[Files.indowebster.com] TBI

7/27/2019 [Files.indowebster.com] TBI

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CEREBROSPINAL INJURY

Dr. Suherman, SpS


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Brain Injury

As defined by the National Head Injury

Foundation

a traumatic insult to the brain capable ofproducing

physical, intellectual, emotional,social and vocational changes.


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Causes of TBI

49%

25.8%

10%8% 7.4%

0.6%

0%

5%

10%

15%

20%

25%

30%

35%

40%

45%

50%

Trans

porta

tion

Falls

Firea

rms

Othe

r Assa

ults

Othe

r

Unkn

own


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Direct Brain Injury Types

Coup

Injury at site

of impact

Contrecoup

Injury on

opposite side

from impact


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CEREBRAL EDEMA

1). CYTOTOXIC

- occurs as a result of cell death

(failure of the Na+/K+ ATPase)

- the classic cause of cytotoxic edema is stroke

- also occurs with global hypoxia and hypoosmolar states

2). VASOGENIC- results from injury to the Blood Brain Barrier (BBB)

- classic cause is a brain tumor

- yet, stroke and hypertensive encephalopathy can

cause BBB injury vasogenic edema3). INTERSTITIAL (HYDROSTATIC)

- results from obstructive hydrocephalus and extravasation

of CSF into periventricular brain tissue


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Cerebral autoregulation

CBF depends on CPP and CVR

CPP = MAP ICP

Cerebral autoregulation maintainsconstant CBF by compensating forchanges in ICP unless:

ICP such that CPP < 40 mm Hg

MAP > 160 mmHg or < 60 mmHg Brain injury/ trauma


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Intracranial hypertension

Normal ICP: 6-15 mm Hg

ICP > 20 mm Hg for > 5 minutes

72% of patients with severe traumatic brain

injury

Inversely related to outcome

Lower BP limit of CBF auto regulation less in

children than adults However, even mod ICP may adversely affect

cerebral perfusion


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Pathophysiology ofICP

Early hours: CBF, hypoperfusion, ischemia

24 -48h post trauma: Some areas remain hypoperfused and infarcted Other areas: relative hyperemia despite no in

cerebral metabolic demands (uncoupling)

BBB injury cerebral edema

4872 h: CBF and CBV ICP Pain, agitation, seizures cerebral metab CBV ICP


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Assessment of Impaired Consciousness

Use practical scaleGlasgow Coma Scale

Three features are in dependently observed :

Points* EYE OPENING

Spontaneous 4

To speech 3

To pain 2

None 1* BEST MOTOR RESPONSE

Obeys commands 6

Localized to pain stimuli 5

Withdraws from pain stimuli 4

Decorticate flexion 3

Decerebrate extension 2None 1

* VERBAL RESPONSE

Oriented 5

Confused conversation 4

Inappropriate words 3

Incomprehensible sounds 2None 1


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CLINICAL FEATURES + IMAGING

Clinical Features Radiological Exam Pathologic name

Mild Head Injury unconsc < 10 brain CT normal Concussion

GCS 1315

no neuro deficit

Moderate Head Injury unconsc 10- 6 hrs brain CT abnormal Contusion

GCS 39pos neuro deficit

SIMPLE HEAD INJURY GCS 15

no neuro deficit

no unconsc

CRITICAL GCS 3-4


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BASAL SKULL FRACTURE

Signs

Battles Signs

RetroauricularEcchymosis

Raccoon Eyes

Bilateral PeriorbitalEcchymosis


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BASAL SKULL FRACTURE

May tear dura

Permit CSF todrain through anexternalpassageway

May mediaterise of ICP

Evaluate forTarget or

Halo sign


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CONTUSION

Bruising of brain tissue

May be caused by coup or contracoup injuries

Most commonly involve the tips of the frontal

and temporal lobes

Often enlarge over the first 2448 hours

after injury

Important to check :

