TBI Flashcards
TBI rates by age:
Rates of TBI-related deaths per 100,000 population:
- ~75 in adults aged ≥75 years
- ~25 in those aged 65-74 years
- ~20 in those aged 55-64 years
- Unintentional falls (highest in older adults aged ≥75 years )
- Suicide (highest in older adults aged ≥75 years )
SURVIVAL RATES and PROGNOSIS
-80% mild
100% survival
-10% moderate
93% survival
-10% severe
42% survival
Survivors of severe traumatic brain injury constitute a small percentage of the total group of TBI survivors, but they account for the majority of those who receive acute TBI rehabilitation.
-prognosis is highly variable
FACTORS FOR PROGNOSIS:
-initial severity of injury
-age (yougner and >75 years worse prognosis)
-CT abnormalities
-concomitant injuries
-length of PTA
PTA
-inability to create new memories
-mild: <24 hours
-moderate: 1-7 days
-severe: > 7 days
> 2 week PTA–> less optimistic
-persistent PTA- amnestic syndrome
What scale is used to classify the severity of TBI?
GLASGOW COMA SCALE
What two scales are used to stage TBIs?
Disorders of Consciousness Scale
Rancho Los Amigos Scale
GLASGOW COMA SCALE
verbal response
-oriented 5
-confused orientation-4
-inappropriate words-3
-incomprehensible sounds- 2
-nil- 1
eye-opening
-spontaneous- 4
-to speech - 3
- to pain-2
-nil -1
motor response
-obeys simple command- 6
-localizes (pushes away from a painful stimulus) - 5
-withdraws- 4
-abnormal flexion- 3 (UE flex LE extend) -decorticate
-extensor response-2 (UE extend LE extend ) -decerebrate
-Nil- 1
MILD: 13-15
**note CT abnormalities as well - mTBI
MODERATE: 9-12
SEVERE: 3-8
**lowest score possible is a 3
Primary brain injury
- Concussion
- Diffuse Axonal Injury (DAI) * Anoxic/hypoxic brain injury
- Contusion
- Laceration
- Hemorrhage
Secondary brain injury
- Hypotension
- Hypoxia
- Increased ICP
- Cerebral edema
- Vasospasm
- Failure of autoregulation
- Excitotoxicity
- Production of free
radicals
Diffuse brain injury
-concussion
-DAI
-anoxic/hypoxic brain injury
-metabolically active areas —> hippocampus, cerebellar purkinje cells, basal ganglia
Focal brain injury
-contusion
-laceration
-hemorrhage
–EDH
–SDH
–subarachnoid hemorrhage
–intracerebral hematoma
Closed vs Open brain injury
CLOSED
* Closed injury means the skull is intact
* Coup-contre coup is one
example of a closed injury
OPEN
* Open injury means the skull is fractured or broken
* This could be due to impact, explosion, projectiles, gunshot
* need to consider risk of infection
What can a CT scan help to identify?
acute injury, blood, bone, edema
-chronic or late stage blood detection
What can an MRI help to identify?
-MRI is more sensitive
-FLAIR- an inflammatory process; Fluid-attenuated inversion recovery (FLAIR) is an advanced magnetic resonance imaging sequence that reveals tissue T2 prolongation with cerebrospinal fluid suppression, allowing detection of superficial brain lesions.
-diffusion weighted- ischemia, WM
–DWI is commonly used to detect and stage tumors, and also to monitor tumor response to treatment over time.
-Gradient Echo-hemosiderin- DAI
—Hemosiderin deposition is the consequence of recurrent or persistent hemorrhage in the subarachnoid space. There are two types of SS. In “classical”-type SS, hypointense MRI signals are observed in the brainstem and cerebellum with diffuse and symmetrical margins.
