Herniation Syndromes

Types of Herniation

  1. Subfalcine herniation
    • supratentorial mass lesions may lead to cingulate gyrus hernation
    • often in supratentorial metastasis, low- or high-grade gliomas
    • pericallosal branches of ACA along free edge of falx may be compressed leading to infarction
  2. Uncal herniation
    • most common type
    • presents as: impaired consciousness, fixed dilated ipsilateral pupil, hemiparesis contralaterally
    • uncus herniates over tentorial edge, compresses CN III
    • uncus can also herniate into midbrain and into posterior fossa, compressing corticospinal tract
    • PCA may be compressed between uncus and midbrain causing occipital lobe infarct
  3. Central herniation
    • generalized cerebral mass effect
    • entire mid-brain herniates downward
    • presentation: obtunded with altered breathing pattern, pinpoint pupils, loss of upward gaze
  4. Tonsillar herniation:
    • infratentorial tumors cause cerebellum to herniate through foramen magnum compressing the medulla
    • presentation:  cardiorespiratory dysfunction, altered breathing patterns, impaired consciousness

Treatment:

  1. positioning:  elevate head 30° (decrease CSF hydrostatic pressure, facilitate venous drainage), head facing straightforward (decrese IJ vein compression), remove constricting garments or devices around neck
  2. avoid hypoxia and hypercapnia – target PaCO2 35-40 mm Hg, intubate if declining neurologic status or GCS <8 or requiring sedation / GA for ICP control
  3. hemodynamic support – maintain euvolemia (use isotonic fluids); avoid CPP<50mm Hg; initiate treatment if CPP fall <60 to avoid CPP<50mm Hg; vasopressors, avoid vasodilators (nitroglycerine and nitroprusside – exacerbates cerebral edema through cerebral hyperemia)
  4. avoid fever, hypothermia may be effective in lowering ICP but long-term outcome still unclear; target normothermia for now
  5. anticonvulsants – seizures affect airway, increases PaCO2, exacerbates cerebral edema and ICP; seizure prophylaxis after crani for tumor resection still unclear but prudent to start prophylaxis for supratentorial brain tumors; prefer newer generation anticonvulsants
  6. Mannitol 25% at 0.5-1.5 g/Kg – reduces ICP, peak effect 15-35 mins after infusion, duration several hours; osmotic diuresis may lead to hypovolemia and electrolyte imbalance (check q6-8h); given peripheral or through central IV catheter over 10-20minutes;  high osmotic levels may produce renal damage; upper limit to safely administer mannitol is 320 mOsm/L; may leak into brain parenchyma and exacerbate vasogenic edema if used over sustained time
  7. hypertonic saline – continuous infusion (2-3%) or bolus (23.4%); central venous catheter needed for concentrations 3% or higher; complications include fluid overload (CHF); do not abruptly stop infusion to avoid rebound ICP; wean over 12-24h
  8. Steroids – reduces permeability of tumor capillaries, dexamethasone is drug of choice (low index of Na and water retention, long half life, low mineralocorticoid activity, low tendency to induce psychosis, controls tumor-associated pain, limits n/v, improves appetite in cancer); 10-20mg IV x1 if with acute nruologic symptoms, maintenance dose of oral or IV 4-24mg in divided doses; expect improvement in 48 hours, use lowest effective dose; use GI prophylaxis
  9. Surgery – resection, intraventricular catheterization

Future Therapies

  1. inhibition of VEGF – SU5416 (semaxanib), AZD2171
  2. COX-2 inhibitors – inhibits production of prostaglandins involved in inducing cerebral edema, also found to induce apoptosis and prevent anigogenesis; SC-236, rofecoxib, PPAR-γ

 

References

Esquenazi, Y., V. P. Lo, and K. Lee. “Critical Care Management Of Cerebral Edema In Brain Tumors”.Journal of Intensive Care Medicine (2015): n. pag. Web.

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