Vascular diseases

A 76-year-old woman reported a fishbone stuck in her throat, but no foreign body was identified. Eight weeks later, she experienced a transient ischaemic attack, and a stingray barb was subsequently removed from the right common carotid artery. To our knowledge, this is the first report of the migration of an ingested stingray barb. Clinical recordWhile holidaying in Queensland, a 76-year-old woman presented to an emergency department, reporting a fishbone stuck in her throat after a meal of snapper. A neck x-ray showed a vague 1 cm linear opacity. She was referred to an ear, nose and throat surgeon who performed a laryngoscopy and rigid oesophagoscopy under general anaesthesia. This revealed bruising to the right hypopharynx without mucosal trauma, but no foreign body was identified. The patient was discharged the following day, and subsequently returned home to Victoria. Two weeks later, the patient presented to her local doctor with ongoing dysphagia. A repeat x-ray of her neck showed a linear area of calcification of up to 1cm in length on the lateral film among patchy areas of calcification in the thyroid cartilage and carotid bifurcations (Box 1, A and B). No further action was taken. Six weeks later, the patient re-presented reporting transient left facial droop, left arm weakness and paraesthesia that resolved completely after 10 minutes. She also reported persistent dysphagia, a painful lump on the right side of her neck, and weight loss of 5 kg since her trip to Queensland. An urgent carotid duplex ultrasound examination revealed a linear foreign body traversing the right common carotid artery, 2 cm proximal to its bifurcation. The patient was transferred to our hospital. She was fit and her only comorbidities were hypertension, hypercholesterolaemia and anxiety disorder. On examination, she had raised blood pressure (165/70 mmHg) and was in sinus rhythm. There was a palpable mass in the right anterior triangle of the neck, with no audible bruit. Neurological examination was unremarkable. A computed tomography scan with intravenous contrast medium confirmed the presence of a 34 mm linear foreign body traversing the right common carotid artery, with a surrounding soft tissue mass consistent with a haematoma. There was no extravasation of contrast medium (Box 1, C). A small filling defect, consistent with an adherent thrombus, was noted on the intravascular segment of the foreign body. The patient underwent exploratory surgery with awake, regional anaesthesia, which permitted continuous neurological monitoring. This enabled safe distal cross-clamping of the internal and external carotid arteries and proximal cross-clamping of the common carotid artery before the foreign body and the traumatised carotid artery were manipulated. A 1 cm segment of the right common carotid artery (which was 2 cm proximal to the carotid bifurcation and included the foreign body) was resected and an end-to-end anastomosis with 6-0 Prolene (Ethicon, Piscataway, NJ, USA) was carried out. The foreign body was subsequently identified as a stingray barb (Box 2). There was no neurological compromise during or after the surgery. A Gastrografin (Bayer AG, Berlin, Germany) swallow fluoroscopy study undertaken 1 day after surgery showed no leak of contrast from the pharynx. The patient was discharged 4 days after the surgery, had recovered by 6-week follow-up, and was well at a 12-month review. DiscussionForeign bodies that migrate from the pharynx and oesophagus into the neck are often reported;1-7 most common among adults are fishbones.1,2 To our knowledge, this is the first report of the migration of an ingested stingray barb. The harpoon-like structure of the barb facilitates its migration in one direction, similar to observations in cases of migrating saw-toothed fishbones.3 Stingray injuries are common in tropical regions of Australia;8 envenomation is a concern in acute injuries, due to the necrotising properties of the venom, and pseudoaneurysm of the superficial femoral artery is a reported complication of this.9 It is not surprising that envenomation did not occur in our patient, as the stingray barb may have been lodged in the snapper for some time, and any remaining venom was probably destroyed during cooking. Previously reported cases of foreign bodies migrating into the common carotid artery were not associated with an ischaemic cerebrovascular event.4-6 In a case reported in 1958, the foreign body (a needle) was extracted directly by endoscopy;4 two other cases required open exploration and cross-clamping of carotid arteries.5,6 Ingested foreign bodies that migrate outside the pharynx and oesophagus are difficult clinical scenarios to diagnose. Migration may occur within 24 hours of injury.1 Investigation usually begins with an x-ray to locate the foreign body, but this is not entirely sensitive, even for fish bones.2 Although stingray barbs have been reported to be radio-opaque on x-ray,10 they may not be detected as stingray skeletons are cartilaginous and the spine contains vasodentine.11 In our patient, the stingray barb was visualised as a radio-opaque body in the x-ray, but the findings were uncertain because of calcification in the thyroid gland and carotid arteries. When a foreign body is seen on x-ray, an oesophagoscopy showing oedema, bruising or abrasion should raise suspicion of a migrating foreign body.7 Computed tomography is the investigation of choice, and should be performed as soon as possible to prevent catastrophic complications of migration into structures of the neck.1,2 1 Radiographic findings from a patient who ingested a stingray barb A,B: X-rays 2 weeks after the patient reported a fishbone stuck in her throat, showing linear area of calcification in the lateral film (arrow). C: Computed tomography scan after the patient experienced a transient ischaemic attack, showing linear foreign body (arrow). 2 Stingray barb removed from common carotid artery

Desmond C C Gan MB BS, BMedSci · Ravi L Huilgol MB BS, FRACS · Mark J Westcott MB BS, FRACS

Objective: To assess the efficacy of endovenous laser therapy (EVLT) for treating varicose veins with saphenous reflux.Design: A trial of treatment, with results assessed by ultrasound surveillance.Setting: Outpatient clinics with sonographer and nursing support.Main outcome measures: Control of reflux; occlusion or obliteration of the saphenous veins assessed by ultrasound.Results: EVLT was used to treat 404 veins in 308 patients. Univariate life table analysis showed primary success in 80% (95% CI, 69%–87%) and secondary success after further treatment of recurrent saphenous vein reflux by ultrasound-guided sclerotherapy in 88% (95% CI, 78%–95%) at 3 years. On multivariate Cox regression analysis, none of the covariates studied were associated with ultrasound failure.Conclusions: Early results indicate that EVLT effectively controlled saphenous reflux. Its advantages are that it is performed as an outpatient procedure under local anaesthesia with immediate mobilisation, causes minimal disruption of activities, and avoids surgical trauma.

Kenneth Myers MS, FRACS, FACS · Robert Fris FRACS, FACS · Damien Jolley MSc(Epidemiol)

The prevalence of peripheral arterial disease (PAD) in people aged over 55 years is 10%–25% and increases with age; 70%–80% of affected individuals are asymptomatic; only a minority ever require revascularisation or amputation. Patients with PAD alone have the same relative risk of death from cardiovascular causes as those with coronary or cerebrovascular disease, and are four times more likely to die within 10 years than patients without the disease. The ankle–brachial pressure index (ABPI) is a simple, non-invasive bedside tool for diagnosing PAD — an ABPI less than 0.9 is considered diagnostic of PAD. About half of patients with PAD (defined by an abnormal ABPI) have symptomatic coronary or cerebral vascular disease. The ABPI is an independent predictor of coronary and cerebrovascular morbidity and mortality. Patients with PAD require medical management to prevent future coronary and cerebral vascular events. There are currently insufficient data to recommend routine population screening for asymptomatic PAD using the ABPI.

