Papilledema

Neuro-ophthalmologic Urgencies and Emergencies Introduction Papilledema is optic disc swelling from increased intracranial pressure. Patients presenting with papilledema often have symptoms of increased intracranial pressure, including headache, transient visual obscurations, and pulse synchronous tinnitus, and may have diplopia from 6th nerve palsies. If the raised intracranial pressure is acute, nausea and emesis is also often present. Patients with papilledema will  typically  have  bilateral  optic  disc  edema  and  preserved  central  vision,  unlike other optic neuropathies associated with disc edema, such as ischemic optic neuropathy, which typically causes loss of central visual acuity. A sudden rise in intracranial pressure secondary to acute subarachnoid or intraparenchymal hemorrhage may cause acute onset papilledema, though these changes typically occur after 1–5  days of elevated intracranial pressure. Papilledema can have associated peripapillary retinal hemorrhages and cotton wool spots representing nerve fiber layer ischemia.  Venous pulsations will disappear secondary to compression of the central retinal vein resulting in retinal venous engorgement and tortuosity. Severe disc  swelling can cause  subretinal fluid extension  to the macula that will result in reduction in visual acuity and metamorphopsia. Patients may also be noted to have retinal or choroidal folds. Papilledema typically causes blind spot enlargement. Papilledema can lead to visual field defects,  most commonly  inferior nasal defects, but severe  or persistent papilledema can cause significant field loss and even blindness if left untreated. The most common acute causes of papilledema in the emergency department include hydrocephalus, venous sinus thrombosis, meningitis, intracranial hemorrhage, and idiopathic intracranial hypertension. Malignant hypertension should be on the differential. History and the remainder of the neurologic exam should help identify the correct etiology. Intracranial  Hypertension Intracranial hypertension can either be chronic, as with idiopathic intracranial hypertension  (pseudotumor cerebri), or  acute,  often occurring  secondary  to a  tumor, obstructive hydrocephalus, traumatic brain injury, intracranial hemorrhage, or venous sinus thrombosis (Fig.  5.4). Head CT scan may demonstrate small ventricles and cistern and sulcal effacement. Brain MRI and MR venogram will provide more detail  and  help  eliminate  secondary  causes  of  raised  intracranial  pressure.  A  patient with focal neurological deficits in association with signs of meningismus and/or fevers should be worked up for meningitis, encephalitis, and abscess. Since papilledema indicates increased intracranial pressure, neuroimaging should be performed prior to lumbar puncture to rule out a mass lesion that could increase the risk of iatrogenic herniation.