The second important point concerns attitudes. It is true that we must avoid creating "half trained scientists and half baked clinicians," but it is equally important to affirm that it is wrong to use either laboratory or clinical training in a purely instrumental way. To this end is linked the need for a firm commitment to the job in hand, whether it is a clinical task or a problem in basic research, and respect for those who do this job every day. Only in this way can we avoid engendering in colleagues who are "pure" scientists or clinicians the feeling that they are being used. I have found this feeling to be particularly strongly held among non-clinical scientists in several settings, but I am grateful to have experienced it to a lesser extent among clinician colleagues. Finally, it is important to remember the impact of abrupt career changes on family life. My children were born during my period as a preclinical lecturer and were of school age when I suddenly started doing resident on call duties. The first few months were painful for all concerned and, even after a period of three years in which to acclimatise, they still complain bitterly-although no longer tearfully-about each month's weekend on call. TEIFION DAVIES
Bexlev Hospital, Bexley, Kent DA5 2BW
1 Weatherall DJ. The physician scientist: an endangered but far from extinct species. BMJ 1991;302:1002-5. (27 April.) 2 Davies TW. When things go wrong again. BMJ 1987;295:929.
Anatomy past and present SIR,-As Dr Bruce Charlton clearly outlines, anatomy, once regarded as "the single most useful study a doctor could make," is now crammed and reduced to a preliminary subject.' Dr Charlton emphasises that to survive anatomy must reintegrate with clinical medicine and provide a relevant teaching role. A recent study of 40 senior house officers in accident and emergency medicine in the Oxford region assessed their knowledge of applied hand anatomy. This is an area of practical importance as hand injuries account for 15-20% of all attendances at accident and emergency departments. The results (table) are disturbing or reassuring depending on one's perspective. To a hand specialist they are disturbing-but then accident and emergency senior house officers are not hand specialists. The results are reassuring if one considers that these doctors have not studied anatomy for 5-15 years. Yet they still have an 80% diagnostic accuracy rate in assessing hand injuries. If we are to expect qualified doctors to have a good working knowledge of
Knozwledge of anatomv ofthe hand ofsenior house officers in accident and emergency departments in Oxford reg:ion No(%) answering correctly (n=40) Bones:
Name the bones in the finger Tendons: What is the function of flexor digitorum profundus?
29 (72) 31 (78)
What does flexor digitorum superficialis insert into? 8 (20) What tendon lies over the median nerve? 15 (38) What can be damaged by a penetrating wound to the dorsum of the MCP joint? 31(78) What is a mallet finger? 34 (85) Nerves: Shade in the area of the hand supplied by the ulnar nerve 33(83) How would you test the motor function of the ulnar nerve? 33 (83) Indicate the site of the median nerve at the wrist 33 (83) How would you assess a patient's ability to oppose the thumb? 36(90) Draw the course of the ulnar digital nerve in the index finger 14 (35)
BMJ
VOLUME
302
1
JUNE
1991
applied anatomy then we must provide appropriately tailored postgraduate anatomy classes. The anatomy department must carry its valuable teaching role into the postgraduate curriculum, targeting the teaching of relevant anatomy to each clinical specialty. A familiar knowledge of applied anatomy may once again become one of the most useful studies a doctor could make. NOELLE M MURPHY
another imidazole derivative (ketoconazole or metronidazole). A cross sensitisation between different imidazole derivatives and an anaphylactic reaction to these has been reported.' To our knowledge this is the first published report of an anaphylactic reaction to fluconazole. I Van Dijke CPH, Veerman FR, Haverkamp HCH. Anaphylactic rcactions to ketoconazole. BM7 1984;287:1673.
Middlesbrough General Hospital, Middlesbrough TS5 5AZ DAVID OLNEY Milton Keynes (General Hospital, Milton Keynes MK6 5LD 1 Charlton B. Anatomy past and present. BMJ 1991;302:1001-2. (27 April.) 2 Wilson P. A spectrum of hand injuries. BritishJournal ofAccident and Emergencv Medtctne 1986;1:25-7.
Drug Points Azapropazone and warfarin Dr LINDA BEELEY (Drug and Therapeutics Unit, Queen Elizabeth Hospital, Birmingham B15 2TH) writes: Lest another drug interaction myth becomes established I should like to correct a small point in the drug point by Drs Nay Win and D C Mitchell.' They say that azapropazone potentiates warfarin because it alters the renal clearance of R and S isomers of warfarin. This is not the case. Warfarin is eliminated almost entirely by hepatic metabolism,2 and azapropazone, like phenylbutazone, probably inhibits the metabolism of the warfarin isomers. 1 Win N, Mitchell DC. Azapropazone and warfarin. BM_J 1991;302:969-70. (20 April.) 2 Banfield C, O'Reilly R, Chan E, Rowland M. Phenvlbutazonewarfarin interaction in man. Br J Clin Phartnacol 1983;16: 669-75.
