induced coma scales' or mental scoring systems,4 or both, may be of more value but require further evaluation. Although the authors mention epilepsy as a.
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Damaging diagnoses of myalgic encephalitis in cHildren SIR,-We are being referred, from consultants and family doctors, a small but nevertheless worrying number of children and very young teenagers in whom a diagnosis of myalgic encephalitis has been made or suggested-in some cases because the mother has been diagnosed as having myalgic encephalitis. Some of these young subjects have received management and treatment which has not been put to the generally accepted tests of clinical efficacy or safety. Virtually all have had their quality of life further and seriously impaired by the application ofthe myalgic encephalitis label. The consequences have been serious with withdrawal from school, loss of contact with social peers, somatising of psychological problems, and lack of rational medical treatment, whether it be from a paediatrician or child psychiatrist. In most cases the diagnoses have been made or offered by parents with harassed practitioners acquiescing in the diagnosis without making the necessary rigorous clinical appraisal. In other cases the proffered diagnosis has led to extensive and unnecessary investigation. We believe that there is a more responsible role to be played by the ME Society. It should reconsider carefully whether it should encourage parents to consult doctors sympathetic to the diagnosis of myalgic encephalitis in adults, who are not necessarily best equipped to diagnose and manage these young patients. We have exercised forebearance by writing in these restrained terms, but we are concerned that a diagnosis of myalgic encephalitis may seriously damage a child's health. FRANK HARRIS
Department of Child Health, Royal Liverpool Children's Hospital, Alder Hey, Liverpool L12 2AP L S TAITZ
Department of Child Health, Children's Hospital, Sheffield
Comatose patients smelling of alcohol SIR,-The leading article by Dr .Gerardine Quaghebeur and Mr Peter Richards' addresses a difficult problem that is commonly encountered but falls short of giving an adequate overview. That neurosurgeons should fall prey to using the vague terms coma and comatose throughout such an article is surprising. Perhaps this reflects the inability of standard neurosurgical scoring scales to reflect levels of intoxication.2 The use of poison
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induced coma scales' or mental scoring systems,4 or both, may be of more value but require further evaluation. Although the authors mention epilepsy as a complicating factor in diagnosis, hypoglycaemia, hyperglycaemia, drugs (80% of overdoses are associated with alcohol), subarachnoid haemorrhage, and acute cardiac events, which are all common, have been omitted. History and examination, as stated in the article, may lead to diagnosis in these patients, but neglect of blood sugar estimation is, in our view, a serious oversight.' Blood gas tensions, temperature, and electrocardiography may also be important indicators in diagnosis in unconscious patients smelling of alcohol. Finally, the implication that all patients with altered consciousness who smell of alcohol should be admitted for eight hours' observation (presumably to a neurosurgical ward) is hardly realistic and would not receive widespread support.
an altered level of consciousness is concerned, if there has been a recent head injury any patient who has confusion or any other depression of the level of consciousness should be admitted; any doctor who sends a patient home from casualty who is less than fully alert for whatever reason should be absolutely certain of his or her diagnosis and that the patient will receive adequate care outside of hospital before doing so. The point of our comment about observing the patient was, of course, that drunk patients within eight hours should be starting to get better and if the patient does not improve then it is essential to rethink the diagnosis.
STEPHEN CUSACK RUPERT EVANS
SIR,-Much as we enjoyed the interesting editorial by Dr Gerardine Quaghebeur and Mr Peter Richards, as consultants in accident and emergency medicine who have to deal most nights with comatose patients smelling of alcohol we think that they have omitted an important investigation. All such patients arriving in our department have routine stick testing for blood glucose concentration (BM Stix estimation). We have accumulated a series of six type I diabetic patients who have missed their meals and taken small amounts of alcohol, rendering them comatose. The other types of patients are the chronic alcoholics who restrict their food intake and have impaired gluconeogenesis. We therefore advocate that estimating the serum glucose concentration is of greater importance in the comatose patient smelling of alcohol than estimating the alcohol concentration.
