- Email: [email protected]
Recent aspects of bronchopulmonary dysplasia after hyaline-membrane disease
417
8. KauppilaA, Hartikainen-SorriA-L, Koivisto M, Ryhiinen P. Cell-mediated immunocompetence of children exposed in utero to short-term or long-term action of glucocorticoids. Obstet Gynecol, in press.
Relevance of lecithin/sphingomyelin the obstetrical decision
C. Tchobroutsky,
Mater&P
(L/S)
ratio measurement
in amniotic fluid for
Port Royal, 123 Boulevard Port Royal, Paris 14e, France
A major advance in obstetrics is the development of an amniotic fluid test to estimate the maturity of the fetal lungs. However, in some conditions such as intra+uterine growth retardation (IUGR), awaiting fetal lung maturity is less important today than it was 10 yr ago. In other conditions such as diabetes, delivery after 38 wk is now generally accepted and the importance of the determination of fetal lung maturity loses its relevance. In a retrospective study we compared the number of amniocenteses performed in the years 1973 and 198 1: the percentage of patients given amniocentesis fell from 2.3 to 1.3 (P -C 0.05). Moreover, the mean number of amniocenteses per patient fell from 1.7 to 1.0. Very few pregnancies complicated by HTA and/or IUGR have been subjected to amniocentesis. The main candidates for amniocentesis remain the insulin-treated diabetics. According to the literature, the predictive value of the L/S ratio in diabetics is much lower than in other pregnancies. In our experience, however, the frequeny of a false mature L/S ratio was less than 1% in more than 300 diabetics. This change in attitude is probably due to (1) a better estimation of gestational age and fetal growth with the advent of ultrasound; (2) a better estimation of fetal distress with the non-stress test; and (3) the advances in neonatal intensive care. In a second retrospective study we analysed the role of the determination of fetal lung maturity in the decision leading to elective termination of pregnancy of very-low-birthweight infants (VLBW) or to abstention. Only 6 amniocenteses were performed in 26 patients. Fifteen pregnancies were electively terminated. Only once were we able to delay delivery for 10 days and wait for a near-mature L/S ratio. In the other cases the determination of pulmonary maturity was not the leading reason for our decision. We believe that the value of the determination of pulmonary maturity holds mainly for those cases with a reactive non-stress test, but then when elective delivery is considered.
Recent aspects of bronchopulmonary
dysplasia after hyaline-membrane
M. Couchard, Mater&P
123 Bd. de Port-Royal,
Port-Royal,
disease
F-75014 Paris, France
This review about BPD is aimed at recalling recent answers to the following questions. What is the current rate of BPD in HMD, and are there modifying trends? What is the present knowledge of the pathology and pathogenesis? Which
418
special clinical features should be focused upon from now on? Also, to date, which recommendations could be used for better management and prevention? Rate The current rate of BPD in HMD remains high, i.e. from 24 to 28% in survivors to 3 1% in non-survivors, with a strong effect of the duration of ventilation: 74% above 14 days, to 100% beyond 28 days. BPD appears to be a major factor in late neonatal deaths (concurrently with intracranial haemorrhage) [ 11. Pathology Recent reports on the pathology show that a simple uncomplicated premature birth takes place in the midst of a complex process of lung development together with pulmonary tissue maturation. Experimental HMD in monkeys shows the early and extensive lesions which are superimposed on this normal process. When the post-HMD reparative process evolves, it may follow a healing mode with catch-up growth, or it may deviate to a scarring process resulting in deeply disturbed lung tissues and altered growth. The pathogenesis most probably is multifactorial [l] and includes the effect of lengthy aggressions on lung epithelium and bronchioles; impairment of the mucociliar-y clearance system; oxygen toxicity, especially the role of superoxide and other highly reactive cytotoxic free-radicals; the prime role of capillary lesions; the variable level of antioxidant defense systems; insufficient macrophage activity; the type of respirator used (barotrauma); and the role of complications such as pneumothorax, emphysema, infections, hypersecretion, atelectasis, and patent ductus arteriosus [l-3]. In summary: oxygen plus pressure plus time in a vicious circle. Clinical features At present, special