Anaesthetics

Inside chronic pain. An intimate and critical account . Lous Heshusius. New York: Cornell University Press, 2009 (xvii + 167 pp). ISBN 978 0 8014 4796 9. The lessons contained in this concise, personal narrative of an articulate patient crippled by chronic pain present a number of challenges to all who read it. There is a brief, scholarly foreword by David Morris, Professor of English at the University of Virginia, that sets the scene — conceptually, all chronic illness must be constructed at the crossroads of biology and culture. And there is an excellent coda by Scott Fishman, Professor of Anesthesiology and Pain Medicine at the University of California, Davis, which emphasises that the story you’ve just read is not unique. We have to ask ourselves, how can we consistently access all the options to put it together for these patients? How often do we even say, “I will go through this journey with you, and be your consultant”? More often than we care to admit, we neglect the social, spiritual and cultural dimensions of our patients’ experience in favour of a medical model of disease. The patients bear the largest burden on the journey towards recovery. How does one competently advocate for oneself when emotion and dysfunctional cognitions unduly influence the processes? Support systems are needed to negotiate a maze of clinicians, contradictory information and advice, and adversarial bureaucracies, yet time has to be spent alone in the present — not in the past or future — practising individualised coping strategies. This book will make you annoyed and frustrated — with the writer, her health care professionals, yourself, and with the system. Perhaps, you may also reflect on your management of chronic pain, and open new communication channels with your patients and your colleagues. Even undergraduates can learn from this little book, but I think it would be best read and digested by experienced clinicians. The only real downside is its North American setting. However, I can assure readers it all happens here too.

Robert D Helme

To the Editor: Treatment of critically ill pregnant women is challenging, and information on medication use during pregnancy is scant. We describe the case of a pregnant woman who required extracorporeal membrane oxygenation (ECMO), prolonged sedation and paralysis to treat acute respiratory distress syndrome secondary to pandemic (H1N1) 2009 influenza. A 34-year-old pregnant woman (G2P1) at 21 weeks’ gestation presented to a metropolitan hospital with level 1 intensive care unit facilities. She had known Grade 2 placenta praevia, a 5-day history of influenza-like symptoms, and no history of asthma, chronic disease or recent travel. On examination, she was severely hypoxic (PaO2, 27 mmHg on 15 L/min O2), conscious, tachypnoeic and speaking in single words. A chest x-ray showed extensive bilateral infiltrates (Box). She needed urgent endotracheal intubation but remained hypoxic despite maximal intensive mechanical ventilation. The patient was transferred to St Vincent’s Hospital, Sydney, where venovenous ECMO was commenced on arrival. Her oxygenation status improved and remained satisfactory. Mechanical ventilation was reduced (tidal volume, < 6 mL/kg; peak pressure, < 30 cm H2O) to avoid ventilator-induced lung injury. The patient required very high doses of morphine, fentanyl, midazolam, propofol, dexmedetomidine, cisatracurium and heparin during ventilation and ECMO. In addition, empirical treatment with oseltamivir (150 mg twice a day, Days 1–8), azithromycin and ceftriaxone was started on admission, before a bronchoalveolar lavage specimen tested positive for influenza A and pandemic influenza. Furthermore, a multiresistant Escherichia coli caused ventilator-associated pneumonia, which was treated with meropenem (1 g three times a day, Days 17–30). ECMO was discontinued on Day 19, when lung function had improved. No other organ failure developed. On Day 21, a tracheostomy was performed for severe weakness and weaning failure. The patient was weaned from the ventilator on Day 35 and was discharged home 2 weeks later, after making a full recovery. She gave birth by caesarean section at 35 weeks’ gestation. The baby was in good health and the patient recovered well — both left hospital 3 days after the birth. Information on the use of medication in pregnant women who require intensive care is limited, especially the use of neuraminidase inhibitors.1 We found little evidence on the safety of long-term use of neuromuscular blockers and sedation in pregnancy, with or without ECMO.2 Most literature on this topic describes short-term use of neuromuscular blockers and sedation. Dexmedetomidine has a short postmarketing history, and has therefore had limited use. Data from Australia and New Zealand indicate that 9% of patients admitted to an intensive care unit with pandemic influenza are pregnant. An estimated inhospital mortality rate of more than 16% in this population indicates the severity of the infection.3,4 Single-organ lung failure is a common feature of complicated pandemic influenza, and venovenous ECMO should be considered in these circumstances.2,4,5 Our case demonstrates that ECMO and the drugs necessary for its use can be used during pregnancy in a patient with influenza-associated acute respiratory distress syndrome, and that survival of the patient and fetus is possible. Chest x-ray of a pregnant woman with influenza-associated acute respiratory distress syndrome showing extensive bilateral infiltrates

Susan A Welch · Leone N Snowden · Hergen Buscher

Objective: To evaluate national practice for antibiotic prophylaxis in cardiac surgery with respect to the use of protocols, agent selection and duration of administration.Design, setting and participants: Two point-prevalence surveys of intensive care units in 24 public and 27 private hospitals performing cardiac surgery in Australia, conducted in 2004 and 2008, using a structured telephone questionnaire of the attending senior intensive care clinician in each unit.Main outcome measures: Existence of a protocol in the unit for antibiotic prophylaxis, specific antibiotic agents used and their duration of administration.Results: Between 2004 and 2008, reported protocol use increased from 58% to 80% (P = 0.02), while concordance with version 13 of the Australian Therapeutic guidelines: antibiotic for both choice of agent and timing (duration of administration) remained around 10%. Use of multiple agents was common, as was continued antibiotic administration after completion of surgery. Over 4 years, the proportion of cardiac surgical units reporting vancomycin administration for routine valve surgery prophylaxis doubled to 62% (P < 0.001).Conclusion: Despite an increase in reported protocol use for antibiotic prophylaxis in cardiac surgery, concordance with national antibiotic guidelines remained low, with duration of antibiotic administration deviating most from recommendations. Prophylactic vancomycin use appears to have increased substantially in recent years. Clinical implementation of recommended perioperative cardiac surgical antibiotic prophylaxis may not occur until supported by evidence from either a large prospective randomised study or standardised national surveillance of cardiac surgical site infection rates.

Timothy P Haydon FRACP, FJFICM, FANZCA · Jeffrey J Presneill MB BS, MBiostat, PhD · Megan S Robertson FRACP, FJFICM, FANZCA

Pregnancy and delivery are critical times for women with bleeding disorders, with mothers, and possibly their affected infants, being exposed to a variety of haemostatic challenges. Management of women with bleeding disorders during pregnancy involves a multidisciplinary team including, but not limited to, an obstetrician, an anaesthetist and a haematologist. This consensus document from the Australian Haemophilia Centre Directors’ Organisation (AHCDO) provides practical information for clinicians managing women with bleeding disorders during pregnancy. Included are: the expected physiological response in pregnancy in such women; management of pregnancy, labour and delivery, as well as obstetric anaesthesia issues, postpartum care, and reducing and treating postpartum haemorrhage; and management of infants at risk of a bleeding disorder and of bleeding in neonates. The guidelines were developed after extensive consultation, face-to-face meetings and revisions. The final document represents a consensus opinion of all AHCDO members. Where evidence is lacking, recommendations are based on clinical experience and consensus opinion.

