Link To And Resources From “Neuroprotection from acute brain injury in preterm infants- CPS podcast” With Additional Resources On Volume Targeted Ventilation

This post contains links to and resources from Neuroprotection from acute brain injury in preterm infants- CPS podcast [Link to podcast] [Link to transcript]. By Larissa.Shapka Jun 23, 2019 from PedsCases.

Here are links to the position statement Neuroprotection from acute brain injury in preterm infants [PubMed Abstract] [Full Text HTML]
Posted: Jun 21 2019 from the Canadian Paediatric Society.

Here are excerpts from the podcast:

Background and pathophysiology:

In Canada, approximately 21% of infants born at or before 32+6 weeks gestational age will have findings consistent with parenchymal lesions or intraventricular hemorrhage on brain ultrasound. These injuries can occur due to ischemia and reperfusion which causes infarction and/or hemorrhage.

Why is it that these preterm infants have such a high
incidence of acute brain injury? Extremely preterm infants have delicate cerebral vessels and immature autoregulatory systems, which means that fluctuations in blood flow can lead to ischemia and hemorrhage.

Two of the most common forms of acquired brain injuries in preterm infants are germinal matrix hemorrhage- intraventricular hemorrhage, more commonly referred to simply as intraventricular hemorrhage (IVH) and periventricular leukomalacia (PVL).

In preterm infants, intraventricular hemorrhages usually arise from the germinal matrix located next to the lateral ventricles. There is wide variation in the clinical presentation of IVH, and some infants can initially appear asymptomatic. Diagnosis is made based on imaging findings,and IVH are classified into 4 grades of severity based on the extent of bleeding, ventricular dilation, and involvement of brain parenchyma.

The other common preterm brain injury is periventricular leukomalacia (PVL), which refers to necrosis of white matter in a characteristic distribution on neuroimaging. The etiology is often ischemia, however PVL may also arise from infection or cytokine exposure. PVL can be classified into cystic and non-cystic forms.

Depending on severity, both IVH and PVL are associated with poor motor
and cognitive outcomes, seizures, and visual disturbances. Specifically, they can both cause cerebral palsy in surviving preterm infants.

The first 72 hours after birth are considered the highest risk time for brain injury to occur. Known as the “critical window,” this is a time period in which neuroprotective interventions can change outcomes. We will review strategies that can be used in this critical window, as
well as those applicable to antenatal, perinatal, and postnatal periods as a whole.

The podcast then goes on to review the various strategies in detail. Perhaps the most important strategy is to have the premature infant delivered at a tertiary care center. 

Location of delivery:

Studies have demonstrated an increased rate of acute brain injury in preterm infants born outside of tertiary care facilities.  .  .  . The CPS advises that when possible, mothers at risk of preterm delivery should be
transferred to a tertiary care facility. If this is felt to be unsafe, then a tertiary care team should be consulted to discuss the administration of maternal corticosteroids and magnesium sulphate.


Volume targeted ventilation* should be the first mode of ventilation for preterm infants within 72 hours of delivery. It has been associated with lower chance of intraventricular hemorrhage compared to pressure-limited ventilation, and lower risk of intraventricular hemorrhage than early high-frequency oscillatory ventilation.

Please see the following resources on volume targeted ventilation

Ventilation (continued):

PaCO2 should be closely monitored in the first 72 hours of life in infants born at or less than 32+6 weeks gestational age. Target PaCO2 should be between 45 mmHg and 55mmHg, to a maximum of 60mmHg. There is increased risk of periventricular leukomalacia when PaCO2 is below 35mmHg, and of intraventricular hemorrhage when PaCO2 is above 60mmHg. The adverse effects of hypercapnea appear to be dose dependent in extremely low birth weight infants. Attention should be paid to metabolic acidosis along with hypercapnia.


  1. Infants born ≤ 32+6 weeks gestation are at increased risk of acute brain injury due to fragile blood vessels and immature autoregulatory systems. Injury can be parenchymal or intraventricular due to ischemia/reperfusion.
  2. The first 72 hours after birth are the highest risk time for brain injury to occur.
  3. Neuroprotection strategies in the antenatal period include administering maternal corticosteroids for delivery expected ≤ 34+6 weeks gestational age, magnesium sulphate for imminent delivery ≤ 33+6 weeks, and antibiotics for preterm premature rupture of membranes and expected delivery ≤ 32+6 weeks.
  4. Perinatal factors with neuroprotective benefit include delivery at a tertiary care centre when safe, delayed cord clamping, and prevention of hypothermia.
  5. Postnatal strategies should include empiric antibiotic treatment for risk of early onset sepsis, cautious use of inotropes for hypotension, and targeted use of prophylactic indomethacin. If ventilatory support is being provided, volume targeted ventilation is the mode of choice. It is also important to ensure neutral head position and provide developmentally appropriate care.
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