- Laboratory studies blood peripherycoagulation test

- Support clinically important abnormalities


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CONCUSSION / MINOR or MILD

HEAD INJURY

May or may not have loss of consciousness

Should have normal (no acute pathology) CT Scans

Commonly complain of :

- Headache

- Dizziness

- Irritability

- Short term memory loss- And / or Short attention span

May have SEQUELAE that may devastating to ADL

(Activities of Daily Living)


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Epidural Hematoma Bleeding between dura

mater and skull

Involves arteries

Middle meningeal arterymost common

Rapid bleeding & reductionof oxygen to tissues

Herniates brain towardforamen magnum

Focal Brain InjuryIntracranial Hemorrhage


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CT scan of an acute

left-sided epdural

hemaoma. Note the

typical convex orlens-shaped

appearance. The

hematoma takes

this shape as thedura strips from the

undersurface of the

cranium, limited by

the suture lines. Amidlineshift of the

ventricular system

exists.


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Subdural Hematoma

Bleeding within meninges

Beneath dura mater &

within subarachnoid space Above pia mater

Slow bleeding

Superior sagital sinus

Signs progress overseveral days

Slow deterioration ofmentation

Focal Brain Injury

Intracranial Hemorrhage


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Acute subdural

hematoma:

Note the bright

(white) image

properties of theblood on this

noncontrast cranial

CT scan.

Note also themidline shift.


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Subacute subdural

hematoma: thecrescent-shaped

clot is less white

than on CT scan of

acute subdural

hematoma


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Subarachnoid Hemorrhage

May not present with physical findings

Head AcheNuchal Rigidity

Blood in CSF


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Brain CT scan

shows subtlefinding of blood at

the area of the

circle of Willis

consistent with

acute subarachnoid

hemorrhage.


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Intracerebral Hemorrhage

Rupture blood vessel within the brain

Presentation similar to stroke symptoms

Signs and symptoms worsen over time

Focal Brain InjuryIntracranial Hemorrhage


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Intracerebral Hematoma

Located in the brain parenchyma

Difficult to distinguish from contusion


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Diffuse Brain Injury

Due to stretching forces placed on axons

Pathology distributed throughout brain

Types

Concussion Mild form

Moderate Diffuse Axonal Injury

Severe Diffuse Axonal Injury


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Brainstem Injury

Significant mechanical disruption of axons

Cerebral hemispheres and brainstem

High mortality rate

Signs & Symptoms

Prolonged unconsciousness

Cushings reflex

Decorticate or Decerebrate posturing

Diffuse Brain InjurySevere Diffuse Axonal Injury


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Cushings Reflex

Late sign of increasing ICP

Bradycardia

Widening pulse pressure/ increasing BP

Changes in respiratory patterns


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MEDICAL COMPLICATION :

1).CARDIOVASCULAR EFFECT :* SIGN OF SYMPHATHETIC HYPERACTIVITY ELEVATED LEVELS OF PLASMA NOREPINEPHRINE

CARDIOVASCULAR CHANGES

HYPERTENSION

TACHYCARDIA

INCREASED CARDIAC INDEX

DECREASED PERIPHERAL VASCULAR RESISTANCE

2).RESPIRATORY SYSTEM COMPLICATION* RESPIRATORY DYSFUNCTION IS COMMON AFTER TBI

* POTENSIAL PROBLEM :

NEUROGENIC PULMONARY EDEMA (NPE)

HYPOXEMIA

HYPOCARBIA

NOSOCOMIAL PNEUMONIA

PULMONARY EMBOLISM

ASPIRATION


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3). DEEP VEIN THROMBOSIS

AND PULMONARY EMBOLUS (PE)

* RISK FACTOR : - COAGULATION COMPLICATION

- IMMOBILITY

- TRAUMA TO THE PELVIS OR LEGS

- AGE OVER 40 YEARS

- OBESITY

4). COAGULOPATHY DIC

* LOCAL CONTROL BLEEDING, RESULTING FROM :

