Intracranial Pressure in Traumatic Brain Injury Özlem Korkmaz Dilmen Associate Professor of...
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Transcript of Intracranial Pressure in Traumatic Brain Injury Özlem Korkmaz Dilmen Associate Professor of...
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