15 terms

Cranial Trauma


Terms in this set (...)

Closed head injury
primary (contusions, concussions, etc) vs secondary (hypoxia, hypotension)
- cerebral hypoxia -> ATP depletion -> failure of Na/K pump -> intracellular accumulation of Na & Ca -> acidosis, decreased NT uptake -> glycolysis inhibition, increased extracellular glutamate -> activation of NMDA channel -> increased intracellular Ca -> protease/phospholipase activation -> free fatty acid (free radical accumulation)
- impairment of autoregulation of cerebral blood flow, decoupling of cerebral metabolism & cerebral blood flow
Monro-Kellie hypothesis
brain parenchyma, blood, CSF in fixed box (skull)
with increasing ICP, CSF production decreases, CSF is pushed into the spinal compartment & resorption increases -> intracranial blood volume decrease by venous compression -> compliance decreases and small increases in volume lead to expontentially higher increases in ICP ->culminating in parenchyma herniation, occlusion of arterial supply with resulting infarcts
Cerebral Edema
disruption of BBB (vasogenic) or primary intracellular edema (cytotoxic)
Cerebral Perfusion Pressure
normal 50mmHg
should be > 60 mmHg in TBI
malignant cerebral edema
in pediatrics with severe hyperemia, refractory increases in ICP, high morbidity/mortality
- many have electrolyte, endocrine, & cardiopulmonary function abnormalities
Describe treatment considerations for severe head trauma
1. Neuro
2. CV
3. Pulm
4. GI
5. GU
6. Heme
7. ID
8. FEN
9. MSK
10. Dispo
1. frequent neuro exams (q1hr), ICP monitoring device for GCS <8, prophylactic anticonvulsant therapy, consideration of evacuation of symptomatic mass lesions or hemicraniectomy

2. SBP > 90 < 160 (depending on baseline BP & ICP), place arterial & central line

3. intubation (GCS < 8; inability to maintain adequate ventilation, impending airway loss from neck or pharyngeal injury, poor airway protection ass'd w/depressed level of consciousness &/or the potential for neurological deterioration)

4. stomach ulcer proph

5. place foley

6. cbc, type & cross

7. abx proph if bolt or EVD is in place, tetanus, hemophilus, PCV if indicated

8. NPO, NS goal of euvolemia, e-'s, mannitol to temporize elevated ICP for refractory intracranial HTN hold for serum osm > 320, hypertonis saline goal Na > 145

9. Ensure adequate tertiary survey, maintain C spine until cleared

10. Dispo
describe Concussion
1. definition
2. si/sx
3. eval
1. traumatic biomechanical force to the brain leading to short lived impairment of neurologic function which resolves spontaneously. no abnormality on standard neuroimaging studies

2. somatic, cognitive, emotional, LoC, amnesia, behvioral changes, altered level of consciousness

3. stepwise increase in activit
if the pt is asymptomatic at the current level, may advance to the next level. if symptoms recur, the player/pt should return to the prior asymptomatic level for at least 24h before attempting to increase activity
Skull Fractures
1. Dx
2. Rads
3. Rx
1. CT
2. contre coup injury in 30%
3. surgical debridement when wound is open, > 0.5cm of depression or is cosmetically deforming
-increased surgical risk if fx is overa dural sinus
-abx may be indicated for open fx
describe longitudinal temporal bone fracture
more frequent (70-90%) -> facial n paralysis, hearing loss, vertigo, temporal/parietal trauma, epidural hematoma
describe transverse temporal bone fracture
less frequent (10-30%) - > sensorineural hearing loss, equilibrium disorders, facial n injury
- facial n damage more likely w/transverse fx but overall longitudinal fx are more frequent, so most facial n palsies are caused by longitudinal fx
Growing skull fx
children (usually <3yo) w/fx & underlying dural lac, may result in progressive diastatic fx & underlying leptomeningeal cyst
- req's surgical intervention w/repair of underlying dural defect
describe diffuse axonal injury (DAI)
1. etiology
2. clinical
3. location
4. radiology
5. outcome
1. centripetal progression of neuronal disconnection (shear injury) 2/2 severe oblique vector (ie high speed MVA)

2. low GCS w/o obvious lesion on CT scan

3. corpus callosum, internal capsule, midbrain (tectum), basal ganglia, descending corticospinal fibers (pontomedullary junction)

4. punctate hemorrhages on MRI (GRE sequence most sensitive)

5. poor
epidural hematoma
1. rad
2. outcome
3. presentation
4. Rx
5. venous epidural hematoma
1. 70% temporoparietal, 90% w/fx & underlying middle meningeal artery injury
-lenticular, convex shape
-may have delayed enlargement
-rarely ass'd w/other brain injury (in comparison to acute subdural hematoma)

2. 5% mortality, 10-30% delayed enlargement

3. most have hx of severe head trauma
- classically have a "lucid interval" w/resolving confusion after initial injury & then neurological decline ( <30% pt's)

4. surgical evacuation, obs if small & asymptomatic

5. more frequent in children
next to dural sinuses or tentorium
subdural hematoma
1. epidemiology
2. etiology
3. rads
4. Rx
5. outcome
1. 15% of severe head trauma
chronic subdurals are often seen in elderly w/minor trauma esp when on anticoagulation
-predisposition w/conditions that cause brain atrophy & therefore increased tension on bridging veins (alcohol abuse, dementia)

2. shear injury to bridging cortical veins (ie trauma, intracranial hypotension, severe atrophy, birth trauma)

3. CT
acute = hyperintense (can be isointense w/low hematocrit or rapidly expanding lesions)
subacute = isodense
chronic (>3wks) = hypodense

4. pt's w/symptomatic SDH w/midline shift should be surgically evacuated
-acute SDH req's a trauma craniotomy
-chronic SDH may be amenable to evacuation w/burr holes

5. 35-90% mortality, depending on chroniciy, pt age, & comorbidities
- reaccumulation of chronic SDH in up to 45%
penetrating cranial injury
1. pathophys (GSW)
2. radiology
3. rx
4. outcome
1. direct & indirect (temporary cavitation) injury
- pressure waves lead o stretch injury in adjacent brain w/high velocity projectiles

2. CT scan - may see skull fragments, debris

3. consider surgery for GCS 3-5 w/large EDH
GCS 6-8 w/o transventricular or bihemispheric injury
or GCS 9-15

4. mortality 70-80%
2/3 victims die at scene
post-traumatic epilepsy in 50% of survivors. if comatose at time of presentation, mortality is > 90%