Idiopathic Respiratory Distress Syndrome In Newborns

(Syndrome of hyaline membranes)

Idiopathic respiratory distress syndrome is most commonly caused by a lack of pulmonary surfactant in the lungs of newborns <37 weeks. The risk increases with the degree of immaturity. Symptoms and signs include groaning breathing, the use of respiratory muscles and nostrils shortly after birth. The diagnosis is made clinically. Prenatally can tested the lung maturity and the risk can be estimated. The treatment consists of the administration of surfactant and supportive measures.

Idiopathic respiratory distress syndrome is most commonly caused by a lack of pulmonary surfactant in the lungs of newborns <37 weeks. The risk increases with the degree of immaturity. Symptoms and signs include groaning breathing, the use of respiratory muscles and nostrils shortly after birth. The diagnosis is made clinically. Prenatally can tested the lung maturity and the risk can be estimated. The treatment consists of the administration of surfactant and supportive measures. Since etiology surfactant is produced only at the end of pregnancy (34th to 36th week) in sufficient quantity, the risk of idiopathic respiratory distress syndrome increased (IAS), the sooner the child is born. Other risk factors include multiple pregnancy, maternal diabetes, male sex, and a fair skin type. The risk is reduced with fetal growth restriction, pre-eclampsia or preeclampsia, maternal hypertension, premature rupture of membranes and maternal Corticosteroideinnahme. There are rare inherited cases, caused by a mutation of the surfactant protein (SP-B and SP-C) and a mutation of the ABC transporter A3 (ABCA3) arise. The pathophysiology of pulmonary surfactant is a mixture of phospholipids and lipoproteins, which are secreted by the type II pneumocytes (Perinatal Physiology: Lung function). It reduces the surface tension of the water film lining the alveoli, thereby reducing the tendency of alveoli to collapse as well as the force required to inflate them. In Tensidmangel a greater pressure is required to open the alveoli. Without adequate breath pressure, the lungs are diffuse atelectasic and resolve inflammation and pulmonary edema (pulmonary edema) from. Since the blood that flows through the atelectatic areas, is not oxygenated (intrapulmonary right to left shunt), the child is hypoxic. The lung compliance is reduced, the work of breathing is increased. In severe cases, the diaphragm and intercostal muscles get tired, and it comes to CO2 retention. A respiratory acidosis develops. Complications of idiopathic respiratory distress syndrome are an intraventricular hemorrhage (intracranial hemorrhage: intraventricular and / or intraparenchymal hemorrhage), periventricular violation of the white matter, tension pneumothorax (pneumothorax (voltage)), bronchopulmonary dysplasia (bronchopulmonary dysplasia (BPD)), sepsis (sepsis in newborns ) and neonatal death. The intracranial complications with hypoxia, hypotension, and changes in blood pressure and a decreased cerebral blood flow (intracranial bleeding intracranial haemorrhage; hemorrhagic shock and encephalopathy syndrome hemorrhagic shock and encephalopathy syndrome (HSES)) associated. Symptoms and signs Symptoms are fast, moaning breaths, beginning immediately or a few hours after birth, with suprasternalen and substernal retractions and nasal flaring. Once the atelectasis and respiratory failure progress, the symptoms of cyanosis, irregular breathing and apnea worse. Newborns <1000 g can have as stiff lungs, that they are unable to start in the delivery room with breathing or to maintain it. On examination, breath sounds are reduced. Peripheral pulses may be reduced with edema peripheral extremities and reduced urine output. Diagnosis Clinical evaluation ABG (hypoxemia and hypercapnia) chest radiograph blood, cerebrospinal fluid and cultures from tracheal aspirate The diagnosis is due to the clinical presentation, an assessment of the risk factors and blood gases show hypoxia and hypercapnia and asked chest x-ray. The radiograph shows diffuse atelectasis, classically described as milk turbidity Aerobronchogramm; the changes correlate approximately with the severity of the disease. The differential diagnosis includes a B-streptococcal pneumonia and sepsis, transient tachypnea in neonates (transient tachypnea of ??the newborn), persistent pulmonary hypertension, aspiration, pulmonary edema, and congenital heart disease. There are bled cultures Liquorkulturen the newborn and perhaps cultures of Trachealsekrets. Clinically, the streptococcus pneumonia Group B is very difficult to distinguish from IAS, so should be initiated at outstanding culture results already with the antibiotic treatment. The screening idiopathic respiratory syndrome can be predicted prenatally by determination of lung maturity, given by way of amniotic fluid, which can be obtained by amniocentesis or collected after the rupture of membranes in the vagina. This helps in determining the optimal delivery timing. this is important for elective deliveries before the 39th week of pregnancy when gestational age can not be confirmed by the fetal heart sounds, the hCG levels and ultrasound