ORTHO: PRELIM 2- HEAD AND CERVICAL SPINE CONDITIONS Incidence rate Causes leading to death (2010)

1. Falls (54.4%) in elderly

2. Self-inflicted in >15y/o
Traumatic Brain Injury (TBI) 3. MWA in children & young adults
4. Assault for 0-4yrs
1. Concussion
2. Contusion Classification of TBI
3. Coup-counter-coup injury
❖ Severity
Cervical Spine Trauma ❖ Pathoanatomic
❖ Mechanism / Etiology
1. Whiplash
❖ Symptom / Clinical

Based on Severity
TRAUMATIC BRAIN INJURY
Severity GCS LOC PTA
❖ Partial or total impairment of cognitive abilities and Mild 13-15 <20min- 1 hr <24 hrs
physical functioning caused by injury to the brain from ❖ 2013 : 10.6% of all injuries Moderate 9-12 1-24 hrs >1-7 days
direct or indirect bump, blow or jolt to the head. ❖ 2015: 0.2% of Americancs Severe 3-8 >24 hrs > 7 days
❖ M>F
Brain Injury ❖ Age group:
o >75 yrs (25%)
1. Acquired Brain Injury o 0-4 yrs (18%)
✓ Chemical / Toxic / Metabolic o 15-24 yrs (12%)
✓ Anoxia & Hypoxia (lack of oxygen)
✓ Tumors
✓ Infections

Signs and Symptoms

❖ Contusion
❖ Depression
❖ Dizziness or balance problems
❖ Double or fuzzy vision
❖ Feeling foggy or groggy
❖ Headache
❖ Memory loss
❖ Nausea
❖ Sleep disturbances
❖ Lightheadedness
❖ Slurred speech ❖ Mortality (2013) : 2.2% of TBI patients die.
❖ Slow breathing rate o Most common: >75 y/o
❖ Swelling at site of injury o Least common: 5-14 y/o
o M (74%) > F (26%)

Causes (2013)

1. Falls (47.2%)
2. Struck by or against an object ( 15.4%)
3. MVA (13.7%)
4. Assault
 Contusions/lacerations Diffuse vascular injury
Intracranial hemorrhage Brain swelling
Based on Mechanism of Injury Focal lesions 2ᵒ to ↑ICP

Mechanism Main pathology

Impact Vascular (hemorrhage) Based on Integrity of Skull
Traumatic axonal injury
Inertial Loading (rapid Traumatic axonal injury
acceleration-deceleration
Penetrating Local tissue necrosis Mechanism
Blast Brain swelling
Localization
Clinical Classification of TBI
Based on Onset of Symptoms
Primary Brain Damage
Immediate
Scalp laceration
Skull fracture
Concussion
Contusions/lacerations
Coup-Countercoup
Whiplash injury
Intracranial hemorrhage
Diffuse axonal injury
❖ Concussion
Open Brain Closed Brain o Aka mild traumatic brain injury (MTBI)
Damage Damage o Common among contact and collision
Penetrating Impact sports participants ranging from 0.1 to 21.5
Inertial Loading per 1000 athletic exposures.
Blast o Immediate, usually reversible, traumatically
Focal Diffuse induced physiologic disruption in brain
function that is manifested by LOC (<10%),
memory loss, alteration of mental state or
personality, or focal neurologic deficits.
o Anatomic bases: axonal disruption resulting
in disconnection between areas involved in
Secondary Brain Damage consciousness: cerebral cortex, brainstem
Minutes to days RAS, thalamus & hypothalamus.
Intracranial hemorrhage
Brain swelling / edema Concussion VS. Contusion
↑ ICP
Brain damage associated Concussion Contusion
w/ lack of oxygen Diffuse, widespread Bruise; often associated
Infection homogenous impairment of with swelling (edema)
Chemical changes leading functioning of brain tissue & ↑ICP
to cell death Widespread Localized (single/multiple)
Hydrocephalus Microscopic Macroscopic

PRIMARY BRAIN DAMAGE Contusion VS. Laceration

❖ Scalp Laceration Surface Laceration

o OPEN head injury with cognitive deficits. Intact arachnoid-pia Torn arachnoid-pia
o Caused by sharp or blunt forces
❖ Skull Fracture
o Hallmark of brain damage
o OPEN head injury with cognitive deficits
o Moderate (78%)
o Incidence
o Severe (10%)
▪ 3% mild
o Mild (6%) contusions found in 94% of
▪ 65% in those requiring admission
fatalities
▪ 80% in fatal injury
o Most likely location of cortical contusions:
Linear Depressed frontal & temporal lobe

