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Common Neuromuscular Diseases Assess

-field of view
Head Trauma -observe pt is visually attentive
- Closed Head Injuries -clearly command tell me your name
- Traumatic Intracranial Hematomas -lift up two fingers on each side sequentially, And wiggle
Spine Trauma the toes.
- Patterns of Injury
- Neurologic Syndromes Visually or verbally unresponsive
-assess for response to peripheral stimuli
CLOSED HEAD INJURY - Nail bed pressure
- Deep central stimulation
Primary Injury
-firm twisting pinch to supraclavicular skin
-Immediate injury to neurons from transmission of the
Note for external signs of head injury
force of impact
-bleeding, deformation of the skull
Secondary Injury
- Subsequent neuronal damage due to the sequelae of
Medical management
-CHI and IC hemorrhage or depressed skull fracture
- hypoxia, hypotension, hydrocephalus, IC Hpn, hematoma
-17 mg/kg loading does
Initial assessment
-300-400 mg/d maintenance
-ABCDs of resuscitation
-Blood glucose monitor, control by sliding scale insulin
-hypoxia & hypotension -> worsen outcome
-Fever antipyretic
-intubation pt who cant follow commands
-hyperglycemia + hyperthermia
may contribute to 2nd ry injury
-Head injury increase prevalence to peptic ulcer, GI bleed
-compression stocking or athrombic pumps
-pt who cant be mobilized rapidly

Low risk for intracranial injury:
- Head trauma patients who are asymptomatic:
headache, dizziness, or scalp lacerations, (-)
- May be discharged home without a head CT scan
- Printed discharge instructions
- should return to ER for symptoms: Confusion,
Persistent nausea, Weakness, or Speech difficulty

Moderate risk for intracranial injury:

- (+) Altered consciousness, amnesia, progressive
headache, skull or facial fracture, vomiting, or
- Prompt head CT.

High risk for intracranial injury:

Severe head injury: GCS score is 3 to 8 - Depressed consciousness, focal neurologic deficits,
Moderate head injury: GCS score is 9 to 12 penetrating injury, depressed skull fracture, or
Mild head injury if the GCS score is 13 to 15 changing neurologic examination
- Immediate head CT and admission for observation
or intervention as needed.

1. Concussion 1. epidural hematoma

- temp. neuronal dysfunction ff non-penetrating trauma - accumulation of blood between skull and dura
- CT is NORMAL - meningeal artery disruption
- deficits resolves minutes to hours - classic 3 stage clinical presentation
- transient loss of consciousness 1. unconscious
- alteration of mental status 2. awakens and lucid interval - hematoma expands
- memory difficulties are common 3. lethargic
- COLORADO grading system: - uncal herniation ipsilateral 3rd nerve palsy and
o grade 1 confusion only contralateral hemiparesis
o grade 2 amnesia - CT: clot is bright; BICONVEX (lentiform), well defined
o grade 3 loss of consciousness border usually respects cranial suture lines
- second-impact syndrome - clot forms over convexities but rarely in post. Fossa
- 1st 1 to 2 weeks after injury - open craniotomy
- criteria for conservative management:
2. Contussion - clot volume <30 cm3
- a bruise of the brain, when the force from trauma is - maximum thickness <1.5 cm
sufficient to cause breakdown of small vessels and - GCS >8
extravasion of blood into the brain - prognosis: EDH>SDH
- CT appear bright
- Frontal, Occipital, Temporal poles most involved 2. Acute subdural hematoma
- may enlarge to frank hematoma 1st 24 hrs - accumulation of blood bet arachnoid membrane and dura
- rarely cause significant mass effect as they represent - results from venous bleeding tearing or bridging vein
small amounts of blood in injured parenchyma rather than from cerebral cortex to the dural sinus
coherent blood clots (acceleration/deceleration)
- Edema may develop around a contusion, causing mass - CT scan: clot is bright or mixed density;
effect CRESCENT-SHAPED (lunate); less distinct border;
does not cross midline due to presence of falx
- occur at cerebral hemispheres, between hemispheres or
layer over tentorium
- open craniotomy
- thickness > 1cm
- midline shift >5mm
- GCS drop by 2
- nonoperatively managed hematomas may stabilize and
3. Diffuse Axonal Injury
eventually evolve to chronic SDHs
- damage to axon due to rotational acceleration and then
- prognosis is worse than EDH
- axons may completely disrupt->retract-> axon balls
3. Chronic Subdural hematoma
- severe MRI small hemorrhages in corpus callosum and
- collection of blood breakdown products atleast 2-3 wks
dorsolateral midbrain
- acute hematomas (hyperdense) for 3 days then
hypodensity after 2-3 weeks
4. Penetrating injury
- CT scan: dark as CSF; traces of white small hemorrhages
- types: Missile bullests or fragment devices
- acute-on-chronic SDH
Nonmissile knives or ice picks
-small bleeds may expand -> symptomatic
- skull Xray and CT scan
-alcoholics, elderly and pt on anticoagulation high risk
- cerebral angiography if passes major artery
- pt: headache, seizure, confusion, contralateral
- operative exploration
hemiparesis or coma
- small objects left in parenchyma left in place to avoid
- chronic SDH >1cm surgically drained
iatrogenic secondary brain injury
- consist of viscous fluid motor oil texture
- antibiotics to decrease chances of meningitis or abscess
- simple burr hole drain chronic SDH THE MECHANICS OF SPINE TRAUMA
- anterior burr hole if collection does not drain
- open craniotomy if SDH is too congealed for irrigation FLEXION/EXTENSION
- strategies to prevent reaccumulation of blood - bending the head and body forward flexes the spine
- subdural or subgaleal drains left 1-2 days - flexion loads the spine anteriorly, distracts posteriorly
- mild hydration and bedrest with head of bed flat - flexion loads the spine posteriorly, distracts anteriorly
- high levels of inspired oxygen draw nitrogen out
- follow up ct postoperatively and 1 month later COMPRESSION/DISTRACTION
4. Intraparenchymal Hemorrhage - force applied along the axial axis (axial loading)
- associated with Hypertensive hemorrhage or AVMs compresses the spine
- may occur in contused area of brain - loads the spine anteriorly and posteriorly
- mass effect from developing hematomas may present as - falling object strikes head or shoulders, when landing in
delayed neurologic deficit the feet, buttocks, or head after fall
- delayed traumatic intracerebral hemorrhage first 24 hrs
- pt with contusion should reimaged 24 hrs after trauma Distraction
- craniotomy if: - a pulling force in line with the spinal axis
- clot volume >50 cm3 - unloads the spine anteriorly and posteriorly
- clot volume >20 cm3 w/ GCS 6-8 and - during a hanging, when chin or occiput strikes an object
Midline shift >5 mm first during fall, or when passenger submarines under loose
- basal cistern compression seatbelt

