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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 Suction: lungs Intubation CPR: – Epinephrine: ETT Establish IV access – IV (intravenous) – UVC (umbilical venous catheter) – UAC (umbilical arterial catheter). 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. RDS Surfactant 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 RDS Surfactant 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. 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 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. 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 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 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 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 Neonatal Sepsis Congenital vs Nosocomial Congenital source: – Vaginal flora – transplacental (viral infections) Nosocomial ( > 7 days) – Environment – Instrumentation Neonatal Risk Factors Low birth weight /preterm Instrumentation: – IV lines, intubation changes Immune defense Skin integrity Maternal Risk Factors Prolonged rupture of membranes >24hr Intrapartum fever Peripartum infection: – Chorioamnionitis, UTI Group B Strep positive (carrier) Neonatal Sepsis Signs: non-specific – lethargy, temperature instability – poor feeding, poor colour and tone – apneas, increased ventilation requirements, increased blood glucose. 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 Neonatal Sepsis WBC (8-34 x109/Litre) – trends – relative increase Differential: left shift= immature neutrophils > 0.20(20%) total neutrophils immature neutr: bands, metamyelocytes, 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. 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 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 Patent Ductus Arteriosus 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-toright shunt. 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 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 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 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 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. 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 Questions?