❖ COUP CONTRE COUP

o CLOSED head injury with cognitive deficits.
Patho-anatomic Classification of TBI o Brain contusion at the site of impact (coup)
& opposite to site of impact (countercoup)
Based on Extent of Damage

Localized / Focal Damage Diffuse Damage Diastatic Basilar

Scalp laceration Global ischemic injury
Skull fracture Traumatic axonal injury
 Sub- Common(?) May be Basilar or Diffuse Axonal / Shearing Injury
arachnoid High associated vertebral
mortality with base of arteries ❖ Clinical syndrome of axonal tearing with supporting
skull fracture neuroradiological changes
Intra- 16-23% Multiple Blood ❖ The changes in the brain are often microscopic and
cerebral fatalities contusions vessels in may not be evident on CT scan or MRI
brain
Treatment

Intracranial hemorrhage: ❖ Prevention of TBI is the best approach since there is no

cure.
❖ Stages of treatment:
Response to TBI o Initial
o Acute
❖ Vascular damage -> Hemorrhage o Surgical
❖ Nerve damage - > Traumatic axonal injury o Rehabilitation

Intracranial Hemorrhage / Hematoma Initial Treatment

❖ Most common cause of clinical deterioration in ❖ Address all life threatening conditions
patients with lucid interval o CAB
❖ Types: ❖ Surgery for injuries
o Extradural / Epidural ❖ Transfer to specialized trauma care unit
o Subdural ❖ A psychologist familiar with acute trauma & a trauma
o Subarachnoid social worker will assist the patient and family in
o Intracerebral decision making.
❖ EARLY stabilization reduces the incidence of
hypotensive brain injury but NOT that of diffuse
ischemic injury

Acute Treatment

Traumatic Axonal Injury

Incidence Common Source of ❖ Contributes to atleast 35% of morbidity & mortality in