Paul E Norman DS, FRACS · John W Eikelboom MB BS, FRACP · Graeme J Hankey MD, FRACP

To the Editor: We read with interest the case report of Ward and colleagues, describing methicillin-resistant Staphylococcus aureus with reduced susceptibility to vancomycin in a patient being treated for lower-limb ischaemia.1 We conclude that this antibiotic resistance may not have developed if the patient had been treated with conventional vascular therapy. The patient had diabetes, was haemodialysis-dependent and continued to smoke. Bilateral lower-limb ischaemia in such a patient is an indication for early vascular assessment, including angiography, debridement of non-viable tissue and, if possible, revascularisation. The option of early below-knee amputation should always be considered for such a patient. Broad-spectrum antibiotics administered over a long period to patients with ischaemic tissue can provide the ideal medium for development of multiresistant organisms. In this patient, 41 days of chronic infection, combined with the decreasing nutritional status typical of haemodialysis patients, contributed to the breakdown of both below-knee amputation sites and the ongoing sepsis. The difficult decision to preserve or amputate an ischaemic limb is best made by a vascular surgeon in consultation with the patient. Amputation should not be seen as treatment failure but as another stage of vascular disease. Early amputation preserves the physical condition and nutrition of patients and allows earlier transfer to rehabilitation units, with an improved result.2

Anthony J Grabs · Reginald SA Lord

Objective: To summarise recent evidence from case reports (published January 1995 – September 2001) of adverse events after cervical spine manipulation.Data sources: Five computerised literature searches (MEDLINE – Pubmed; EMBASE, the Cochrane Library, AMED [Allied and Complementary Medicine Database], and CISCOM [Centralised Information Service for Complementary Medicine]) were performed. No language restrictions were applied.Study selection: All case reports containing original data of adverse events after cervical spine manipulation were included.Data extraction: All articles were evaluated and key data extracted according to pre-defined criteria: patient's age, sex and diagnosis; type of therapist; type of treatment; nature of adverse event; method of diagnosis; and clinical outcome.Data synthesis: Thirty-one case reports (42 individual cases) were found. The patients were equally distributed between the sexes (21 male, 20 female, one unknown) and mostly middle-aged (range, 3 months to 87 years). Most were treated by chiropractors. Arterial dissection causing stroke was reported in at least 18 cases.Conclusions: Serious adverse events after cervical spine manipulation continue to be reported. As the incidence of these events is unknown, large and rigorous prospective studies of cervical spine manipulation are needed to accurately define the risks.

Edzard Ernst MD, PhD, FRCP(Edin)

Thoracic aorta injury secondary to blunt chest trauma accounts for 10% to 20% of fatalities from high-velocity accidents, and the subsequent mortality rate in untreated survivors is high.1 Standard management is based on prompt radiological diagnosis and surgical repair by thoracotomy, usually with partial left heart bypass. Despite technical advances, these procedures carry significant mortality and postoperative paraplegia rates (up to 30% and 10%, respectively),2 and severe traumatic comorbidity or coincidental chest disease in many patients makes their aortic injury inoperable. Endovascular stent-graft repair is emerging as an alternative for treating thoracic aortic injury, with a number of potential advantages.3,4 These include the ability to treat patients with contraindications to thoracotomy, and the potential to reduce neurological complications. However, clinical experience with this procedure is limited. The procedure involves deploying a self-expanding, fabric-covered metal stent from within the diseased vessel to exclude an aneurysmal segment, and is performed by means of a dedicated delivery system retrogradely inserted through the femoral artery. We report a case of immediate stent-graft repair of a traumatic false aneurysm of the thoracic aorta in a patient for whom thoracotomy was relatively contraindicated. We also review the published data and discuss technical issues. Clinical recordA 47-year-old professional motorcyclist was thrown from his bike against a rubber tyre wall at high speed. He did not lose consciousness, but immediately noticed low back pain and lower-limb tingling. His vital signs were stable, and he was transferred to the trauma unit with full spinal precautions. Subsequent evaluation showed a pulse rate of 65 beats per minute, blood pressure of 150/65 mmHg, 30 respirations per minute, and a Glasgow Coma Score of 15. He had absent left knee and ankle jerks, reduced light touch sensation in L2–S1 dermatomes on the left and L2–L3 on the right, with normal power and anal tone. Chest and spine radiographs showed an abnormal mediastinal contour consistent with haemorrhage, and a fracture-dislocation of the lumbar spine at the L2–L3 level. Computed tomography (CT) angiography showed thoracic aortic injury with intimal flap and false aneurysm of the proximal descending aorta. We felt that turning the patient to the lateral thoracotomy position for conventional surgical repair would risk further neurological deficit. Therefore, after discussing therapeutic options with the patient and his family, emergency endovascular stent-graft repair of the thoracic aortic injury was performed (see Box for technical details). CT angiography confirmed absence of extraluminal flow after the procedure. The patient subsequently underwent fixation of the lumbar spine injury using posterior rods, pedicle screws and bone graft. He made a complete neurological recovery. Three days after stent-graft insertion, he underwent video-assisted thoracoscopic evaluation of the left side of the chest for drainage of a large haemoserous pleural effusion. The thoracic aortic contour was normal, with minimal peri-aortic haematoma. Repeat CT angiography at six and 12 months confirmed thrombosis of the false aneurysm, with no complication related to the stent-graft repair, and the patient remains well 18 months after the injury. DiscussionA number of centres have published encouraging initial results for elective endovascular stent-graft repair of chronic thoracic aortic aneurysms, usually related to atherosclerosis or chronic dissection.4-7 The largest study, of more than 100 patients, reported an initial technical success rate (aneurysm thrombosis) of 85%, one-month mortality of 10% and morbidity of 30%, and two-year actuarial survival of 70%.4 Stent-graft repair has been used to treat established traumatic thoracic aortic aneurysms,8,9 but there are few reports of immediate stent-graft repair of thoracic aortic injury.10-12 This case demonstrates the feasibility of emergency endovascular stent-graft repair for thoracic aortic injury. Stent-graft repair is an option for patients who are unable to undergo thoracotomy because of associated injuries or pre-existing chest disease. The endovascular strategy may reduce early surgical morbidity. In particular, the minimal requirement for anticoagulation and avoiding aortic cross-clamping may lower the risks of cerebral haemorrhage and paraplegia.2 For our patient with coincidental spinal injury, stent-graft repair minimised the chance of neurological deterioration secondary to lateral positioning for thoracotomy. Continuing improvements in devices and delivery systems are likely to increase the familiarity, ease of use and availability of "off-the-shelf" thoracic aortic stent-graft systems. However, the role of emergency endovascular repair of thoracic aortic injuries requires further clarification. Medium-term follow-up data for endovascular repair of chronic thoracic aortic aneurysms suggest a small incidence of endoleak, delayed rupture and paraplegia,4,13 but very limited information is available for traumatic false aneurysms. In particular, the role of stent-graft repair in the context of intensive medical management of thoracic aortic injury needs to be defined.14 Stent-graft deployment technique The diameter of the isthmic (26 mm) and descending (24 mm) thoracic aorta and the longitudinal extent of intimal injury were determined from computed tomography, and an appropriately sized "off-the-shelf" stent-graft (Zenith, 28 mm diameter, 120 mm length, Cook Australia) was obtained. The procedure was performed with the patient in the supine position in the angiography suite under general anaesthesia, commencing eight hours after the accident. Diagnostic aortography via the right common femoral artery confirmed a transverse intimal tear 2 cm distal and opposite to the left subclavian artery origin (Figure a). Formal left common femoral arteriotomy was performed, followed by placement of the stent-graft device within its 24 F delivery system to the aortic arch over a stiff Lunderquist guide wire (Cook Australia). Precise proximal positioning of the device was aided by intermittent angiography of the left subclavian artery origin using a 4 F Omni-flush catheter (Angiodynamics, USA) inserted via the left brachial artery. (In this case there was sufficient length of normal isthmic aorta to achieve a seal with the proximal stent-graft without compromising the left subclavian artery origin. Where there is insufficient distance it may be necessary to position the stent-graft across the subclavian artery origin, and to perform left carotid to distal subclavian bypass at a later stage should ischaemic symptoms ensue.) The self-expanding stent-graft was deployed in stages to allow recoil of the Z-stent sections to accommodate the inner radius of curvature of the aortic arch. Optimal apposition of the proximal stent-graft was achieved with secondary dilatation ("moulding") using a compliant latex balloon (Cook Australia), resulting in successful exclusion of the false aneurysm, and patency of the subclavian artery (Figure b). The left common femoral arteriotomy was repaired.