clinical features should be kept in mind. These include the increased work of breathing [4] and the role of diaphragm fatigue in the patient’s tolerance for BPD; the repeated upper respiratory tract infections or bronchitis or pneumonia in the first year of life [1,3,5,6]; the impairment of pulmonary tests; the occurrence of car pulmonale; the variations of the pulmonary status and cardiac tolerance during sleep states [7]; the importance of EKG and echocardiography; and the general regression of symptoms and radiologic features without a total functional normalization [3,4,8]. Management is aimed at ‘secondary prevention’ in babies requiring artificial ventilation: early fine resuscitation; perfect monitoring; routine chest physiotherapy; moderate fluid therapy; early closure of patent ductus arteriosus; meticulous asepsis; and an all-time concern that ‘the shorter the better’, If BPD had developed despite all precautions the case should be handled as follows: avoid additional complications at any rate; feed by gavage for a longer time than is usual in normal premature infants; adjust supplemental oxygen to the minimal levels required to relieve hypoxia with adjusted raises during sleep; apply chest physiotherapy; and administer bronchodilators and vitamin E. Later measures include the careful organization of discharge, family life,infant care, and immunizations. However, BPD is the result of scarring on a developing immature tissue and even the very best intensive care can do much but not miracles in very-low-birthweight babies. Therefore, we must think in terms of primary prevention, i.e. struggle to avoid the large number of premature deliveries that are preventable through better prenatal care. All physicians involved in prenatal care, public offices, and government must be aware that this heavy medical burden and very costly social problem can be lessened by the prevention of preterm birth.
419
References 1. Monset-Couchard
M. Pediatric Updates, in press, 1983 (107 references, up to December 1981). 2. Arlart IP. Rontgenologische Aspekte des Atemnotsyndroms und der bronchopulmonalen Dysplasie. Roentgenblaetter 1982; 35: 84-89. 3. Monset-Couchard M, Henry E, Larroche JCI, Moriette G, Bomsel F. Dysplasia broncho-pulmonaire. Analyse de 565 cas de ventilation artificielle chez le nouveau-&. Ann Radio1 (Paris) 198 1; 24: 55-65. 4. Morray JP, Fox WW, Kettrick RG. Downes JJ. Improvement in lung mechanics as a function of age in the infant with severe bronchopulmonary dysplasia. Pediatr Res 1982; 16: 290-294. 5. Vohr BR, Bell EF, Oh W. Infants with bronchopulmonary dysplasia. Am J Dis Child 1982; 136: 443-447. 6. Weinstein MR. Oh W. Oxygen consumption in infants with bronchopulmonary dysplasia. J Pediatr 1981; 99: 958-961. 7. Wei’tzenblum E, Muzet A, Ehrhart M, Ehrhart J. Sautegeau A, Weber L. Variations nocturnes des gaz du sang et de la pression arterielle pulmonaire chez les bronchitiques chroniques insuffisants respiratoires. Nouv Press Med 1982; 11: 1119-1122. 8. Wong YC, Beardsmore JH, Meek J, Stocks J, Silverman M. Bronchial hypersecretion in preterm neonates. Arch Dis Child 1982; 57: 117-122.
The CPAP-test for an exact indication of CPAP-therapy
D. Gmyrek and R. Schwarze, Medical Academy ‘Carl Gustav Carus’, Department of Neonatology of the Pediatric Clinic, Fetscher-Strasse 74, DDR-8019 Dresden, D.D.R. Introduction Without doubt the CPAP-therapy is a great advantage in the treatment of the respiratory distress syndrome of premature infants. For deciding the question in the individual case: ‘Is the CPAP-therapy indicated or not?’ we developed the so-called CPAP-test. Material and Methods We carry out the CPAP-test in the following way [ 11: -first we make the usual hyperoxia-test (HOT) by increasing the fraction of inspired oxygen concentration (Fi4) up to 100%; -following a CPAP of 5 cm H,O (= 0.5 kPa) is employed and the FiO, is again increased up to 100%. During the whole examination the transcutaneous PO, (tcPq) is continuously recorded. Thus, the whole test consists of the HOT plus a HOT performed under CPAP conditions, Results We performed more than 150 examinations according to this method. The measurement results were analysed by classifying them into two criteria: (1) the tcPO&ue in the HOT; and (2) the additional increase in the tcP0, in the CPAP-test. This additional increase, called AtcPO,, results from the tcP0, in the CPAP-test minus the tcP0, in the HOT. When plotting both criteria on a coordinate system we succeeded in separating five types of cardiorespiratory disturbances from each other (Fig. 1).
