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Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
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Respiratory Distress Syndrome (Rds)

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  • 1. Respiratory distress syndrome (RDS) Mbbs.weebly.com
  • 2. RDS = HMD RDS: Respiratory distress syndrome HMD: Hyaline membrane disease
  • 3. Introduction
    • Acute lung disease of the newborn caused by Pulmonary surfactant deficiency.
    • Tends to occur in neonates younger than 32 weeks GA
    • Outcome of RDS has improved with the increased use of antenatal steroids and early postnatal surfactant therapy
  • 4. Etiology
    • Prematurity
    • Pulmonary surfactant (PS) deficiency
  • 5. Incidence
    • Increase in incidence with decreasing gestational age
    • <28wk: 60-80%
    • 32-34wk: 15-30%
    • 37wk: 5%
    • Infant of diabetic mother (IDM): 5-6 times higher than non-IDM
  • 6. Constituents of PS
  • 7. Functions of PS
    • lower surface tension
    • maintain alveolar stability
    • prevent the collapse of small air spaces at end expiration
  • 8. Capillary permeability↑ Pulmonary hypertension Hyaline membrane formation R->L shunting
  • 9. Hyaline membrane
  • 10. Hyaline membrane
  • 11. Clinical manifestation
    • symptoms: progressive respiratory distress within 2-6h tachypnea, intermittent expiratory grunting (from partial closure of glottis)
    • signs: nasal flaring( 鼻扇 ), cyanosis, subcostal and intercostal retractions ( 三凹征 ), fine rales can be heard, systolic murmur can be heard at left border of sternum in some patients.
  • 12. Chest retraction
  • 13. Laboratory examinations 1. foam test (胃液泡沫稳定试验〕 2. measurement of the levels of PS amniotic fluid or tracheal aspirate L / S (lecithin / sphingomyeline)  2  maturity of lungs 3. blood gas : pH  , PaO 2  , PaCO 2  , HCO 3 -  (mixed acidosis)
  • 14. X-ray of RDS
    • ground glass change
    • (fine reticular granularity of the parenchyma)
    • air bronchogram
    • white lung
  • 15. Severe RDS- white lung
  • 16. Echocardiography Color flow Doppler  PDA and PPHN PDA = Patent ductus arteriosus( 动脉导管未闭 ) PPHN = Persistent Pulmonary Hypertension of newborn ( 新生儿持续性肺动脉高压 )
  • 17. Differential diagnosis
    • wet lung(transient tachypnea of newborn, TTN )
    • group B streptococcal (GBS) pneumonia
    • diaphragmatic hernia
  • 18. X-ray of Wet Lung
  • 19. Defect in the diaphragm
  • 20. X-ray of diaphragmatic hernia
  • 21. Infant of diaphragmatic hernia
  • 22. Treatment-General therapy I 1. Temperature maintenance: T:36.5  C 2. Monitoring: T, R, HR, S a O 2 ,BP and blood gas 3. Fluid therapy:
    • 5%GS 65-75ml/kg/d (D1)
    • electrolyte supplement
    • start feeding if stable
    • parenteral nutrition (肠道外营养〕 when feeding intolerance and poor energy intake
  • 23. Treatment-General therapy II 4.    Correction of acidosis 5.   Closure of PDA 6.    Antibiotics
    • fluid restriction
    • diuretics
    • Indomethacin, ibuprofen
    • surgical ligation
  • 24. Treatment Oxygen therapy and assist ventilation 1.oxygen therapy
    • nasal cannula, mask or headbox oxygen
    • keep PaO 2 50-70mmHg, S a O 2 90-95%
    • Prevent alveolar collapse at end expiration
    • Indication: FiO 2. > 0.4, PaO 2 < 50 mmHg or S a O 2 < 85%
    • Pressure: 4-6 cmH 2 O
    2. CPAP (continuous positive airway pressure)
  • 25. CPAP
  • 26. Treatment - CMV Conventional mechanical ventilation (CMV) 1. Indication
    • CPAP>8cmH 2 O and FiO 2 >0.6,PaO 2 <50mmHg or S a O 2 <85%
    • PaCO 2 >60mmHg and PH<7.25
    • Frequent apnea
    • Pulmonary air leak (PAL)
    • Chronic lung disease (CLD=BPD)
    • Retinopathy of prematurity (ROP)
    • Ventilator-associated pneumonia (VAP)
    2. Complications of CMV
  • 27. Conventional mechanical ventilation
  • 28. Pulmonary air leak
  • 29. PS replacement therapy PS
  • 30. PS replacement therapy 1.Clinical effect 2.natural PS: Survanta synthetic PS: Exosurf 3.method: via endotracheal tube within 2h of life dosing: 2-4 doses
    •  RDS mortality
    •  pneumothorax
    •  lung compliance and gas exchange
  • 31. PS treated RDS
  • 32. Prevention
    • Prevention of prematurity
    • Antenatal corticosteroid therapy
    • Dexamethasone or betamethasone
    •  RDS mobidity and mortality
    • PS prophylatic therapy
  • 33.
