TBI Flashcards
Traumatic Brain Injury
mechanisms of injury includes penetrating or blunt trauma to the head
penetrating trauma: can be result of penetration from foreign object (e.g. bullet) that causes direct damage to cerebral tissue
blunt trauma: can be result of deceleration, acceleration, or rotational forces
*with all head injuries, you must assume cervical spine injury until it has been ruled out
Acceleration and Deceleration Injuries
acceleration injuries: occur when brain has been hit by something and brain moves forward to the point of impact (initial injury)
deceleration injuries: cause the brain to crash against the skull after it has hit something (brain hitting back of skull)
ex) whiplash
Primary Injury
occurs at the moment of impact as a result of mechanical forces to the head
includes: contusion laceration shearing hemorrhage
Secondary Injury
occurs when the biochemical and cellular response to the initial trauma that can exacerbate the primary injury and cause loss of brain tissue not originally damaged
includes: ischemia hypercapnia hypotension cerebral edema sustained HTN
Contusion
bruising of brain r/t accel/decel aka coup/contrecoup injuries
contusions can progress over 3-5 days following the injury
small contusion tx: neuro exams and ICP monitoring
large contusion tx: surgical intervention to prevented increased edema and ICP
Concussion
a brain injury accompanied by a brief loss of neurologic function, esp loss of consciousness (seconds to an hour)
neurologic dysfunction includes:
- confusion
- disorientation
- post-traumatic amnesia
pt w/ loss of consciousness of 5 or more minutes need to be observed for a 24 hour period
Concussion: Clinical Manifestations
- HA
- dizziness
- nausea
- irritability
- inability to concentrate
- impaired memory and fatigue
Skull Fracture Classification
open: dura is torn
* risk of meningitis d/t torn meninges
closed: dura is not torn
Skull Fracture: Clinical Manifestation
CSF otorrhea or rhinorrhea
Battle’s sign
Raccoon eyes
Types of Skull Fractures
simple: a break in a cranial bone without damage to the skin
depressed: a break in a cranial bone w/ depression of the bone in toward the brain
linear: a break in a cranial bone resembling a thin line, without splintering
compound: a break in or loss of skin and splintering of the bone. along w/ the fracture, brain injury like subdural hematoma can occur
* all can be open or closed
Hematomas: Types
Epidural and Subdural: occur outside the brain tissue
Intracerebral: bleeding into brain tissue itself (directly damage neural tissue and can produce further injury as result of pressure and displacement of intracranial contents)
Epidural Hematomas
collection of blood between the inner table of the skull and the outermost layer of the dura
most often associated w/ skull fractures
d/t arterial bleeds
Epidural Hematomas: Clinical Manifestation
- steadily progressive
- rapidly advancing coma (increased ICP)
- unconscious > lucid > unconscious (b/c of way head is bleeding
- seizures common
- can look like stroke sx
- less fatal b/c sx occur faster therefore it’s more noticeable
Subdural Hematoma
collection of blood between the dura and underlying arachnoid membrane
most often related to rupture in the bridging veins
caused by: acel/decel and rotational forces
d/t venous bleeds
commonly seen in: alcoholics (d/t frequent falls) and elderly (aging shrinks brain and stretches vessels w/ falls)
Subdural Hematomas: Clinical Manifestation
- slow to develop sx (don’t show until the end when it’s almost too late which is why mortality rate is high)
- can occur w/ or w/o trauma
- decreased LOC
- ipsilateral pupil dilated
- seizures are less common
Intracerebral Hematoma
bleeding occurs w/in cerebral tissue
caused by:
- depressed skull fractures
- penetrating injuries (bullet, knife)
- sudden accel/decel motion
Missile Injuries
caused by objects that penetrate the skull which causes focal damage but little accel/decel or rotational injuries
depressed injuries: caused by fractures of the skull w/ penetration of bone into the cerebral tissue
