Head injuries

HEAD INJURIES
Tracy Bedford, CRNA, MSN
MedLaw Consulting
312-525-1700

Tracy Bedford MedLaw Consulting 312-525-1700 www.medlaw-consulting.com

HEAD INJURY – “an injury clinically evident on physical examination and is recognized by the presence of ecchymoses, lacerations, deformities, or cerebrospinal fluid leakage.”
TBI – “injury to the brain itself and is not always clinically evident; if unrecognized, it may result in an adverse outcome.”

TBI
CDC definition – “craniocerebral trauma, specifically, an occurrence of injury to the head (arising from blunt or penetrating trauma or from acceleration/deceleration forces) that is associated with any of these symptoms attributable to injury: decreased level of consciousness, amnesia, other neurologic or neuropsychological abnormalities, skull fracture, diagnostic intracranial lesions, or death.”

Who gets TBI?

STATISTICS

ANATOMY

CEREBRUM
Largest part of the brain
2 hemispheres (left and right)
Lobes of the brain
2 layers
Gray matter of cerebral cortex
White matter

FRONTAL LOBE
Problem solving
Judgment
Inhibitions
Planning
Motor
Personality
Emotions
Organization
Attention and concentration
Expressive language/speaking

TEMPORAL LOBES
Memory
Hearing
Receptive
language/
understanding
Organization
Sequencing

PARIETAL LOBE
Sense of touch
Identification of shapes, colors
Spatial perceptions
Visual perceptions

OCCIPITAL LOBE
Vision

BRAINSTEM
Regulatory control of heart rate, respirations, BP
Arousal
Consciousness
Sleep & wake cycles
Attention and concentration

CEREBELLUM
Balance
Coordination
Skilled motor

MENINGES
Dura mater
Arachnoid
Pia mater

NEURONS
Nerve cells that carry impulses to and from the brain
Axons transmit electrical impulses, stimulating sensory and motor responses throughout the body

MECHANISMS OF INJURY
Blunt force trauma
Acceleration/
deceleration
Coup-contrecoup
Car accident
Fall
Penetrating injury
Gun shot wounds
Shock waves
Stab wounds
Usually on left side

PATHOPHYSIOLOGY
Primary injury
Initial injury sustained
Secondary injury
Metabolic changes occurring due to primary injury that further damage

SEVERITY OF INJURY = amount of brain tissue damage
How to measure:
Duration of loss of consciousness
Initial GCS
Length of
posttraumatic
amnesia
Rancho Los Amigos Scale

GLASGOW COMA SCALE
EYE OPENINGPOINTS
Eyes open spontaneously 4
Eyes open verbal command 3
Eyes open only with painful stimuli 2
No eye opening 1
VERBAL RESPONSE
Oriented and converses 5
Disoriented and converses 4
Inappropriate words 3
Incomprehensible sounds 2
No verbal response 1
MOTOR RESPONSE
Obeys verbal commands 6
Response to painful stimuli
localizes pain 5
withdraws from pain 4
flexor posturing 3
extensor posturing 2
no motor response 1

MILD INJURY
Disruption of
brain function
Alteration in
consciousness
GCS 13-15
PTA < 24 hours
Symptoms can
occur days, weeks,
or months after injury

Concussions Class I TBI
Minimal TBI Low-risk TBI
Grade I TBI

MTBI

Post-MTBI
Increased risk for seizures
Headaches
Cranial nerve injuries
Loss of smell
Loss of taste
Diplopia
Facial pain
Occipital neuralgia
Vertigo

CONCUSSION
Classic signs – confusion and amnesia
On CT, little to no abnormality due to no gross or microscopic tissue abnormalities
Most recover fully within weeks/months
High risk for secondary injury: Second Impact Syndrome
Post concussion syndrome
Higher morbidity with repeat injuries

POST CONCUSSION SYNDROME
Headaches
Dizziness
Fatigue (physical and mental)
Visual changes
Sensitive to noise and light
Decreased concentration and memory problems
Anxiety/depression
Irritability
Mood swings
Sleep disturbances