Anaphylactic reaction after oral fluconazole Drs GABRIELLE NEUHAUS, N PAVIC, and M PLETSCHER (Gynecological Hospital, University of Basle, CH-4031 Basle, Switzerland) write: We would like to report an unusual side effect of treatment with fluconazole. A healthy 22 year old woman with no previous. allergy was given 150 mg fluconazole orally to treat a vulvovaginal candidiasis. A few minutes after intake she developed pruritus and paraesthesia of hands and feet, oedema of the feet, and a feeling of constriction of the airways and lack of air. About two hours later she was brought to the hospital with the following symptoms: generalised erythema, oedema of all the extremities, and hypotension (blood pressure 95/30 mm Hg) with her pulse hardly detectable. She lost consciousness for a short time, recovering after intravenous injection of 100 mg hydrocortisone, 125 mg methylprednisolone, and 4 mg clemastine. She reported no intake of any other potential allergen in the 12 hours before the event. Two and a half years previously she had been treated with ketoconazole and twice, one year and one week before the event, with metronidazole (vaginally and orally). She had had no previous contact with fluconazole. Results of a prick test with fluconazole solution were positive at a 1:10 dilution (reaction to histamine positive, reaction to sodium chloride negative). With such low molecular weight compounds, however, this is of questionable significance. For ethical reasons we did not perform the more informative re-exposure test. From the history and the skin test result it seems very likely that this was an allergic reaction to fluconazole, possibly caused by a cross sensitisation through
Sensorineural hearing loss with low dose erythromycin DR EVELYN KEMP, Dr SHLOMO KEIDAR and Professor J G BROOK (Department of Medicine D, Rambam Medical Centre, Haifa, Israel) write: A 77 year old woman with a two week history of fever up to 38 5°C and dry cough was prescribed a nine day course of oral erythromycin 1-5 g daily. A day after starting the treatment she noticed a profound deterioration in her hearing. An audiogram showed symmetrical mainly high tone sensorineural hearing loss. A chest radiograph showed a moderate left sided pleural effusion, presumed to be postpneumonic. The erythromycin was stopped after nine days (total dose of erythromycin 13 5 g) and she was given oral amoxycillin instead. Her hearing improved two days later, which was confirmed by an audiogram performed a week later. At follow up two weeks later she felt well without cough or fever, and subjectively her hearing had completely returned. A repeat chest radiograph showed normal results. Renal function and liver function were normal throughout the course of her condition. The patient was taking no other drugs and we found no other predisposing factors to her hearing loss. Reports of patients taking erythromycin who developed sensorineural ototoxicity show that they were suffering from renal dysfunction'" or renal and liver dysfunction," or were receiving high dose intravenous erythromycin.' In these cases temporary deafness is presumed to have been caused by accumulation of the drug leading to ototoxicity. Originally erythromycin was thought not to require dose reduction in renal failure as only 2% of oral and 12-15% of intravenous erythromycin is excreted in the urine./ Pharmacokinetic studies in patients with renal failure, however, show enhanced bioavailability of the drug. "' There is also gross disturbance of hepatic metabolism in end stage renal failure leading to erythromycin accumulation.2 Erythromycin toxicity generally causes a reversible moderate sensorineural hearing loss, particularly at frequencies above 4000 cycles per second, and low pitched tinnitus. To the best of our knowledge, ours is the first case report of reversible idiosyncratic hearing loss associated with low dose oral erythromycin therapy with normal renal and liver function. I Kroboth PD, McNeil MA, Kreeger A, Dominguez J, Raymond R. Hearing loss and crythromycin pharmacokinetics in a patient receiving hemodialysis. Arch Inter itfed 1983;143: 1263-5. 2 Taylor R, Schofield IS, Ramos JM, Bint AJ, Ward MLK. Ototoxicity of erythromrcin in perutotLal dialysis patients.
Lancet 1981;ii:935-6. 3 Mery JP, Kanfer A. Ototoxicity of erythromycin in patients with renal insufficiency. VNEnglJ7Mled 1979;301:944. 4 Van Manon WVF, Van der Meer JMW1', Kalf MW, Schicht SM. Ototoxicitv of erythromycin. Laticet 1978;ii:214. 5 Eckman M, Johnson T, Reiss R. Partial deafness after ervthromycin. N Engl j Med 1975;649:292. 6 Quinnan G, McCabe W. Ototoxicitv of ervthromvcin. I.ancet 1978;i: 1 160-1. 7 Schweitzer VG, Olsoni NR. Ototoxic effect of crvthromrvci therapy. Arch Otolarvngol 1984;110:258-60. 8 Mintz U, Amir J, Pinkhas J, de Vries A. Transicnt perceptive deafness due to erythromycin lactobionate. JAMA 1973;225: 112-23. 9 Karmodv CS, Weinstein L. Reversible sensorineural hearing loss with intravenous ervthromvcin lactobionate. Ann Otol Rhinol Larvngol 1977;86:9-1 1. 10 Merv JP, Kanfer A. Hearing loss and erythromycin pharmacokinetics in patients receiving hemodialysis. Arch Intern Med 1984;144:4 19-20.
