Monro-Kellie hypothesis
• adult skull is rigid with a constant intracranial volume
• contents (CSF, blood, brain) are incompressible
Vbrain (glial 44%, neuronal 36%) + Vblood (10%)+ VCSF (10%) + Vlesion = Vskull (constant)
increase in one constituent/space-occupying lesion = increase in ICP
ICP < 15 mmHg (adults); 3-7 mmHg (children);
Vskull - 1400 - 1700ml (adults)
however, ICP does not rise initially due to compensatory mechanisms (autoregulation):
immediate: displacement of CSF to lumbar theca, displacement of blood from venous sinuses
delayed: displacement of ECF or ICF; displacement of brain tissue into compartments under less pressure (herniation)
Compensatory mechanisms of ↑ ICP
Displacement of CSF, blood, extracellular fluid, ICF
once compensation is exhausted, ICP rises exponentially
Intracranial volume versus pressure.
Stage 1 (compensation)
↑ in 1 of 3 vol. (blood, CSF, or tissue) → compensated by ↓ in 1 or 2 other vol. Usually ↓CSF production or ↑ reabsorption → arterial constriction (↓ blood); Sx - drowsiness, slight confusion.
Stage 2
volume continues ↑ → constricting cerebral arteries → ↓ blood flow (hypoxia and hypercapnia) - Sx ↓ of consciousness, pathologic breathing, pupillary changes.
Stage 3 (decompensation)
hypoxia and hypercapnia → arteries reflex dilation → blood volume ↑ → ↑ ICP → compresses the arterioles and capillaries → ↑hypoxia and the hypercapnia → damage to brain tissue (↑ Sx) → reflexes ↑ BP → ↑ ICP
Stage 4
↑ swelling and pressure → herniation - When ICP = sBP → cerebral perfusion stops.