5-4. INTRACRANIAL PRESSURE (ICP)

a. Changes Caused by Intracranial Pressure. A patient with head injury may experience an alteration in his level of consciousness. Other symptoms associated with a severe head injury may include convulsions, delirium, coma, paralysis, and increased intracranial pressure, which will be discussed here. The skull (a container that cannot expand) holds the brain, vascular tissue, and cerebrospinal fluid. Any problem (trauma, edema, tumor, infection, or bleeding) which adds to the contents of the skull will result in an increase in intracranial pressure in the skull. That increased pressure sets off the changes listed below:

(1) As the intracranial pressure increases, the blood vessels are squeezed from the outside, restricting blood flow throughout the arteries.

(2) As the brain notes a drop in blood pressure, the sympathetic defenses respond, causing the blood pressure to increase.

(3) Respiratory changes occur due to the chemoreceptors that sense changes in the blood chemistry.

(4) The vagus nerve is affected, causing the pulse to slow.

(5) Cushing's response - Increased blood pressure characterized by slow pulse. This is a clear but late sign of increased intracranial pressure.

(6) As the intracranial pressure progresses, the level of consciousness is altered. Eventually, unconsciousness occurs because the body's vital functions cannot operate properly. Ultimately, there is brain death due to loss of adequate cerebral perfusion (passage of fluid through the brain).

(7) Once the brain's ability to compensate is exhausted, the areas of the brain shift, causing herniation.

NOTE: Compression may be from above (central syndrome) or from the side (lateral syndrome). The central syndrome progresses in a more orderly manner and causes unconsciousness early.

b. Progressive Levels of Intracranial Pressure. Three progressive levels of intracranial pressure can be identified.

(1) Progressive level one.

(a) Involves cerebral cortex and upper brain stem.

(b) Blood pressure rises, pulse slows.

(c) Pupils appear small but are reactive.

(d) Abnormal respiratory pattern noted (possibly Cheyne-Stokes).

(e) Initially, patient will try to remove painful stimuli. Later, the patient withdraws from pain.

(f) As progression occurs, the pain will cause decorticate posturing (flexion of the upper extremities with lower extremities becoming rigid and extended).

(g) Still reversible.

(2) Progressive level two.

(a) Middle portion of the brain stem is involved.

(b) Blood pressure increases.

(c) Pulse slows.

(d) Pupils become fixed at 3 to 5 mm and nonreactive or only sluggishly reactive to light.

(e) Abnormal respiratory pattern: fast, shallow panting (neurogenic hyperventilation).

(3) Progressive level three.

(a) Pupils become fixed and dilated.

(b) If only one "blown" pupil, it will be on the same side as the hematoma or swelling. (Crossover of nerves occurs at about the lip level.)

c) Document which pupil dilates first.

(d) Respiratory ataxia (erratic, no rhythm) or absent. No response to painful stimuli.

(e) Pulse is rapid and irregular.

(f) Decreased blood pressure.