Hypoxic-ischemic encephalopathy in preterm infants

Abstract

Objective: To determine both the incidence of perinatal hypoxic ischemic encephalopathy (HIE) in a group of preterm infants 32–36 weeks gestational age at a single center and the outcomes of these patients.

Study design: The number of infants 32–36 weeks gestational age without major congenital anomalies born at Vanderbilt University Hospital between January 1, 2002 and June 30, 2008 was determined and a retrospective chart review was performed on those infants with a 5-minute Apgar score of less than 6. Infants were considered to have experienced perinatal HIE if they met all of the following criteria:

5-minute Apgar score less than 6

Cord or initial patient blood pH less than 7.00 or base deficit greater than 15 (mmol/L)

Evidence of encephalopathy at or shortly after birth (seizures, hypotonia)

History of a sentinel event at the time of delivery

No other cause of encephalopathy (sepsis, hypermagnesemia, hemorrhage, hyponatremia, drug induced)

Preterm infants with 5-minute Apgar score less than 6 not meeting all of the criteria were considered not to have had perinatal HIE. A poor outcome was defined as death, or cerebral palsy, or neurodevelopmental impairment, or bilateral deafness, or bilateral blindness. If no follow-up data was available, the patient was recorded as being alive at discharge and considered to be normal.

Results: Between January 1, 2002 and June 30, 2008 there were 1,325 infants 32–36 weeks gestational age born at Vanderbilt University Medical Center. The incidence of perinatal HIE in these patients was 12/1325 (0.9%). 58.33% of these patients suffered poor outcomes.

Conclusion: With a similar incidence and experience of adverse sequelae as the term infant, preterm infants 32–36 weeks in gestation with perinatal HIE should be considered for future randomized controlled studies for treatment of this potentially devastating injury.