9.4 · General effects: Increased intracranial pressure

Increased intracranial pressure (IICP)

Rise in pressure from anything taking up volume in the brain, such as a tumour, hemorrhage, edema, or excess CSF

Monro-Kellie hypothesis

To adjust for increased pressure there must be a reduction in another cranial content: blood volume, CSF volume, or tissue volume

First compensation for rising ICP

Loss of CSF, as it is most easily decreased

ICP Stage 1

May be asymptomatic; CSF displaced into spinal subarachnoid space with increased reabsorption, and blood removed by external compression of the venous system

Limit on blood buffering in ICP Stage 1

Increased carbon dioxide in brain tissue causes vasodilation

ICP Stage 2

Significant decrease in perfusion of brain tissue and hypoxia, resulting in confusion, restlessness, and drowsiness

Cushing's reflex

Vasomotor center neurons cause systemic vasoconstriction, increasing systemic blood pressure to overcome decreased flow in the brain

ICP Stage 3

ICP begins to equal mean arterial pressure; hypoxia and hypercapnia cause rapid deterioration with decreased arousal, small sluggish pupils, and hyperventilation; all compensatory mechanisms are used up

ICP Stage 4

Herniation: brain is squeezed across structures to lower-pressure compartments including the tentorium and foramen magnum

End point of herniation

ICP equals systolic arterial pressure, cerebral blood flow ceases, causing death

Clinical manifestations of herniation

Coma, fixed dilated pupils, death

Uncal herniation signs

Ipsilateral pupil dilation, hemiparesis, visual field loss, respiratory arrest, and decreased consciousness

Cerebral edema

Increase in fluid content causing an increase in brain tissue volume; occurs after trauma, infection, hemorrhage, tumour, ischemia, infarct, or hypoxia

Effects of cerebral edema

Distorts blood vessels, displaces brain tissues, and causes herniation

Vasogenic edema

Increased permeability of the blood-brain barrier lets plasma proteins leak from capillaries, increasing tissue water content; occurs mainly in white matter

Cytotoxic edema

Toxins or hypoxia cause failure of the cell transport mechanism, so more sodium and therefore more water is inside the cell; occurs mainly in gray matter

Hydrocephalus

Excess cerebrospinal fluid in the ventricles, subarachnoid space, or both, from excess production or too little reabsorption

Noncommunicating (obstructive) hydrocephalus

Blockage in the ventricular system from tumour, inflammation, or hemorrhage prevents CSF from reaching the arachnoid villi to be reabsorbed

Communicating hydrocephalus

Failure of reabsorption due to reduced number or scarring of arachnoid villi from meningitis; rarely from CSF overproduction by choroid plexus adenoma