- Email: [email protected]
ENDOSCOPIST PROTECTION FROM BIOPSY VALVES
1341
intravenously per day, in a 50-year-old man with chlordiazepoxideresistant delirium tremens associated with fat embolism.2 The mechanism of action remains elusive. Steroids stabilise membranes and inhibit the release of arachidonic acid from phospholipids, thereby diminishing the formation of prostaglandins known to have an important role in inflarnmation.3,4 Because of the significant mortality of untreated delirium tremens, we suggest a trial of parenteral dexamethasone in patients unresponsive to benzodiazepine and supportive fluid therapy. Departments of Neurosurgery, Biochemistry, and Surgery, Baylor College of Medicine and Ben Taub General Hospital, Houston, Texas 77030, USA
DUNCAN K.FISCHER RICHARD K. SIMPSON, JR F. AMES SMITH, JR KENNETH L. MATTOX
1. Flink EB, Lizarralde G, Jacobs W. Therapy of delirium tremens with urea (or dexamethasone) and magnesium sulfate J Lab Clin Med 1971; 78: 990. 2 Horowitz I, Klingenstein RJ, Levy R, Zimmerman MJ. Fat embolism in delirium tremens Am J Gastroenterol 1977, 68: 476-80. 3. Gryglewski RJ, Panczenko B, Korbut R, Grodzinska L, Ocetkiewicz A. Corticosteroids inhibit prostaglandin release from perfused mesentenc blood vessels of rabbit and from perfused lungs of sensitized guinea pig. Prostaglandins 1975, 10: 343-55. 4. Hong SL, Levine L. Inhibition of arachidonic acid release from cells as the biochemical action of anti-inflammatory corticosteroids Proc Natl Acad Sci USA 1976, 73: 1730-34.
ENDOSCOPIST PROTECTION FROM BIOPSY VALVES
SiR,—The device Mr Harrison and Mr Morris describe (May 7, to protect the endoscopist and assistant from possible contamination by fluid emitted from the biopsy valve during insertion or withdrawal of accessory instruments through this valve. As they say this is mostly due to positive pressure within the biopsy channel, induced by insufflation of air into the organ under study and by positive pressure generated by the patient. A much simpler method, however, is to keep the suction button depressed during insertion and particularly withdrawal of an p
1024) is designed
accessory
instrument, which will then have the
device described
same
effect
as
the
by Harrison and Morris.
Gastro-Intestinal Unit, Leicester Royal Infirmary, Leicester LE1 5WW
D. L. CARR-LOCKE
INTOXICATION BY BENZODIAZEPINES DURING PREGNANCY
SIR,-Although benzodiazepines cross the placenta and accumulate in the fetal compartment, it is not easy to establish a relation between the exposure to the drug and possible toxic effects. Most studies have analysed the correlation of long-term intake of benzodiazepines at therapeutic doses during the second trimester with lesions such as haemangioma or heart and vascular malformations. Recently we observed multiple accidental poisoning with these drugs. Five pregnant women, four in the second trimester (weeks 20, 22, 22, and 23) and one in the third (week 35), who should have had an O’Sullivan test, received about 10 g of benzodiazepine orally in one dose, because of a mistake in the labelling of the glucose delivered to our laboratory. The four women in the second trimester vomited part of the dose after ingestion. They had variable sensory depression, but not loss of consciousness. Only one of the fetuses showed a diminution in the variability of the fetal heart rate in a non-stress test. 24 h after admission for observation, they were discharged and followed up weekly as outpatients. Benzodiazepines in urine became negative between 4 and 6 weeks and assessments of fetal well-being were normal. The patient in the third trimester did not vomit and had respiratory depression with bronchospasm, which caused admission to the intensive care unit for 2 days with assisted ventilation. Over the next 5 days, she had neurological depression with severe drowsiness and light muscular hypotony; she recovered spontaneously. The fetus, in a non-stress test, showed a significant