-T2- brainstem
-diffusion tensor- experimental, WM
–detects the white matter fibers that connect different parts of the brain
-MRA- vasculature (dissection)
–The MRA scan is a form of an MRI and is performed with the same machine. The only difference is that the MRA takes more detailed images of the blood vessels than the organs or tissue surrounding them
T1 vs T2 imaging on MRI
T1-weighted MRI enhances the signal of the fatty tissue and suppresses the signal of the water
T2-weighted MRI enhances the signal of the water
Epidural hemorrhage/hematoma
-arterial bleeding FAST
-bleeding between the dura and the skull
-middle meningeal artery laceration from temporal fracture
-urgent evacuation usually required
-“lucid interval”- blood accumulates in epidural space
-The typical presentation is an initial loss of consciousness following trauma, a complete transient recovery (“often termed as a lucid interval”), culminating in a rapid progression of neurological deterioration. 14-21% of patients with EDH
–pupillary problems
—reflex problems
–thunderclap headache
SD hemorrhage/hematoma
-venous bleeding–> slower than arterial
-bleeding between dura mater and brain surface
-can occur with minimal force in elderly or chronic alcoholics
-may require evacuation if causing mass effect or worsening of symptoms —> perform serial CT scan to determine
What is a midline shift in the brain?
A midline shift occurs when the pressure exerted by the buildup of blood and swelling around the damaged brain tissues is powerful enough to push the entire brain off-center. This is considered a medical emergency and is an ominous sign.
-can be a result of a collection of blood between the dura mater and the brain tissue (SUBDURAL HEMATOMA)
SAH
-subarachnoid hemorrhage
-bleeding directly into the brain parenchyma (functional tissue of the brain)
-arterial bleeding
-often due to a burst aneurysm
-usually presents as the worst headache of your life
-COMMON CAUSES:
–head trauma
–burst aneurysm
Brain contusion
-occurs from the brain impacting the skull
-causes bleeding and swelling inside of the brain around the area where the head was struck
-most vulnerable structures: inferior frontal lobes, anterior and medial temporal lobes, ventral brainstem
-cortical areas overlying basal skull structures are particularly vulnerable
Diffuse axonal injury (DAI)
-widespread stretching of axons caused by rotation of the brain around its axis
-differential effect of acceleration/deceleration forces
-multifocal
-white matter throughout the brain is affected
-if deeper structures such as corpus callosum and brainstem affected–> higher severity
-not easily imaged
Axonic or hypoxic injury of the brain
-DEF: The term “anoxia” refers to the complete lack of oxygen delivery to an organ. The term “hypoxia” applies when an organ experiences oxygen delivery that is insufficient to meet the metabolic needs of the tissue; oxygenation status very important
-MECH OF INJURY: asphyxiation (suffocation), drowning, anaphylaxis
-SUSCEPTIBLE BRAIN AREAS: parietal and occipital cortices, hippocampus, cerebellum, BG
Poor prognostic factors for TBI
HYPOTENSION
* SBP<90 mmHg
* MAP<60 mmHg
HYPOXIA
* PaO2<60 mmHg (normal: 75-100 mmHg)
* O2 sat<90%
–> can be caused by apnea
–> may lead to cyanosis
INCREASED ICP
-Monroe-Kelly Doctrine
–> * Brain is surrounded by non- distensible tissue
* 80% Brain
* 10% CSF
* 10% Blood
–increased volume in one area decreases the volume in another area
–when a person is unable to auto-regulate pressure, ICP increases
ICP and CPP normal values and abnormal values
INTRACRANIAL PRESSURE:
–> NORMAL: 0-15 mmHg
–> KEEP BELOW: <20 mmHg (acute management)
CEREBRAL PERFUSION PRESSURE:
-pressure at which brain tissue is perfused
-NORMAL: 60-100 mmHg
-MAP-ICP= CPP
What can be a result of increased ICP?
midline shift
herniation
-both could be life threatening
MED MANAGEMENT OF INCREASED ICP
- Use of a monitoring device – a “bolt” monitor
- Surgery- Decompression, debridement, bone flap
OTHER:
-elevate HOB
-cooling
-ventriculostomy- withdraw fluid or monitor amount of fluid (hole into ventricular space)
-diuretics- move water from the extracellular space to the intravascular, increased cerebral blood flow and O2 delivery
- delicate balance because want to decrease ICP but keep systolic pressure high so there is perfusion of brain tissue
What is a bolt monitor for ICP:
This method is used if monitoring needs to be done right away. A hollow screw is inserted through a hole drilled in the skull. It is placed through the membrane that protects the brain and spinal cord (dura mater). This allows the sensor to record from inside the subdural space.
What medical interventions/medications are used to decrease brain metabolism and brain energy needs?
