Ear, nose and throat

Otitis media typically presents as either acute otitis media (AOM), with symptoms including fever, otalgia, otorrhoea or irritability and short duration; or as otitis media with effusion (OME), which is often asymptomatic and characterised by accumulation of fluid in the middle ear. Diagnostic certainty of otitis media is challenging, given the young age of patients and variability of symptoms. Otitis media predominantly occurs as coincident to viral upper respiratory tract infections and/or bacterial infections. Common viruses that cause upper respiratory tract infection are frequently associated with AOM and new-onset OME. These include respiratory syncytial virus, rhinovirus, adenovirus, parainfluenza and coronavirus. Predominant bacteria that cause otitis media are Streptococcus pneumoniae, Moraxella catarrhalis, and non-typeable Haemophilus influenzae. Antibiotic therapy does not significantly benefit most patients with AOM, but long-term prophylactic antibiotic therapy can reduce the risk of otitis media recurrence among children at high risk. In Australia, 84% of AOM is treated with antibiotic therapy, which contributes to development of antibiotic resistance. Vaccine development is a key future direction for reducing the world burden of otitis media, but requires polymicrobial formulation and ongoing monitoring and modification to ensure sustained reduction in disease burden.

Helen M Massa PhD · Allan W Cripps PhD · Deborah Lehmann MB BS, MSc

Otitis media is a common childhood illness associated with hearing loss, social disadvantage and medical costs. Prevalence and severity are high among Indigenous children. Respiratory bacterial and viral pathogens ascend the eustachian tube from the nasopharynx to the middle ear, causing inflammation, fluid accumulation, and bulging of the tympanic membrane, with or without pain. Among Australian Indigenous children, ear disease commences earlier in life, and involves multiple strains of bacterial pathogens at high density that persist longer. Persistent nasal discharge, overcrowded living conditions (particularly exposure to many children) and poor facilities for washing children perpetuate a vicious cycle of transmission and infection. Risk factors include environmental tobacco smoke, season, lack of breastfeeding, younger age and immature immune system, and possibly genetic factors. The innate immune system is a critical first response to infection, particularly as passive maternal antibodies decline and during the maturation of the infant adaptive immune response. The relative contributions of innate factors to protection from otitis media are currently not well understood. A diversity of antibodies that target strain-specific and conserved antigens are generated in response to natural exposure to otitis media pathogens (or to vaccines). Deficiencies in these antibodies may explain susceptibility to recurrent infections. Incremental contributions from all these elements are likely to be important in otitis media susceptibility versus protection. Effective medical and social strategies to prevent early age of onset are urgently needed.

Selma P Wiertsema PhD · Amanda J Leach PhD

Acute otitis media (AOM) is diagnosed on the basis of acute onset of pain and fever; a red, bulging tympanic membrane; and middle ear effusion. AOM is managed with analgesia (paracetamol or non-steroidal anti-inflammatory drugs). Antibiotic therapy is minimally effective for most patients; it is most effective for children < 2 years with bilateral otitis media and for children with discharging ears. National guidelines recommend antibiotic therapy for Indigenous children with AOM. Evidence for corticosteroids, topical analgesia and xylitol are scant. Otitis media with effusion (OME) is diagnosed as the presence of middle ear effusion (type B tympanogram or immobile tympanic membrane on pneumatic otoscopy) without AOM criteria. Well children with OME with no speech and language delays can be observed for the first 3 months; perform audiological evaluation and refer to an ear, nose and throat (ENT) specialist if they have bilateral hearing impairment > 30 dB or persistent effusion. Children with effusions persisting longer than 3 months can benefit from a 2–4-week course of amoxycillin. Chronic suppurative otitis media is a chronic discharge through a tympanic membrane perforation. It is managed with regular ear cleaning (dry mopping or povidone–iodine [Betadine] washouts) until discharge resolves; topical ear drops (eg, ciprofloxacin); audiological evaluation; and ENT review.

Hasantha Gunasekera DCH, FRACP, MIPH(Hons) · Tony E O’Connor AFRCSI, FRCS(ORL-HNS) · Shyan Vijayasekaran MB BS, FRACS · Christopher B Del Mar MD, FRACGP

Otitis media with effusion and recurrent acute otitis media are ubiquitous among Indigenous children. Otitis media causes conductive hearing loss that may persist throughout early childhood and adversely affect social interactions, language acquisition and learning. Control of otitis media usually restores hearing to adequate levels. Surgery is to be considered when otitis media has not responded to medical treatment. In non-Indigenous populations, tympanostomy tubes (“grommets”), with or without adenoidectomy, can control otitis media; how these findings relate to Indigenous Australians is not known. Tympanic membrane perforation is a frequent sequela of early childhood otitis media among Indigenous children. It occurs as early as 12 months of age and causes conductive hearing loss. Perforation is associated with recurrent aural discharge, particularly in the tropics and in desert regions. Medical and public health management is required until a child is old enough to undergo surgical closure of the perforation, usually by an age of 7–10 years. Surgical closure of the tympanic membrane stops the aural discharge and improves the hearing sufficiently to avoid the need for hearing aids in most cases. The success rate of surgery conducted in rural and remote Australia is below urban benchmarks; improving this will probably require funding for community-based follow-up.

Stephen J O’Leary BMedSc, PhD, FRACS · Ross D Triolo BSc(MedSci), MB BS

Otitis media is a common disease in childhood that can adversely affect cognitive and educational outcomes. The literature in this area is equivocal, and findings may be influenced by research design. The impact of otitis media on individual children’s development appears to depend on the inter-relationship between several factors. Children who have early-onset otitis media (under 12 months) are at high risk of developing long-term speech and language problems. Otitis media has been found to interact negatively with pre-existing cognitive or language problems. For biological or environmental reasons, some populations have a pattern of early onset, higher prevalence and episodes of longer duration; this pattern leads to a higher risk of long-term speech and language problems. These factors suggest that Indigenous children may be at higher risk of cognitive and educational sequelae than non-Indigenous children.

Corinne J Williams PhD · Ann M Jacobs BAppSc(Speech and Hearing)

Otitis media affects nearly all children worldwide. Despite an enormous amount of research, our understanding of this common condition continues to be challenged. New pathogens involved in otitis media are still being identified. The importance of interactions between viral and bacterial infection and the role of new vaccines need to be clarified. The proposal that bacteria can become more resistant to therapy through biofilm formation and intracellular infection could have important implications for treatment. The most important clinical research findings have been summarised in systematic reviews. In developed countries, research supporting “watchful waiting” of otitis media with effusion and acute otitis media have had most impact on evidence-based clinical practice guidelines. Indigenous Australian children remain at risk of more severe otitis media. Research programs targeting this population have been well supported. Unfortunately, interventions that can dramatically improve outcomes have remained elusive. For children at high risk of otitis media, health care services should concentrate on accurate diagnosis, antibiotic treatment of suppurative infections, and scheduled follow-up of affected children. Despite the lack of recent studies, strategies to minimise the impact the hearing loss associated with otitis media are important. Improvements in education, hygiene practices, and living conditions are likely to reduce the incidence and severity of otitis media. Studies of these types of interventions are needed.

