Neonatal Encephalopathy

Invited guests* attended part of the PMMRC meeting on 22 February 2007 for a discussion on neonatal encephalopathy. The PMMRC agreed to include in its Work Plan for 2007/08 (which is submitted to the Minster of Health for approval) funding to establish a Neonatal Encephalopathy Working Group.

Neonatal Encephalopathy Working Group Background Information

Reducing Neonatal Encephalopathy in New Zealand (PDF, 48 KB)

Neonatal Encephalopathy Working Group Meeting Minutes

8 November 2007 (PDF, 41 KB)

More information on Neonatal Encephalopathy
Below is an excerpt taken from the Newborn Services Clinical Guideline on the Auckland DHB website.

Neonatal Encephalopathy (NE) is “a clinically defined syndrome of disturbed neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, sub normal level of consciousness and often seizures”.

NE occurs in approximately 3.5 - 6/1000 live births and usually affects the full term infant. The terminology NE is preferred to Hypoxic Ischemic Encephalopathy (HIE) as it is not always possible to document a significant hypoxic-ischemic insult and there are potentially several other aetiologies.

Specifically, it is important to exclude metabolic disease, infection, drug exposure, nervous system malformation and neonatal stroke as possible causes of the encephalopathy. The requirement for investigation to exclude these possibilities will depend on the presentation, history and clinical features of the individual case.

Three Clinical Stages of Encephalopathy

Stage 1

Duration < 24 hours with hyperalertness.
Uninhibited Moro and stretch reflexes.
Sympathetic effects.
Normal electroencephalogram.

Stage 2

Obtundation.
Hypotonia.
Decreased spontaneous movements with or without seizures.

Stage 3

Stupor.
Flaccidity.
Seizures.
Suppressed brain stem and autonomic functions.
The EEG may be isopotential or have infrequent periodic discharges.

Notes:

Stage 3 or persistence of stage 2 for more than seven days or failure of the EEG to revert to normal is associated with neurodevelopmental impairment or death.
Full-term infants who develop long-term neurologic sequelae from intrapartum asphyxia may not have low Apgar scores but will demonstrate neurological dysfunction within 48 hours.

* Malcolm Battin, Neonatologist Auckland; Glenda Oben, Senior Information Analyst, New Zealand Health Information Service (NZHIS), Ministry of Health; Teresa Sullivan, Patient Safety Development Manager and Melissa Field, Senior Business Analyst, Accident Compensation Corporation (ACC); Vaughan Richardson, Neonatologist Wellington and ACC Assessor.

Page last updated: 21 april 2008