penetrating injuries: caused by a missile that enters the cranial cavity but does not exit
perforating injuries: caused by missile injuries that enter and then exit the brain
risk of infection and cerebral abscess d/t fragments embedded w/in the brain
Head Injury and C-Spine Injury
all cases of head injury, assume c-spine injury also until it’s ruled out
- stabilize pt on spine board using log roll maneuver
- neck should be immobilized in well fitted c-collar and padded head immobilization device
- avoid tight c-collar (any pressure on the external jugular veins will increase ICP)
Neurological Exam of TBI Pts
- glasgow coma scale
- brainstem exam
- motor exam
- sensory exam
- peripheral reflex exam
*many pt’s w/ TBI have significant alterations of consciousness and/or pharmaceuticals present that limit the scope of the exam
**if muscle relaxants have been administered, the only aspect of the neuro exam that may be evaluated is the pupillary exam
Glasgow Coma Scale
screening exam that involves:
- eye opening
- verbal response
- motor response
highest score = 15
score interpretation:
<9 = severe head injury
9-12 = moderate head injury
13-15 = minor head injury
coma = 3
Response to Painful Stimuli
flexor posturing/decordicate posturing
extensor posturing/decerebrate posturing
flaccid (indicates brain stem herniation)
Brainstem Exam
pupillary exam
ocular movement
corneal reflex
gag reflex
may not get corneal reflex esp in those who wear contacts b/c putting in contacts dulls corneal reflex so we don’t totally rely on this
Motor Exam
when a pt is not alert enough to cooperate w/ strength testing, motor exam is limited to assessment of asymmetry in exam demonstrated by asymmetric response to pain stimulation or a difference in muscle tone between sides
Sensory Exam
pt’s with altered levels of consciousness are unable to cooperate w/ sensory testing, and findings from a sensory examination are not reliable in pt who are intoxicated or comatose
pt needs to be awake, cooperative, and talkative
Peripheral Reflex Exam
can be helpful to identify gross asymmetry in the neurological exam
Mild Head Injury
usually doesn’t progress
usually require minimal observation after they are assessed carefully
typically concussions
PCS
post concussive syndrome
consists of persistence of any combination f the following after head injury for 2-4 months:
- HA
- N/V
- memory loss
- dizziness
- diplopia
- blurred vision
- emotional lability
- sleep disturbances
Moderate and Severe Head Injury
tx:
- initial cardiopulmonary stabilization by ACLS guidelines
- prevent hypoxia and hypotension
- once stabilized > ABCs and neuro exam, head CT
*if they’ve received muscle relaxants, the only neuro response that may be evaluated is the pupillary response
TBI: Tx
decrease ICP:
- osmotic diuretics
- drain extra CSF
- craniotomy
- induce hypothermia to decrease metabolic rate (barbiturates to put them in coma)
- increase rate of mechanical ventilation if they are hypercapnic
meds:
- anticonvulsant to prevent seizure activity (dilantin, phenobarb, Keppra)
- vasoactive meds: want high perfusion and high MAP to ensure brain is adequately perfused (Nipride is BP is too high)
Penetrating Brain Injury: Tx
involves two parts:
- tx TBI
- tx debridement and removal of penetrating object
wounds are frequently dirty as pathogens are introduced into the brain from the scalp surface and from the surface of the penetrating object
meninges are torn > pt at high risk for meningitis
Mild Concussion w/o Loss of Consciousness: Discharge Instructions
- problems frequently don’t occur until 24 hours after injury
- watch for increased sleepiness; waken q 2-3hrs
- immediately return to ED or call EMS if:
- any change in LOC
- unable to arouse
- seizures occur
- bleeding/clear drainage from ear/nose
- loss of sensation or movement in any extremity
- blurred vision, slurred speech, vomiting
Head Injury: Nursing Priority
maintain adequate respiratory function
prevent hypoxia and respiratory acidosis