8. KauppilaA, Hartikainen-SorriA-L, Koivisto M, Ryhiinen P. Cell-mediated immunocompetence of children exposed in utero to short-term or long-term action of glucocorticoids. Obstet Gynecol, in press.
Relevance of lecithin/sphingomyelin the obstetrical decision
C. Tchobroutsky,
Mater&P
(L/S)
ratio measurement
in amniotic fluid for
Port Royal, 123 Boulevard Port Royal, Paris 14e, France
A major advance in obstetrics is the development of an amniotic fluid test to estimate the maturity of the fetal lungs. However, in some conditions such as intra+uterine growth retardation (IUGR), awaiting fetal lung maturity is less important today than it was 10 yr ago. In other conditions such as diabetes, delivery after 38 wk is now generally accepted and the importance of the determination of fetal lung maturity loses its relevance. In a retrospective study we compared the number of amniocenteses performed in the years 1973 and 198 1: the percentage of patients given amniocentesis fell from 2.3 to 1.3 (P -C 0.05). Moreover, the mean number of amniocenteses per patient fell from 1.7 to 1.0. Very few pregnancies complicated by HTA and/or IUGR have been subjected to amniocentesis. The main candidates for amniocentesis remain the insulin-treated diabetics. According to the literature, the predictive value of the L/S ratio in diabetics is much lower than in other pregnancies. In our experience, however, the frequeny of a false mature L/S ratio was less than 1% in more than 300 diabetics. This change in attitude is probably due to (1) a better estimation of gestational age and fetal growth with the advent of ultrasound; (2) a better estimation of fetal distress with the non-stress test; and (3) the advances in neonatal intensive care. In a second retrospective study we analysed the role of the determination of fetal lung maturity in the decision leading to elective termination of pregnancy of very-low-birthweight infants (VLBW) or to abstention. Only 6 amniocenteses were performed in 26 patients. Fifteen pregnancies were electively terminated. Only once were we able to delay delivery for 10 days and wait for a near-mature L/S ratio. In the other cases the determination of pulmonary maturity was not the leading reason for our decision. We believe that the value of the determination of pulmonary maturity holds mainly for those cases with a reactive non-stress test, but then when elective delivery is considered.
Recent aspects of bronchopulmonary
dysplasia after hyaline-membrane
M. Couchard, Mater&P
123 Bd. de Port-Royal,
Port-Royal,
disease
F-75014 Paris, France
This review about BPD is aimed at recalling recent answers to the following questions. What is the current rate of BPD in HMD, and are there modifying trends? What is the present knowledge of the pathology and pathogenesis? Which
418
special clinical features should be focused upon from now on? Also, to date, which recommendations could be used for better management and prevention? Rate The current rate of BPD in HMD remains high, i.e. from 24 to 28% in survivors to 3 1% in non-survivors, with a strong effect of the duration of ventilation: 74% above 14 days, to 100% beyond 28 days. BPD appears to be a major factor in late neonatal deaths (concurrently with intracranial haemorrhage) [ 11. Pathology Recent reports on the pathology show that a simple uncomplicated premature birth takes place in the midst of a complex process of lung development together with pulmonary tissue maturation. Experimental HMD in monkeys shows the early and extensive lesions which are superimposed on this normal process. When the post-HMD reparative process evolves, it may follow a healing mode with catch-up growth, or it may deviate to a scarring process resulting in deeply disturbed lung tissues and altered growth. The pathogenesis most probably is multifactorial [l] and includes the effect of lengthy aggressions on lung epithelium and bronchioles; impairment of the mucociliar-y clearance system; oxygen toxicity, especially the role of superoxide and other highly reactive cytotoxic free-radicals; the prime role of capillary lesions; the variable level of antioxidant defense systems; insufficient macrophage activity; the type of respirator used (barotrauma); and the role of complications such as pneumothorax, emphysema, infections, hypersecretion, atelectasis, and patent ductus arteriosus [l-3]. In summary: oxygen plus pressure plus time in a vicious circle. Clinical features At present, special clinical features should be kept in mind. These include