Peter S Morris MB BS, FRACP, PhD · Peter Richmond MB BS, FRACP · Deborah Lehmann MB BS, MSc · Amanda J Leach MAgSci, PhD · Hasantha Gunasekera DCH, FRACP, MIPH(Hons) · Harvey L C Coates AO, MS, FRACS

To the Editor: We both are ear, nose and throat (ENT) specialists at a tertiary university hospital and cover 1–2 nights of emergency calls each month. Over 8 months in 2008, we witnessed four emergency patients (aged 25–39 years; three men, one woman) who had sore throat, mild fever and pain on swallowing, without any respiratory distress symptoms. One patient presented with “hot potato voice”. All had had a palatine tonsillectomy in childhood. On examination, the oral pharynx appeared normal to mildly hyperaemic, without any suppuration. To exclude potentially fatal epiglottitis, all patients underwent transnasal flexible laryngoscopy, which revealed swollen lingual tonsils covered with fibrinous exudate typical of streptococcal infection. Distal structures, including the epiglottis and endolarynx, were normal. Acute lingual tonsillitis was diagnosed, and the patients quickly responded to penicillin therapy. Some degree of infection of the lingual tonsils probably occurs when the pharynx is otherwise infected, but is usually left undiagnosed because it is not easily visible without laryngoscopy.1 Although none of our patients had any life-threatening symptoms, this condition could potentially cause upper airway compromise, and the course would certainly be more arduous without antibiotics. The flexibility of our health care system in Croatia allows for some emergency patients’ to refer themselves to the relevant specialty services. If these patients had presented to general practice rather than to our department, where we performed transnasal laryngoscopy, this diagnosis would have probably gone unnoticed, and antibiotic therapy would not have been prescribed. Thus, is acute lingual tonsillitis a neglected cause of severe sore throat? A search of the current literature and ENT textbooks did not reveal many reports of this disease.2,3 Even if our observations referred to rare cases, considering our hospital catchment population for ENT emergencies of more than 300 000, they still outnumbered all cases of epiglottitis treated at our emergency service during the same period. Therefore, it is our opinion that acute lingual tonsillitis should be at least kept in mind as a condition that can cause severe sore throat that is oropharyngoscopically silent or mimics simple viral infection, but is effectively and readily treated with antibiotics.4 Because the base of the tongue cannot be visualised by routine intraoral examination, confirmation of the diagnosis must be made by an ENT specialist who will perform laryngoscopy.

Sasa Janjanin · Drago Prgomet

Clinical record A 68-year-old man presented to our general district hospital in December 2006 with the chief complaint of sore throat, which had started abruptly 2 hours earlier. The pain was described as intense with a stabbing character. He reported minimal improvement after being given 10 mg of morphine subcutaneously. The patient did not report experiencing any cardiac or pulmonary discomfort, and he had no pertinent past medical history. His family history included one sister who had died of a ruptured aortic aneurysm. The patient was a non-smoker and denied any recent medication use. Physical examination showed that the patient’s vital signs were stable, with a normal level of consciousness, a regular pulse of 61 beats/min, and a blood pressure equal at both arms of around 115/70 mmHg. He was slightly tachypnoeic and diaphoretic. An ear, nose and throat examination did not provide any diagnostic clues as to the cause of the pharyngeal pain. Findings of a cardiovascular examination were normal apart from an audible right carotid artery bruit. No other physical abnormalities were detected. Results of laboratory tests were unremarkable, except for a markedly elevated d-dimer level (8.41 mg/L; upper limit of normal, 0.50 mg/L). Routine chest radiography was suggestive of mediastinal widening (Figure A). On the basis of these findings, a thoracic computed tomography scan was performed, which showed a 5.4 cm dissecting ascending aortic aneurysm (Figure B). The dissection involved the aortic root, ascending part of the aorta and aortic arch, and propagated into the right brachiocephalic trunk and left common carotid artery (Figure C). Transthoracic echocardiography additionally showed the presence of a bicuspid aortic valve with moderate grade 2/4 aortic insufficiency. Thoracic aortic dissection was diagnosed, classified as a Stanford type A dissection, given the involvement of the ascending aorta. A congenital bicuspid aortic valve and an ascending aortic aneurysm were predisposing factors for aortic dissection. The patient successfully underwent emergency surgery with graft replacement of the aortic valve and the dissected aortic segment. A: Chest x-ray showing mediastinal widening. The upper normal mediastinal width is defined as a mediastinum to chest-width ratio of over 0.25, measured at the level of the aortic arch (illustrated by the length of the solid line); this is noticeably exceeded in our patient (dashed line). B: Computed tomography scan showing an aneurysmatic dilatation of the ascending aorta with a classical dissection flap (black arrowhead) separating a true and false lumen. C: Propagation of the dissection process into the supra-aortic vessels (white arrows). The clinical presentation in our case was rather trivial, but the combined results from two basic investigations — an elevated d-dimer level and an abnormal chest x-ray — heightened our clinical suspicion for aortic dissection and led us to perform aortic imaging. Thoracic aortic dissection generally results from a laceration of the intimal lining of the aorta. This allows blood leakage into the aortic wall resulting in a propagating separation of the aortic media, thereby creating a false blood-filled lumen.1 Hence, the major criterion for definitive diagnosis of aortic dissection includes visualisation of a so-called intimomedial flap that divides the aorta into a true and a false lumen. Several aortic imaging techniques can be used for this purpose, of which contrast-enhanced computed tomography (CT) and transoesophageal echocardiography (TOE) are the most feasible to perform in an emergency department setting.1,2 Moreover, these investigations help to localise the dissection, thereby allowing appropriate classification. Currently, the Stanford classification of aortic dissection is the most widely adopted system.1,2 This system has the virtue of merely dividing aortic dissection into two subtypes, depending on whether the ascending aorta is involved (type A) or not (type B).1,2 While the definitive diagnosis of aortic dissection is usually straightforward, making the initial clinical diagnosis can be extremely challenging. Aortic dissection is associated with a dramatic rate of misdiagnosis and delayed recognition.3 This is no doubt partially explained by the highly variable clinical presentation of the condition. Our case is a striking illustration of why acute aortic dissection is colourfully called a “clinical chameleon”.1 Although most patients with aortic dissection present with severe chest or back pain (Box 1), the pain can be variably localised to the neck, jaw or throat.4 Throat pain occurs most often in cases of a dissection of the aortic arch, particularly when the supra-aortic vessels are involved. Our patient complained only of a sore throat, and denied having thoracic pain. Only two similar cases have been previously reported.5,6 Moreover, findings on physical examination can be very subtle.1 Classical signs consistent with the diagnosis of thoracic aortic dissection, such as an aortic insufficiency murmur or decreased femoral arterial pulsation, were not present in our patient. According to the International Registry of Acute Aortic Dissection,7 these so-called typical findings are infrequently detected during physical examination (Box 1). In our case, the only notable features of the physical examination were diaphoresis and a right carotid artery murmur. The latter was presumably the result of propagation of the dissection into the right brachiocephalic trunk. Because symptoms and signs of aortic dissection can be diverse and sometimes treacherously trivial, the initial diagnostic suspicion might rely on abnormalities observed during the basal diagnostic work-up. This routinely consists of laboratory testing with d-dimer analysis and chest radiography. d-dimer analysis has only recently come to the fore, with several studies focusing on the stringent association between the d-dimer level and aortic dissection.3,8,9 The pathophysiological mechanism for this relationship is well explained by the release of tissue factor from the dissected aortic wall. This sets off a cascade of events — activation of the extrinsic coagulation system, generation of fibrin, and secondary fibrinolysis with d-dimer formation.8 The d-dimer assay is reported to have an excellent sensitivity and negative predictive value for aortic dissection (Box 1). The quoted sensitivity is equal for both types of dissection, although absolute d-dimer values tend to be higher in type A aortic dissections as they are usually more extended.10 Given its high sensitivity and negative predictive value, d-dimer testing is an attractive tool for the diagnostic work-up of aortic dissection, particularly in the setting of a low pretest probability for aortic dissection. In such cases, a normal d-dimer result can reliably exclude the presence of aortic dissection, hence obviating the need for further investigations.9,10 Besides elevation of the d-dimer level, the clinical suspicion for aortic dissection should also be heightened if the chest radiograph is abnormal (Box 1). Mediastinal widening (relative mediastinum to chest-width ratio > 0.25;11 Figure A) is the most common radiographic finding in aortic dissection.7 Of note, absolute estimations of the mediastinal width are practically inaccurate, as these measurements are influenced by the distance between the roentgenographic source and the thorax.12 It is worth mentioning that one in three patients with aortic dissection has a normal chest x-ray.11 Thus, relying on chest radiography alone as the initial diagnostic modality is inefficient as it clearly carries a high risk of misdiagnosis. When readily available, contrast-enhanced CT and TOE are the preferred imaging modalities in an acute care setting. Both investigations have a comparable diagnostic accuracy and allow a definitive diagnosis of aortic dissection to be established.1,2 However, the diagnosis must first be suspected before it can be confirmed — this case serves as a reminder of this life-threatening condition’s wide variability in clinical presentation, and the need to maintain continuing vigilance. 1 Clinical and basic diagnostic features of thoracic aortic dissection, and percentages of patients presenting with these features who are subsequently diagnosed with Stanford type A or B aortic dissection1,2 Stanford classification Features Type A* Type B† Clinical symptoms and signs7 Presence of any pain 94% > 95% Retrosternal pain 71% 44% Interscapular pain 33% 41% Back pain 47% 64% Abdominal pain 22% 43% Blood pressure Hypotension or shock/tamponade < 25% < 5% Hypertension 35% 70% Aortic insufficiency murmur < 45% < 15% Decreased or absent peripheral pulsations < 20% < 10% Laboratory analysis8,9 d-dimer sensitivity (cutoff, 0.50 mg/L) > 95% > 95% d-dimer negative predictive value (cutoff, 0.10 mg/L) 100% Not reported Chest radiography7 Mediastinal widening 63% 56% Abnormal or blurred aortic contour 47% 53% Other radiographic features‡ < 25% < 25% * Dissection with involvement of the ascending aorta. † Dissection of the descending aorta without involvement of the ascending aorta. ‡ Such as displaced aorta, aortic calcification, tracheal displacement, pleural effusion. Lessons from practice Thoracic aortic dissection is characterised by a highly variable clinical picture, which has led to the condition being called a “clinical chameleon”. d-dimer testing can be of value in excluding aortic dissection. A normal chest x-ray does not rule out the possibility of aortic dissection. Advanced aortic imaging should be performed early in patients who have symptoms suggestive of aortic dissection in order to prevent misdiagnosis.

