Increased intracranial pressure and herniation

Question 1

Glasgow coma scale

Answer 1

Question 2

What is decorticate posturing

Answer 2

Question 3

Mechanism and clinical signs of Subfalcine herniation

Answer 3

Question 4

Mech and signs of Transtentorial-Uncal herniation

Answer 4

Mech: Uncus of temporal lobe pushes downward causing compression of the midbrain against the tentorial notch

Sign: Ipsilateral fixed blown pupil, ophthalmoplegia, contralateral hemiparesis, decerebrate posturing, diminished level of consciousness

Question 5

Mech and signs of Transtentorial-Central herniation

Answer 5

Mech: Downward displacement of the cerebral hemispheres compressing the diencephalon and midbrain against the tentorial notch

Signs: Fixed mid-position pupils, early coma, decorticate posturing, Cheyne-Stokes respirations, central DI

Question 6

Mech and signs of tonsillar herniation

Answer 6

Mech: Cerebellar tonsils push downward through the foramen magnum, causing compression of the medulla and superior cervical spinal cord

Signs: Cushing’s Triad (erratic bradypnea, bradycardia, hypertension), respiratory arrest, coma, bilateral arm numbness/parasthesias

Question 7

Types of herniations

Answer 7

Question 8

What is cerebral perfusion pressure

Answer 8

cerebral perfusion pressure = mean arterial pressure - intracranial pressure

Falls in cerebral perfusion pressure may result in brain ischemia and neuronal death. Cerebral perfusion pressure crisis occurs when the pressure is <60 mm Hg.

Question 9

Normal intracranial pressure

Answer 9

ormal intracranial pressure (ICP) is 5-15 mm Hg and typically mirrors jugular venous pressure

Question 10

causes of elevated intracranial pressure

Answer 10

Trauma, Large ischemic stroke, intracranial hemorrhage, hydrocephalus, diffuse cerebral edema, brain neoplam

Question 11

Relationship between bp and intracranial pressure

Answer 11

As the ICP rises, blood pressure elevates as a compensatory reflex to try to maintain adequate cerebral perfusion pressure.

Question 12

symptoms of increased intracranial pressure

Answer 12

Headache, nausea, vomiting, papilledma in an awake patients and may progress to coma over time.

Question 13

What is the Monroe-Kellie doctrine?

Answer 13

There is a fixed total intracranial volume made up of several partial volumes. Any increase in one volume compartment requires a decrease in the others. It is expressed with the following formula:

V intracranial = V brain + V blood + V csf + V x

Where Vx represents some unknown volume, such as a mass lesion, abscess, edema, hygroma, or foreign object. To accommodate a new volume, one of the other components must be displaced. CSF exits through the arachnoid granulations in to the venous sinuses first as a temporary measure.

Question 14

When does ischemia occur

Answer 14

Normally, cerebral blood flow is held constant by a mechanism of cerebrovascular autoregulation. However, with acute brain injury, the ability to autoregulate can be lost. If cerebral blood flow drops below 20 mL/100g/min, ischemia can ensue.

Question 15

Management of Increased Intracranial Pressure

Answer 15

Airway monitoring

Breathing monitoring

Cerebral perfusion pressure optimization: ICP<20 and CPP>65

Osmotherapy with either mannitol or hypertonic saline

Sedation

Hypothermia (reduces cerebral metagolism and cerebral blood flow)

Neurosurgical intervention

Question 16

What type of surgical interventions can be done for increased intracranial pressure?

Answer 16

Decompressive hemicraniectomy, hematoma evacuation, ventricular intracranial pressure monitor

Question 17

When is hyperosmolar therapy suggested

Answer 17

For lesions producing cytotoxic edema in which the blood-brain barrier is relatively preserved (like with ischemic stroke, subdural or epidural hematomas)

Hyperosmotic therapy is effective ONLY for symptomatic management or for measured intracranial pressure >30 cmH2O

Question 18

Management of vasogenic edema

Answer 18

steroids are recommended for reduction of intracranial pressure. It is thought that steroids tighten the gaps between epithelial cells in capillaries, leading to reduced fluid leak from the intravascular to intercellular space.

Question 19

Use of mannitol

Answer 19

Mannitol works as an osmotic diurectic and increases the serum osmolality. This removes brain water to reduce ICP and increases cerebral blood volume. It is widely available and easy to administer through a peripheral IV.

Cons include electrolyte depletion (potassium), volume depletion, and possible transient volume overload (by adding to the circulating blood volume) for those with severe congestive heart failure. Those with end stage renal disease cannot excrete it.

Question 20

Use of hypertonic saline

Answer 20

This does not work as a diuretic likely mannitol (therefore, volume depletion is not a major adverse effect), but may increase total body sodium. It does create an osmotic gradient between the serum and the intracranial compartment to reduce ICP.

Question 21

Use of hyperventilation

Answer 21

Hyperventilation is used as a temporary intervention. Carbon dioxide is a potent vasodilator and can increase ICP. Hyperventilation decreases carbon dioxide and therefore reduces ICP but the vasoconstriction can cause ischemia. Goal is PaCO2 of 32-34 mm Hg.

Question 22

What is the cushings triad

Answer 22

Bradycardia, bradypnea, hypertension