Download - 009 youmans cerebral edema
• Blood-Brain barrier (BBB) is exceptionally active system
• Endothelial cells can inactivate neuroactivate or neurotoxic substances
• Regulate microenvironment of the brain, fluid and ions between circulation and brain
• Interstitial fluid of the brain
• lower Ca2+ and K+ and higher Mg2+
Cerebral edema
• Four categories
• Cytotoxic edema
• Vasogenic edema
• Interstitial edema
• Osmotic edema
• Cause of cytotoxic edema
• Cerebral infarction or ischemia
• Meningitis
• Reye’s syndrome
• Trauma
• Seizure
• Water intoxication
• Mechanisms
• Osmotic gradient from metabolic failure of the Na+, K+-ATPase pump cause cellular swelling of neurons, glia and endothelial cells
• Loss of ATP and excess glutamate after cerebral ischemia or TBI cause influx of calcium into cell then apoptosis and sodium exchange (3 Na+ per Ca3+) occur
• Nitric oxide (NO) from nitric oxide synthase (NOS)
• Neuronal NOS produces toxic free radical (early after cytotoxic injury)
• Endothelial NOS cause vasodilatation and increase blood flow
• Inducible NOS produce NO and free radical at 24-48 hr after injury
• NCCa-ATP channel (nonselective cation channel) opened after depletion of ATP, cause cytotoxic edema after ischemia
• Regulated by sulfonylurea receptor 1 (can be blocked by low dose glibencamide)
• Diffuse-weighted MRI signal change within minute after events occur (very early)
• In first 12 hour, loss of visible gray-white matter junction and gyral edema occur
• 12-24 hour , increase signal in T2-weighted MRI
• Cause of vasogenic edema
• Primary or secondary brain tumour
• Brain abscess and encephalitis
• Trauma
• Lead poisoning
• Late stage of cerebral infarction
• Mechanisms
• Blood-tumor barrier has abnormal micro vessels that lacks of tight junctions cause plasma leakage into brain’s extracellular space
• Macromolecular protein produced by tumor has been identified as vascular permeability factor (VPF) and vascular endothelial growth factor (VEGF)
• Glucocorticoids can block permeability-enhancing effects of VPF and VEGF and inhibit tumor cell production of VPF and VEGF
• High VPF and VEGF gene expression found in glioblastomas, meningiomas and metastases
• Hypodensity lesion in CT scan and decrease signal in T1-weighted MRI mostly involve only white matter
• Increase signal in T2-weighted and FLAIR MRI
• Cause of interstitial edema
• Hydrocephalus
• Mechanism
• Transependymal flow of water and solute into periventricular extracellular space
• Hypodensity area around periventricular white matter in CT scan
• Increased signal in FLAIR MRI at interstitial brain surrounding ependyma
• Cause of osmotic edema
• Hemodialysis
• SIADH
• Hypertensive crisis
• Water intoxication
• Rapid reduction of blood glucose in hyperglycaemic crisis
• Mechanism
• Hyperosmolarity in brain relatively to circulatory then water move into brain along osmotic gradient
• Specific treatment
• Direct treatment of causative disease or conditions
• Glucocorticoids have effect to peritumoral edema (mostly vasogenic edema) but less effect to cytotoxic and interstitial edema
• Diuretics can cause systemic dehydration and increase circulatory osmolarity and carbonic anhydrase inhibitor (acetazolamide) can reduce CSF production
• Mannitol and other osmotic agents temporality reduce cerebral edema (used in acute setting and prepare for definite treatments)