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