on behalf of the Australian Haemophilia Centre Directors’ Organisation

New guidelines and a multidisciplinary approach have the potential to help patients in need while minimising inappropriate use of opioids With an estimated community prevalence of about 20%, chronic non-malignant pain represents a significant but neglected and often poorly managed problem in Australia. In 2007, the cost of chronic pain to the community was estimated at $34 billion, which included burden of disease and productivity costs, each accounting for one-third of the total, and one-fifth ($7 billion) attributed to health system costs.1 Its prevalence and associated costs will rise as the population ages. The causes of chronic non-malignant pain are many, including rheumatic disorders, injuries and musculoskeletal degenerative disorders, and vary greatly with age, sex and other demographic characteristics. Many doctors currently approach such pain from a narrow biomedical perspective. This too often defaults to the use of opioids under pressures including time constraints, patient demands, and limited access to supports such as pain clinics and physical therapies. The introduction of sustained-release prescription opioids in Australia two decades ago promised a new era in chronic pain management. These agents were preferred because they offered prolonged analgesia with a potentially lower risk of dependence and drug-seeking behaviour. Previously, short-acting opioids had often been prescribed, causing problems when peak effects of analgesia and euphoria alternated frequently with troughs marked by pain and opioid withdrawal. This created conditions conducive to dose escalation and the eventual development of dependence. The shining promise of the sustained-release prescription opioids has been dulled by two main problems. First, the long-term effectiveness and net benefit of opioids in the management of patients with chronic non-malignant pain remain uncertain, reflecting the biopsychosocial complexity of the underlying conditions and the difficulties of performing clinical trials in such heterogeneous populations.2 Second, increasing consumption of sustained-release prescription opioids has been accompanied by some disturbing developments, first reported from the United States. In 2000, drug overdose deaths from prescription opioids, especially from unsanctioned use, began to outnumber deaths from heroin and cocaine.3 Between 1997 and 2007, admissions for treatment of “abuse” rose by 456% for opioid analgesics and 5% for heroin.4 Australia may be starting to follow these US trends, with substantial increases in consumption of oral prescription opioids since 1990,5 and reports of diversion, injection and related harms.6 However, the extent of inappropriate opioid prescribing and of unsanctioned opioid use in Australia cannot currently be determined. Our information systems are not standardised across jurisdictions, are unable to capture all prescriptions (both private and funded by the Pharmaceutical Benefits Scheme), and are not available to intending prescribers and pharmacists. Three overlapping groups — patients with chronic non-malignant pain, patients with malignant pain, and illicit users (of heroin or prescription opioids) — form a potential common market for opioids, with flow-on effects if any group is inadequately managed. The idea of a continuum between opioid use for pain management and addiction underpins the idea of “universal precautions in pain medicine”.7 Inappropriate prescription can lead to problematic use and opioid dependence. The heroin shortage that started in 2000 in Australia was followed by increasing injection of prescription opioids, especially in rural areas and jurisdictions where heroin was scarcest.8 Increasing demand for prescription opioids may arise where there is unmet demand for opioid substitution treatment with methadone or buprenorphine. People on low incomes may be tempted to request and on-sell prescription drugs to the black market as demand and prices increase. These considerations underpin the desirability of a broader biopsychosocial framework for the assessment of patients with chronic non-malignant pain, and a greater role for non-pharmacological interventions. Such interventions are scarce and underfunded in primary care. Australia has the most developed training program for pain medicine worldwide, but there are too few specialists and there is great demand for pain clinics. In an effort to bring these complex issues to the fore, the Royal Australasian College of Physicians (RACP) has released a prescription opioid policy;9 the Box contains a summary of its recommendations. Reflecting the complex nature of the subject, the report was prepared by an interdisciplinary group, including representatives from the RACP, the Royal Australian College of General Practitioners, the Royal Australian and New Zealand College of Psychiatrists and the Faculty of Pain Medicine of the Australian and New Zealand College of Anaesthetists. The challenge is to provide a better balance between two, sometimes competing, objectives — encouraging more appropriate opioid prescription for patients with chronic non-malignant pain while reducing unsanctioned use of opioids, whether by patients or illicit users. No single health discipline can overcome these complex problems, but a truly multidisciplinary approach has the potential to achieve great advances. The current situation not only results in frustration for patients and families, but also undermines the good standing of the medical profession. The present unhappy cocktail includes patients with chronic, complex painful conditions; doctors who lack succinct uniform guidelines, real-time prescription monitoring information and ready access to relevant specialist advice; and a setting where authorities must minimise diversion of prescription opioids. In 2008, unmet demand for opioid substitution treatment was estimated to exceed the 39 000 patients then in such programs.10 Better tailoring of such treatment to also meet the needs of people dependent on pharmaceutical opioids, many of whom have never previously sought help, may attract and retain more patients in effective treatment. This would most likely decrease the demand for black-market prescription opioids. Australia has a unique opportunity to improve management of patients with chronic non-malignant pain and people who become dependent on opioids; to reduce inappropriate prescribing of opioids; and to avoid the problems that have bedevilled the US. The most important step required is establishing a group with sufficient authority to achieve wide consensus on an action plan and then implement and coordinate national change across jurisdictions, professions and disciplines (especially general practitioners and pharmacists). As most management of chronic non-malignant pain occurs in general practice, little will be achieved unless and until GPs are provided with more support and better linkages to critical specialties. Summary of recommendations of the Royal Australasian College of Physicians report9 1. Establish a national expert advisory group to develop a coordinated approach to implementing the recommendations below, to improve management of chronic non-malignant pain and reduce problematic use of pharmaceutical opioids. 2. Develop guidelines for management of chronic non-malignant pain appropriate for and accepted by general practitioners, integrating non-pharmacological elements of treatment with pharmacological approaches within a biopsychosocial framework, and providing widely accepted standards for audit and feedback. 3. Enhance clinical practice, with improved support for GPs and better linkages to relevant specialties, especially pain medicine and addiction medicine. 4. Improve information systems, with one national, web-based system that includes private and Pharmaceutical Benefits Scheme prescriptions and provides information for prescribers and pharmacists in real time. 5. Standardise regulation and control across jurisdictions. 6. Minimise unmet demand for opioid substitution therapy, and revise it for people dependent on pharmaceutical opioids to decrease the demand for black-market prescription opioids. 7. Improve integration of College training programs in the fields of pain medicine, addiction medicine, psychiatry and general practice. 8. Increase applied research to reduce gaps in knowledge and improve health service delivery.

Alex D Wodak FRACP, FAChAM, FAFPHM · Milton L Cohen MD, FRACP, FFPMANZCA · Malcolm D H Dobbin PhD, FAFPHM, MPH · Richard A Hallinan BMed, FAChAM · Mary Osborn MPubHlth