MODERATE INJURY
Unconscious for
20 minutes to
6 hours
GCS 9 – 12

SEVERE INJURY
Unconsciousness greater than 6 hours
GCS 3 - 8
About 20% of head injuries results in severe TBI
30% risk of death
25% achieve long-term functional independence
Management is aimed at preventing secondary brain injury

Causes of TBI

STATISTICS
Risk of death after head injury remains significantly increased for up to 13 years
Death rate is highest in the 1st year after head injury and is the greatest in moderate and severe TBI
Years 2 – 13: mortality is the same in all groups (mild, moderate, severe)

ACCELERATION/DECELERATION

Acceleration/deceleration forces alone are enough to cause severe TBI
Damage to the axons can result in swelling (edema) and axonal separation
With severe injury, axons can rupture

DIFFUSE AXONAL INJURIES
Visible only on MRI
High index of suspicion with multiple small cerebral contusions on CT

MECHANISMS OF INJURY
Acceleration – when a moving object strikes the head
Deceleration – when the head is in motion and strikes a stationary object
Acceleration/deceleration – brain moving rapidly within the skull, resulting in a combination of injury -causing forces.
Nerve fibers may be stretched, torn, or completely severed
Diffuse head injury
Coup-contrecoup

Monro-Kellie doctrine
The three components of the brain create a fixed volume
Brain tissue (80%)
CSF (10%)
Blood (10%)
*Any change in volume in one requires the others to decrease volume to compensate, or ICP will rise

IMPENDING HERNIATION
Symptoms
Ipsilateral dilated pupil
Cushing’s reflex
Hypertension
Bradycardia
Respiratory depression/irregularity

VASCULAR TRAUMA

EPIDURAL HEMATOMA (EDH)
A blood clot that forms under the skull on top of the dura
Lens-shaped on CT scan
Usually arterial bleed
Earlier surgical intervention associated with decreased mortality

EDH
Acute, symptomatic
-neurologic emergency
1-4% of TBI cases
Highest incidence in
adolescents and
young adults
Most are due to head trauma from MVAs, falls, and assaults
Associated with skull fracture in 75-95%

EDH symptoms
Severe head trauma
– comatose
Lesser injury
– momentary loss
of consciousness
Lucid interval
Headache
Vomiting
Drowsiness
Confusion
Seizures
Hemiparesis (paralysis affecting only one side of the body)

EDH – venous bleed
Neurologic decline occurs over days to weeks
DEATH

SUBDURAL HEMATOMA (SDH)
Bleeding below dura
Usually venous bleed
Crescent-shaped on CT
50% are comatose after the injury
Up to 38% have a lucid interval

Acute traumatic SDH
Those at increased risk
Incidence highest in middle-aged men
Preexisting significant cerebral atrophy
Elderly
Chronic alcohol abuse
Previous TBI
Use of antithrombotics

Chronic SDH
Symptoms evident days or weeks after the initial trauma and may be intermittent
May c/o headaches, lightheadedness, cognitive impairment, apathy, somnolence, seizures, change in consciousness

Diagnosis and treatment - SDH
Diagnosed via CT scan
Treatment based on neuro exam
Surgical evacuation of clot
Acute SDH > 10mm thick
Midline shift > 5mm
Control of bleeding

Subarachnoid hemorrhage (SAH)
Bleeding below the arachnoid membrane
Sudden, severe
headache

Intracerebral hematomas
Bleeding in the cerebral tissue
Caused by
Depressed skull fractures
Penetrating injuries
Acceleration/deceleration injuries
Medical and/or surgical management

PENETRATING INJURIES
Simple closure
Superficial debridement and dural closure
Antibiotics
Surgery

SKULL FRACTURES
Linear
Most heal spontaneously
Depressed
Great force required
Surgical treatment
Basilar
Serious blow to the back of the head
Raccoon eyes – bruising around the eyes
Battle’s sign – bruising behind the ear
Observation for 24-48 hours
Open
Scalp laceration allows direct exposure
of brain tissue
Increased risk for infection

Left-sided brain injury
Language reception – difficulty understanding
Expressive language – difficulty trying to say what they are thinking
Verbal memory deficits
Impaired logic
Decreased control over the right side of the body

Right-sided brain injury
Visual-spatial impairment
Visual memory deficits
Decreased control over the left side
Altered creativity and music perception
Loss of “the big picture”

