neonates Flashcards
Indication for MgSO4 for neuroprotection
What is the dose ?
In woman at risk of imminent birth use MgSO4 for neuroprotection
Viable – 30 weeks
Planned or expected within 24 hours
Aim for MGSo4 within 4 hours as close as possible
IV 4 g loading dose over 20-30 minutes then 1g / hr via IV route – continue until birth or 24 hours
Regardless of pleurality, parity, MOD, steroids or not
What monitoring is needed on MgSO4
Monitoring
Loading
checking pulse, blood pressure, respiratory rate and patellar reflexes before loading dose, 10 minutes after loading dose infusion has started and at the end of the loading dose infusion (20-30 minutes).
The infusion should be stopped if respiratory rate decreases more than 4 breaths per minute below baseline, or is less than 12 breaths per minute; or diastolic blood pressure decreases more than 15 mm Hg below baseline level.
Maintenance
While the maintenance infusion is running, observe for any adverse effects.
The minimum assessments should include checking pulse, blood pressure, respiratory rate, patellar reflexes and urine output 4-hourly.
Stop infusion if respiratory rate is less than 12 breaths per minute; if patellar reflexes are absent, if hypotension occurs or if urine output is less than 100 mL over 4 hours.
Who to be concerned about for MgSO4 toxicitiy?
How to manage toxicity?
Magnesium toxicity is unlikely with the regimens recommended in these guidelines and serum magnesium concentrations do not need to be routinely measured (RCOG 2006). In women with renal compromise, serum magnesium monitoring is recommended. Calcium gluconate (1 g (10 mL of 10% solution) slowly via intravenous route over 10 minutes) can be given if there is clinical concern over respiratory depression
What is cerebral palsy?
What is the rate?
Cerebral palsy (CP) is a group of disorders characterised by motor and/or postural dysfunction of a non-progressive nature commonly associated with cognitive impairment 2:1000
Risks for CP
Risks
PTB (less then 34 weeks)
VLWB (less the 1500g)
Also chorioamnionitis, APH, complications of multiples, placental insufficiency and perinatal asphyxia
Neonatal risk factors (inversely associated with gestational age)
IVH
Periventricular leucomalacia
Proposed mechanism of action for MgSO4 in neuroprotection
Magnesium sulphate reduces neuronal injury by ‘down regulation’ of excitatory stimuli. Damaged neurons are sensitive to the excitatory neurotransmitter glutamate, but the blocking of N-methyl-D-aspartate (NMDA) receptors by magnesium prevents the influx of calcium that causes cell death.12
The vasoactive properties of magnesium may result in increased cerebral blood flow due to cerebral vasodilatation, thus minimising hypoxic-ischaemic damage.
In an inflammatory model of preterm birth inducing pro-inflammatory cytokines, magnesium sulphate has been shown to prevent neuronal injury.
Magnesium may have anti-apoptotic (programmed cell death) effects, thus directly reducing neuronal loss.
What is the evidence for MgSO4 for preventing CP
Cochrane review included 5 trials, 6145 babies,
RCT that MgSO4 used for neuroprotective intent and not
No increase in mortality
Decrease in absolute risk of cerebral palsy RR 0.68
Absolute risk 3.7 treated, 5.4 in Placebo group
31% risk reduction
NNT 29 in very preterm, 63 overall
Some trials went up to 34 weeks – resourcing decision and lack of solid data limits guidelines
Respiratory distress syndrome RDS
Pathophysiology
RDS is caused by deficiency of surfactant, the phospholipid mixture (predominantly desaturated palmitoyl phosphatidyl choline) that reduces alveolar surface tension, which decreases the pressure needed to keep the alveoli inflated, and maintains alveolar stability
Diffuse atelectasis leads to low compliance and low functional residual capacity. Hypoxemia results primarily from mismatching of ventilation and perfusion as blood bypasses atelectatic air spaces (intrapulmonary shunting). Right-to-left shunting that occurs through the ductus arteriosus and foramen ovale, because of increased pulmonary vascular resistance (PVR), also contributes to decreased oxygenation. Hypoxemia is often accompanied by respiratory and/or metabolic acidosis
Inflammatory response to epithelial injury leaking to oedema and increase further in airway resistance – this can trigger cytokines that further deactivate surfactant production exacerbating the problem further
Surfactant deficiency likely genetic / Pre term babies made less and not as good quality surfactant
How to manage RDS
Long term risks
Preterm Tx -
antenatal glucocorticoid therapy, early intubation for surfactant therapy, and/or administration of continuous positive air pressure (CPAP) or positive end-expiratory pressure (PEEP) in the delivery room to provide adequate lung volume
Risk bronchopulmonary dysplasia
What is Transient tachypnea of the newborn (TTN)
A failure of adequate lung fluid clearance at birth, resulting in excess lung liquid. The liquid fills the air spaces and moves into the extra-alveolar interstitium, where it pools in perivascular tissues and interlobar fissures until it is cleared by the lymphatic or vascular circulation. decreasing pulmonary compliance
Reduced activation of Na channels that clear lungs of excess fluid
Reduction of inflation
Who gets TTN
How to treat it ?
Usually between 34 and 37 weeks, often ElLSCS
Term and postterm babies are also at risk for TTN.
occurs within two hours after delivery
Lasts <24 hours (potentially <72)
What is Persistent pulmonary hypertension of the newborn (PPHN).
abnormal persistence of elevated PVR that leads to right-to-left shunting of deoxygenated blood through the foramen ovale and the ductus arteriosus, resulting in hypoxemia.
underdevelopment, maldevelopment, or maladaptation of the pulmonary vascular bed. PPHN is also often associated with nonacute conditions due to a structural abnormality (eg, congenital diaphragmatic hernia) or chronic in utero stress (eg, meconium aspiration syndrome). These concurrent findings suggest that a structural etiology (eg, increased musculature of pulmonary vessels), rather than simply a functional change in pulmonary vascular reactivity at birth, contributes to PPHN in many cases.
Who gets PPHN
How does it present
Usually occurs in term infants, (can be late preterm or postterm)
Present tachypnea and cyanosis. Differential pre- and postductal saturation is a common finding or systolic murmur of tricuspid insufficiency.
metabolic acidosis may be present due to lactic acidosis from poor perfusion or severe hypoxemia, in addition to the respiratory acidosis that accompanies respiratory failure.
What are the effects of corticosteroids?
Overall reduction in Neonatal death Cerebrovascular haemorrhage Necrotising enterocolitis Respiratory support ICU admissions Systemic infections within the first 48hrs of life
No increase in maternal death, puerperal sepsis or chorio-amnionitis.
Also effective in PROM and hypertension related syndromes.
No difference in SGA, birthweight, apgars, admission to NICU, length of neonatal hospitalisation
Hw to manage preterm RDS
Manage temperature Preterm infants are at risk of hypothermia Use radiant above warmers Avoid burns (less then 28 weeks put them in a bag) Ambient temp 26 degrees Warmed humidified air Exothermic mattresses Cover the head
Handling and skin protection
Respiratory support
CPAP
If spontaneous effort then for CPAP – preferred by ANZCOR over intubation and ventilation
Pressures of at least 5cm H20
Blended air (up to 30% oxygen) or room air and titrate
Use pulse ox
If HR below 60 then for CRP – IV access through umbilical line, adrenaline
