ICP + TBIs Flashcards
brain metabolic activity
20% of cardiac output
25% of total body glucose
autoregulation
ability of brain to maintain a constant perfusion despite wide variations in blood pressures
ensures cerebral blood vessels dilate in response to a perceived increase in requirements
MonroKellie Hypothesis
intracranial volume (VIC) = brain volume + blood volume + CSF volume + lesion volume
cerebral perfusion pressure (CPP)
CPP = MAP-ICP
normal CPP = 50-60
normal MAP
60-90
normal ICP
5-15
low CPP
CPP < 40-50 leads to hypoxia of cerebral tissue and loss of autoregulation
increased ICP results in
decreased CPP
primary causes of IICP
brain tumor trauma nontraumatic cerebral hemorrhage ischemic stroke hydrocephalus post operative cerebral edema meningitis
secondary causes of increased ICP
airway obstruction hypoxia/hypercarbia HTN/hypotension position hyperthermia seizures metabolic disorders (hyponatremia)
hourly neuro assessment includes
GCS
pupillary response to light
motor function
vitals
GCS
assesses level of consciousness, motor response to stimulus
reliable if it has been obtained prior to intubation or sedating medications
GCS categories
eye opening (4) motor response (6) verbal response (5)
GCS values
13-15 mild/no brain injury
9-12 moderate brain injury
< 8 severe brain injury
causes of small pupils
bright room
glaucoma meds
opiates
damaged pons
causes of dilated pupils
fear
anxiety
cocaine use
brainstem compression
blown pupil
> 4mm
3 types of downward herniation
uncal
central
tonsillar
Cushing response triad
bradycardia
hypertension (widened pulse pressure)
respiratory variation
suspected herniation requires immediate response
indications for ICP monitoring
severe head injury with GCS 3-8 subarachnoid hemorrhage hydrocephalus brain tumor stroke meningitis
leading causes of TBI
falls
MVCs
assaults
sports related injury
TBI patho
direct damage to cerebral parenchyma and axonal injury 2/2 impact to the head
concussion
caused by sudden deceleration of brain against the skull
not associated with underlying parenchymal damage
MBI sx
amnesia headache anxiety dizziness fatigue
cerebral contusions and diffuse axonal injuries
often result of acceleration/deceleration injuries
contusions
brain accelerates against fixed skull
disruption of underlying cerebral parenchyma and blood vessels
brain may recoil and impact skull on opposite side
coup/countercoup injury
cerebral edema develops in 24-72 hrs
may result in IICP
diffuse axonal injuries
deceleration and shearing between different densities of white and grey matter in the brain
graded from I-III
linear skull fracture
nondisplaced
occur from low velocity impact
depressed skull fracture
depression of bone at point of impact
may be closed or open
basilar fractures
occur at base of skull
vascular injuries
may result from bleeding of arteries and veins between the brain and the skull or in the brain tissue
bleeding that occurs between the brain and the skull is a surgical emergency !!!