Sébastien Anguille MD · Aurélie M Derweduwen MD · Jeroen Lenz MD · Luc Vanuytsel MD, PhD · Frank J Cools MD

A 45-year-old man presented with marked, progressive bulging of the right tonsil (Figure, A) and slight swelling of the right submandibular region. Gadolinium-enhanced magnetic resonance imaging of the head and neck showed a large (5 × 4 × 3 cm) neoplasm, occupying the right parapharyngeal space, extending from the deep parotid lobe to the ipsilateral tonsillar region (Figure, B). The neoplasm was removed via an incision in the neck and identified, by histological examination, as a pleomorphic adenoma. In many cases, the first clinical sign of a deep-lobe parotid neoplasm is enlargement of the tonsillar region. Other differential diagnoses of tonsillar swelling include peritonsillar abscess, tonsillar neoplasm and internal carotid aneurysm.

Matteo Alicandri-Ciufelli · Gabriele Molteni · Domenico Villari · Francesco Mattioli · Livio Presutti

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

David Leake was born on 5 September 1907 at “Euroka”, in Walgett, northern New South Wales. In 1919, he was enrolled as a boarder at Cranbrook School in Sydney, where he excelled in several sports, including rugby, rowing and cross-country running. Encouraged by his father to study medicine, David enrolled at the University of Sydney in 1926 and graduated in 1932. In the same year, following the family tradition of breeding livestock, he purchased his first Hereford cows, which he ran with his brother Louis’s poll stud at Cudgewa in the upper Murray region. David left for England in 1934 to work as a Resident Medical Officer in London, returning in 1937 to work in general practice at Canowindra, in central NSW. He enlisted in 1940 and became a member of the 2/5th Australian General Hospital. The following year, he was imprisoned in Salonika, Greece, in the infamous Dulag 183, a German transit camp for prisoners of war (POWs). In 1942, he was sent to Obermansfeld, a POW camp near Frankfurt in Germany, to care for seriously injured POWs. He became the ear, nose and throat (ENT) surgeon there. In the book Escape to live, by Wing Commander Edward Howell, David received special praise: “Our doctors were a young and lively gang . . . Outstanding among them was David Leake . . . He was one of those rare doctors whose interest in their patients is more than professional. He was a philosopher and friend to them as well”. The day David arrived back in Australia in 1945, he married Phyllis Byrne, whom he had met before the war. After training in ENT surgery at Royal Prince Alfred Hospital in Sydney, he moved to Tamworth in 1947. He was probably the first ENT specialist practising in “the bush”. In 1949, he purchased “Bahreenah”, on Goonoo Goonoo Creek near Tamworth, and established what is now the oldest Poll Hereford stud in family ownership. David didn’t suffer fools gladly, and was respected for his “bloody-mindedness”, determination, self-reliance, resilience, dedication to the task in hand, and skill at improvisation — characteristics forged during his time as a POW. On one occasion when a bronchoscopic forcep was not available, he made one from no. 8 fencing wire! But in spite of his “no nonsense” exterior, he was dedicated to and loved by his patients and staff for his care and compassion, attending emergencies at all hours. David retired reluctantly at the age of 80, mumbling that he’d been “given the sack”. He was awarded the Medal of the Order of Australia in 1994 for services to surgery and Poll Hereford breeding. David died peacefully in a nursing home on 30 June 2006. His wife Phyllis had predeceased him in 1990. He is survived by his daughter Jane, who continues to breed Poll Herefords. A loyal friend and colleague, David is affectionately remembered for his dedication, idiosyncracies and marvellous uniqueness.