decrease of variability in heart rate, with periods of silent rhythm, which disappeared in a few hours. The fetal assessments were later normal. Benzodiazepines in the mother’s urine remained positive until delivery. The five patients delivered at term vaginally. All the Apgar responses were present in the first minute of life. All babies were morphologically normal, without apparent deficiencies in psychomotor development, their course being normal at 6 months of life. Ma. J. CERQUEIRA C. OLLE J. BELLART Department of Obstetrics and Gynaecology, F. BARO and Biochemistry, L. CABERO de la Santa i Creu Sant Hospital Pau, J. M. QUERALTO Autonomous University of Barcelona, 08025 Barcelona, Spam J. RODRIGUEZ ESPINOSA
ALLERGIC BRONCHOPULMONARY MYCOSIS
SIR,-Your April 16 editorial on pulmonary aspergillosis (p 864) explains some of the difficulties encountered in serological tests for aspergillosis and allergic bronchopulmonary aspergillosis (ABPA). An additional problem is that several different fungi have now been implicated in causing a syndrome similar to ABPA. These include Candida albieans,l Helminthosporium spp,2 Curvularia lunata and Drechslera hawaiiensis,3 Mucor Spp,4 and Aspergillus spp other than Afumigatus.5 The following case illustrates the uncertainty that can occur. A 62-year-old non-asthmatic farmer presented with what was thought to be an atypical pneumonia. Sputum culture and a routine serological screen failed to reveal a cause. Treatment with a variety of antibiotics was associated with a worsening of symptoms, increased shadowing on chest X-ray, and the finding of large numbers of C albicans and Absidia eorymibifera in sputum. Intravenous amphotericin with hydrocortisone cover led to considerable improvement within 2 weeks. His eosinophil count was never raised, his aspergillus skin-prick test was negative on several occasions, and he had precipitin lines to rhizopus and C albicans, but not to Afumigatus nor to an extract of his own absidia (done by the Mycology Reference Laboratory, Colindale). Neither clinical features nor serological tests were consistent with allergic alveolitis. There was no evidence of immunodeficiency. About 6 months after discharge he had a second symptomatic episode of chest X-ray shadowing with sputum yielding C albieans and Abs corymibifera. Precipitin lines were present against candida, rhizopus, penicillium, and pseudallescheria but not to his absidia or aspergillus. His symptoms and chest X-ray cleared within 11 days of starting intravenous amphotericin with prednisolone cover. This rapid resolution of symptoms and shadowing after amphotericin and steroids on two occasions suggests that the response was due to steroids and that the patient’s illness was probably due to hypersensitivity to the fungi in his sputum. Because of the number of organisms that may be responsible for allergic bronchopulmonary mycosis, the presence of cross-reacting antigens, and the potential absence of detectable antibody, it is probably unsafe to place great reliance on current serological techniques for diagnosis or confirmation of this condition. Public Health Laboratory, Heavitree, Exeter EX2 5AD
IVAN MUSCAT
Department of Medicine, Royal Devon and Exeter Hospital,
SUSAN OXBORROW
Exeter EX2 5T
JOHN SIDDORN
SK, Khan ZU, Singh MM. Role of aspergillus and candida species allergic bronchopulmonary mycoses: a comparative study. Scand J Resp Dis 1979; 60: 235-42. 2. Hendrick DJ, Ellithorpe DB, Lyon F, Hattier P, Salvaggio JE. Allergic bronchopulmonary helminthosporiosis. Am Rev Resp Dis 1982; 126: 935-38. 3. McAleer R, Kroenert DB, Elder JL, Froudist JH. Allergic bronchopulmonary disease caused by Curvularia lunata and Drechslera hawaiiensis. Thorax 1981; 36: 338-44. 4 Kino T, Yamada Y, Honda K, et al. Diagnosis and treatment of a case of allergic bronchopulmonary mycosis caused by mucor-like fungus. Nippon Kyobu Shikkan 1. Sandu RS, Mehta m
Gakkai Zasshi 1983; 9: 896-903. K, Takizawa H, Suzuki M, Miyachi S, Ichinohe M, Yanagihara Y. Allergic bronchopulmonary aspergillosis due to Aspergillus oryzae. Chest 1987; 91: 285-86
