8. Head Injury
High potential for poor outcome
Deaths occur at three points in time
after injury:
– Immediately after the injury
– Within 2 hours after injury
– 3 weeks after injury
10. Types of Head Injury
Scalp injury : minor injury
resulting in laceration, abrasion
& hematoma
Skull injury : may occur with
or without damage to brain.
Brain injury
11. Head Injuries
Closed or blunt: blunt object damages
the brain and its coverings without actually
perforating the skull or dura.
Penetrating: when the skull and brain
are directly lacerated by an object such as a
bullet, or piece of bone.
Coup-Contrecoup Injuries : same
blow causes injury on opposite sides
of the brain.
12. Skull Fractures
Linear Skull Fracture: is a break in the continuity
of the bone, appear as thin lines on X-ray.
Depressed Skull Fracture - The broken piece
of skull bone is pressed towards or embedded in the
brain.
Comminuted and Compound Skull Fracture -
The scalp is cut and the skull is splintered, multiple
fractures.
Basilar Skull Fracture
The skull fracture is located at the base of the skull
and may include the opening at the base of the skull
15. Some Signs of Skull
Fractures
– CSF or fluid draining from ear (“halo”
sign)
– Blood behind tympanic membrane
– Raccoon Eyes: periorbital ecchymoses
– Battles Sign: bruise over mastiod process
– Cranial nerve and inner ear damage
16. Battles’ sign
Often occurs in
fractures at base of
skull (posterior cranial
fossa).
Large "black and blue
mark" looking areas
below the ear, on the
jaw and neck.
It may include damage
to the nerve for
hearing.
CSF Otorrhea:
cerebral spinal fluid
may leak out of the
17. Raccoon Eyes
The skull fracture
produces "black and
blue" mark looking
areas around the
eyes.
CSF Rhinorrhea:
cerebral spinal fluid
may leak into the
sinuses and out of
nose.
20. Traumatic brain injury (TBI) is
An insult to the brain, caused by an
external physical force, that may
produce physical, intellectual,
emotional, social and vocational
changes.
Major causes of TBI motor vehicle
accidents, falls, acts of violence, sports
& recreational injuries, blows to head,
child abuse (shaken baby syndrome).
21.
22. Mechanisms of Brain
Injury
Acceleration injury occurs
when the immobile head is struck
by a moving object.
Deformation injury : the force
results in deformation and
disruption of the impacted part,
(skull fracture)
23. Mechanisms Cont’d
Deceleration injury : head is moving
and hits an immobile object (car
accident-hitting steering wheel)
Acceleration-deceleration injury :
moving object hits immobile head and
then head hits immobile object.
Associated with rotation injury where
brain is twisted in the skull (whiplash).
26. Types of Brain Injury
Concussion: is a head trauma that may or
may not result in loss of consciousness (for 5
minutes or less) and retrograde amnesia.
Contusion: is a severe injury in which the
brain is bruised resulting in swollen brain
tissue, areas of hemorrhage, infarction,
necrosis, edema. Results in loss of
consciousness and symptoms of shock.
27. Concussion
May experience only dizziness and feel “dazed”.
Retrograde amnesia
Treatment involves observing patient for headache,
dizziness, lethargy, irritability and anxiety.
Client should resume normal activities slowly and the
following should be watched for: difficulty in awakening or
speaking, confusion, severe headache, vomiting or
weakness on one side of the body.
May or may not show up on CAT scan.
Blood clot can occasionally occur causing death
Months to years to heal
28. Contusion
Depends on which areas of the brain
damaged – cerebral hemispheres, brain stem
(RAS)
Can cause diffuse axonal type injury resulting
in permanent or temporary damage
If widespread injury, abnormal eye movement
and motor function, increased intracranial
pressure and herniation - poor outcome.
May have residual damage, seizures
30. Diffuse Axonal
Injury:
severe widespread
injury to axons in
the cerebral
hemispheres,
corpus collosum
and brain stem.
31. Diffuse Axonal Injury
Extensive tearing of nerve tissue throughout the brain
causing the release of chemicals, causing additional
injury.
