The Massachusetts General Hospital Handbook of Neurology

Authors: Flaherty, Alice W.; Rost, Natalia S.

Title: Massachusetts General Hospital Handbook of Neurology, The, 2nd Edition

Copyright 2007 Lippincott Williams & Wilkins

> Table of Contents > Adult Neurology > Intracranial Pressure

Intracranial Pressure

A. See also

CT appearance of herniation, p. 180.

B. Sx and progression of herniation

• 1. Central supratentorial herniation: Usually subacute, from tumor. Diencephalon is forced down through tentorium.

  • a. Diencephalic stage (reversible): Small pupils with light-near dissociation, roving eyes with decreased upgaze, obtundation, yawning. Progresses to Cheyne-Stokes breathing and decorticate posture.

  • b. Pontine stage (not reversible): Midsized fixed pupils (even though pontine lesions cause pinpoint nonreactive pupils). Cheyne-Stokes progresses to tachypnea. Decreased doll's eyes and calorics. Disconjugate gaze intranuclear ophthalmoplegia. Decorticate posture becomes decerebrate, then flaccid.

  • c. Medullary stage: Dilated pupils. Slow, irregular respirations.

• 2. Uncal supratentorial herniation: Usually rapid, often from hematoma of temporal lobe, malignant cerebral edema following an acute ischemic stroke, encephalitis (e.g., HSV).

  • a. First stage: Unilateral pupil dilation often before mental status change. Uncal herniation can pinch off PCAs.

  • b. Second stage: Ophthalmoplegia and hyperventilation. May see Kernohan's false localizing sign: ipsilateral hemiplegia as contralateral peduncle is compressed.

  • c. Third stage: Midposition pupils and decerebrate posture.

  • d. Fourth stage: Sx of central herniation (see *above).

• 3. Cingulate herniation (subfalcine): Often seen in malignant cerebral edema of ischemic stroke, ICH, GBM. Can pinch off ACA and present with abulia, poor concentration, LE weakness.

• 4. Subtentorial herniation: Often presents with respiratory arrest, so prophylaxis is more useful than monitoring. Rapid and devastating; often requires emergent neurosurgical intervention (suboccipital decompression).

  • a. Upward cerebellar herniation: May see dorsal midbrain syndrome.

  • b. Tonsillar herniation: Compresses medulla.

C. Causes of high ICP

Mechanism determines rx.

• 1. Mass lesion: E.g., blood, tumor, trauma. Use osmolar agent, mass resection, EVD, VP shunt.

• 2. Poor CSF resorption: E.g., pseudotumor cerebri (see p. 69). Rx with acetazolamide (decreases CSF production), osmolar agent, shunt.

• 3. Cerebral edema:

  • a. Vasogenic: From tumor, abscess. Use steroids, osmolar agent, resection, shunt.

  • b. Ischemic (cytotoxic): From stroke, trauma (diffuse axonal injury). No role for steroids. Use osmolar agent, shunt, resection.

  • c. Granulocytic: From infection.

  • d. Interstitial: From obstructive hydrocephalus.

P.68

D. Tests to assess ICP

• 1. CT: see p. 180 for CT appearance of high ICP.

• 2. CSF pressure:

  • a. Methods: See neurosurgical decompression techniques, p. 85.

    • 1) LP is often contraindicated if you suspect high ICP from mass lesion, posterior fossa process, or obstructive lesion in spinal canal. Okay to assess pseudotumor.

    • 2) External ventricular drain (EVD): Allows pressure measurements as well as CSF drainage.

    • 3) ICP monitor: (AKA bolt, subarachnoid screw) Allows only pressure measurements and short-lived measurement capacity (~5 d).

  • b. Values: Normal <7 mm Hg (100 mm water). Needs rx if >18 mm Hg (200 mm water). Life threatening if >25 mm Hg (350 mm water) and mean arterial pressure <85.