Peter R C Wakeford · Douglas J Harbison

Objective: To determine agreement between diagnoses and management plans made during an initial videoconference appointment and subsequent face-to-face consultations in paediatric ear, nose and throat (ENT) surgery.Design and setting and participants: A paediatric ENT clinic servicing patients from Bundaberg, Queensland, was conducted through the Centre for Online Health at the Royal Children’s Hospital (RCH) in Brisbane. Between January 2004 and February 2006, 152 consultations with 97 patients were carried out. We retrospectively audited patients’ charts to compare the diagnosis and management plan formulated at the initial videoconference and the eventual diagnosis and surgical management after face-to-face consultation. The clinical outcomes for children who were not recommended for surgery at the RCH were ascertained by telephone survey.Main outcome measures: Agreement between videoconference and face-to-face consultation findings.Results: Of the 97 patients, 75 were recommended for surgical management at the RCH. The remaining patients were either referred back to their general practitioner (9), followed up by the regional paediatrician (10) or lost to follow-up (3). At the conclusion of the study, seven patients were still awaiting surgery and were excluded. Among the 68 patients seen via videoconference and in person, the recorded diagnosis was the same in 99% of cases (67). Surgical management decisions were the same in 93% of cases (63). Telephone follow-up with paediatricians and GPs confirmed that there were no missed diagnoses or ongoing ENT-related problems in the 19 patients referred back to their care.Conclusions: Decisions about ENT surgical interventions for children assessed during videoconference clinics are in close agreement with decisions made by the same surgeon at face-to-face consultation. The way is open to employ telemedicine more widely for pre-admission ENT assessment. However, as in any telemedicine work, widespread application requires care.

Anthony C Smith MEd, BN, PhD · Samuel Dowthwaite BBiomedSc, MB BS · Julie Agnew MB BS(Hons), FRACS · Richard Wootton PhD, DSc

Objective: To investigate the effectiveness and safety of acupuncture in persistent allergic rhinitis (PAR)Design: Randomised, single-blind, sham-controlled trial conducted from May 2004 to February 2005.Participants and intervention: 80 patients with PAR (age, 16–70 years) were randomly assigned to receive real or sham acupuncture. After a 1-week baseline period, participants were treated twice weekly for 8 weeks and followed up for another 12 weeks.Main outcome measures: Nasal obstruction, sneezing, rhinorrhoea and nasal itch were each self-assessed daily on a 5-point scale, and scores were aggregated weekly. The sum of the symptom scores (total nasal symptom score, TNSS) was also determined. A secondary outcome was use of PAR relief medication.Results: After 8 weeks’ treatment, the weekly mean difference in TNSS from baseline was greater with real (−17.2; 95% CI, −24.6 to −9.8) than with sham acupuncture (−4.2; 95% CI, −11.0 to 2.7) (P = 0.01). The decrease in individual symptom score was also greater with real acupuncture for rhinorrhoea (P < 0.01) but not the other symptoms. At the end of follow-up, the greater difference in TNSS from baseline in the real acupuncture group was still apparent: real, −21.0 (95% CI, −29.1 to −12.9) versus sham, − 2.3 (95% CI, −10.2 to 5.6) (P = 0.001). Moreover, the differences from baseline in all four individual symptom scores were greater for the real than for the sham group (P < 0.05). Real and sham acupuncture were both well tolerated.Conclusion: Our findings suggest that acupuncture is effective in the symptomatic treatment of PAR.Trial registration: Australian Government Therapeutic Goods Administration CTN 034/2004.

Charlie C L Xue BMed, PhD · Xuedong An BMed, MApplSc · Thomas P Cheung MSc · Cliff Da Costa PhD · George B Lenon PhD · Frank C Thien MD · David F Story PhD

Derek Farrar, a respected Otolaryngology, Head and Neck Surgeon, was one of the few who brought ear, nose and throat (ENT) surgery to Tasmania in the mid 20th century. Derek was born in Portsmouth, UK, on 27 December 1921. He was educated in Hong Kong and Plymouth, and studied medicine at St Bartholomew’s Medical School at the University of London. On graduating in 1943, he entered the Royal Navy as Surgeon-Lieutenant. After the War, he undertook further training at St Bartholomew’s and obtained a Fellowship of the Royal College of Surgeons in 1949. He developed an interest in ENT surgery and qualified for a Diploma in Laryngology and Otology of the Royal College of Physicians and Surgeons in 1955. Derek came to Australia in 1956 to take up a position in a private ENT practice with Dr Mills Bates in Launceston, and qualified for Fellowship of the Royal Australasian College of Surgeons in the following year. He also worked as an Honorary ENT Surgeon at Launceston General Hospital. After practising in Launceston for 20 years, Derek moved to Hobart, where he worked in private practice and at the Royal Hobart and Repatriation General Hospitals as an Honorary ENT Surgeon, while continuing to visit Launceston regularly. He was also an enthusiastic teacher of medical students, residents and ENT registrars. Derek attended the Hobart and Launceston branches of the Peter MacCallum Clinic (later W P Holman Clinic) for three decades as a Head and Neck Surgeon. He gave generously of his opinion and skills to the younger generation of Otolaryngology, Head and Neck surgeons who came to practise in Tasmania in the early 1980s. In his leisure time, Derek was very active in the Cruising Yacht Club of Tasmania (CYCT). During his period as Commodore, he instigated the publication (by the CYCT and the Tasmanian Lands Department) of D’Entrecasteaux waterways, a book of maps and local guidance for cruising yachts. This book, detailing the area from Recherche Bay in Tasmania’s southwest to the upper Derwent River at New Norfolk, remains a classic guide to locals and visitors cruising these waters. In the late 1980s, Derek retired and had more time for sailing. Northern Queensland was his destination on a number of occasions, the last being in 1997, when he saw his yacht sunk from under him, probably as a result of hitting a submerged container. Thereafter, he pursued a quiet retirement, but his health ailed in later years and he died of pneumonia on 14 February 2007. He is survived by his wife Rhonwen and also by his sons Alan and Nigel. He will be sadly missed and long remembered by his colleagues.

Philip J Moore

A 47-year-old woman presented with a 6-month history of fever, redness and pain in her ears and nose, and hoarseness of voice. She had redness and thickening of both ears (Figure A, solid arrow) with sparing of the lobule (hollow arrow), and a collapsed nasal bridge (Figure B). A computed tomography neck scan revealed destruction of the thyroid cartilage (Figure C). Antineutrophil cytoplasmic antibodies were negative, ruling out Wegener’s granulomatosis. A diagnosis of relapsing polychondritis was made, and prednisolone and azathioprine were commenced. After 7 months of follow-up, there have been no further episodes of cartilagenous inflammation. Features of relapsing polychondritis A: Redness and thickening of the ear (solid arrow) and sparing of the lobule (hollow arrow). B: Collapsed nasal bridge. C: Computed tomography neck scan showing destruction of the thyroid cartilage.

