ICP and Herniation Syndromes Flashcards
Monroe Kellie Doctrine
States that the total volume of intracranial contents is constant.
In adults, this is about 1700cc. VBrain + Vcsf + Vblood + Vmass = constant
As Vmass increases, body compensates by lowering Vcsf and Vblood (esp venous blood) - increased CSF absorption at arachnoid villae
Normal ICP
5-20cm measured by ventriculostomy
Rate of CSF formation
500cc/day in choroid plexus
4 causes of increased ICP
1) Increased intracranial volume (cerebral or extracerebral) - mass or hemorrhage
2) Acute generalized brain swelling - anoxia, hepatic encephalopathy, Reyes, hypertensive encephalopathy
3) CSF flow obstruction or impaired absorption - obstructive hydrocephalus
4) Increased CSF production - choroid plexus papilloma
General symptoms of increased ICP
HA, nausea, vomit, lethargy, visual changes
Papilledema** (all patients with increased ICP) - blurring of optic disc margins
Specific - related to anatomic consequence (types of herniation)
Subfalcine herniation
When ipsilateral cingulate gyrus is pushed under the falx cerebri to contralateral side.
This causes compression of contralateral frontal lobe and bilateral anterior cerebral arteries
This can lead to bilateral ACA infarcts presenting as leg weakness, incontinence, and mental status changes
Uncal herniation
When the uncus (medial projection of parahippocampal gyrus on basal surface of cerebellum) herniates under the tentorial notch
This causes compression of the ipsilateral posterior cerebral artery and the adjacent oculomotor nerve - causes ipsilateral mydriasis
As syndrome progresses, PCA infarcts (ipsilateral or bilateral) occur as well as complete ipsilateral oculomotor palsy
Interestingly, this syndrome can lead to an ipsilateral hemiparesis by compressing the contralateral cerebral peduncle against the tentorium at the so-called Kernohan’s notch. This is a false localizing sign as the culprit lesion causes a hemiparesis on the ipsilateral side of the body by compressing contralateral structures
Cerebellar tonsilar herniation
When increased ICP causes the cerebellar tonsils to displace inferiorly through the foramen magnum, causing medullary compression. This leads to respiratory depression and is usually a fatal event.
Treatment of elevated ICP
Through decreasing volume of intracranial contents and by increasing cerebral blood floow
1) Elevate head of bed to 30deg. This assists in CSF flow and absorption
2) Administer osmotic agent like mannitol which works immediately by increasing plasma volume, thereby increasing MAP and CBF. It also acts as osmotic diuretic drawing fluid from the cranial circulation as it does not cross the BBB. Dose related tox is renal failure.
3) Hyperventilation in intubated patient will cause immediate drop in ICP by vasoconstriction of cerebral small vessels. These vessels are exquisitely sensitive to local pH and constrict in the presence of a high pH, as in the case of decreased pCO2. Downside is that in long run, it will decrease CBF and is therefore only used in acute, emergent setting
4) Barbs - no longer routinely recommended
5) Hypothermia - maybe
6) Steroids - not used for routine reduction of ICP. They are useful only when there is a component of vasogenic edema usually in setting of a mass (tumor or abscess)
Cerebral blood flow
AKA Cerebral Perfusion Pressure
MAP minus ICP
The higher the ICP the lower the CBF
Brain elastance
Ratio of change in ICP to change in CSF volume. In normal brain, infusion of 1cc of CSF causes rise in ICP by 0-2mmHg, resulting in elastance of 1mmHg/mL
In a swollen brain that has already employed its compensatory mechanisms, the elastance can be 10-20