Immediate coma, decerebrate & decorticate posturing,
and global edema
The tearing of the nerve tissue disrupts the brain’s
regular communication and chemical processes
producing temporary or permanent widespread brain
damage, coma, or death.
A person with a diffuse axonal injury could present a
variety of functional impairments depending on where
the shearing (tears) occurred in the brain.
32. Intracranial
Hemorrhage
Intracranial hematomas
are collections of blood
that develop within the
cranial vault.
Three kinds: epidural,
subdural & intracerebral
34. Meninges
Epidural
Scalp
Hematoma:
mostly arterial
Skull (blood collects
Dura matter b/t the skull &
Arachnoid the dura mater
of the brain)
Pia
Brain tissue
grey
white
35. Subdural
hemorrhage
- usually
Scalp
venous (blood
Skull
collects b/t the
Dura matter dura & the
arachnoid
mater). May be
classified as
acute, subacute
or chronic.
36. Acute & Subacute Subdural
Hematoma
Usually result from brain or blood vessel
laceration
Symptomatic within 24 to 48 hours of injury
Symptoms include loss or variable levels of
consciousness, headache, irritability,
increasing signs of increased ICP (increased
BP, decreased pulse, slowing respiratory
rates)
Requires prompt treatment!
38. Diagnostic Tests
CT or MRI: data on structural causes such
as tumor or hemmorhage.
-Metabolic – will be unremarkable
LP: infection or bleeding (cloudy or
bloody)
EEG: structural or metabolic, seizure
activity
Lab tests: LFTs, kidney function, glucose
levels, toxicology, ABGS
39. Diagnostic Tests for
Abnormal Reflexes
Oculocephalic reflex
response – abnormal
if eyes remain in fixed
position when head
turned
Oculovestibular reflex
response – absence
of eye movement
when water instilled in
ear = brain death
40. * Level of consciousness is
*
the single most important
indicator of neurological
function and change*
41. Medical Management
Prompt recognition and treatment of
hypoxia & acid-base disorders (why?)
Control of increasing ICP resulting from
increased cerebral edema and
expanding hematoma
Surgical treatment
– Burr holes
– Craniotomy
46. Post Head Injury
Observe for 24 hrs
Take to emergency if any of following::
– decreasing LOC (confusion, drowsy)
– loss of consciousness/inability to wake
– vomiting
– convulsions
– bleeding or drainage from ears/nose
– weakness or loss of sensation in arm or leg
– blurring of vision/slurring of speech
– changes in pupil
47. Nursing Assessment:
Brain Injury
ABCDs
Maintaining airway
History if possible
Determine LOC, ability to respond to verbal
commands, reactions to tactile stimuli, status of
reflexes.
Glasgow Coma scale
Fluid and electrolyte balance
Monitoring/managing potential complications
48.
49.
50.
51. The Glasgow Coma Scale
The Glasgow Coma Scale (GCS) is a
universally used neurological
assessment tool to assess degree of
consciousness impairment. CGS
measures eye, verbal, and motor
response. It is an excellent scale to
measure arousal. It is less helpful
related to content measurement.
Know the difference b/
content & arousal
52. GLASGOW COMA SCALE SCORE (GCS)
Eyes 1 Closed at all times
2 Opens to pain
3 Opens to voice command A score of 10 or less
4 Open spontaneously indicates a need for
Motor 1 No response emergency
2 Extension (decerebrate) attention
3 Flexion posturing (decorticate) 15 (top score)
4 Flexion withdrawal
5 Localizes painful stimulus A score less than 7
6 Obeys commands is interpreted as
Verbal 1 No response coma
2 Incomprehensible sounds
3 Inappropriate words
4 Disoriented and converses
5 Oriented and converses
53. Nursing Diagnoses
– Altered Tissue Perfusion
– Risk for Suffocation/Aspiration
– Altered Oral Mucous Membranes
– Risk for Impaired Skin Integrity
– Risk for Contractures
– Altered Nutrition: Less than Body
Requirements
– Fluid volume deficit
– Risk for Injury
– Altered family processes
54. Nursing management
– Maintaining the airway
– Protecting the patient
– Fluid balance
– Mouth care, skin and joint integrity
– Corneal integrity
– Thermoregulation
55. Emergency Care
ABCs
Airway maintenance, intubation with oxygenation
(PO2 > 90mmHg), mild hyperventilation – avoid
hypercapnia.