Accident and Emergency Department, Royal Infirmary of Edinburgh, Edinburgh EH3 9YW 1 Quaghebeur G, Richards P. Comatose patients smelling of alcohol. BrMedJ 1989;299:410. (12 August.) 2 Galbraith S, Murray WR. The relationship between alcohol and head injury and its effects on the conscious lesel. Br]f Surg 1976;63: 128. 3 Matthew H, Lawson AAH. Acute barbiturate poisoning-a review of two years experience. Q3J Med 1966;35:539. 4 Merigian KS, Hedges JP, Roberts JR. Use of abbreviated mental status examination in the initial assessment ofoverdose patients. Arch Emerg Med 1988;5: 139. 5 Tennant WG, Robertson CE. Alcohol induced hypoglycemia. British3journal of Accident and Emergency Medicine 1987;2:16.
AUTHORS' REPLY,-Drs Stephen Cusack and Rupert Evans seemed to have missed the point of our short editorial in that it was a reminder to doctors working in casualty that not all unconscious patients who are smelling of alcohol are drunk and that special attention must be given to other causes of coma. We assumed that any doctor with sufficient knowledge to pass his or her qualifying exams would understand the need to exclude metabolic disorders, poisoning, and acute cardiac events as causes of comas, and therefore we concentrated on giving advice on how to differentiate between patients who have a surgically treatable cause of their coma from those who do not. The use of the terms coma and comatose throughout the article, although imprecise, was of practical necessity. When you are limited to 600 words, as we were, to use our preferred term "Glasgow coma score of eight or less" rather than the term coma would have used up too many words. Finally, as far as admission of patients with
PETER RICHARDS
Charing Cross Hospital, Londoni W6 8RF GERARDINE QUAGHEBEUR Brook Hospital, London SEIX 4L>'
D F McGEEHAN J A A MARYOSH
North Staffordshire Royal Infirmary, Stoke on Trent ST4 7LN 1 Quaghebeur G, Richards P. Comatose patients smelling of alcohol. BrMedJ 1989;299:410. (12 August.)
SIR,-We agree with the points made by Dr Gerardine Quaghebeur and Mr Peter Richards in their editorial.' Comatose patients smelling of alcohol, however, may also be suffering from alcohol induced hypoglycaemia.2 This problem is likely to occur in patients who have ingested alcohol after a period of fasting, which may occur more commonly in chronic alcoholics. We think, therefore, that in the comatose patient smelling of alcohol stick testing of a capillary blood sample for glucose is extremely
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important. It is cheap, easily performed, and will identify patients who have a rapidly reversible cause for their neurological disorder. W G TENNANT
Vascular Studies Unit, Bristol Royal Infirmar\, Bristol BS2 C E ROBERTSON
Roval Infirmarv, Edinburgh EH3 I Quaghebeuir Gi, Richards P'. Comatose patients smelling of alcohol. BrlecdJ 1989;299:410. ( 12 August.) 2 Tennant W'G, Robertson CE. Alcohol induced hypoglycaemia. Bntish Journal of .lccideni and Emrgencv Medicitne 1987;2: 16-7.
culitis, however, is often absent in biopsy specimens from these sites.2 With the introduction of the antineutrophil cytoplasmic antibody assay the diagnosis hopefully can be made earlier, even when the ear, nose, and throat biopsy is not pathognomonic, and referral to a lupus arthritis research unit may be unnecessary. We disagree with the term subacute Wegener's granulomatosis used by the authors and prefer instead the concept of a limited form of the disease as proposed by Carrington and Liebow3 and substantiated by Cassan et al.4 GEORGE E MURTY Department of Ear, Nose, and rhroat, Freeman Hospital, Newcastle upon Tyrnc BRIAN T MAINS
Ear, nose, and throat symptoms in subacute Wegener's granulomatosis SIR,-The paper by Dr D P D'Cruz and colleagues' raises several interesting points that deserve comment. I have experience of 57 patients with Wegener's granulomatosis who also had symptoms and signs relevant to the ear, nose, and throat, although all except three also had lesions elsewhere in the body. Each was treated with a combination of oral prednisolone and azathioprine; one died three years after treatment from glomerulonephritis in a badly damaged kidney. None of these 57 patients had side effects attributable to azathioprine in contrast to the 50% of Dr D'Cruz and colleagues' patients who had side effects with cyclophosphamide. The term "total remission" should be used with care (no duration times are included in their paper) as one woman, whom I first treated at the age of 16, eventually had two normal pregnancies while in "remission" and six years later suffered a near fatal pulmonary recurrence when she was pregnant again. Fortunately, her condition was controlled, and last week I removed the tonsils of her first born. As yet I have not published this comprehensive series of patients who were treated over 24 years as I thought that the numbers were too small. Obviously this was a mistake as the advantages of azathioprine over cyclophosphamide seem to be as yet unappreciated-except by patients. D F N HARRISON Institute of Laryngology and Otology, University College and Mliddlesex School of Mledicine, London I D'Cruz DP, Baguley E, Asherson RA, Hughes GRV. Ear, nose, and throat symptoms in stubacute Wegener's granulomatosis. Br MedJ 1989;299:419-22. (12 August.)