A 49-year-old man presented with verapamil toxicity complicated by hypotension and a junctional rhythm, in the context of deliberate self-poisoning with multiple drugs. The patient’s hypotension normalised following the early use of high-dose insulin euglycaemic therapy (HIET), without the need for additional vasopressors; it recurred when HIET was prematurely stopped, and again stabilised when HIET was recommenced. Consideration should be given to the early use of HIET in treating severe calcium channel blocker toxicity, rather than as a last resort after other therapies have failed. (MJA 2009; 191: 350-352) Clinical recordA 49-year-old man presented to a peripheral hospital emergency department 1–1.5 h after deliberately ingesting multiple medications: verapamil (unknown amount), controlled-release morphine sulfate (20 × 30 mg), diazepam (50 × 5 mg) and tramadol (15 × 200 mg). He was a smoker with a history of depression, ethanol misuse, chronic back pain, hypertension and a previous instance of deliberate self-poisoning with multiple drugs. At initial assessment, the patient’s vital signs were: temperature, 36.8°C; pulse, 84 beats/min; respiratory rate, 19 breaths/min; blood pressure (BP), 115/80 mmHg; oxygen saturation, 95% on room air; and Glasgow Coma Scale score, 14/15. He was drowsy, disorientated to time, and had 2 mm pupils that were equal and reactive. He had ataxia, dysarthria and was generally weak. His breath ethanol concentration was 0.172 mg%. Thirty minutes later, the patient was hypotensive (BP, 85/45 mmHg; pulse, 72 beats/min). He was treated with oxygen, 2 L intravenous (IV) 0.9% saline, a naloxone IV infusion (400 μg/h), and 10 mL IV 10% calcium gluconate. He was transferred to a tertiary referral centre and, on arrival (at 2.25 h after initial presentation), his BP was 85/45 mmHg, pulse was 64 beats/min, and an electrocardiogram (ECG) showed a junctional rhythm. Rapid sequence intubation (with propofol 40 mg + 20 mg IV and suxamethonium 100 mg IV) was performed for airway protection and ongoing management of haemodynamic instability, while metaraminol IV boluses (total, 0.7 mg) were administered. Activated charcoal (50 g) was given, and sedation was maintained with a propofol infusion. The patient remained hypotensive (BP, 75/45 mmHg; pulse, 56 beats/min) after intubation, so high-dose insulin euglycaemic therapy (HIET) was commenced at 3.5 hours after presentation. He was given dextrose (50 mL 50% glucose) and a 30 IU short-acting insulin IV bolus (~ 0.5 IU/kg), followed by a further bolus of 50 mL 50% glucose and a short-acting insulin IV infusion (30 IU/h) (Box 1). His BP improved to 110/70 mmHg at 4 hours, with a pulse of 82 beats/min and sinus rhythm on ECG, and he remained stable during transfer to the intensive care unit (ICU). The insulin infusion was abruptly stopped 5.5 hours after presentation, on arrival in the ICU. The patient’s hypotension subsequently recurred (systolic BP, 70 mmHg; pulse, 75 beats/min), prompting administration of 500 mL IV Gelofusine (a colloidal plasma volume substitute; B. Braun, Sydney, NSW) and commencement of an adrenaline IV infusion (20 μg/min). The insulin infusion (30 IU/h) was restarted at 8.5 hours, and his BP again stabilised (Box 1). The propofol IV infusion was gradually increased from 50 mg/h to 150 mg/h between 5.5 hours and 11.5 hours after presentation, and a noradrenaline IV infusion was commenced at 9.5 hours to maintain normotension. At 15.5 hours, pulmonary artery catheter measurements showed a high cardiac index (5.1 L/min/m2; reference range [RR], 2.5–4.0 L/min/m2) and a low systemic vascular resistance index (1047 dynes·s/cm5/m2; RR, 1900–2400 dynes·s/cm5/m2); the patient’s pulse was 85 beats/min and BP was 140/60 mmHg. HIET was continued and the patient remained haemodynamically stable. Adrenaline and noradrenaline were weaned off (at 17.5 hours and 23.5 hours, respectively), despite the propofol infusion rate being increased to 500 mg/h at 18.5 hours. Once sedation was withdrawn, the patient was extubated at 26.5 hours. Insulin was weaned over 5 h and discontinued at 30.5 hours; dextrose was stopped 1 h later. The patient was transferred to the observation ward and discharged well later that day, after psychiatric clearance. During treatment with HIET, the patient’s blood glucose levels were checked hourly and ranged from 6.6 mmol/L to 13.2 mmol/L (RR, 3.5–5.5 mmol/L). He received about 25 g/h of dextrose (mostly as 50% dextrose infusions). Potassium and magnesium levels were also serially monitored; the minimum potassium level was 2.7 mmol/L (RR, 3.5–5.0 mmol/L) at 8.75 hours, and the magnesium level troughed at 0.5 mmol/L (RR, 0.75–1.05 mmol/L) at 15 hours. These were corrected with a total of 200 mmol of potassium chloride and 20 mmol magnesium chloride. DiscussionHIET is an increasingly accepted therapy for calcium channel blocker (CCB) toxicity, but reports of its use are limited and it remains controversial. Indeed, the scarcity of severe CCB poisoning cases means that a randomised controlled trial of HIET may not be feasible.1 Treating clinicians who seek advice from clinical toxicologists are often hesitant about the high doses required and the potential for adverse effects. Such hesitancy is potentially harmful, as a hypotensive patient with a CCB overdose who otherwise appears well is at risk of abrupt lethal cardiovascular collapse.1 HIET is traditionally recommended after other therapies have failed.2,3 This case report aims to raise awareness of HIET for the treatment of CCB toxicity and supports its early use, rather than as a last resort.4 Verapamil binds the alpha-1 subunit of L-type calcium channels, preventing the intracellular influx of calcium.5 These channels are functionally important in cardiac myocytes, vascular smooth muscle cells, and islet beta cells.5 Verapamil’s cardiac toxicity results from excessive negative inotropy, negative chronotropy and negative dromotropy, characterised by myocardial depression, sinus bradycardia, and atrioventricular node blockade.4 Vascular smooth muscle tone is impaired, resulting in decreased afterload, systemic hypotension, and coronary vasodilation.5 Less well known are the metabolic effects of CCBs such as verapamil. Under the stress of the drug-induced shock state, the cardiac myocytes shift from using free fatty acids, their favoured “resting state” energy substrate, to carbohydrates.3,4 CCB toxicity also impairs the uptake of glucose and free fatty acids by cardiac myocytes3,4 and inhibits calcium-dependent mitochondrial activity required for glucose catabolism.3,4 Furthermore, insulin release is dependent on calcium influx into islet beta cells through L-type calcium channels.3,4 Thus, CCB toxicity can cause hypoinsulinaemia,3,4 which, in conjunction with CCB-induced insulin resistance, may lead to hyperglycaemia and a ketoacidotic state.6 Atropine, calcium boluses and infusions, glucagon, inotropes, vasopressors, and cardiac pacing have all been advocated for managing CCB toxicity, despite questionable efficacy.3,4,7-9 For instance, the evidence for glucagon is limited to small, non-blinded animal studies where no survival benefit or improvement in mean arterial pressure was shown, although heart rate improved in some cases.7 Rarely, heroic measures such as extracorporeal circulatory support and intra-aortic balloon counterpulsation have been successfully employed.5,10 HIET was first used to treat verapamil toxicity in humans in 1993, with a favourable outcome.6 Since then, in addition to animal studies, there have been nearly 70 cases reporting the beneficial use of HIET in humans, with an overall survival rate of 85%.8 However, to our knowledge, use of HIET in humans before the administration of glucagon or vasopressors has only been reported once.6 There have been some reports of HIET failure in treating CCB toxicity, although the dosing of insulin was low or uncertain, or it was used late.6,8 Early use of HIET may be more effective than HIET rescue therapy, as CCB-induced insulin resistance is greatest in the first 24 hours2 and the maximal haemodynamic benefit of HIET may not occur immediately.6 HIET may allow the heart to overcome metabolic starvation in CCB toxicity, which compounds the direct CCB impairment of myocardial contractility.3,4 Insulin increases glucose and lactate uptake by myocardial cells and improves function without increased oxygen demand.11,12 It also induces pyruvate dehydrogenase, hastening myocardial lactate oxidation, and helps clear the cytosol of glycolytic byproducts that impair calcium handling and cause diastolic dysfunction.3 Insulin promotes excitation–contraction coupling and contractility because enhanced glycolysis promotes increased sarcoplasmic reticulum-associated calcium ATPase activity and increased cytoplasmic calcium concentrations, and promotes calcium entrance into mitochondria and sarcolemma.3 HIET may be best used adjunctively with other measures such as catecholamines, for two reasons. First, insulin-mediated inotropy is not catecholamine-mediated, and is not affected by β blockers.3 Second, although insulin appears to improve myocardial contractility, it has no chronotropic effect and may cause vasodilation.3,8 HIET is safe, and adverse events are predictable, uncommon, and easily managed.2,8 The maximum safe dose of insulin is unknown, but loading doses of 0.5–1.0 IU/kg followed by infusions of 0.1–2.5 IU/kg/h are typically used.8 Interestingly, neither the inadvertent administration of a 1000 IU insulin loading dose for verapamil toxicity13 nor treatment of toxic cardiogenic shock for 2 days with a 6 IU/kg/h insulin infusion had any adverse effects.14 Adverse effects of HIET include hypoglycaemia, hypokalaemia, hypomagnesaemia, and hypophosphataemia.2,6,8 Although these are rarely clinically significant, they necessitate careful monitoring. Hypoglycaemia (blood glucose < 3.3 mmol/L) occurred in 16% of 55 published cases,8 and no cases of hypoglycaemia within 24 hours of CCB overdose were noted in Greene and colleagues’ series of seven cases.2 Greene et al also reported a mean dextrose requirement of 0.05 g/kg/h (range, 0–0.17 g/kg/h), although the mean blood glucose level exceeded the euglycaemic range.2 Some cases of severe CCB toxicity in patients presenting with hyperglycaemia do not require any additional glucose administration despite high-dose insulin therapy,15 and hypoglycaemia may be more likely in milder cases without marked hypotension.8 In addition, hypokalaemia (potassium < 3.5 mmol/L) was noted in only two patients in Greene et al’s small series, with a minimum potassium level of 2.8 mmol/L.2 Excessive correction of hypokalaemia should be avoided, because it reflects the intracellular shift of potassium from the extracellular compartment due to the action of insulin, rather than a potassium-depleted state.4 Interestingly, hypokalaemia in HIET may augment myocardial contractility by enhancing calcium entry during systole, and increased intracellular potassium may have a membrane-stabilising effect in excitable cells.4,6 In conclusion, we advocate consideration of the early use of HIET (as detailed in Box 2) for the prevention and treatment of life-threatening complications from potentially lethal CCB overdoses. HIET is safe, inexpensive and freely available, and suitable for use even in remote settings before transfer to a referral centre. 1 Early changes in the patient’s systolic blood pressure (SBP) and heart rate, relative to treatment with high-dose insulin and adrenaline infusions Following administration of a 0.5 IU/kg short-acting insulin bolus 3.5 hours after presentation, a short-acting insulin intravenous infusion (0.5 IU/kg/h) was commenced (black line), and the patient’s blood pressure improved. The infusion was abruptly discontinued 2 hours later and the patient again became hypotensive. This resolved following commencement of an adrenaline infusion (20 μg/min) (grey arrow), and the insulin infusion (0.5 IU/kg/h) was restarted 8.5 hours after presentation (black arrow). 2 Recommended high-dose insulin euglycaemic therapy protocol,3,4,9 based on the clinical experience of the Western Australian Toxicology Service, published case reports, reviews and animal studies Commence therapy with: Glucose 25 g (50 mL of 50% solution) IV bolus, unless marked hyperglycaemia (blood glucose > 22 mmol/L) is present Short-acting insulin 1 IU/kg bolus to maximally saturate insulin receptors Continue therapy with: Short-acting insulin infusion starting at 0.5 IU/kg/h and titrated every 30 min to a maximum of 5 IU/kg/h* Dextrose 25 g/h IV infusion titrated to maintain euglycaemia (blood glucose, 5.5–14 mmol/L); central venous access may be required to allow use of concentrated solutions (eg, 50% dextrose) and limit excess volume administration Monitor: Glucose — every 20 min for first hour, then every 1 h Potassium — replace only if < 2.5 mmol/L and there is a source of potassium loss Therapeutic end points: Improvement in myocardial ejection fraction (> 50%); increased BP (systolic BP > 90 mmHg in adults) Adequate heart rate (> 60 beats/min) Resolution of acidaemia; euglycaemia; adequate urine output (1–2 mL/kg/h) Reversal of cardiac conduction abnormalities (QRS interval < 120 ms) Improved mentation Therapy is weaned after the withdrawal of other vasopressors, as cardiotoxicity resolves. Dextrose may be required after cessation of insulin. IV = intravenous. BP = blood pressure. * The maximum safe and effective rate of infusion is unknown but may be even higher than 5 IU/kg/h. In animal studies, insulin infusions as high as 10 IU/kg/h have been safely used.11

