Intracranial Pressure in Traumatic Brain Injury

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

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

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

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

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

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

8. Airway - A • Clearance (aspiration) • Oral/Nasal Airway • Intubation

9. Breathing - B • Symmetry • Breathing Sounds • Tidal Volume • Respiratory rate

10. 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

11. Circulation - C • Pulse • Rate • Rhytme • Arterial Pressure • Hypertension • Hypotension

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

13. GLASGOW COMA SCALE • I. Motor Response6 - 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

14. Exposure andEnvironment - E The patient’s clothes should be removed or cut in an appropriate manner so that any injuries can be seen.

15. Severity of TBI

16. Prognosis • Type of lesion • Age • Severity of injury as defined by GCS

17. Head Injury Primary Injury Secondary Injury

18. 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)

19. Causes of Secondary Brain Injury • Hypotension • Hypoxia • Anemia • Hyper/Hypoglycemia • Hyperthermia • Hyper/Hypocapnia • Intracranial hypertension • Cerebral edema • Compression from expanding masses • Vasospasm • Seizures

20. Systemic Effects of Head Injury • TBI is a multisystem disorder with profound systemic complications: • Respiratory • Cardiovascular • Hematological • Electrolyte • Neuroendocrinological disorders

21. Human Brain • Dependent on aerobic metabolism • Weight: 2 % of BW • CBF: 15% of cardiac output

22. Components of Cranium • Brain • CSF • Blood V1+ V2+ V3+

23. Intracranial Content • Brain: 1300-1400 g • CSF= 150-175 mL • CBF = 50 mL/100 g tissue/min

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

25. 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

26. Diffuse Brain Swelling

27. Cerebral Blood Volume(CBV) • CBF • Venous out-flow obstruction • Orthostatic effects • Local factors

28. CBF determinants • CMR • Arterial Pressure • PaCO2 • PaO2

29. Cerebral Autoregulation CBF(mL/100g/min) 50 Diameter of cerebral vassels MAP 50 mmHg 150 mmHg PaCO2 55 mmHg 20 mmHg

32. Otoregülasyon Eğrisi

33. 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.

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

35. 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 O2 ➜ Neuron: CPP

41. Right MCA infarct

42. After decompresive surgery and ICP monitoring.

43. CT scan showing cerabral contusions, hemorhagee within the hemispheres, subdural hematoma and scull fracture.

44. Epidural hematoma

45. Subdural hematoma

47. Any questions?

48. Thank you for your attention