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![Page 1: Intracranial Pressure in Traumatic Brain Injury Özlem Korkmaz Dilmen Associate Professor of Anesthesiology and Intensive Care Cerrahpasa School of Medicine.](https://reader036.fdocuments.us/reader036/viewer/2022062305/56649d165503460f949ecc00/html5/thumbnails/1.jpg)
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
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Learning ObjectivesLearning Objectives
•First aid for TBI
•Prevention of secondary brain injury
•Basic neurophysiology
•Treatment of increased ICP
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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
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Head InjuryHead Injury
• 46 years old, male
• Injured in a car crash
• Unconscious
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•A (Airway)
•B (Breathing)
•C (Circulation)
•D (Disability)
•E (Exposure)
First AidFirst Aid
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AirwayAirway - A - A
• Head tilt, chin lift
• Jaw trust (SCI)
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• Clearance
(aspiration)
• Oral/Nasal Airway
• Intubation
AirwayAirway - A - A
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• Symmetry
• Breathing Sounds
• Tidal Volume
• Respiratory rate
BreathingBreathing - B - B
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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
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• Pulse
• Rate
• Rhytme
• Arterial Pressure
• Hypertension
• Hypotension
CirculationCirculation - C - C
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DisabilityDisability - D - D
Disability is determined from the patient
level of consciousness according to the
Glasgow Coma Score.
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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
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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.
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GCS
Severe 3-8
Moderate 9-12
Mild 13-15
Severity of TBISeverity of TBI
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PrognosisPrognosis
•Type of lesion
•Age
•Severity of injury as defined by GCS
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Primary Injury
Secondary Injury
Head InjuryHead Injury
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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)
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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
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Systemic Effects of Head InjurySystemic Effects of Head Injury
• TBI is a multisystem disorder with profound systemic
complications:
Respiratory
Cardiovascular
Hematological
Electrolyte
Neuroendocrinological disorders
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•Dependent on aerobic metabolism
•Weight: 2 % of BW
•CBF: 15% of cardiac output
Human BrainHuman Brain
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Components of CraniumComponents of Cranium
•Brain
•CSF
•Blood
V1+
V2+
V3+
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Intracranial ContentIntracranial Content
•Brain: 1300-1400 g
•CSF= 150-175 mL
•CBF = 50 mL/100 g tissue/min
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Volume of Brain ParenchymaVolume of Brain Parenchyma
•Brain
•Inflammatory/neoplastic tissue
•Bleeding (Hematoma)
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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
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Diffuse Brain Swelling
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Cerebral Blood VolumeCerebral Blood Volume(CBV)(CBV)
•CBF
•Venous out-flow obstruction
•Orthostatic effects
•Local factors
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CBF determinantsCBF determinants
•CMR
•Arterial Pressure
•PaCO2
•PaO2
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Cerebral AutoregulationCerebral Autoregulation
MAMAPPPaCO2
50 mmHg55 mmHg
20 mmHg
150 mmHg
Diameter of cerebral vassels
50
CB
F(m
L/1
00g
/m
in)
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Otoregülasyon EğrisiOtoregülasyon Eğrisi
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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.
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Impaired Cerebral AutoregulationImpaired Cerebral Autoregulation
• Trauma,
inflammation,
seizure activity and
conditions causing
raised ICP may
abolish auto-
regulation and the
CPP
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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
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Right MCA infarct
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After decompresive
surgery and ICP
monitoring.
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CT scan showing
cerabral contusions,
hemorhagee within
the hemispheres,
subdural hematoma
and scull fracture.
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Epidural hematoma
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Subdural hematoma
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Any questions?
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Thank you for your attention