Aman Sharma MD · Pradeep Bambery MD, FRCP(Glas) · Ajay Wanchu MD, DM · Surjit Singh MD · Naresh K Panda MS, FRCS(Edin)

A 50-year-old woman presented to her dermatologist in 1999 with a 6-month history of recurrent pruritic scaly plaques on the abdomen, arms and hairline. The rash, which was presumed to be seborrhoeic dermatitis, improved after treatment with systemic prednisolone. No skin biopsies were taken at the time. In 2004, she developed a leonine facies (Box, A), widespread erythroderma, alopecia, generalised peripheral lymphadenopathy, hyperkeratosis of the palms, and bilateral swollen pinnae with otorrhoea (Box, B). Punch biopsies revealed Pautrier microabscesses containing atypical CD4+ lymphocytes. A peripheral blood film showed Sézary cells, confirming Sézary syndrome. The patient’s condition deteriorated despite treatment with methotrexate, prednisone, bexarotene, interferon, psoralen and ultraviolet A, as well as extracorporeal photopheresis. Radical palliative radiotherapy to the head and neck improved her leonine facies and otitis externa (Box, C). The patient died in 2006, 8 years after initial presentation. Sézary syndrome is a rare, aggressive, cutaneous T-cell lymphoma characterised by widespread erythroderma, atypical peripheral lymphocytes (Sézary cells) and lymphadenopathy. Cutaneous T-cell lymphomas typically present as indolent cutaneous eruptions and are often misdiagnosed at initial presentation, as the skin lesions mimic common dermatological disorders such as eczema or psoriasis. A: Leonine facies. B: Oedematous right pinna. C: Left pinna after radiotherapy.

David R Waterhouse MB ChB · Subhaschandra Shetty MB BS, MS(ENT) · Jeremy S Gathercole MRCS, LRCP, FRACS · Christopher J Seeley MB ChB, FRACS

Acutaneous dental sinus tract is a channel which leads from a dental focus of infection to drain onto the face or neck.1 These tracts tend to occur more frequently from infected mandibular teeth (80%) than maxillary teeth (20%).2 Hence, they are more common in the submandibular or submental regions of the face.3 Sinus tracts may result from localised infections, such as an infected tooth, periodontal disease, actinomycosis or osteomyelitis.4 There are numerous reports of cutaneous dental sinus tracts in the dental literature,1,4-10 but comparatively few reports in the medical literature.2,3 Patients with these lesions often present first to general practitioners rather than to dentists,1-7 possibly because they do not associate lesions of the face with teeth and often have no associated dental pain. Lessons from practice Dental infection can present with cutaneous lesions of the face and neck. Dental assessment is recommended for non-healing face and neck lesions, particularly in submandibular and submental regions. Biopsies or excisions are not necessary and can cause scarring. Management of the dental focus of infection through endodontic (root canal) treatment or tooth extraction will resolve the sinus tract. Clinically, a cutaneous dental sinus tract may resemble a pimple, ulcer, nodule, or indurated cystic area. Because these tracts have a similar clinical appearance to other facial lesions and are relatively uncommon, they may be misdiagnosed, leading to inappropriate antibiotic therapy, aspiration or surgery. Unless the dental focus of infection is treated, recurrence is likely.1-10 When surgical intervention is attempted, breakdown of the wound can leave scarring and wound contracture.2-8 In our three patients, the dental sinus tracts occurred because of delays in diagnosis or management. The differential diagnosis includes pyogenic granuloma, furuncle, foreign body reaction, and cysts, such as sebaceous, epidermoid and thyroglossal cysts.3 Neoplastic causes, such as basal and squamous cell carcinomas, should also be considered,1 as well as other infective causes, including osteomyelitis, actinomycosis and tertiary syphilis gumma.2 Intraoral radiographic examination is a crucial diagnostic tool. A carious tooth or periapical radiolucency on a dental radiograph suggests a possible dental focus of infection. Dental assessment will confirm diagnosis. Usually, dental sinus tracts drain within the mouth, commonly in the vestibule adjacent to the affected tooth. However, they may drain onto the face, depending on the relationship of the muscle attachments and tissue planes of the face to the focus of infection. In the maxilla, if the focus of infection is superior to the muscle attachment, or in the mandible, inferior to the muscle attachment, a sinus tract may form on the face. Pus travels via the route of least resistance along facial planes until exiting cutaneously. When cutaneous sinus tracts are involved, the infected tooth is often free of pain as the tract provides an outlet for inflammatory exudates, allowing decompression.6 The infected, non-vital (ie, necrotic) tooth may be slightly tender to percussion. Histologically, sinus tracts show inflammatory tissue, granulation tissue or abscess formation. The tract may have an epithelial lining.4 Elimination of the source of infection by endodontic treatment or tooth removal results in resolution of the sinus tract, typically within 2 weeks.4,7,8 In most cases, the result is cosmetically acceptable, as in our Patients 1 and 2, but wound contraction and scar tissue may necessitate surgical revision (as in Patient 3).3 Biopsy should be avoided as it may lead to exacerbation of infection or scarring. Antibiotic therapy is indicated when there are signs of systemic involvement (eg, pyrexia or lymphadenopathy). Clinical records Patient 1 A healthy 40-year-old man presented to his general practitioner complaining of a non-healing pustule, and a swelling on his chin with an associated purulent discharge. The patient was referred by his GP to a hospital for excision of the lesion under the care of a surgeon. The surgeon believed the lesion to be a sebaceous cyst and attempted to remove it. Following the procedure, the patient developed fever, malaise, and marked swelling of the mental region. He was admitted to hospital for 2 days for intravenous antibiotic therapy. A dental origin for the lesion was then considered, and the patient was referred to a dental specialist (an endodontist) for assessment. The patient had a history of a car accident which caused trauma to the teeth 15 years previously. He did not receive dental treatment at the time. Clinical examination revealed an erythematous lesion on the chin measuring 0.5 cm in diameter, from which pus drained freely (Figure 1A). Routine clinical dental tests were conducted, including tooth percussion and CO2 dental pulp testing. Radiographic examination revealed a broad radiolucency associated with three of the lower incisor teeth (Figure 1B). These findings led to a diagnosis of chronic apical periodontitis caused by pulpal necrosis and infection of two lower incisor teeth (teeth 31 and 32). Tooth 41 was vital. The patient underwent endodontic (root canal) therapy to the lower incisor teeth (31 and 32) and reported that the discharge ceased a week later. Photographs taken at 3-month follow-up showed resolution of the tract (Figure 1C and 1D). Patient 2 A healthy 41-year-old woman presented to her GP with a non-healing pimple on her right nasolabial fold (Figure 2A). The GP referred the patient to a surgeon who attempted to excise the lesion. Reportedly, the lesion resolved, only to recur 3 months later. By this time, the surgeon suspected a dental aetiology, and referred the patient to an endodontist. Radiographic examination suggested that the lesion was related to an infected upper canine. A radiolucent area around the root of the tooth was characteristic of a periapical abscess (Figure 2B). The tooth was treated endodontically (Figure 2C), and the skin tract resolved. Patient 3 A 7-year-old girl presented to a dentist with toothache and a developing skin lesion under her chin. She had a history of trauma to her lower lip and teeth at 3 years of age. The lower right lateral incisor tooth was slightly tender to percussion, and radiographic examination revealed a radiolucency associated with the root of the tooth. The dentist referred her to an endodontist, who confirmed the diagnosis of chronic apical periodontitis with facial sinus tract. Endodontic treatment was begun, but, because of a dental phobia, the girl delayed completion of this treatment. She presented again 6 months later because the skin lesion had worsened, becoming raised, firm and erythematous (Figure 3A). Endodontic treatment was completed (Figure 3B), and the skin lesion began to heal. At 6-month follow-up, wound contracture had caused dimpling of the skin in the affected area (Figure 3C). This may require surgical revision.

