Poor outcome after hypoxia-ischemia in newborns is associated with physiological abnormalities during early recovery. Possible relevance to secondary brain injury after head trauma in infants.
"Secondary hypoxia/ischemia" (i.e. regional impairment of oxygen and substrate delivery) results in secondary deterioration after traumatic brain injury in adults as well as in children and infants. However, detailed analysis regarding critical physiological abnormalities resulting from hypoxia/ischemia in the immature brain, e.g. acid-base-status, serum glucose levels and brain temperature, and their influence on outcome, are only available from non-traumatic experimental models. In recent studies on hypoxic/asphyxic cardiac arrest in neonatal piglets, we were able to predict short-term outcome using specific physiologic abnormalities immediately after the insult. Severe acidosis, low serum glucose levels and fever after resuscitation were associated with an adverse neurologic recovery one day after the insult. The occurrence of clinically apparent seizure activity during later recovery increased mortality (epileptic state), and survivors had greater neocortical and striatal brain damage. Brain damage after transient hypoxia/ischemia and "secondary brain injury" after head trauma may have some mechanistic overlap, and these findings on physiological predictors of outcome may also apply to pathologic conditions in the post-traumatic immature brain. Evaluation of data from other models of brain injury will be important to develop candidate treatment strategies for head-injured infants and children and may help to initiate specific studies about the possible role of these physiological predictors of brain damage in the traumatically injured immature brain.
Brambrink
A M
AM
Department of Anaesthesiology, Johannes Gutenberg University, Mainz, Germany. brambrin@mail.uni-mainz.de
Ichord
R N
RN
Martin
L J
LJ
Koehler
R C
RC
Traystman
R J
RJ
D000138:Acidosis / Q000503:physiopathology; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001930:Brain Injuries / Q000503:physiopathology* / Q000628:therapy; D002545:Brain Ischemia / Q000503:physiopathology*; D006259:Craniocerebral Trauma / Q000503:physiopathology* / Q000628:therapy; D007003:Hypoglycemia / Q000503:physiopathology; D007036:Hypothermia, Induced; D000860:Hypoxia / Q000503:physiopathology*; D012640:Seizures / Q000503:physiopathology; D013552:Swine