55274777 respiratory-distress-in-newborn

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55274777 respiratory-distress-in-newborn

  1. 1. RESPIRATORY DISTRESS SYNDROME PRESENTER:JOY W. KAMAUFACILITATOR:DR. SONGOK
  2. 2. OUTLINE•Distinguish between respiratory distress andRDS•Definition of RDS•Incidence and risk factors•Pathogenesis•presentation•Diagnosis•Treatment•Complications•Prognosis
  3. 3. Respiratory distress is a symptom complex arisingfrom disease processes that cause failure tomaintain adequate gaseous exchange•Tachypnea (>60bpm)•Grunting, Flaring, Retractions/ recessions (GFR)•Cynosis•Reduced air entry
  4. 4. CAUSES OF RESPIRATORY DISTRESS Obstruction of the airway Lung parenchymal disease1- Choanal atresia 1- Meconium aspiration2- Congenital stridor 2- Respiratory distress syndrome3- Tracheal or bronchial stenosis 3- Pneumonia 4- Transient tachypnea of the newborn (retained lung fluid) 5- Pneumothorax 6- Atelectasis 7- Congenital lobar emphysema Non-pulmonary causes Miscellaneous1- Heart failure 1- Disorders of the diaphragm e.g.2- Intracranial lesions (diaphragmatic hernia)3- Metabolic acidosis 2- Pulmonary haemorrhage 3- Pulmonary hypoplasia
  5. 5. DOWNE’s SCORING OF RESPIRATORY DISTRESS 0 1 2 Cyanosis None In room air In 40% FIO2 Retractions None Mild Severe Audible with Audible without Grunting None stethoscope stethoscope Air entry Clear Decreased or delayed Barely audible Respiratory Under 60 60-80 Over 80 or apnea rateScore:> 4 = Clinical respiratory distress; monitor arterial blood gases> 8 = Impending respiratory failure
  6. 6. •(RDS) is a condition of increasing respiratorydistress, commencing at, or shortly after, birth andincreasing in severity until progressive resolutionoccurs among the survivors, usually around 2nd to7th day•Maybe primary or secondary•Incidence and severity is inversely proportional togestational age •<28wks- 60-80% •28-32wks- 25-50% •32-36wks- 15-30% •>37 wks- 5% •rare at term
  7. 7. RISK FACTORS•Neonates younger than 33-38 weeks•Weight less than 2500g•Maternal diabetes•Cesarean delivery without preceding labor•Precipitous labor•Fetal asphyxia•Second of twins•Cold stress•Previous history of RDS in sibling•Males•whites
  8. 8. DECREASED RISK•Use of antenatal steroids•Pregnancy-induced or chronic maternalhypertension•Prolonged rupture of membranes•Maternal narcotic addiction•Chronic intrauterine stress•IUGR or SGA•Thyroid hormones•Tocolytic agents
  9. 9. ETIOLOGY AND PATHOPHYSIOLOGY.• Surfactant deficiency is the 1O cause of RDS.• Low levels of surfactant cause high surface tension• High surface tension makes it hard to expand the alveoli.• Tendency of affected lungs to become atelectatic at end-expiration when alveolar pressures are too low to maintain alveoli in expansion• Leads to failure to attain an adequate lung inflation and therefore reduced gaseous exchange
  10. 10. PATHOPHYSIOLOGYPulmonary Surfactant decreases surfacetension
  11. 11. Structure of lung surfactantmajor constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin),phosphatidylglycerol, apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol
  12. 12. • With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells .• Wk 20: start of surfactant production and storage. Does not reach lung surface until later• Wk 28-32: maximal production of surfactant and appears in amniotic fluid• Wk 34-35; mature levels of surfactant in lungs• The amounts produced or released may be insufficient to meet postnatal demands because of immaturity.• Surfactant inactivating states eg maternal DM may lead to surfactant of lower quality/ immature
  13. 13. • Rare genetic disorders may cause fatal respiratory distress syndrome eg.• Abnormalities in surfactant protein B and C genes• gene responsible for transporting surfactant across membranes (ABC transporter 3 [ABCA3]) are associated with severe and often lethal familial respiratory disease
  14. 14. Prematurity, BA, hypoxemia, hypotension, iatrogenic lung injury, cold stress Low surfactant, high ST Hyaline Proteinaceous Small alveolarDifficulty membrane outflow & unitsexpanding edemaalveoli withincreasedrecoil atelectasis Decreased lung compliance
  15. 15. atelectasis Decreased lung Chest wall: compliance •Hyper- compliant •Indrawing •Low resistance toV-Q mismatch lung recoil Greater work of breathingPulmonaryvasoconstriction ExhaustionHigh P.V. resistance apnoea Right- left shunt More hypoxia, worsening lung injury Hypercapnia, acidosis
  16. 16. pathologyInflammation so accumulation of neutrophils in the lungAtelectasis and hyaline membraneDecrease fluid absorption and lung edema; liver-like lungHemorraghe & interstitial emhysema esp if ventilated
  17. 17. CLINICAL COURSE• Signs of RDS in minutes to hours after birth• Tachypnea, prominent (often audible) Grunting, Flaring, Retractions, (GFR) and Cyanosis relatively unresponsive to oxygen• Breath sounds normal or harsh bronchial• Crepitations esp over posterior lung bases• Natural course is worsening cyanosis and dyspnea