Christopher P Nickson MB ChB, DTMH, GCertClinTox · Mark Little FACEM, DTMH, MPHTM

To the Editor: Duke and colleagues recently reported the excess mortality and extra bed-days caused by intensive care access block in metropolitan Melbourne.1 Access block is an important patient safety issue, and we report here additional data that support their results. The Australasian Clinical Indicator Report: 2001–2007, published by the Australian Council on Healthcare Standards (ACHS), reported that the national rate of intensive care access block was 5.9% in 2007, a statistically significant (P < 0.001) increase from 5.3% in 2001.2 There were large differences between states, with higher rates in Victoria in 2006 and 2007. In 2007, the rate of cancellation or postponement of elective major surgery due to lack of intensive care beds was 3.1%, and the rate of interhospital transfer was 1.3%.2 Other rates reported were: the rate of discharge from the intensive care unit delayed more then 12 hours (16.6%) and the rate of after-hours (between 18:00 and 06:00) discharge (17.5%).2 The Victorian rate of after-hours discharge from the intensive care unit, calculated from seven participating hospitals in 2007 (21.6%),2 is comparable with the rate of after-hours step-down to a low-acuity ward found in Duke et al’s study — 18.6% for the period July 2004 to June 2006.1 The ACHS Clinical Indicator Program provides national and peer-group benchmarking to health services participating in its accreditation program, the Evaluation and Quality Improvement Program (EQuIP). Through its annual Clinical Indicator Report, the data are analysed and allow identification of unsatisfactory rates and wide variations in practice. Such national data can help health policymakers identify areas for potential improvement in the standards of health care delivery, particularly in areas where indicators address access. Duke and colleagues’ salient article illustrates the importance of such data being utilised for this purpose.

Helen E Stark · Chris N Maxwell · Robert W Gibberd

Extracorporeal membrane oxygenation (ECMO) is a technique that involves oxygenation of blood outside the body, and provides support to selected patients with severe respiratory or cardiac failure. The two major ECMO modalities are venoarterial and venovenous. Data from several randomised trials support the use of ECMO in neonatal respiratory failure, and a recent randomised controlled trial of ECMO in adults has produced encouraging results. The evidence base for ECMO use in cardiac disease is developing, but progress has been slowed by considerations of clinical equipoise and evolving indications for ECMO. Advancing ECMO technology and increasing experience with ECMO techniques have improved patient outcomes, reduced complications and expanded the potential applications of ECMO. Awareness of the indications and implications of ECMO among doctors managing patients with severe but potentially reversible respiratory or cardiac failure may help facilitate better communication between health care teams and improve patient recovery.

Steven J Lindstrom MB BS(Hons), BMedSc(Hons) · Vincent A Pellegrino MB BS, FRACP, FJFICM · W Warwick Butt MB BS, FRACP, FJFICM

Objective: To examine the response of the Victorian State Trauma System to the February 2009 bushfires.Design and setting: A retrospective review of the strategic response required to treat patients with bushfire-related injury in the first 72 hours of the Victorian bushfires that began on 7 February 2009. Emergency department (ED) presentations and initial management of patients presenting to the state’s adult burns centre (The Alfred Hospital [The Alfred]) were analysed, as well as injuries and deaths associated with the fires.Results: There were 414 patients who presented to hospital EDs as a result of the bushfires. Patients were triaged at the emergency scene, at treatment centres and in hospital. National and statewide burns disaster plans were activated. Twenty-two patients with burns presented to the state’s burns referral centres, of whom 18 were adults. Adult burns patients at The Alfred spent 48.7 hours in theatre in the first 72 hours. There were a further 390 bushfire-related ED presentations across the state in the first 72 hours. Most patients with serious burns were triaged to and managed at burns referral centres. Throughout the disaster, burns referral centres continued to have substantial surge capacity.Conclusions: Most bushfire victims either died, or survived with minor injuries. As a result of good prehospital triage and planning, the small number of patients with serious burns did not overload the acute health care system.

Peter A Cameron MB BS, MD, FACEM · Biswadev Mitra MB BS, MHSM, FACEM · Mark Fitzgerald MB BS, FACEM · Carlos D Scheinkestel FRACP, FJFICM, DipDHM · Andrew Stripp BBSc(Hons), MSc · Chris Batey CCRN · Louise Niggemeyer RN, ICCert, MEd · Melinda Truesdale MB BS, FACEM, GradDipHSM · Paul Holman ASM, GradDipHealthAdmin, MACAP · Rishi Mehra MB BS, PGDipEcho, FANZCA · Jason Wasiak MPH, BN, GradDipCritCareNurs · Heather Cleland MB BS, FRACS

Objectives: To measure the prevalence of interventions used to circumvent intensive care access block and to estimate the attributable mortality and additional hospital bed-days associated with them.Design and setting: Retrospective observational study of 11 adult public hospital intensive care units (ICUs) in Melbourne, Victoria, July 2004 – June 2006.Main outcome measures: Prevalence of five interventions in response to access block; attributable fatalities and/or increased length of stay associated with each.Results: 21 896 ICU admissions and 3039 inhospital deaths (13.9%) were screened. All hospitals reported ICU access block. There were 6787 interventions for access block (mean, 9.3/day) — 4070 (18.6% of admissions) instances of after-hours step-down from an ICU to a low-acuity ward; 1115 (5.1%) delays in an emergency department > 8 hours; 895 (4.1%) postponed major surgeries; 487 (2.2%) interhospital transfers; and 220 (1.0%) instances of premature cessation of intensive care. Based on published risk estimates, these interventions may have resulted in 91.1 (95% CI, 34.7–147.2) attributable deaths and 4368 (95% CI, 333–10 050) additional hospital bed-days each year.Conclusions: Intensive care access block is frequent, and measures to circumvent it increase mortality and length of stay. Further study of the health and financial implications of access block are warranted.

Graeme J Duke MD, FJFICM, FANZCA · Michael D Buist MD, FRACP, FJFICM · David Pilcher FRACP FJFICM, MRCP · Carlos D Scheinkestel FRACP, FJFICM, DipDHM · John D Santamaria MD, FRACP, FJFICM · Geoff A Gutteridge FJFICM, FANZCA · Peter J Cranswick FJFICM, FANZCA · David Ernest FRACP, FJFICM, MHlth · Craig French FJFICM, FANZCA · John A Botha MMed, FRACP, FJFICM

To the Editor: Sondergaard is essentially correct in his criticism of the Australian and New Zealand College of Anaesthetists (ANZCA).1 And ANZCA president Leona Wilson’s obfuscatory response to the criticism provided me with little reassurance.2 We all know that our health care system is “highly complex” and involves multiple jurisdictions, but these points have no relevance in determining whether Sondergaard is adequately trained and competent to work in Australia as a specialist. To decide that someone with his history and qualifications cannot give anaesthesia unsupervised is patently nonsensical, as is the insistence that experienced overseas specialists must take the College’s final exams. All of us who were Fellows of the ANZCA precursor, the Faculty of Anaesthetists of the Royal Australasian College of Surgeons, were granted automatic Fellowship of the ANZCA on its formation in 1992, as were some senior practitioners who had never sat the Faculty exams. The College can, it seems, arbitrarily waive the exam requirement for some, and it regularly awards Honorary Fellowships to distinguished overseas visitors. However, these doctors are not the competent working clinicians with overseas qualifications who would, if they could, take up vacant positions in rural areas, such as Katoomba just outside Sydney. Here, in October last year, a woman in labour was turned away from a hospital for want of an anaesthetist and gave birth in an ambulance by the roadside. I worked as a specialist anaesthetist in Sweden for nearly 2 years and can verify that Scandinavia produces competent anaesthetists. The attitude of the ANZCA to overseas-trained specialists seems elitist and denies the Australian people access to the services of competent people who happen to have learned this essential specialty elsewhere.