Roland A Barrowman BDS · Mehdi Rahimi BSc, BDS · Mark D Evans MDSc, GradDipClinDent · Arun Chandu MDSc, MB BS, FRACDS(OMS) · Peter Parashos MDSc, PhD

Does allergy predispose to acute infectious sinusitis? Some patients report sinus infections during the hayfever season, and it is commonly supposed that congestion associated with allergic rhinitis can predispose to infectious sinusitis by interfering with the function of the sinus ostia. However, there is no good evidence to support this hypothesis, and no good evidence that specific treatment by allergen avoidance or immunotherapy (or even non-specific treatment with continuous topical corticosteroids) can prevent acute infectious sinusitis in people who do not have underlying chronic sinusitis. Most episodes of acute sinusitis are sequelae to viral upper respiratory tract infections. However, topical corticosteroids are an effective adjunct to antibiotic therapy in cases of acute infectious sinusitis, with or without coexisting allergy (Level II).1 Does allergy cause chronic rhinosinusitis or nasal polyposis? Chronic rhinosinusitis (CRS) (ie, inflammation of the mucosa of the nose and the paranasal sinuses) can be subdivided into two types according to the presence or absence of nasal polyposis (NP).2 The mucosal inflammation in CRS without polyposis is usually neutrophil predominant, but when NP is present (CRS/NP) it is usually eosinophil predominant. The tissue eosinophilia and frequent association of CRS/NP with asthma3 have led to the assumption that CRS/NP is caused by allergy. However, most studies have shown that the presence of IgE to environmental allergens (atopy) is no more common in people with CRS (with or without NP) than in the general population, and the symptoms of CRS are not affected by seasonal changes or allergen exposure. Thus it is now thought that allergy is not the cause of CRS in most cases. Atopy may coexist with CRS, and symptoms of allergic rhinitis can be superimposed on symptoms of CRS. There is no evidence that allergen avoidance or immunotherapy can alleviate CRS, but it may relieve superimposed hayfever symptoms. A subset of CRS/NP associated with chronic fungal infection and systemic fungal allergy has been termed “allergic fungal sinusitis”, but the exact parameters of this entity remain unclear. Antifungal treatments have been disappointing, and the evidence for effectiveness of immunotherapy for fungal allergy in this condition is limited. In most cases, the cause of CRS is not apparent. Bacterial infection frequently coexists, but may not be causative. Current theories of causation include bacterial biofilms, fungal hypersensitivity, sensitivity to bacterial superantigens, and genetic factors. What is the relationship between aspirin sensitivity and sinus disease? About a third of adults with CRS/NP and asthma also have aspirin sensitivity, in which the ingestion of aspirin or another non-steroidal anti-inflammatory drug (NSAID) causes an acute exacerbation of asthma or nasal symptoms or both. This is not an IgE-mediated allergy, but rather a pharmacological intolerance due to dysregulation of prostaglandin and leukotriene metabolism. Patients with CRS may also note symptom exacerbation after intake of alcohol or sulphites, or from aeroirritants such as smoke and fumes. Because these are not true allergies, skin prick testing and allergen desensitisation are not applicable. Aspirin desensitisation by graded oral doses can be effective, but must only be carried out by a specialist under controlled, supervised conditions. Investigation and referral. CRS can cause symptoms similar to perennial allergic rhinitis, and may be indistinguishable on history alone. Anosmia and the presence of nasal polyps seen on anterior rhinoscopy (Figure) are good predictors of chronic sinusitis. However, the complaint of “sinus headache” is not a good predictor of a radiographic finding of sinusitis. Investigation for CRS is appropriate when symptoms of perennial rhinitis occur in the absence of allergy; when allergy is present but not relevant (eg, when there is allergy to seasonal pollens, but symptoms are perennial); or if the symptoms fail to respond adequately to allergy-directed treatment. A computed tomography scan of the sinuses is a useful diagnostic test and is more accurate and informative than a plain sinus x-ray. Evidence-based practice tip Surgery is an effective treatment for chronic rhinosinusitis in patients who have failed medical treatment, with improvement in 75%–85% of patients (Level III).* * NHMRC levels of evidence. Patients with CRS should be reviewed by both an allergist/immunologist and an ear, nose and throat surgeon for consideration of a range of issues including bacterial or fungal infection, coexistent allergy, immunoglobulin deficiency, aspirin/NSAID sensitivity, comorbidities (eg, asthma, Wegener granulomatosis, Churg–Strauss vasculitis, ciliary dyskinesia, cystic fibrosis), or surgery to restore sinus ostial patency. Management. The mainstay of medical therapy is corticosteroids, which act on both allergic and non-allergic inflammation. Topical corticosteroids are effective for treating NP and concomitant allergic symptoms (Level II).4 Brief courses of systemic corticosteroids can significantly reduce inflammation in CRS/NP and alleviate symptoms temporarily (Level III),5 facilitating maintenance therapies or surgical intervention. Although polyp regrowth after surgery occurs quite frequently, surgery remains an important part of overall management.

William B Smith PhD · Peter-John Wormald MD

To the Editor: The Ear, Nose and Throat Department at the Royal Darwin Hospital services an area of about 550 000 km in the Northern Territory. As part of our remit involves dealing with conditions affecting the organs of speech and hearing, a proportion of our patients have communication handicaps. We have frequently encountered the use of “Hand Talk” among Indigenous patients with communication handicaps, and we feel this merits highlighting to your readership. Hand Talk is an established sign language within and between Aboriginal groups in the NT. Although various groups have different signing systems, there are enough similarities between them to enable inter-group communication. Its existence is thought to date as far back as other spoken Aboriginal languages that have now been lost. Theories about its conception include a means of overcoming language barriers between different language groups, a silent form of communication during hunting expeditions, a means of conversation for women during long periods of mourning when speech is prohibited, and a means of communication for deaf or aphonic individuals.1 While completely separate from established Western sign languages, Hand Talk is a sophisticated and intricate means of communication that allows complex interactions to take place and proficient individuals to integrate into their society.2 In the course of our service delivery in Darwin and to outlying districts, we have been struck by both the frequency with which Hand Talk is used in an impromptu manner and the proficiency users exhibit in communicating with it. The significance of this requires an appreciation of the difficulties of applying Western-type communication rehabilitation to Indigenous Australians in remote regions. For example, providing hearing aids, a basic and standard form of communication rehabilitation in urban areas of Australia, can face numerous obstacles in a remote setting. These include lack of a service provider and technical and maintenance support, poor compliance, and logistical problems (something as simple as running out of hearing aid batteries can be a major problem for those in remote areas). While no data are available on the ubiquity of Hand Talk, it clearly represents a valuable part of Aboriginal culture with an important practical function in a situation where Western models of communication rehabilitation are difficult to apply. While attempts to improve conventional communication rehabilitation should continue, these should be combined with efforts to foster Hand Talk through education and facilitating its dissemination by existing users so it does not suffer the fate of other lost Indigenous languages.3

