Farewell lecture by Prof. Herting: Progress in premature babies!

Today is June 27th, 2025

Date: June 27, 2025 – Source 1 ():
– Farewell lecture by Prof. Dr. Egbert Herting on July 11th at 4 p.m. s.t. in the lecture hall of the Central Hospital Z1/Z2.
– Topic of the lecture: “The role of surface tension” and advances in the treatment of respiratory distress syndrome in premature babies through the use of surfactant.
– Prof. Dr. Egbert Herting has been a professor of pediatric and adolescent medicine at the University of Lübeck since August 2004.
– He was director of the clinic for pediatric and adolescent medicine at the University Hospital Schleswig-Holstein, Lübeck campus.
– Scientific focus: diseases of newborns and premature babies as well as infectious diseases in children.

Source 2 ():
– Synonyms: respiratory distress syndrome of the newborn, hyaline membrane syndrome
– English: neonatal respiratory distress syndrome (NRDS), infant respiratory distress syndrome (IRSD, IRS)
– Definition: Respiratory distress syndrome of prematurity (IRDS) is a pulmonary disease in premature infants caused by lung immaturity and surfactant deficiency.
– ICD-10 code: P22.0

**Epidemiology:**
– 60-80% of premature babies (< 28 weeks of gestation) develop respiratory distress syndrome.
– Mature newborns (> 37 weeks of gestation) show IRDS in < 5% of cases.
– Overall, 1% of newborns develop respiratory distress syndrome.
– Most common cause of death in the neonatal period.

**Etiology:**
– Lung most affected by lack of intrauterine maturation.
– Deficient surfactant formation leads to alveolar collapse and impaired gas exchange.

**Pathophysiology:**
– Surfactant production begins from the 20th week of pregnancy, sufficient concentration only from the 35th week of pregnancy.
– Without surfactant: Lungs collapse after expiration, leading to atelectasis and hypoxia.
– Hypoxia increases surfactant production and leads to damage to the alveolar epithelium.

**Symptoms:**
– Occurrence of respiratory distress syndrome immediately or a few hours after birth.
– Symptoms: nostrils, retractions of the sternum and intercostal spaces, tachypnea (> 60/min), groaning expiration, pale gray to cyanotic skin color.

**Diagnosis:**
– Based on gestational age and typical clinical presentation.
– Diminished breathing sounds on auscultation.
– Blood gas analysis shows hypoxemia, normocapnia, in severe cases hypercapnia and respiratory lactic acidosis.

**Prenatal diagnosis:**
– Amniocentesis and lecithin-sphingomyelin ratio to assess the risk of lung maturation.

**Stage classification:**
– I: fine-grained reduction in transparency (microatelectasis)
– II: positive aerobronchogram
– III: further reduction in transparency, blurring of the diaphragm and heart contours
– IV: White lung, no differentiation of the heart contours from the lung parenchyma

**Therapy:**
– Treatment in specialized perinatal centers.
– Principle of “minimal handling”.
– Non-invasive or invasive ventilation depending on the severity.
– CPAP ventilation with PEEP from 3 to 8 cmH2O.
– Intratracheal application of surfactant possible.
– Controversially discussed intubation for prophylactic surfactant administration.

**Complications:**
– Long-term ventilation can lead to pneumothorax and bronchopulmonary dysplasia.
– Retinopathy of prematurity as a result of oxygen administration.

**Prevention:**
– Delay premature birth by tocolysis.
– Glucocorticoid betamethasone for lung maturation 24-48 hours before birth.

**Forecast:**
– Mortality averages 30%.

Source 3 ():
– Respiratory distress syndrome (IRDS) is common in premature babies.
– Cause: Insufficient lung maturity due to premature birth, leading to surfactant deficiency.
– Preterm births with a known risk of preterm birth previously received therapy with glucocorticoids to mature the lungs.
– Studies show that repeated administration of steroids does not improve lung maturation and can cause fetal growth disorders.
– Prenatal surfactant administration is no longer recommended because it is associated with changes in brain development and later mental abnormalities.
– Frequency of IRDS in premature babies before 30 weeks of pregnancy: 60%.
– Surfactant is normally produced from the 35th week of pregnancy.
– Lack of surfactant leads to lung alveoli sticking together (secondary atelectasis).

**Respiratory Distress Syndrome (IRDS) Symptoms:**
– Accelerated breathing (tachypnea) with over 60 breaths per minute.
– Difficult breathing (dyspnea) with groaning when exhaling.
– Nasal breathing and contractions in the upper abdomen, between the ribs and under the larynx.
– Stopping breathing (apneas).
– Pallor of the skin or cyanosis (bluish discoloration of the skin).
– Weakness and reduced muscle tone.

**Stages of Respiratory Distress Syndrome (IRDS):**
1. Fine-grained transparency reduction.
2. Positive aerobronchogram beyond the heart contour.
3. Further reduction in transparency with blurring of the diaphragm and heart contours.
4. White lung, cardiac contours cannot be differentiated from lung parenchyma.

**Treatment:**
– Prenatal: delayed birth (e.g. through tocolysis).
– Postnatal: administration of surfactant into the trachea, supportive oxygen administration, CPAP or SIMV ventilation, infusion treatment, minimal handling, fluid balancing, antibiotics if necessary.

**Possible Complications or Secondary Conditions:**
– Chronic lung disease (bronchopulmonary dysplasia, BPD).
– Eye damage (retrolental fibroplasia, retinopathy of prematurity).
– Pneumothorax, pulmonary emphysema, bronchial malformations, asthma, chronic lung problems.
– Cerebral hemorrhages and resulting consequential damage.