*** helps to limit secondary injury of the brain
Paralytics - act at NMJ, decrease stimulation, on mechanical ventilator and in medically-induced coma, protected airway
Barbituates - decrease metabolic rate by putting whole NS to “sleep”
Hypothermia- decreased metabolic rate (more evidence for children)
Reasons for immediate neurosurgery after TBI:
- Removal of debris
- Removal of blood
- Stop hemorrhage
- Clean and disinfect
- Stabilize any fractures
- Possible bone removal
- Plate placement
Possible Sequelae of TBI
-Focal deficits based on location of injury
* Occipital contusions -> visual
processing difficulties or cortical blindness
* Motor cortex injury -> contralateral paresis or paralysis
* Brainstem injury -> disruption in cardiac and respiratory function
-cranial nerve damage
* Lack of smell (I)
* Blindness (II)
* Depth perception problems and diplopia (III, IV and VI)
* Swallowing problems (IX)
-cognitive and neurobehavioral issues
* due to frontal lobe injury, whole brain trauma, or lack of oxygenation/metabolic issues
Management of Cognitive and Behavioral Issues
FRONTAL SYNDROMES
* Orbital frontal- disinhibition
* Medial frontal- initiation
SLEEP-WAKE CYCLE DISRUPTIONS
* Sleeping meds
* Environment
* Education
AMPLIFICATION OF PERSONALITY TRAITS
* OCD
* Impulsivity
REGULATE MOOD
* Amantadine –> It has also been improve focus, impulse control, and even mood swings related to ADHD and disruptive mood dysregulation disorder
INCREASE/STIMULATE BRAIN ACTIVITY
* Provigil (Dopamine agonists)
INCREASE AROUSAL AND ATTENTION
* Ritalin
COMPLICATIONS FOLLOWING TBI:
HETEROTOPIC OSSIFICAITON
* Risk factors- whole body trauma, immobility, spasticity,
long bone fractures, prolonged coma
* Pain, decreased ROM, edema/erythema
–> Phosphatase levels, Xray,
–> Bone scan gold standard
TREAT:
-bisphosophates, NSAIDs, ROM
INTRACRANIAL INFECTION
-esp open TBI
SEIZURES
-esp open TBI and hemorrhagic injuries
Post traumatic seizures:
- Immediate <24 hr from time of injury
- Early 1-7 days from time of injury
- Late >7 days from time of injury (post-traumatic epilepsy)
- First 2 years after injury - 3x greater risk of seizure
development compared to 2-12 years post-injury - If epilepsy develops, medications are needed for life
-5-19% of those with mod-severe TBI–> develop late post traumatic epilepsy
When are prophylactic measures indicated for post-traumatic seizures?
only in the first 7 days
*want to limit amount of seizures in the first few days
–As seizure prophylaxis has not been found to be effective in preventing late seizures occurring after seven days post-TBI, the continuation of seizure prophylaxis identified in this group of patients incurs higher risk for adverse effects and greater cost without providing any additional benefits in seizure prevention
no beneftis for continued prophylaxis after 7 days
What is a seizure?
As seizure prophylaxis has not been found to be effective in preventing late seizures occurring after seven days post-TBI, the continuation of seizure prophylaxis identified in this group of patients incurs higher risk for adverse effects and greater cost without providing any additional benefits in seizure prevention
FINITE, BRIEF
-A spontaneous, sustained, highly synchronous discharge that disrupts normal brain activity–> seizure
Presentation and cause of seizures:
-result in transient brain impairment or LOC
-if underlying cause eliminated, seizures stop
-most often unpredictable and no relationship to activity
-Can be provoked by flashing lights or flickering TV
Ictal period
period in which the seizure occurs (ictus or ictal)
post-ical- period after seizure ends but before full return to baseline mental status
Status epilepticus (SE)
-can be fatal
-adults and children 5 years or older
-more common in those with known cause of seizures: tumor, infection of CNS, drug abuse
-5 MINUTES OF CONTINUOUS SEIZURE
-EMC needed for intubation, anesthesia, IV meds, EEG (brain activity)
** must have EEG–> otherwise flight for life transfer
-if seizure > 60 min (clinically or by EEG) –> put patient in pentoarbital coma
—-> (barbituate induced coma) Refractory status epilepticus is often treated with third-line therapy, such as pentobarbital coma. However, its use is limited by side effects. Recognizing and preventing major and minor adverse effects of prolonged pentobarbital coma may increase good outcomes.
