Increased intracranial pressure and herniation Flashcards
Glasgow coma scale
What is decorticate posturing
Mechanism and clinical signs of Subfalcine herniation
Mech and signs of Transtentorial-Uncal herniation
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
Mech and signs of Transtentorial-Central herniation
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
Mech and signs of tonsillar herniation
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
Types of herniations
What is cerebral perfusion pressure
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.
Normal intracranial pressure
ormal intracranial pressure (ICP) is 5-15 mm Hg and typically mirrors jugular venous pressure
causes of elevated intracranial pressure
Trauma, Large ischemic stroke, intracranial hemorrhage, hydrocephalus, diffuse cerebral edema, brain neoplam
Relationship between bp and intracranial pressure
As the ICP rises, blood pressure elevates as a compensatory reflex to try to maintain adequate cerebral perfusion pressure.
symptoms of increased intracranial pressure
Headache, nausea, vomiting, papilledma in an awake patients and may progress to coma over time.
What is the Monroe-Kellie doctrine?
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.
When does ischemia occur
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.
Management of Increased Intracranial Pressure
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
What type of surgical interventions can be done for increased intracranial pressure?
Decompressive hemicraniectomy, hematoma evacuation, ventricular intracranial pressure monitor
When is hyperosmolar therapy suggested
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
Management of vasogenic edema
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.
Use of mannitol
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.
Use of hypertonic saline
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.
Use of hyperventilation
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.
What is the cushings triad
Bradycardia, bradypnea, hypertension