5. Akiyama
intravenously per day, in a 50-year-old man with chlordiazepoxideresistant delirium tremens associated with fat embolism.2 The mechanism of action remains elusive. Steroids stabilise membranes and inhibit the release of arachidonic acid from phospholipids, thereby diminishing the formation of prostaglandins known to have an important role in inflarnmation.3,4 Because of the significant mortality of untreated delirium tremens, we suggest a trial of parenteral dexamethasone in patients unresponsive to benzodiazepine and supportive fluid therapy. Departments of Neurosurgery, Biochemistry, and Surgery, Baylor College of Medicine and Ben Taub General Hospital, Houston, Texas 77030, USA
DUNCAN K.FISCHER RICHARD K. SIMPSON, JR F. AMES SMITH, JR KENNETH L. MATTOX
1. Flink EB, Lizarralde G, Jacobs W. Therapy of delirium tremens with urea (or dexamethasone) and magnesium sulfate J Lab Clin Med 1971; 78: 990. 2 Horowitz I, Klingenstein RJ, Levy R, Zimmerman MJ. Fat embolism in delirium tremens Am J Gastroenterol 1977, 68: 476-80. 3. Gryglewski RJ, Panczenko B, Korbut R, Grodzinska L, Ocetkiewicz A. Corticosteroids inhibit prostaglandin release from perfused mesentenc blood vessels of rabbit and from perfused lungs of sensitized guinea pig. Prostaglandins 1975, 10: 343-55. 4. Hong SL, Levine L. Inhibition of arachidonic acid release from cells as the biochemical action of anti-inflammatory corticosteroids Proc Natl Acad Sci USA 1976, 73: 1730-34.
ENDOSCOPIST PROTECTION FROM BIOPSY VALVES
SiR,—The device Mr Harrison and Mr Morris describe (May 7, to protect the endoscopist and assistant from possible contamination by fluid emitted from the biopsy valve during insertion or withdrawal of accessory instruments through this valve. As they say this is mostly due to positive pressure within the biopsy channel, induced by insufflation of air into the organ under study and by positive pressure generated by the patient. A much simpler method, however, is to keep the suction button depressed during insertion and particularly withdrawal of an p
1024) is designed
accessory
instrument, which will then have the
device described
same
effect
as
the
by Harrison and Morris.
Gastro-Intestinal Unit, Leicester Royal Infirmary, Leicester LE1 5WW
D. L. CARR-LOCKE
INTOXICATION BY BENZODIAZEPINES DURING PREGNANCY
SIR,-Although benzodiazepines cross the placenta and accumulate in the fetal compartment, it is not easy to establish a relation between the exposure to the drug and possible toxic effects. Most studies have analysed the correlation of long-term intake of benzodiazepines at therapeutic doses during the second trimester with lesions such as haemangioma or heart and vascular malformations. Recently we observed multiple accidental poisoning with these drugs. Five pregnant women, four in the second trimester (weeks 20, 22, 22, and 23) and one in the third (week 35), who should have had an O’Sullivan test, received about 10 g of benzodiazepine orally in one dose, because of a mistake in the labelling of the glucose delivered to our laboratory. The four women in the second trimester vomited part of the dose after ingestion. They had variable sensory depression, but not loss of consciousness. Only one of the fetuses showed a diminution in the variability of the fetal heart rate in a non-stress test. 24 h after admission for observation, they were discharged and followed up weekly as outpatients. Benzodiazepines in urine became negative between 4 and 6 weeks and assessments of fetal well-being were normal. The patient in the third trimester did not vomit and had respiratory depression with bronchospasm, which caused admission to the intensive care unit for 2 days with assisted ventilation. Over the next 5 days, she had neurological depression with severe drowsiness and light muscular hypotony; she recovered spontaneously. The fetus, in a non-stress test, showed a significant