SIR, -We would like to add our experience of the presenting features of 42 patients with Wegener's granulomatosis to that of Dr D P D'Cruz and colleagues' 22 patients. ' The mean age at presentation of our patients was 49 4 years (range 15-72 years) and the mean time from onset to diagnosis was 23 weeks (range three days-four years). The prevalences of involvement at presentation were as follows: renal 26 (62%); nasal cavity and paranasal sinuses 22 (52%); pulmonary 21 (50%); ear 10 (24%); skin eight (19%); joints eight (19%Yo); mouth and oropharynx five (12%); nervous system four (10%); eye three (7%); larynx two (5%); and others five (12%). Five patients presented with lesions of their ear, nose, and throat system alone. Of 29 biopsy specimens taken from an ear, nose, and throat site, only 12 enabled a definitive diagnosis to be made. We therefore agree that renal disease need not necessarily be a presenting feature and that disease of the ear and throat occurs perhaps more commonly than is widely appreciated. The classic histopathological picture of granulomatous vas-
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Department of Ear, Nose, and 'I'hroat, Royal Victoria Hospital, Belfast I D'Crtuz DP, Baguley E, Asherson RA, Hughes GRV. Ear, nose, and throat svmptoms in subacute Wegener's granulomatosis. Br.VedJ7 1989;299:419-22. ( 12 August.) 2 Fauci AS, Haynes BF, Katz P, Wolff SNM. Wegener's granulomatosis: prospectise clinical and therapeutic experience with 85 patients for 21 years. Ann Intern Med 1983;98:76-85. 3 Carrington CB, Liehow AA. Limited forms of angeitis and granulomatosis of Wegener's type. Am 7 Med 1966;41: 497-527. 4 Cassan SM, Coles DJ, Harrison EG Jr. 'I'he concept of limited forms of Wegener's granulomatosis. Am J Med 1970;49: 366-79.
SIR,-In the article on ear, nose, and throat symptoms in Wegener's granulomatosis Dr D P D'Cruz and colleagues' rightly draw attention to the fact that this condition may present with symptoms of the ear, nose, and throat before progressing to systemic manifestations. Emphasis on the delay in giving adequate treatment was highlighted by their finding of a mean period of 3 6 years from the presentation of original symptoms to making the final diagnosis. A previous article2 drew attention to the need for vigilance and suspicion of an underlying systemic vasculitis in cases of unremitting otitis media. Two patients recently presented to our department with evidence of secretory otitis media with effusion and an apparent mixed sensorineural and conductive hearing loss. The first patient was an 18 year old man whose mean bone conduction over four frequencies (500 Hz, 1 KHz, 2 KHz, and 4 KHz) was 65 dB. The second patient was a 57 year old man whose mean bone conduction was 70 dB. In the first patient the diagnosis became clear when he developed renal failure over four weeks. In the second patient the diagnosis was made when he developed renal failure 18 months after presenting with otological symptoms. Both had dramatic improvement of the sensorineural loss, their mean bone conduction falling to 30 dB. In the second patient this may represent pre-existing ear disease, as he had a grade III pars tensa retraction pocket in one ear. The treatable causes of sensorineural hearing loss are few, and for the long term wellbeing of the patient preservation of hearing is of enormous importance. The reversibility of sensorineural hearing loss in Wegener's granulomatosis is well documented.4 The delay in starting adequate treatment in our two patients emphasises that the diagnosis of Wegener's granulomatosis should be a clinical one. Reliance on any particular disease pattern is unsound.' This is especially so in ear, nose, and throat manifestations as secondary infection of the middle ear or the paranasal sinuses, or both, may lead the investigating clinician astray. He or she may believe erroneously that such infection is the primary problem. Reliance on specimens obtained for histological confirmation is also unsafe as the results are inconclusive in up to 50% of cases, even in patients with renal involvement.6 Histological specimens were not helpful in our patients, and it would be erroneous to suggest that the biopsy specimens in this condition give inconclusive