What are the 4 main categories that can cause acute seizures?
metabolic
drug induced
illness
neurologic
-acute head trauma, esp penetrating wound
-meningitis
-encephalitis
-stroke
-brain abcess
-brain tumor
Drugs that can induce seizure
haloperidol - antipsychotic medication
ephedrine - treats hypotension, CNS stimulant
methotrexate - DMARD
cyclosporine - immunosuppressive agent used to treat organ rejection post-transplant
cocaine
amphetamines
alcohol withdrawal
What is Epilepsy? Risk Factors?
DEF: Epilepsy refers to recurrent seizures from known or
unknown causes
RISKS: family hx, developmental disability, head trauma, stroke hx
PRENATAL AND PERINATAL FACTORS:
* Hypoxia-ischemia
* congenital infections
* inborn errors of metabolism
* prematurity
POSTNATAL CONDITIONS:
* CNS infections
* head trauma
* hypoxic- ischemic encephalopathy
-FEBRILE SEIZURES- most common seizure disorder in childhood; good prognosis; workup still warranted due to underlying acute infectious disease (sepsis, bacterial meningitis)
What is the prognosis of epilepsy?
-increased mortality compared to gen pop
-death from asphyxia is greatest concern during eating
-drowning during seizure is consequence of bathing or swimming alone
-correlation between depression and epilepsy
—> higher suicide attempt
—> more likely hospitalized for dep
Focal onset vs generalized onset seizure
FOCAL
* Abnormal electrical discharge clearly begins in one specific part of the brain (a seizure focus/locus)
GENERALIZED
* Abnormal electrical
activity is widespread throughout the brain very early in the seizure
*loss of consciousness
Focal seizure (non-dyscognitive)
- retained awareness
- preservation of consciousness and unilateral hemispheric involvement
- used to be called “simple partial seizure”
- manifestations: jerking, sensory symptoms (paresthesias, tingling) that spread to other body areas
- cog and affective changes–> illusions, hallucinations, sudden sense of fear
auras- affect 60%; sensory and psycho-illusory phenomena
Focal Dyscognitve Seizure
- Awareness is ALTERED or loss of consciousness
- about 70-80% arise from:
-temporal lobe- deja vu, oral or manual automatisms (chewing, picking, rubbing thumb and fingers)
-occipital lobe - aura or a visual disturbance
*appears dazed and confused with random
walking, mumbling, head-turning, or pulling at clothing
- may or may not have post-ictal confusion
*seizure lasting 45-90 seconds –> followed by confusion or disorientation for several minutes
Absence Seizure- type of focal seizure
-sudden cessation of ongoing conscious activity
-minor convulsive muscular activity or loss of postural control
-previous name: “petit mal” seizure
-staring, with or without eye blinding
-NO posictal phase
-common in children, often disappear by teenage years
Generalized Myoclonic seizure
*MYOCLONIC- sudden, brief, single, or repetitive ms. contractions involving one body part or the entire body
–> bilateral, convulsive, tonic or clonic
* Quick muscular jerky movement of the body, face, trunk extremity or
entire body
* May be unilateral or bilateral
* May be injurious (fall, hit objects)
* +/- loss of consciousness
* Duration of seconds, may cluster (more than one seizure in a 24 hour period)
* common to have long, post-ictal period —> headache, muscle soreness, mental dulling, lack of energy, mood changes lasting 24 hours
Difference between tonic and clonic phases of generalized myoclonic seizure
TONIC
-rigidity
-full body extension with wrist flexion
CLONIC
-generalized jerking movements
-flexion of UE and LE
Possible complications resulting from generalized myoclonic seizure:
- oral trauma
- vertebral compression fractures
- shoulder dislocation
- aspiration -> pneumonia
- sudden death
Generalized atonic seizure
-ATONIC- brief losses of consciousness and postural tone not
associated with tonic muscular contractions
-“drop attacks”
-MOST IN CHILDREN with diffuse encephalopathies
-sudden loss of muscle tone –> falls with injury
-common to have short post ictal period
Diagnosis of seizure and epilepsy
EEG- key role with dx of epilepsy
-observe seizure and EEG recording simultaneously
-normal reading DOES NOT rule out dx
-performance of metabolic study helpful during seizure occurrence
-BRAIN IMAGING: indicated to rule out mass effect or vascular disease
Common EEG montage:
DOUBLE BANANA-
The bipolar longitudinal pattern, also called the “double banana,” is a commonly used bipolar montage. It consists of a display in which each channel connects adjacent electrodes from anterior to posterior in two lines, essentially covering the parasagittal and temporal areas bilaterally.
