Traumatic Head Injury
(Relates to Chapter 63 “Management of Patients with Neurologic Trauma” in the textbook)
• Differentiate head injuries according to mechanism of injury and clinical signs and symptoms
• Identify diagnostic testing, and treatment options
• Describe the nursing management of patients with head injury
• Discuss the need for injury prevention
Head Injury
• Any trauma to the
– Scalp
– Skull
– Brain
• Head trauma includes an alteration in consciousness, no matter how brief
Causes
– Motor vehicle accidents
– Falls
– Assaults
– Firearm-related injuries
– Sports-related injuries
– Recreational accidents
• Highest risk age group is 15-24 (males twice as likely)
• <5 or >75 are at very great risk for traumatic head injury
•
Advise drivers to obey traffic laws, and to avoid speeding or driving when under the influence of drugs or
alcohol.
• Advise all drivers and passengers to wear seat belts and shoulder harnesses. Children younger than 12 years of
age should be restrained in an age/size-appropriate system in the back seat.
• Caution passengers against riding in the back of pickup trucks.
• Advise motorcyclists, scooter riders, bicyclists, skateboarders, and roller skaters to wear helmets.
• Promote educational programs that are directed toward violence and suicide prevention in the community.
• Provide water safety instruction.
• Teach patients steps that can be taken to prevent falls, particularly in the elderly.
• Advise athletes to use protective devices. Recommend that coaches be educated in proper coaching techniques.
• Advise owners of firearms to keep them locked in a secure area where children cannot access them.
• High potential for poor outcome
• Deaths occur at three points in time after injury
– Immediately after the injury (initial trauma)
– Within 2 hours after injury (progressive injury/internal bleeding)
– 3 Weeks after injury (MODS)
PRIMARY INJURY – IMMEDIATE INJURY
SECONDARY INJURY – EVERYTHING ELSE ( POSSIBLY DUE TO INCREASED ICP, LACK OF O2 ETC….)
Types of Head Injuries
• Scalp lacerations (most common)
– Can bleed profusely
– Can be hematoma, lg evulsion under the scalp
• Skull fractures
– Linear or depressed (break in bone without alteration of parts- low velocity injury)
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Simple, comminuted, or compound (can be with our without fragments- low to moderate impact injury.
Comminuted – direct blow – high momentum impact – bone fragmented into many pieces. Compound –
severe head injury, usually a depressed skull facture, scalp laceration with a communicating pathway
into the intracranial cavity-open)
– Closed or open
Frontal fx – may see air in the forehead tissue, may see CSF rhinorrea
Orbital fx – Raccoon eyes, optical nerve injury – will have nerve intrapment
Parital fx – facial paralysis, battle signs
Basilar skull fx – CSF leakage (ears, nose) battle sign, difficulty hearing, facial paralysis, gazed stare, veritgo – due
to open pathway - could lead to menenigel(sp) infection
Minor head trauma (temporary LOC with no apparent structural damage)
– Concussion
– Mild and Classic (MILD - memory laps, may see LOC, can include seizure, HA, dizziness. CLASSIC – will
result in LOC- lasting <6hrs, always followed by some degree of post injury amnesia. NO structural
damage on either)
Major head trauma
– Contusion – moderate to severe head injury – bruise on brain – impact of brain against the skull –
characterized by LOC (stupor/confusion)
– Lacerations – involve actual tearing of brain tissue
Diffuse axonal injury (DAI)
– Widespread axonal damage occurring after a mild, moderate, or severe TBI
– Process takes approximately 12 to 24 hours
– Damage occurs around
• Axons in subcortical white matter of the cerebral hemispheres
• Basal ganglia
• Thalamus
• Brainstem
Diffuse axonal injury (DAI) – responsible for most cases of post traumatic disorders. Also in conjucntion with
hypoxic ischemic injury. Lesions occur from sudden accelerations/deceleration injury. Most common cause of
vegetative state
– Clinical signs
• Decreased LOC
• Increased ICP
• Decerebration or decortication
• Global cerebral edema
Epidural hematoma
– Results from bleeding between the dura and the inner surface of the skull
– Neurologic emergency**
– Venous or arterial origin – usually 99% a tear in the arterial origin (middle meningel)
– More common in young people, because the dura is not attached
– Classic signs include
• Initial period of unconsciousness
• Brief lucid interval followed by decrease in LOC
• Headache
• Nausea, vomiting
• Focal findings
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Subdural hematoma
– Occurs from bleeding between the dura mater and arachnoid layer of the meningeal covering of the
brain
– Most common source is the veins that drain the brain surface into the sagittal sinus
– Usually venous in origin
• Much slower to develop into a mass large enough to produce symptoms
– May be caused by an arterial hemorrhage
– Acute subdural hematoma
• Signs within 48 hours of the injury
• Similar signs and symptoms to brain tissue compression in increased ICP
• Patient appears drowsy and confused
• Ipsilateral pupil dilates and becomes fixed
*High rate of mortality due to secondary injury related to it.