James F Wilkinson

Objective: To estimate the effect of day of the week on the odds of being discharged alive from an intensive care unit (ICU).Design: A longitudinal analysis of risk of discharge by day of the week.Setting and patients: 4569 patients admitted to the ICU of St Thomas’ Hospital, London, from 2002 to 2006.Results: The odds of being discharged alive were lowest on the weekend and literally climbed during the week.Conclusion: Our results show a frightening pattern of discharge from an ICU ward, most likely caused by a complex web of specialist availability and patient demand.

Adrian G Barnett BSc(Hons), GStat, PhD(Maths) · Nicholas Graves BA(Hons), MA, PhD(Econ) · Ben S Cooper BSc, MSc, PhD · Rahul Batra BS, MD · Jonathan D Edgeworth MB BChir, BSc, PhD

Objective: To identify current prescribing and administration practices in relation to intravenous potassium chloride (IV KCl).Design and setting: A prospective multicentre assessment of IV KCl prescribing and administration at six public hospitals (three large metropolitan hospitals, a smaller metropolitan specialty hospital, and two rural hospitals) in Victoria between August and December 2006. Data were collected for either a 4-week period or for 200 IV KCl orders, whichever occurred first, in clinical areas where concentrated KCl ampoules were available.Main outcome measures: Number and type of IV KCl prescriptions and dose administrations; method of preparation and administration of each dose.Results: A total of 888 prescriptions and 1088 administrations were assessed across the six hospitals. There were 69 different types of orders for IV KCl, varying in either concentration or volume. KCl ampoules were used in 59% of all administrations of IV KCl. In instances where the prescription matched an available premixed IV KCl infusion, the premix was used on 89% of occasions.Conclusions: There is significant variability in the prescribing and administration of IV KCl in these Victorian hospitals. New formulations of premixed IV KCl infusions may enable the removal of ampoules from patient care areas. The medical profession can play a major role in driving the adoption of consistent practice and supporting and leading this important safety initiative.

Melita A Van de Vreede BPharm, MHSM, GradDipHospPharm · Sally G Wilson BPharm, PhD, GradDipHospPharm · Michael J Dooley BPharm, GradDipHospPharm

Australia is an attractive workplace for overseas-trained specialist (OTS) anaesthetists. The path to recognition of the qualifications and experience of OTS anaesthetists is, in my opinion, bogged down in an overzealous assessment procedure. The Australian and New Zealand College of Anaesthetists (ANZCA) is a self-proclaimed professional body that is not subject to regulation by the federal government. Medical authorities such as the Australian Medical Council and state medical boards have no influence on ANZCA’s assessment criteria and procedures. In my opinion, the current state of affairs with regard to assessment of OTS anaesthetists can not be justified.

Soren Sondergaard DMSc, MD

To the Editor: It has been well established that traditional inhalational anaesthetic agents can cause mild and sometimes fulminant liver failure.1 However, while newer inhalational agents are a theoretical cause of hepatotoxicity, such cases have rarely been reported.2,3 We describe desflurane-induced acute liver failure in a 53-year-old woman with achalasia, hypertension, type 2 diabetes mellitus and hyperlipidaemia. She underwent a Heller myotomy for treatment of the achalasia in late 2004. During anaesthesia, desflurane was administered (1.2 minimum alveolar concentration [MAC]) via a Datex–Ohmeda Aestiva/5 anaesthesia delivery system (GE Healthcare, Sydney, NSW). After the operation, her serum alanine aminotransferase (ALT) concentration peaked at 943 U/L (reference range, < 35 U/L). This was attributed to antibiotic toxicity. As the initial myotomy was inadequate, the surgery was repeated 10 days later with desflurane (0.9 MAC) anaesthesia. The patient developed acute liver failure 96 hours after surgery (serum ALT level, 11 600 U/L; pH, 7.06; international normalised ratio, 3.7) and died despite supportive management. A postmortem examination confirmed massive hepatic necrosis and significantly elevated trifluoroacetyl chloride-specific IgG4 antibodies (optical density, 0.585; reference range, < 0.233) — consistent with an inhalational agent being the cause of the necrosis. There are few similar cases of desflurane-induced acute liver failure in the literature to date2,3 and none, to our knowledge, in Australia. Fulminant hepatic necrosis induced by halothane, the original offending agent, occurs in about one in 35 000 adults. This is thought to be immune-mediated and appears to be directly correlated with the metabolism of the anaesthetic, catalysed by cytochrome P450 2E1, to trifluoroacetylated hepatic proteins. The altered protein is seen as “non-self”, generating an immune response that, on re-exposure, leads to inflammation and cellular death.4 Desflurane is metabolised to inorganic fluoride and trifluoroacetyl chloride. However, due to a lower blood : gas partition coefficient and its resistance to degradation (as a result of replacement of chlorine by fluorine at the α-carbon position), desflurane is metabolised by hepatic enzymes to a lesser extent than halothane, enflurane and isoflurane.4 Thus, the degree of hepatic metabolism appears to be related to the potential for hepatic injury, as seen clinically. Evidence for immune-mediated, allergic sensitisation continues to emerge. Identification of IgG4 antibodies, the rarest and most IgE-like immunoglobulins, strongly suggests an allergic component in the pathophysiology of this disease.5 Although hepatotoxicity is a rare complication of the newer inhaled volatile agents, it may have devastating consequences. Anaesthetic agents should be considered in the differential diagnosis of hepatotoxicity, especially in the context of extreme elevation of serum transaminases, suggesting the presence of massive hepatic necrosis. In this case, postoperative ALT elevation was attributed to antibiotic — rather than desflurane — toxicity, with disastrous results following re-exposure, a scenario that might have been prevented if recognised earlier. A full incident report was made at the tertiary hospital involved, and the death was reported to (and examined by) the coroner. The main recommendation made from the case was that inhalational agents should be avoided in the setting of hepatitis.

Marcus W Chin · Dolores B Njoku · Gerard MacQuillan · Wendy S Cheng · Nickolas Kontorinis

The level of documentation of vital signs in many hospitals is extremely poor, and respiratory rate, in particular, is often not recorded. There is substantial evidence that an abnormal respiratory rate is a predictor of potentially serious clinical events. Nurses and doctors need to be more aware of the importance of an abnormal respiratory rate as a marker of serious illness. Hospital systems that encourage appropriate responses to an elevated respiratory rate and other abnormal vital signs can be rapidly implemented. Such systems help to raise and sustain awareness of the importance of vital signs.

Michelle A Cretikos MB BS, MPH, PhD · Rinaldo Bellomo MD, FJFICM · Ken Hillman MB BS, FRCA, FJFICM · Jack Chen MB BS, MBA · Simon Finfer MB BS, MRCP, FRCA · Arthas Flabouris MB BS, FANZCA, FJFICM

Textbook of regional anesthesia and acute pain management. Admir Hadzic, editor. New York: McGraw-Hill Medical, 2007 (xviii + 1259 pp). ISBN 978 0 07 144906 X. In this text, Hadzic aims to provide the scientific basis for the practice of regional anaesthesia, integrating it into the multimodal approach to acute pain management. He has selected 126 contributors, most of whom are American, to write the 83 chapters, nearly all of which are multiauthored. The result is a well coordinated treatise on every aspect of regional anaesthesia, serving as an excellent introduction to the postgraduate study of the subject. No topic is ignored — community practice, the austere environment, and the principles of statistical methods of research are unique inclusions. As well, the new techniques of ultrasound-guided nerve blocks are well covered. The management of postoperative pain introduces latest concepts including multimodal analgesia (although the organisation of an acute pain service has a rather rigid North American approach). The book is very well laid out, punctuated with coloured boxes containing “Clinical pearls” and tabular summaries. It is profusely illustrated with anatomical diagrams, photographs of positioned patients, equipment and some anatomical dissections. While these break up the text into easily readable bites, the photographs are occasionally overdone; repetitive images showing slightly different needle positions add little to the clear descriptions. Some anatomical drawings are too diagrammatical and do not give an easy understanding of the point being made. A final minor criticism: there are slight inaccuracies in the description of the surface anatomy of some nerve blocks, particularly those of the ilioinguinal and iliohypogastric nerves, and of the greater occipital nerve. A newcomer to the art of regional anaesthesia needs three guides — clear textbooks, access to accurate recent concepts and helpful teachers. This textbook admirably fills the first two requirements.

