Papilledema after Acute Head Injury

Abstract

Low grade papilledema after acute, severe head injury was identified in 15 (3.5%) 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 (ICP) was monitored continuously for 3 or more days in 9 patients; it was mildly elevated (20 to 40 mm Hg) in 7 patients and moderately elevated (40 to 60 mm Hg) 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 (chi square-4.327; P less than 0.04). Papilledema did not occur in 6 patients with sustained, severely elevated ICP (greater than 60 mm Hg) for 3 or more days. Each of these patients died. The severity of the trauma apparently accounts for the failure of papilledema to develop, possibly by arresting axoplasmic production and transport in retinal nerve fibers.

Severe Papilledema Identified 3 Weeks After Head Injury. Case Report.

“…6) Impaired axoplasmic flow of optic nerve fibers also contributes to papilledema. 11,12) Papilledema may also be caused by venous congestion of the optic nerve due to impaired sinus drainage. 1,[3][4][5] Generalized intraocular venous congestion and cavernous sinus thrombosis (or stenosis) …”

“…The incidence of posttraumatic papilledema is about 3.5% to 30%, 9,11) in contrast to 50% to 60% in patients with brain tumor 13) and 50% to 75% in patients with chronic subdural hematoma. 2) The appearance of papilledema is not always correlated with the severity of head injury, suggesting that sustained increase of intracranial pressure (ICP) is essential for the development of papilledema, 13) usually within a few days following trauma or hemorrhagic ictus.…”

“…2) The appearance of papilledema is not always correlated with the severity of head injury, suggesting that sustained increase of intracranial pressure (ICP) is essential for the development of papilledema, 13) usually within a few days following trauma or hemorrhagic ictus. 11,12) Rapid appearance of papilledema after intracranial hemorrhage is exceptional, 10) whereas appearance of papilledema may be delayed after cerebral hemorrhage for as long as 13 days after the hemorrhagic event with acute increase of ICP. 8) We report a case of visual impairment associated with papilledema that rapidly progressed 3 weeks after head injury, the longest delay in the appearance of papilledema so far reported.…”

Papilledema: epidemiology, etiology, and clinical management

“…In one study of patients with acute head injury, the presence of papilledema had little correlation with the degree of high ICP and it was found only in 3.5% of patients 20. Thus, the absence of papilledema does not necessarily rule out high ICP in these patients.…”

Brain death and intraocular pressure

“…Thus, the fact that our patients were routinely given dexamethasone can explain the lack of ODE in our series. Furthermore, since ODE first appears some days after ICP elevation [9,16] and our severly head-injured patients died early, ODE had no chance to develop. Retinal hemorrhages, a funduscopic evidence of raised ICP, were found frequently in our study.…”