Intracranial Pressure

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.



The Massachusetts General Hospital. Handbook of Neurology
The Massachusetts General Hospital Handbook of Neurology
ISBN: 0781751373
EAN: 2147483647
Year: 2007
Pages: 109

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