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Respiratory problems in premature infants Dr. Rozin Ilya Department of Neonatology Kaplan Medical Center.

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Presentation on theme: "Respiratory problems in premature infants Dr. Rozin Ilya Department of Neonatology Kaplan Medical Center."— Presentation transcript:

1 Respiratory problems in premature infants Dr. Rozin Ilya Department of Neonatology Kaplan Medical Center

2 Respiratory problems Respiratory Distress Syndrome (RDS) or Hyaline Membrane Diseases (HMD) Broncho-Pulmonary Dysplasia (BPD)

3 Respiratory Distress Syndrome

4 Definition Also known as hyaline membrane disease Deficiency of pulmonary surfactant in an immature lung Common respiratory disorder of premature infants RDS can also be due to genetic problems with lung development

5 Epidemiology Major cause of morbidity and mortality in preterm infants 20,000-30,000 newborn infants each year ( in US) Incidence and severity of RDS are related inversely to gestational age of newborn infant (most case before 37 weeks) weeks gestation : 50% weeks gestation : <30%

6 Epidemiology Overall incidence in grams: 42% grams: 71% grams: 54% grams: 36% grams: 22%

7 Other risk factors for RDS Increased Risk Prematurity Male gender Familial predisposition Cesarean section without labor Perinatal asphyxia Caucasian race Infant of diabetic mother Chorioamnionitis Non-Immune hydrops fetalis Multiple pregnancy (twins or more) Decreased Risk Chronic intra-uterine stress Prolonged rupture of membranes Maternal hypertension or toxemia IUGR/SGA Antenatal glucocorticoids Maternal use of narcotics/cocaine Tocolytic agents Hemolytic disease of the newborn

8 Phases of Lung Development

9 Lung Development

10 Surfactant Complex lipoprotein Composed of 6 phospholipids and 4 apoproteins Surfactant contains 70-80% phospholipids, 8-10% protein, and 10% neutral lipids

11 Surfactant Metabolism


13 4 surfactant apoproteins Surfactant protein B (SP-B) Surfactant protein C (SP-C) for preventing atelectasis, and Surfactant protein A (SP-A) - facilitates phagocytosis of pathogens by macrophages and their clearance from the airways Surfactant protein D (SP-D) – if absent - increased surfactant lipid pools in the airspaces and emphysema in mice

14 Assessment of Fetal Lung Maturity Lecithin / sphingomyelin (L/S) ratio Lamellar body counts Phosphatidylglycerol After 35 weeks gestation

15 L/S Ratio

16 Pathophysiology


18 Etiology Preterm delivery Mutations in genes encoding surfactant proteins SP-B SP-C ATP-binding cassette (ABC) transporter A3 (ABCA3) - is critical for proper formation of lamellar bodies and surfactant function and may also be important for lung function in other pulmonary diseases

19 Lung Compliance

20 Normal Lung

21 Hyaline Membranes

22 Surfactant Inactivation Meconium and blood can inactivate surfactant activity (Full-term > Preterm) Proteinaceous edema and inflammatory products increase conversion rate of surfactant into its inactive vesicular form Oxidant and mechanical stress associated with mechanical ventilation that uses large TV

23 Clinical Manifestations Tachypnea Nasal flaring Grunting Intercostal, sub xiphoid, and subcostal retractions Cyanosis Apnea

24 Differential Diagnosis TTN MAS Pneumonia Cyanotic Congenital Heart Disease Pneumomediastinum, pneumothorax Hypoglycemia Metabolic problems Hematologic problems Anemia, polycythemia Congenital anomalies of the lungs

25 Diagnosis Onset of progressive respiratory failure shortly after birth Characteristic chest radiograph Laboratory tests – rule out infection Analysis of blood gas: Hypoxia Hypercarbia

26 Chest X Ray “ground glass”

27 Prevention Antenatal glucocorticoids Enhances maturational changes in lung architecture and inducing enzymes Stimulate phospholipid synthesis and release of surfactant All pregnant mothers at risk for preterm delivery between 24 and 34 weeks gestation should receive ACS

28 Treatment Surfactant Therapy Assisted Ventilation Techniques and Oxygen therapy (be careful) Supportive Care Thermoregulation Fluid Management Nutrition Antibiotic therapy Gentle handling

29 Prognosis Acute complications of respiratory distress syndrome : Alveolar rupture Infection Intracranial hemorrhage and periventricular leukomalacia Patent Ductus Arteriosus (PDA) with increasing left-to-right shunt Pulmonary hemorrhage Necrotizing enterocolitis (NEC) and/or gastrointestinal (GI) perforation Apnea of prematurity

30 Prognosis Chronic complications of respiratory distress syndrome : Broncho pulmonary dysplasia (BPD) Retinopathy of prematurity (ROP) Neurologic impairment

31 Bronchopulmonary dysplasia Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that develops in preterm neonates treated with oxygen and positive-pressure ventilation (PPV). The pathogenesis of this condition remains complex and poorly understood.