1341
Bexlev Hospital, Bexley, Kent DA5 2BW
1 Weatherall DJ. The physician scientist: an endangered but far from extinct species. BMJ 1991;302:1002-5. (27 April.) 2 Davies TW. When things go wrong again. BMJ 1987;295:929.
Anatomy past and present SIR,-As Dr Bruce Charlton clearly outlines, anatomy, once regarded as "the single most useful study a doctor could make," is now crammed and reduced to a preliminary subject.' Dr Charlton emphasises that to survive anatomy must reintegrate with clinical medicine and provide a relevant teaching role. A recent study of 40 senior house officers in accident and emergency medicine in the Oxford region assessed their knowledge of applied hand anatomy. This is an area of practical importance as hand injuries account for 15-20% of all attendances at accident and emergency departments. The results (table) are disturbing or reassuring depending on one's perspective. To a hand specialist they are disturbing-but then accident and emergency senior house officers are not hand specialists. The results are reassuring if one considers that these doctors have not studied anatomy for 5-15 years. Yet they still have an 80% diagnostic accuracy rate in assessing hand injuries. If we are to expect qualified doctors to have a good working knowledge of
Knozwledge of anatomv ofthe hand ofsenior house officers in accident and emergency departments in Oxford reg:ion No(%) answering correctly (n=40) Bones:
Name the bones in the finger Tendons: What is the function of flexor digitorum profundus?
29 (72) 31 (78)
What does flexor digitorum superficialis insert into? 8 (20) What tendon lies over the median nerve? 15 (38) What can be damaged by a penetrating wound to the dorsum of the MCP joint? 31(78) What is a mallet finger? 34 (85) Nerves: Shade in the area of the hand supplied by the ulnar nerve 33(83) How would you test the motor function of the ulnar nerve? 33 (83) Indicate the site of the median nerve at the wrist 33 (83) How would you assess a patient's ability to oppose the thumb? 36(90) Draw the course of the ulnar digital nerve in the index finger 14 (35)
BMJ
VOLUME
302
1
JUNE
1991
applied anatomy then we must provide appropriately tailored postgraduate anatomy classes. The anatomy department must carry its valuable teaching role into the postgraduate curriculum, targeting the teaching of relevant anatomy to each clinical specialty. A familiar knowledge of applied anatomy may once again become one of the most useful studies a doctor could make. NOELLE M MURPHY
another imidazole derivative (ketoconazole or metronidazole). A cross sensitisation between different imidazole derivatives and an anaphylactic reaction to these has been reported.' To our knowledge this is the first published report of an anaphylactic reaction to fluconazole. I Van Dijke CPH, Veerman FR, Haverkamp HCH. Anaphylactic rcactions to ketoconazole. BM7 1984;287:1673.
Middlesbrough General Hospital, Middlesbrough TS5 5AZ DAVID OLNEY Milton Keynes (General Hospital, Milton Keynes MK6 5LD 1 Charlton B. Anatomy past and present. BMJ 1991;302:1001-2. (27 April.) 2 Wilson P. A spectrum of hand injuries. BritishJournal ofAccident and Emergencv Medtctne 1986;1:25-7.
Drug Points Azapropazone and warfarin Dr LINDA BEELEY (Drug and Therapeutics Unit, Queen Elizabeth Hospital, Birmingham B15 2TH) writes: Lest another drug interaction myth becomes established I should like to correct a small point in the drug point by Drs Nay Win and D C Mitchell.' They say that azapropazone potentiates warfarin because it alters the renal clearance of R and S isomers of warfarin. This is not the case. Warfarin is eliminated almost entirely by hepatic metabolism,2 and azapropazone, like phenylbutazone, probably inhibits the metabolism of the warfarin isomers. 1 Win N, Mitchell DC. Azapropazone and warfarin. BM_J 1991;302:969-70. (20 April.) 2 Banfield C, O'Reilly R, Chan E, Rowland M. Phenvlbutazonewarfarin interaction in man. Br J Clin Phartnacol 1983;16: 669-75.