epidural hematoma
bleeding between dura mater and skull associated with skull fx 2/2 laceration in middle meningeal artery develops rapidly requires surgical evacuation
epidural hematoma sx
initial LOC
lucid interval
sudden re-LOC
rapid deterioration in neurologic status
subdural hematomas
usually 2/2 countercoup injuries and a venous bleed
classified as acute, subacute, and chronic
acute subdural hematoma
develops within 24-48 hrs of injury initial LOC followed by deteriorating GCS hemiparesis dysphagia IICP requires evacuation
subacute subdural hematoma
develops days-weeks following injury
clot usually liquefies
evacuation is on an elective basis
chronic subdural hematoma
more common in older adults
develops weeks after injury
nonspecific sx (headache, confusion, speech deficits)
may require burr holes for drainage
subarachnoid hemorrhage
bleeding between arachnoid and pia mater
can be traumatic or 2/2 preexisting aneurysm
factors that predict death/disability for severe TBI
age GCS prior to intubation pupillary size/reaction to light presence of extracranial injury CT findings presence of hypotension
severe TBI collaborative care
early intubation transport fluid resuscitation CT scan immediate evacuation of mass/lesion ICU care with ICP monitoring
TBI oxygenation and perfusion
maintain PaO2 >60, SpO2 >90 positioning, supplemental O2 avoid hypercarbia (increases ICP)
TBI sedation and pain relief
agitation + pain increase BP and ICP
benzos (except midazolam) for sedation
propofol decreases ICP and can be titrated for neuro assessments
morphine for pain
osmotherapy
can decrease ICP
mannitol (diuretic)
hypertonic saline
CSF drainage
intraventricular catheter and a pressure transducer can drain
negligible effects on cerebral blood flow
should lower ICP immediately
high dose barbiturate therapy nursing considerations
used for refractory IICP assess for: hypotension continuous ICP monitoring mechanical ventilation pneumonia ileus protect corneas
therapeutic hypothermia
AKA target temperature mgmt
decreases ICP
prevent shivering
adverse effects: arrhythmias, coagulopathies, pulmonary infection, electrolyte imbalances, hypothermia induced diuresis
decompressive craniectomy
may be used in conjunction with duroplasty
indicated if continuous deterioration and s/s herniation
maintain adequate cerebral perfusion and oxygenation
TBIs and seizures
risk factors: GCS < 10 cortical contusion depressed skull fx subdural, epidural, or intracranial hematomas penetrating head wounds a seizure within 24 hrs post injury
TBIs and nutrition
TBI pts have increased metabolic needs
TBI increases metabolic rate to 120-240% of expected
begin enteral feedings within 72 hrs
monitor blood glucose 80-120
TBI complications
pneumonia
ARDS
DVT
sodium imbalance
TBI recovery predictive factors
duration and severity of coma
duration of posttraumatic amnesia
location/size of contusions and hemorrhages in brain
other injuries
earliest sign of increasing ICP
change in level of consciousness
slowed speech, delayed responses to verbal suggestions
vitals changes with IICP
increased systolic pressure widened pulse pressure decreasing HR wide fluctuations in HR hyperthermia
late s/s IICP
Cushing triad (bradycardia, HTN, bradypnea)
projectile vomiting
deterioration of LOC
hemiplegia, decortication, decerebration, flaccidity
Cheyne-Strokes respirations
loss of reflexes (pupil, gag, corneal, swallowing)
IICP nursing dx
ineffective airway clearance ineffective breathing pattern ineffective cerebral perfusion deficient fluid volume r/t fluid restriction risk for infection r/t ICP monitoring
IICP complications
brainstem herniation
diabetes insipidus
SIADH
pt goals
maintain patent airway normalize respirations adequate cerebral tissue perfusion fluid balance absence of infection absence of complications
IICP interventions
elevate HOB to 60 degrees to promote venous drainage
frequent respiratory assessment and maintain patent airway
maintain calm atmosphere
monitor fluid status every hour I&O
use strict aseptic technique for ICP monitoring system
IICP things to avoid
hip flexion
valsalva maneuver
abdominal distention
any stimuli that may increase ICP
craniotomy
opening of skull to remove tumor, relieve IICP, evacuate clot, control hemorrhage
craniectomy
remove portion of skull
cranioplasty
repair of cranial defect using a plastic or metal plate
Burr holes
circular openings for exploration or diagnosis to provide access to ventricles or for shunting procedures , to aspirate a hematoma or abscess, or make a bone flapp
preoperative care for cranial surgery
corticosteroids, fluid restriction, mannitol/diuretics to reduce cerebral edema
abx
diazepam
pt care after cranial surgery
monitoring of respiratory fxn frequent vitals/LOC assess dressing for bleeding/CSF drainage monitor for potential seizures monitor fluid status
cranial surgery nursing dx
ineffective cerebral tissue perfusion risk for imbalanced body temperature potential for impaired gas exchange disturbed sensory perception body image disturbance impaired communication (aphasia) risk for impaired skin integrity impaired mobility
maintaning cerebral perfusion actions
monitor respiratory status to prevent hypoxia/hypercapnia
vitals q15 min
strategies to reduce cerebral edema (peaks 24-36 hrs)
avoid extreme head rotation