Ken W Sleeman

Objective: To assess the outcomes for chronic dialysis patients requiring admission to an intensive care unit (ICU) or high dependency unit (HDU).Design: Retrospective audit of prospectively collected data from local and national databases.Setting: The ICU and HDU at a tertiary referral hospital.Participants: 70 chronic dialysis patients admitted between 2001 and 2006.Main outcome measures: Unit and hospital mortality, recurrent admission patterns and median survival after discharge from hospital.Results: For patients’ last admissions, mortality in the ICU or HDU was 17% and in hospital was 29%. The 12 deaths in the ICU or HDU occurred a median of 18 hours (range, 3–203 hours) after admission, reflecting the severity of their underlying illness. The independent predictors of death in hospital were age and the number of non-renal organ systems failing. Patients with pulmonary oedema had a lower risk of death than patients admitted for other reasons. Although 21 patients accounted for 55 of 104 admissions (53%), recurrent admissions to the ICU or HDU generally occurred during different hospital admissions. They were not associated with a higher risk of death in hospital. Patients discharged home had a median survival of 2.25 years, and a median survival of 3.5 years from starting dialysis. The median survival for patients on dialysis in Australia in general is 4.5 years (Australia and New Zealand Dialysis and Transplant Registry).Conclusion: Dialysis patients discharged home after an ICU or HDU admission have survival similar to that of Australian dialysis patients generally.

Sivagnanavel Senthuran FRCA, FJFICM · Hiran Bandeshe BSc, BEng(Biomed) · Dwarakanathan Ranganathan FRCP, FRACP · Robert Boots PhD, FRACP, FJFICM

Christmas this year will be marked for us by the arrival of our first grandchild, so as a mother and obstetrician I am receiving a steady stream of questions from my daughter on pregnancy-related matters — not the least of which relate to the use of analgesia in labour. At her antenatal classes, the advice has been to draw up a birth plan: warm baths, movement, partner support, and later, possibly, reluctantly, epidural ... But if I do want an epidural, she asks, will it be available even at Christmas? Christmas is also the time for celebrating the birth of Christ — which led me to wonder about the obstetric details of this event. There is little precise information available to us. Luke 2:4-7, though the author was himself a physician, gives but a brief historical account: ... Joseph ... went up ... unto ... Bethlehem ... with Mary his espoused wife, being great with child ... while they were there, the days were accomplished that she should be delivered. And she brought forth her firstborn son, and wrapped him in swaddling clothes, and laid him in a manger ... (All Bible quotations given here are from the King James Version.) Although there was clearly a birth plan, this was heavenly and long-term, rather than a matter of maternal choices. Presumably the delivery was a spontaneous vaginal one, with a cephalic presentation and rapid labour — possibly initiated by the long donkey ride to Bethlehem. There would have been few facilities for intrapartum care in a stable, and, although angels were in evidence, we are not told of the presence of any human support other than Mary’s husband. The third stage of labour was probably uncomplicated — depictions in religious art always show the mother of Jesus as serene postpartum, with no hint of exhaustion or exsanguination. What can be said with certainty is that for the Madonna there was little in the way of pain relief in labour, and that this situation would continue for women in childbirth for nearly two thousand years. Not only was effective medication lacking, women also had to contend with the curse of Eve — a belief that the pain of labour was women’s lot following Eve’s succumbing to temptation and her subsequent banishment from the Garden of Eden. In Genesis 3:16, God declares sternly, “... in sorrow thou shalt bring forth children”. And so, for hundreds of years, women brought forth children with only the support of other women for relief from pain, and many men, particularly clergy, regarded pain in childbirth as evidence of God’s moving in mysterious ways that should not be questioned. The Nativity, by Petrus Christus, circa 1450. Fortunately, all this finally began to change in the middle of the 19th century, thanks largely to Queen Victoria and a remarkable medical practitioner named John Snow. Victoria, mother of nine, has often been depicted as disliking sex (“lie back and think of England!” is frequently attributed to her), but immediately after her marriage in February 1840 she wrote to her Uncle Leopold, King of the Belgians, that she was the “... happiest Being that ever existed”, and within days she conceived her first child, the Princess Royal, born in November that year.1 She was no wimp — despite “all the ennuies” of pregnancy, she worked until close to each birth — but she was not amused by the experience of labour.1 After her first delivery, she remonstrated with Leopold that “men never think ... what a hard task it is for us women to go through this very often”.1 Later, when her eldest daughter was herself married, Victoria wrote to her of the “heavy trials” and “cruel sufferings” that labour entailed,2,3 and commented that: ... the pride of giving life to an immortal soul is very fine ... but I own I cannot enter into that; I think much more of our being like a cow or a dog at such moments; when our poor nature becomes so very animal and unecstatic.2 Nevertheless, her letters show that she adored her “Angel” — her consort, Prince Albert — and was devoted to all her children.1 In London in 1847, Dr John Snow began to experiment with ether, which dentist William Morton had successfully demonstrated as an anaesthetic to an interested Boston audience the previous year.4 Born in 1813 to a poor Yorkshire family and apprenticed at age 14 to a surgeon, Snow later studied medicine at the Hunterian School of Medicine in London.5 He was a vegetarian, a teetotaller and, by his own admission, celibate all his life, devoting his energies entirely to his profession.6 Snow was one of the first to calculate appropriate dosages of ether; he devised his own apparatus for its administration and soon had “the busiest ether practice in London”.6 He was also interested in chloroform, introduced by James Simpson of Edinburgh in 1847 for obstetric and surgical anaesthesia, and he wrote about both drugs.7,8 Simpson, as well as taking a clinical interest in pain relief for childbirth, also confronted the Church’s objections, quoting from Genesis 2:21-22 the story of Eve’s creation from Adam’s rib: ... the Lord God caused a deep sleep to fall upon Adam ... and He took one of his ribs ... and the rib ... made he a woman. Thus, said Simpson to his opponents, did God condone the use of anaesthesia.9 Victoria and Albert initially expressed interest in chloroform for childbirth in 1848. However, the Royal physicians, Dr Charles Locock and Sir James Clark (a man described as “a walking medical calamity”), had grave concerns about the safety of the drug, so the birth in 1850 of Victoria’s seventh child, Prince Arthur, took place without anaesthesia.6 Over the next 3 years, Snow’s reputation as a safe anaesthetist grew, and, in early April 1853, with the arrival of another child imminent, Albert summoned him to Buckingham Palace for a private conversation. Three days later, the Queen commenced labour, and Snow was again called to the Palace. Subsequently he wrote: April 7, 1853 — Administered ... to the Queen in her confinement ... a little chloroform with each pain ... on a folded handkerchief .... Her Majesty expressed great relief from the application [and] appeared very cheerful and well, expressing herself much gratified with the effect ...6 The Queen indeed found chloroform “delightful beyond measure”, and the child, Prince Leopold, was born healthy. The editors of the Lancet, however, were not amused. “Intense astonishment ... has been excited throughout the profession by the rumour that her Majesty during her last labour was placed under the influence of chloroform, an agent which has unquestionably caused instantaneous death in a considerable number of cases”, they thundered.10 The British Medical Journal hit back at its rival, asserting that “when well controlled and supervised, the use of chloroform is safe”, and by the 1860s, using chloroform in both obstetrics and general surgery was standard practice.11 In 1857, at the birth of her last child, Princess Beatrice, the Queen again used chloroform, once more administered by Dr Snow. “Her Majesty is a model patient”, Snow declared, but very properly declined to comment further on his conduct of either case. The Royal approval much enhanced his professional reputation, and chloroform in childbirth became respectable, being referred to as anaesthesia à la reine. The notion of pain relief in labour was here to stay.12 Snow died in 1858, aged just 45, but left an enduring medical legacy not just confined to his contribution to anaesthesia. In 1854, he had investigated an outbreak of cholera in his London neighbourhood of Soho, becoming convinced — well before the germ theory of disease was accepted — that the source could be traced to water from a public pump in Broad Street. He persuaded a sceptical municipality to remove the pump’s handle — whereupon the epidemic abated. He thus made a significant contribution to epidemiology, as well as to the realisation that plagues and epidemics were not, in fact, the work of a wrathful God.6 Chloroform continued to be used in childbirth until the 1970s, joined by narcotics such as pethidine, nitrous oxide–oxygen mixtures, and other self-administered analgesics. Since the 1960s, increasingly sophisticated techniques of epidural analgesia have been developed.5,12 Currently, 90% of Australian women having their first child have some form of pharmacological pain relief in labour.13-15 However, with the growth since the 1980s of a movement critical of the medicalisation of childbirth, opinions on the acceptability of pain relief in labour have become polarised. Now, instead of the doctrine of the divine necessity of pain in labour, we have the view that experiencing pain is a woman’s right, and that accepting analgesia diminishes the experience of childbirth. “The easy availability of analgesia”, says one advocate of this viewpoint, “can reinforce the medical notion that women’s bodies are intrinsically defective”.16 Not so, respond some obstetric anaesthetists — epidurals are “the gold standard ... you can participate in the experience, you can push the baby out, and it takes the pain away”.17 Had it been possible, Queen Victoria would almost certainly have ordered one. So, what advice should I give my daughter? The same that I would give all women. There is no right or wrong way to have a baby, be it in a stable or a tertiary-level hospital — there is just the best way for you. Epidurals are effective and safe, and available even on Christmas Day. Be well informed, keep an open mind, make the decisions that seem right for you at the time, and do not be tempted to regret them later; the most important thing is a healthy baby and a healthy mother. We will welcome our Christmas arrival with joy.

