B112 Pathology of increased ICP Flashcards
What are the compensatory mechanisms for raised intracranial pressure?
The venous plexus draining the blood, increased pressure increass CSF fluid filtration into the veins.
There is a small amount of elasticity and compliance of the dura mater.
The compensatory mechanisms are only useful to relieve slow increases in ICP, and acute increases will result in herniation.
What are the types of pathologies that increase ICP?
What is the normal ICP range?
At what values do symptoms appear?
Cerebral edema
Hydrocephalus
Normal range” 7-15 mmHg
symptoms at 30 mmHg
brain death at 60 mmHg.
Pathogenesis of cerebral edema
Vasogenic Edema:
- Due to damage and increased vascular permeability of the blood brain barrier
- Fluid shifts from blood into the Intracellular space.
- Can be localized or generalized
- example is localized brain abscess - causes increased local permeability and local vasogenic edema
Cytotoxic Edema:
- Cellular damage in the CNS, as in hypoxic or ischemic injury or due to toxin exposure.
- Cells lakcing ATP or with mitochondrial damage can’t operate their NA/K pumps effectivley, and can’t maintain osmotic regulation. Accumulate ions and swell with water.
What is the groos morphology of cerebral edema
Flattened Gyri
Narrowed, compressed Sulci
Compressed, small ventricles
What is the pathologic consequence of brain edema?
How does it cause damage to the CNS?
Brain herniation is the major risk.
Three types:
- Subfalcine
- Transtentorial
- Tonsillar
Herniation causes cell death due to compromised blood supply, ie, the herniated tissue becomes infarcted.
What are regions are damaged by each of the 3 types of herniation, and what are the causes of each type?
Subfalcine herniation
- Caused by unilateral or assymetric swelling of the cerebral hemispheres. (epidural hematoma, very rapid. Subdural hematoma, slow, over days to weeks)
- Pushes the cingulate gyrus under the falx, compresses the anterior cerebral artery, causing ischemic infarct of the anterior cerebrum.
Tentorial herniation
- When the medial side of the temproal lobe is pushed into the free margin of the tentorium cerebelli
- This has the notable neurologic sign of compressing CN 3 oculomotor nerve.
- Causes an ipsilateral pupil dilation ‘blown pupil’ and impaired movement of that eye.
- It may also compress the posterior cerebral artery, resulting in ischemic infarction of the occipital lobe and visual cortex
Tonsillar herniation
- Displacement of the cerebellar tonsils through the foramen magnum
- Is immediately life threatening, due to brain stem compression of the medullary respiratory and cardiac centers.
What are the types/classifications of hydrocephalus?
Communicating hydrocephalus:
- There is no blockage of CSF flow or interuptions in the ventricular system.
- Caused by decreased CSF reabsorption in the arachnoid granulations
- Idiopathic
- Meningitis
- Can result from scarring due to previous infection,
- Causes general dilation of the entire ventricular system
Non-communicating hydrocephalus:
- When there is a localized obstruction
- Causes dilation in one specific part.
- Caused by masses obstructing the interventricular foramen of Monro or the Cerebral Aqueduct.
Hydrocephalus ex vacuo
- Generalized dilation of the ventricles and increased CSF around the brain, compensating due to generalized or local areas of brain atrophy and degeneration.
Hydrocephalus internus
- expansion of the ventricles
- expansion of the CSF surrounding the brain, compressing the brain (generalized brain atrophy of hydrocephalus ex vacuo)
Pesentation and Symptoms of hydrocephalus,
Treatment
In infants, prior to suture closure, the
- rapid expansion of the head
- vomiting, seizures
- sleeping, fatigue
In adults
- Headaches
- double vision
-
Hakim’s triad:
- gait ataxia
- urinary incontinence
- mental impairment/dementia
- Focal neurologic deficits
Treatment:
Surgical shunt procedure draining the CSF into the abdominal cavity.