  18. 18. • If inadequately treated, hypotension, fatigue, cyanosis, and pallor increase• grunting decreases or disappears as the condition worsens• Apnea as infants tire: OMINOUS needs immediate intervention• mixed respiratory-metabolic acidosis, edema, ileus, and oliguria (end-organ damage and complications)
  19. 19. • Respiratory failure may occur• Usually illness peaks in 3 days, then gradual improvement• Improvement is often heralded by spontaneous diuresis and the ability to oxygenate the infant at lower inspired oxygen levels or lower ventilator pressures• Death may occur esp from day2-3
  20. 20. MORTALITY• Death is rare on the 1st day,• usually occurs between days 2 and 7• causes are: – alveolar air leaks (interstitial emphysema, pneumothorax), – pulmonary hemorrhage – Intracranial hemorrhage• Late mortality from bronchopulmonary dysplasia
  21. 21. Is a Clinical diagnosis: respiratory distress occurring soon after birth.Pay attention to risk factors! Pulse Oximetry: aim for SPO2 >85%.ROUTINE!Full blood count and Cultures to check for sepsis: rem culture onlypositive 40-50% of the time!! gastic aspirates/ buffy smears for GBSChest radiograph: air bronchogram, reticular/ ground-glass appearanceafter 6-12 hrs to full opacity later on.Blood gases: hypoxia, hypercapnia, acidosis. Signs of RESP FAILUREdetermine mgmt eg CPAP vs ventilation etc Electrolytes, glucose, renal and liver function Echocardiogram: diagnosing PDA, determine the direction and degreeof shunting, making the diagnosis of pulmonary hypertension andexcluding structural cyanotic heart disease
  22. 22. Treatment of RDS Supportive mgmt:Oxygen at the minimum FiO2 to maintain arterial O2 at 60-80mmhg equivalent to 85-95% SPO2.Thermoregulation: baby in humidified (60-80%)incubator. Aimfor core temp of 36.50 CIVF (10% dextrose; avoid fluid overload so dont go above140ml/kg!)Adequate caloric intakeBroad spectrum antibiotics in all infants with RDS after takingsamples for septic screen (Xpen-Genta)Correct electrolyte imbalancesPrevent and correct anemiaMay need NaHCo3 in severe acidosis (3-5mEq but based on pHie the lower the ph, the higher the dose)Vitamin A 5,000 IU 3times/ wk for 4wks; reduces BPD Endotracheal Surfactant (100mg/kg)
  23. 23. Surfactant Laboratory Container Concentration Recommended doseCurosurf Farmalab-Chiesi 1.5 & 3 ml 80 mg/ml 100 to 200 mg/kgPorcineSurvanta Abbott 4ml & 8 ml 25 mg/ml 100 mg/kgBovineAlveofact Boeringer 1.2 ml 40 mg/ml 100 mg/kgBovineExosurf Wellcome 13.5 mg/ml(DPPC) 5 ml/kgSyntheticProphylaxis of infants >1350g but with pulmonary immaturityPropylaxis of infants <1350g at risk of RDSRescue therapy of infants with RDS
  24. 24. PREVENTION OF RDSAvoid neonatal hypothermiaGood control of maternal Diabetes mellitus in pregnancyActive mgmt of labour to avoid birth asphyxiaPrenatal corticosteroids 48hrs before deliveryAvoid unnecessary CS/ inductionSingle dose surfactant to at risk, premature infants at birthPrenatal assessment of fetal lung maturity Lecithin –sphingomyelin ratio <1.5 prior to delivery suggests prematurity. If >2.0, has PPV of 95-100% Absence of phospatidylglycerol means immaturity: if present, has PPV of 96-100% Surfactant albumin ratio >0.47 has PPV of 95% Lamellar body counts >30-40000 has PPV of 97%
  25. 25. COMLICATIONSacute chronicApnea ROP PPH &Air leak BPD infection Neurodevep. impairment ICHPDA & foramen ovaleEnd-organ hypoxic injury
  26. 26. Transient Tachypnea of the NewbornResults from slow absorption oflung fluidTerm born by LSCS/IDM /maternalasthmaMild respiratory distressPeaks at about 36 hours of lifeResolve spontaneously
  27. 27. NEONATAL PNEUMONIAPneumonia & Sepsis have various manifestationsincluding typical signs of distress as well astemperature instabilityCommon pathogen- Group B Streptococcus,Staph aureus, Streptococcus aureus,Streptococcus Pneumoniae,Gm neg rodsRisk factors- prolonged rupture of membranes,prematurity,& maternal feverCXR- bilateral infiltrates suggesting in uteroinfection.
  28. 28. MECONIUM ASPIRATION SYNDROME Incidence- 1.5- 2 % in term or post term infants. Meconium is locally irritative, obstructive & medium for for bacterial culture Meconium aspiration causes significant respiratory distress. Hypoxia occurs because aspiration occurs in utero. CXR- Patchy atelectasis or consolidation.
  29. 29. Apnea of prematurity> 50% of infants <1500g requireintervention for apneaTreatments• Stimulation• CPAP• Intubation• Medication: Caffeine Methylxanthines Theophylline Doxapram• Oxygen
  30. 30. pneumothoraxSpontaneous -1-2%MAS ,hypoplasticlung,aggressiveresuscitation,CPAP,ventilationTension pneumothorax-immidiate drainage
  31. 31. Prognosis• Bad prognosis

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