Respiratory distress syndrome of the newborn
| Classification according to ICD-10 | |
|---|---|
| P22.0 | Respiratory distress syndrome of the newborn |
| ICD-10 online (WHO version 2019) | |
The newborn respiratory distress syndrome (ANS) (also hyaline membrane syndrome , surfactant deficiency syndrome , infant respiratory distress syndrome (IRDS)) is a lung function disorder in newborns . The dysfunction is one of the leading causes of death in newborns. It used to be called idiopathic respiratory distress syndrome , but this name is now out of date. The cause was discovered in 1959 by Mary Ellen Avery . Surfactant administration therapies were introduced by Tetsuro Fujiwara from the 1970sdeveloped in Japan and Bengt Robertson in Sweden.
frequency
About 60% of premature babies below the 30th week of pregnancy develop respiratory distress syndrome. Overall, 1% of newborns develop respiratory distress syndrome. Respiratory distress syndrome is the most common cause of death in premature babies. By lung maturity induction before birth, the incidence of respiratory distress syndrome was reduced. In premature babies before the 28th week of pregnancy, however, respiratory distress syndrome is still the most important cause of death.
The disease can also be an essential characteristic of rare syndromes, such as the brain-lung-thyroid syndrome .
Pathophysiology
In premature births, the adrenal cortex is usually not yet fully developed (only happens in the 35th week of pregnancy). This is why the fetus is not yet able to produce cortisol there, but this is absolutely necessary for the development of type II pneumocytes, as these form surfactants . Surfactant is produced by the lung surfactant , the surface tension of the liquid film, of the alveoli reduces rests (alveoli) and thus reduces the pressure which is required for their development (→ lung maturation ).
In the case of a surfactant deficiency, the alveoli collapse at normal intrathoracic pressures; high ventilation pressures have to be used to ensure development (and thus ventilation of the lungs) (see also section on therapy ). High ventilation pressures can cause (further) lung damage. A lack of surfactant leads to the formation of hyaline membranes ( mucopolysaccharides and glycoproteins from the blood plasma) in the lungs, and the lungs are less elastic or stiff.
Many authors such as Mayatepek or Muntau define the term ANS relatively narrowly as:
- primary surfactant education disorder in premature infants. In this case, the lung tissue is simply not yet sufficiently mature to produce sufficient surfactant.
In addition, there are other scenarios of a surfactant deficiency with the formation of hyaline membranes and shortness of breath:
- Excessive inactivation of already formed surfactant, such as meconium aspiration syndrome (inhalation of amniotic fluid containing mekonium , but here other aspects such as chemical pneumonia , fibrosis and superinfections play a role).
- Secondary surfactant formation disorder : Hypoxia , circulatory disorders , changes in lung metabolism or structure lead to reduced surfactant production. This phenomenon plays e.g. B. in bronchopulmonary dysplasia / pulmonary hypoplasia , pulmonary hypertension and persistent fetal circulation a role.
Complex interactions exist between surfactant deficiency, many of the above-mentioned disease phenomena and their therapies, so that they can reinforce each other and also with regard to the surfactant deficiency.
Clinical picture
Respiratory distress syndrome occurs immediately after birth or a few hours after birth. Indicative symptoms are increasing shortness of breath in the newborn with cyanosis , indentations in the area between the ribs or above the sternum when breathing, groaning when exhaling, movement of the nostrils when breathing (nostrils) and accelerated breathing ( tachypnea ).
Possible acute complications of respiratory distress syndrome are the formation of emphysema and air accumulation in the body cavities ( pneumothorax , pneumomediastinum , pneumoperitoneum ).
Radiological staging
Characteristic changes can be seen on chest x-rays . Gradual shading occurs up to the full image of the so-called "white lung".
- I. Fine granular lung pattern
- II. I + aerobronchogram extending beyond the contours of the heart
- III. II + blurring or partial obliteration of the contours of the heart and diaphragm
- IV. "White lung"
prophylaxis
Induction of lung maturity : In the event of a threatened premature birth with manifestation of a primary ANS, an attempt is made to put the child's lungs into a more mature state than would correspond to the gestational age by administering betamethasone to the mother twice every 24 hours . This enables a significant increase in the available surfactant to be achieved over a period of days. In addition, this treatment leads to a stabilization of the blood-air barrier and to a reduced inactivation of already synthesized surfactants.
At the same time, attempts are made to delay birth by at least a few days by administering labor-inhibiting agents ( tocolytics ) in order to give the lung maturation therapy the time to “strike”.
Therapy of the manifest ANS
A mild respiratory distress syndrome can be stabilized with CPAP ventilation . For more severe cases, endotracheal intubation and controlled ventilation with increased inspiratory pressure and positive end-expiratory pressure (PEEP) are required. A respiratory distress syndrome often requires long-term ventilation with sometimes high oxygen partial pressures . This can lead to bronchopulmonary dysplasia . Another dreaded complication of forced oxygen administration is retinopathy of premature babies .
In the therapy of manifest ANS, a basic distinction is made between symptomatic and causal therapy . Symptomatic therapy includes:
- Minimal handling: Avoid burdensome care and diagnostics
- careful observation
- regular temperature controls (child, incubator, breathing gas)
- Blood gas analysis (preferably via transcutaneous measurement)
- Oxygen supply via nasal CPAP or respirator
- Nasal CPAP when there is a need for oxygen
- artificial respiration
- Antibiotic treatment
- careful fluid balance
- Ductus arteriosus Botalli : attention to the increased risk of reopening
- Laboratory controls (blood gases, blood glucose, hematocrit, electrolytes, total protein, blood count, platelets, signs of infection)
The causal therapy of respiratory distress syndrome is based on surfactant substitution . This is usually applied directly into the windpipe via the tube. This reduces mortality and alleviates complications.
A combination of close perinatal care (lung maturation, postpartum administration of surfactant, ventilation) and gentle induction of labor can alleviate respiratory distress syndrome and reduce the incidence of complications. The treatment of respiratory distress syndrome in newborns takes place in perinatal centers.
literature
- Marion Kiechle: Gynecology and Obstetrics. Urban & Fischer, Elsevier, Munich 2007, ISBN 978-3-437-42406-9 .
- Ertan Mayatepek: Pediatrics. Urban & Fischer, Munich 2007, ISBN 978-3-437-43560-7 .
- Ania Muntau: Pediatric intensive course. Urban & Fischer, Munich 2009, ISBN 978-3-437-43392-4 .
Web links
- Guideline "Acute, non-obstructive pulmonary failure (ARDS / ALI) in childhood" , guideline of the Society for Neonatology and Pediatric Intensive Care Medicine on awmf.org
Individual evidence
- ↑ Michael Obladen, Rolf F. Maier (Ed.): Neonatal Intensive Care Medicine. Springer, Berlin et al. 2006, ISBN 978-3-540-33738-6 , pp. 205ff.
- ↑ Michael Obladen, Rolf F. Maier (Ed.): Neonatal Intensive Care Medicine. Springer, Berlin et al. 2006, ISBN 978-3-540-33738-6 , pp. 180ff.