- THE VESSEL WALL

- THE CLOTTING FACTORS

- THE PLATELETS

* INJURY TO THE TISSUE RELEASES INTO BLOODSTREAM PHOSPHOLIPOPROTEINS

* PHOSPHOLIPOPROTEINS ACTIVATED CLOTTING FACTORS

* CLOOTING MECHANISM AND PLATELETS ACTIVATED ALSO BY VESSEL WALL DAMAGES BY

HYPOXIA, ACIDOSIS, SHOCK

* 10% - 35% TBI, DEVELOP A COAGULOPATHY

* 8% DEVELOP DCI OF ALL TBI VICTIM, AND 40% FROM THAT IS SWEVERE TBI


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5). WATER AND ELECTROLYTE BALANCE* TOTAL BODY WATER 60% OF THE BODY WEIGHT

52% OF THE BODY WEIGHT

* POTASSIUM, ORGANIC ACIDS,PHOSPHATE AND SULFATE INTRACELLULAR

* SODIUM, CHLORIDE EXTRACELLULAR

* TBI : - SYNDROME IN APPROPRIATE ANTIDIURETIC HORMONE SECRETION

- CEREBRAL SALT WASTING- OTHER ELEKTROLYTE ABNORMALITIES

* ELECTROLYTE ABNORMALITIES OCCUR IN NEARLY 60% OF SEVERE TBI

* MOSTLY HYPONATREMIA OFTEN CAUSED BY SIADH, 5% -12%

6). HYPOTHALAMIC AND PITUITARYDYSFUCTION* TBI PHYSIOLOGY STRESS PROVOKES INCREASED SERUM CORTISOL

-- DUE TO AN ELEVATED ADRENOCORTICOTROPIC HORMONE (ACTH)

* 60% SEVERE AND FATAL TBI INJURY TO THE HYPOTHALAMUS

* 2% DIABETES INSIPIDUS DAN 1% HYPOPITUITARISM


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7). METABOLIC DISTURBANCES* TBI CHANGES IN METABOLISM

* AUTONOMIC AND ENDOCRINE ALTERATION OCCUR

PRODUCING AN INCREASE :

- CATECHOLAMINES

- STEROIDS

- INSULIN

- GLUCAGON

* NEED ADDITIONAL METABOLIC DEMAND :

- ELEVATED CARDIAC OUTPUT

- HYPERVENTILATION

- FEVER

- RESTLESSNESS

- SEIZURE

- SECONDARY INFECTION

8). GASTROINTESTINAL COMPLICATION

* TBI -- INDEPENDENT RISK FACTOR FOR GASTRIC STRESS EROSION


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OTHER COMPLICATION :

1). SEIZURE : IMMEDIATE, EARLY, LATE

2). INFECTION

* EXTRACRANIAL (Including SYSTEMIC

INFECTION)* INTRACRANIAL

3). FRONTAL LOBE DISTURBANCES

* APATHY

* DISINHIBITION -- AGITATED

4). FEVERCOUSED BY PROINFAMATION AGENT (SITOKIN,TNF) OR INFECTION

5). VERTIGO


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PROGNOSTIC VALUE FOR TBI :

Depend on several PREDICTION OUTCOME

VARIABLES, such :

agesGCS

pupil reaction

length of PTA

length of comabrain CT abnormalities

complication


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SPINAL CORD INJURY

3 STAGING :

1). Acute phase

the injurycontinue for hours or even days

2). Recovery phase

period during function returns,

hoursmonths/years

3). Chronic phasefunction reached a plateau


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SPINAL CORD INJURY

Neurological Protection Therapy :

1990 : METHYL PREDNISOLONE, HIGH DOSE

can improve neurological recovery when givenwithin 8 hours

Dose : 30 mg/kg IV over 15 minutes with

subsequent maintenance infusion

of 5 mg/kg/h over the next 24 hours

Other ones : GM 1 (Ganglioside)investigation


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SPINAL CORD INJURY

Rehabilitation- Immobilization :

instability prior to surgical stabilization

- Bladder / Bowel training

- Lung complicationacute phase

- Skin care

- Extremities : 46 weeks prevention of DVT


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