Neonatal and Infantile Apnea

  • Dorothy H. Kelly
  • Daniel C. Shannon

Abstract

Prolonged sleep apnea, defined as apnea greater than 20 sec or less than 20 sec if accompanied by bradycardia,1 has been described in premature infants for many years2–4 and more recently in young infants5–10 and in older children.11–20 Long—term effects attributed to this condition range from neurologic abnormalities to death. Banker and Larroche, in autopsy studies of preterm infants who had experienced repeated episodes of prolonged apnea and cyanosis, noted diffuse neuronal loss in the cerebral cortex, leukomalacia in periventricular watershed zones, and spasticity in two of three infants who survived for longer than 1 month after the cyanotic event. In autopsy studies of full—term infants whose hypoxic episode occurred between 2 and 52 weeks of age, they described subcortical leukomalacia. They theorized that the specific brain lesions in the two groups of infants occur because the affected regions are border zones and have a tenuous arterial blood supply from the anterior, middle, and posterior cerebral arteries.21 Lou recently documented that cerebral perfusion pressure in the premature infant is mainly dependent on systemic blood pressure and that auto—regulation of smooth muscle tone in vessels is not present.22 This observation strengthens the argument that these areas are extremely susceptible to hypoxic injury.

Keywords

Obstructive Sleep Apnea Sleep Apnea Continuous Positive Airway Pressure Premature Infant Patent Ductus Arteriosus 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Aubrey Milunsky, Emanuel A. Friedman, and Louis Gluck 1981

Authors and Affiliations

  • Dorothy H. Kelly
    • 1
    • 2
  • Daniel C. Shannon
    • 1
    • 2
  1. 1.Department of PediatricsHarvard Medical SchoolBostonUSA
  2. 2.Massachusetts General HospitalBostonUSA

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