Caroline M de Costa MPH, FRCOG, FRANZCOG

Born on 5 October 1915 in Sydney, Charles Sara was a well known Sydney anaesthetist. Charles studied medicine at the University of Sydney. After graduating in 1940 and completing his residency at Royal South Sydney Hospital, he saw active military service in World War II, receiving the Pacific Star, War Medal, Defence Medal and Australian Service Medal. Charles gained the Diploma of Anaesthetics of the University of Sydney in 1950. He worked for many years as an Honorary Anaesthetist (and later Consultant) at the Royal Alexandra Hospital for Children, the Royal Prince Alfred Hospital and the United Dental Hospital, Sydney. From 1966 to 1975, he was a Lecturer in anaesthesia in the Faculty of Dentistry at the University of Sydney. In 1975, his pioneering work in dental anaesthesia was acknowledged by his being awarded the Belisario Award of the Australian Society for the Advancement of Anaesthesia and Sedation in Dentistry, for “outstanding contribution in the field of dental anaesthesia and sedation” over 25 years. Charles served the Australian Society of Anaesthetists as Treasurer, then Secretary, from 1954 to 1959, and was Chairman of the New South Wales Section from 1960 to 1961. Elected a Foundation Member and Fellow of the Faculty of Anaesthetists of the Royal Australasian College of Surgeons at its inauguration in 1952, he was a member of the Faculty’s Court of Examiners, then Vice-Chairman of the Court, from 1961 to 1970. As a member of the Board of Faculty from 1967 to 1974, Charles contributed enormously to the establishment of the Faculty’s training program in anaesthesia. On his retirement from the Board, he was fittingly awarded the Robert Orton Medal for meritorious service to anaesthesia, the highest honour of the Faculty. He was also the Faculty representative to the Standards Association of Australia and was consultant to the Coronial Investigation Unit for Anaesthetic and Drug-Related Mortality. Charles was a skilful, thoughtful and helpful colleague who was greatly respected by the surgeons he worked with. He was an encouraging mentor with an outgoing, genial personality and a hearty laugh. He published original articles on a wide range of topics and took a scientific approach to the many challenges in the developing specialty of anaesthesia. His leisure interests were many and varied. In his youth, Charles was a keen and competitive surf lifesaver, and participated in the rescue of well over 100 people swept out to sea on Black Sunday (6 February 1938) at Bondi Beach. Reading, amateur radio and film-making were other pursuits. Sadly, he became progressively disabled by complications following surgery for a meningioma and died on 28 December 2005. He is survived by his wife Barbara, son Antony and daughter Angela.

Jeanette Thirlwell

Objective: To investigate the change in pattern of discharge of patients from an intensive care unit (ICU) to hospital wards and to determine the impact of discharge time on subsequent hospital mortality.Design and participants: A retrospective cohort study of 10 903 patients discharged alive from a single ICU between 1 January 1992 and 31 December 2002.Main outcome measure: In-hospital mortality.Results: Of the 10 903 patients discharged alive from the ICU, 486 (4.5%) died in hospital wards. When discharge times were categorised according to nursing shift (morning, 07:00–14:59; afternoon, 15:00–21:59; and night, 22:00–06:59), patients were more likely to be discharged on an afternoon shift (odds ratio, 3.63; 95% CI, 3.05–4.30) or night shift (4.52; 95% CI, 3.15–6.64) in 2000–2002 compared with 1992–1994. In a multiple logistic model, hospital mortality after discharge from the ICU was increased by higher APACHE II score (1.14; 95% CI, 1.12–1.16); admission to ICU from the operating room (1.47; 95% CI, 1.11–1.95) and from the general ward (1.75; 95% CI, 1.37–2.23); and discharge during the afternoon (1.36; 95% CI, 1.08–1.70) and night shifts (1.63; 95% CI, 1.03–2.57).Conclusion: Over an 11-year period, more patients are being discharged from the ICU in the afternoon and night suggesting increasing pressure on ICU beds. Patients discharged on these shifts have an increased risk of death.

Antony E Tobin MB BS, FRACP, FJFICM · John D Santamaria MD BS, FRACP, FJFICM

An Australian document now has an important role in acute pain management worldwide More than 50% of patients continue to have severe pain after surgery and trauma.1 This situation not only results in unnecessary suffering, but occurs despite evidence that inadequate treatment of acute pain increases the risk of postoperative complications and may lead to persistent (chronic) pain. Indeed, operations and injuries are considered to contribute to at least 25% of the burden of chronic pain.1 These points were highlighted at a forum cosponsored by the International Association for the Study of Pain (IASP), the European Federation of IASP Chapters, and the World Health Organization on 11 October 2004. This forum launched the Global Day Against Pain in support of the declaration that in acute, chronic non-cancer and cancer pain, “the relief of pain should be a human right”, and that improvements in the management of pain, including acute pain, require “global education of health professionals, patients and their families”.1 In Australia, there has been long-standing awareness of the need to improve the management of acute pain. This was supported by the publication of the first edition of Acute pain management: scientific evidence by the National Health and Medical Research Council (NHMRC) in 1999.2 At that time, the NHMRC and the Agency for Health Care Policy and Research in the United States were the only organisations worldwide to have produced evidence-based documents on the treatment of acute pain. More recently, this awareness has been highlighted by a number of high-level activities including the Pain Management Project of the National Institute of Clinical Studies,3 the development of the Operational principles for acute pain management by the Victorian Quality Council4 and the release of a Statement on patients’ rights to pain management by the Australian and New Zealand College of Anaesthetists (ANZCA) and the Faculty of Pain Medicine (FPM), a multicollegiate Faculty under ANZCA.5 International awareness of the need to improve the management of pain also continues to grow. The IASP held another Global Day Against Pain on 17 October 2005, which focused on pain in children.6 The Global Day Against Pain is to become an annual event. The IASP is also forming a special interest group on acute pain, which will further promote better management.7 Over recent years there has been an enormous increase in the amount of evidence available on the management of acute pain. Therefore, ANZCA and the FPM convened a working party to oversee a revision of the 1999 NHMRC acute pain document. To summarise the substantial amount of new evidence in a concise and easily readable form to help health care professionals and consumers, a large panel of contributors was appointed to draft sections of the document, and a multidisciplinary consultative committee (including medical, nursing, allied health and complementary medicine providers as well as consumers) was chosen to review drafts of the document and contribute more broadly as required. Evidence was annotated according to the levels recommended by the NHMRC.8 In addition, many practical recommendations for the treatment of aspects of acute pain were included by the working party as “clinical practice points” because of their clinical relevance, even though they are not purely evidence-based. The revised document9 was approved by the NHMRC in June 2005 and launched at the World Pain Congress in Sydney in August 2005. It has already received widespread recognition with formal endorsement by the IASP and the Australian Pain Society. As it forms the basis for the section on acute and postoperative pain in the third edition of the IASP’s Core curriculum for professional education in pain, its use worldwide is ensured.10 It has also been endorsed by the Royal College of Anaesthetists in Britain and recommended by the American Academy of Pain Medicine to its members. Much of the evidence relating to acute pain management comes from the hospital setting, but many of the principles can be extrapol-ated to other acute pain settings, such as managing pain from renal colic or migraine or the use of opioids and non-steroidal antiinflammatory drugs (NSAIDs). Examples of updated key messages and clinical practice points for the use of opioids, paracetamol, NSAIDs and cyclo-oxygenase-2 (COX-2) inhibitors are listed in the Box. As the field of acute pain medicine is changing rapidly, new information emerging in areas considered to be of importance will be reviewed by the working party and posted periodically on the ANZCA website (http://www.anzca.edu.au/publications/acutepain.htm). A third edition of Acute pain management: scientific evidence is planned for 2010. A revision of the consumer guide to acute pain management will also be available shortly at the above website. Knowledge about acute pain medicine is growing too rapidly for individuals to keep abreast of it unaided. It is hoped that the updated guidelines will help clinicians and others approach acute pain treatment more effectively and safely, thus going some way towards reducing the suffering and improving outcomes of patients in our community. Selected updated key messages and clinical practice points*9 Opioids Dextropropoxyphene has low analgesic efficacy (Level I evidence). In the management of acute pain, one opioid is not superior over others but some opioids are better in some patients (Level II evidence). Tramadol has a lower risk of respiratory depression and impairs gastrointestinal motor function less than other opioids at equi-analgesic doses (Level II evidence). Pethidine is not superior to morphine for treating pain of renal or biliary colic (Level II evidence). In adults, age is a better predictor of opioid requirements than weight, although there is a large interpatient variation (Level IV evidence). Assessing sedation level is a more reliable way of detecting early opioid-induced respiratory depression than a decreased respiratory rate (clinical practice point). The use of pethidine should be discouraged in favour of other opioids (clinical practice point). Paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs) and cyclo-oxygenase-2 (COX-2) inhibitors Paracetamol is an effective analgesic for acute pain (Level I evidence). NSAIDs and COX-2 inhibitors are effective analgesics with similar efficacy for acute pain (Level I evidence). NSAIDs given in addition to paracetamol improve analgesia (Level I evidence). COX-2 inhibitors and NSAIDs have similar adverse effects on renal function (Level I evidence). Paracetamol, NSAIDs and COX-2 inhibitors are valuable components of multimodal analgesia (Level II evidence). COX-2 inhibitors do not impair platelet function (Level II evidence). Gastric ulceration rates with short-term use of COX-2 inhibitors are similar to those for placebo (Level II evidence). Adverse effects of NSAIDs are significant and may limit their use (clinical practice point). The risk of adverse renal effects of NSAIDs and COX-2 inhibitors is increased in the presence of factors such as pre-existing renal impairment, hypovolaemia, hypotension, use of other nephrotoxic agents and angiotensin-converting enzyme inhibitors (clinical practice point). Levels of evidence designated according to those recommended by the National Health and Medical Research Council.8 * Reproduced with permission from the Australian and New Zealand College of Anaesthetists.

