CEREBROSPINAL INJURY

Dr. Suherman, SpS

Brain Injury
As

defined by the National Head Injury Foundation a traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes.

Causes of TBI
49%
50% 45% 40% 35% 30% 25% 20% 15% 10% 5% 0%

25.8%

10%

8%

7.4% 0.6%

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Direct Brain Injury Types

Coup

Injury at site of impact Injury on opposite side from impact

Contrecoup

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 edema

3). INTERSTITIAL (HYDROSTATIC)

- results from obstructive hydrocephalus and extravasation of CSF into periventricular brain tissue

Cerebral autoregulation
CBF

depends on CPP and CVR CPP = MAP ICP Cerebral autoregulation maintains constant CBF by compensating for changes in ICP unless:

ICP such that CPP < 40 mm Hg MAP > 160 mmHg or < 60 mmHg Brain injury/ trauma

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

Pathophysiology of ICP
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

48 72 h: CBF and CBV ICP Pain, agitation, seizures cerebral metab CBV ICP

Assessment of Impaired Consciousness

Use practical scale Glasgow

Coma Scale

Three features are in dependently observed : Points

* EYE OPENING Spontaneous To speech To pain None * BEST MOTOR RESPONSE Obeys commands Localized to pain stimuli Withdraws from pain stimuli Decorticate flexion Decerebrate extension None * VERBAL RESPONSE Oriented Confused conversation Inappropriate words Incomprehensible sounds None 4 3 2 1 6 5 4 3 2 1 5 4 3 2 1

CLINICAL FEATURES + IMAGING

Clinical Features Mild Head Injury unconsc < 10 GCS 13 15 no neuro deficit Radiological Exam Pathologic name brain CT normal Concussion

Moderate Head Injury unconsc 10-<6hrs brain CT abnormal GCS 9 12 pos neuro deficit Severe Head Injury unconcs > 6 hrs GCS 3 9 pos neuro deficit brain CT abnormal

Contusion

Contusion

SIMPLE HEAD INJURY GCS 15 no neuro deficit no unconsc CRITICAL GCS 3-4

BASAL SKULL FRACTURE

Signs

Battles Signs
Retroauricular Ecchymosis

Raccoon Eyes
Bilateral Periorbital Ecchymosis

BASAL SKULL FRACTURE

May tear dura

Permit CSF to drain through an external passageway May mediate rise of ICP Evaluate for Target or Halo sign

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 24 48 hours after injury

Important to check : - Laboratory studies blood periphery coagulation test - Support clinically important abnormalities

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)

Focal Brain Injury

Intracranial Hemorrhage Epidural Hematoma

Bleeding between dura mater and skull Involves arteries Middle meningeal artery most common Rapid bleeding & reduction of oxygen to tissues Herniates brain toward foramen magnum

CT scan of an acute left-sided epdural hemaoma. Note the typical convex or lens-shaped appearance. The hematoma takes this shape as the dura strips from the undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular system exists.

Focal Brain Injury Intracranial Hemorrhage Subdural Hematoma

Bleeding within meninges Beneath dura mater & within subarachnoid space Above pia mater Slow bleeding Superior sagital sinus Signs progress over several days Slow deterioration of mentation

Acute subdural hematoma: Note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift.

Subacute subdural hematoma: the crescent-shaped clot is less white than on CT scan of acute subdural hematoma

Subarachnoid Hemorrhage

May

not present with physical findings Head Ache Nuchal Rigidity Blood in CSF

Brain CT scan shows subtle finding of blood at the area of the circle of Willis consistent with acute subarachnoid hemorrhage.

Focal Brain Injury

Intracranial Hemorrhage

Intracerebral Hemorrhage

Rupture blood vessel within the brain Presentation similar to stroke symptoms

Signs and symptoms worsen over time

Intracerebral Hematoma
Located
Difficult

in the brain parenchyma

to distinguish from contusion

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

Diffuse Brain Injury

Severe Diffuse Axonal Injury

Brainstem Injury Significant mechanical disruption of axons

Cerebral hemispheres and brainstem

High mortality rate Signs & Symptoms

Prolonged unconsciousness Cushings reflex Decorticate or Decerebrate posturing

Cushings Reflex
Late

sign of increasing ICP

Bradycardia Widening

pulse pressure/ increasing BP

Changes

in respiratory patterns

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

MEDICAL COMPLICATION :
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

MEDICAL COMPLICATION :
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

MEDICAL COMPLICATION :
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

OTHER COMPLICATION :
1). SEIZURE : IMMEDIATE, EARLY, LATE 2). INFECTION * EXTRACRANIAL (Including SYSTEMIC INFECTION) * INTRACRANIAL 3). FRONTAL LOBE DISTURBANCES * APATHY * DISINHIBITION -- AGITATED 4). FEVER COUSED BY PROINFAMATION AGENT (SITOKIN,TNF) OR INFECTION 5). VERTIGO

PROGNOSTIC VALUE FOR TBI : Depend on several PREDICTION OUTCOME VARIABLES, such : ages GCS pupil reaction length of PTA length of coma brain CT abnormalities complication

SPINAL CORD INJURY

3 STAGING : 1). Acute phase the injury continue for hours or even days 2). Recovery phase period during function returns, hours months/years 3). Chronic phase function reached a plateau

SPINAL CORD INJURY

Neurological Protection Therapy : 1990 : METHYL PREDNISOLONE, HIGH DOSE can improve neurological recovery when given within 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

SPINAL CORD INJURY

Rehabilitation - Immobilization : instability prior to surgical stabilization - Bladder / Bowel training - Lung complication acute phase - Skin care - Extremities : 4 6 weeks prevention of DVT