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PULMONARY ŒDEMA IN UPPER AIRWAY OBSTRUCTION
510 PULMONARY ŒDEMA IN UPPER AIRWAY OBSTRUCTION
SIR,-Recent reviews of the pathogenesis of pulmonary oedema do not mention upper airway obstruction (U.A.o.) as a possible cause. 1,2 Acute u.A.o. has been shown by Drinker3 to induce pulmonary oedema in hypoxic dogs. Travis et al.4 described two children in whom pulmonary oedema developed as a complication of severe U.A.o. Both children, one with croup, the other epiglottitis, recovered after treatment by tracheal il1tubation and positive-pressure ventilation or continuous positive airway pressure. Pulmonary cedema is a rare complication of acute u.A.o. in children, but its occurrence should occasion no surprise when one considers the methanics of upper airway obstruction. In u.A.o., wherever its anatomical site, dynamic inspiratory extrathoracic airway is likely to occur as a result of the pressure drop across the obstruction. When airway collapse does occur, transpulmonary pressure rapidly increases with only a small resultant increase in inspiratory gasflow. On expiration, on the other hand, airway pressure is above atmospheric and the obstructed portion of the upper airway tends to dilate. The change in transpulmonary pressure is therefore smaller on expiration than on inspiration, the reverse of the situation in lower airway obstruction. The net effect is a mean subatmospheric ("negative") transpulmonary pressure, which will tend to pull water from pulmonary capillaries into alveoli. Whether the hydrostatic forces which develop in U.A.o. are sufficient to produce pulmonary oedema is a question which has not to my knowledge been studied in man. I have measured the intratracheal pressure changes in an 18-month old male with croup severe enough to require tracheostomy. Upon removal of the tube 3 days later digital occlusion of the stoma produced sternal retraction and inspiratory stridor necessitating reinsertion of the tube. Before reinsertion a sterile catheter connected to a Sanborn pressure transducer was placed in the stoma. The pressure changes in the trachea were recorded on a Hewlett-Packard physiological monitor. Breath-by-breath inspiratory pressures (referred to atmospheric pressure) varied from -24 to -50 cm H2O, with a mean of -37 cm H2O. Expiratory pressures ranged from +5 to +15 cm H2O, with a mean of + 11 cm H2O. The mean intratracheal pressure (calculated from the area under the pressure curves) was-l0.l cmH2O. These pressures would seem large enough to account for a transcapillary pressure gradient sufficient to produce at least interstitial pulmonary oedema. Indeed it is possible that the hypoxaemia described in croup,5 which does not improve immediately after relief of obstruction,6 is mediated by interstitial pulmonary oedema, clearance of which may take some hours. Pulmonary oedema has been observed in this hospital in some patients with fulminant hepatic failure who hyperventilate with an obstructed upper airway. It is possible that hydrostatic forces play a role in the pathogenesis here also. Upper airway obstruction deserves more consideration as a pathogenetic mechanism in pulmonary oedema.
collapse of part of the
Respiratory Care Unit, Fairfield Hospital for Communicable Diseases, Melbourne, Victoria, Australia
H.
NEWTON-JOHN
1. Robin, E. D., Cross, C. E., Zelis, R. New Engl. J. Med. 1973, 288, 239, 292. 2. Staub, N. C. Physiol. Rev. 1974, 54, 3. 3. Drinker, C. K., Pulmonary Edema and Inflammation: Analysis of Processes Involved in Formation and Removal of Pulmonary Transudases and Exudates. Cambridge, Massachusetts, 1945. 4. Travis, K. W., Todres, I. D., Shannon, D. C. Pediatrics, 1977, 59, 695. 5. Newth, C. J. L., Levison, H., Bryan, A. C. J. Pediat. 1972, 81, 1068. 6. Taussig, L. M., Castro, O., Beaudry, P. H., Fox, W. W., Bureau, M. Am. J. Dis. Child, 1975, 129, 790.