measurements, as well as for nichtelektive deliveries between 34th and 36th week of pregnancy. (The more surfactant in the amniotic fluid, the greater the stability of the resulting foam, if the amniotic fluid combined with ethanol and shaken is) to the amniotic fluid tests include lecithin / sphingomyelin ratio Foam Stability Index test surfactant / albumin ratio, the risk is low when the lecithin / sphingomyelin ratio> is 2, phosphatidylglycerol is present, there is a foam-stability index of 47 or Surfactant- / albumin ratio is> 55 mg / g. Surfactant treatment O2 supply as needed Mechanical ventilation required The prognosis with treatment is excellent, the mortality is <10%. With adequate ventilation, Surfactantsekretion starts. If the secretion begins, the idiopathic respiratory distress syndrome disappears within 4 or 5 days, but a severe hypoxia can result in the meantime to multiple organ failure and death. No specific treatment is intratracheal administration of surfactant. However, this treatment requires intubation can also be necessary for the ventilation and oxygenation. Less premature newborns (> 1 kg) and those with a lower O2 demand (percentage of inspired O2 [FiO 2] <40-50%) are sometimes good (to the sole replacement dose of O2 or to treatment with nasal, continued positive airway pressure ventilatory support in newborns and infants: Continuous positive airway pressure (CPAP)) on. A treatment strategy with an early (within 20-30 minutes after birth) surfactant therapy is a big reduction in the duration of mechanical ventilation, a lower incidence of air leak syndrome (Pulmonary Air leak syndrome) and a lower incidence of bronchopulmonary dysplasia connected. Surfactant accelerates recovery and reduces the risk of pneumothorax, interstitial emphysema, intraventricular hemorrhage, bronchopulmonary dysplasia, neonatal hospital and 1-year mortality. Infants who get surfactant for a diagnosed IAS, however, have a higher risk of prematurity apnea (apnea of ??prematurity). Among the options for the Tensidersatz include berectant berectant Poractant alfa Calfactant Lucinactant is a lipid-bovine lung extract, there is enriched with the proteins B and C, Colfosceril palmitate, palmitic acid, and tripalmitin; the dose is 100 mg / kg every 6 hours as needed up to 4 doses. Poractant alfa is a modified porcine-derived crushed lung extract containing phospholipids, neutral lipids, fatty acids and surfactant-associated proteins B and C; the dose is 200 mg / kg, followed by up to 2 doses of 100 mg / kg at intervals of 12 hours as needed. Calfactant is a calf lung extract containing phospholipids, neutral lipids, fatty acids and surfactant-associated proteins B and C; the dose is 105 mg / kg every 12 hours as needed up to 3 doses. Lucinactant is a synthetic pulmonary surfactant having a surfactant protein B analogue Sinapultid- (KL4) peptide, phospholipids and fatty acids; the dose is 175 mg / kg every 6 hours up to 4 doses. The lung compliance quickly improved after treatment. The highest value of the inspiratory pressure the ventilator may need to be lowered quickly in order to reduce the risk of pulmonary air leak syndrome. The other ventilation parameters (z. B. FiO2, frequency) must be quickly reduced if possible also. Prevention If a fetus is delivered in the 24th to 34th week of pregnancy, the mother should be at least 48 h before the birth of 2 doses of 12 mg betamethasone at intervals of 24 hours or 4 doses of dexamethasone, 6 mg i.v. or i.m. every 12 hours, are added. This induces fetal Surfactantsekretion and reduces the risk of an IAS or the severity of the disease. (Preterm labor.) Studies have shown that prophylactic intratracheal surfactant in newborn with a high risk of developing IAS (infants <30 weeks of completed pregnancy especially in the absence of prenatal corticosteroid exposure) the risk of neonatal death and certain forms of pulmonary diseases (e.g., B. pneumothorax) reduced. Important points that idiopathic respiratory distress syndrome (IAS) is caused by a deficiency of pulmonary surfactant, which usually occurs only in neonates <37 weeks; the defect is severe with increasing immaturity. When a surfactant deficiency, the alveoli close or not open and the lungs are diffuse atelectasic and resolve inflammation and pulmonary edema from. In addition to causing respiratory failure IAS increases the risk of intraventricular hemorrhage, tension pneumothorax, bronchopulmonary dysplasia, sepsis and death. The diagnosis is made clinically and with chest X-ray; Pneumonia and sepsis ruled out by appropriate cultures. When a premature baby is expected that lung maturity is evaluated by testing the amniotic fluid to the lecithin / sphingomyelin ratio, foam stability or the surfactant / albumin ratio. Treatment is with intratracheal surfactant and a breathing support is provided if needed. The mother be given multiple doses of a parenteral corticosteroid (betamethasone, dexamethasone), when the delivery must take place between the 24th and 34th week of pregnancy; Corticosteroids stimulate the fetal surfactant production and reduce the risk and / or severity of the IAS.

Health Life Media Team

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