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Dobutamine-atropine stress echocardiography and central anticholinergic syndrome
continuum has clouded our understanding of pre-eclampsia for some time.’ Unlike pre-eclampsia, isolated gestational hypertension without proteinuria does not increase maternal and perinatal mortality.2,3 Biochemical changes in women with proteinuric pre-eclampsia and isolated gestational hypertension also indicate a different pathophysiology. Although endothelial activation, as indicated by increased circulating concentrations of cellular fibronectin, can be shown in women with pre-eclampsia up to 10 weeks before clinically evident disease, there is no increase in hypertensive women without proteinuria, even at the time of increased blood pressure.4 Epidemiological data also indicate that the long-term outlook for women who do have pre-eclampsia is quite different from those with hypertension alone during pregnancy. There is no increase in eventual fixed hypertension in truly pre-eclamptic women,5 whereas hypertension without proteinuria predicts the eventual development of hypertension.’ It is pre-eclampsia, rather than PIH, that should be the focus of any investigation with implications for maternal and fetal health. We would be interested in the duration of sexual cohabitation before conception in the 19 subjects who developed pre-eclampsia.
Profuse growths of N meningitidis were isolated from 19 of 1510 (1-26%) throat swabs taken from patients with sore throats during 1993 and 1994. Group A haemolytic streptococci were also isolated from 2 of the 19 specimens, mixed anaerobes from another 2, group B streptococci and pneumococci from 2 further individual specimens, and 1 case subsequently was shown to have glandular fever. When these findings were discussed with the medical officers looking after the patients, it was notable that their sore throats had been present for more than five days; 1 patient had an ephemeral rash. It was decided that a single dose of ciprofloxacin would be the most appropriate treatment in those cases in which no other presumed pathogen than N meningitidis had been isolated. Other pathogens were treated with oral penicillin. Our results merit further investigation. Many patients with severe meningococcal disease give a history of having had a sore throat a week before onset of the meningitis. Is it possible that the simple treatment of a prolonged sore throat might in some cases abort the progression to meningitis?
Philip N Baker, James M Roberts Magee-Womens Research Institute and Departments of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA 15213, USA
Microbiology Laboratory,
1 2
3
4
5
Chesley LC. Mild preeclampsia: potentially lethal for women and for the advancement of knowledge. Clin Exp Hypertens 1989; B8: 3-12. Dunlop W. General management of mild and moderate hypertensive diseases in pregnancy. In: Sharp F, Symonds EM, eds. Hypertension in pregnancy. New York: Perinatology Press, 1987: 263-78. Page EW, Christianson R. Influence of blood pressure changes with and without proteinuria upon the outcome of pregnancy. Am J Obstet Gynecol 1976; 126: 821-33. Taylor RN, Crombleholme WR, Friedman SA, Jones LA, Casal DC, Roberts JM. High plasma cellular fibronectin levels correlate with biochemical and clinical features of preeclampsia but cannot be attributed to hypertension alone. Am J Obstet Gynecol 1991; 165: 895-901. Fisher KA, Luger A, Spargo BH, Lindheimer MD. Hypertension in pregnancy: clinical-pathological correlations and remote prognosis. Medicine 1981; 60: 267-76.
Do
meningococci
cause sore
throats?
SiR-There are times when investigating one’s own family reveals interesting anomalies. After the wife of a microbiologist had suffered from a sore throat for a week he decided to do a "curative" throat swab. He inoculated various plates in his laboratory and was informed the next day that there was an almost pure growth of Neisseria meningitidis that his staff recognised with standard techniques. Two aspirins improved the clinical picture, and a few tactical telephone calls confirmed that the patient was not developing meningococcal meningitis. Does this organism act as a primary pathogen and cause a sore throat of unusual duration and severity? It is recognised that it is easy to isolate small numbers of N meningitidis from the normal throat in up to a quarter of the fit adult population.’1 However, detection of this organism is not part of the routine investigation of throat swabs submitted to the laboratory. We concentrate on the presence of haemolytic streptococci and the organisms that cause Vincent’s angina. Under specific circumstances we seek for the presence of N gonorrhoeae, Corynebacterium diphtheriae, and perhaps C haemolyticum. It is also recognised that a range of virus infections may present as a sore throat. Following the observation above, the two laboratories in Somerset were persuaded to look for high numbers of N meningitidis when throat swabs were being examined. 1636
J V S Pether, R J D Scott, P Hancock Public Health Laboratory,
1
Musgrove Park Hospital, Taunton TA1 5DB, UK; and Yeovil District Hospital, Yeovil
Pether JVS, Lightfoot NF, Scott RJD, Morgan J, Steele-Perkins AP, Sheard SC. Carriage of Neisseria meningitidis: investigations in a military establishment. Epidemiol Infect 1988; 101: 21-42.