TRANSVERSE
REFERENTIAL
AVERAGE
*EEG MONTAGE:
Montages are logical, orderly arrangements of electroencephalographic derivations or channels that are created to display activity over the entire head and to provide lateralizing and localizing information. Most often, bipolar and referential montages are used for routine electroencephalographic recordings.
Description of anti-seizure medication Gabapentin (neurontin)
An anticonvulsant is used as an add-on drug for individuals with
refractory complex partial and secondarily generalized tonic-clonic seizures
Gabapentin is in a class of medications called anticonvulsants. Gabapentin treats seizures by decreasing abnormal excitement in the brain.
Description of anti-seizure medication Lamotrigine (Lamictal)
Drug acts at voltage-sensitive sodium channels to stabilize neuronal membranes and inhibit neuronal release, particularly of glutamate
Description of anti-seizure medication Topiramate (Topamax)
Blocking voltage-dependent sodium channels
Description of anti-seizure medication Tiagabine (Gabitril)
Blocking reuptake of the neuroinhibitory transmitter GABA into neuronal and glial cells; an add-on drug
By slowing the reuptake of synaptically-released GABA, it prolongs inhibitory postsynaptic potentials. (inhibits the excitatory activity of the brain)
Other anti-seizure medications
- Levetriacetam (Keppra)
*Divalproex sodium (Depakote) - Valproic Acid/Valproate
Surgical procedures for seizure
- Lobectomies
- Cortical resections
- Sectioning of corpus
callosum
Vagal nerve stimulation for seizures:
-through implantable pulse generator
-stimulation of left vagal nucleus–> inhibitory projection influences cerebral cortex
-reported to result in 50% reduction in seizure
PROTOCOL FOR SEIZURE
DO THIS
-call out help or push code button
-secure patient: catch or help them be seated, slowly lower to ground if able, clear space around them and place pillow behind head , attempt log roll to prevent aspiration
DON’T DO THIS
-put anything in their mouth
-hold the patient down –> fractures or injury possible
NOTE this if you witness seizure
-duration
-observation of fall
-type
-respiratory status
-behavior before
-responsiveness, unresponsiveness, aphasia
-movements: vocalization, oral automatisms, manual automatisms, head turns, eye blinks, eye deviation, extension or flexion of limbs, shaking of extremities (all, unilateral, upper body, lower body)
-postictal confusion or agitation, wandering, etc
When is it okay to NOT tranpsort to ED?
-known epilepsy
-quickly return to baseline cognitive status
-no phys injury that needs additional eval
-the fall with seizure onset was witnessed
-no neck pain, concussion, vomiting, or new neurologic deficit (numbness, weakness)
-call EMS if unsure
PT and exercise with hx/risk of seizure:
✓History of seizure diagnosis
✓Medications (timing and which ones)
✓Patient education for consistency in medications
✓Seizure triggers
✓Type and frequency of seizures
✓Refer if signs of depression are present
NEW DIAGNOSIS OF SEIZURES:
* Activity restrictions for the first 2-3
months
* Recs for safest activities *
Medical treatment must be
initiated and monitored
* If antiepileptic drugs are
discontinued–> monitor activity initially
*epilepsy can progress in children–> exercise limitations may change over time
SEs of seizure meds and implications
-slowed cognition
-altered reaction time
-nystagmus
-ataxia
-dysarthria
-lethargy
-nausea
-irritability
-skin rash
AFTER ACTIVITY AND USE OF MEDS:
-loss of fluid (sweat)–> can affect blood levels of med
-loss of fluid can increase the metabolism of liver enzymes
-ask the neurologist if vigorous activity is safe!
Colorado law and epilepsy/seizure when driving
- A doctor is not required to report that a person has a seizure disorder to the DMV
- A doctor can report a medical condition that then may be followed up when a
license needs renewal
Department of Revenue: The department can only seek a medical opinion when they have reason to believe that the driver is physically or mentally unable to operate a vehicle
safely.
-if the DMV is aware of your diagnosis–> they may request periodic medical updates
-other states have different laws