PREHOSPITAL

Evaluation of head trauma in the ED setting
GOAL – to identify which patients have an acute traumatic injury and which patients can safely be sent home
Assessment
GCS
Neuro exam
Pupillary signs
Neuroimaging results
VS

Primary survey
ABCDE
Airway – assess, protect , maintain cervical stabilization
Breathing – adequately oxygenate
Circulation – control hemorrhage, maintain organ perfusion (HR, BP)
Disability assessment – basic neuro evaluation
Exposure

SECONDARY SURVEYgoal – identify injuries
Full head-to-toe assessment
Detailed history
Mechanism of injury
History of injury
Physical exam
Specific diagnostic studies

GOALS
Stabilize the patient
Identify who needs surgical intervention
Prevent secondary injury
Hypoxia
Hypercarbia
Hypotension
Hypovolemia
Electrolyte abnormalities
Hyperthermia

Intracranial hypertension (ICH)
Medical emergency
Goal – to address the underlying cause
Ways to reduce ICP
Sedation
Positioning
Normothermia
CSF drain
Antiepileptic medications
Osmotic diuretics
Decompressive craniectomy

Symptoms of increased ICP
Global
Neurologic deterioration
Vomiting
Cushing’s triad
Focal
Local effects

ICP monitoring
Comatose with GCS 3-8 and abnormal neuroimaging
Comatose with normal
imaging with at least one of the following:
>40 years old
Motor posturing
Systolic BP <90

CT scan
Widely used
Speed
Simplicity
Availability
Neurosurgical abnormalities are visible on CT
Better imaging of high velocity penetrating wounds (bullets vs. knife)

Up to one-third of patients with normal scans developed CT abnormalities within the first few days after closed head injury

Limitations of CT
Small lesions may not be detected
SDH < 3mm
Possible that CT limits the diagnosis of lesions responsible for PCS
Low velocity penetration causes less tissue damage, so not as visible on CT

Benefits of MRI
Better visualization of axonal injury
More specific for soft tissue damage
More sensitive for detection of small lesions (SDH, areas of contusion, hematomas)
Used in the presence of a negative CT but a high suspicion for intracranial hemorrhage

MRI
Done to exclude other causes for those with persistent, disabling complaints who did not have MRI during acute injury evaluation
As MRIs technologically advance, they may play an important future role in MTBI diagnosis and management

Limitations of MRI
Cost
Availability
Accessibility
Safety in use with metal implants (ex. pacemakers)
Life-saving devices may not be compatible (ventilator, etc.)
Patient motion

WHAT AFFECTS RECOVERY
Increased age
Area and extent of injury
Lower GCS
Longer coma duration (>4 weeks)
Length of PTA
Imaging studies
Time since injury
Skills and behavior before injury
Motivation for recovery
Substance abuse/alcohol
Past bruising/concussion

RECOVERY
Full recovery
New baseline of cognitive function
Life-long deficits
Rehabilitation team
Physical therapy
Occupational therapy
Speech therapy
Neuropsychologist
Persistent vegetativestate
Death

“Traumatic brain injury is the most misunderstood, misdiagnosed, underfunded public health problem our nation faces.”
- Susan Connors, president of the Brain Injury Association of America

BONUS MATERIAL

MILITARY
Blasts
Blunt force trauma
Increased survival due to advancements in protective equipment and body armor
Falls
MVAs
Fragment, shrapnel, bullet wounds
Complications
Shock
Hypoxia
Skull fracture
SDH
EDH
seizures

CHILDREN
Most frequent up to 1 year of age
Usually prior abuse
Frequent delayed diagnosis
Perpetrators are generally male and frequently the father of the child
Abusive head trauma – most common cause of death
skull fractures
Retinal hemorrhages – alone is not definitive evidence for child abuse
Intracranial bleeding
Subdural hematomas
Initial CT, then follow-up with MRI
MRI to document the pattern, extent, and timing of injuries

Children
Initial clinical presentation is often nonspecific with no outward sign of trauma
Child may present with irritability, lethargy, feeding difficulties
Head trauma is associated with
SDH
SAH
Massive cerebral edema