cause bleed TBI cases without space occupying lesions
Extradural 0.2-4% 85% of skull Middle ❖ Refers to the pathologic demonstration of damaged
Epidural 5-22% fracture meningeal axons in a pattern supporting traumatic etiology
fatalities (squamous artery ❖ Degrees of injury
part of the damage o Grade 1 : microscopic changes in white
temporal matter of cerebral cortex, corpus callosum, ❖ Aimed at minimizing secondary injury and life support.
bone) brainstem & cerebellum. o Mechanical ventilation
Subdural 5% 70% of skull Torn o Grade 2 : gross focal lesions isolated in o Intracranial pressure monitoring
20-63% fractures; superficial ❖ Medications
corpus callosum
fatalities often bridging o Sedatives to minimize agitation and
o Grade 3: focal lesion in dorsolateral
contralateral veins
quadrant of the rostral brainstem secondary injury
o Anticonvulsants
 o Coma-inducing medications to decrease
oxygen requirements of the brain
o Glucocorticoids & diuretics to reduce
cerebral edema
o For attention problems and aggressive
behavior
❖ To decrease ICP:
o Hyperventilation
o IV mannitol
o IV furosemide
o Reverse Trendelenburg position (if no
contraindication)
Surgical Treatment
❖ Overall goal: to prevent secondary injury by helping to
maintain blood flow and oxygen to the brain and
minimize swelling and pressure.
❖ Includes
o Hematoma evacuation
o Fracture repair
o De compressive craniotomy
Rehabilitation goals are to:
❖ Stabilize the medical and rehabilitation issues related
to brain injury and the other injuries
❖ Prevent secondary complications.
o Pressure sores
o Pneumonia
o Contractures
❖ Restore lost functional abilities.
o Limited ability to move
o Use the bathroom
o Talk, eat and think
Hyperbaric Oxygen
❖ 100% oxygen for one hour at 1.5 atmosphere absolute
❖ Induces neuroplasticity, cerebral angiogenesis and
improve both white and gray microstructures
indicating regeneration of nerve fibers
❖ Result
o Rapid improvement of headaches and sleep
disturbances, improvement in all symptoms
and resolution of most symptoms.
Prognosis
❖ 66% make a full recovery and 2% are permanently
disabled.
❖ Factors associated with poor outcome:
o Pre-injury back pain
o High frequency of GP attendance
o Evidence of pre-injury depression or anxiety
symptoms
o Front position in the vehicle
o Pain radiating away from the neck after
injury.
❖ Recovery from a TBI varies based on the individual and
the brain injury
o Moderate to severe TBI may cause lasting
cognitive and behavioural impairments.
❖ Indicators for prognosis:
o Duration of coma
▪ The shorter the trauma, better
the prognosis
o Post-traumatic amnesia
▪ Shorter the amnesia, better the
prognosis
o Extent of generalized atrophy
o Location & depth of focal cerebral lesions
o Age
▪ Patients over 60 or under age 2
have the worst prognosis
❖ The majority of sports-related concussions (80-90%)
resolve within 7-10 days.
❖ Recovery period is usually longer for children,
adolescent and athletes with a previous history of
injury.
Long Term Sequelae of TBI
❖ Vegetative state
o Seen in 71% of cases with grade 2/3 axonal
injury & 80% of thalamic pathology.
❖ Long term cognitive problems
o Possible neurodegeneration at a late stage
o Even mild head injury is associated with
higher-than-expected incidence of
disability.
CERVICAL SPINE TRAUMA
❖ Varies from minor ligamentous damage to ovet osteo-
ligamentous instability and spinal cord injury
❖ Incidence : 2-3% of all cases of blunt trauma
❖ Age & Sex : 20-30 yrs male ; elderly females
❖ Common cause: accidental fall, RTA
❖ Common site: atlantoaxial region and C6-C7 in the
subaxial cervical spine.
WHIPLASH INJURY
❖ Damage to both the cervical vertebrae and soft tissues
following a force that causes excessive hyperextension,
hyper flexion or rotation of the neck
❖ Most common injury resulting from rear-end vehicle
collisions at speeds of less than 14 miles per hour.
Types of Injury
1. Typical cervical hyperextension injuries
o Body is thrown forward but the head lags ->
neck hyperextensions till maximum
extension - > neck snaps into flexion
2. A rapid deceleration injury
o Head thrown forward into hyper flexion ->
cause longitudinal distraction and
neurological damage. Hyperextension may
occur in the subsequent recoil.
Epidemiology
❖ Trauma and sports injuries are more common in young
adults.
❖ Rates of whiplash are higher in
o Persons using a seatbelt with shoulder
restraint that with no restraints but
seatbelts often prevent more serious
injuries.
o Poor posture
o Poorly-fitted head restraints
o Women sustain higher rates of whiplash.
Probably because their neck muscles are
less well developed than men’s.
o Narrowing of the cervical spinal canal due
to acquired or congenital disorders
predisposes to spinal cord damage.
Symptoms
❖ May not develop until 6-12 hrs after the injury, or even
after a few days
❖ Include
o Neck pain, jaw pain
o Paraspinal muscle tightness and muscle
spasm
o Headache, fatigue, dizziness, vertigo,
blurring of vision, nausea
o Numbness or weakness in shoulders & arms
= injury to nerve root
o There may be retropharyngeal swelling and
dysphagia
o Insomnia, anxiety or depression
 o Leg weakness, hyperactive tendon reflexes ❖ Exercise
in the legs, up going plantar response, o Effectiveness of exercise for neck pain is
and/or sphincter disturbances = damage to questionable
the spinal cord. o Using specific strengthening exercises as a
part of routine practice for chronic neck
WHIPLASH-ASSOCIATED DISORDERS (WAD) pain, cervicogenic headache and
radiculopathy may be beneficial.
❖ Risk factors for serious injury
o Immediate onset of neck pain following the
event
o Age 65 years or older
o Dangerous mechanism of injury (a fall
greater than 1 m) or a side impact collision.
o Unable to walk about or sit following the
injury.
❖ Classification
o Grade 0: No complaints or physical signs.
o Grade 1: Indicates neck complaints but no
physical signs.
o Grade 2: Indicates neck complaints and
musculoskeletal signs
o Grade 3: Neck complaints and neurologic
signs
o Grade 4: Neck complaints and
fracture/dislocation.

Management

❖ Reassurance that whiplash-associated disorder is

usually benign and self-limiting.
❖ Encouragement of early return to usual activities and
early mobilization.
❖ Discouragement of rest, immobilization and the use of
soft collars.
❖ Provision of adequate analgesia:
o IM Lidocaine for chronic mechanical neck
disorders & IV methylprednisone for acute
whiplash.
o NSAIDs and muscle relaxants have limited
evidence of effectiveness
o Acupuncture treatment for patients with
chronic neck pain
o Multiple cervical manipulation sessions may
provide better pain relief and functional
improvement than certain medications at
immediate/long term follow up.
▪ There is a risk of very rare but
serious adverse events for
manipulation, arterial dissection,
myelopathy, vertebral disc
extrusion and epidural
hematomas.