The next step for the management of uncal herniation if clinical signs do not resolve with interventions to reduce intracranial pressure is to consider decompressive surgical options. Hypertonic saline can be administered as a continuous infusion at 0.5-1.5 mL/kg/hr. 3% hypertonic saline is given as a bolus dose of 5-10 mL/kg in patients with acute elevations of intracranial pressure or with signs of brain herniation. Mannitol is given as a bolus dose of 0.5-1 g/kg and can be administered every four hours as needed for intracranial pressures above 20 mmHg, maintaining the osmolar gap less than 20 mOsm. Hyperosmolar therapy with mannitol or 3% hypertonic saline is administered to patients with intracranial pressure elevations above 20 mmHg or when there is suspected brain herniation. Hyperventilation is typically reserved for situations where there is life-threatening intracranial hypertension, such as in uncal herniation. We look forward to working with you to determine the best eye surgery or nonsurgical treatment for your individual needs. Hyperventilation works to reduce the intracranial pressure by decreasing arterial carbon dioxide levels which will induce vasoconstriction to reduce the cerebral blood volume this is achievable by increasing tidal volume or respiratory rate with a target PaCO2 of 30-35 mmHg. Hyperosmolar therapy with either mannitol or hypertonic saline Ultimately if untreated, uncal herniation progresses to central herniation. Further compression of the midbrain due to uncal herniation can then progress to lethargy, coma, or death. Over time, the patient may develop impaired ocular motility which will give the eye a classic down-and-out appearance. ![]() In patients who present with isolated anisocoria, this could be a sign that there is impending uncal herniation. The hallmark unilateral dilated pupil can be the first symptom to appear without severe impairment in the level of consciousness or contralateral hemiparesis. The cardinal signs of uncal herniation are an acute loss of consciousness associated with ipsilateral pupillary dilation and contralateral hemiparesis. These symptoms are due to compression or displacement of ascending arousal pathways, the oculomotor nerve (CN III), and the corticospinal tract. A late finding on an ophthalmologic exam in a patient with increased ICP is papilledema, which presents with a blurring of the optic disc margin and decreased venous pulsations. These symptoms include headache, nausea, vomiting, and altered mental status. Physical exam in increased ICP will reveal Cushing's triad of hypertension, bradycardia, and irregular respiration or apnea. A patient with impending uncal herniation will initially present with symptoms of increased intracranial pressure.
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