CNS traumatic injury Flashcards
1
Q
Concussion
A
- A complex pathophyiosological process affecting the brain, induced by traumatic biomechanical forces
- Rapid onset and short-term impairment of function that resolves spontaneously
- May not loose consciousness
- No abnormalities found on CT or MRI
2
Q
Concussion Sx
A
- Severity can only be determined in retrospect: after symptoms clear, after neuro exam is normal, after cognitive function returns
- Concussion signs: poor concentration, easily distracted, ringing in ears, sadness, seeing stars, noise/light sensitivity, glassy eyes/vacant stare, vomiting and sleep disturbances
- Sleep disturbances: hypersomnia, trouble falling asleep, restless sleep
3
Q
Pathophysiology
A
- Impaired neurotransmission: excessive release of glutamate leads to neurotoxicity
- Dysregulation of ions: opening of ion channels puts strain on ion pumps and increases energy demand
- Hypermetabolic state
- Reduction in cerebral blood flow + hyper metabolic state results in energy crisis
4
Q
Dx of concussion
A
- Detailed concussion history (too many don’t report it and then return to sport prematurely- can lead to sudden death due to second impact syndrome)
- Appearance of Sx’s might be delayed several hours following a concussive episode
- Potential biomarkers: S100B elevates 3 hrs post trauma and clears in a week
- SCAT imPACT BESS, eye matrix
- Rx: none, but best is to rest brain (avoid lights, noise, stress), regular sleep pattern, meds on low doses
5
Q
Types of injury
A
- Abraisions: scrapping injuries to skin
- Contusions (bruises): blood vessels rupture under intact epidermis
- Lacerations: blunt trauma causing a tear in tissue (non-clean edges)
- Incision: a sharp force injury w/ clean edges (longer than it is deep)
- Stab: a sharp force injury w/ clean edges (deeper than it is long)
- Gun shot wounds (GSW): penetrating (entrance) and may be perforating (exit)
6
Q
Dating of contusion
A
- Based on the color of the contusion (early-> late)
- Red/purple, bluish brown, greenish brown, green, yellow
- Blood products: hemoglobin, hemosiderin, biliverdin, bilirubin
7
Q
Types of skull fractures 1
A
- Linear: fracture often extending through entire thickness of calvarium
- In adults is often clinically insignificant, but may cause epidural hematoma by severing the middle meningeal artery
- In children 75% of skull fractures are linear, and complications include subgaleal hematoma (bleeding btwn aponeurosis and periosteum of skull) and epidural hematoma
- Displaced/nondisplaced: loss of normal anatomic alignment (or not)
8
Q
Types of skull fractures 2
A
- Depressed: bone is pressed into cranial vault
- Complications include post traumatic seizures, infection, loss of consciousness
- Open/closed: absence or presence of overlying laceration
- Complications may include communication of CSF
- Comminuted: multiple linear fractures (from repeated blows, seen in child abuse)
- Diastatic: separation of skull structures (can be growing fracture)
- Hinge: skull is fractured at base and has hinge mobility
9
Q
Basilar skull fracture
A
- Fracture of bones of base of skull
- Temporal bone is weak, fracture could rupture middle meningeal artery and cause epidural hematoma
- Can produce CSF leaks (dural tearing)
- Produces variety of effects: nausea/vomiting (brainstem), oculomotor defects (III, IV, VI), facial nerve palsies and hearing loss (VII and VIII)
- Clinical signs: battle sign (retroauricular hematoma), raccoon eyes, rhinorrhea/otorrhea (CSF leaking out nose/ear), hemotympanicum (blood on ear drum)
10
Q
Sites of contusion
A
- Direct (coup) injury: at the site of impact
- Indirect (contrecoup): opposite to site of impact
- Can be both when there is acceleration to deceleration
- Ex: head hitting windshield causes coup in frontal lobes then contrecoup in occipital lobes
11
Q
Traumatic diffuse axonal injury (TDAI)
A
- Non-traumatic causes of widespread injury to axons
- Due to rotational acceleration/deceleration of head (shearing, twisting)
- Usually causes unconsciousness, which may or may not be reversible
- Damages white matter
- Often affects corpus callosum, but can affect any structure w/ white matter
- Gross evidence: gliding contusions, petechiae in corpus callosum, focal lesions in brain stem
- Microscopic damage: axon spheroids (swollen damaged axons), amyloid plaques
12
Q
Epidural hematoma
A
- Breaking the temporal bone can tear the middle meningeal artery and cause an epidural hematoma
- Smoothly-encapsulated hematoma that collects btwn dura and skull (calvarium)
- Causes mass effect-> cerebral edema and/or herniation
13
Q
Subdural hemorrhage
A
- More common than epidural hemorrhage, due to tearing of bridging veins
- Caused by substantial head injury
- Usually not as smoothly encapsulated as epidural hemorrhage
- Can form a membrane then re-bleed (usually slow bleeds)
- Bleeds btwn dura and the arachnoid layer (into the now formed subdural space)
- Causses mass effect-> cerebral edema and/or herniation
- Chances are increased w/ drugs
14
Q
Subarachnoid hemorrhage
A
- More common than subdural and epidural
- No mass effect
- Other symptoms: worst headache ever, stiff neck, vomiting, deteriorating mental status, sudden death
- Ruptured berry aneurysm, VA laceration, AVM all cause subarachnoid hemorrhage
- Can also be caused by trauma
- Blood in CSF causes hydrocephalus (prevents reuptake of CSF), and other vasospasms
15
Q
Increased intracranial pressure (ICP)
A
- Can be caused by hydrocephalus, mass effects, cerebral edema
- 2 types of cerebral edema
- Vasogenic edema: breakdown of BBB (tumors)
- Cytotoxic edema: due to energy failure (infarction)
- Cerebral edema will cause large, flat gyri, narrowing of sulci
- ICP is what causes herniation
