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The Preterm Neonate Phm 456 Michael Heffer BSc.Phm.MHSc.

The Preterm Neonate Phm 456 Michael Heffer BSc.Phm.MHSc. What does it mean to be preterm?. Gestational age: age in weeks dated from the first day of the mother’s last menstrual period. Full term: 37-42 weeks Preterm: <37weeks Viability: 23-24 weeks (400-500g). Resuscitation.

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The Preterm Neonate Phm 456 Michael Heffer BSc.Phm.MHSc.

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  1. The Preterm NeonatePhm 456 Michael Heffer BSc.Phm.MHSc.

  2. What does it mean to be preterm? • Gestational age: • age in weeks dated from the first day of the mother’s last menstrual period. • Full term: 37-42 weeks • Preterm: <37weeks • Viability: 23-24 weeks (400-500g)

  3. Resuscitation • Suction: lungs • Intubation • CPR: • Epinephrine: ETT • Establish IV access • IV (intravenous) • UVC (umbilical venous catheter) • UAC (umbilical arterial catheter).

  4. Respiratory Distress Syndrome (RDS) • Primary cause: surfactant deficiency • Clinical picture: • atelectasis (deflated balloons) hypoxemia, poor lung compliance, alveolar epithelial damage, pulmonary edema. • Progresses to fibrous membranes and development of chronic lung disease. • Requires high ventilation support: risk of broncho-pulmonary dysplasia.

  5. RDSSurfactant production • Endogenous cortisol stimulates synthesis at 30-32 weeks in-utero. • Normal lung function (34-36wks) • Clinical test: amniocentesis • Lamellar Body Count: LBC • surfactant containing particles in amniotic fluid • reflection of lung maturity

  6. RDSSurfactant production • Surfactant: • synthesized in Type II cells in alveolus. • composed of 80-90% lipid DPPC (dipalmitoyl phosphatidylcholine) • 10-20% Proteins (spreading action) • lowers surface tension in alveolus • -stability on expiration.

  7. RDS Prevention and Treatment • Risk of preterm delivery? • Betamethasone 6mg x2 dose q24h • stimulates surfactant production in the fetus • significant reduction in incidence of RDS • Multiple courses? • MACS study

  8. RDS Prevention and Treatment • Exogenous surfactant replacement: • Synthetic: • Exosurf: contains DPPC and spreading agents. No proteins. • Natural source: • Survanta: minced bovine lung product contains proteins. • BLES: bovine lung exogenous lipid extract- Investigational Lung lavage. Contains proteins.

  9. Apnea of Prematurity • Apnea • cessation of breathing for 15-20 seconds. • complicated by cyanosis, pallor, hypotonia , bradycardia • Nursing scale • severity grade 1-4 depending on bradycardia and oxygen required. • amount of stimulation required gentle (G) vs vigorous (V) ie. 3G apnea

  10. Apnea of Prematurity • Primary cause: immature systems: • decreased sensitivity of chemoreceptors to CO2. • diaphragm muscle fatigue • Secondary causes: (Rule out) • infection • low hemoglobin • medications (morphine) • ventilator related: blocked tube/positioning of infant

  11. Apnea of Prematurity: Treatment • Methylxanthines: Caffeine / Theophylline • Doxapram infusion(off market-Mar 2001) • Mechanism: • increased sensitivity of medullary respiratory centre to CO2 • stimulates central respiratory drive • increases diaphragmatic contractility

  12. Apnea of Prematurity: Treatment • Caffeine: • longer 1/2 life: 65-100hrs • once daily dosing • Side Effects: • tachycardia, jitteriness • rarely seen • caffeine levels if symptomatic (40-100 micromoles/L) • CAP study: long term effects

  13. Neonatal Sepsis • Congenital vs Nosocomial • Congenital source: • Vaginal flora • transplacental (viral infections) • Nosocomial ( > 7 days) • Environment • Instrumentation

  14. Neonatal Risk Factors • Low birth weight /preterm • Instrumentation: • IV lines, intubation changes • Immune defense • Skin integrity

  15. Maternal Risk Factors • Prolonged rupture of membranes >24hr • Intrapartum fever • Peripartum infection: • Chorioamnionitis, UTI • Group B Strep positive (carrier)

  16. Neonatal Sepsis • Signs: non-specific • lethargy, temperature instability • poor feeding, poor colour and tone • apneas, increased ventilation requirements, increased blood glucose.