  • 34. Hypoxic Ischemic Encephalopathy (HIE)
  • 35.
    • Definition
    • Perinatal asphyxia
    • hypoxic-ischemic brain injury
    • significant mortality and long-term morbidity
    • permanent neurologic impairment
    • (mental retardation, epilepsy and cerebral palsy)
  • 36. Etiology
    • Hypoxic factors--- perinatal asphyxia, severe respiratory disease
    • Ischemic factors---severe heart failure,severe bradycardia
  • 37. Pathological changes
    • Diffuse cerebral edema, necrosis and hemorrhage
    • Term infants: necrosis of cerebral cortex,basal ganglia,thalamic nuclei
    • Preterm infants:
    • Periventricular hemorrhage (PVH)
    • Intraventricular hemorrhage (IVH)
    • Periventricular leukomalacia ( PVL, 脑室周围白质软化 )
  • 38. Lesions of HIE
  • 39. Pathogenesis Alteration of cerebral blood flow
  • 40. Pathogenesis
    • 2. Alteration of metabolism of brain tissue
    • Hypoxia  anaerobic glycolysis↑  Na–K-ATPase pump insufficiency  cerebral edema
    • Free radical formation
    • Calcium influx
    • Toxic effect of excitatory amino acids
    • Neuronal apoptosis and necrosis
  • 41. Clinical manifestation
    • Altered level of consciousness
    • Irritability– somnolence (嗜睡〕 -- lethargy (昏睡〕 -- coma
    • Muscle tone--- hypotonic or flaccid (肌力松软〕
    • Primary reflex--- diminish or disappear
    • Seizures
    • Increased intracranial pressure
  • 42. Clinical manifestation
  • 43. Diagnosis
    • History: perinatal asphyxia
    • Profound metabolic or mixed acidemia (pH <7) in an umbilical artery blood sample
    • Persistence of an Apgar score of 0-3 for longer than 5 minutes
    • Clinical manifestation
    • Neonatal neurologic sequelae (eg, seizures, coma, hypotonia)
  • 44. Diagnosis
    • Laboratory examination
    • Cranial ultrasound
    • CT scanning (decrease of tissue attenuation)
    • MRI
    • EEG abnormalities
    • Biochemical markers (serum CK-BB and plasma NSE  )
  • 45. CT scanning of HIE
  • 46. Treatment-I
    • Supportive care
    • Maintain adequate ventilation PaO 2 50-70mmHg PaCO 2 <40mmHg
    • maintain adequate tissue perfusion (normal HR,BP)
    • correction of electrolyte and acid-base disorder
    • correction of hypoglycemia
    • correction of hypotension Dopamine and Dobutamine
    • fluid therapy 60-80ml/kg/d
  • 47. Treatment-II
    • 2.Control seizures
    • Sodium luminal (first choice)
    • loading dose 15-20mg/kg IV
    • maintenance dose 3-5mg/kg/d
    • Diazepam (安定〕
    • Chloral hydrate
  • 48. Treatment-III
    • 3.Treatment of cerebral edema
    • Frusemide (first choice)
    • Albumin
    • Mannitol
  • 49. Intracranial hemorrhage of the newborn
  • 50.