– Subacute subdural hematoma
• Occurs within 2 to 14 days of the injury
• After initial bleeding, subdural hematoma may appear to enlarge over time
– Chronic subdural hematoma
• Develops over weeks or months after a seemingly minor head injury
• Peak incidence in sixth and seventh decades of life – due to brain atrophy
– Chronic subdural hematoma
• Presenting complaint often focal symptoms, not signs of increased ICP
• Delay in diagnosis in older adults because symptoms mimic those of vascular disease and
dementia
• Intracerebral Hematoma
– Occurs from bleeding within the parenchyma (unreachable bleed)
• Usually occurs within the frontal and temporal lobes
• Size and location of hematoma determine patient outcome
• Will have neurological symptoms – HA, systemic HTN…etc
• Often seen with bullet injuries
• Subarachnoid Hematoma
– Bleeding into the subarachnoid space
• Most common causes are subarachnoid aneurysm, head trauma, or hypertension
• Can happen with trauma, especially in the elderly
Vasospasms – development of cerebral vasospasm – constriction - occurs 3-14 days after initial hemorrhage – s/s –
horrible HA, decreased LOC, confusion, focal deficit. Will be medicated with Nimotop**, triple H therapy : hypervolemia,
induce arterial HTN, hemodilution
Intracerebral and Subarachnoid Hematoma
• Berry aneurysm
• Berry aneurysm
Diagnostic Studies and Collaborative Care
• CT scan
– Best diagnostic test to determine craniocerebral trauma
• MRI
• PET
• Transcranial Doppler studies – looking for vasospams
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Cervical spine x-ray (1-7)
Glasgow Coma Scale (GCS)
Treatment principles
– Prevent secondary injury
– Timely diagnosis
– Surgery if necessary
• Craniotomy
• Craniectomy
• Cranioplasty
• Burr-hole
Nursing Management
• Nursing assessment
– Airway
– Glasgow Coma Scale score
– Neurologic status
– Presence of CSF leak
– Collaborative problem: Increased ICP
GLASGOW COMA SCALE
Eye
opening
response
Best
verbal
response
Best
motor
response
Spontaneous
4
To voice
3
To pain
2
None
1
Oriented
5
Confused
4
Inappropriate
words
3
Incomprehensible
sounds
2
None
1
Obeys command
6
Localizes pain
5
Withdraws
4
Flexion
3
Extension
2
None
1
Total
**Base it on mental integrity not mechanical ability
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Planning
– Overall goals
• Maintain adequate cerebral perfusion
• Remain normothermic
3
to
15
• Be free from pain, discomfort, and infection
• Attain maximal cognitive, motor, and sensory function
• Nursing implementation
– Acute intervention
• Maintain cerebral perfusion
• Prevent secondary cerebral ischemia
• Monitor for changes in neurologic status
• Treatment of life-threatening conditions will initially take priority in nursing care
• Nursing implementation
– Ambulatory and home care
• Nutrition, Bowel / bladder control
• Seizure disorders, Personality changes
• Family participation and education
Pathologic reflexes
• Babinski’s sign
• Grasp
• Snout – tap on lip…purse their lips. That’s pathological. Know something is going on
• Oculocephalic Reflex
“Doll’s Eye Movement”
– Normal Doll’s Eye (brainstem intact)
• Eyes move opposite direction of head rotation (remain focused on what pt may be viewing)
– Abnormal Doll’s Eye (brainstem injury)
• Eyes follow direction of head rotation
• Poss. loss of gag & cough reflex
• http://medstat.med.utuh.edu
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“Cold Caloric Testing”
Intact brainstem
– Nystagmus, w/ eyes slowly move toward ear irrigated w/ cold water & rapid movement away
• Severe brainstem damage
– Both eyes fixed midline position
• Inhibition of reflex
– Neuromuscular blockers
– Barbiturates
– Persistent Vegetative State
• absence of awareness of self and environment
• inability to interact with others
• no voluntary responses
• lack of language comprehension
• brain stem function to maintain life
• condition has continued for at least 1 month**
Brain Death
• Brain death is defined as the irreversible loss of function of the brain, including the brain stem
• Brain death is a clinical diagnosis, and a repeat evaluation at least 6 hours later is recommended
• Medical documentation should include cause and irreversibility of the condition
– Corneal reflex absent
– Gag reflex absent
– Apnea
– Angiography
– Consider an EEG
• CARDINAL SIGNS OF BRAIN DEATH ARE – ABSENCE OF BRAINSTEM FUNCTION, APNEA AND COMA
• Life Gift
• 806-798-5568
• www.lifegift.org
Tissue
One donor can help 70 people
– Bone
– Skin
– Tissue – ligaments, tendons
– Veins
– Heart valves
– Eyes/corneas
– Organs
One donor can save 8 lives!
– Heart
– Lung (can be single or double)
– Liver
– Kidneys (2)
– Pancreas
– Intestine
Pt must be intubated, on a vent, no sedation, GCS <5, posturing, no painful stimuli
Background
• Texas law: you are brain dead “when your doctor says you are brain dead”
– Family doesn’t have the choice to leave a brain-dead pt on vent indefinitely
Brain Death Testing
• Clinical exam
– GCS 3
– No brain stem reflexes
• Apnea test
– Baseline ABG is obtained
– Vent removed, supplemental O2 provided (lasting for 5-8mins)
• Cerebral Blood Flow
– Scan assesses for entry of dye into brain
• Cerebral Arteriogram
– 4 vessel study
– Absolute determination**
• EEG
– Artifact may cause false interpretation
– Slow turnaround on results of study
Donor Management
• “What’s good for the patient is good for the donor”
– Normal labs, ABGs, CXRs
– Normal vital signs
– Urine output 50-300 ml/hour
• Adequate oxygenation
• How do You sign up?
• Register as a donor at www.donatelifetexas.org
– Centralized state registry
– First person consent
– Coordinators can search the registry with the pt’s information, speeding up the donation process
Summary
• Maintain airway
• Early diagnosis and treatment
• Prevention of secondary injury
• Maintain cerebral perfusion pressure