Respiratory distress syndrome
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Respiratory Distress Syndrome (RDS), formerly known as hyaline membrane disease, is a life-threatening lung disorder that results from underdeveloped lungs and insufficient pulmonary surfactant. It occurs most commonly in preterm infants and results in inadequate lung inflation and collapse. Management involves providing warm oxygen supplementation and potentially ventilator support. Surfactant replacement therapy is also used to reduce mortality and complications like bronchopulmonary dysplasia. With appropriate treatment, prognosis is good especially for infants weighing over 1000 grams.
Respiratory distress syndrome
- 1. RESPIRATORY DISTRESS SYNDROME MIRITI M.D MASTER OF CLINICAL MEDICINE: ACCIDENTS AND EMERGENCY June 2018
- 2. Specific Learning Objectives • Definition • Etiology • Pathogenesis and Pathophysiology • Clinical Features • Management • Complications
- 3. RESPIRATORY DISTRESS SYNDROME • Respiratory Distress Syndrome (RDS) formerly known as hyaline membrane disease, is a life threatening lung disorder that results from underdeveloped and small alveoli and insufficient level of pulmonary surfactant that leads to atelectasis. • It is the leading cause of death in preterm infants • Occurs in 50% babies born at26-28 weeks and 25% of babies born at 30-31 weeks
- 5. Etiology/ Causes • RDS occurs as a result of insufficient production of surfactant which is seen in: Prematurity (more common) Maternal diabetes (Inadequate utilization of glycogen for surfactant production) Meconium aspiration syndrome Caesarian section (Due to lack of adrenergic and steroid hormones released during labour) Pulmonary Causes: Congenital malformation, pneumonia, edema of lungs, bleeding from lungs, pleural effusion Non Pulmonary causes: Sepsis, Exposure to cold, acute blood loss.
- 6. Pathogenesis and Pathophysiology • Surfactant production starts at around 20 weeks of gestation and peaks at 35 weeks. (Any neonate <35 weeks is prone to develop RDS) • Surfactant is the substance produced by type II alveolar cells composed of 90% phospholipids and 10 % protein. It has two major components: lecithin (L) and sphingomyelin (S). Lecithin is a fatty protein necessary for absorption of oxygen by lungs and sphingomyelin, phospholipid helps to reduce surface tension. • After 35 weeks of gestation, normal L/S ratio detected in amniotic fluid is 2:1 which indicates fetal lungs are mature.
- 7. •Surfactant is a substance that has detergent properties, thus reduce surface tension of the fluids that line the alveolar and respiratory passages, resulting in increased pulmonary compliance at low intra alveolar pressure. Deficient surfactant production causes unequal inflation of alveoli on inspiration and collapse of alveoli on end expiration. •Without surfactant, infants are unable to keep their lungs inflated and thus produce widespread atelectasis. It has been estimated that each breath requires as much negative pressure (60-75cm H2O) as the initial lung expansion at birth. Blood flow through the atelectatic portion of the lungs is compromised leading to hypoperfusion to the lung tissue and increased pulmonary vascular resistance.
- 8. •Inadequate pulmonary perfusion and ventilation produce hypoxemia and hypercapnia which causes pulmonary vasoconstriction, resulting to partial reversion of fetal circulation (Right to left shunting of blood through the ductus arteriosus and foramen ovale). •Prolonged Hypoxemia activates anaerobic glycolysis which produce increased amount of lactic acid eventually causing metabolic acidosis. Inability of atelectatic lungs to flow off excess CO2 produce respiratory acidosis. Lower pH causes further vasoconstriction.
- 9. •Deficient Pulmonary Circulation and Alveoli perfusion, PO2 continues to fall, pH falls and alveoli are necrosed, this further reduces surfactant production. Ischemic damage to the alveoli, cause transudation of proteins into the alveoli that forms hyaline membrane which makes the lungs stiff and inelastic, thereby inhibiting gas exchange in lungs and is characterized by clinical triad of: Tachypnea Respiratory grunt Inspiratory retractions •Eventually the neonate goes into respiratory Failure
- 11. Clinical Presentation A) Initial manifestation • Tachypnea and Labored breathing • Audible expiratory grunting • Intercostal/ Substernal retractions • Nasal Flaring • Cyanosis/ pallor • Fine respiratory crackles B) Manifestation as disease progresses • Apnea • Flaccidity • Unresponsiveness • Diminished breath sounds • Mottling
- 13. Clinical Features C) In severe Condition • Shock like state • X-ray shows reticulogranular pattern ( Ground Glass appearance) of lung fields that represent alveoli atelectasis
- 15. Diagnostic measures • Details of Antenatal and Prenatal History • Assessment and Evaluation of Clinical manifestation • Arterial Blood gas analysis: PCO2 above 65mmHg PO2 of 40mmHg pH below 7.15 • X-ray shows ground glass appearance of lung fields that represent alveolar atelectasis • Pulse oximetry: Decreased SPO2 • Shake test • Prenatal diagnosis of RDS can be made by determining Lecithin/sphingomyelin ratio in amniotic fluid after 35 weeks of gestation.