    • remains a significant cause of both morbidity and mortality in infants born prematurely.
    • Sequelae include life-long neurological deficits, such as cerebral palsy, developmental delay, and seizures.
    • PVH-IVH remains a serious problem for preterm infant
    Intracranial hemorrhage of the newborn
  • 51. Etiology and pathogenesis
    • Vascular factor
    • < 32wk premature infant
    • immature blood vessels in germinal matrix
    • (subependymal region)
    • perinatal hypoxia and blood pressure fluctuations
    • subependymal hemorrhage(SEH)
    • periventricular – intraventricular hemorrhage
    • (PVH-IVH)
  • 52. Where is germinal matrix ?
  • 53. Etiology and pathogenesis
    • 2.Pressure factor
    • Hypoxia, acidosis, wide fluctuation of cerebral blood flow velocity
    • impairment of vascular auto-regulation
      • “ pressure passive circulatory state”
    • capillary injury
  • 54. Etiology and pathogenesis 3. Birth trauma Laceration of tentorium cerebelli,falx cerebri and cerebral superficial vein  Rupture of cerebral vein  Subdural hemorrhage(SDH)
  • 55. Subdural hemorrhage ( SDH)
  • 56. Etiology and pathogenesis
    • 4. Other factors
    • Vit k deficiency, coagulopathy
    • Maternal ITP
    • Maternal medication (phenytoin, phenobarbital, rifampicin)
    • Infusion of hyperosmotic solution
  • 57. Clinical manifestation-I
    • Non-specific features
    • Hypothermia
    • Anemia
    • Jaundice
    • Frequent apnea,
    • Hypovolemia shock
  • 58. Clinical manifestation-II
    • Neurologic dysfunction
    • Increased intracranial pressure
    • bulging anterior fontanel, BP  ,seizures,
    • opisthotonus( 角弓反张 ),high pitched shrill cry
    • Abnormal respiration
    • Altered level of consciousness
    • irritability, somnolence( 嗜睡 ) , lethargy( 昏睡 ) , coma
  • 59. Clinical manifestation-III
    • Neurologic dysfunction
    • Abnormal eye signs
    • gaze, limitation of upward gaze, nystagmus (眼球震颤〕
    • Pupil : dilated and poorly reactive pupil
    • Primary reflex (rooting, sucking, grasp, Moro) diminish or disappear
    • Muscle tone
  • 60. Periventricular- Intraventricular Hemorrhage
    • Grading based on cranial ultrasound or CT scan
    • Grade I: GMH (confined to GM- subependymal region)
    • Grade II: Intraventricular hemorrhage( IVH)
    • Grade III: Grade II + dilated ventricles
    • Grade IV: Grade III + intraparenchymal hemorrhage
  • 61. Periventricular- Intraventricular Hemorrhage CT ultrasound PVH IVH PVH-IVH
  • 62. Primary Subarachnoid Hemorrhage(SAH)
    • Associated with birth trauma
    • Post hemorrhage hydrocephalus (communicating or obstructive hydrocephalus)
  • 63. Intraparenchymal Hemorrhagel (IPH) hemorrhage  liquefied  cyst formation  porencephalic cysts ( 脑穿通性囊肿 )
  • 64. Treatment-I
    • Supportive care
    • minimal handling
    • fluid therapy
    • maintain blood pressure ,temperature
    • Hemostasis
    • fresh frozen plasma (FFP),
    • Vit k 1, ethamsylate, reptilase
  • 65. Treatment-II
    • Control seizures
    • sodium luminal
    • Diazepam
    • Decrease of intracranial pressure
    • frusemide
    • low dose mannitol
  • 66. Treatment-III
    • Management of hydrocephalus
    • Pharmacologic: acetazolamide
    • serial lumbar punctures
    • permanent ventricular –peritoneal shunt
  • 67. Prevention
    • Avoidance of premature birth
    • Prevention of perinatal asphyxia
    • Avoidence of wide fluctuation of BP
    • Prophylatic therapy
    • Antenatal steroid
  • 68. Questions?
  • 69. Thank You!

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