Published online June 1, 2005
PEDIATRICS
Vol. 115
No. 6
June 2005, pp.
1765-1767
(doi:10.1542/peds.2005-0665)
Mechanical Ventilation and Cerebral Palsy
Hany Aly, MD
Department of Neonatology
George Washington University and Children’s National Medical Center
Washington, DC 20037
Abbreviations: CP, cerebral palsy • NDD, neurodevelopmental delay • ELBW, extremely low birth weight • MV, mechanical ventilation • ENCPAP, early nasal continuous positive airway pressure
The article by Laptook et al1 in the March 2005 issue of Pediatrics offered an interesting analysis of varying risk factors related to the development of cerebral palsy (CP) and neurodevelopmental delay (NDD) in extremely low birth weight (ELBW) infants. Despite having normal head ultrasound results, the incidence of CP and NDD in ELBW infants was almost 30%. Factors associated with CP/NDD were male gender, multiple births, decreasing birth weight, and increasing duration of conventional mechanical ventilation (MV). The relation of MV duration and CP retained its significance after controlling for other possible confounders in a multiple-regression model. For example, in a group of ELBW infants with the same gestational age, birth weight, gender, race, prenatal history, socioeconomic status, insurance type, use of surfactant and postnatal steroids, and incidence of pneumothorax, necrotizing enterocolitis, and late-onset sepsis, an infant would have a 20% higher chance of developing CP/NDD if he or she were maintained an additional 10 days on MV. The impact of birth weight on outcomes (for the sake of comparison) was not dissimilar. For each 100-g decrease in birth weight, the odds of an ELBW infant developing CP increased by 30%.1
Several reasons validate the association of MV and CP. MV produces positive intrathoracic pressure that can impede venous return and thus decreases cardiac preload. Subsequently, cardiac output can be compromised and cerebral blood flow fluctuates.2 In addition, exchange of carbon dioxide (CO2) in MV-supported infants is typically manipulated by the managing team using predetermined parameters. The impact of overriding an infant’s ability to control arterial pressure of CO2 (PaCO2) on cerebral blood flow in mechanically ventilated infants has not been studied. Furthermore, the association of mechanical ventilation and lung inflammation is well established.3 Such inflammation may trigger a systemic response that can injure the brain or other organs.4 Another reason for the compromised brain development in ELBW infants supported by MV could be the exposure to sedatives that are often used in these infants. Morphine, when administered to pregnant rats, aborted the dendritic arborization and axonal branching in the fetal brain with an overall decrease in neuronal density of the cortex in offspring. Benzodiazepines are not any safer.5 An inverse relationship was established recently between the intensity of care provided to ELBW infants and their outcomes.6 Premature infants of similar severity of illness, birth weight, gender, and race reportedly had higher incidences of mortality and neurologic morbidities when provided with higher neonatal therapeutic intensity. Premature infants managed with MV suffer from frequent sleep interruption, pain, and discomfort during routine procedures such as tracheal suctioning, heel sticks, and blood draws.7 In addition, current ventilator alarms significantly exceed the recommended noise level in the NICU and can be a potential hazard to the developing brain.8 Other developmental risks related to MV in premature infants include their loss of self-regulatory behaviors to control stress, the delay in oral readiness for feeds while being orally intubated, and maternal deprivation caused by physical limitation. Conversely, shorter duration of MV, less use of opiates, and possibly earlier discharge from hospital were reported when a strategy of individualized, developmentally oriented care was provided to premature infants.9
Therefore, how can we translate these data on the developing neonatal brain into practical steps? One step would be to consider conducting a clinical trial to test the effect of postnatal steroids on the brain of premature infants with and without the presence of chronic lung diseases. Despite its known association with CP, postnatal steroids can decrease ventilator days and chronic lung diseases that can subsequently ameliorate the risk for CP/NDD.10 However, brain development remains suboptimal with or without steroids. In other words, such a prospective trial will determine which is the lesser of 2 evils on the premature brain: steroids or ventilators. A less invasive and less expensive approach would be to examine the need for intubation and MV in the first place. Early nasal continuous positive airway pressure (ENCPAP) was demonstrated recently as a feasible strategy for respiratory support in ELBW infants. Lower incidences of chronic lung diseases were reported from neonatal units adopting ENCPAP strategies.11,12 It may be that a change in the concept of management will lead to a significant decrease in the number of intubation procedures and that an even-more aggressive approach to earlier extubation will shorten the duration of MV. Randomized, controlled trials to compare neurodevelopmental outcomes of premature infants supported with ENCPAP to those supported with MV are urgently needed, especially because evidence that directly or indirectly links MV with brain compromise is growing. In the absence of such a trial, ventilator days should be kept to a minimum.
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ACKNOWLEDGMENTS
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I thank Dr Penny Glass, director of the Child Development Clinic (Children’s National Medical Center, Washington, DC), for reviewing this commentary.
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FOOTNOTES
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Accepted Mar 22, 2005.
Reprint requests to (H.A.) Department of Neonatology, George Washington University Hospital, 900 23rd St NW, Suite G-2092, Washington, DC 20037. E-mail: haly{at}mfa.gwu.edu
No conflict of interest declared.
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PEDIATRICS (ISSN 1098-4275). ©2005 by the American Academy of Pediatrics
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