Julian A Hanson · D Mark Brooks · Jai S Raman

To the Editor: Carotid stenting is a new application of endovascular therapy. Its efficacy in preventing strokes is yet to be established, by contrast with the proven Level 1 evidence of benefit from carotid endarterectomy. The risks of implanting carotid stents at present appear greater than the risks of carotid endarterectomy. An overview of carotid endarterectomies in Australia is maintained by vascular surgeons, through audits such as the ongoing Melbourne Vascular Surgeons Association Audit and the New South Wales Carotid Endarterectomy Audit. The technique of carotid stenting, the stents themselves and the brain-protective devices used during the implanting of stents are expensive and still evolving. The long-term durability of stents is unknown. Australian vascular surgeons, neuroradiologists and neurologists are awaiting the outcome of two major international randomised trials of carotid stenting versus endarterectomy (the US Carotid Revascularization Endarterectomy versus Stent Trial and the European International Carotid Stenting Study). These seek Level 1 evidence of the comparative risks and success of the new stenting procedures in stroke prevention and aim to document the late outcome of stenting, particularly the incidence of restenosis, which is a significant problem in other arteries after stenting. While these definitive trials are in progress, vascular surgeons of the Royal Australasian College of Surgeons wish to add their note of caution to the reservations expressed in the NHMRC guidelines on stroke prevention1 and the recommendations of the Australian Association of Neurologists.2 A recent commentary by Spence and Eliasziw3 illustrates the disparate nature and the limitations of existing studies of carotid stenting. We consider carotid stenting is not yet appropriate for widespread use in Australia. Experienced endovascular and neurology teams should continue to evaluate the new procedure. Stenting of symptomatic carotid atheroma should only be conducted with the consent of patients who are fully informed about stenting's known hazards and unproven status and who understand that the established treatment is carotid endarterectomy.4 Clinicians should audit closely the immediate outcome and long-term complications of any carotid stenting they perform.

Peter L Field

To the Editor: I read with interest the article by Hender and colleagues recently published in the Journal.1 I agree with the authors' conclusion that there is presently insufficient evidence to suggest the widespread use of endoluminal treatment for carotid artery disease. However, there are a number of problems with the authors' interpretation of our recent article comparing the outcome of surgical and endoluminal treatment of symptomatic carotid stenosis.2 Firstly, the figures in the Box are completely misleading. The percentages of adverse outcome quoted for patients undergoing endoluminal treatment are those that were found for cases receiving endarterectomy, while the figures quoted for endarterectomy are the findings for endoluminal treatment. [A correction of this error was published in the 3/17 December 2001 issue of the Journal, page 672.] Hence, any reader simply looking at the Box would be left with the false conclusion that the outcome of endoluminal treatment is superior. Secondly, the authors refer to our article2 as a "meta-analysis". In our article we went to some trouble to explain that a meta-analysis was not possible, as only one small randomised trial had been published at that time. Instead, we had to use reports from single centres and we discussed the difficulties of comparing the results when patients had not been randomised. Thirdly, the results of the CAVATAS trial were published in June 2001.3 A surprising finding was that the perioperative stroke rate (defined as a neurological deficit lasting seven days or more) for patients undergoing either carotid angioplasty (with or without stenting) or conventional endarterectomy was the same (around 10%). In fact, the disabling stroke rate of around 6% after either endovascular treatment or endarterectomy was three times higher than that found in the North American randomised trial of endarterectomy.4 Finally, the authors refer to our patients undergoing carotid stenting, whereas the majority of the patients referred to in fact received angioplasty alone.

Jonathan Golledge

The prevalence of vascular disease in our society has led to innovations in vascular surgery that focus increasingly on less invasive techniques to diagnose and treat disease. Prevention. There has been little progress with prevention of arterial or venous disease. Conventional risk factors for atherosclerosis appear to be as prevalent as ever, but new risk factors have emerged. Homocysteinaemia may be just as important as lipid disorders, is present in 10% of the population, and can be controlled by vitamin supplements. Other factors identified are metalloproteases for aneurysms, and cytokines, growth factors and inflammatory cells responsible for atherogenesis and venous ulceration, yet none have yet led to tangible therapeutic advances. Diagnosis. Duplex ultrasound scanning is replacing angiography for preliminary assessment and may become the definitive investigation for some conditions. It is simple, relatively inexpensive, and non-invasive, and can be applied to disease at most sites. It is used by many surgeons in Australasia as the sole investigation to select patients for carotid endarterectomy.1 Computer analysis of carotid plaque echogenicity by ultrasound promises to better define plaques that pose an increased risk for stroke. Ultrasound scanning can be used to select techniques for femoral artery bypass grafting, and most surgeons now use it to predict whether endovascular therapy is a realistic option. Regular ultrasound surveillance improves results after femoral artery vein bypass grafting, although its value for other interventional techniques has yet to be proven. For chronic venous disease, up to 30% of important deep to superficial connections can be missed by clinical examination alone, inviting early recurrence.2 Many surgeons now scan most patients before treating varicose veins. Treatment. There has been great interest in endovascular therapy. Until recently, surgeons' enthusiasm has outstripped the manufacturers' ability to produce suitable systems, resulting in valid criticism. A Sydney team leads the world in assessing outcome for endoluminal grafting for aortic aneurysms.3 Relatively atraumatic insertion of a stent or graft through the femoral arteries is a most attractive alternative to major open repair for abdominal or thoracic aortic aneurysms. The technique has been limited by difficulties in sealing grafts to normal arteries above and below aneurysms to prevent "endoleak" into the aneurysm sacs. Surgeons in Perth and Adelaide have pioneered innovative techniques to incorporate vital arterial branches (just above and below most aneurysms) with side stents or grafts.4 This will allow the main graft to be taken above the renal and visceral arteries in the abdomen or carotid arteries in the thorax. Studies show that aneurysms can shrink to produce strains on grafts that can lead to their late disruption, and this has influenced newer graft designs. It has yet to be determined whether the current fabric cover and stent scaffold is sufficiently strong to withstand repeated pulse deformation over long periods. The debate is even more lively as to whether endovascular stenting for carotid stenosis has advantages over conventional carotid endarterectomy.5 The open operation is far less traumatic than that for aneurysms and is probably safer than current techniques for carotid stenting, so that enthusiasm for the latter has evolved slowly. However, new filter devices that trap embolised material passing up the carotid arteries after balloon dilatation have advanced the endovascular approach in its inevitable incursion into traditional management. A more prosaic but potentially explosive development has been the introduction of minimally invasive techniques to treat varicose veins. Ultrasound follow-up after all forms of treatment has shown that residual or recurrent connections are frequent. Surgical stripping is not universally popular with patients, although specialist phlebologists obtain excellent long-term results with good cosmetic appearance and minimal morbidity. Endovenous alternatives are attractive but have not been objectively assessed. These began with sclerosant injection into major saphenous veins under ultrasound guidance. This gained considerable impetus when it was appreciated that the detergent sclerosants can be injected as a foam which stays in the vein for far longer and is easy to track with ultrasound. More recently, techniques are being evaluated for obliterating the saphenous vein with radiofrequency or laser probes introduced by percutaneous puncture. Quality. ASERNIPS (the Australian Safety and Efficacy Register of New Interventional Procedures – Surgical) has done well to introduce an effective audit for assessing safety and efficacy after endoluminal grafting for aorto-iliac aneurysms. The challenge for the vascular surgical community is to better audit and evaluate all existing and new techniques for diagnosis and treatment to ensure that they are effective.

