Elevated intracranial pressure

Increased intracranial pressure common in neurological insults including intracranial hemorrhage, traumatic brain injury, brain tumors, and strokes.

Almost all acute and catastrophic brain diseases increase intracranial pressure.

Intracranial hypertension can be a medical or surgical emergency.

Traumatic brain injury, intracerebral and extracerebral hematomas, cerebral infarction, and brain swelling associated with liver failure, and brain tumors associated with increased ICP.

Elevated intracranial pressure consistently associated with poor outcomes.

10 to 15% of traumatic brain injuries are severe, and most are associated with raised intracranial pressure.

The rate of death is 18.4% for patients with traumatic brain injury and increased intracranial pressure of less than 20 mmHg and 55.6% of those within intracranial pressure for more than 40 mmHg.

May int2242upt cerebral blood flow, and brain herniation with disability and death.

Requires serial examination to permit detection of progression of the process to prevent herniation and death.

Can cause shift of the brain.

Brain composed of noncompressible tissue and it is perfused by CSF and blood which are also noncompressible and they lie within the rigid skull.

Because the skull is essentially a fixed vault, any increase in brain volume results in increased intracranial pressure.

Expansion of intracranial components of the brain including intravascular blood and CSF, must be at the expense of a reduction in another component, this is ref2242ed to as the Monro-Kellie hypothesis.

In a response to increased brain volume, CSF is initially forced from the cranial subarachnoid spaces and lateral ventricles into the spinal subarachnoid space.

As this compensatory mechanism fails, pliable blood vessels are compressed and cerebral blood flow is reduced.

An intracranial pressure of 50 to 60 mmHg approaches the arterial pressure in the vessels of the circle of Willis and brings about global brain ischemia, the end of which results in brain death.

Within the cranium pressure-volume relationships approximate and exponential curve, with in the inflection point ranging from 20-25 mmHg in adults, and a lower range in children due to the higher ratio of brain volume to intracranial volume.

Therefore the goal of care is to keep intracranial pressure below these levels.

Brain parenchyma is 80% water, making brain volume very responsive to changes in water content.

When increased intracranial pressure occurs in the cerebral hemisphere results from a mass or edema the midline structures, subfalcine and uncus, are downwardly displaced and the manifestations are decreased consciousness, ipsilateral third cranial nerve palsy, and contralateral hemiplegia.

Posterior fossa lesions with compression of the medulla may be associated with impaired consciousness, hypertension, bradycardia and increased risk of sudden death from respiratory or cardiac arrest.

Cerebral perfusion pressure is equal to the mean arterial pressure minus the pressure in the cerebral veins and subarachnoid space.

Increased mean arterial pressure increases the cerebral perfusion pressure.

Reductions in the mean arterial pressure decreased cerebral perfusion pressure.

When cerebral perfusion pressure decreases the cerebral arterioles dilate to maintain cerebral blood flow and delivery of oxygen and nutrients.

When cerebral perfusion pressure increases, blood vessels constrict and keeps the cerebral blood flow stable, the process known as autoregulation.

Autoregulation may be impaired with brain trauma and a fall in cerebral perfusion pressure below 60 mm Hg leads to brain ischemia.

Cerebral perfusion pressure is a marker for cerebral blood flow and the former is measured by the presence of an intracranial pressure monitor.

Management includes; elevating the head of the bed to 30 degrees or greater, avoiding jugular vein compression, avoiding hypercapnea which causes vasodilatation and increases intracranial pressure, avoid agitation and use of mannitol intravenously at 0.75-1.5 mg/kg.

The effectiveness of an osmolar agent in creating water egress from the brain depends on the extent to which the solute is excluded by the blood brain barrier.

Hyperosmolar therapy benefit requires an intact blood brain barrier.

In areas of brain tissue damage, such as seen in traumatic contusion brain injuries, the blood brain barrier is disrupted and allows equilibration of molecules between blood and the interstitial fluid of the brain.

Hyperosmolar agents exert their effect largely by removing water from the remaining normal brain tissue, and such therapy reduces intracranial pressure pressure in proportion to the volume of undamaged brain tissue.

Hyperosmolar therapy has limited effect on brain edema surrounding a mass lesion.

With hyperosmolar therapy most of the reduction in brain volume occurs during and soon after the maximal osmolarity is induced by the infusion of a hyperosmolar agent.

Sustaining the reduction in intracranial pressure depends on maintaining serum hyperosmolarity with the hyperosmolar agent.

The brain accommodates to serum hyperosmolarity by increasing intracellular solute concentrations.

Sodium has a reflection coefficient of 1.0 making it an ideal agent for inducing an osmotic gradient between blood and brain tissue.

Mannitol has a reflection coefficient of 0.9 and is a highly effective agent in reducing brain water content.

Mannitol lowers blood viscosity causes a reactive constriction of cerebral conductance vessels, and reduces intracerebral blood volume and intracranial pressure.

As hypercapnia raises intracranial pressure by causing vasodilation, noninvasive positive pressure ventilation may be helpful or intubation may be necessary.

Efforts to prevent coughing or vomiting to prevent further elevation of intracranial pressure.

Monitoring of ICP is standard of care in patients with severe traumatic brain injury, however it lacks efficacy.

In a controlled trial of patients with traumatic brain injury, with care focused on maintaining monitored ICP at 20 mm Hg or less, there was no superiority to care based on imaging and clinical examination (Chesnut RM et al).

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