Spine Trauma ROTATION

- Provides structural support for the body as the principal - force applied tangential to spinal axis rotates the spine
component of the axial skeleton, while protecting the - depends on the range of motion of intervertebral facet
spinal cord and nerve roots joints
- Damage to these elements reduces the strength of the - occur during off-center impacts to the body or head or
spine and may cause instability, which compromises both during glancing automobile accidents
supportive and protective functions
- Spine trauma may occur with or w/out neurologic injury.
-Incomplete or complete.
Incomplete: If there is some residual motor or sensory
Neurologic function below the level of the lesion
Complete: Neurologic dysfunction persisting 24 hours
after injury has a very low probability of return of function
in the involved area.
- immediate neurologic injury may be due to direct
damage to the spinal cord or nerve roots from penetrating
injuries, especially from stab wounds or gunshots.
- Blunt trauma may transfer sufficient force to the spine to
cause acute disruption of bone and ligament, leading to
subluxation, which is a shift of one vertebral element in
relation to the adjacent level.
*Subluxation decreases the size of the spinal canal and
neural foramina and causes compression of the cord or
*Such neural impingement can also result from
retropulsion of bone fragments into the canal during a
- Transection, crush injury, and cord compression impairing
perfusion are mechanisms leading to SCI.

JEFFERSON FRACTURE 1. Injury to the entire cord at a given level results in

- bursting fracture of the ring C1 (atlas) due to compression anatomic or functional cord transection with total loss of
motor and sensory function below the level of the lesion.
forces The typical mechanism is severe traumatic vertebral
subluxation reducing spinal canal diameter and crushing
- result from flexion forces
- classified to three types 2. Injury to half the cord at
a given level results in
Type I fracture involves the tip only.
Brown-Squard syndrome,
Type II fracture passes through the base of the with loss of motor control
odontoid process. and proprioception
Type III fracture passes through the body of C2. ipsilaterally and loss of
nociception and
HANGMANS FRACTURE contralaterally.
- hyperextension/distraction injury angle of the jaw The typical mechanism is a
- hyperextension/compression diving accidents stab or gunshot wound.
- hyperflexion
- define by bilateral C2 pars interarticularis fractures
3. Injury to the interior gray matter of the cord in the cervical spine
results in a central cord syndrome, with upper extremity worse than
lower extremity weakness and
- stabilize by rib cage varying degrees of numbness.
- lumbar spine large vertebrae The typical mechanism is transient
Thoracolumbar higher threshold for injury than cervical compression of the
3 column model for categorizing thoracolumbar injury cervical cord by the ligamentum
flavum buckling during
a. anterior column - anterior half of vertebral body traumatic neck hyperextension.
b. middle post. Half + post. Longitudinal ligament This syndrome occurs in
c. posterior pedicles, facet joints, laminae, spinous patients with pre-existing cervical
process, and interspinous ligaments stenosis.

- compression/flexion injury anterior column only
- stable and not asc. w/ neurologic deficit
4. Injury to the ventral half of the
cord results in the anterior cord
BURST FRACTURE syndrome, with paralysis and loss
- pure axial compression anterior and middle column of nociception and thermoception
- unstable bilaterally.
- half of pt have neurologic deficit due to compression of The typical mechanism is an acute
disc herniation or
cauda equine from fragments retropulsed to spinal canal ischemia from anterior spinal
artery occlusion.
- flexion/distraction middle and posterior, rare ant wedge
- lap seatbelt hyperflexion
- unstable and associated with neurological deficit

- flexion/distraction, shear, or compression forces
- anterior, middle, posterior columns
- neurological deficit can result from retropulsion of mid.
Column bone fragments into spinal canal, or from
subluxation causing decreased canal diameter