results simply because of difficulties in gaining access to the affected site of inflammation. Hopes that a serological test such as that employing antineutrophil cytoplasmic antigen7 would be specific for Wegener's granulomatosis have not been realised. In both our patients the results of this test were negative. False positive results are also known to occur. The clinical impression of an ill patient with a raised white cell count, anaemia, and a considerably raised erythrocyte sedimentation rate certainly points to an underlying systemic disorder. Treatment with steroids alone allows progression of the disease, albeit at a reduced rate. Dramatic improvement was seen in our patients with the addition of cyclophosphamide. This drug may have to be given in the absence of absolute confirmation of the diagnosis. RICHARD VAUGHAN-JONES NIGEL PADGHAM Ear, Nose, and Throat Department, Dundee 1 D'Cruz DP, Baguley E, Asherson RA, Hughes GRV. Ear, nose, and throat symptoms in subacute Wegener's granulomatosis. Br MedJf 1989;299:419-22. (12 August.) 2 Ridley MG. Recurrent otitis media and pulmonary infiltrates as presenting features in Wegener's granulomatosis. Br Med _7
1988;297:352-3.
3 Tos M. Upon the relationship between secretory otitis media and chronic otitis and its sequelae in adults. 7 Lar-ngol Otol 1981;95:101 1-22. 4 Clements MR. Recovery from sensori-neural deafness in Wegener's granulomatosis.. Laryngol Otol 1989;103:515-8. 5 Deremee RA. Wegener's granulomatosis anatomical correlates, a proposed classification. Mayo Clin Proc 1976;51:777-8. 6 Pinching AJ. Wegener's granulomatosis: observations on 18 patients with severe renal disease. QJ Med 1983;52:435-60. 7 Lockwood CM. Association of alkaline phosphatase with an
autoantigen recognised by circulating antineutrophil antibodies in systemic vasculitis. Lancet 1987;i:716-9.
Surgeons and trauma care SIR, -I recently suggested that accident and emergency specialists have a central role in the resuscitation of victims of major trauma.' This is not to say, as implied by another correspondent,2 that other practitioners are "lacking" in this or any other regard. Major trauma has not been uniformly well managed in the past,' and defence of erstwhile systems and standards is inappropriate. No one disputes that rapid intervention by senior surgeons saves lives after trauma.4 Despite this, or perhaps because of it, general surgeons may not be best placed to supervise the totality of the resuscitation effort. Consultant led resuscitation produces unexpected survivors among seriously injured patients. The most important actions contributing to this are not surgical procedures but the administration of anaesthetic drugs to permit intubation and elective ventilation.' Accident and emergency consultants are best suited to direct the coordinated approach to acutely injured patients for the following reasons. Firstly, they are likely to be available and free from other duties. Secondly, they interact constantly with all relevant specialists, notably in critical care. Middle grade staff often rotate between the two departments, and access to intensive care beds presents no problem to consultants working in this kind of environment. Thirdly, continuity of care is at least as important in the earliest stages of trauma care as it is later on. These begin immediately after injury and comprise the rapid response to the incident, extrication, field stabilisation, and expeditious transfer to definitive treatment. Many accident units operate a flying squad system to deliver resuscitation skill to the scene of a serious accident. Once back in the resuscitation room continuity is assured by the rescuing doctor retaining his or her responsibility for the patient. The 200 full time consultants in accident and emergency in Britain receive in their departments about two million injured patients a year. In addition, there are many thousands of victims of
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