Pamela E Macintyre MB BS, FANZCA, FFPMANZCA · Stephan A Schug MD, FANZCA, FFPMANZCA · David A Scott MB BS, PhD, FANZCA

Clinical intensive care and acute medicine. 2nd ed. Kenneth M Hillman, Gillian F Bishop. Cambridge: Cambridge University Press, 2004 (xvi + 685 pp). ISBN 0 521 78980 X. The practice of intensive care medicine is forever evolving to meet the demands of critically ill patients. Of particular importance has been the recent increasing advocacy for critical care outreach through improved surveillance outside intensive care units, and the provision of medical emergency teams. The authors of this book have been pioneers in this evolutionary process, and in this second edition the reader is presented with a very practical, commonsense approach to the care of the acutely unwell patient. The format is very easy to follow, and information about both generic and specific aspects of critical care medicine is easily accessed. The major emphasis of the book, however, is on general, practical topics rather than comprehensive reviews of diseases or specific organ failures (although these are very adequately covered). A junior hospital doctor wanting to refresh his or her knowledge of fluid and electrolyte therapy is as well served as a consultant in a peripheral centre who needs to urgently review planning priorities before transporting a sick patient. The text is concise and contains the right balance between practical and theoretical issues. There are troubleshooting sections at the end of selected chapters, and there is a further reading section at the end of every chapter. Clinical intensive care and acute medicine will be used widely by postgraduate medical trainees rotating through intensive care but will also be a very welcome companion for critical care vocational trainees and consultant intensive care physicians. Although there is a chapter on quality assurance and clinical audit, there is relatively little information about complications. This is partly due to the deliberate omission of descriptions of procedural techniques. Importantly, the authors have managed to provide an authoritative, practical guide to clinical decision making in this rapidly changing area of acute medicine. Larry P McNicol Director of Anaesthesia, Austin Hospital, VIC

Larry P McNicol

Raymond F Raper,* Elizabeth Fugaccia,† Yahya Shehabi‡ * Board Member, † Member, ‡ Chairman, NSW Regional Committee, Joint Faculty of Intensive Care Medicine, 117 Alexander Street, Crows Nest, NSW 2065. yshehabiATozemail.com.au To the Editor: We are writing in response to the pejorative, unhelpful and somewhat misleading editorial “The shortage of kidneys for transplantation in Australia”.1 There are many possible reasons for lower organ donation rates in Australia. Several Australian initiatives have led the way in reducing the incidence of severe, traumatic brain injuries. These include the compulsory wearing of seat belts and helmets, random breath testing, and a zero blood alcohol limit for inexperienced drivers. Intensive care medicine is better structured and organised in Australia and New Zealand than in most of the countries cited by Mathew et al, with higher organ donation rates. Intensive care outcomes in Australia are world-leading. So the donor rate may be lower because patient outcomes are better. A comprehensive chart audit of donor potential in New South Wales carried out under the supervision of the Organ Donation Network NSW/ACT, identified very few missed donors (T Wills, Manager, Organ Donation Network NSW/ACT, personal communication), and a Victorian audit has suggested that the donor pool may be much lower in Australia than previously estimated.2 Similarly, organ donation rates will appropriately vary considerably among hospitals. To improve outcomes, critically ill patients are transported to centres with specific experience and expertise, resulting in a preponderance of potential donors in hospitals with trauma and neurosurgical services compared with hospitals lacking these. The intensive care community supports these life-saving initiatives, notwithstanding the effect they may have on organ donation potential. In fact, the principal “barrier” to organ donation in Australia appears to be the consent rate. From 2000 to 2004, 44% of families declined organ donation when faced with an actual rather than a hypothetical request.3 The intensive care community represents the interests of critically ill patients and their families. We will continue our best endeavours to improve both the survival and quality of life of patients suffering devastating brain injuries (our performance standard). When all brain function ceases, despite our best efforts, we will continue to facilitate organ donation, in discussion with the family, and in consideration of the patient’s known or projected wish. The intensive care community has led the way in developing organ donation-related practice guidelines4 and in related education. Australian Donor Awareness Program — Training (ADAPT) workshops are now a compulsory component of Fellowship of the Joint Faculty of Intensive Care Medicine training. The editorial implication of poor performance and lack of commitment is inaccurate and offensive.

Raymond F Raper · Elizabeth Fugaccia · Yahya Shehabi

Timothy H Mathew,* Randall J Faull,† Paul L Snelling‡ * Medical Director, Kidney Health Australia, GPO Box 9993, Adelaide, SA 5001; † Nephrologist, Royal Adelaide Hospital, Adelaide, SA; ‡ Nephrologist, Royal Prince Alfred Hospital, Camperdown, NSW. tim.mathewATkidney.org.au In reply: We regret that Raper et al have misinterpreted our editorial on the shortage of donor kidneys in Australia.1 We are particularly concerned and indeed mystified by their last statement, where they state that we implied that “poor performance and . . . lack of commitment” were to blame. This was in no manner our message. Rather, we sought to emphasise that all possibilities to optimise local donation rates should be explored, so desperate patients seeking grafts from potentially dangerous overseas sources need not expose themselves to serious potential morbidity and mortality. We consider that our intensive care colleagues perform superbly under the most difficult of circumstances when managing potential organ donation. We understand they are often unsupported with managing potential donations while they must at the same time deal with the grieving family, and the immediate demands of treating other seriously ill patients. We simply suggest that problems within the system (for example, differences between states in the number of intensive care beds per head of population or in the provision of specifically funded donor coordinators) that might hinder increasing organ donation should be carefully examined. We believe it is unhelpful to suggest that the South Australian experience should simply remain unexplained. In the article by Opdam and Silvester (cited by Raper et al), of 112 potential donors, 46 were considered medically suitable unrealised potential donors, and their estimated maximal potential donor rate was 30 per million,2 remarkably similar to the rates seen in Spain (the country with the highest organ donor procurement rate) and South Australia. We agree with the conclusions of Opdam et al that “an increase in the organ donation rate may be possible through increasing consent and the identification and support of potential donors”. As they also state, this would require substantial changes in clinical practice, with resource and ethical complications We did not mean to offend our intensivist colleagues. We merely suggest that we all need to assess the systems in which donation occurs and attempt to improve donation rates, for the sake of the many desperate people awaiting organ transplants in this country.

Timothy H Mathew · Randall J Faull · Paul L Snelling