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LET SLEEPING GIAIARDIA LIE
872 The buccal mucosa was also strikingly swollen. Her tongue was painful and swollen, resulting in dysphagia. Oesophageal radiographs showed notable buccal-lingual oedema partly obstructing the oropharynx. The patient’s response to withdrawal of mianserin treatment was dramatic, with disappearance of the facial oedema and macroglossia within four days. The time between initiation of mianserin and the oedematous reaction, and between discontinuation of the drug and disappearance of the oedema, is strongly suggestive of a cause-andeffect relation between the two. It is unlikely that diazepam or atenolol caused these reactions since symptoms did not occur until the addition of mianserin to her drug regimen. Although moderate glossitis has been recorded in two patients treated with mianserin,6 severe buccal-facial-lingual oedema has not been documented and should be added to the potential side-effects of this drug. Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel
G. LEIBOVITCH Y. MAARAVI O. SHALEV
Kopera H. Lack of anticholinergic and cardiovascular effects of mianserin. Acta Psychiatr Scand 1983; 302 (suppl): 81-89. 2. Clink HM. Mianserin and blood dyscrasias. Br J Clin Pharmacol 1983; 15: 291-93S. 3. Quraishy E. Erythema multiforme during treatment with mianserin: a case report. Br J Dermatol 1981; 104: 481. 4. Braye SG, Copplestone JA, Gartell PC. Neutropenic enterocolitis during mianserininduced agranulocytosis. Br Med J 1982; 285: 1117. 5. Boetscher B. Tolvon and toxic epidermal necrolysis. Med J Aust 1980; i: 280-81. 6. de al Fuente JR, Berlanga C. Glossitis associated with mianserin. Lancet 1984; i: 233. 1.
LET SLEEPING GIAIARDIA LIE
SIR,—Dr Gibb (July 22, p 216) reports the examination of faeces specimens for Giardia lamblia microscopy. We take issue on the value of this presenting data from Manchester Public Health
unselective
by wet-film practice by Laboratory
(PHL). In 1988, 62 patients from two neighbouring Manchester health districts with a total population of 307 000 were reported as showing evidence of G lamblia infestation. Of these, 55 (89%) were diagnosed at Manchester PHL which receives nearly all "community-generated" samples, and the other 7 were reported by four hospital laboratories. One laboratory examines wet-films from all the (about 1000) paediatric faeces specimens it receives annually and reported two positives. The remainder, like ourselves, do wet-film microscopy only if it is requested by a clinician or if the patient history suggests contact with giardiasis, travel abroad, or prolonged diarrhoea. In our laboratory this amounts to just over half the specimens received whereas in the hospital laboratories the proportion is somewhat less. As in Edinburgh, we find that most (over 95%) of our positives are diagnosed without recourse to a faecal concentrate. The 62 cases represent an incidence of 20-2 cases per 100 000 population per year, which exceeds the notional annual rate of 172 cases per 100 000 population served by the Edinburgh Medical School department of microbiology (calculated from the data presented by Gibb and those available from census statistics). Our figure, however, is an average which conceals a more than threefold difference in rates (11’0 per 100000 versus 344 per 100000 population) between the two Manchester districts. Since 85-90% of positives from both districts were reported on samples examined in our laboratory, bias resulting from variations in reporting habits, selection of specimens for testing, or laboratory technique and competence is excluded. Dr Gibb is therefore right to have some reservation about ascribing the higher identification rate of G lamblia in Edinburgh, compared with the rest of Scotland, solely to the practice of unselective examination of all faeces specimens by wet film since an almost identical difference in rates in the Manchester districts plainly results from factors independent of
laboratory practice. Our laboratory also examines for parasites and bacterial pathogens in stool samples from applicants for employment by food manufacturers. Faeces from 835 such individuals, who each submitted three samples as part of routine pre-employment