TERMS
Contusion – bruising of the brain
Coup – initial site of impact
Contrecoup – rebound site of impact (opposite of coup injury)
Ecchymosis – bruising
Edema –swelling
Epistaxis – nose bleed
Deceleration injury – the head is moving and strikes a stationary object
Acceleration injury – the object strikes the head

TERMS
Deformation forces – force great enough to change the shape of the skull and cause compression of the brain tissue
Focal – localized area
Hemiplegia – paralysis on one side of the body
Apraxia – inability to perform purposeful movements (although no sensory or motor deficit is present)
Tinnitus – ringing in the ears
Cognition – thinking capability
Foramen magnum – opening in the occiput bone at the base of the skull where the spinal cord passes

TERMS
Hypertension – increased blood pressure
Bradycardia – low heart rate (<60)
Cushing’s triad – hypertension, bradycardia,
Anisocoria – unequal pupil size
Contralateral – (affecting) the opposite side
Ipsilateral – on the same side
Hematoma – swelling of blood in a confined space (caused by broken blood vessel)
Ecchymosis – bruising
Meninges – membranes of the spinal cord and brain (dura, arachnoid, pia)

TERMS
Hypothermia – body temperature below normal
Retrograde amnesia – loss of memory just before the trauma took place
Antegrade amnesia – loss of memory just after
Coup – primary site of impact
Contrecoup – secondary impact
Antithrombotic agent – medication that interferes with blood coagulation (blood thinner)
Encephalopathy – any dysfunction of the brain
Papilledema – edema and inflammation of the optic nerve
Periorbital – around the eye

TERMS
Vasospasm – spasm of a blood vessel
LeForte fracture – a type of facial fracture. The grade (I, II, or III) will summarize the location and severity of fracture
Ventriculostomy – a catheter placed in the ventricle of the brain, allowing for measurement of ICP and drainage of CSF
Hypoxia – oxygen deficiency
Hypercarbia – increased carbon dioxide in the blood (from hypoventilation)
Hypovolemia – low blood volume
Hypoglycemia – decreased blood sugar (glucose in the blood)

TERMS
Hyponatremia – low sodium in the blood
Hypernatremia – elevated sodium
Hydrocephalus – increased CSF in the brain ventricles
Orbital – bony cavity of the skull the contains and protects the eyeball
Hyphema – blood in the anterior chamber of the eye
Proptosis – orbital hematoma
(cerebrospinal) rhinorrhea – CSF leak as evidenced by clear fluid from the nose
(Brain) herniation – protrusion of brain through an opening in the skull
Decompressive craniectomy – removal of a portion of the skull to relieve increased ICP

TERMS
Pyrexia – fever
Morbidity – a disease state
Mortality – death rate
Hemotympanum – blood in the middle ear
Neuralgia – severe, sharp pain along the course of a nerve
Anosmia – loss of smell
Syncope – decreased level of consciousness due to decreased blood flow to the brain
Hygroma – a sac containing fluid
Bilateral – both sides
Unilateral – pertaining to one side

ABBREVIATIONS
TBI – traumatic brain injury
GSW – gunshot wound
GCS – Glasgow coma scale
CSF – cerebral spinal fluid
HR – heart rate
RR – respiratory rate
BP – blood pressure
ICP – intracranial pressure
HTN – hypertension
LOC – loss of consciousness
PERL – pupils equal and reactive to light

ABBREVIATIONS
PTA – posttraumatic amnesia
Fx – fracture
SDH – subdural hematoma
EDH – epidural hematoma
SAH – subarachnoid hemorrhage
IVH – intraventricular hemorrhage
ICH – intracranial hypertension or intracerebral hemorrhage
DAI – diffuse axonal injury
CT – computed tomography
MRI – magnetic resonance imaging
c/o – complaint of

ABBREVIATIONS
HA – headache
MVA – motor vehicle accident
CPP – cerebral perfusion pressure
MAP – mean arterial pressure
PCS – postconcussion syndrome
AHT – abusive head trauma
CBF – cerebral blood flow
SIS – second impact syndrome
NAI – nonaccidental injury (in children)
ABX – antibiotics
CN – cranial nerve
B/L - bilateral

