Brain Injury & Sci

7/29/2019 Brain Injury & Sci

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SARAh S. TAUPAN, RN, MN, DPA



What is Traumatic Brain Injury?

Closed – head collides with another object but there

is no opening through the skull and dura

Open–

object penetrates the skull, enters the brainand damages the soft brain tissue in its path. Exposes

the brain



Annual number of people who experience a

traumatic brain injury:

1. 4 million annually in the United States

Deaths: 50,000 Hospitalization: 235,000

Among children ages 0 to 14 years

Deaths: 26, 850

Hospitalizations: 37,000



MILD SEVERE loss of

consciousness

and/or confusion

and disorientationis shorter than 30

minutes

The person looks

normal and oftenmoves normal in

spite of not feeling

or thinking

normal.

loss of consciousness

for more than 30

minutes and memory

loss after the injury

or penetrating skull

injury longer than 24

hours

Results in permanent

neurobiologicaldamage that can

produce lifelong

deficits to varying

degrees.



1. Acceleration- occurs when the head is

struck by a moving object and set in

motion.

2. Deceleration- occurs when the moving headstrikes a solid, immobile object.

3. Acceleration & deceleration

4. Deformation- refers to injuries in which

the force results in deformation anddisruption of the integrity of the impacted

body part(i.e. skull fracture)











A. By description of injury

1. Blunt trauma

2. Penetrating injuries

3. High velocity objects

4. Coup injury

B. According to structures damaged

1.PRIMARY HEAD INJURY

1. SCALP INJURIES

2. SKULL INJURIES



Three types of skull fractures

Linear skull fractures

Depressed skull fractures

Basilar skull fractures – Racoon’s sign, Battle’s sign,

halo’s sign, otorrhea,

rhinorrhea, test CSF



2. SECONDARY HEAD INJURY

- Include Hemorrhage, edema and

infection HEMORRHAGE

EPIDURAL HEMATOMA

SUBDURAL HEMATOMA

ACUTE SUBDURAL HEMATOMA

CHRONIC SUBDURAL HEMATOMA

INTRACRANIAL HEMATOMA

BRAIN SWELLING AND EDEMA

INFECTIONS





C. Brain Injuries

ConcussionContusions

TYPES OF CEREBRAL CONTUSION

A. TEMPORAL LOBE CONTUSIONB. FRONTAL CONTUSION

C. FRONTAL-TEMPORAL

CONTUSION

D. BRAIN STEM CONTUSION



CONCUSSION CONTUSION Temporary loss of

neurologic function

with no apparent

structural damagelasting for a few

seconds to few

minutes

Jarring of the brainthat caused it to

stop functioning

momentarily

More severe injury

in which the brain

is bruised, with

possible surfacehemorrhage

Unconscious for

more than a few

seconds or minutes

Picture is

somewhat similar

to that of shock



INCREASED DROWSINESS AND

CONFUSION

INABILITY TO AWAKEN,lucid intervals

VOMITING

CONVULSION OR FITS

BLEEDING OR DRAINAGE FROM

NOSE OR EARS



BLURRING OF VISION

WEAKNESS ON EITHER ARMS OR LEGS

SLURRED SPEECHSIGNS OF INCREASED ICP

SIGNS OF DIABETES INSIPIDUS :

Increase urine output, dry skin, drymucus membrane – check for urine

specific gravity





Immobilization

Do not attempt to remove

penetrating objectsCover head wounds and apply

pressure

ABC



MAINTAINING THE AIRWAYKeep unconscious patient in a position that

facilitates drainage of oral secretion Establish effective suctioning proceduresGuard against aspiration and respiratory

insufficiency

MAINTAIN HYDRATION & ADEQUATENUTRITION

Maintain fluid and electrolytesA urinary catheter is maintained It is important to maintain the unconscious

patient's blood pressure through IV fluid andmedication.



MAINTAINING SKIN INTEGRITY

The patient is turned and positionedA compression device wrapped around

the legs that prevents blood clots. Daily

injections are also given to preventblood clots.

SEIZURE PRECAUTION

NO OPIOIDS



Duration of Coma. The shorter the

coma, the better the prognosis.

Post-traumatic amnesia. The shorter

the amnesia, the better the

prognosis.

Age. Patients over 60 or under age 2

have the worst prognosis, even if they suffer the same injury as

someone not in those age groups.

Wh t i it?



What is it?

