Intracranial Pressure in Intracranial Pressure in

Traumatic Brain InjuryTraumatic Brain Injury

Özlem Korkmaz Dilmen Özlem Korkmaz Dilmen

Associate Professor of Anesthesiology

and Intensive Care

Cerrahpasa School of Medicine

Learning ObjectivesLearning Objectives

•First aid for TBI

•Prevention of secondary brain injury

•Basic neurophysiology

•Treatment of increased ICP

Epidemiology of Head Epidemiology of Head InjuryInjury

• 1.5 million people sustain

TBI every year in US.

• Adolescent

• Males> females

• Car accidents, motor

vehicle crashes, falls

Head InjuryHead Injury

• 46 years old, male

• Injured in a car crash

• Unconscious

•A (Airway)

•B (Breathing)

•C (Circulation)

•D (Disability)

•E (Exposure)

First AidFirst Aid

AirwayAirway - A - A

• Head tilt, chin lift

• Jaw trust (SCI)

• Clearance

(aspiration)

• Oral/Nasal Airway

• Intubation

AirwayAirway - A - A

• Symmetry

• Breathing Sounds

• Tidal Volume

• Respiratory rate

BreathingBreathing - B - B

Hypoxemia Following Head InjuryHypoxemia Following Head Injury

Immediate or late hypoxemia is common following head injury and is

associated with poor neurological outcome. Causes of hypoxemia

after TBI:

• Airway obstruction

• Abnormal respiratory patterns as a result of cerebral hemispheric

or basal ganglia damage

• Neurogenic alterations in FRC and V/Q matching

• Acute neurogenic pulmonary edema

• Aspiration pneumonia/pneumonitis due to impaired airway reflexes

and subsequent ARDS

• Direct lung trauma, pneumothorax or tracheobronchial injury

• Pulse

• Rate

• Rhytme

• Arterial Pressure

• Hypertension

• Hypotension

CirculationCirculation - C - C

DisabilityDisability - D - D

Disability is determined from the patient

level of consciousness according to the

Glasgow Coma Score.

GLASGOW COMA SCALEGLASGOW COMA SCALE

•I. Motor Response

6 - Obeys commands fully

5 - Localizes to noxious stimuli

4 - Withdraws from noxious stimuli

3 - Abnormal flexion, i.e. decorticate

posturing

2 - Extensor response, i.e.

decerebrate posturing

1 - No response

•II. Verbal Response

5 - Alert and Oriented

4 - Confused, yet coherent, speech

3 - Inappropriate words and jumbled

phrases consisting of words

2 - Incomprehensible sounds

1 - No sounds

•III. Eye Opening

4 - Spontaneous eye opening

3 - Eyes open to speech

2 - Eyes open to pain

1 - No eye opening

Exposure anExposure andd Environment Environment - E - E

The patient’s clothes should be

removed or cut in an appropriate

manner so that any injuries can be

seen.

GCS

Severe 3-8

Moderate 9-12

Mild 13-15

Severity of TBISeverity of TBI

PrognosisPrognosis

•Type of lesion

•Age

•Severity of injury as defined by GCS

Primary Injury

Secondary Injury

Head InjuryHead Injury

Primary & Secondary Brain InjuryPrimary & Secondary Brain Injury

• Primary injury: occurs as an imediate result of

head trauma (not regarded as treatable)

• Secondary injury: occurs following primary

injury with a delay (minutes, hours, days)

Causes of Secondary Brain InjuryCauses of Secondary Brain Injury

• HypotensionHypotension

• HypoxiaHypoxia

• Anemia

• Hyper/Hypoglycemia

• Hyperthermia

• Hyper/Hypocapnia

• Intracranial

hypertension

• Cerebral edema

• Compression from

expanding masses

• Vasospasm

• Seizures

Systemic Effects of Head InjurySystemic Effects of Head Injury

• TBI is a multisystem disorder with profound systemic

complications:

Respiratory

Cardiovascular

Hematological

Electrolyte

Neuroendocrinological disorders

•Dependent on aerobic metabolism

•Weight: 2 % of BW

•CBF: 15% of cardiac output

Human BrainHuman Brain

Components of CraniumComponents of Cranium

•Brain

•CSF

•Blood

V1+

V2+

V3+

Intracranial ContentIntracranial Content

•Brain: 1300-1400 g

•CSF= 150-175 mL

•CBF = 50 mL/100 g tissue/min

Volume of Brain ParenchymaVolume of Brain Parenchyma

•Brain

•Inflammatory/neoplastic tissue

•Bleeding (Hematoma)

Brain Brain EEdemadema

Cytotoxic edema: intracellular water

retention (hypoxia, experimental toxins)

Vasogenic edema: Plasma ultra filtrate

rapidly diffuses into the brain parenchyma

(capillary endothelium, BBB disruption)

Mixed

Diffuse Brain Swelling

Cerebral Blood VolumeCerebral Blood Volume(CBV)(CBV)

•CBF

•Venous out-flow obstruction

•Orthostatic effects

•Local factors

CBF determinantsCBF determinants

•CMR

•Arterial Pressure

•PaCO2

•PaO2

Cerebral AutoregulationCerebral Autoregulation

MAMAPPPaCO2

50 mmHg55 mmHg

20 mmHg

150 mmHg

Diameter of cerebral vassels

50

CB

F(m

L/1

00g

/m

in)

Otoregülasyon EğrisiOtoregülasyon Eğrisi

Cerebral Cerebral AutoregulatiAutoregulationon

• Over a wide range of blood pressure, cerebral

blood flow remains constant if metabolic

demands are unchanged.

• If blood pressure falls, cerebral vasodilatation

occurs to increase flow and thus maintain

cerebral oxygen and nutrient delivery.

• If blood pressure is excessively high the

cerebral vessels constrict, maintaining

cerebral oxygen and nutrient delivery whilst

protecting the brain.

• Trauma, inflammation, seizure activity and

conditions causing raised ICP may abolish

auto-regulation and the CPP therefore

becomes linearly dependent on MAP.

Impaired Cerebral AutoregulationImpaired Cerebral Autoregulation

• Trauma,

inflammation,

seizure activity and

conditions causing

raised ICP may

abolish auto-

regulation and the

CPP

OO22 Neuron: CPP➜ Neuron: CPP➜

• Cerebral Perfusion Pressure

– AP= 110/80, MAP: 90, ICP= 10 CPP= 80 mmHg⇒

– AP= 90/60, MAP: 70, ICP= 30 CPP= 40 mmHg⇒

CPP 50 mmHg CBF= NORMAL (uninjured)⇒

Brain Injury:

– MAP> 90 mmHg, CPP> 70 mmHg

Right MCA infarct

After decompresive

surgery and ICP

monitoring.

CT scan showing

cerabral contusions,

hemorhagee within

the hemispheres,

subdural hematoma

and scull fracture.

Epidural hematoma

Subdural hematoma

Any questions?

Thank you for your attention