NA;Low grade papilledema after acute, severe head injury was identified in 15 lpar;3.5percnt;rpar; of 426 patients. Papilledema was recognized immediately after head injury in 1 patient, during the 1st week in 10 patients, and in the 2nd week or after in 4 patients. Initial computed tomographic scans showed evidence of brain injury in 11 of these patients. The intracranial pressure lpar;ICPrpar; was monitored continuously for 3 or more days in 9 patientssemi; it was mildly elevated lpar;20 to 40 mm Hgrpar; in 7 patients and moderately elevated lpar;40 to 60 mn Hgrpar; in 2 patients. Intracranial hypertension was controllable in each patient. A sudden, severe, but transient increase in ICP best explained the immediate development of papilledema and survival of 1 patient. Sustained but mild to moderately elevated ICP accounted for papilledema appearing in the 1st week. Papilledema in the 2nd week or after occurred from impaired cerebrospinal fluid absorption and consequent communicating hydrocephalus or delayed focal or diffuse cerebral swelling. A lesser degree of head injury in patients with posttraumatic papilledema was suggested by a higher Glasgow coma score, milder and controllable elevations in ICP, and the absence of any fatality in this group. The favorable outcome was significant compared to the mortality of the more severely injured patients lpar;chi squarehyphen;4.327semi; p 0.04rpar;. Papilledema did not occur in 6 patients with sustained, severely elevated ICPlpar;60 mm Hgrpar; for 3 or more days. Each of these patients died. The Severity of the trauma apparently accounts for the failure of pailledema to develop, possibly by arresting exoplasmic production and transport in retinal nerve fibers. lpar;Neurosurgery16colon;357hyphen;363, 1985
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