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MED SURG- ICP

Terms in this set (45)

intracranial pressure
the amount of pressure inside the skull
-brain tissue= 78%
-blood= 12%
-CSF= 10%
factors that influence ICP
-arterial pressure
-venous pressure
-intraabdominal and intrathoracic pressure
-posture
-temperature (fever)
-ABGs (specifically CO2 levels)
-hypertension (headaches due to increased pressure)
Monro-Kellie doctrine
if one component increases, another must decrease to maintain ICP (like blood tissue and CSF)
when ICP increases, brain gets compressed and cells cant work anymore
ICP values
5-15mmHg
normal compensatory adaptions
1. changes in CSF volume (CSF will drain into spinal column to compensate for too much pressure in the brain)
2. Changes intracranial blood flow (will vasoconstrict to decrease blood flow if too much pressure)
3. changes in brain tissue volume (brain tissue will smush and compress)
When ability to compensate is limited...
volume increase continues, ICP rises and brain decompensates which will lead to ischemia
Cerebral blood flow (CBF)
-amount of blood in mL passing through 100g of brain tissue in 1 minute
-autoregulation
brain needs a certain amount of blood to function the right way
autoregulation
-adjusts diameter of blood vessels
-ensures consistent CBF (metabolic needs of brain tissue, maintain CPP)
-only effective if mean arterial pressure (MAP) is 70-150mmHg
What happens if there is too much ICP?
If there is too much ICP, the brain compresses and CSF goes the path of least resistance to the brain stem or respiratory tract
MAP
amount of pressure to get blood to the organs
*if MAP is 65 and ICP is 15, then CPP is 50 which is too low*
cerebral perfusion pressure (CPP)
CPP = MAP - ICP
*to increase CPP, increase MAP*
normal CPP values
-less than 50mmHg is associated with ischemia and neuronal death
-less than 30mmHg is incompatible with life
how to increase MAP
you want to increase MAP if you want to increase CPP
give them vasopressor to vasoconstrict
drain CSF to being ICP down
factors affecting cerebral blood vessel tone
1. CO2:
increase= cerebrovascular dilation (increase risk of increased ICP)
decrease= cerebrovascular constriction (less blood flow to the brain but less ICP)
2. O2:
decrease= cerebrovascular dilation and anaerobic metabolism (hyperventilate to decrease ICP because it blows off CO2)
Increased ICP
-life threatening
-increase in any of the 3 components: blood, brain tissue and CSF)
-increase in cerebral edema
causes of increased ICP
1. mass: hematoma, hemorrhage, contusion, abscess, tumor
2. cerebral edema: tumor, hydrocephalus, head injury, brain inflammation, brain anoxia or ischemia
cerebral edema
-increase extravascular fluid in brain
-variety of causes (mass, tumor, head injury)
-3 types
3 types of cerebral edema
1. vasogenic (bad)
2. cytotoxic (no breakdown in BBB-hypoxia)
3. interstitial (hydrocephalus)
hydrocephalus
accumulation of fluid in the spaces of the brain
ICP s/s
*change in LOC!!* (most reliable indicator of a patient's neuro status and a flattening affect)
change in vitals (Cushing's triad and body temp)
-ocular signs (compressed CNIII)
-impaired swallowing and gag reflexes
-decrease in motor function
-headache (continuous and worse in the morning)
-vomiting (no nausea, PROJECTILE)
-impaired brain stem reflexes
Cushing's Triad
1. systolic hypertension with a widening PP
2. bradycardia with pounding pulses
3. irregular respirations
widening PP
widening difference between systolic and diastolic numbers (ex: 202/50)
ocular s/s of increased ICP
-ipsilateral pupil dilation
-sluggish or no response to light
-inability to move eye upward, adduct
-eyelid ptosis
-fixed unilateral dilated pupil
decorticate
-cerebral cortex impairment
-wrist together on chest and legs stretching out
