There are four main categories of cerebral edema: cytotoxic edema, vasogenic edema, interstitial edema, and osmotic edema. Cytotoxic edema is caused by cellular swelling from metabolic failure of ion pumps due to conditions like ischemia or trauma. Vasogenic edema results from plasma leakage into brain tissue from damaged blood vessels, often due to tumors. Interstitial edema occurs when fluid moves from ventricles into surrounding brain tissue in hydrocephalus. Osmotic edema is caused by hyperosmolarity differences between the brain and circulation in situations like water intoxication or hemodialysis. Treatment focuses on the underlying cause, while diuretics and osmotic agents can temporarily reduce swelling.

1. Cerebral edema
YOUMANS Neurological Surgery
Sixth edition

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

3. The Blood-Brain Barrier

5. • 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+

6. Cerebral edema
• Four categories
• Cytotoxic edema
• Vasogenic edema
• Interstitial edema
• Osmotic edema

7. Cytotoxic edema

8. • Cause of cytotoxic edema
• Cerebral infarction or ischemia
• Meningitis
• Reye’s syndrome
• Trauma
• Seizure
• Water intoxication

9. • 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 Ca
3+
) 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

10. • 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)

12. • 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

13. Vasogenic edema

14. • Cause of vasogenic edema
• Primary or secondary brain tumour
• Brain abscess and encephalitis
• Trauma
• Lead poisoning
• Late stage of cerebral infarction

15. • 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)

16. • 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

18. • 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

19. Interstitial edema

20. • Cause of interstitial edema
• Hydrocephalus
• Mechanism
• Transependymal flow of water and solute into
periventricular extracellular space

21. • Hypodensity area around periventricular white matter in CT scan
• Increased signal in FLAIR MRI at interstitial brain surrounding
ependyma

22. Osmotic edema

23. • 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

26. Treatment

27. • 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

28. • 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)

29. Thank you