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CONTUSION occurs at the time of the accident Primary Brain Injury Primary Brain Injury

FOCAL BRAIN INJURY DIFFUSE BRAIN INJURY

Initial LoC FOCAL BRAIN INJURY CLOSE HEAD INJURY

Secondary Brain Injury

Behavior Changes
MVA

hemorrhage and edema, peak after

about 18 to 36 hours. impact of the brain against the skull
bounces
Belen, Alyssa Loreen
Increase Intracranial Pressure BLUNT FORCE TRAUMA TO THE HEAD
Acceleration-Deceleration Injury Napa, Leona Nicole
BSN 3 - 1

Hyperdense Possible Herniation impact of the brain against the skull

CONTRECOUP
COUP INJURY directly
INJURY
Hypodense

breakage of blood vessels and Vigorously shaking a

CT Scan shearing of bridging veins Acceleration- impact on Pterion region tear intima layer of basilyar
Isodense bleeding into the surrounding tissue young child
Deceleration Injury
develop within 48 hours shearing of middle meningeal
Acute subdural hematoma CONTUSION
of the initial head injury Craniotomy and Burr Bleeding into potential space artery
CT Scan BUN Burr holes
holes between dura and arachnoid
develop 2 days - 2 Subacute subdural blood accumulates
weeks hematoma Crescent Shaped continuously in the potential
Epidural Hematoma SLOW EPIDURAL BLEED
Lucid Interval Initial LoC Subdural Hematoma space between the dura and
develop over weeks or Chronic subdural Crosses Suture lines the skull
months. hematoma as the blood accumulates CT Scan Initial LoC then lucid
damage to cerebral cortex Acute compression of Increase pressure in posterior
*MORE DEADLY* Chronic blood breakdown Lens Shaped
near central sulcus underlying cortex cranial fossa
products ↑ osmotic pressure Osmotic Therapy:
Blood can spread to a Contralateral Hemiparesis Do not Cross Suture Rapidly Increase Intracranial Mannitol
Contralateral Hemiparesis Increase Intracranial Pressure Lines
larger area Pressure
compensatory hemodilation

Nausea
Decreased ↑
leads to effusion
ICP > MAP

LoC Cerebral Edema more blood accumulates

MORPHINE FOR PAIN: CORTICOSTEROIDS
Increase Drowsiness Keep Head and Neck in Neutral
Headache Position
GCS shift of the midline
Maintain airway and ventilation Nausea
Cognitive impairment Semi fowlers position
Prevent secondary injuries
Decrease LoC CUSHING'S TRIAD impending brain
Dizziness
1. Maintaining the airway Agitation herniation Airway Management
2. Maintain head and neck in neutral alignment; immobilized
Vomiting Hypertention
until injury is determined Headache
3. Clear the upper airway; nose and mucus of mouth Benzodiazepines Assess GCS Monitor Vital Signs
4. Suction the airway if needed
Bradycardia Decreased LoC
CUSHING'S TRIAD Propofol (Diprivan), a sedative– Osmotic Therapy: Mannitol Monitor for early signs of IICP
Intraventricular Catheter Calculation of CPP if hypnotic agent IV Prophylaxis
ICP monitor in place Hypoxia check for hypotension and ↓ COMPLICATION
DUE TO (R) IICP Monitor Fluid Status
Rapidly Increase Intracranial CHEST XRAY BUN cardiac output
Pressure ABG ANALYSIS
IICP brain herniates through IICP brain herniates tentorial Check Serum
ABG ANALYSIS CBC foramen magnum notch Osmolality
more blood accumulates ICP > MAP
↑ co2 ↑ Fluid compresses oculomotor
↑ICP compresses respiratory ↑ICP compresses
Hyperventilate
Build up Vasodilation
Leaks
compresses brainstem
nerve (CN III)
centers in medulla
arterioles in brain Worst ↑ BRAIN HERNIATION PAPILLEDEMA
Fundoscopic Eye
ICP Widened pulse Exam
Hypoxia Neurons Baroreceptors in aortic