WHOOPING-COUGH VACCINE
SIR,-It would be helpful if Professor Stewart (July 23, p. or anyone else who shares his view, could give the evi-
189),
dence for his statement that "in every epidemic there are numerous instances (my italics) where B. pertussis is isolated from severely ill children who have been fully vaccinated". This was so with some of the batches of vaccine made before 1968, but it is quite contrary to my own experiencel.2 with vaccine in use for the past ten years. The organism is now rarely isolated from children who have had three doses of vaccine ; and those few occasions tend to be associated with plain vaccine, not the currently recommended absorbed vaccine. In Professor Stewart’s own publications, there is no evidence to support his recent statement. One of them3 does not indicate the number of cases from which the organism was isolated. Anothermentions 10 isolates from children who had received "two or more doses of pertussis vaccine", but does not say how many would remain after exclusion of those who had an incomplete course of only two doses and those who had pre-1968 vaccine. If your readers are to believe that numerous fully vaccinated children develop severe pertussis infection, they need some firm evidence. Department of Bacteriology and Virology, University of Manchester,
Stopford Building, Manchester M13 9PT
NOEL W. PRESTON
HYPOGLYCÆMIC EFFECT OF PENTAMIDINE DETECTED BY GLUCOSE SCREEN
SIR,-The use of biochemical tests for population screening has evolved over the last 15 years5 along with developments in automation. Batteries of laboratory tests (e.g., urea and electrolytes), often called profiles, are justifiable on grounds of economy and because of the physiological relationships between the variables being measured. The case for larger profiles with 10 or more tests is not so strong, however. One test not always included with the usual urea and electrolyte profile is plasma-glucose. We would like to record our experience since the Boehringer glucose-oxidase automated kit was introduced on a Technicon SMA 6/60 ’AutoAnalyzer’ in March of this year. The finding of an unsuspected mild-to-moderate hyperglycxmia is not uncommon and may save a delay of 12-24 h i(or more) in diagnosis in an inpatient and even longer in an outpatient. For example, in the haematology clinic at Addenbrooke’s Hospital, in the past 4 months, three patients on highdose steroid therapy have been found to have an unsuspected hyperglycsemia; all required treatment, one with soluble insulin. One case of hypoglycasmia was detected by the screen: it was an important side-effect of an unusual drug. A man of 66 with non-Hodgkin’s lymphoma was suspected of having Pneumocystis carinii infection, and pentamidine was given for 5 days. 2 days after he stopped taking pentamidine, during the weekend, his condition deteriorated and he became unrousable and cyanosed. The underlying hypoglycaemia was first appreciated when the glucose screen, as part of the urea and electrolyte profile, was reported at 1-1mmol/1. Intravenous glucose led to a rapid recovery. The hypoglycaemic potential of pentamidine (it is a biguanide derivative) was described in 1958 when the drug was used as a treatment for trypanosomiasis.6 However, the drug is not often needed in the U.K., and information about 1. 2. 3. 4. 5. 6.
Preston, N. W., Stanbridge, T. N. Br. med. J. 1972, iii, 448. Preston, N. W. Lancet, 1976, i, 1065. Stewart, G. T. ibid. 1977, i, 234. Bassili, W. R., Stewart, G. T. ibid. 1976, i, 471. Whitby, L. G., Lancet, 1974, ii, 819. Klinkhamer, L. V. Trop. geog. Med. 1958, 10, 332.
SIR,-Recent reviews of the pathogenesis of pulmonary oedema do not mention upper airway obstruction (U.A.o.) as a possible cause. 1,2 Acute u.A.o. has been shown by Drinker3 to induce pulmonary oedema in hypoxic dogs. Travis et al.4 described two children in whom pulmonary oedema developed as a complication of severe U.A.o. Both children, one with croup, the other epiglottitis, recovered after treatment by tracheal il1tubation and positive-pressure ventilation or continuous positive airway pressure. Pulmonary cedema is a rare complication of acute u.A.o. in children, but its occurrence should occasion no surprise when one considers the methanics of upper airway obstruction. In u.A.o., wherever its anatomical site, dynamic inspiratory extrathoracic airway is likely to occur as a result of the pressure drop across the obstruction. When airway collapse does occur, transpulmonary pressure rapidly increases with only a small resultant increase in inspiratory gasflow. On expiration, on the other hand, airway pressure is above atmospheric and the obstructed portion of the upper airway tends to dilate. The change in transpulmonary pressure is therefore smaller on expiration than on inspiration, the reverse of the situation in lower airway obstruction. The net effect is a mean subatmospheric ("negative") transpulmonary pressure, which will tend to pull water from pulmonary capillaries into alveoli. Whether the hydrostatic forces which develop in U.A.o. are sufficient to produce pulmonary oedema is a question which has not to my knowledge been studied in man. I have measured the intratracheal pressure changes in an 18-month old male with croup severe enough to require tracheostomy. Upon removal of the tube 3 days later digital occlusion of the stoma produced sternal retraction and inspiratory stridor necessitating reinsertion of the tube. Before reinsertion a sterile catheter connected to a Sanborn pressure transducer was placed in the stoma. The pressure changes in the trachea were recorded on a Hewlett-Packard physiological monitor. Breath-by-breath inspiratory pressures (referred to atmospheric pressure) varied from -24 to -50 cm H2O, with a mean of -37 cm H2O. Expiratory pressures ranged from +5 to +15 cm H2O, with a mean of + 11 cm H2O. The mean intratracheal pressure (calculated from the area under the pressure curves) was-l0.l cmH2O. These pressures would seem large enough to account for a transcapillary pressure gradient sufficient to produce at least interstitial pulmonary oedema. Indeed it is possible that the hypoxaemia described in croup,5 which does not improve immediately after relief of obstruction,6 is mediated by interstitial pulmonary oedema, clearance of which may take some hours. Pulmonary oedema has been observed in this hospital in some patients with fulminant hepatic failure who hyperventilate with an obstructed upper airway. It is possible that hydrostatic forces play a role in the pathogenesis here also. Upper airway obstruction deserves more consideration as a pathogenetic mechanism in pulmonary oedema.
collapse of part of the
Respiratory Care Unit, Fairfield Hospital for Communicable Diseases, Melbourne, Victoria, Australia
H.
