PATHOPHYSIOLOGY
In adults, the rigid cranial cavity created by the skull is normally filled with three essentially noncompressible elements: the brain (85%), CSF (5%), and blood (10%). |
A state of dynamic equilibrium exists. |
If the volume of any of these components ↑, the volume of the others must ↓ to maintain normal pressures in the cranial cavity. |
Monro-Kellie hypothesis: If volume ↑ in any of brain, CSF, or blood → volume of others must ↓ |
ETIOLOGY
Brain requires constant supply of oxygen and glucose If blood flow interrupted → ischemia, disruption of cerebral metabolism. |
Compensatory mechanisms to maintain blood flow when ICP increases |
‣ Pressure autoregulation |
‣ Chemical autoregulation |
‣ Displacement of some CSF to spinal subarachnoid space |
‣ Increased CSF absorption |
Autoregulatory mechanisms have limited ability to maintain cerebral blood flow |
CAUSES
Head injury |
Cerebral edema |
Hydrocephalus |
‣ Imbalance between production/absorption of CSF |
Excess CSF |
‣ Congenital or acquired |
Brain tumor or abscess |
‣ ‣ Head trauma |
Intracranial hemorrhage |
‣ ‣ Infection |
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‣ ‣ Tumor |
COLLABORATION
Identify and treat underlying cause |
Control ICP to prevent herniation syndrome |
ICP >40 mmHg = life-threatening medical emergency |
Diagnosis made on basis of observation, neurologic assessment |
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Diagnosis made on basis of observation, neurologic assessment |
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CLINICAL MANIFESTATIONS
Loss of autoregulation |
• ICP continues to rise, cerebral perfusion falls |
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• Causes cerebral tissue ischemia, manifestations of cellular hypoxia |
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Changes in cortical function |
Earliest manifestations may be delayed by compensatory measures |
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• If slow onset of IICP, decrease in level of consciousness (LOC) might not be presenting symptoms Instead visual disturbances, vomiting, or headache |
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• Lumbar puncture could cause brain herniation |
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• Cushing triad |
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• Behavior, personality changes |
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• Impaired memory, judgment |
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• Changes in speech pattern |
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• LOC decreases to coma, death |
DX TESTS
Diagnosis made on basis of observation, neurologic assessment |
Lumbar puncture not performed when IICP suspected |
Release of pressure could cause herniation |
Serum osmolality, arterial blood gases (ABGs) |
Electroencephalogram (EEG) may be used to monitor depth of coma or to diagnose brain death |
Transcranial Doppler (TCD) to measure cerebral blood flow velocity |
Especially for patients who have vasospasms related to cerebral hemorrhage |
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ASESSMENT
Observation and patient interview |
- LOC using GCS |
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- Any loss of motor control |
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- Primary complaints |
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- Events leading up to current condition |
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- Basic medical hx |
Physical examination |
- Assessment of neurologic status |
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- Pupillary size, reaction to light |
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- V/S, incl. temp. |
Ongoing monitoring |
- Assess for, report manifestations of IICP every 15–60 minutes |
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- Look for trends |
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- Sudden changes may indicate deterioration |
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- Subtle change may be early sign of declining neurologic condition |
Monitor pulse oximetry, ABGs |
If device to monitor IICP is in place |
- Recording readings |
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- Assess patency of catheter |
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- Monitor insertion site for s/s of infection |
IMPLEMENTATION
Ensure adequate oxygenation |
Reduce intracranial pressure |
Reduce environmental stimulation |
Reduce environmental stimulation |
Prepare patient and family for discharge |
EVALUATION
Expected outcomes may include |
- Patient’s ICP returns to acceptable limits following treatment |
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- Patient’s LOC improves with reduction of ICP |
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- Patient experiences no infection as result of ICP monitoring |
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- Family describes appropriate outcome expectations |
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- Patient and family institute, maintain adequate safety measures after discharge |
Some patients require days, weeks, or months of monitoring for ICP changes |
- Reassess plan of care to be relevant to patient’s current condition |
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