L34 - Pathology of raised intracranial pressure and cerebrovascular disease Flashcards
Definition of ICP and normal range?
Definition: pressure of the CSF within the cranial cavity.
Normal range: less than 10 mm Hg (150 mm water).
Definition of raised ICP?
elevation of the mean CSF pressure above 15 mm Hg (200 mm water)
when measured with the patient in the lateral decubitus position (Lumbar puncture position)
List the 2 primary categories of causes in Increased ICP?
Depends on the volume and pressure of intra-cranial content against the rigid cranium:
* Rigid cranium (exception = infant): Separated into compartments by tough dura*
- Space-occupying lesions (e.g. haematoma, tumour, abscess, etc.)
- Secondary effects: Brain swelling / cerebral edema or obstruction to CSF flow (Hydrocephalus)
List 4 factors that may impact the effect/ manifestation of increased ICP?
- age - elderly, infancy (e.g. infants have more distensible cranium)
- stage of spatial compensation (e.g. old people have more atrophied brains with more space to compensate)
- rate of increase ICP
- pressure gradient
How does age impact the effects of raised ICP?
Elderly: cerebral atrophy = more space for compensation
Infant: separation of sutures = can tolerate more increase in ICP
Explain how stage of spatial compensation impacts effects of raised ICP? (think compensations to initial phase, gradual increase in ICP…)
1) Initial phase: reduction in CSF volume in ventricles, venous space (intracranial veins) in dural sinuses
2) Slow increase in space occupying-lesion: compensatory cerebral atrophy, erosion of skull bone etc.
3) After all possible compensation: critical point: further slight increase in intracranial contents volume causes abrupt increase in ICP
Give 2 causes of increased ICP with different rates and how it affects the outcome?
Slow-growing i.e. meningioma = progressive brain atrophy with slow increase in ICP
Acute haematoma = fast increase in ICP without time to compensate
Explain how the structure of the brain is related to the effects of ICP and pressure gradients?
Pressure gradient determines which area of brain is distorted/ displaced by expanding lesions**
- dural folds separate the brain into compartments
- posterior cranial fossa is connected to the spinal cord through foramen magnum
Describe the compartments of the brain formed by dural folds?
Dural folds (falx cerebri, tentorium cerebelli…etc)
> > separate brain into compartments (right and left cerebral hemispheres, anterior, posterior cranial fossa)
How are cerebral herniations classified? List 2 most important classes?
Classified on the part that is herniated and the structure which it has been pushed:
- Transtentorial and uncal herniation
- Cerebellar tonsil herniation (coning)
Describe transtenorial herniation.
Temporal lobe impinged against sharp edge of tentorium cerebelli (dural fold)
Describe cerebellar tonsil herniation? Think about structures affected and symptoms?
Downward displacement of cerebellar tonsils through foramen magnum
> > compression, distortion of medulla oblongata
> > frequently results in apnoea (respiratory arrest)
List the 6 structures that are affected in transtentorial herniation? (3 neuronal, 1 ventricular, 2 vascular structures)
Neuronal:
- ipsilateral oculomotor nerves
- optic nerve and retinal vein
- Contralateral cerebral peduncle
Ventricular:
- aqueduct of Sylvius (3rd to 4th ventricle)
Vascular:
- posterior cerebral artery
- haemorrhage and infarction of midbrain and pons
Clinical manifestation of transtentorial herniation impinging on the 3 specific neuronal structures?
- Compress ipsilateral oculomotor nerves – fixed and dilated pupils, ptosis
- Compress optic nerve and retinal vein – papilloedema
- Contralateral cerebral peduncle pushed against free edge of the tentorium - hemiplegia in same side of body as the space occupying lesion (false localising sign)
Clinical manifestation of transtentorial herniation impinging on the vascular and cerebral ventricular structures?
- Compress posterior cerebral artery – infarction of ipsilateral occipital cortex (cortical blindness) (bilateral in severe case)
- Compress aqueduct of Sylvius – hydrocephalus
- haemorrhage and infarction of midbrain and pons (loss of consciousness, depression of heart rate, changes in respiration, elevated blood pressure due to increased sympathetic activity)
List some early signs of raised ICP apart from those seen in herniation?
1) Headache (stretching of meninges)
2) Projectile vomiting (distortion of brainstem)
3) Separation of sutures of the vault (in infants, children)
4) Erosion of skull bone (in long, sustained moderate increase in ICP)
Compare and contrast primary and secondary hydrocephalus?
Primary hydrocephalus:
- Obstruction to CSF flow from choroid plexus… aqueduct… subarachnoid space
- Increased production + Impaired absorption
Secondary hydrocephalus:
- Compensatory increase in CSF
Define hydrocephalus.
increase in CSF volume in ventricles / subarachnoid space / both
Define the different causes of brain swelling?
(1) cerebral edema: 3 classes:
a) vasogenic
b) cytotoxic
c) hydrocephalic
(2) Congestive brain swelling from vasodilatation
What causes of congestive brain swelling?
Hypoxia, hypercapnia causes loss of vasomotor tone»_space; vasodilation»_space; complicate acute brain injury
Cause of cerebral vasogenic edema? What are the accompanying pathologies?
Cause:
- increased filtration pressure and/or permeability of the capillaries and venules
- Defective BBB»_space; water, sodium,
protein extravasated into the extracellular space
Accompanying cerebral contusions, recent infarcts, brain abscess and tumours
Cause of cerebral cytotoxic edema?
Acute hypoxia»_space; Loss of cellular osmoregulation (increased intracellular water, sodium)
