theroutine use of invasive haemodynamic monitoringin this disease is scientifically unproven and therefore,should be discouraged, although there may be veryrare instances where it may be required.

The comments regarding airway management aremuch appreciated. In preparing this article we decidedto concentrate on controversial areas relevant to emerg-ency management, which had been recently researchedin the international literature. Our primary aim was togive emergency physicians an update in this area. Wedecided that there was no controversy regarding theimportance of establishing and maintaining an airwayin severe pre-eclampsia or eclampsia (or indeed in anyemergency), although we are grateful to Reid and Confor bringing this up. There is no doubt that the eclampticpatient represents a difficult airway and an in-depthdiscussion of management of this was beyond the scopeof the paper. Similarly we did not go into depth onventilation of such patients. As we stated: ‘Key pointsin the ED management of severe pre-eclampsia andeclampsia are: resuscitation and treatment of complica-tions, prompt consultation and appropriate dispositionfor delivery of the foetus and placenta’. Implicit in thisstatement is immediate consultation with our obstetric,anaesthetic and intensive care colleagues.

Conflicts of interest: None.

Reference1. Clark SL, Cotton DB. Clinical indications for pulmonary artery

catheterization in the patient with severe preeclampsia. Am.J. Obstet. Gynecol. 1988; 158: 453–8.

Martin Lew, MBBS, DRANZCOG, FACEMEmergency Physician

Maroondah Hospital Emergency DepartmentMelbourne, Vic., Australia

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February 2004161Letters to the EditorLetters to the EditorLetters to the EditorLetters to the EditorAcute urinary retention secondary to kava ingestion

Kava extracted from the pepper plant (Piper methy-sticum), a shrub cultivated throughout the South pacific,is used as a medicinal extract or ceremonial beverage. InAustralia, it is widely taken as a drink in Northern Terri-tory Aboriginal cultures and in Tongan communities.

I report a case of a 61-year-old Tongan male whopresented to our emergency department with acuteurinary retention secondary to kava ingestion. Heattended after drinking one litre of kava that eveningas part of a community gathering and had returnedhome to find he was unable to pass any urine. Hehad been well the day prior to admission. He tried toovercome this problem by drinking a litre of milk,and presented to the department a few hours laterdistressed and complaining of suprapubic pain.On abdominal examination he had a large palpablebladder and the rest of the physical examination wasnormal. A 16 French indwelling catheter (IDC) wasinserted which drained 900 mLs of clear urine withimmediate relief of symptoms. Further history fromthe patient included adenocarcinoma of the lung, butthere was no history or symptoms of prostatic disease,nor dysuria. A full blood count, urea and electrolytesand a urinalysis were normal. At 6 hours postpresentation, the IDC was removed and the patientwas allowed to ambulate and drink fluids. He was ableto void twice that afternoon and was discharged home.A follow-up phone call confirmed the patient hadnot developed any further urinary difficulties. He did,however, recall that he had experienced similar lesssevere problems following previous meetings whichwere held at six-monthly intervals and involved largeamounts of kava consumption.

Kava has been classified as a non-narcotic, non-opiate,non-fermenting, non-alcoholic and physiologically non-addictive beverage.1 Although exact mechanisms ofaction remain ill defined, kava may exert its effects byblockade of voltage-gated sodium channels2 and by γ-aminobutyric acid (GABA) receptor and dopaminereceptor antagonism.3 Kavalactones are a heterogeneousgroup of lipid-like compounds found in the plant rootsand stems, which are responsible for the therapeuticeffects seen with kava use.

The desirable effects of kava are as an anxiolyticand spasmolytic, as well as imparting a sense of tran-quillity and euphoria on its drinker. Adverse effects

associated with chronic use or acute consumptionof large quantities have been documented in a smallnumber of case reports and letters1,4 and a pilot studyin an aboriginal community.5 These include delirium,choreoathetosis, dystonic reactions, ichthyotic eruptions,hepatic derangement, breathlessness, and non-specifichaematological and biochemical abnormalities.

This case reminds readers that the pharmacologicalproperties of kava are still poorly understood, andthat an additional mechanism of action may includeanticholinergic activity as well as other receptorantagonism. The paucity of research and literaturein this area indicates the need for ongoing identificationand publication of cases of kava toxicity.

The Therapeutic Goods Administration (TGA) an-nounced the recall of all 87 kava containing medicinalpreparations in August 2002, due to this incompletedata on kava and its uses, in the light of a few reportsof fatal hepatic injury.6 The plant is also listed asan import prohibited good and its availability isnow severely limited. In spite of this, it remains readilyavailable in those communities that historically haveused it and it will continue to lead to a potentially widespectrum of emergency department presentations.Kava ingestion should therefore be recognized andincluded in the routine history taking and examinationfor all at risk groups such as Tongan and NorthernTerritory Aboriginal populations.

Conflicts of interest: None.

References1. Chanwai G. Kava toxicity. Emerg. Med. 2000; 12: 142–5.

2. Gleitz J, Beile A, Peters T. Kavain inhibits veratridine activatedvoltage-dependent Na+-channels in synaptosomes preparedfrom rat cerebral cortex. Neuropharmacology 1995; 34: 1133–8.

3. Schelosky L, Raffauf C, Jendroska K et al. Kava and dopamineantagonism. J. Neurol. Neurosurg. Psych. 1995; 58: 639–40.

4. Spillane P, Fisher D, Currie B. Neurological manifestations ofkava toxicity. Med. J. Aust. 1997; 167: 172–3.

5. Matthews J, Riley M, Fejo L et al. Effects of the heavy usageof kava on physical health: Summary of a pilot survey in anaboriginal community. Med. J. Aust. 1988; 148: 548–55.

6. Therapeutic Goods Administration. TGA recalls over thecounter medicines containing kava. Media release TW/20,15th August 2002.

Nicola Leung, B. Med.Emergency Registrar, Toxicology Registrar

Department of Clinical Toxicology and PharmacologyNewcastle Mater Hospital, NSW, Australia