Ensure adequate fluid however avoid lowering the
blood osmolarity.
Initial neuro assessment and Glasgow Coma Scale
Etiology of the brain injury will dictate further
evaluation & treatment
58. Nursing Management Cont’d
Administer prescribed meds to reduce ICP:
barbituates, mannitol analgesics, narcotics
Maintain fluid balance with NaCl or RL solution
Avoid noxious stimuli (explain)
Maintain cerebral perfusion pressure >70mmHg
Maintain normal body temperature – avoid
hyperthermia
59. Osmotic Diuretic (Mannitol)
Reduces cereberal edema by osmotic dehydration.
Preferred b/c it is confined to extracellular space & does
not normally cross an intact blood brain barrier.
Carefully monitor vitals, CVP, B.P, intake & output,
catheter patency, signs of fluid overload, eye response
/acuity & electrolyte imbalance?? Why??
NOTE: If blood-brain barrier is damaged the medication
enters the brain and increases swelling!!
Hinweis der Redaktion
Diastatic Skull Fracture The skull of infants and children are not completely solid until they grow older. The skull is composed of jigsaw-like segments (cranial fissures) which are connected together by cranial sutures. Skull fractures that separate the cranial sutures in children prior to the closing of the cranial fissures are termed "diastatic skull fractures". Cribiform Plate Fracture The cribiform plate is a thin structure located behind the nose area. If the cribiform plate is fractured, cerebral spinal fluid can leak from the brain area out the nose. Can cause damage to the nerves and blood vessels that pass through the opening at the base of the skull
Fractures occurring in posterior cranial fossa – temporal bone. Figure 63-2 Basilar fractures allow cerebrospinal fluid to leak from the nose and ears. Adapted from Hickey, J. V. (2003). The clinical practice of neurological and neurosurgical nursing (5th ed.). Philadelphia: Lippincott
Halo sign: testing for CSF when blood is mixed with possible CSF. Place drop of fluid on white pad – blood will coalesce and CSF will leave a yellowish ring if possible.
Otorrhea signifies a tear in the dura
Periorbital ecchymosis Nerve damage for the sense of smell or eye functions may occur.
Of clients admitted to ER, 50% have evidence of alcohol or substance abuse. Most are male< 30 years of age.
Mechanism of Injury. The brain is somewhat mobile within the spiny interior of the skull. Under normal circumstances the delicate brain is protected from contact with the spiny contours of the skull. This protective barrier is known as cerebrospinal fluid. It surrounds the brain, and under normal circumstances, cushions the brain from contact with its hard, spiny shell. However, when the head is subjected to violent forces, such as those exerted in: automobile accidents; violent shaking or whiplash; forceful falls and blows; the brain may sustain permanent damage. Such damage results from the delicate brain being forcibly rotated and battered within the spiny skull, also known as, the brain vault. During such episodes brain tissue is ripped, torn, stretched, battered and bruised. Such battering is followed by bleeding, swelling and bruising of brain tissue. Sometimes the brain can recover from such insults without any apparent consequences. In other cases the resultant difficulties can last a lifetime.
Concussion: ( a sudden transient mechaincal head injury with disruption of neural activity and a change in loc) May experience only dizziness and feel “dazed”. Retrograde amnesia Treatment involves observing patient for headache, dizziness, lethargy, irritability and anxiety. Client should resume normal activities slowly and the following should be watched for: difficulty in awakening or speaking, confusion, severe headache, vomiting or weakness on one side of the body. May or may not show up on CAT scan. Can cause diffuse axonal type injury resulting in permanent or temporary damage Blood clot can occasionally occur causing death Months to years to heal
Contusion: Depends on which areas of the brain damaged – cerebral hemispheres, brain stem (RAS) If widespread injury, abnormal eye movement and motor function, increased intracranial pressure and herniation - poor outcome. May have residual damage, seizures
The image below shows a lateral view of the brain with contusions (hemorrhagic necrosis) at the frontal poles, and along the temporal lobes.