Kenneth A Myers MS, FRACS, FACS

Letter Economy class syndrome: a forgotten lesson MJA 2001; 175: 669-670 To the Editor: The editorial by Gallus and Baker,1 and subsequent correspondence which speculated about prolonged calf pressure contributing to causing deep vein thrombosis,2 reminded me of an undergraduate lecture in 1948 about pulmonary embolism in people who slept in deck chairs in London air raid shelters during World War II. This lecture was given by Simpson, then a lecturer in forensic medicine (and later a respected authority in this specialty), who reported a significant increase in deaths from pulmonary embolism (to 24) in September and October 1940, soon after serious night air-attacks on London began.3 This compared with only four in September and October 1939. Twenty-one of these 24 deaths occurred in, or soon after leaving, air raid shelters. The pople who died were mostly elderly, obese and often had varicosities of the leg veins. A typical case was that of an overweight, 60-year-old woman who complained of numb legs and swollen ankles after sitting for 10 hours in a deck chair — she dropped dead in the street while walking home, eight minutes after leaving the shelter. Autopsy showed multiple small pulmonary embolisms and small tags of very fresh antemortem clot in the tibial veins. Simpson concluded that the process was mainly mechanical (calf compression causing obstruction, stasis, oedema and thrombosis), as sleeping in deck chairs causes compression of calf veins against the front edge of the chair for many hours. He proposed that people in air raid shelters should therefore be given provision for lying down. Indeed, by the time his letter was published, in December 1940, he noted that the number of cases of fatal pulmonary embolism were already decreasing, coinciding with the provision of bunks in the shelters. Stasis remains the precipitating factor in Virchow's triad of thrombus formation (abnormal blood flow [stasis], endothelial injury and hypercoagulability). Venous flow rate while lying down slows to half on standing and a third on sitting,4 even before calf compression is added. In 1940, civil authorities acknowledged the cause of an excess of cases of fatal pulmonary embolism and preventive measures were implemented, with documented success within two months. In 1954, Homans reported venous thromboembolism "probably due to sitting travel" by air and car.5 In 1988, calf pressure in cramped seating was blamed by the originators of the popular but restrictive term "economy class syndrome".6 In the 1990s, and in relation to the 2000 Olympic Games, a host of cases of flight-related pulmonary embolism were reported.1 But, in 2001, it seems the evidence for a causative effect must still be considered "circumstantial".1 Lloyd K Morgan Retired General Practitioner, PO Box 150, Lorne, VIC 3232 Gallus AS, Baker RI. Economy class syndrome [editorial]. Med J Aust 2001; 174: 264-265. Slonim L. Economy class syndrome Med J Aust 2001; 175: 176 Simpson K. Shelter deaths from pulmonary embolism. Lancet 1940; 2: 744. Ferrari E, Chevallier T, Chapelier A, Baudouy M. Travel as a risk factor for thromboembolic disease: a case-control study. Chest 1999; 115: 440-444. Homans J. Thrombosis of the deep leg veins due to prolonged sitting. N Engl J Med 1954; 250: 148-149. Cruickshank JM, Gorlin R, Jannett B. Economy class syndrome. Lancet 1988; 2: 497-498. Make a comment

Lloyd K Morgan

Snapshots Traumatic false aneurysm in the popliteal artery of a child Dorothy J Radford Deputy Director of Cardiology The Prince Charles Hospital, Brisbane, QLD MJA 2001; 175: 658

Dorothy J Radford

Letter Improving the treatment of leg ulcers MJA 2001; 175: 670 To the Editor: The article by McMullin emphasises the importance of compression in the treatment of ulcers.1 External pressure equal to that inside the veins will collapse varicosities, which can easily be seen by standing in a swimming pool with water up to the chest. As one cannot spend one's life standing in a pool, it seemed to me that there should be some way of duplicating this in a more convenient form. After some experimentation, I have found a reasonably easy way is to use two sphygmomanometer cuffs, with the tubes connected by suitable plastic tubing, and containing enough water to about 3/4 fill one of the bladders. An insert is put in the canvas of one, to enable it to be worn around the waist (theoretically it should be at the height of the heart, but in practice there seems little difference if it is worn at waist height), and the other is wrapped around the ankle with the ulcer (see Box). The leg cuff is applied first, while still empty, over whatever dressing is preferred on the ulcer, and maybe a layer of cotton wool, as the cuff material can be rather coarse. Then the waist cuff is put on; this contains the water, which can be felt running down and expanding the lower cuff. The importance is that the pressure exerted will balance that in the veins, cannot exceed this, and will vary according to whether one is standing, sitting, or lying down, when water will run back into the upper cuff. As an ophthalmologist I don't get to treat many people with leg ulcers, but I have had vein problems myself for a number of years, with periodic small ulcers, none of which have ever grown to any size, and have healed in four weeks, most in rather less time, with the above management. Obviously, I don't claim it will cure everyone, but it does provide a more scientific pressure which is equal all round the leg, and balances the venous pressure at all times. In my case the pressure, when standing, works out at 66 mm Hg. Even if there is arterial insufficiency, the pressure is only that which is in the veins. No doubt, a purpose-made appliance which is easier to apply and covers a larger area could be produced. Graeme W Johnson Ophthalmologist, 4th Floor, 39 East Esplanade, Manly, NSW 2095. grapamATnsw.bigpond.net.au McMullin GM. Improving the treatment of leg ulcers. Med J Aust 2001; 175: 375-378. Make a comment Device for applying appropriate and even pressure in the management of leg ulcers A: The two connected sphygmomanometer cuffs, one extended to allow it to fit around the waist. B: The device as it is worn. Back to text

