Transcript Neonatal TPN: Feel satiated in the process

The Preterm Neonate
Phm 456
Michael Heffer BSc.Phm.MHSc.
What does it mean to be
preterm?
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Gestational age:
– age in weeks dated from the first day of
the mother’s last menstrual period.
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Full term: 37-42 weeks
Preterm: <37weeks
Viability: 23-24 weeks (400-500g)
Resuscitation
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Suction: lungs
Intubation
CPR:
– Epinephrine: ETT
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Establish IV access
– IV (intravenous)
– UVC (umbilical venous catheter)
– UAC (umbilical arterial catheter).
Respiratory Distress Syndrome
(RDS)
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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
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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
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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
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Risk of preterm delivery?
– Betamethasone 6mg x2 dose q24h
– stimulates surfactant production in the
fetus
– significant reduction in incidence of RDS
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Multiple courses?
– MACS study
RDS Prevention and Treatment
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Exogenous surfactant replacement:
Synthetic:
– Exosurf: contains DPPC and spreading
agents. No proteins.
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Natural source:
– Survanta: minced bovine lung product
contains proteins.
– BLES: bovine lung exogenous lipid
extract- Investigational
Lung lavage. Contains proteins.
Apnea of Prematurity
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Apnea
– cessation of breathing for 15-20 seconds.
– complicated by cyanosis, pallor,
hypotonia , bradycardia
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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
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Primary cause: immature systems:
– decreased sensitivity of chemoreceptors
to CO2.
– diaphragm muscle fatigue
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Secondary causes: (Rule out)
– infection
– low hemoglobin
– medications (morphine)
– ventilator related: blocked
tube/positioning of infant
Apnea of Prematurity: Treatment
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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
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Caffeine:
– longer 1/2 life: 65-100hrs
– once daily dosing
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Side Effects:
– tachycardia, jitteriness
– rarely seen
– caffeine levels if symptomatic (40-100
micromoles/L)
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CAP study: long term effects
Neonatal Sepsis
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Congenital vs Nosocomial
Congenital source:
– Vaginal flora
– transplacental (viral infections)
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Nosocomial ( > 7 days)
– Environment
– Instrumentation
Neonatal Risk Factors
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Low birth weight /preterm
Instrumentation:
– IV lines, intubation changes
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Immune defense
Skin integrity
Maternal Risk Factors
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Prolonged rupture of membranes
>24hr
Intrapartum fever
Peripartum infection:
– Chorioamnionitis, UTI
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Group B Strep positive (carrier)
Neonatal Sepsis
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Signs: non-specific
– lethargy, temperature instability
– poor feeding, poor colour and tone
– apneas, increased ventilation
requirements, increased blood glucose.
Neonatal Sepsis
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Full Septic work up
– Cultures: blood, urine, ETT, swab, LP
– WBC (white blood cell count) and
differential
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Cultures:
– Gram stain
– bacteria: 48hours
– ureaplasma: 4-5 days
Neonatal Sepsis
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WBC (8-34 x109/Litre)
– trends
– relative increase
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Differential:
left shift= immature neutrophils > 0.20(20%)
total neutrophils
immature neutr: bands, metamyelocytes,
Neonatal Sepsis
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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
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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)
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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
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Patency of the DA in utero:
– Maintained through high levels of circulating
prostaglandins
Patent Ductus Arteriosus
Pathophysiology
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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
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Increased pulmonary blood volume
– reduced lung compliance
– pulmonary hemorrhage
– chronic lung disease
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Reduced systemic circulation
– hypotension/ poor systemic perfusion
– gut: Necrotizing enterocolitis
– kidneys: renal failure
– cerebral ishemia: Intra ventricular
hemorrhage
Clinical Presentation
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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
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Premature infants with:
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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
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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
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Short course:
– most commonly used
– 0.2mg/kg Q12H x 3 doses
– >20% reopening rates:repeat courses
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Long course:
– 0.1mg/kg Q24H x 5-7 doses
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Best approach not yet determined.
Indomethacin: Side Effects
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 Renal Function (urine output, creatinine,
urea)
– decreased renal blood flow
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Necrotizing Enterocolitis (NEC)
– decreased mesenteric blood flow
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Hyponatremia
– water retention
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 platelet aggregation
– COX inhibition
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 bilirubin levels
– displacement from binding site
Questions?