Diffuse Axonal Injury There is extensive tearing of nerve tissue throughout the brain. This can cause brain chemicals to be released, causing additional injury. Experiences immediate coma, decerebrate & decorticate posturing, and global edema The tearing of the nerve tissue disrupts the brain’s regular communication and chemical processes. This disturbance in the brain can produce temporary or permanent widespread brain damage, coma, or death. A person with a diffuse axonal injury could present a variety of functional impairments depending on where the shearing (tears) occurred in the brain.
Hematomas . often have delayed effects as the subsequent swelling of the brain causes increased intracranial pressure, distortion and herniation of the brain. Signs and symptoms depend on size of area affected and the speed with which the hematoma develops.
Locations of intracranial hemorrhages.
Epidural hematomas occur between the skull and the dura. Occurs in 10% head injuries and usually associated with skull fracture Often caused by a rupture or lacerations of the menigeal artery that leads to continuous bleeding, separation of dura from skull and compression of brain. Usual sequence is loss of consciousness, client awakens followed by change in LOC, change in pupil reactivity and eye movement paralysis on same side as hematoma., then coma.
Onset of symptoms is somewhat slower because bleeding is venous.
Bleeding directly into the brain tissue Often caused by things that stab wounds, bullet wounds, and may be caused by systemic hypertension. May be difficult to treat surgically because of location. Rx includes supportive care, management of ICP, fluids, electrolytes, and anti-hypertensives.
Oculocephalic (Doll’s Eye reflex) Only done on unconscious patients, & never in unconscious pts with ? C-spine injury Is movement of the eyes in the direction opposite to that in which the head is moved. Abnormal reaction: eyes remain in fixed position in skull when head is turned. The reflex is absent or impaired in patients with brain stem problems. Oculovestibular (caloric test) Only performed if oculocephalic responses are absent. Tests CN III, IV, VI, & VII Instillation of ice water or warm water should result in deviation of eyes either toward (ice water) or away (warm) from irrigated ear. Absence of movement indicates brain death. Do not perform in conscious Pt. or ruptured tympanic membrane.
Change in vital signs is a late manifestation! Ongoing monitoring for changes is imperative!!
Read and know the care of clients post-craniotomy!
Ongoing assessment: Level of consciousness and responsiveness with the Glasgow Coma Scale. Level of cognitive functioning (example pg 1683, Smeltzer & Bare) Vital Signs Other neurologol signs
Because the GCS is based on client’s ability to respond and communicate, you would not use it under the following conditions: Client is Intubated Eyes are swollen shut Client is unable to speak English Blindness Aphasic Paralyzed or hemiplegic
The total of the 3 scores can range from 3-15. Example: client who is unresponsive to painful stimuli; does not open eyes; & has complete muscle flaccidity has a score of 3. A score of less than 7 is interpreted as coma. Neuro assessment sheets will include along with the Glasgow Coma: Voluntary motor control - In the cooperative alert client voluntary motor is assessed for symmetry vs. symmetry – right and left side. 2) Cranial nerve function pupils EOMS Blink reflex Facial symmetry 3) Vital signs including temperature & respiratory pattern 4) Speech – clear, slurred, rambling, aphasic
IICP is associated with decreased LOC, hypercapnia, and potential for PE. Hypotonic solutions move water into the cell!
Goals of ICP Monitoring: Maintain CPP 50-70mmHg Maintain ICP < 20 Monitor for evanta (rebleed, herniation)
Sedation to reduce metabolic demand
It acts by increasing osmotic pressure of the glomerular filtrate, inhibiting reabsorption of water and electrolytes. This elevates blood osmolality, drawing fluid from the interstitial spaces & brain cells into the blood. Diuresis is expected.