Dobutamine-atropine stress echocardiography and central anticholinergic syndrome SiR-Picano and colleagues (Oct 29, p 1190) describe their experience with dobutamine-atropine stress echocardiography to diagnose coronary artery disease, and report the rare complication of atropine poisoning. They do not describe the underlying pathogenesis of this condition, nor its management. From their description, I presume atropine poisoning is the central anticholinergic syndrome-a condition in which atropine acts on central nervous system cholinergic receptors to cause confusion or longlasting coma.’ This condition is well known to anaesthetists, who are occasionally confronted with such cases during postoperative recovery after administration (usually as premedication) of atropine or hyoscine. It is thought to be in elderly patients, and the classic more common presentation is unexplained confusion or prolonged sedation. Physostigmine 0-5-2 mg intravenously can reverse these central effects because, unlike neostigmine, it can cross the blood-brain barrier, 1,2 This is because of its high lipid solubility. I have used this treatment on several occasions in postoperative recovery. Administration of physostigmine, therefore, also acts as a diagnostic test: rapid improvement rules out other causes of confusion and coma in this age group (in particular stroke). Such treatment can reduce anxiety to all concerned, as well as the requirement for long hospital care and additional health care resources. An alternative would be to avoid atropine use in the elderly and to give glycopyrrolate, a quaternary anticholinergic drug that does not cross the blood-brain barrier and so cannot cause central anticholinergic syndrome. Paul Myles Department of Anaesthesia, Alfred Hospital, Melbourne 3181, Australia 1 2
Moss J, Craigo PA. The autonomic nervous system. In: Miller RD, ed. Anesthesia. 4th ed. Melbourne: Churchill Livingstone, 1994; 566-67. Crowell EB, Ketchum JS. The treatment of scopolamine-induced delirium with physostigmine. Clin Pharmacol Ther 1967; 8: 409-14.
Profuse growths of N meningitidis were isolated from 19 of 1510 (1-26%) throat swabs taken from patients with sore throats during 1993 and 1994. Group A haemolytic streptococci were also isolated from 2 of the 19 specimens, mixed anaerobes from another 2, group B streptococci and pneumococci from 2 further individual specimens, and 1 case subsequently was shown to have glandular fever. When these findings were discussed with the medical officers looking after the patients, it was notable that their sore throats had been present for more than five days; 1 patient had an ephemeral rash. It was decided that a single dose of ciprofloxacin would be the most appropriate treatment in those cases in which no other presumed pathogen than N meningitidis had been isolated. Other pathogens were treated with oral penicillin. Our results merit further investigation. Many patients with severe meningococcal disease give a history of having had a sore throat a week before onset of the meningitis. Is it possible that the simple treatment of a prolonged sore throat might in some cases abort the progression to meningitis?
