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Papilledema after acute head injury
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Low grade papilledema can occur after severe head injury, often indicating milder trauma and better outcomes. This finding suggests papilledema is a potential indicator of less severe traumatic brain injury.
Area of Science:
- Neuroscience
- Ophthalmology
Background:
- Traumatic brain injury (TBI) can lead to various complications.
- Papilledema, swelling of the optic disc, is a known sign of increased intracranial pressure.
Observation:
- Low grade papilledema was observed in 3.5% of patients following acute, severe head injury.
- Papilledema onset varied, appearing immediately, within the first week, or later.
- Computed tomography scans revealed brain injury in most affected patients.
Findings:
- Intracranial pressure (ICP) was mildly to moderately elevated and controllable in patients with papilledema.
- Papilledema timing correlated with ICP patterns: sudden increases for immediate onset, sustained elevations for later onset.
- Patients with papilledema had higher Glasgow Coma Scores and no fatalities, suggesting less severe TBI compared to non-papilledema cases.
Implications:
- Papilledema in TBI patients may indicate a less severe injury with a favorable prognosis.
- The absence of papilledema in non-survivors with extreme ICP suggests trauma severity can prevent its development.
- Further research into papilledema as a prognostic marker in TBI is warranted.
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.