CHEYNE'S STROKE
↓ Cerebral Blood flow will die arch detect ↑
BP
Supportive measures Fixed Dilated pupils = no PERRLA
Decreased LoC
1. ventilatory support respond to light
1. Monitor Respiratory rate as
arteries in the body Stimulates vagus nerves 2. seizure prevention
needed if the pt is not on a
3. fluid and electrolyte Asymmetric Pupil(s)
ventilator; Breath sounds constrict to divert blood Coma or Death
maintenance "DOWN AND OUT"
2. Monitor O2 saturation and Flow to the brain
releases of acetylcholine 4. nutritional support
ABG for increase Pa02
5. management of pain and
3. Prepare o2 administration or Ineffective airway clearance Decreased Intracranial Ineffective Breathing Pattern
anxiety.
intubation Hypertention Adaptive Capacity
Bradycardia
4. Preparation for cranial surgery
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GLASCOW COMA SCALE (TBI) FOCAL BRAIN INJURY

tear intima layer of basilar 9-8 = SEVERE HEAD INJURY
artery More blood = Worst

Within SULCI
Outcome

OPEN HEAD INJURY Penetrating Injuries

blood accumulates on 92 o2 sat
subarachnoid space
Blood in the
between arachnoid mater and Ventricular cisterns Skull X-ray KNIFE WOUND | GUN SHOT WOUND FORCEFUL TRAUMA
pia mater

CEREBRAL LACERATION the bones of the skull are forcefully

blood accumulates the csf displaced downward
CT SCAN Aneurysm Repair
rapidly
enters the brain, and damages the
can vary from a slight depression to
Risk for Infection soft brain tissue in its path
COMPLICATION after 2 days - 2 bones of the skull
Subarachnoid Hemorrhage
week AFTER SAH splintered and embedded within
contusion or shearing of small Close Observation
Calcium Channel Blocker: Older Adults brain tissue
blood vessels
Thunderclap Headache Nimodipine
POST-TRAUMATIC VASOSPASM elevation of the
DEPRESSED SKULL FRACTURES skull and
CT Scan/MRI blood into the brain tissue débridement
Rapid LoC
Cerebral Ishemia supportive care; control of CSF LEAK:
ICP; and careful yellow wish
administration of fluids, Expanding Clot Intracerebral Hematoma
with mixed
Rebleeding Frequent electrolytes, and nose, pharynx, or ear with blood
HYDROCEPHALUS
antihypertensive
medications BUN
CT Scan/MRI
Hyponatremia IICP and herniation may occur
Fluid Resuscitation Serum Electrolytes Headache Wound care and
Risk for Infection wound dressing
Assess GCS
Fever Temperature Regulation
CBC
Craniotomy/Crainectomy Decreasing LoC Seizure
Phenytoin seizure prophylaxis
Seizures
(decrease the risk of early
Osmotic diuretics such as
posttraumatic seizures) IFC Hemiplegia on contralateral side meningitis
mannitol
Seizure Precaution:
1. O2 Prophylaxis:
2. SUCTION Deteriorating consciousness to Stiffneck
Diazepam BUN
Carbamazepine deep coma

Open Injury

Decerebrate HEAD TRAUMA SUCH AS HAIR COMBING

Types of Skull Fracture LACERATION
OR BRAIDING ON CHILD/NEWBORN

Simple (Linear) Fracture is a break in the bone without abnormal accumulation of blood
Direct Damage on Scalp
damage to the skin under the galeal aponeurosis of the
internal fixation scalp

A comminuted skull fracture refers to a splintered or Blood vessels constrict poorly and
caused by rupture of emissary
multiple fracture line scalp bleeds profusely
veins.