Graeme W Johnson

Short-stay carotid endarterectomy Does the risk of complications warrant more than overnight stay? MJA 1998; 168: 149-150 Each year an estimated 32 000 Australians suffer a first-ever stroke1 (about 80% of which are ischaemic2 ), and a similar number are affected by transient ischaemic attacks (TIAs).3 About 40% of patients with ischaemic stroke syndromes have extracranial arterial lesions accessible to surgery,4 most commonly carotid stenosis. Significant carotid stenosis is present in an estimated 80 000 Australians aged 50-74 years.2 For many with this condition, carotid endarterectomy is the treatment of choice.2 The operation of carotid endarterectomy is more or less standardised, although controversies persist over technical issues (eg, local versus general anaesthesia, need for monitoring of cerebral perfusion or brain function, indications for shunting to maintain carotid flow during carotid clamping, and closure of the arteriotomy directly versus with a patch).5 Nevertheless, for most patients, the operation is straightforward. In this issue of the Journal, Bourke and Crimmins report 59 patients who underwent carotid endarterectomy with short hospital stay.6 Patients were admitted on the morning of the operation (performed under local anaesthesia) and discharged the next day. Before admission, patients were counselled about possible complications and how to respond. Six were excluded from overnight hospital stay for good reasons. No strokes or major complications occurred among the 59, although one developed the reperfusion syndrome which threatened a haemorrhagic stroke, another developed headaches severe enough to prolong hospital stay, and a third was returned to the operating theatre because of complications in the groin wound. The major conclusion of the report is that patients can safely undergo carotid endarterectomy with only an overnight stay. Short-stay carotid endarterectomy is practised in some other Australian institutions, notably Victorian teaching hospitals, probably in response to management efficiencies driven by casemix funding. In the United States, overnight carotid endarterectomy has been usual for several years, with some groups even advocating same-day carotid endarterectomy (with discharge the afternoon or evening of the operation). What are the main disadvantages of overnight carotid endarterectomy? Apart from inconvenience, there is the possibility that longer hospital stay might allow the complications of the surgery to be prevented or better treated. Firstly, stroke may follow carotid endarterectomy. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) found perioperative stroke rates of 1%-5%,7 while rates are considerably higher in many institutions.8 The neurologic deficit may be evident on conclusion of the operation, but more often there is a latent period during which the patient is awake and neurologically intact. For example, unpublished data from the European Carotid Surgery Trial (ECST) show that, among 1807 patients who underwent carotid endarterectomy, 85 had a perioperative stroke or died within the first 24 hours after surgery, 14 on the second day, five on the third day, eight on the fourth day, and 13 from the fifth day onwards (Dr Graeme J Hankey, Neurologist, Royal Perth Hospital, Perth, WA, personal communication, 1997). Most delayed strokes are caused by thrombotic occlusion of the internal carotid artery or by embolism of thrombus formed at the site of the reconstruction. 9 Stroke progression will be halted, and about half the patients returned to normal, by urgent repeat disobliteration of the carotid reconstruction.9 Therefore, based on the ECST data, remaining in hospital a second night might mitigate or prevent perhaps 5% of perioperative strokes. Cerebral haemorrhage occurs in about one per 400 patients, typically from the fifth day onwards.10 Often there is preceding hypertension, headaches, and sometimes epileptiform convulsions. These are attributed to cerebral hyperperfusion, and treated by reduction of blood pressure to normal, bedrest, and pain relief. If a late stroke occurs, urgent cerebral computed tomography is needed to distinguish cerebral haemorrhage from infarction, as treatment otherwise usually includes heparin and perhaps redo carotid reconstruction. A second complication after carotid endarterectomy is temporary instability in control of blood pressure and heart rate, which occurs in a little over half of patients.11 In 60% of these, hypertension (presumably due to interference with carotid baroreceptors) persists and may lead to cerebral oedema and stroke. The other 40% develop hypotension and/or bradycardia and may require heparin to minimise the chance of carotid thrombosis, although fluid replacement and atropine are usually effective. The cardiovascular instability usually resolves within 24 hours of surgery, and patients may be discharged when their blood pressure has returned to the usual preoperative level. A third early hazard after carotid endarterectomy is bleeding into the neck wound. At St Vincent's Hospital, Sydney, haemorrhage from the carotid suture line or other vessels needs to be corrected urgently in the operating theatre after about one per 200 operations (unpublished data), while at the Cleveland Clinic, United States, cervical haematoma requiring drainage developed after 1.5% of operations.12 Although most developed within the first 24 hours after surgery, some were delayed to the second or third day. A neck haematoma can rapidly obstruct the airway, and, as laryngeal oedema makes endotracheal intubation difficult, an expert anaesthetist and facilities for urgent tracheotomy should be available. Sudden disruption of the arterial suture line with heavy bleeding can be fatal or lead to a stroke through impaired carotid flow. None of these complications affected the patients reported by Bourke and Crimmins, although one patient was urgently readmitted for the reperfusion syndrome. The authors also had the advantage of treating local patients, facilitating postdischarge supervision and care. However, complications do occur for other surgeons, and, in general, patients should remain in hospital while complications are a real risk. Same-day carotid endarterectomy is inappropriate for most Australian institutions, as most patients return home on discharge from hospital rather than transfer to a nearby hospital-affiliated domiciliary service, as in the United States. Bourke and Crimmins also reported using duplex ultrasonography routinely instead of cerebral angiography to assess carotid stenosis before surgery. Duplex ultrasonography of the cervical vessels is indicated when carotid stenosis is suspected or the significance of a neck bruit is uncertain. It accurately confirms the presence of carotid stenosis, and measures its degree, but caveats apply. It cannot directly assess the arteries within the chest or cranial cavity, its accuracy depends on operator experience, and it is less reliable when the carotid arteries are tortuous or rotated or when the internal carotid artery is completely, or apparently completely, occluded. Angiography is more comprehensive, allowing visualisation of the intrathoracic and intracranial vessels, as well as the neck vessels, and nowadays can be performed on outpatients using a fine catheter introduced into the brachial or femoral artery by percutaneous puncture. Further, intra-arterial digital subtraction angiography reduces the volume of contrast medium, but, even so, angiography is invasive and potentially dangerous, causing stroke in about one per 200 patients, even in good centres,11 and more in less-skilled hands.13 Magnetic resonance angiography is a safer alternative, but current Federal Government policies restrict its availability. The cost of a carotid endarterectomy in Australia has been variously estimated as $56002 and $7000.5 This can be reduced by eliminating unnecessary investigations and by shortening hospital stay. Nevertheless, safety demands that patients are properly advised and their suitability assessed before they enter an overnight program. Short