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Embryology of Bronchial Atresia
REFERENCES 1 Kraft SC, Earle RH, Roesler M, Esterly JR. Unexplained bronchopulmonary disease with inflammatory bowel disease. Arch Intern Med 1976; 136:454-59 2 Jones GR, Malone ON. Sulphasalazine induced lung disease. Thorax 1972; 27:713-17 3 Theodoropoulos G, Archimandritis A, Davaris ~ Plataris J, Mellisinos K. Ulcerative colitis and sarcoidosis: a curious associationreport of a case. Dis Colon Rectum 1981; 24:308-10 4 James DG, Williams WJ. Immunology of sarcoidosis. Am J Med
1982; 72:5-8 5 Godin NJ, Sachar DB, Wmchester R, Simon C, Janowitz HD.
Loss of suppression T-cells in active inJIammatory bowel disease. Gut 1984; 25:743-47
10 De Haan RL, O'Rahiely R. Embryology of the heart. In: Hurst ~ ed. The heart. New York: McGraw Hill, 1978; 6-18 11 Stocker.n: Drake RM, Madewell JE. Cystic and congenital lung disease in the newborn. Perspect Pediatr Patholl978; 4:93-154
Hypokalemia from Usual
SSlbutamol Dosage To the Editor:
It is well known that both salbutamol and theophylline poisoning produce hypokalemia and and hyperglycemia, and that in both cases these changes have been reversed by administration of proprano-
101. 1••
Embryology of Bronchial Atresia To the Editor: We were interested by the report by Williams and Schuster on the association of bronchial atresia and bronchogenic cyst (Chest 1985; 87:396-98). We are aware of two similar cases in previous publications. Case 2 ofTsuji et all showed bronchial mucocele and hyperinflation of the right upper lobe, together with a mediastinal bronchogenic cyst. Case 2 of Brocard and Gallouedeei had bronchial atresia and mucocele ofthe posterior segmental bronchus ofthe left lower lobe and a bronchogenic cyst in paraesophageal position, as was confirmed pathologically. Other congenital anomalies have been associated with bronchial atresia: pericardial defect,3.4 atrium septum defect and left-sided inferior vena cava, 5 congenital cystic adenomatoid malformation (CCAM) Stocker type 111, 6 unilateral agenesis of the kidney, 7 anomalous venous drainage of the left upper lobe, 8 pulmonary sequestration, 3 and fusion of apophyseal joints C2-C3. 8 These associated defects occur early in embryologic developn'ient; eg, the pericardium is normally fOrmed in the fifth week8 and the interatrial septum is normally complete in the eighth week. 10 CCAM Stocker type III is believed to result from an injury at the time of early budding ofthe lung. 11 Renal agenesis occurs prior to 31 days. 11 These associations indeed point towards the early phases of budding of the lung (fourth to sixth week) as the origin of bronchial atresia, at least for a number of cases.
Hypokalemia induced by salbutamol has been described only during overdosage. t.3 However it might be possible, we think, that therapeutic concentrations ofsalbutamol also produce hypokalemia. We describe a case of a 34-year-old male nurse and football player who took 6 mg (0.08 mglkg) salbutamol half an hour befOre a 30 min, 100 W exercise test, which was performed as described by 1llrssanen et aI, 4 in order to study serum potassium changes during exercise with medication. As we knO\1v, potassium concentration normally rises during exercise.4-! However, after taking salbutamol, our patient's serum potassium concentration rised remarkably less than during the exercise test without medication. Serum potassium concentration was 0.5 f.Lmollllower than before the exercise and the patient became hypokalemic (3.4 fAomolll) 30 min after the exercise (Fig 1). The patient palpitation and he received 40 mg propranolol. About two hours later, he went to play football. Thereafter, he felt unusual palpitation and tiredness that, we suppose, might be due to profound hypokalemia. Due to our exercise test results, we suggest that hypokalemia may be noticeable also during ordinary salbutamol treatment. Rapid potassium changes, especially hypokalemia, during exercise may achieve dangerous rhythm disturbances.
fen
Ikka Kantola, M.D.
7brku UnWer8ity Central H08pital, Leo Tansanen, M.D., Miklceli Central Hospital, Suomi, Finland
4.8
Dirk Van Renterghem, M.D. Bmgge, Belgium
REFERENCES 1 Tsuji S, Held S, Sato A. The syndrome ofbronchial mucocele and regional hyperinflation of the lung. Chest 1973; 64:44-447 2 Brocard H, Gallouedec Ch. Les formes radiocliniques de l'atresie bronchique. Rev Fr Mal Respir 1976; 4:953-62 3 Montaque Nl: Shaw HR. Bronchial atresia. Ann Thorac Surg 1974; 18:337-45 4 Jones ~ Developmental defects in the lungs. Thorax 1955; 10:205-13 5 Medelli J, Lattaignant JC, BertollX J~ Pietri J, Caudot B, Remond A. L'atresie bronchique segmentaire. Poumon 1979;
35:53-58
6 Cacia R, Sobonya RE. Congenital cystic adenomatoid malformation of the lung with bronchial atresia. Hum Pathol 1981; 12:947-50 7 Vaghei R. Bronchial atresia ofupper lobe ofthe lung. Chest 1970; 57:91-94 8 Desvignes C, Hummel J, Jamet G, Levasseur ~ Rojas-Miranda A, Verley J, et aI. Emphyseme pulmonaire et atresie bronchique. Ann Chir Thorac Cardiovasc 1974; 13:135-38 9 Hudson REB. Diseases of the pericardium. In: Hurst ~ ed. The heart. New York: McGraw Hill, 1978, P. 1636-40
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EXCERCISE
30 I
10
20
30
TIME (MIN)
FIGURE 1. Serum potassium levels during exercise with salbutarnol6 mg (- - - - - -) and without medication ( - - ) . CHEST I 89 I 4 I APRIL, 1986
818
1982; 72:5-8 5 Godin NJ, Sachar DB, Wmchester R, Simon C, Janowitz HD.
