Reactive mydriasis
Specialty: Neurology.
Why it occurs
- Uncal herniation of the temporal lobe (direct compression of the third cranial nerve against the tentorium cerebellum due to massive intracranial hypertension secondary to hematoma, tumor or cerebral edema)
- Ruptured or giant aneurysm of the posterior communicating artery
- Ischemia or infarction of the brainstem (midbrain) with nuclear damage to the third nerve
- Closed ocular trauma with paralysis of the pupillary sphincter muscles
- Intoxication by atropinic or other topical or systemic anticholinergics
Initial workup
Immediate pupillary examination with a medical examination flashlight to document non-reactivity to direct and indirect light (consensual); Urgent computed tomography (CT) of the head to rule out mass effect, subarachnoid hemorrhage or brain herniation; Emergency brain CT angiography or MRI angiography if a posterior communicating artery aneurysm is suspected.
red flags
Presence of a unilateral non-reactive mydriasis of acute onset associated with progressive deterioration of alertness (stupor, coma), rigidity of decerebration or contralateral hemiparesis. It constitutes a sign of extreme neurological alarm that denotes brain stem involvement and imminent risk of brain death.
Standard management
- Mannitol 20% — 0.5-1 g/kg rapid intravenous bolus) or 3% or 7.5% hypertonic saline (urgent osmotic therapy to reduce intracranial pressure and reverse uncal herniation
- Emergency decompressive surgery (decompressive craniotomy, hematoma evacuation) or endovascular aneurysm embolization.
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Neurology
- Listed causes
- 5
- Treatment options
- 2