hospital stay is not appropriate if patients cannot be accommodated close to the hospital after discharge. It is also inadvisable when patients have persisting cardiovascular instability, questionable neurologic status or will be returning to unsupervised solitary accommodation. Short-stay policies must be designed to provide ongoing supervision by the clinical team, including domiciliary nurses during convalescence. Further, short-stay policies from institutions with demonstrated excellent outcomes and well organised postdischarge supervision and care cannot be translated to others with inferior or uncertain standards. In the case of carotid endarterectomy, most of the postoperative hazards needing urgent intervention are unlikely after 48 hours. Therefore, hospital discharge two days after the operation is a reasonable compromise and, in my opinion, safer than discharge a day earlier. Reginald S A Lord Professor of Surgery University of New South Wales, and St Vincent's Hospital, Sydney, NSW Reprints: Professor RSA Lord, Surgical Professorial Unit, Level 17, O'Brien Building, St Vincent's Hospital, Darlinghurst, NSW 2010. Anderson CS, Jamrozik KD, Burvill PB, et al. Ascertaining the true incidence of stroke: experience from the Perth Community Stroke Study, 1989-1990. Med J Aust 1993; 188: 80-84. National Health and Medical Research Council. Clinical practice guidelines: prevention of stroke. Canberra: NHMRC, 1996. Dennis MS, Bamford J, Sandercock P, Warlow C. Incidence of transient ischaemic attacks in the Oxford Shire, England. Stroke 1989; 20: 333-339. Robins M, Baum HM. The national survey of stroke. Incidence. Stroke 1981; 12 (2 Pt 2 Suppl 1): I45-I57. Lord RSA. Carotid endarterectomy: options and outcomes. Aust N Z J Surg 1995; 65: 151-159. Bourke BM, Crimmins DC. Overnight stay for carotid endarterectomy. Med J Aust 1998; 168: 157-160. North American Symptomatic Carotid Endarterectomy Trial (NASCET) collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325: 445-453. Rothwell PM, Slattery J, Warlow CP. A systematic review of the risk of stroke and death due to endarterectomy for symptomatic carotid stenosis. Stroke 1996; 27: 260-265. Lord RSA, Chao A. Urgent carotid reconstruction for the neurologically unstable patient. Proceedings of Seminar on Acute Carotid Interventions, Rome, Italy, 12 December 1997. Hafner DH, Smith RB, King OW, et al. Massive intracerebral hemorrhage following carotid endarterectomy. Arch Surg 1987; 122: 305-310. Lord RSA. Surgery of occlusive cerebrovascular disease. St Louis, Mo: CV Mosby, 1986. Hertzer NR, Bevan EG, O'Hara PJ, Krajewski LP. A prospective study of vein patch angioplasty during carotid endarterectomy. Three-year results for 801 patients and 917 operations. Ann Surg 1987; 206: 628-635. Hankey GJ, Warlow CP, Sellar AG. Cerebral angiographic risk in mild cerebrovascular disease. Stroke 1990; 21: 209-222. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Overnight hospital stay for carotid endarterectomy Bernard M Bourke and Denis C Crimmins MJA 1998; 168: 157-160 For editorial comment see Lord Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - ©MJA1998 Abstract Objective: To determine if overnight hospital stay after carotid endarterectomy (CEA) is feasible and safe in the Australian setting. Design: Case series with follow-up of 4-11 months (mean, 7 months). Patients and setting: All patients undergoing primary CEA performed by a vascular surgeon (B M B) between 30 May and 11 November 1996. Surgery was performed in one of four hospitals (a district general public hospital with about 400 beds and three private hospitals) in the Gosford area of New South Wales. Interventions: CEA using regional anaesthesia and sedation, after diagnosis by duplex ultrasound scan, avoiding cerebral angiography and intensive care; planned discharge after overnight hospital stay; review at one month and duplex ultrasound scan at four months. Outcome measures: Length of hospital stay and complications. Results: 65 patients were admitted for CEA during the study period and 59 were scheduled for overnight stay (one had "re-do" surgery, two remained longer for reasons unrelated to carotid artery disease, and three had been scheduled before the change to overnight stay). 54 (92%) were discharged on the first postoperative day, and only three required readmission within 30 days (for urinary retention, angina and reperfusion syndrome). There were no deaths, no myocardial infarctions and no recognised instances of cerebral ischaemia during follow-up. Conclusion: CEA can be performed safely without cerebral angiography or intensive care, with over 90% expectation of a single night's stay in hospital. Introduction Carotid endarterectomy, once controversial, has now been established by major prospective trials as highly efficacious in preventing cerebral ischaemic events in patients with carotid artery disease.1-4 Reflecting this evidence, the annual number of carotid endarterectomies performed in Australia increased from 3384 in the 1991-92 financial year to 5427 in 1994-95.5 Nevertheless, use of carotid endarterectomy in asymptomatic patients is still questioned, because of its potential for serious complications6 and claims that it is not cost effective.7 In addition, the operation is now facing challenges from new procedures -- carotid angioplasty and stenting -- which are claimed to be effective, with shorter hospital stays.5 However, studies in the United States have shown that the traditional four- to six-day hospital stay after carotid endarterectomy can be reduced and postoperative intensive care avoided without compromising patient safety.8-10 Further, recent major advances in non-invasive methods of diagnosing extra cranial carotid disease (eg, duplex ultrasound)11,12 have raised questions about the need for cerebral angiography (itself carrying about 1% risk of stroke13) before surgery. In addition, although general anaesthesia is used for carotid endarterectomy at most Australian centres (with notable exceptions14), many major overseas centres favour regional cervical or local anaesthesia.15,16 These have the advantage of allowing the procedure to be performed in patients who are unfit for general anaesthesia. We tested the hypothesis that carotid endarterectomy can be performed in the Australian setting with reduced resources (avoiding cerebral angiography and intensive care) while maintaining an acceptable standard of care. We report the outcomes for the first 59 patients scheduled for carotid endarterectomy with overnight hospital stay in the practice of the surgical author (B M B). Methods Subjects and setting Subjects were all patients who had primary carotid endarterectomy performed by B M B between 30 May and 11 November 1996. All were scheduled for overnight postoperative hospital stay, unless longer stay was indicated for management of conditions unrelated to carotid artery disease. Surgery was performed in one of three private hospitals or the major district general public hospital in the Gosford area of New South Wales. Patients had either been referred by general practitioners or other specialists with symptoms of internal carotid artery disease, or signs such as audible cervical bruit, or had been undergoing regular ultrasound monitoring of the internal carotid artery (eg, patients with coronary artery disease or previously treated contralateral coronary disease). Carotid endarterectomy was offered to: Patients with typical symptoms of internal carotid artery disease (retinal ischaemia, cerebral hemispheric transient ischaemic attacks or completed stroke) and 60% or greater stenosis at the origin of the appropriate internal carotid artery; Patients with typical symptoms but less than 60% stenosis, if duplex ultrasound examination showed carotid plaque to be the likely cause of symptoms; Asymptomatic patients with 80% or greater stenosis; and Asymptomatic patients with 60%-79% stenosis, if the stenosis had progressed from less than 60% within six months or they specifically requested surgery. No patients who fulfilled these criteria were considered "medically