  17. Neonatal Sepsis • Full Septic work up • Cultures: blood, urine, ETT, swab, LP • WBC (white blood cell count) and differential • Cultures: • Gram stain • bacteria: 48hours • ureaplasma: 4-5 days

  18. Neonatal Sepsis • WBC (8-34 x109/Litre) • trends • relative increase • Differential: left shift= immature neutrophils > 0.20(20%) total neutrophils immature neutr: bands, metamyelocytes,

  19. Neonatal Sepsis • Treatment: always mg/kg • Congenital infection: • Prophylaxis: gram +ve and -ve coverage. • Ampicillin plus aminoglycoside • Nosocomial infection: • Prophylaxis: Cloxacillin and aminoglyc. • Methicillin (Beta lactamase) resistant? Switch to vancomycin and aminoglyc.

  20. Neonatal Sepsis • Pharmacist follow up: DRP’s • Gram stain,cultures, sensitivities: • Coagulase negative staph. Staph. epidermidis: contaminant? • LP positive? 3 weeks treatment • consider better penetration: Cefotaxime • Therapeutic drug monitoring: • gentamicin, vancomycin

  21. Patent Ductus Arteriosus (PDA) • Ductus arteriosus (DA) connects the pulmonary artery and the descending aorta • In utero: • Output of the right ventricle bypasses the unexpanded lungs by way of the DA and subsequently travels to the placenta for oxygenation • Patency of the DA in utero: • Maintained through high levels of circulating prostaglandins

  22. Patent Ductus Arteriosus

  23. Pathophysiology • At birth changes occur in the neonate’s circulation • umbilical cord is clamped resulting in an increase in systemic vascular resistance • lungs expand and pulmonary vascular resistance drops • results in switch from right-to-left shunting across the PDA during fetal life to a left-to-right shunt.

  24. Risk with untreated PDA • Increased pulmonary blood volume • reduced lung compliance • pulmonary hemorrhage • chronic lung disease • Reduced systemic circulation • hypotension/ poor systemic perfusion • gut: Necrotizing enterocolitis • kidneys: renal failure • cerebral ishemia: Intra ventricular hemorrhage

  25. Clinical Presentation • Increased heart rate/tachycardia • widened pulse pressure • bounding pulses • hyperactive precordium • continuous murmur • Echocardiographic diagnosis • diastolic turbulence on Doppler in the pulmonary artery

  26. Risk Factors for PDA • Premature infants with: • Respiratory Distress Syndrome (RDS) • Hypoxia • Acidosis • Fluid Overload • incidence of PDA inversely related to the gestational age • spontaneous closure occurs more frequently in larger and healthier babies than smaller and sicker babies

  27. PDA Treatment • Supportive Measures: • fluid restriction (80% of TFI requirements) • diuretics to control pulmonary edema if fluid restriction isn’t adequate • correction of anemia with transfusions • treatment of hypoxia and acidosis

  28. PDA treatment: Indomethacin • Short course: • most commonly used • 0.2mg/kg Q12H x 3 doses • >20% reopening rates:repeat courses • Long course: • 0.1mg/kg Q24H x 5-7 doses • Best approach not yet determined.

  29. Indomethacin: Side Effects •  Renal Function (urine output, creatinine, urea) • decreased renal blood flow • Necrotizing Enterocolitis (NEC) • decreased mesenteric blood flow • Hyponatremia • water retention •  platelet aggregation • COX inhibition •  bilirubin levels • displacement from binding site

  30. Questions?

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