brain injury Flashcards
2 categories of brain injury
primary
secondary
primary brain injury
occurs immediately at onset of brain injury
- trauma: shearing, tearing, stretching
- stroke, ischemia: necrosis
secondary brain injury
development of further neurologic damages and changes subsequent to primary injury
- leads to progressive neuro-degeneration and delayed cell death, damage some distance away form primary injury
increased intracranial pressure
normal: 0-15 mmHg
increased: acute brain injury, impaired neuro function: compression of brain.
3 components of brain volume
brain tissue
CSF
blood
- slight increase in one will be offset by a decrease in others.
common causes of increased ICP
stroke
trauma
tumor
S/S of increased ICP
HA vomiting altered LOC blurry vision -later stages: decreased pupil response altered respiratory pattern unresponsive
brain compression
complication of increased ICP
brain herniation
protrusion of brain tissue through opening in supporting dura
traumatic brain injury
characterized by severity, location, and mechanism of injury
- concussion
- contusion
- intracranial hematomes
severity of brain injury
GCS on admission or lowest in 48 hours
nontraumatic brain injury
cerebrovascular disease
cerebral aneurysm
arteriovenous malformation
CNS infection
contusion
an area of brain tissue damage
- focal injury
- polar injury
- diffuse axonal injury
focal injury
coup
localized to site of impact
polar injury
coup-countercoup
due to acceleration-deceleration movement
diffuse axonal injury
due to movement of brain within the skull
intracranial hematoma: 3 types
epidural
subdural
subarachnoid
epidural hematoma
blood between dura and skull
brief period of disturbed consciousness followed by a period of normal cognition (lucid interval) then consciousness rapidly deteriorates
-typically involves artery
subdural hematoma
blood between dura and outer layer of arachnoid membrane
-typically involves veins, onset may be slower
Acute: s/s in 24hours
Subacute: increased ICP 2-10days later
Chronic: variable presentation days to weeks later
subarachnoid hemorrhage
blood between arachnoid and pia mater
Traumatic: due to rupture of bridging veins
Nontraumatic: rupture of cerebral aneurysms or arteriovenous malformations
-blood spreads through CSF causing meningeal irritation, hydrocephalus, HA, vasospasms, ischemia
cerebrovascular disease and stroke
abnormal cerbral perfusion
- TIA
- ischemic stroke
- hemorrhage stroke
s/s of stroke
- numbness/ weakness in face, arm, leg, unilateral
- confusion, trouble talking
- visual disturbance
- dizzy. loss of balance
Transient ischemic attacks (TIA)
neuro symptoms typically last only minutes, but the may last as long as 24 hours.
-warning signs of thrombotic disease and carry a significant risk for subsequent stroke
ischemic stroke
sudden occlusion of cerebral artery secondary to thrombus or embolization
- thrombus: atherosclerosis and hypercoagualbe states
- emboli: cardiac source: a-fib
acute ischemia in brain
neuro deficit within 1 minutes
can have infarct and necrosis
hemorrhagic stroke
hemorrhage in brain parenchyma
- due to HTN
parenchyma
functional tissue
stroke Tx
assure airway, resp. status and CV function
assess neuro deficit
CT to determin ischemic or hemorrhagic
Hemorrhagic stroke tx
returning BP to normal could result in ischemia
- return to normal slowly once pt is stable
ischemic stroke tx
aspirin: affects platelet aggregation and inhibits thrombus size
thrombolytic therapy
BP management
anticoagulant therapy
Stroke sequelae
Motor:
- flaccidity or paralysis: recovery about 6wks
sensory:
- may involve neglect or visual impairment
Language
- aphasia
Cognitive deficit
- impaired language skills, spatial relationship skills, concentration, reasoning, and short-term memory
cerebral aneurysm
lesion of an artery that results in dilation and ballooning of a segment of vessel
- HTN, acute alcohol use, recreational drug use ( cocaine)
cerebral aneurysm s/s
increased ICP distorts intracranial structures secondary cerebral vasospasm (constriction around rupture) -reduced blood flow - increased ischemia, possible infarct risk for rebleed risk for hydrocephalus
cerebral aneursym tx
surgical stabilization
arteriovenous malformation
vascular lesions though to be congenital
failure of capillary system to develop, arteries shunt blood directly to veins.
- high pressure causes vessels to progressively enlarge
- risk of rupture and hemorrhage
vascular steal syndrome
abnormal shunting of blood to arteriovenous malformation results in ischemia in normal tissue
- neuro dysfunction
arteriovenous malformation tx
surgically removed
shrink with gamma radiation
bacterial meningitis
microbial invasion of CNS
most common cause: streptococus pneumoniae
usually bacterial
s/s of bacterial meningitis
headache
fever
stiff neck
cerebral dysfunction
CNS infections organisms gain acces to CNs by
hematogenous: blood
middle ear or paranasal sinuses
vertical: maternal fetal exchange
encephalitis
inflammation of the brain commonly causes by viruses -west nile -western equine - herpes simplex
treatment of encephalitis
supportive with control of symptoms antiviral steroids anti-seizure fluid resuscitation
brain abscess
localized collection of pus in brain parenchyma
-penetrating wounds
-direct extension or retrograde thrombophlebitis neighboring structure
-blood-borne form distant site
s/s 1-4 weeks after initial infection
brain abscess tx
drainage or excision
IV abx
post infection: neuro deficits
-cognitive, motor, sensory