decerebrate
-midbrain and brainstem impairment
-poor prognosis
-hyperproning
cerebral herniation
-inadequate cerebral perfusion
-CSF moves to the path of least resistance and herniates towards the midbrain
diagnostic studies
-CT scan/MRI/PET
-EEg
-cerebral angioplasty
-ICP and brain tissue oxygenation measurement (LICOX cath)
-doppler and evoked potential studies
-NO LUMBAR PUNCTURE
Glasgow Coma Scale
highest score (good)= 15
lowest score (bad)= 3
3 indicates no response whatsoever
"he went from a 13 to a 5" is an indication of increased ICP
ICP monitoring devices
-subarachnoid (burr holes)
-ventricular (more common, fed through ventricle and shows increased volume that isn't supposed to be there)
-subdural (burr holes)
-epidural (below bone above brain in dura)
-intraparenchymal (in tissue, not used today)
Ventriculostomy
Gold standard for monitoring ICP
-catheter inserted into lateral ventricle
-coupled with an external transducer
-can be done at bedside or in OR
leveling a ventriculostomy
level to tragus of ear where "foramen of monro" is
measurement of ICP
-measure as a mean pressure (monitor over time)
-waveform should be recorded
-prevent and monitor for infection (ASEPTIC!!)
-transducer shows the increase pressure on the monitor
-evaluate changes with patient condition
-can control ICP by removing CSF (not too much!)
-intermittent or continuous drainage
inaccurate readings of ICP are caused by:
CSF leaks
obstruction in catheter or kinks in tubing
differences in height of bolus/transducer
incorrect height of drainage system
bubbles/air in tubing
*treat patient, not number on screen*
interprofessional care
-treat underlying cause first!
-support brain function
-adequate oxygenation
-surgery
drug therapy
-mannitol
-hypertonic 3% saline
-corticosteroids
-ant seizure meds
-antipyretics
-sedatives and analgesics (manage agitation)
-barbituates
-IV NaCl over NSS
mannitol
-decreases ICP
-plasma expansion
-osmotic effect (diuretic)
-monitor fluid and electrolyte status
hypertonic 3% saline
-moves water out of cells and into blood
-monitor BP and serum sodium levels
corticosteroids
-vasogenic edema
-helps improve cerebral blood flow
-monitor fluid intake
-monitor serum sodium and glucose levels
-concurrent antacids, H2 receptor blockers and proton pump inhibitors
nutritional therapy
1. hypermetabolic and hypercatabolic state so increased need for glucose!!
2. enteral or parenteral nutrition
3. early feeding (within 3 days of injury)
4. keep patient normovolemic
nursing assessment for increased ICP
1. LOC (glasgow coma scale)
2. cranial nerves
3. motor strength (pronator drift test)
4. motor response
5. vital signs
Nursing Goals/Planning
1. maintain paten airway
2. ICP within normal limits
3. normal fluid and electrolyte balance
4. prevent complications secondary to immobility and decreased LOC
Respiratory function
1. maintain patent airway
2. elevate HOB 30 degrees (helps to drain)
3. suctioning PRN and only for less than 10 seconds
4. minimize abdominal distention
5. monitor ABGs
6. maintain ventilary support
*DO NOT CLUSTER CARE*
Pain and anxiety management
1. opioids
2. propofol (awake but calm)
3. dexmedtomidine (arousable but sleeping)
4. neuromuscular blocking agents (paralyzing)
5. benzodiazepines (don't wear off quickly so we do not use often, especially in older adults)
Fluid and electrolyte balance
1. monitor IV fluids
2. daily electrolytes
3. monitor for DI or SIADH
4. monitor and minimize increases in ICP
**diabetes insipidus can increase ADH and can cause herniation and urine output from 30mL/hr to 100mL/hr)
Interventions to optimize ICP and CPP
HOB elevated appropriately
Prevent extreme neck flexion
Turn slowly
Avoid coughing, straining, Valsalva
Avoid hip flexion
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