the increased work of breathing [4] and the role of diaphragm fatigue in the patient’s tolerance for BPD; the repeated upper respiratory tract infections or bronchitis or pneumonia in the first year of life [1,3,5,6]; the impairment of pulmonary tests; the occurrence of car pulmonale; the variations of the pulmonary status and cardiac tolerance during sleep states [7]; the importance of EKG and echocardiography; and the general regression of symptoms and radiologic features without a total functional normalization [3,4,8]. Management is aimed at ‘secondary prevention’ in babies requiring artificial ventilation: early fine resuscitation; perfect monitoring; routine chest physiotherapy; moderate fluid therapy; early closure of patent ductus arteriosus; meticulous asepsis; and an all-time concern that ‘the shorter the better’, If BPD had developed despite all precautions the case should be handled as follows: avoid additional complications at any rate; feed by gavage for a longer time than is usual in normal premature infants; adjust supplemental oxygen to the minimal levels required to relieve hypoxia with adjusted raises during sleep; apply chest physiotherapy; and administer bronchodilators and vitamin E. Later measures include the careful organization of discharge, family life,infant care, and immunizations. However, BPD is the result of scarring on a developing immature tissue and even the very best intensive care can do much but not miracles in very-low-birthweight babies. Therefore, we must think in terms of primary prevention, i.e. struggle to avoid the large number of premature deliveries that are preventable through better prenatal care. All physicians involved in prenatal care, public offices, and government must be aware that this heavy medical burden and very costly social problem can be lessened by the prevention of preterm birth.
419
References 1. Monset-Couchard
M. Pediatric Updates, in press, 1983 (107 references, up to December 1981). 2. Arlart IP. Rontgenologische Aspekte des Atemnotsyndroms und der bronchopulmonalen Dysplasie. Roentgenblaetter 1982; 35: 84-89. 3. Monset-Couchard M, Henry E, Larroche JCI, Moriette G, Bomsel F. Dysplasia broncho-pulmonaire. Analyse de 565 cas de ventilation artificielle chez le nouveau-&. Ann Radio1 (Paris) 198 1; 24: 55-65. 4. Morray JP, Fox WW, Kettrick RG. Downes JJ. Improvement in lung mechanics as a function of age in the infant with severe bronchopulmonary dysplasia. Pediatr Res 1982; 16: 290-294. 5. Vohr BR, Bell EF, Oh W. Infants with bronchopulmonary dysplasia. Am J Dis Child 1982; 136: 443-447. 6. Weinstein MR. Oh W. Oxygen consumption in infants with bronchopulmonary dysplasia. J Pediatr 1981; 99: 958-961. 7. Wei’tzenblum E, Muzet A, Ehrhart M, Ehrhart J. Sautegeau A, Weber L. Variations nocturnes des gaz du sang et de la pression arterielle pulmonaire chez les bronchitiques chroniques insuffisants respiratoires. Nouv Press Med 1982; 11: 1119-1122. 8. Wong YC, Beardsmore JH, Meek J, Stocks J, Silverman M. Bronchial hypersecretion in preterm neonates. Arch Dis Child 1982; 57: 117-122.
The CPAP-test for an exact indication of CPAP-therapy
D. Gmyrek and R. Schwarze, Medical Academy ‘Carl Gustav Carus’, Department of Neonatology of the Pediatric Clinic, Fetscher-Strasse 74, DDR-8019 Dresden, D.D.R. Introduction Without doubt the CPAP-therapy is a great advantage in the treatment of the respiratory distress syndrome of premature infants. For deciding the question in the individual case: ‘Is the CPAP-therapy indicated or not?’ we developed the so-called CPAP-test. Material and Methods We carry out the CPAP-test in the following way [ 11: -first we make the usual hyperoxia-test (HOT) by increasing the fraction of inspired oxygen concentration (Fi4) up to 100%; -following a CPAP of 5 cm H,O (= 0.5 kPa) is employed and the FiO, is again increased up to 100%. During the whole examination the transcutaneous PO, (tcPq) is continuously recorded. Thus, the whole test consists of the HOT plus a HOT performed under CPAP conditions, Results We performed more than 150 examinations according to this method. The measurement results were analysed by classifying them into two criteria: (1) the tcPO&ue in the HOT; and (2) the additional increase in the tcP0, in the CPAP-test. This additional increase, called AtcPO,, results from the tcP0, in the CPAP-test minus the tcP0, in the HOT. When plotting both criteria on a coordinate system we succeeded in separating five types of cardiorespiratory disturbances from each other (Fig. 1).