Philip N Baker, James M Roberts Magee-Womens Research Institute and Departments of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA 15213, USA
Microbiology Laboratory,
1 2
3
4
5
Chesley LC. Mild preeclampsia: potentially lethal for women and for the advancement of knowledge. Clin Exp Hypertens 1989; B8: 3-12. Dunlop W. General management of mild and moderate hypertensive diseases in pregnancy. In: Sharp F, Symonds EM, eds. Hypertension in pregnancy. New York: Perinatology Press, 1987: 263-78. Page EW, Christianson R. Influence of blood pressure changes with and without proteinuria upon the outcome of pregnancy. Am J Obstet Gynecol 1976; 126: 821-33. Taylor RN, Crombleholme WR, Friedman SA, Jones LA, Casal DC, Roberts JM. High plasma cellular fibronectin levels correlate with biochemical and clinical features of preeclampsia but cannot be attributed to hypertension alone. Am J Obstet Gynecol 1991; 165: 895-901. Fisher KA, Luger A, Spargo BH, Lindheimer MD. Hypertension in pregnancy: clinical-pathological correlations and remote prognosis. Medicine 1981; 60: 267-76.
Do
meningococci
cause sore
throats?
SiR-There are times when investigating one’s own family reveals interesting anomalies. After the wife of a microbiologist had suffered from a sore throat for a week he decided to do a "curative" throat swab. He inoculated various plates in his laboratory and was informed the next day that there was an almost pure growth of Neisseria meningitidis that his staff recognised with standard techniques. Two aspirins improved the clinical picture, and a few tactical telephone calls confirmed that the patient was not developing meningococcal meningitis. Does this organism act as a primary pathogen and cause a sore throat of unusual duration and severity? It is recognised that it is easy to isolate small numbers of N meningitidis from the normal throat in up to a quarter of the fit adult population.’1 However, detection of this organism is not part of the routine investigation of throat swabs submitted to the laboratory. We concentrate on the presence of haemolytic streptococci and the organisms that cause Vincent’s angina. Under specific circumstances we seek for the presence of N gonorrhoeae, Corynebacterium diphtheriae, and perhaps C haemolyticum. It is also recognised that a range of virus infections may present as a sore throat. Following the observation above, the two laboratories in Somerset were persuaded to look for high numbers of N meningitidis when throat swabs were being examined. 1636
J V S Pether, R J D Scott, P Hancock Public Health Laboratory,
1
Musgrove Park Hospital, Taunton TA1 5DB, UK; and Yeovil District Hospital, Yeovil
Pether JVS, Lightfoot NF, Scott RJD, Morgan J, Steele-Perkins AP, Sheard SC. Carriage of Neisseria meningitidis: investigations in a military establishment. Epidemiol Infect 1988; 101: 21-42.
Dobutamine-atropine stress echocardiography and central anticholinergic syndrome SiR-Picano and colleagues (Oct 29, p 1190) describe their experience with dobutamine-atropine stress echocardiography to diagnose coronary artery disease, and report the rare complication of atropine poisoning. They do not describe the underlying pathogenesis of this condition, nor its management. From their description, I presume atropine poisoning is the central anticholinergic syndrome-a condition in which atropine acts on central nervous system cholinergic receptors to cause confusion or longlasting coma.’ This condition is well known to anaesthetists, who are occasionally confronted with such cases during postoperative recovery after administration (usually as premedication) of atropine or hyoscine. It is thought to be in elderly patients, and the classic more common presentation is unexplained confusion or prolonged sedation. Physostigmine 0-5-2 mg intravenously can reverse these central effects because, unlike neostigmine, it can cross the blood-brain barrier, 1,2 This is because of its high lipid solubility. I have used this treatment on several occasions in postoperative recovery. Administration of physostigmine, therefore, also acts as a diagnostic test: rapid improvement rules out other causes of confusion and coma in this age group (in particular stroke). Such treatment can reduce anxiety to all concerned, as well as the requirement for long hospital care and additional health care resources. An alternative would be to avoid atropine use in the elderly and to give glycopyrrolate, a quaternary anticholinergic drug that does not cross the blood-brain barrier and so cannot cause central anticholinergic syndrome. Paul Myles Department of Anaesthesia, Alfred Hospital, Melbourne 3181, Australia 1 2
Moss J, Craigo PA. The autonomic nervous system. In: Miller RD, ed. Anesthesia. 4th ed. Melbourne: Churchill Livingstone, 1994; 566-67. Crowell EB, Ketchum JS. The treatment of scopolamine-induced delirium with physostigmine. Clin Pharmacol Ther 1967; 8: 409-14.