- 16. Diagnosis Chest x-ray: Grade 1 (mild cases):Thelungs show fine homogenousground glassshadowing.
- 17. Grade2: Widespread air bronchogrambecome visible.
- 18. Grade3: Confluent alveolar shadowing.
- 19. Grade4: Complete white lung fields with obscuringof the cardiacshadow.
- 20. Management • Neonate should be placed in Newborn Unit (NBU) and nursed in warm incubator. The infant must be kept warm (36.50C). • Oxygen administration- Adequate, warm and humidified O2 in high concentration is given through plastic hood to maintain arterial PO2 between 50-90mmHg is given. • If oxygen saturation of blood cannot be maintained at a satisfactory level and carbon dioxide level rises, Infant will require ventilator support.
- 21. Management cont……. • Mild distress can be managed without ventilator. Moderate and severe RDS need ventilator support. • Frequent monitoring of the PO2, PCO2,pH and arterial blood gas are to be done to diagnose metabolic and respiratory acidosis. • Ventilator support- Infant with RDS are handicapped by decreased lung compliance and alveolar collapse during expiration. Administration of oxygen under positive pressure would prevent alveolar collapse and ensure gas exchange throughout respiratory cycle. • Continuous Positive Airway Pressure (CPAP) is indicated and useful in infant with decreased lung compliance.
- 23. Management cont….. • After weaning from ventilator, Oxygen should be administered via hood. • Maintenance of nutrition and hydration by IV route. • Maintenance of acid base balance • IV administration of 7.5% Sodium bicarbonate in dose of 3-8 meq/kg in 24 hours in 1:1 dilution with distilled water.
- 24. Management cont….. • Surfactant therapy-Via Endotracheal tube is indicated in all neonates with RDS and prophylaxis can be given in all premature infants. Adequate oxygenation, ventilation and monitoring should be started before administration of surfactant. • Dose 100mg/kg body weight in 2 to 4 divided doses at 6 to 12 hours apart. • Depending upon the babies condition, repeated dose of surfactant need to be administered • The adverse effect of surfactant therapy include: Apnea, Hypotension, Pulmonary hemorrhage , lung tissue damage from oxygen pressure and Bradycardia. • Arterial Blood gases and CXR should be monitored .
- 25. Surfactant replacement therapy Surfactant replacement therapy canreduce mortality and incidence of Chronic pulmonarydisease. There are 2 types of surfactant: 1. Natural surfactant extract Bovine(Survanta), Porcine(Curosurf) Natural surfactants appear to be superior, perhaps of their surfactant-associated protein content. Natural surfactants have amore rapid onset and are associated with alower risk ofpneumothorax and improved survival.
- 26. Cont… 2. Syntheticsurfactant Exosurf and ALEC (Artificial Lung Expanding Compound) 3. Newer surfactant • Synthetic surfactants with synthetic peptides modelled on surfactant proteins, Aerosolized surfactants. Dose: •Survanta 100mg/kg for the first and subsequent doses. •Curosurf 200mg/kg for the first dose and 100mg/kg for the subsequent doses or 100mg/kg for all the doses.
- 27. Management cont….. • IV antibiotics • Administration of Vitamin E- Low birth weight or preterm babies receiving oxygen therapy may be administered vitamin E at a dose of 100 IU/Kg/day IM from birth onwards.
- 28. Prognosis • Prognosis is good with appropriate and timely treatment • Survival can be as 60-80% in infant > 1000grams. In the absence of ventilatory support, neonate with severe disease will die. • If there is no complication during the first 48 hours, infant begins to improve by 72 hours and if they survive for 96 hours chances of survival is higher.
- 29. Complications • Patent ductus arteriosus • Congestive cardiac failure • Retrolental fibroplasia • Intraventricular hemorrhage • Bronchopulmonary dysplasia • Neurological abnormalities • Pneumonia • Sepsis
- 30. REFERENCES • Basic Paediatric Protocols: for ages upto 5 years. (2016). Republic of Kenya Ministry of Health. • Robert, N.R.C (1988) Textbook of neonatology (1st ed.) Liberty of congress cataloguing publication, Singapore (pp:274-306) • Rodriguez RJ, Martin RJ, Fanaroff AA. Respiratory distress syndrome and its management. In: Fanaroff AA, Martin RJ, eds. Fanaroff and Martin’s Neonatal-Perinatal Medicine: Diseases of the Fetus and Infant. 7th ed. St. Louis, MO: Mosby; 2002:1001–1011.