unfit" for the procedure. All agreed to surgery. Duplex ultrasound Stenosis of the internal carotid artery was assessed by duplex ultrasound examination (combination of Doppler and B-mode ultrasound) performed according to internationally recognised standards17 either by B M B or by one of two fully accredited vascular technologists. Stenosis was graded as none to moderate (< 60%), severe (60%-79%) or critical (80%-99%), according to the haemodynamic parameters of Zwiebel18 (Box 2, below). As degree of stenosis determined by duplex ultrasound examination may differ from that determined by cerebral angiography, we also applied the more stringent haemodynamic criteria of Carpenter et al19 to ultrasound results. The decision to use duplex ultrasound examination routinely instead of cerebral angiography was based on comparison of the results of the two tests and the atheromatous plaque removed at carotid endarterectomy (the "ultimate" gold standard) in about 400 of B M B's previous patients (unpublished data). Since then, duplex ultrasound had been used routinely instead of cerebral angiography for a further 400 patients before the present study. Surgery At the preoperative consultation, B M B explained that the patient would be admitted on the day of surgery and discharged on the first postoperative day. The availability of a relative or friend competent to care for the patient was also assessed. Preadmission assessment (full blood count, coagulation screen, estimation of blood urea, creatinine and electrolytes, electrocardiography and chest x-ray) were performed in the week before surgery. All procedures were performed in conscious patients with regional cervical block and sedation given by the method of Davies et al.14 After surgery, patients were nursed in the recovery room for four to six hours and then either sent back to a general surgical ward (in the public hospital), or assigned a special nurse in a general or high dependency ward (in the private hospitals). All patients were reviewed by medical staff twice on the first postoperative day and discharged in the care of a relative or friend that afternoon with instructions to contact the surgeon about any concerns, unless complications requiring further hospitalisation were apparent. The first 12 patients in the series were telephoned by B M B on the second postoperative day, but this practice was discontinued as it was considered unnecessary and alarming for the patient. Follow-up All patients were followed up with a consultation with B M B a month after surgery and a duplex ultrasound scan four months after surgery, to assess symptom recurrence and development of disabling stroke or significant surgical or medical complications. Patients continue to be followed up at 6- to 12-month intervals. An independent clinician (D C C) retrospectively reviewed all patients' hospital records to verify major morbidity (stroke or myocardial infarction), mortality and consecutiveness of the series, usually within a month of patient discharge. Results Subjects Of the 65 patients who had carotid endarterectomy between 30 May and 11 November 1996, 59 were scheduled for overnight postoperative stay. The other six were not scheduled for overnight stay as they were undergoing "re-do" surgery (one patient), had been scheduled before the change to overnight stay and therefore had not been counselled about a short stay (three patients), or needed longer hospital stay for reasons unrelated to carotid artery disease (two patients). One of these asked to remain in hospital for cataract surgery, and the other was taking warfarin and was admitted under the care of a cardiologist four days before surgery, and remained four days after, for stabilisation of this drug. Independent assessment of these patients' records by D C C to verify the reason for exclusion showed that none experienced complications which would have prolonged their stay more than a night had they been entered into the study. The 59 patients scheduled for overnight stay comprised 38 men and 21 women. Their characteristics are shown in Box 2, and the indications for carotid endarterectomy in Box 3. Forty of the 59 patients had symptoms of carotid artery disease (either typical, such as carotid transient ischaemic attacks, or possible, such as non-hemispheric ischaemia) plus 60% or greater stenosis of the internal carotid artery, according to the criteria of Zwiebel.18 All but three of these also met the criteria of Carpenter et al19 for 60% or greater stenosis. Of the five patients with typical symptoms but less than 60% stenosis, duplex scan showed the carotid plaque to be hypoechoic and, in B M B's opinion, the likely cause of the symptoms. At operation in all five, the plaque was found to be soft, friable and ulcerated, supporting this assessment (Figure 1). All but two of the asymptomatic patients had either a critical (80%-99%) stenosis or a severe (60%-80%) and progressive stenosis (Figure 2). The two exceptions had severe but non-progressive stenosis and requested surgery after the risks and benefits and results of recent trials had been explained to them . Cerebral angiography was used to confirm duplex ultrasound results in one of the 65 patients, as heavy calcification made imaging less than optimal. Of the 54 patients with 60% or greater stenosis by the criteria of Zwiebel,18 all but three also met the criteria of Carpenter et al19 for this degree of stenosis. Therefore, we were confident that almost all would have fitted the criterion of at least 60% stenosis by angiography as applied in the Asymptomatic Carotid Atherosclerosis4 and North American Symptomatic Carotid Endarterectomy1 trials. Hospitalisation and surgery Thirty-six of the operations were performed in a public hospital and 23 in private hospitals. Fifty-three of the 59 patients were admitted on the day of surgery. Another two were already in hospital for investigation of cerebral symptoms under the direction of a neurologist, and four were admitted the previous day (two because of transport difficulties that prevented them reaching hospital early enough on the morning of surgery and two because of administrative errors). In five operations, the arteriotomy was closed primarily, while in 53 operations (90%) a vein patch was inserted; no synthetic patches were used. The remaining operation was aborted after the skin incision, as the patient had an extreme panic attack. Nine patients (15%) required cerebral protection with a shunt after evidence of intraoperative cerebral ischaemia. Average operation times were: without patch, 77 minutes (range, 65-105 minutes), and with patch, 98 minutes (range, 70-145 minutes). Two patients with angina were sent to the intensive care unit for the first post- operative night. Outcome measures Hospital discharge: 54 of the 59 patients were discharged on the first postoperative day (Day 1), and four on Day 2 (two were kept in hospital because of angina and one because of nausea, and one refused to go home on the first day, despite agreeing preoperatively). The remaining patient was not discharged until Day 3 because of prolonged headache. Complications: Complications are shown in Box 4. There were no deaths or cases of cerebral ischaemia or myocardial infarction. All complications, except the reperfusion syndrome, became apparent within one day of surgery. The patient with reperfusion syndrome was readmitted with a generalised seizure on Day 5 and required ventilatory support for 13 hours, but made a complete recovery after 24 hours. Cerebral computed tomography showed frontal oedema associated with a small area of possible cerebral haemorrhage, but no evidence of cerebral ischaemia. Clinically, there were no neurological deficits. Two other patients were readmitted within 30 days, one on Day 3 for urinary retention, which had not been present at discharge, and one on Day 23 for unstable angina. The latter had known inoperable coronary artery disease and had been admitted several times before carotid endarterectomy for angina. Patient acceptance of overnight stay: Discharge on Day 1 was very well accepted by all but one