cerebral edema

Introduction

Brain swelling due to increased extravascular water in the neuropil & white matter.

Etiology

• acute brain injury
  • ischemic stroke
  • traumatic brain injury
  • brain metastases
  • encephalopathy due to severe hyponatremia [2-5]
• high-altitude cerebral edema

Monitor

• serial neurological exams
• intracranial pressure as indicated [2-5]

Radiology

• neuroimaging with non-contrast brain CT 1st line
  • CT to identify early hypodensity, involvement of >= 1/3 of the middle cerebral artery territory, & midline shift, predictive of cerebral edema & severity
  • CT scans also used to monitor progression of cerebral edema
• MRI of brain is more sensitive than CT
  • diffusion-weighted imaging can quantify water mobility & detect early cytotoxic edema
  • T2-weighted imaging is useful for later changes due to vasogenic edema
• diagnostic features on neuroimaging include sulcal effacement, ventricular compression, midline shift, & effacement of basal cisterns or 4th ventricle [2-5]

Complications

• increased intracranial pressure
• diminished cerebral perfusion
• increased riskk of brain herniation [2-5]

Management

• general supportive measures [2-5]
  • elevation of the head of the bed to 30 degrees facilitates venous outflow & & reduces intracranial pressure
  • optimizing ventilation to achieve normocapnia of mild hypocapnia if acute increased intracranial pressure
  • avoid systemic hypotension
  • maintenance of normal body temperature
• osmotic agents mannitol, hypertonic saline & glycerol reduce intracranial pressure by creating an osmotic gradient drawing water out of the brain parenchyma
• glucocorticoids indicated for vasogenic edema associated with brain tumors & brain metastases
  • dexamethasone preferred due to long 1/2-life & minimal mineralocorticoid activity
    • severe symptoms: 10 mg IV bolus followed by 16 mg/day in divided doses prn
    • milder symptoms: 4-8 mg/day
    • consider gradual taper to minimize adrenal insufficiency if therapy > 5 days
  • glucocorticoids may be harmful in cerebral edema due to trauma, stroke, or other non-neoplastic causes
• CSF removal (ventricular shunt) for hydrocephalus or increased intracranial pressure with ventricular enlargement.
• adjunctive investigational agents include glibenclamide, bumetanide & conivaptan which target molecular pathways involved initiation of edema
• decompressive craniectomy for malignant cerebral edema unresponsive to medical therapy
• seizure prophylaxis is not routinely indicated unless seizures have occurred [2-5]
• high-altitude cerebral edema
  • immediate return to lower elevation
  • supplemental oxygen
  • dexamethasone as indicated

More general terms

• edema (swelling, tumefaction, tumescence)

More specific terms

• high-altitude cerebral edema (HACE)