Spinal injuries cause

myelopathy or damage towhite matter or myelinated

fiber tracts that carry

signals to and from thebrain. It also damages gray

matter in the central part of

the spine, causingsegmental losses of

interneurons and

motorneurons.



CAUSE: TRAUMA AS VEHICULAR AND DIVINGACCIDENTS, FALLS AND BULLET SHOT WOUNDS;LESS OFTEN BY TUMORS WITHIN THE SPINALCORD OR OUTSIDE OF THE CORD THAT COMPRESSIT

TYPESA. CONCUSSION WITHOUT DIRECT TRAUMA TOTHE CORD

B. COMPRESSION, CONTUSION OR LACERATION OF

THE CORDC. HEMORRHAGE INTO THE CORD

D. COMPRESSION OF THE BLOOD SUPPLY TO THECORD.







CAUSE- VIOLENT HYPEREXTENSION ANDFLEXION OF THE NECK USUALLY AS A RESULT

OF A TEAR DUE TO AUTOMOBILE ACCIDENT

SIGNS AND SYMPTOMS: PALE AAND DAZED ;

RARELY LOSES CONSCIOUSNESS; MAY EXHIBITWEAKNESS, GAIT DISTURBANCES; DIZZINESS

AND VOMITING; OCCIPITAL HEADACHE,

NUCHAL RIGIDITY AND PAIN RADIATING THE

ARM. RX: BED REST, ANALGESIC AND HOT PACKS,

PLASTIC COLLAR



CAUSE: LIFTING HEAVY OBJECTS OR A FALL

ON THE BACK

SIGNS AND SYMPTOMS: BACK PAINS THAT

RADIATES ON THE BACK OF A LEG, DIFFICULTY

IN WALKING, MUSCLE SPASM, AND DISORDERSOF A SENSATION

RX: IF A SINGLE DISK IS INVOLVED, IT MAY BE

SURGICALLY REMOVED. HOWEVER, SPINAL

FUSION (UNITING TWO VERTEBRAE) ISUSUALLY PERFORMED.



CAUSE: loss of function inflictedat the time of injury

SIGNS AND SYMPTOMS: absence

of perspiration, retention of feces and urine, hypotension

with slow steady pulse and dry

skin



Stage of spinal shock sensation and motor power localized below the

vertical height of the lesion are lost. This stagelasts for 2 to 3 weeks .

Stage of recovery after a period typically ranging from 2 to 3

weeks of injury, the nerves partially recover,and the return of segmental reflexes produceparaplegia-in-flexion.

Stage of reflex failure after a period of days the recovered reflexes

again start to give way due to completedegeneration of nerve cells.



C5 – Observed respiratory status

C6 – quadriplegia= priority is

atelectasis

C8 – neurogenic shock : hypotension,

bradycardia, warm dry skin

Thoracic & below – paraplegia

Cauda equina syndrome –

compression in the nerve roots that

can lead to permanent loss of

bladder and bowel control and

paraplegia, refer to the physician

STAT



Sacral SCI:

1. Higher than S2 – with erection ,no

ejaculation

2. S2-S4 – no erection, no ejaculation

3. High lesion – increase probability to

perform sexually

4. Below lesion – decrease probability

to perform sexually

5. Paraplegia

6. Bowel and bladder incontinence



The location of the injury

In general,

injuries that arehigher in yourspinal cordproduce more

paralysis.

The severity of the injury.

Spinal cordinjuries are

classified aspartial orcomplete,depending on

how much of thecord width isdamaged.



Thrombophlebitis

Measures such as ROM exercises, thigh-high elasticcompression stockings, adequate hydration andanticoagulation medications (heparin and warfarin ) asprescribed are given

Orthostatic Hypotension Activity should be planned in advance and adequate

time given for a slow progression of position changes

Autonomic Dysreflexia

Stimuli that may trigger this: distended bladder ( mostcommon ); distention or contraction of visceral organs,especially the bowel; or stimulation to the skin, gooseflesh



MANAGEMENT :

1. Keep supine in neutralalignment

2. Immobilized apply C collar

3.Use log rolling technique inturning

4. ABC, Brief neurologic exam

5. Bladder program

6. Baclofen

7. Methylprednisolone



MEDICAL – SURGICAL MGT :

1. Skeletal Traction:A. Minerva vest – provides

significant immobilization

including lateral flexion

B. Gardner wells – reduce

dislocation, subluxation, pain &

spasm

C. Halo vest – immobilize theneck, opening must be attached

to the client

2. Decompression,3. Spinal fusion









Clinitron Bed Tilt Bed





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Brain Injury & Sci