Loss of suppression T-cells in active inJIammatory bowel disease. Gut 1984; 25:743-47
10 De Haan RL, O'Rahiely R. Embryology of the heart. In: Hurst ~ ed. The heart. New York: McGraw Hill, 1978; 6-18 11 Stocker.n: Drake RM, Madewell JE. Cystic and congenital lung disease in the newborn. Perspect Pediatr Patholl978; 4:93-154
Hypokalemia from Usual
SSlbutamol Dosage To the Editor:
It is well known that both salbutamol and theophylline poisoning produce hypokalemia and and hyperglycemia, and that in both cases these changes have been reversed by administration of proprano-
101. 1••
Embryology of Bronchial Atresia To the Editor: We were interested by the report by Williams and Schuster on the association of bronchial atresia and bronchogenic cyst (Chest 1985; 87:396-98). We are aware of two similar cases in previous publications. Case 2 ofTsuji et all showed bronchial mucocele and hyperinflation of the right upper lobe, together with a mediastinal bronchogenic cyst. Case 2 of Brocard and Gallouedeei had bronchial atresia and mucocele ofthe posterior segmental bronchus ofthe left lower lobe and a bronchogenic cyst in paraesophageal position, as was confirmed pathologically. Other congenital anomalies have been associated with bronchial atresia: pericardial defect,3.4 atrium septum defect and left-sided inferior vena cava, 5 congenital cystic adenomatoid malformation (CCAM) Stocker type 111, 6 unilateral agenesis of the kidney, 7 anomalous venous drainage of the left upper lobe, 8 pulmonary sequestration, 3 and fusion of apophyseal joints C2-C3. 8 These associated defects occur early in embryologic developn'ient; eg, the pericardium is normally fOrmed in the fifth week8 and the interatrial septum is normally complete in the eighth week. 10 CCAM Stocker type III is believed to result from an injury at the time of early budding ofthe lung. 11 Renal agenesis occurs prior to 31 days. 11 These associations indeed point towards the early phases of budding of the lung (fourth to sixth week) as the origin of bronchial atresia, at least for a number of cases.
Hypokalemia induced by salbutamol has been described only during overdosage. t.3 However it might be possible, we think, that therapeutic concentrations ofsalbutamol also produce hypokalemia. We describe a case of a 34-year-old male nurse and football player who took 6 mg (0.08 mglkg) salbutamol half an hour befOre a 30 min, 100 W exercise test, which was performed as described by 1llrssanen et aI, 4 in order to study serum potassium changes during exercise with medication. As we knO\1v, potassium concentration normally rises during exercise.4-! However, after taking salbutamol, our patient's serum potassium concentration rised remarkably less than during the exercise test without medication. Serum potassium concentration was 0.5 f.Lmollllower than before the exercise and the patient became hypokalemic (3.4 fAomolll) 30 min after the exercise (Fig 1). The patient palpitation and he received 40 mg propranolol. About two hours later, he went to play football. Thereafter, he felt unusual palpitation and tiredness that, we suppose, might be due to profound hypokalemia. Due to our exercise test results, we suggest that hypokalemia may be noticeable also during ordinary salbutamol treatment. Rapid potassium changes, especially hypokalemia, during exercise may achieve dangerous rhythm disturbances.
fen
Ikka Kantola, M.D.
7brku UnWer8ity Central H08pital, Leo Tansanen, M.D., Miklceli Central Hospital, Suomi, Finland
4.8
Dirk Van Renterghem, M.D. Bmgge, Belgium
REFERENCES 1 Tsuji S, Held S, Sato A. The syndrome ofbronchial mucocele and regional hyperinflation of the lung. Chest 1973; 64:44-447 2 Brocard H, Gallouedec Ch. Les formes radiocliniques de l'atresie bronchique. Rev Fr Mal Respir 1976; 4:953-62 3 Montaque Nl: Shaw HR. Bronchial atresia. Ann Thorac Surg 1974; 18:337-45 4 Jones ~ Developmental defects in the lungs. Thorax 1955; 10:205-13 5 Medelli J, Lattaignant JC, BertollX J~ Pietri J, Caudot B, Remond A. L'atresie bronchique segmentaire. Poumon 1979;
35:53-58
6 Cacia R, Sobonya RE. Congenital cystic adenomatoid malformation of the lung with bronchial atresia. Hum Pathol 1981; 12:947-50 7 Vaghei R. Bronchial atresia ofupper lobe ofthe lung. Chest 1970; 57:91-94 8 Desvignes C, Hummel J, Jamet G, Levasseur ~ Rojas-Miranda A, Verley J, et aI. Emphyseme pulmonaire et atresie bronchique. Ann Chir Thorac Cardiovasc 1974; 13:135-38 9 Hudson REB. Diseases of the pericardium. In: Hurst ~ ed. The heart. New York: McGraw Hill, 1978, P. 1636-40
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4.2
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4.0
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0
CL ~
::>
3.8
0::
IJJ
l/)
3.6 3.4
10 5 0 I
10
20
EXCERCISE
30 I
10
20
30
TIME (MIN)
FIGURE 1. Serum potassium levels during exercise with salbutarnol6 mg (- - - - - -) and without medication ( - - ) . CHEST I 89 I 4 I APRIL, 1986
818