  • c. Conversions: 1 mm water = 0.07 mm Hg.

  • d. Cerebral perfusion pressure (CPP) = MAP (mean arterial pressure) - ICP (intracranial pressure).

E. Rx of acute ICP

• 1. Guidelines for hyperosmolar therapy: Monitor the following features:

  • a. Exam: Tie therapy to clear change in exam, e.g., dilated pupil or decreased consciousness.

  • b. ICP: Keep ICP <18-20 mm Hg, CPP >70 mm Hg.

  • c. Blood: Check electrolytes and serum osmolality q6h while on an agent. Hold the next dose for Na >160, serum osm >310, or osmolal gap (measured minus calculated serum osmolality) >10.

• 2. Miscellaneous: HOB up 30 degrees, airboots or SQ heparin.

• 3. Mannitol: Tolerance may develop to mannitol after ~48 h of use; thus, some advocate delay in use.

  • a. Dose: 25-100 g (not mg) IV bolus for average-sized person, or 0.25-1 g/kg. Then 25-50 g q4h.

  • b. Contraindications: Low BP, severe hyponatremia (will initially lower Na, then increase it), serum osm >310. If there is a large volume of damaged blood-brain barrier, there is little effect from mannitol. Rebound is rare; never use rebound as a reason not to give mannitol.

  • c. To discontinue mannitol: Typical taper is 25 g q6h 1 d, 25 q8h 1 d, 25 q12h 1 d, 25 q24h 1 d, then stop.

• 4. Hypertonic saline: Well tolerated; does not cause initial hyponatremia.

  • a. Contraindications: Na >160.

  • b. Infusion: 3% NaCl, ~40-50 cc/h; can go through peripheral IV for up to 12 h, then needs central line.

  • c. Bolus: 23% NaCl, 15-30 cc q6h via central line.

  • d. D/c: Requires taper to prevent rebound.

• 5. Dexamethasone: Helps if high ICP is from tumor or some infections, not stroke or head trauma. 10 mg IV, then 4 mg q6h.

• 6. Hyperventilation: Last-ditch, temporary effect. Keep pCO₂ ~30.

  • a. Danger of ischemia: pH >7.5 transiently decreases cerebral blood flow through vasoconstriction.

  • b. Danger of rebound: Can occur when you raise pCO₂ after pH has compensated, so wean slowly (increase pCO₂ range by 5 U q8h).

• 7. Barbiturates: Raise brain perfusion by lowering ICP more than BP. Often require IV pressors. They also lower brain metabolism.

P.69

• 8. Surgery: E.g., EVD, VP shunt, hemicraniectomy. See neurosurgical decompression techniques, p. 85.

• 9. Choice of antihypertensives when ICP is high:

  • a. Avoid: Nitroprusside, nitroglycerine, hydralazine, and Ca channel blockers, which raise ICP via vasodilation and, therefore, decrease cerebral perfusion.

  • b. Use: -blockers or ACE-I for BP control. Nicardipine is one Ca channel blocker that is well tolerated and effective.

F. Pseudotumor cerebri

(benign intracranial hypertension):

• 1. H&P: Headache, papilledema, constricted visual fields. More common in obese young women or pts with rapid weight gain.

• 2. Tests: LP shows high opening pressures, symptom relief after large-volume tap. Pt should have periodic visual field checks.

• 3. Causes: Obesity, steroid use, hyper-/hypovitaminosis A, drugs [tetracycline, nitrofurantoin, isotretinoin (Accutane)], anemia.

• 4. DDx: Dural sinus thrombosis, mass lesion, meningitis, inflammation (SLE, sarcoid, Beh et's dz).

• 5. Rx: Primary goal is preventing visual loss. Acetazolamide 250-1000 mg PO qd-tid (check electrolytes); repeated LPs, weight loss. Consider VP shunt or optic nerve fenestration. The latter protects against visual loss better but is less effective at controlling CSF pressure and HA.