009 youmans cerebral edema

Cerebral edemaYOUMANS Neurological Surgery

Sixth edition

• Accumulation of excess fluid in the intracellular or extracellular spaces of the brain

The Blood-Brain Barrier

• 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

Cytotoxic 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

Vasogenic edema

• 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

Interstitial edema

• 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

Osmotic edema

• 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

Treatment

• 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)

Thank you