patient, who had agreed to it preoperatively, but in the event refused to go home until Day 2. Most patients were relieved in that discharge the day after surgery seemed to "defuse" the magnitude of the procedure for them. Follow-up: All patients were followed up, for an average of 7 months (range, 4 to 11 months). At one-month follow-up, all previously symptomatic patients reported relief of symptoms, including eight who had had non-hemispheric ischaemia. None reported new neurological symptoms, and there were no significant medical or surgical complications (ie, requiring hospitalisation or outpatient treatment). Four-month duplex scanning showed that three patients had evidence of intimal hyperplasia (peak systolic velocity in the internal carotid artery greater than 130 cm/s), and one patient had asymptomatic occlusion of the internal carotid artery. The remaining endarterectomised vessels were widely patent without abnormality. Discussion The results of this case series show that carotid endarterectomy can be performed safely with basic resources, avoiding both carotid angiography and intensive care, and with reduced postoperative hospital stay. Complications in this series compared favourably with those found in previous, major surveys (0-7.5% major complication rate,1,3,21 depending on the type of patient). No deaths or strokes occurred in our series. The only major complication was one case of reperfusion syndrome. This is a rare event after carotid endarterectomy (incidence, 0.4%), and is thought to be caused by revascularisation of a chronically ischaemic cerebrovascular bed. It may occur up to seven days after operation and may progress to seizures, cerebral haemorrhage and death.22 It is usually preceded by a headache, and, although minor headache is common after carotid endarterectomy, patients with severe headaches should not be discharged. Importantly, all complications except the reperfusion syndrome became apparent within one day of surgery, supporting the proposal that longer monitoring in hospital is not needed for patients who have shown no signs of complications within this time. Avoiding cerebral angiography and intensive care and shortening postoperative hospital stay reduces the cost of carotid endarterectomy. In the United States, Ascer et al showed that averting standard angiography and limiting hospital stay to one night saves US$6900 per patient.23 Avoiding cerebral angiography also reduces costs indirectly; the investigation itself can cause stroke,11 which must be included in the overall cost analysis. According to an NHMRC cost analysis, a stroke costs the community $40 243.5 Reducing the cost of carotid endarterectomy could make the procedure more cost effective in asymptomatic patients. In symptomatic patients with high grade stenosis, it is highly cost effective because of its great efficacy in reducing stroke (17% absolute risk reduction).1 In contrast, in asymptomatic patients, it is calculated that 19 carotid endarterectomies are needed to prevent one stroke in five years,4 leading commentators to question its cost effectiveness in these patients.7 However, the dilemma is that most patients experience no warning symptoms of stroke, and if preventive measures are to have an impact they need to be directed to the asymptomatic population as well as the symptomatic population.24 As our study involved only 59 patients, it can be regarded as only a pilot study. However, it confirms the conclusions of overseas studies that carotid endarterectomy can be performed safely with use of only basic resources.8-10,12,13 Since this study, a further 108 consecutive patients have undergone carotid endarterectomy performed by B M B with overnight stay. We have had no reason to alter the overnight policy. Proponents of alternative treatments for carotid bifurcation disease, such as carotid angioplasty and stenting, will not only have to prove the efficacy of these procedures, but will also need to justify the costs of using cerebral angiography (often more than once), disposables (sheaths, wires, angiography catheters, angioplasty balloons, contrast agents) and stents, together with the costs of any short or long term complications. References North American Symptomatic Carotid Endarterectomy Trial Collaborators: Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991; 325: 445-453. North American Symptomatic Carotid Endarterectomy Trial (NAS-CET) Steering Committee: North American Symptomatic Carotid Endarterectomy Trial: Methods, patient characteristics, and progress. Stroke 1991; 22: 711-720. European Carotid Surgery Trialists' Collaboratory Group: MRC European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet 1991; 337: 1235-1243. Asymptomatic carotid atherosclerosis study group. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995; 273: 1421-1428. National Health and Medical Research Council. Clinical practice guidelines: prevention of stroke -- the role of anti-coagulants, anti-platelets and carotid endarterectomy. Canberra: NHMRC, 1996. Easton JD, Serman DG. Stroke and mortality rate in carotid endarterectomy: 228 consecutive operations. Stroke 1977; 8: 565-568. Hankey GJ. Asymptomatic carotid stenosis: how should it be managed? Med J Aust 1995; 163: 197-200. Hirko MK, Morasch MD, Burke K, et al. The changing face of carotid endarterectomy. J Vasc Surg 1996; 23: 622-627. Collier PE. Are one-day admissions for carotid endarterectomy feasible? Am J Surg 1995; 170: 140-143. Calligaro KD, Dougherty MJ, Raviola CA, et al. Impact of clinical pathways on hospital costs and early outcome after major vascular surgery. J Vasc Surg 1995; 22: 649-660. Goodson SF, Flanigan P, Bishara RA, et al. Can carotid duplex scanning supplant arteriography in patients with focal carotid territory symptoms? J Vasc Surg 1987; 5: 551-557. Kuntz KM, Skillman JJ, Whittemore AD, Kent KC. Carotid endarterectomy in asymptomatic patients -- is contrast angiography necessary? A morbidity analysis. J Vasc Surg 1995; 22: 706-716. Hankey GJ, Warlow CP, Sellar RJ. Cerebral angiographic risk in mild cerebrovascular disease. Stroke 1990; 21: 209-222. Davies MJ, Mooney PH, Scott DA, et al. Neurologic changes during carotid endarterectomy under cervical block predict a high risk of post-operative stroke. Anesthesiology 1993; 78: 829-833. Imparato AM, Ramirez A, Riles T, Minzer R. Cerebral protection in carotid surgery. Arch Surg 1982; 117: 1073-1078. Connolly JE. Carotid endarterectomy in the awake patient. Am J Surg 1985; 150: 159-165. Thiele BL, Jones AM, Hobson RW, et al. Standards in non-invasive cerebrovascular testing: report from the Committee on Standards for Non-invasive Vascular Testing of the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery. J Vasc Surg 1992; 15: 495-503. Zwiebel WJ. Introduction to vascular ultrasonography. 3rd ed. Philadelphia: WB Saunders, Harcourt Brace Jovanovich, 1992: 123-132. Carpenter JP, Lexa FJ, Davis JT. Determination of sixty percent or greater carotid artery stenosis by duplex Doppler ultrasonography. J Vasc Surg 1995; 22: 697-705. Rosenberg N. CRC handbook of carotid artery surgery: facts and figures. 1st ed. Boca Raton, Fla: CRC Press, 1989. Riles TS, Fisher FS, Lamparello PJ, et al. Immediate and long term results of carotid endarterectomy for asymptomatic high grade stenosis. Ann Vasc Surg 1994; 8: 144-149. Reigel MM, Hollier LH, Sundt TM, et al. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy. J Vasc Surg 1987; 5: 628-634. Ascer E, Pollina RM, Lorensen E, et al. Carotid endarterectomy for asymptomatic stenosis. A safe simplified cost effective approach [abstract]. Cardiovasc Surg 1995; 1 : 46. 3 Suppl. Bock RW, Gray-Weale AC, Mock PA, et al. The natural history of asymptomatic carotid artery disease. J Vasc Surg 1993; 17: 160-171. (Received 20 Feb, accepted 26 Sep, 1997) Authors' details Gosford Hospital, Holden Street, Gosford, NSW. Bernard M Bourke, FRACS, DDU, Vascular Surgeon; Denis C Crimmins, FRACP, Neurologist. Reprints: Dr B M Bourke, 213 Albany Street North, Gosford, NSW 2250. Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Bernard M Bourke · Denis C Crimmins