TRAUMATIC BRAIN INJURY.pptxaffddf5ffhfssf

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1. PRIMARY SURVEY FOR TRAUMATIC BRAIN INJURY AND PREVENTION OF SECONDARY BRAIN DAMAGE TEAM KOCHERS : DR KULRAJ DR QASIM DR MILAN DR PRINCE DR RADHIKA DR YESHWANT DR ARIF DR BRAJ BHUSHAN

2. What is TBI ? TBI is defined as an brain function impairment that results from an external force.

3. PATHOPHYSIOLOGY Factors affecting cerebral blood flow: 1. Autoregulation 2. Cerebral perfusion pressure (CPP) 3. Mean arterial pressure ( MAP ) 4. Intracranial pressure 5. CPP = MAP - ICP

4. Normally, autoregulation regulates the local cerebral blood flow to maintain the cerebral oxygenation. CPP is maintained at 50 to 150mmhg by auto regulation This autoregulation is lost in TBI and hence even a small drop in blood pressure decreases the brain perfusion and CPP.

5. INTRACRANIAL PRESSURE The Monro – Kellie doctrine Increase in ICP reduces CPP and exacerbates the ischemia Normal ICP is maintained at 5-15mmhg ICP more than 22mmhg is associated with poor outcomes

6. PRIMARY BRAIN INJURY SECONDARY BRAIN INJURY Contusions Occurs due to chemicals and neurotoxins released as a result of brain damage Hematomas SECONDARY BRAIN INSULTS like: Diffuse axonal injury HYPOXIA ,HYPONATREMIA, HYPERGLYCEMIA which accelerate the secondary neurotoxic effects Loss of blood brain barrier Direct cellular damage Loss of the electro chemical function

7. PATHOPHYSIOLOGY OF SECONDARY BRAIN DAMAGE Occurs as a result of decreased oxygen delivery to the brain Severe trauma causes alteration in cerebral blood vessel auto-regulation. Systemic hypotension with this altered autoregulation results in decreased CBF and decreased O2 delivery. This ischemia is exacerbated even further by systemic hypoxemia and IC HTN; which decreases CBF even further and a cascade of events involving mediators of inflammation, excitotoxicity, calcium influx and Na+ K+ ATPase dysfunction leads to neuronal cell dysfunction and death.

8. SUBDURAL HEMATOMA EXTRADURAL HEMATOMA

9. SUBARACHNOID HEMORRHAGE CEREBRAL CONTUSION

10. DIFFUSE AXONAL INJURY CEREBRAL EDEMA

11. PRIMARY SURVEY: AIRWAY AND BREATHING Includes Cervical spine stabilization Stepwise approach: suctioning , jaw thrust or chin lift maneuver , oro /nasopharyngeal airways Auscultation and pulse oximetry Transient respiratory arrest and hypoxia : SBI Perform early ET intubation in GCS < 8, persistent hypoxia, compromised airway, difficulty in breathing Maintain PcO2 approx. 35-45mmhg, O2 saturation > 90%, PaO2 >60mmhg

12. Prolonged hyperventilation with PcO2<25mmhg is not recommended Tension pneumothorax, massive haemothorax and flail segment should be identified and managed : further compromise the ventilation and can exacerbate secondary brain injury

13. CIRCULATION Traumatic hypotension leads to ischemia within low flow regions of injured brain. Ischemia amplifies the neurotoxic cascade and increases cerebral edema Identification of shock: skin cool, sweaty, tachycardia, hypotension Pelvic binder: hemodynamically unstable followed by a blunt trauma Hypotension is treated as hypovolemic until proven otherwise Aggressive fluid resuscitation : two large bore IV cannulae /central or intraosseous venous access, Blood/FFP/Platelets/Normal saline

14. Excess Iv Crystalloids/colloids avoided: hemodilution, increase coagulopathy and increase risk of adult respiratory distress syndrome Tranexamic acid 1g over 10 minutes f/b 1g dose over 8 hrs ( pulse >110/min or SBP < 110mmhg) Ideally given within 1 st hr from injury For suspected head injury: Maintain SBP >100mmhg for 50-69yrs of age SBP > 110mmhg for 15-49yrs and > 70yrs of age Permissive hypotension worsens the outcome in patients with brain injury

