Intracranial Pressure in Traumatic Brain Injury Özlem Korkmaz Dilmen Associate Professor of Anesthesiology and Intensive Care Cerrahpasa School of Medicine

Learning Objectives First aid for TBI Prevention of secondary brain injury Basic neurophysiology Treatment of increased ICP

Epidemiology of Head Injury 1.5 million people sustain TBI every year in US. Adolescent Males> females Car accidents, motor vehicle crashes, falls

Head Injury 46 years old, male Injured in a car crash Unconscious

A (Airway) B (Breathing) C (Circulation) D (Disability) E (Exposure) First Aid

Airway - A Head tilt, chin lift Jaw trust (SCI)

Clearance (aspiration) Oral/Nasal Airway Intubation Airway - A

Symmetry Breathing Sounds Tidal Volume Respiratory rate Breathing - B

Hypoxemia 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 Circulation - C

Disability - D Disability is determined from the patient level of consciousness according to the Glasgow Coma Score.

GLASGOW 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 and Environment - E The patient’s clothes should be removed or cut in an appropriate manner so that any injuries can be seen.

GCS Severe3-8 Moderate9-12 Mild13-15 Severity of TBI

Prognosis Type of lesion Age Severity of injury as defined by GCS

Primary Injury Secondary Injury Head Injury

Primary & 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 Injury Hypotension Hypotension Hypoxia Hypoxia Anemia Hyper/Hypoglycemia Hyperthermia Hyper/Hypocapnia Intracranial hypertension Cerebral edema Compression from expanding masses Vasospasm Seizures

Systemic 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 Brain

Components of Cranium Brain CSF Blood V1+ V2+ V3+

Intracranial Content Brain: g CSF= mL CBF = 50 mL/100 g tissue/min

Volume of Brain Parenchyma Brain Inflammatory/neoplastic tissue Bleeding (Hematoma)

Brain Edema ✤ 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 Volume (CBV) CBF Venous out-flow obstruction Orthostatic effects Local factors

CBF determinants CMR Arterial Pressure PaCO 2 PaO 2

Cerebral Autoregulation MAP PaCO 2 50 mmHg 55 mmHg20 mmHg 150 mmHg Diameter of cerebral vassels 50 CBF(mL/100g/min)

Otoregülasyon Eğrisi

Cerebral Autoregulation 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 Autoregulation Trauma, inflammation, seizure activity and conditions causing raised ICP may abolish auto-regulation and the CPP

O 2 ➜ 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

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