32 Pathogenesis

33 Definition 1967, Northway et al. : premature infants with RDS, resaved prolonged ventilation, with high concentration of oxygen and high peak inspiratory pressure All require oxygen at 28 days after birth and progressive change on chest x-ray

34 Definition 1979, Bancalari: same to Northway + tachypnea and crackles or retraction. 1988, new criterion: oxygen supplementation at 36 weeks postmenstrual age (PMA) - more accurately predicted abnormal pulmonary outcome at 2 years of age - with medical care more infant with oxygen at 28 days

35 Definition 2000, National Institute of Child Health and Human Development (NICHD)

36 Definition Because of absent specified in the consensus BPD definition, it was recommended that a physiologic test confirming the need for supplementation oxygen be performed

37 Epidemiology Incidence: 42-46% (BW g) 25-33% (BW= g) 11-14% (BW=1001=1250g) 5-6% (BW= g) Risk factors: Prematurity, low BW White boys Genetic heritability

38 Epidemiology By the NICHD at 2010 from Neonatal Research Network BW gr GA 22 0/7 – 28 6/7 weeks BPD of all diagnosis - 68% Mild - 27% Moderate – 23% Severe – 18%

39 Pathology “Old” BPD:  Airway inflammation  Fibrosis  Smooth muscle hypertrophy “New” BPD:  Lung development arrests before alveolarization: lung have larger but fewer alveoli than normal lung  Pulmonary vasculature to be dysmorphic

40 Pathology “Old BPD” (before surfactant and steroids) Cystic changes, heterogeneous aeration “New BPD” (after surfactant and steroids) More uniform inflation and less fibrosis, absence of small and large airway epithelial metaplasia and smooth muscle hypertrophy Some parenchymal opacities, but more homogenous aeration and less cystic areas PATHOLOGIC HALLMARKS: larger simplified alveoli and dysmorphic pulmonary vasculature

41 Pathology Old BPD: Airway injury, inflammation and parenchymal fibrosis due to mechanical ventilation and oxygen toxicity New BPD: Decreased septation and alveolar hypoplasia leading to fewer and larger alveoli, so less surface area for gas exchange Dysregulation of vascular development leading to abnormal distribution of alveolar capillaries and thickened muscular layer of pulmonary arterioles

42 Pathogenesis

43 Chorioamnionitis – caused by an ascending infection, as possible cause But histologic chorioamnionitis to be protective ( same umbilical vasculitis) – potential role of transcription factor nuclear factor kB and inflammation Ureaplasma colonization Bacterial sepsis

44 Pathogenesis Hemodynamic significantly PDA and surgery ligation Mechanical ventilation ( volutrauma and barotrauma ) Oxygen toxicity High volume of fluids intake n the first few days after birth Lower serum cortisol level ( in VLBW ) – early adrenal insufficiency

45 Outcomes Higher rate recurrent hospitalization in the first year after birth Lung disease in adulthood: airway obstruction, reactive airways, emphysema Affect growth Cardiovascular sequelae: pulmonary artery hypertension, cor pulmonale, systemic hypertension Poor neurodevelopmental outcomes: language delay, increased fine and gross motor impairment

46 Prevention and therapy Antenatal:  corticosteroids administration standard of care – 24 – 34 weeks effect on the incidence of BPD controversial in animals studies – arrest alveolarization and microvascular development

47 Prevention and therapy Postnatal:  postnatal corticosteroids therapy decreased time to extubation early use – poor neurodevelopmental outcomes (CP) adverse effects: hyperglycemia, hypertension, GI bleeding, hypertrophic cardiomyopathy, infection

48 Prevention and therapy  Azithromycin macrolides antibiotic anti-inflammatory effect active against Ureaplasma infection in a RCT no statistic significance ( for 6 weeks of therapy )

49 Prevention and therapy  Vitamin A: regulation of lung development injury repair low level – increased risk to BPD  Vitamin E and Selenium: study result have been mixed selenium works synergistically with Vit E to prevent peroxide formation – not show to reduce risk to BPD

50 Prevention and therapy  Caffeine: significant reduce in BPD  Pentoxiphilline: non specific phosphodiesterase inhibitor decreased pulmonary inflammation  Cromolyn: mast cell stabilizer non protective effect

51 Prevention and therapy  Nitric Oxide: benefit on oxidative stress and lung development – in animal studies not support the use in routine care  Surfactant: not decreased incidence of BPD improving respiratory care prophylactic therapy is associated with lower risk of BPD

52 Prevention and therapy  Ventilatory strategies: permissive hypercapnia ( pH>7.20 and pCO2 from 45 to 55 mmHg ) gentle ventilation ( SIMV, HFV, Volume-targeted ventilation, NSIMV (NIPPV) or NCPAP ) INSURE used adequate oxygenation – difficult

53 Prevention and therapy  Nutrition: excessive fluids intake – more risk for BPD if BPD – infant may need up to 20%-40% more kilocalories

54 Prevention and therapy Therapy of established BPD :  Inhaled steroids : evidence supporting is mixt RCT for early therapy – no support  Diuretics : for decreased pulmonary alveolar and interstitial edema routine used loop diuretics not recommended Thiazide + Spironolactone  Bronchodilators : most commonly β adrenergic agonist short term improvement for acute exacerbation care only


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