TBI: Complications
Diabetes Insipidus:
- pituitary gland affected
- decreased ADH > polyuria, thirst
- watch fluid/electrolyte balance
Hydrocephalus (drain or shunt)
Labile VS (fluctuations; control ICP)
Post Traumatic Syndrome:
- vague ongoing sx; may interfere w/ work
- may need cognitive rehab
Cognitive/Personality Changes
- short term memory loss
- can’t work, go to school, learn new tasks
- impaired judgment > safety risk
Meningeal Tear > infection/meningitis
Monroe- Kelly Doctrine
the pressure-volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP)
CPP
measurement of cerebral blood flow
CPP = MAP - ICP
Causes of increased ICP
- SAH
- Intracranial hematoma
- brain tumors
- aneurysms
- cerebral edema
- encephalitis
- TBI
- stroke
- brain abscess
- hydrocephalus
- meningitis
Cushing’s Triad
indicator of increased ICP
decreased RR
decreased HR
increased BP (systolic HTN - widening pulse pressure)
Indications for Craniotomy
- severe TBI when there is fear of brainstem herniation from high ICP
- aneurysmal SAH
- removal of brain tumors
- thrombosis
- encephalitis
- intracerebral hematoma
Craniotomy
head shaved
positioned face down for entire procedure > periorbital edema
Craniotomy: Post Op
bulky dressing placed, MD changes it first
-if pt is bleeding through dressing, let provider know and reinforce it
neuro checks:
-q1hr for first 24 hrs, then q2hrs after that
suctioning increases ICP
control things that increase ICP (monitor ICP)
no NG tube w/ basilar skull or facial fracture (will typically have OG tubes)
no heavy narcotics b/c you can’t do neuro checks
seizure precautions
SCDs
Spinal aligned
pt wears helmet (pt placed on unaffected side if ICP is not an issue)
External Ventricular Drain (EVD) or Ventriculostomy
- catheter inserted into the lateral ventricle to drain CSF in external bag
- monitors ICP, can adjust to level to drain if ICP gets too high
- re-zero frequently to ensure ICP is accurate
Transphenoidal Surgery
- procedure for removing pituitary tumor
- access to gland w/o craniotomy
Post-Craniotomy Meds
- mannitol: hypertonic sugar solution, crystallizes when cold
- paralytics
- diprivan (propofol): “milk of amnesia”, used for induction, short procedures, rapid onset
Persistent Vegetative State
- no awareness or cognition
- no reflexes
- different than brain death
Criteria Used to Determine Brain Death
- absence of spontaneous respiration
- absence of spontaneous movement
- cessation of brain function (no response on neuro exam)
- flat EEG
- bilateral absence of cortical response to median somatosensory
- no blood flow to brain in doppler
one of the following:
- 2 exams at least 6hrs apart
- 2 flat EEGs at least 2hrs apart
- 2 dopplers at least 2 hrs apart
- extensive facial/cranial damage prohibits testing (all tests that can be done are done and confirmed apnea test)
Brain Tumor: Dx Studies
- careful hx and physical exam
- new onset seizure disorder may be the first indication of a brain tumor (or visual disturbances)
- MRI
- CT
- PET scan
Meningitis
acute inflammation of the meningeal tissues surrounding the brain and spinal cord
infection of the arachnoid mater and the CSF
medical emergency
Meningitis: Clinical Manifestations
- fever
- severe HA
- n/v
- nuchal rigidity
- Brudzinski’s sign
- Kernig’s sign
- photophobia
- decreased LOC/irritability
- seizures
Meningitis: Dx
- blood cultures
- lumbar puncture
- CT scan
- MRI
- CBC
Meningitis: Tx
- antibiotic therapy
- antipyretics (acetominophen)
- seizure precautions
- frequent neuro exams
- droplet precautions
Encephalitis
acute inflammation of the brain
serious, sometimes fatal
Encephalitis: Cause
virus
or complication from: measles, chickenpox, mumps
Encephalitis: Clinical Manifestations
- fever
- HA
- n/v
- hemiparesis
- tremors
- seizures
- personality changes
- memory impairment
- dysphagia
Encephalitis: Dx
CT
MRI
PET
Encephalitis: Tx
- mosquito control
- acyclovir and vidarabine
- antiseizure meds (Keppra, dilantin, phenobarbital)
Brain Abcesses
Cause: tooth infection, sinus infection, ear infection
Dx: CT scan
