In relation to diffuse cerebral oedema; discuss the pathophysiology, and the clinical and CT manifestations.
(30%- 30%- 40% marks)
Cerebral oedema is often classified based on 3 different mechanisms by which oedema results:
Cytotoxic oedema: failure of ionic pumps to maintain cellular homeostasis, accumulation of water and swelling of cells. Blood brain barrier (BBB) is intact. Metabolic derangements and ischaemia most common causes. E.g. CVA, post cardiac arrest, encephalopathy e.g. due to hepatic impairment.
Vasogenic oedema: breakdown of endothelial junctions of the BBB allowing intravascular proteins and fluid into extracellular space. Due to trauma, tumours, inflammation (e.g. infection), late stage of ischaemic insults, high altitude sickness. Mechanism relates to hydrostatic pressure in arterial HT, tumour released endothelial destructive factors (e.g. vascular endothelial growth factor - secretion reduced by Dexamethasone).
Osmotic oedema: Dilution of plasma leading to shift of water down the osmolarity gradient to the brain.
E.g. Excess H2O intake, SIADH, dialysis, rapid decrease in blood glucose when treated for a hyperosmolar hyperglycaemic state.
Cytotoxic and vasogenic oedema often coexist e.g. in setting of infarction or trauma.
May be similar to and superimposed on manifestations of the underlying cause
Related mostly to elevated ICP or mass effect
Agitation, delirium early
Hypertension, bradycardia (Cushing’s response)
Pupillary dilatation and decreased light reflex Papilledema
(Lateralising signs may be present with unilateral uncal/cerebellar herniation)
Loss of sulci
Loss of grey-white differentiation
Basal cistern/lateral ventricle effacement
Herniation of cerebellar tonsils into foramen magnum.
There are several agreed-upon mechanisms which can generate cerebral oedema:
- Cellular oedema
- Cytotoxic oedema (disturbance of cellular osmoregulation due to Na/K ATPase failure), due to interrupted energy supply eg. ischaemia hypoxia or trauma
- Metabolic storage (due to abnormal intracellular accumulation of molecular products), eg. in hyperammonaemia or inherited cell storage diseases suhc as Pompe's disease (glycogen), Hurler's disease (mucopolysaccharides), Gaucher's disease (glycosyl ceramide), etc.
- Extracellular oedema
- Vasogenic oedema (an increase in brain capillary permeability), eg. due to infection
- Osmotic oedema (due to an osmotic gradient between the plasma and the interstitial fluid, across an intact blood-brain barrier), eg. in the context of dialysis disequilibrium, or due to rapid loring of the blood glucose in a hyperglycaemic hyperosmolar state
- Hydrocephalic oedema (obstruction of CSF flow pathways), where CSF infiltrates periventricular white matter due to increased intraventricular pressure, through a damaged ependymal lining.
For the majority of the clinical features listed below, the main source was the UpToDate article on high altitude cerebral oedema, as that seemed like a cause of diffuse oedema which was sufficiently insidious in onset to produce symptoms instead of immediate coma.
- Neck stiffness
- Irritability and confusion
- Agitation, delirium
- Decreased level of consciousness
With raised ICP:
- Loss of light reflex
- Papilledema on fundoscopy
- Primarily affecting white matter
- Indentations of edema with frond-like projections into normal gray matter
- Enhancement following contrast
- Usually focal, i.e. due to some local lesion
- Usually diffuse
- Does not enhance with contrast
- Involves subcortical nuclear gray matter structures (e.g., basal ganglia, thalamus).
Hydrocephalus-associated "interstitial" oedema
- Transependymal fluid: low attenuation periventricular changes around the lateral ventricles. These are usually most prominent surrounding frontal and occipital horns.
Oedema in general
- effacement of the sulci
- effacement of the ventricles
- loss of grey-white differentiation
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