Raocon eyes Inspection and palpation abrasion (brush wound)

Basilar Skull Fracture - Fracture of the base of the skull
such as temporal bones but may also involve the Battle's Sign
occipital, sphenoid, ethmoid, and orbital plate of the
frontal bone. Subgaleal hematoma Non-opioid analgesic such as
CSF Otorrhea
naproxen and ibuprofen
Halo sign 1. The area is irrigated before the laceration
is sutured to remove foreign material and
Risk for Intracranial Infection
yellow wish with mixed with to reduce the risk for infection
blood 2. Wound Care and Wound Dressing CT Scan
Belen, Alyssa Loreen
Napa, Leona Nicole
BSN 3 - 1 SCALP INJURY BUN
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FALLS AND ACCIDENT | HIGH RISK ACTIVITIES | ELDERLY (RISK FOR LOSE BALANCE AND FALL) | DOMESTIC VIOLENCE | BABY |

Belen, Alyssa Loreen DIFFUSE BRAIN INJURY CLOSE HEAD INJURY

Napa, Leona Nicole
BSN 3 - 1

RAPID Acceleration-Deceleration Injury Shaken Baby Syndrome

shearing, tearing, or stretching of nerve

fibers in the midbrain

Symptoms last less than 15 minutes " small, bead-like swellings" alont their
BUN and entail no loss of consciousness Damage to axons
length

CT Scan / MRI headache temporary axonal disturbances decreases the speed of information
processing and responding, and
disrupts attention
Craniotomy Disorientation rapid release of neurotransmitters
widespread disruption of axons in the
white matter of brain
loss of reflexes cause ionic disequilibrium across
Multiple Small,
neuronal membranes
DIFFUSE AXONAL INJURY (DAI) Hyperdense, Punctate
MRI
lesion along the gray-
loss of balance CLASSIC CONCUSSION white matter junction
Immediate LoC

GCS Short Term Amnesia cognitive, psychologic, and

coma lasts 6 to 24 hours
sensorimotor deficits may persist
MILD DAI

Impaired physical mobility injury and impairment is spread

during 24 hrs acetaminophen (
tylenol) After 24hrs Ibuprofen (
Advil) or naproxen sodium
hydration
1. Povide passive ROM
2. Promote proper nutrition and
coma lasting more than 24 hours, and
throughout the cerebral cortex and
MODERATE DAI often incomplete recovery.
Elevate the head of the patients bed to diencephalon
reduce gravitational pressure on the
brain.
axonal injury occurs in both cerebral
Rest including resting your brain after Profound cognitive and sensorimotor
SEVERE DAI hemispheres, the diencephalon, and the
concussion. deficits
brainstem

Impaired and disturbed sensory

perception

Encouraging the patient to do as

much as self care as possible using
physical exercise.

CLINICAL EXAMINATION FOR DETERMINATION OF

Physical Examination: BRAIN DEATH

3 CARDINAL SIGNS
INDUCED COMA 1. Neurologic Assessment: GCS 1. coma
(MEDICALLY INDUCED COMA) 2. Assess the Reflexes: Eye, Gag, cough 2. the absence of brainstem reflexes

3. Response to Pain 3. and apnea.
Barbiturate Coma Therapy 4. Vital signs

5. Skull and Face: Deformity, Laceration, Bruising, Adjunctive Test
Dosing Regimens: bleeding 1. cerebral blood flow studies
Pentobarbital 6. Movement of Extremeties 2. electroencephalogram (EEG)
Thiopental 7. Assess Respiratory 3. transcranial Doppler
4. brainstem auditory-evoked potential,
 Physical Examination:

1. Neurologic Assessment: GCS

2. Assess the Reflexes: Eye, Gag, cough
3. Response to Pain
4. Vital signs: MAINTAIN BP
5. Skull and Face: Deformity,
Laceration, Bruising, bleeding
6. Movement of Extremeties
7. Assess Respiratory

Epidural Hematoma Subdural Hematoma