Patrick Jassar · Garrett F Hunter

Ken Vincent was born in Waverley, Sydney, on 18 December 1916 and died peacefully in Bowral, on 22 February 2005, after a protracted illness. He was the only son of Ernest and Ethel Vincent. Except for a period during World War II, Ken spent his entire life living and working within the Sutherland shire. He attended Cronulla Public School and Canterbury Boys High School. In his last year at Canterbury, he was school captain and captain of the Rugby XV team. He studied medicine at the University of Sydney, graduating in 1941. In 1953, after working for a number of years as a general practitioner, Ken took leave from general practice to specialise in otolaryngology at the Royal Ear, Nose and Throat Hospital in London. He eventually opened his own ENT practice in Caringbah, Sydney, in 1959. He was a Visiting Medical Officer at both St George and Sutherland hospitals. It was through the support of Ken and other doctors in the Sutherland shire that the Sutherland Hospital was originally built in the 1950s, and it was there that he developed an interest in rhinoplastic and ear surgery. He was State President of the Otolaryngology Society from 1974 to 1976. Early in his career, Ken joined Sydney Legacy, caring for the widows and children of ex-servicemen, a very active interest he maintained until the last few years of his life, when poor health prevented further participation and involvement. Another part of his work was his voluntary involvement with the Aboriginal communities of western New South Wales, particularly the Murrin Bridge community at Lake Cargelligo, visiting them on a monthly basis in his capacity as an ENT surgeon. He also visited Papua New Guinea and Fiji to undertake voluntary medical work. Many of the older Cronulla locals will remember him not only as the GP who delivered their babies but also as the one who took out their tonsils, or cured their glue ears or sinus problems. Ken’s great love was his family and his life-long partner Nan, whom he adored. He had a remarkable memory, never forgetting a name or a patient’s details, even well into retirement. As an operating surgeon he was meticulous and unforgiving, especially of himself. Ken is survived by his two children, Peter and Pam, and their families. Ian E Cole

Ian E Cole

Allergic rhinitis (AR) is one of the most prevalent medical conditions. It has significant effects on quality of life and can have considerable socioeconomic effects. The traditional classification of perennial and seasonal rhinitis does not distinguish between provoking factors, nor does it indicate the most appropriate treatment. A more useful classification is based on symptoms, which may be intermittent or persistent, and vary widely in severity. The goal of management is to achieve optimal symptom control. Therapeutic options include allergen avoidance, pharmacotherapy and immunotherapy. Antihistamines and intranasal corticosteroids (INCS) have become the cornerstones of therapy. A variety of effective treatments are available for consumers to self-select, without the advice of a doctor or pharmacist. INCS are widely recognised as the most effective pharmacotherapy for AR, in both adults and children. The efficacy of various preparations is similar, but those with low systemic bioavailability are preferred for children and for patients who are also receiving inhaled, topical or systemic corticosteroids.

Ronald S Walls DPhil, FRACP, FRCPA · Robert J Heddle PhD, FRACP, FRCPA · Mimi L K Tang MBBS, PhD, FRACP, FRCPA · Ben J Basger MSc, BPharm, DipHPharm · Graham O Solley MBBS FACP · Guan T Yeo FRACGP, MBBS

Paul Walker Paediatric Otolaryngologist, John Hunter Children’s Hospital, PO Box 293, New Lambton, NSW 2305; and Conjoint Associate Professor, Disciplines of Surgery and Paediatrics, University of Newcastle. walkerpATtpgi.com.au To the Editor: The study by Paradise et al on tympanostomy tubes for persistent otitis media,1 which was expertly reviewed by Morris and Leach in the Journal recently,2 has since been updated.3 The findings of both studies from Pittsburgh should only be applied with caution in Australia. Indications for inserting ventilating tubes (VTs) can be divided into three: bilateral hearing loss of more than 25–30 dB continuously for 3 months after failed non-operative management; structural damage to the tympanic membrane (TM) which may lead to irreversible hearing loss or cholesteatoma; and a miscellany which includes under-lying sensorineural hearing loss or learning difficulties or similar conditions with deterioration associated with bilateral middle ear effusion (MEE), and recurrent middle ear infections with use of VTs as an alternative to antibiotic prophylaxis, among others. The conclusion of the more recent article by Paradise et al3 — that there was no difference in expressive or receptive speech or cognition between children in whom VTs were inserted early or late — is valuable, but may not readily be extended to Australian practice. Although 6350 children were enrolled, only 397 were actually randomly allocated into the early or late treatment groups. Thus, the numbers are not large. Of more concern is that only 18% of those analysed had bilateral continuous MEE (40 in the early and 32 in the late treatment group), with the remaining 82% having unilateral (continuous or discontinuous) or bilateral discontinuous MEE. Only the 18% with bilateral continuous MEE would ordinarily be candidates for VTs in Australia, as Paradise et al underline the fact that intermittent and/or unilateral MEE is not associated with speech and language difficulties in the absence of other handicaps to learning. An abnormal hearing test result was identified by the study as a 15 dB loss. This could well fall in the normal range for the Australian Hearing Service for children wearing headphones, and a minimum threshold of 25-30 dB should typically be required for considering VTs in Australia. As Morris and Leach2 pointed out for the earlier study,1 the later study also excludes children “not otherwise healthy”,3 and the results cannot be generalised to such children, or to those with moderate rather than mild hearing loss. Pointing to studies such as that of Paradise et al can be very helpful in reassuring parents who want VTs for their child with unilateral or intermittent hearing loss that not having VTs does not place the child’s speech and language development at risk.