decrease of variability in heart rate, with periods of silent rhythm, which disappeared in a few hours. The fetal assessments were later normal. Benzodiazepines in the mother’s urine remained positive until delivery. The five patients delivered at term vaginally. All the Apgar responses were present in the first minute of life. All babies were morphologically normal, without apparent deficiencies in psychomotor development, their course being normal at 6 months of life. Ma. J. CERQUEIRA C. OLLE J. BELLART Department of Obstetrics and Gynaecology, F. BARO and Biochemistry, L. CABERO de la Santa i Creu Sant Hospital Pau, J. M. QUERALTO Autonomous University of Barcelona, 08025 Barcelona, Spam J. RODRIGUEZ ESPINOSA
ALLERGIC BRONCHOPULMONARY MYCOSIS
SIR,-Your April 16 editorial on pulmonary aspergillosis (p 864) explains some of the difficulties encountered in serological tests for aspergillosis and allergic bronchopulmonary aspergillosis (ABPA). An additional problem is that several different fungi have now been implicated in causing a syndrome similar to ABPA. These include Candida albieans,l Helminthosporium spp,2 Curvularia lunata and Drechslera hawaiiensis,3 Mucor Spp,4 and Aspergillus spp other than Afumigatus.5 The following case illustrates the uncertainty that can occur. A 62-year-old non-asthmatic farmer presented with what was thought to be an atypical pneumonia. Sputum culture and a routine serological screen failed to reveal a cause. Treatment with a variety of antibiotics was associated with a worsening of symptoms, increased shadowing on chest X-ray, and the finding of large numbers of C albicans and Absidia eorymibifera in sputum. Intravenous amphotericin with hydrocortisone cover led to considerable improvement within 2 weeks. His eosinophil count was never raised, his aspergillus skin-prick test was negative on several occasions, and he had precipitin lines to rhizopus and C albicans, but not to Afumigatus nor to an extract of his own absidia (done by the Mycology Reference Laboratory, Colindale). Neither clinical features nor serological tests were consistent with allergic alveolitis. There was no evidence of immunodeficiency. About 6 months after discharge he had a second symptomatic episode of chest X-ray shadowing with sputum yielding C albieans and Abs corymibifera. Precipitin lines were present against candida, rhizopus, penicillium, and pseudallescheria but not to his absidia or aspergillus. His symptoms and chest X-ray cleared within 11 days of starting intravenous amphotericin with prednisolone cover. This rapid resolution of symptoms and shadowing after amphotericin and steroids on two occasions suggests that the response was due to steroids and that the patient’s illness was probably due to hypersensitivity to the fungi in his sputum. Because of the number of organisms that may be responsible for allergic bronchopulmonary mycosis, the presence of cross-reacting antigens, and the potential absence of detectable antibody, it is probably unsafe to place great reliance on current serological techniques for diagnosis or confirmation of this condition. Public Health Laboratory, Heavitree, Exeter EX2 5AD
IVAN MUSCAT
Department of Medicine, Royal Devon and Exeter Hospital,
SUSAN OXBORROW
Exeter EX2 5T
JOHN SIDDORN
SK, Khan ZU, Singh MM. Role of aspergillus and candida species allergic bronchopulmonary mycoses: a comparative study. Scand J Resp Dis 1979; 60: 235-42. 2. Hendrick DJ, Ellithorpe DB, Lyon F, Hattier P, Salvaggio JE. Allergic bronchopulmonary helminthosporiosis. Am Rev Resp Dis 1982; 126: 935-38. 3. McAleer R, Kroenert DB, Elder JL, Froudist JH. Allergic bronchopulmonary disease caused by Curvularia lunata and Drechslera hawaiiensis. Thorax 1981; 36: 338-44. 4 Kino T, Yamada Y, Honda K, et al. Diagnosis and treatment of a case of allergic bronchopulmonary mycosis caused by mucor-like fungus. Nippon Kyobu Shikkan 1. Sandu RS, Mehta m
Gakkai Zasshi 1983; 9: 896-903. K, Takizawa H, Suzuki M, Miyachi S, Ichinohe M, Yanagihara Y. Allergic bronchopulmonary aspergillosis due to Aspergillus oryzae. Chest 1987; 91: 285-86
5. Akiyama