TBI Intro Flashcards
Patient population of typical TBI
- Children and older adults (>75 YO)
- Males > females
- Race: American Indian/Alaskan Native, Black, Hispanic population
- Service members/veterans
- Homeless
- Incarcerated
- Domestic abuse survivors
- Rural area dwellings
The MOST common cause of TBI?
FALLS
(MVA/MVC, acts of violence and sports)
Children will most likely suffer a TBI due to:
fall, abuse
Adolescents & young adults will most likely suffer a TBI due to:
falls, assault, MVA
Open TBI
penetrating wound, skull fracture, meningeal compromise
Closed TBI
no skull fracture, only cortical tissue, meninges remain intact
Focal injury
localized to area under site of impact or site opposite to site of impact.
Types of Focal TBIs
- Hematomas
- Hemorrhage
- Contusion
- Coup-contrecoup injuries
Common sites of focal injuries.
Anterior-inferior temporal lobes, prefrontal lobes
Which type of TBI often have stroke-like presentation.
Focal TBI
Your patient was struck in the head and had a brief syncope episode then regained consciousness. Later on they suddenly went unconscious. What type or TBI are you suspecting and what is the potential treatment?
Epidural hematoma, craniotomies and hematoma evacuation
Your elderly patient fell and hit their head. EMS was called and the patient refused transport. They did not loose consciousness. Now it is the next morning and they are not waking up. What kind of TBI do you expect they have and what is the treatment?
subdural hematoma, smaller clots will be reabsorbed by the body, larger clots will require surgical removal.
What is the most life threatening type of TBI and a common sequela?
Subarachnoid hemorrhage (SAH), vasospasm
A common sequela of intracerebral hemorrhage includes
seizures
Coup lesion
contusion on the same size of the brain as the impact.
Contrecoup lesion
surface hemorrhages on the opposite side of the brain trauma as a result of deceleration
Which is associated with more damage, coup or countercoup damage?
Contrecoup
Most common structures involved with coup-contrecoup injuries include:
anterior poles, underside of temporal and frontal lobes
A diffuse axonal injury is:
widespread shearing and retraction of damaged axons resulting in traumatic micro-bleeds
Diffuse axonal injury are associated with significant neurological involvement and a poor prognosis. They most commonly result from damage where?
corpus callosum
basal ganglia
brainstem
cerebellum
T/F secondary brain damage post-TBI occurs much like a stroke via apoptosis and/or necrosis.
False, TBI secondary damage only occurs through apoptosis
Why is increased ICP more dangerous when associated with secondary brain damage compared to primary?
Associated with higher rates of herniation and death
The areas most vulnerable to anoxic/hypoxic brain injuries include
-Hippocampus
-Cerebellum
-Basal Ganglia
Primary cause of anoxic or hypoxic brain injuries?
cardiac arrest (also, CO2, toxicity, near drowning, severe bleeding = systemic hypotension)
Primary blast injuries
direct effect of blast overpressure on organs
What type of blast injury results in diffuse brain damage?
primary
Secondary and Tertiary blast injuries are characterized by:
2ND: shrapnel
3RD: direct blow to head
Imaging in the acute management stage of a TBI consists of:
MRI/CT, PET, EEG
Acute medical management of TBI includes
↓ BP/ICP/IC bleeding/body temp/infection rate/seizure risk
If a patient is in induced hypothermia to decrease ICP, are they a candidate for PT?
NO
The primary acute TBI concern
Increased ICP
Abnormal ICP Value
≥20 mmHg (NOT PT CANDIDATE)
Your pt ICP has been steady around 15 mmHg. Are they a candidate for PT?
Yes, but proceed carefully avoiding interventions that increase ICP.
Activities that increase ICP
- Percussion + vibration
- Fully supine or Trendelenburg
- Cervical flexion
- Valsalva
- Exertional activities (quick elevation HOB, supine>sit)
S&S of ICP
↓ responsiveness
↓ consciousness
- Seizures
- Severe HA
- Vomiting
- Irritability
- Papilledema, pupillary changes, impaired eye movement
- Speech changes
- Posturing
*Cushing’s Triad: ↑ BP/↓ HR, irregular RR
Treatment of ICP
Careful monitoring
Pharmacological agents
Ventricular peritoneal shunt
When can you mobilize a patient who has post-TBI seizures?
a. ≥24 hours seizure free
b. 24-48 hours seizure free
c. ≥ 72 hours seizure free
d. 24-72 hours seizure free
a. ≥24 hours seizure free
Common S&S of seizure
- focal/diffuse twitching, jerking, stiffening
-potential LOC
-Absent staring, “zoned out”
Paroxysmal Autonomic Instability and Dystonia (PAID)
severe medical instability, overdrive of nervous system (“Sympathetic Storming”)
GCS associated with PAID
3-8
Medical management of PAID
Symptom management (CNS depressant meds) “ride the storm out”
Patients are at an increased morbidity risk with PAID…
w/o management/appropriate treatment
S&S Paid:
Tachypnea
Tachycardia
Fever (hyperthermia)
HTN
Diaphoresis
Rigidity +/- decorticate posturing / *decerebrate posturing
Agitation
How do symptoms of PAID present
Cyclicly, at least one cycle/day ~3h long
T/F Decorticate posturing is associated with PAID syndrome d/t damage above red nucleus
False, decerebriate posturing is associated with the sympathetic involvement lower in the brainstem.
What posturing is associated with damage in relation to the red nucleus
Above: decorticate
Below: decerebrate
Polytrauma TBI patient’s have an increased risk of
Heterotopic ossification most common in large joints
It is 8 weeks post-TBI for your patient. They also suffered from multiple fractures d/t an MVC. They are now complaining of knee pain and decreased ROM. You also note erythema, pain with movement, selling and warmth. When you are assessing how will you differentiate between a DVT and HO?
End feel! (DVT: empty or normal end feel, HO: hard end feel)
HO PT Treatment
PROM and stretching to maintain ROM and prevent further complications.