Paul Walker

QuestionIs early surgical referral for children with persistent otitis media with effusion (OME) appropriate? Trial details Design: Randomised, assessor-blinded, controlled trial. Setting: Two hospitals and six private paediatric group practices from the Pittsburgh region in the United States. Participants: 429 children aged less than 3 years who had otitis media with effusion (OME) that had persisted despite treatment with antimicrobial drugs for the equivalent of: 90 days in the case of bilateral effusion; or 135 days in the case of unilateral effusion. Interventions: Children assigned to the early treatment group were scheduled to have ventilation tubes (grommets) inserted as soon as possible. Children assigned to the late treatment group were scheduled to undergo the operation 6 months later if bilateral effusion persisted (or 9 months later if unilateral effusion persisted). Children in the late treatment group could receive grommets earlier if their parents requested the operation. Main outcome measures: Standardised assessment of cognitive ability, receptive language ability, expressive language ability, parenting stress, and child behaviour at 3 years of age. Main results: 169 children in the early treatment group (82%) and 66 children in the late treatment group (34%) had had ventilation tubes (grommets) inserted by 3 years of age. There were no significant differences (mean ± standard deviation) for early treatment versus late treatment in the General Cognitive Index of McCarthy's Scales of Children's Abilities (99 ± 14 v 101 ± 13); Peabody Picture Vocabulary Test–Revised (92 ± 13 v 92 ± 14), Number of Different Words Test (124 ± 32 v 126 ± 30), Percentage of Consonants Correct–Revised Test (85 ± 7 v 86 ± 7), Total Parenting Stress Index, Short-form–Total Stress (66 ± 18 v 68 ± 21), and Child Behaviour Checklist–Total Problems (50 ± 10 v 49 ± 10). Conclusion: In young children with persistent OME, prompt insertion of ventilation tubes (grommets) does not measurably improve developmental outcomes by 3 years of age. CommentaryRationale for the trialOtitis media with effusion (OME) is the most prevalent form of middle ear disease in young children. It is defined as the presence of fluid behind the tympanic membrane without the symptoms or signs of acute otitis media (AOM).1 It is usually associated with some hearing loss. OME with persistent hearing loss may contribute to delays in speech and language development.2 Recommended interventions include the use of antibiotics and the insertion of ventilation tubes (grommets).2-4 There have been concerns about the overuse of grommet surgery. Substantial variation in rates of this procedure have been documented.5,6 Clinical practice guidelines have recommended that grommets are an option for children who have bilateral OME associated with a hearing loss of > 20 decibels for at least 3 months.2-4 The intervention is most likely to benefit younger children (during the most critical phase of language development) and those with most hearing loss. Trial methodsThis trial was part of the largest otitis media cohort study ever conducted.7 The study was generally well designed and well reported.8,9 A total of 6350 healthy infants were enrolled in their first 2 months of life and were evaluated monthly for otitis media; 588 of these children had persistent or very frequent OME. They were regarded as typical of children who might receive surgery in the United States. The aim of the study was to determine the benefits of early referral for surgery compared with delayed referral (where “watchful waiting” continued for an additional 6 months). Random assignment was made by designated non-clinical staff using separate, computer-generated lists of random numbers. Children were stratified according to site, age (in 6-month categories), and whether the eligibility criteria were met on the basis of bilateral or unilateral effusion. Assignment within each of the predetermined strata occurred in permuted blocks of four. This ensured that the allocation was balanced after every four new children (in a stratum) were randomly allocated. Children underwent developmental assessment as soon as possible after their third birthday (and always within 2 months). Standardised assessment tools were used. Assessors were unaware of the child’s medical history, health insurance status, and mother’s level of education. The investigators proposed that a difference of 0.33 standard deviations between groups on any outcome measure could be clinically important. Follow-up of participants over a prolonged period was reasonably good (95% and 92% of the early- and late-treatment groups, respectively). All analyses were based on the intention-to-treat principle (although children who were not assessed could not be included in the analysis). Any weaknesses in the methods and the quality of reporting were relatively minor. Ideally, the authors should have also described (i) how random allocation was concealed from the investigators, (ii) how block size was concealed from investigators (so they couldn’t guess which intervention would be allocated next), (iii) the adequacy of blinding, (iv) the primary outcome for the study, and (v) an assessment of adverse outcomes. The choice of a 0.33-standard- deviation difference between the groups in any of the assessments as the minimal clinically important difference was controversial. While this approach should be able to identify reasonably small statistical differences attributable to the intervention, the clinical importance of such a difference is not easily understood. In the end, because there were no statistically significant differences in any of the outcome measures, this issue did not arise. New informationThis is the largest randomised trial to evaluate ventilation tubes in children with persistent OME. Previous studies had shown that surgery improved hearing by around 12 dB at 6 months and 6 dB at 12 months.5 Most of these studies involved older children and did not include an assessment of speech and language (which is generally regarded as the most important outcome). The results of this study are consistent with those of previous studies in demonstrating that grommet surgery will substantially reduce the amount of time that a child has OME, and modestly improve hearing. However, by 3 years of age, early referral for surgery had no beneficial effect on development or behaviour. The consistent lack of effect for a range of outcome measurements was striking. These findings were not changed by the subsequent subgroup analyses.10 The results of this study are unlikely to be explained by a biased estimate of effect or by chance. Similar results have also been documented in other recent well designed studies in different populations.11-13 Implications for clinical practiceIdentifying young children with persistent OME is a common problem for general practitioners in Australia. For children who are otherwise well, this study shows that early referral for surgery does not improve developmental outcomes at 3 years of age. For individual families affected by long waiting times or preferring to avoid an operation, parents can be reassured that the child will not be disadvantaged by delaying the decision about surgery. The duration of “watchful waiting” can be extended to 9–12 months without serious consequences. Although hearing loss will persist longer, many episodes of persistent OME will resolve and potential complications of surgery (otorrhoea, chronic perforation) will be avoided. It is still possible that the insertion of ventilation tubes will improve developmental outcomes in some children. The results of this study are not applicable to: children with established speech and language delay (or conditions known to be associated with speech and language delay); children with bilateral OME that persists longer than 9–12 months; and children with more substantial conductive hearing loss. Parents of these more severely affected children can be advised that this simple and safe operation will improve their child’s hearing. However, whether it will improve their speech and language development is still uncertain. Further trials targeting these specific subgroups should be supported.

Peter S Morris FRACP, PhD · Amanda J Leach PhD

Objectives: To compare the effectiveness of ototopical ciprofloxacin (0.3%; CIP) with framycetin (0.5%), gramicidin, dexamethasone (FGD) eardrops (5 drops twice daily for 9 days) together with povidone-iodine (0.5%) ear cleaning as treatments for chronic suppurative otitis media (CSOM) in Aboriginal children.Design and participants: Aboriginal community-controlled, community-based, multicentre, double-blind, randomised controlled trial in eight Aboriginal Community Controlled Health Services across northern Australia, involving 147 Aboriginal children with CSOM.Main outcome measures: Resolution of otorrhoea (clinical cure), proportion of children with healed perforated tympanic membrane (TM) and improved hearing, 10–21 days after starting treatment.Results: 111 children aged 1–14 years (CIP, 55; FGD, 56) completed treatment. CSOM cures occurred in 64% (CIP, 76.4%; FGD, 51.8%), with a significantly higher rate in the ciprofloxacin group (P = 0.009, absolute difference of 24.6% [95% CI, 15.8%–33.4%]). TM perforation size and the level of hearing impairment did not change. Pseudomonas aeruginosa was the most common bacterial pathogen (in 47.6%), while respiratory pathogens were rare (in 5.7%).Conclusions: Twice-daily ear cleaning and topical ciprofloxacin is effective at community-level in achieving cure for CSOM. Healthcare providers to Aboriginal children with CSOM should be given special access to provide ototopical ciprofloxacin as first-line treatment.

Sophie Couzos FRACGP, FACRRM, FAFPHM · Traven Lea MAEIH, DipPHTM · Margaret Culbong · Reinhold Mueller MSc, PhD · Richard Murray FRACGP, MPH

Clinical questionA 43-year-old woman sought advice about the treatment of her sea-sickness. A sea-kayaking enthusiast, she suffers disturbing motion sickness in big seas. The usual remedies have either been ineffective or made her drowsy. A scuba-diving instructor recommended that she try taking phenytoin the night before going kayaking, and she wonders whether there is any evidence to support this recommendation. Search questionThe primary search question was ...

Edi G Albert MSc FRACGP