Ch. 25 Loss of Consciousness Following Head Trauma Flashcards
What is the differential dx for a severe (GCS < 8) traumatic brain injury?
What is the definition of a TBI?
TBI results in a disruption of brain function
To meet the definition of TBI, the following criteria must be met:
- Period of loss of consciousness
- Loss of memory for events immediately before or after the accident
- Alteration in mental state at the time of the accident and/or
- FND
How do you calculate GCS?
Composed of three components: eye opening, verbal response, motor response
By definition, a neurologically intact person has GCS score of 15 (GCS score of 3-8 = severe TBI) –> considered to be in a coma and mandates establishment of an airway
What are Raccoon Eyes?
What is Battle’s Sign?
Raccoon Eyes = bilateral periorbital ecchymosis
Battle’s sign = retroauricular ecchymosis
Both should raise suspicion of basilar skull fracture
What is the implication of abnormal arm flexion/leg extension with pain stimulation? Arm/leg extension?
Abnormal flexion in upper extremity and extension in lower extremity in response to painful stimuli = decorticate posturing
Abnormal extension in UE and LE in response to painful stimuli = decerebrate posturing
These are primitve reflexes mediated by the brain stem when high brain fxn = absent
While both are grave signs, decortiate posturing = better prognosis
What is uncal herniation?
Occurs when a space-occupying lesion above the tentorium displaces the uncus of the temporal lobe medially and inferiorly over tentorial incisure impacting on ipsilateral oculomotor nerve (CN III) and ipsilateral cerebral peduncle, which contains the ipsilateral corticospinal tract.
Result: ipsilateral blown pupil and contralateral paralysis
What is the pathophysiology of an epidural hematoma?
Accumulation of blood between the dura and skull
Temporal bone fracture from a head injury results in laceration of the MMA (most common source) resulting in EDH
EDHs have a biconvex appearance on CT
Because the hematoma is from an arterial source, it may expand rapidly and may require urgent surgical evacuation
What is the pathophysiology of an acute subdural hematoma?
Acute subdural hematoma is the accumulation of blood between the dura and arachnoid membrane. It results from tearing of the bridging veins, which run from the cortex to the dural venous sinuses.
SDHs have a crescent-shaped appearance on CT
**elderly, alcoholics, pts on anticoagulation therapy are particularly susceptible**
What is the formula for cerebral perfusion pressure?
What other factors affect cerebral perfusion pressure? What is the most powerful intracranial vasodilator?
CPP = MAP-ICP
Other factors affecting CPP:
B/c brain is encased by rigid bony cranium, three components contribute to ICP: brain tissue, CSF, and blood… in order to maintain constant ICP, an increase in one must result in a decrease in the volume of the other two. This may lead to complications such as reduced CBF leading to brain ischemia.
The most powerful vasodilator = blood CO2 level
Lowering CO2 via mild hyperventilation provides temporary therapeutic benefit for elevated ICP
Cushing’s Triad?
What does it mean? What is the pathophysiology?
- HTN
- Bradycardia
- Irregular RR
Physiologic response to increased ICP
In the presence of elevated ICP, systemic BP increases in order to maintain CPP. The increased P results in negative feedback at the carotid sinus –> bradycardia
The respiratory center is located in the medulla and will become impaired as a result of elevated ICP
What is a coup vs contrecoup injury?
Coup = injury to brain tissue directly below the skull at the point of impact
However, the force of impact may thrust brain tissue against the skull on opposite site and cause injury. This is referred to as contrecoup.
What is normal ICP range?
Between 5-15 mm Hg
What is generally the first-line drug used for reducing intracranial HTN and how does it work?
Mannitol = osmotic diuretic
Increases tonicity of extracellular space, which causes a shift of water from the intracellular space (brain parenchyma) to extracellular space
Additionally, by expanding the plasma volume, it reduces hematocrit and blood viscosity which increases cerebral blood flow (O2 delivery) and reduces ICP
**Avoid in pts with hypotension or hypovolemia due to its volume-depleting effects**
Is there a role for corticosteroids in the treatment of TBI? What is the difference between vasogenic and cytotoxic edema?
No role in setting of TBI – corticosteroids such as dexamethasone are routinely used in the tx of cerebral edema caused by brain tumors and other inflammatory CNS processes
Mechanisms of edema in tumor and in trauma are fundamentally different. Tumors produce edema by causing inflammation (cytotoxic edema) and will respond to corticosteroids.
Trauma, in contrast, causes cerebral edema by triggering abnormal vasoregulation adn by causing brain capillaries themselves to become abnormally leaky (vasogenic edema) and is not responsive to corticosteroids.
When should a craniotomy be performed for acute EDH or SDH? What about craniectomy?
Craniotomy (removing skull flap to evacuate hematoma) is indicated for acute subdural and epidural hematomas that are associated with:
midline shift > 10 mm
hematoma thickness > 5 mm
ICP > 20 mm Hg
Bone flap is returned after hematoma is evacuated
With a craniectomy, the scalp is closed without replacing the bone flap… this allows the brain parenchyma to swell beyond confines of the skull. The bone flap is usually stored for possible reimplantation at a later time.
Overall initial mgmt steps