medicals and who gave no history of recent gastrointestinal symptoms, were examined during the 12 months starting in July, 1988. Fifteen excretors of G lamblia cysts were identified among them. In 13 applicants only one of the three specimens examined was positive and from the others two of three specimens proved to contain cysts, suggesting that the passage of detectable numbers of organisms by these individuals is intermittent and may be transient. It should also be noted that no household or secondary cases were identified as a result of follow-up of this group. This finding contrasts with our observations in subjects whose symptoms suggest giardiasis when samples are consistently positive and both secondary and household cases are observed. Our finding indicates that 1-8% of our normal adult population may prove to carry the organism if it is diligently sought, and this rate does not differ significantly from the positivity rate of 2-3% seen in this laboratory among patients who were tested because their clinical history suggested G lamblia infection. The consequences of a positive report for those identified at our laboratory, whether with symptoms or not, involves further medical and environmental health department inquiries, antimicrobial treatment, and follow-up to assess efficacy of therapy. Such subjects may need to take time off work for these investigations and may even be, unjustifiably in some cases, excluded from work. These services and the inconvenience to the patient must be priced and this figure added to the laboratory cost of the additional examination. We have no doubt that if faeces from patients whose symptoms do not suggest giardiasis were to be examined for the presence of cysts then positives would be seen among them; however, we are uncertain about the value of these individuals being identifed. We are all being exhorted to make the best use of available resources, and the significant costs of examining unselected specimens must place the onus on those advocating this policy to show a benefit to either the patients or the community. Our experience suggests it will be very hard to do so. Public Health
Laboratory, Withington Hospital, Manchester M20 8LR
E. B. KACZMARSKI D. M. JONES
LIGNOCAINE PROPHYLAXIS FOR REPERFUSION ARRHYTHMIAS DURING TREATMENT WITH STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION
SIR,-Some protocols of fibrinolytic therapy in acute myocardial include routine administration of lignocaine as prophylaxis for reperfusion arrhythmias.1 Clinical experience has shown that such arrhythmias are benign and, consequently, the need for prophylaxis has been questioned.2-4 We report our experience in five Spanish hospitals. We analysed retrospectively 386 patients who had clinical and electrocardiographic (ECG) evidence of acute myocardial infarction with a rise in ST segment of more than 0-2 mV in two or more electrocardiographs for 30 min or more, even after sublingual administration of nitroglycerin, within 4-6 h of the onset of pain. Patients were excluded if they were aged more than 70 years or if they had insulin-dependent diabetes, high blood pressure of more than 3 months’ duration or on admission (systolic greater than 200 mm Hg and/or diastolic greater than 120 mm Hg), peptic ulcer, cerebrovascular stroke in the past 2 months, surgery or recent severe trauma, or severe hepatic or renal failure. The total dose of streptokinase ranged between 800 000 and 15 million IU given intravenously in 30-90 min. Before streptokinase corticosteroids were given routinely in four hospitals, acetylsalicylic acid in two, and an additional 50 mg intravenous bolus of sodium heparin in one. Patients whose reperfusion arrhythmia was first detected between 5 and 120 min after the start of streptokinase infusion were examined. Reperfusion arrhythmias were present in 215 (56%) patients. 149 had premature ventricular complexes, 71 sinus bradycardia, 59 accelerated idioventricular rhythm, and 22 ventricular tachycardia. At two hospitals prophylaxis with lignocaine (227 patients) was given routinely. The frequency of reperfusion arrhythmia was 47% in these patients and 67% in those infarction
G. LEIBOVITCH Y. MAARAVI O. SHALEV
Kopera H. Lack of anticholinergic and cardiovascular effects of mianserin. Acta Psychiatr Scand 1983; 302 (suppl): 81-89. 2. Clink HM. Mianserin and blood dyscrasias. Br J Clin Pharmacol 1983; 15: 291-93S. 3. Quraishy E. Erythema multiforme during treatment with mianserin: a case report. Br J Dermatol 1981; 104: 481. 4. Braye SG, Copplestone JA, Gartell PC. Neutropenic enterocolitis during mianserininduced agranulocytosis. Br Med J 1982; 285: 1117. 5. Boetscher B. Tolvon and toxic epidermal necrolysis. Med J Aust 1980; i: 280-81. 6. de al Fuente JR, Berlanga C. Glossitis associated with mianserin. Lancet 1984; i: 233. 1.