MECHANISMSwith their associatedINJURIES

MECHANISMINJURIES
Head-on collision facial injuries
Windshield damage closed head
injuries, coup
contrecoup injuries
Restraint/seat belt head and facial
fractures/injuries

PEDESTRIAN VS. AUTOMOBILE
High speed craniofacial injuries
Bicycle vs. car closed head injuries
FALLS
Vertical impact closed head injuries
Horizontal impact craniofacial fractures

REFERENCES
Bradley, W. G., Daroff, R. B., Fenichel, G. M., & Jankovich, J. (5th ed.). (2008). Neurology in clinical practice. Philadelphia, PA: Butterworth Heinemann.
Brain Trauma Foundation, American Association of Neurological Surgeons, and Congress of Neurological Surgeons. (2007). Guidelines for the management of severe traumatic brain injury. Journal of Neurotrauma; 24:Suppl 1. doi: 10.1089/neu.2007.9994
DeLee, J., Drez, D., & Miller, M. D. (3rd ed.). (2010). Orthopaedic Sports Medicine: Principles and practice. Philadelphia, PA:Saunders.

REFERENCES
Jagoda, A. S., Bazarian, J. J., Bruns, J. J., Cantrill, S. V., Gean, A. D., Howard, P. K.,…Whitson, R. R. (2008). Clinical policy: Neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Annals of Emergency Medicine, 52(6), 714-748.
Marx, J. A., Hockberger, R. S., Walls, R. M., Adams, J., & Rosen, P. (7th ed.). (2010). Rosen’s emergency medicine: Concepts and clinical practice. Philadelphia, PA: Mosby.
Report of (VA) consensus conference: Practice recommendations for treatment of veterans with comorbid TBI, pain, and PTSD. (2010). Retrieved from http://www.ptsd.va.gov/professional/pages/handouts-pdf/TBI_PTSD_Pain_Practice_Recommend.pdf

REFERENCES
Thomas, C. L. (16th ed.). (1989). Taber’s cyclopedic medical dictionary. Philadelphia, PA: F. A. Davis.
U.S. Department of health and human services: Centers for disease control and prevention. Heads up: Facts for physicians about mild traumatic brain injury (MTBI). Retrieved from http://www.cdc.gov/concussion/headsup/pdf/Facts_for_Physicians_booklet-a.pdf

REFERENCES
FULL ARTICLES OBTAINED FROM THE DATABASE UpToDate, found at www.uptodate.com
Blackwell, T. (2010, May 17). Prehospital care of the adult trauma patient. Retrieved from http://www.uptodate.com/contents/prehospital-care-of-the-adult-trauma-patient?source=search_result&selectedTitle=1%7E150
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REFERENCES
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REFERENCES
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REFERENCES
Heegaard, W. G., & Biros, M. H. (2009, October 15). Skull fractures in adults. Retrieved from http://www.uptodate.com/contents/skull-fractures-in-adults?source=search_result&selectedTitle=2%7E55
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McBride, W., & Brock, D. G. (2010, January 13). Subdural hematoma in adults: Etiology, clinical features, and diagnosis. Retrieved from http://www.uptodate.com/contents/subdural-hematoma-in-adults-etiology-clinical-features-and-diagnosis?source=search_result&selectedTitle=2%7E93

REFERENCES
McBride, W., & Brock, D. G. (2010, January 13). Subdural hematoma in adults: Prognosis and management. Retrieved from http://www.uptodate.com/contents/subdural-hematoma-in-adults-prognosis-and-management?source=search_result&selectedTitle=1%7E93
Neuman, M. I., & Bachur, R. G. (2010, December 17). Orbital fractures. Retrieved from http://www.uptodate.com/contents/orbital-fractures?source=search_result&selectedTitle=1%7E14
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REFERENCES
Raja, A., & Zane, R. D. (2010, September 27). Initial management of trauma in adults. Retrieved from http://www.uptodate.com/contents/initial-management-of-trauma-in-adults?source=search_result&selectedTitle=4%7E150
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Siddiq, F., & Brock, D. G. (2010, April 16). Nonaneurysmal subarachnoid hemorrhage. Retrieved from http://www.uptodate.com/contents/nonaneurysmal-subarachnoid-hemorrhage?source=search_result&selectedTitle=3%7E149
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