Loss of Adrenocortical Suppression after Acute Brain Injury: Role of Increased Intracranial Pressure and Brain Stem Function*

1983 ◽  
Vol 57 (6) ◽  
pp. 1245-1250 ◽  
Author(s):  
JOHN FEIBEL ◽  
MARY KELLY ◽  
LOUYSE LEE ◽  
PAUL WOOLF
PEDIATRICS ◽  
1988 ◽  
Vol 82 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Brian A. Lupton ◽  
Alan Hill ◽  
Elke H. Roland ◽  
Michael F. Whitfield ◽  
Olof Flodmark

The role of brain swelling following acute hypoxic-ischemic insult in the genesis of brain injury in the term newborn is controversial. Recent experimental animal studies suggest that it may result from prior irreversible cerebral necrosis and therefore represents a consequence as opposed to a cause of major brain injury. In this study, 32 asphyxiated term newborns were studied during the first week of life with serial intracranial pressure measurements. A total of 26 infants had scans during the first five days of life. Seven patients had two CT scans within this period. These investigations were correlated with outcome at 18 months of age. Seven infants had increased intracranial pressure (> 10 mm Hg) that reached a maximum between 36 and 72 hours of age. Cerebral perfusion pressures remained normal, which makes ongoing ischemic injury unlikely as a cause. The seven patients with increased intracranial pressure had decreased attenuation on CT that was generalized in six infants and patchy in one infant. Of the infants with increased intracranial pressure and severe CT abnormalities, three died and four had severe neurologic sequelae. In seven infants, a second CT scan at three to four days of life demonstrated progression of the decrease in tissue attenuation. Most of the infants with normal intracranial pressure (23/25) had no or had only minor neurologic abnormalities at follow-up. These data suggest that brain swelling is relatively uncommon in the asphyxiated term newborn. The temporal profile of increased intracranial pressure and CT abnormalities, with maximum abnormalities at 36 to 72 hours of age, is most consistent with cerebral necrosis as a cause that, in turn, implies a poor prognosis.


1983 ◽  
Vol 91 (4) ◽  
pp. 399-403 ◽  
Author(s):  
Arnold Komisar ◽  
Stephen Weitz ◽  
Robert J. Ruben

CSF rhinorrhea can have many causes: traumatic, neoplastic, and iatrogenic origins are common. Most traumatic rhinorrhea ceases after a trial of conservative management. While obvious erosion or traumatic destruction of vital structures may be the underlying cause, other pathophysiologic mechanisms may be working in the formation of CSF rhinorrhea, which may require the combined skills of the otolaryngologist and the neurosurgeon. Leakage of CSF is seen in “high-pressure rhinorrhea,” a pathophysiologic state wherein the underlying problem is poor CSF resorption. The result is increased intracranial pressure and eventual rhinorrhea or otorrhea. Areas of CSF leakage correspond to sites of congenital weakness in the cribriform plate region, the parasellar region, or the temporal bone. Weak areas in old base-of-skull fracture sites may leak with increased intracranial pressure. The initial management should stress correction of the deranged pathophysiology, namely shunting. Surgical repair is secondary to controlling the abnormal CSF dynamics.


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