LET SLEEPING GIAIARDIA LIE
SIR,—Dr Gibb (July 22, p 216) reports the examination of faeces specimens for Giardia lamblia microscopy. We take issue on the value of this presenting data from Manchester Public Health
unselective
by wet-film practice by Laboratory
(PHL). In 1988, 62 patients from two neighbouring Manchester health districts with a total population of 307 000 were reported as showing evidence of G lamblia infestation. Of these, 55 (89%) were diagnosed at Manchester PHL which receives nearly all "community-generated" samples, and the other 7 were reported by four hospital laboratories. One laboratory examines wet-films from all the (about 1000) paediatric faeces specimens it receives annually and reported two positives. The remainder, like ourselves, do wet-film microscopy only if it is requested by a clinician or if the patient history suggests contact with giardiasis, travel abroad, or prolonged diarrhoea. In our laboratory this amounts to just over half the specimens received whereas in the hospital laboratories the proportion is somewhat less. As in Edinburgh, we find that most (over 95%) of our positives are diagnosed without recourse to a faecal concentrate. The 62 cases represent an incidence of 20-2 cases per 100 000 population per year, which exceeds the notional annual rate of 172 cases per 100 000 population served by the Edinburgh Medical School department of microbiology (calculated from the data presented by Gibb and those available from census statistics). Our figure, however, is an average which conceals a more than threefold difference in rates (11’0 per 100000 versus 344 per 100000 population) between the two Manchester districts. Since 85-90% of positives from both districts were reported on samples examined in our laboratory, bias resulting from variations in reporting habits, selection of specimens for testing, or laboratory technique and competence is excluded. Dr Gibb is therefore right to have some reservation about ascribing the higher identification rate of G lamblia in Edinburgh, compared with the rest of Scotland, solely to the practice of unselective examination of all faeces specimens by wet film since an almost identical difference in rates in the Manchester districts plainly results from factors independent of
laboratory practice. Our laboratory also examines for parasites and bacterial pathogens in stool samples from applicants for employment by food manufacturers. Faeces from 835 such individuals, who each submitted three samples as part of routine pre-employment
medicals and who gave no history of recent gastrointestinal symptoms, were examined during the 12 months starting in July, 1988. Fifteen excretors of G lamblia cysts were identified among them. In 13 applicants only one of the three specimens examined was positive and from the others two of three specimens proved to contain cysts, suggesting that the passage of detectable numbers of organisms by these individuals is intermittent and may be transient. It should also be noted that no household or secondary cases were identified as a result of follow-up of this group. This finding contrasts with our observations in subjects whose symptoms suggest giardiasis when samples are consistently positive and both secondary and household cases are observed. Our finding indicates that 1-8% of our normal adult population may prove to carry the organism if it is diligently sought, and this rate does not differ significantly from the positivity rate of 2-3% seen in this laboratory among patients who were tested because their clinical history suggested G lamblia infection. The consequences of a positive report for those identified at our laboratory, whether with symptoms or not, involves further medical and environmental health department inquiries, antimicrobial treatment, and follow-up to assess efficacy of therapy. Such subjects may need to take time off work for these investigations and may even be, unjustifiably in some cases, excluded from work. These services and the inconvenience to the patient must be priced and this figure added to the laboratory cost of the additional examination. We have no doubt that if faeces from patients whose symptoms do not suggest giardiasis were to be examined for the presence of cysts then positives would be seen among them; however, we are uncertain about the value of these individuals being identifed. We are all being exhorted to make the best use of available resources, and the significant costs of examining unselected specimens must place the onus on those advocating this policy to show a benefit to either the patients or the community. Our experience suggests it will be very hard to do so. Public Health
Laboratory, Withington Hospital, Manchester M20 8LR
E. B. KACZMARSKI D. M. JONES
LIGNOCAINE PROPHYLAXIS FOR REPERFUSION ARRHYTHMIAS DURING TREATMENT WITH STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION
SIR,-Some protocols of fibrinolytic therapy in acute myocardial include routine administration of lignocaine as prophylaxis for reperfusion arrhythmias.1 Clinical experience has shown that such arrhythmias are benign and, consequently, the need for prophylaxis has been questioned.2-4 We report our experience in five Spanish hospitals. We analysed retrospectively 386 patients who had clinical and electrocardiographic (ECG) evidence of acute myocardial infarction with a rise in ST segment of more than 0-2 mV in two or more electrocardiographs for 30 min or more, even after sublingual administration of nitroglycerin, within 4-6 h of the onset of pain. Patients were excluded if they were aged more than 70 years or if they had insulin-dependent diabetes, high blood pressure of more than 3 months’ duration or on admission (systolic greater than 200 mm Hg and/or diastolic greater than 120 mm Hg), peptic ulcer, cerebrovascular stroke in the past 2 months, surgery or recent severe trauma, or severe hepatic or renal failure. The total dose of streptokinase ranged between 800 000 and 15 million IU given intravenously in 30-90 min. Before streptokinase corticosteroids were given routinely in four hospitals, acetylsalicylic acid in two, and an additional 50 mg intravenous bolus of sodium heparin in one. Patients whose reperfusion arrhythmia was first detected between 5 and 120 min after the start of streptokinase infusion were examined. Reperfusion arrhythmias were present in 215 (56%) patients. 149 had premature ventricular complexes, 71 sinus bradycardia, 59 accelerated idioventricular rhythm, and 22 ventricular tachycardia. At two hospitals prophylaxis with lignocaine (227 patients) was given routinely. The frequency of reperfusion arrhythmia was 47% in these patients and 67% in those infarction