Anaphylactic reaction after oral fluconazole Drs GABRIELLE NEUHAUS, N PAVIC, and M PLETSCHER (Gynecological Hospital, University of Basle, CH-4031 Basle, Switzerland) write: We would like to report an unusual side effect of treatment with fluconazole. A healthy 22 year old woman with no previous. allergy was given 150 mg fluconazole orally to treat a vulvovaginal candidiasis. A few minutes after intake she developed pruritus and paraesthesia of hands and feet, oedema of the feet, and a feeling of constriction of the airways and lack of air. About two hours later she was brought to the hospital with the following symptoms: generalised erythema, oedema of all the extremities, and hypotension (blood pressure 95/30 mm Hg) with her pulse hardly detectable. She lost consciousness for a short time, recovering after intravenous injection of 100 mg hydrocortisone, 125 mg methylprednisolone, and 4 mg clemastine. She reported no intake of any other potential allergen in the 12 hours before the event. Two and a half years previously she had been treated with ketoconazole and twice, one year and one week before the event, with metronidazole (vaginally and orally). She had had no previous contact with fluconazole. Results of a prick test with fluconazole solution were positive at a 1:10 dilution (reaction to histamine positive, reaction to sodium chloride negative). With such low molecular weight compounds, however, this is of questionable significance. For ethical reasons we did not perform the more informative re-exposure test. From the history and the skin test result it seems very likely that this was an allergic reaction to fluconazole, possibly caused by a cross sensitisation through
Sensorineural hearing loss with low dose erythromycin DR EVELYN KEMP, Dr SHLOMO KEIDAR and Professor J G BROOK (Department of Medicine D, Rambam Medical Centre, Haifa, Israel) write: A 77 year old woman with a two week history of fever up to 38 5°C and dry cough was prescribed a nine day course of oral erythromycin 1-5 g daily. A day after starting the treatment she noticed a profound deterioration in her hearing. An audiogram showed symmetrical mainly high tone sensorineural hearing loss. A chest radiograph showed a moderate left sided pleural effusion, presumed to be postpneumonic. The erythromycin was stopped after nine days (total dose of erythromycin 13 5 g) and she was given oral amoxycillin instead. Her hearing improved two days later, which was confirmed by an audiogram performed a week later. At follow up two weeks later she felt well without cough or fever, and subjectively her hearing had completely returned. A repeat chest radiograph showed normal results. Renal function and liver function were normal throughout the course of her condition. The patient was taking no other drugs and we found no other predisposing factors to her hearing loss. Reports of patients taking erythromycin who developed sensorineural ototoxicity show that they were suffering from renal dysfunction'" or renal and liver dysfunction," or were receiving high dose intravenous erythromycin.' In these cases temporary deafness is presumed to have been caused by accumulation of the drug leading to ototoxicity. Originally erythromycin was thought not to require dose reduction in renal failure as only 2% of oral and 12-15% of intravenous erythromycin is excreted in the urine./ Pharmacokinetic studies in patients with renal failure, however, show enhanced bioavailability of the drug. "' There is also gross disturbance of hepatic metabolism in end stage renal failure leading to erythromycin accumulation.2 Erythromycin toxicity generally causes a reversible moderate sensorineural hearing loss, particularly at frequencies above 4000 cycles per second, and low pitched tinnitus. To the best of our knowledge, ours is the first case report of reversible idiosyncratic hearing loss associated with low dose oral erythromycin therapy with normal renal and liver function. I Kroboth PD, McNeil MA, Kreeger A, Dominguez J, Raymond R. Hearing loss and crythromycin pharmacokinetics in a patient receiving hemodialysis. Arch Inter itfed 1983;143: 1263-5. 2 Taylor R, Schofield IS, Ramos JM, Bint AJ, Ward MLK. Ototoxicity of erythromrcin in perutotLal dialysis patients.
Lancet 1981;ii:935-6. 3 Mery JP, Kanfer A. Ototoxicity of erythromycin in patients with renal insufficiency. VNEnglJ7Mled 1979;301:944. 4 Van Manon WVF, Van der Meer JMW1', Kalf MW, Schicht SM. Ototoxicitv of erythromycin. Laticet 1978;ii:214. 5 Eckman M, Johnson T, Reiss R. Partial deafness after ervthromycin. N Engl j Med 1975;649:292. 6 Quinnan G, McCabe W. Ototoxicitv of ervthromvcin. I.ancet 1978;i: 1 160-1. 7 Schweitzer VG, Olsoni NR. Ototoxic effect of crvthromrvci therapy. Arch Otolarvngol 1984;110:258-60. 8 Mintz U, Amir J, Pinkhas J, de Vries A. Transicnt perceptive deafness due to erythromycin lactobionate. JAMA 1973;225: 112-23. 9 Karmodv CS, Weinstein L. Reversible sensorineural hearing loss with intravenous ervthromvcin lactobionate. Ann Otol Rhinol Larvngol 1977;86:9-1 1. 10 Merv JP, Kanfer A. Hearing loss and erythromycin pharmacokinetics in patients receiving hemodialysis. Arch Intern Med 1984;144:4 19-20.
1341