NEWTON-JOHN
1. Robin, E. D., Cross, C. E., Zelis, R. New Engl. J. Med. 1973, 288, 239, 292. 2. Staub, N. C. Physiol. Rev. 1974, 54, 3. 3. Drinker, C. K., Pulmonary Edema and Inflammation: Analysis of Processes Involved in Formation and Removal of Pulmonary Transudases and Exudates. Cambridge, Massachusetts, 1945. 4. Travis, K. W., Todres, I. D., Shannon, D. C. Pediatrics, 1977, 59, 695. 5. Newth, C. J. L., Levison, H., Bryan, A. C. J. Pediat. 1972, 81, 1068. 6. Taussig, L. M., Castro, O., Beaudry, P. H., Fox, W. W., Bureau, M. Am. J. Dis. Child, 1975, 129, 790.
WHOOPING-COUGH VACCINE
SIR,-It would be helpful if Professor Stewart (July 23, p. or anyone else who shares his view, could give the evi-
189),
dence for his statement that "in every epidemic there are numerous instances (my italics) where B. pertussis is isolated from severely ill children who have been fully vaccinated". This was so with some of the batches of vaccine made before 1968, but it is quite contrary to my own experiencel.2 with vaccine in use for the past ten years. The organism is now rarely isolated from children who have had three doses of vaccine ; and those few occasions tend to be associated with plain vaccine, not the currently recommended absorbed vaccine. In Professor Stewart’s own publications, there is no evidence to support his recent statement. One of them3 does not indicate the number of cases from which the organism was isolated. Anothermentions 10 isolates from children who had received "two or more doses of pertussis vaccine", but does not say how many would remain after exclusion of those who had an incomplete course of only two doses and those who had pre-1968 vaccine. If your readers are to believe that numerous fully vaccinated children develop severe pertussis infection, they need some firm evidence. Department of Bacteriology and Virology, University of Manchester,
Stopford Building, Manchester M13 9PT
NOEL W. PRESTON
HYPOGLYCÆMIC EFFECT OF PENTAMIDINE DETECTED BY GLUCOSE SCREEN
SIR,-The use of biochemical tests for population screening has evolved over the last 15 years5 along with developments in automation. Batteries of laboratory tests (e.g., urea and electrolytes), often called profiles, are justifiable on grounds of economy and because of the physiological relationships between the variables being measured. The case for larger profiles with 10 or more tests is not so strong, however. One test not always included with the usual urea and electrolyte profile is plasma-glucose. We would like to record our experience since the Boehringer glucose-oxidase automated kit was introduced on a Technicon SMA 6/60 ’AutoAnalyzer’ in March of this year. The finding of an unsuspected mild-to-moderate hyperglycxmia is not uncommon and may save a delay of 12-24 h i(or more) in diagnosis in an inpatient and even longer in an outpatient. For example, in the haematology clinic at Addenbrooke’s Hospital, in the past 4 months, three patients on highdose steroid therapy have been found to have an unsuspected hyperglycsemia; all required treatment, one with soluble insulin. One case of hypoglycasmia was detected by the screen: it was an important side-effect of an unusual drug. A man of 66 with non-Hodgkin’s lymphoma was suspected of having Pneumocystis carinii infection, and pentamidine was given for 5 days. 2 days after he stopped taking pentamidine, during the weekend, his condition deteriorated and he became unrousable and cyanosed. The underlying hypoglycaemia was first appreciated when the glucose screen, as part of the urea and electrolyte profile, was reported at 1-1mmol/1. Intravenous glucose led to a rapid recovery. The hypoglycaemic potential of pentamidine (it is a biguanide derivative) was described in 1958 when the drug was used as a treatment for trypanosomiasis.6 However, the drug is not often needed in the U.K., and information about 1. 2. 3. 4. 5. 6.
Preston, N. W., Stanbridge, T. N. Br. med. J. 1972, iii, 448. Preston, N. W. Lancet, 1976, i, 1065. Stewart, G. T. ibid. 1977, i, 234. Bassili, W. R., Stewart, G. T. ibid. 1976, i, 471. Whitby, L. G., Lancet, 1974, ii, 819. Klinkhamer, L. V. Trop. geog. Med. 1958, 10, 332.