15. DISABILITY GCS Pupillary size and reaction Thoracolumbar spine protection using log roll technique If pelvic fracture hasn’t been ruled out: 20degree roll with inline spinal stabilization is done

16. EXPOSURE Adequately exposed for examination Record core temperature Hypothermia further increases coagulopathy Minimise exposure for longer period of time and unnecessary exposure Use warmed blankets, trolleys, warmed fluids

17. SECONDARY SURVEY AMPLE history ( allergies, medications, past illness, pregnancy, last meal, events/environment relating to injury) External injuries- fractures, lacerations, , CSF otorrhea, rhinorrhea , hemotympanum Neck-trachea, carotid pulsation, jugular venous distension, posterior cervical pain/spinous process step off EYES: pupils , haemorrhage, racoon eyes, orbital rim fracture

18. Classification of Head Injuries Minor head injury: GCS 15 with no LOC Mild head injury: GCS 14 or 15 with LOC Moderate head injury: GCS 9-13 Severe head injury: GCS 3-8

19. Indications of CT in mild head injury History of LOC, definite amnesia AND any one of the following GCS score less than 15 at 2 hours after injury Loss of consciousness ( more than 5 mins) Suspected open or depressed skull fracture Amnesia before impact ( more than 30 minutes ) Sign of basilar skull fracture ( hemotympanum, raccoon eyes, CSF otorrhea or rhinorrhea , battle’s sign) Dangerous mechanism ) pedestrian struck by motor vehicle, occupant ejected from vehicle, fall from height more than 3 feet or five stairs. Vomiting ( more than 2 episodes) Age more than 65 years Anticoagulant use

20. Management of MODERATE head injury 15 % of head injury patients They still are able to follow simple commands, but usually are confused or somnolent and can have focal neurological deficits such as hemiparesis. Approximately 10% to 20 % will deteriorate and lapse into coma A head CT is obtained in all moderate head injury patients. A follow up CT scan with in 24 hours is recommended if the initial CT scan is abnormal or if there is deterioration of patient’s neurologic status.

21. Management of SEVERE head injury These patients are unable to follow even a simple command because of impaired consciousness even after cardiopulmonary stabilization Greater risk of significant morbidity and mortality Do not delay patient to transfer to obtain a CT scan.

22. BRAIN TRAUMA FOUNDATION RECOMMENDATIONS FOR TBI Hyperosmolar therapy Mannitol is effective for control of raised ICP ( 0.25-1g/kg) Prophylactic hypothermia EARLY ( with in 2.5 hrs) SHORT TERM ( 48hrs post injury ) Hypothermia is not recommended in patients with diffuse injury Infection prophylaxis Routine external ventricular catheter exchange not recommended Oral care is not recommended to reduce ventilator associated Pneumonia Antimicrobial ventricular EVD catheters decrease infection

23. ICP monitoring I f GCS is 3-8 on admission with abnormal CT I n SEVERE traumatic head injury and normal CT, it is indicated with two or more of the following: 1. age > 40yrs 2. unilateral posturing 3. hypotension with sbp < 90 Brain oxygen monitoring and thresholds Jugular venous saturation (50%) or above

24. Blood pressure and oxygenation SBP as described before Saturation (<90%) or Po2 (<60mmhg) should be avoided Nutrition Should be initiated at least 5 days and at most 7 days post injury Sedatives High dose barbiturates to control refractory ICP in hemodynamically stable patient Propofol is also recommended for ICP control but it does not improve mortality.

25. Seizure prophylaxis Decreases early post traumatic seizures ( < 7 days after injury) ; insufficient evidence to recommend levetiracetam over phenytoin. Hyperventillation Recommended as temporising agent Pco2 below 25 mmhg not recommended, avoid in first 24 hrs after injury STEROIDS ARE CONTRAINDICATED

26. REFERENCES Sabiston textbook of surgery 21 st edition Bailey and love’s 28 th edition ATLS 10 th edition