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2. No patientwant to be this ........ No Neurosurgeonlike to plant ....... 3. 4. Classification SeverityAnatomicfindings 5. Classification SeverityMinimal : GCS 15, no LOC or amnesia Mild : GCS 14, or 15 + LOC or amnesiaimpaired alertness or memory Moderate : 9-13 or LOC 5 min orfocal neurological deficit Severe : GCS 5 - 8Critical : GCS 3 - 4 6. Classification Anatomicfindings FocalDiffuse Contusion Coup Countrecoup Gliding Fracture Hematoma EpiduralSubduralIntraparenchymal Intermediary Concussion DAI 7. Marshall CT Grading of Brain Trauma Diffuse Injury Grade CT appearance Mortality I Normal CT scan 9.6% II Cisterns present. Shift < 5mm 13.5% III Cisterns compressed/absent. Shift < 5mm.34% IV Shift > 5mm 56.2% 8. Classification Primary Secondary
Injury sustained by thebrain after the impact Causes:Hypoxia, Hypoperfusion Examples: cerebral edema,herniation 9. Prehospital management
10. Head injury management in A&E room
11. Head injury management in A&E room
12. A B C DE 13. Secondary survey in trauma patients
14. Secondary survey for head trauma GCS Pupillarysize Active bleeding scalp wound 15. GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = incomprehensivesound 3 = inappropriate words 4 = confuse 5 = alert Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command 16. GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries3 = vocal sounds4 = words 5 = orientated to face Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command Pediatric age 1- 5 yrs 17. GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries3 = vocal sounds4 = words Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain Pediatric age upto 6months 18. Pupillary response :
19. Other NeuroExam
20. Other NeuroExam
21. Imaging of head injury
22. Skull Fracture
23. Acute ExtraDural Hemorrhage
24. Acute SubDural Hemorrhage
25. Brain contusion (LEBAM)
26. Diffuse brain injury
27. 28. Management of TBI 29. Monro-Kellie hypothesis
30. 31. Management ofTBI Detection& Monitor Treatment 32. Detection& Monitor GCS Pupillary reflex ICP Monitor Symptoms & sign of herniation 33. Methods of monitoring intracranial pressure . Fiberoptic sensors (Camino),Microchips (internal strain-gauge devices)(Codman)Air pouch technologies (Spiegelberg) 34. Methods of monitoring intracranial pressure . 35. EVD, External Ventricular Drain 36. Primaryinjury Secondary injury HerniationMasslesion ICP ICP ICP ICP 37. Secondary injury Hypoxia Hypovolemia Cerebraledema 38. Howto manageraise ICP? 39. CerebralProtection Sedation 40. Managing raiseICP Generalmeasure Medicalmanagement Surgicalintervention 41. Generalmeasure Head elevation Maintain normal temperature Neck vein compression? ? Chest Physio Hyperventilation Fluid management Glucose monitor Maintain normal Blod pressure 42. Head elevation
43. Neck vein compression?
44. Maintainnormal temperature Keep patientsbody temperaturewithin normal limit 45. ? Chest Physio To give sedation during chest physiotherapy 46. Hyperventilation NO HYPERVENTILATION!!!! Keep patient at the lower limit of normocapnia (32mmHg) Optimal Oxygenation!!! Increased CO2 = Vasoconstriction and Decreased ICP Decreased CO2 = Vasodilatation and Increased ICP 47. Fluid management
48. Glucose monitor
49. Medicalmanagement SedationMuscle relaxant Barbiturate & Propofol analgesic antipyretic Mannitol & Frusemide Hypertonic saline antiepileptics Neuroprotectiveagent BP control 50. Sedationanalgesic Midazolam + Morphine 51. Barbiturate & Propofol Barbiturates appear to exert their ICP-lowering effects through vasoconstriction, which results in a reduction in CBF and CBV secondary to the suppression of cerebral metabolism 52. Muscle relaxant Increase incidence ofaspiration pneumonia 53. Mannitol & Frusemide The administration of mannitol has become the first choice for pharmacological ICP reduction , Mannitol has an immediate plasma-expanding effect that reduces haematocrit and blood viscosity and increases CBF and cerebral oxygenation delivery. Hyperosmotic agents remove more water from the brain than from other organs because the bloodbrain barrier impedes the penetration of the osmotic agent into the brain maintaining an osmotic diffusion gradient.This osmotic effect of mannitol is delayed for 1530 min. Mannitol consistently decreases ICP for 16 h. 54. Mannitol & Frusemide An ultra-early single-shot administration of high-dose mannitol (1.4 g/kg) in the emergency room significantly improves the 6-month clinical outcome after head injury One risk of hyperosmotic agents is the rebound effect, which might increase ICP. To reduce this risk it is recommended that mannitol should be administrated as repeated boluses rather than continuously, only in patients with increased ICP and not longer than 34 days As mannitol is entirely excreted in the urine there is a risk of acute tubular necrosis, particularly if serum osmolarity exceeds 320 mOsmol/l 55. Mannitol & Frusemide Although furosemide itself has only a minimal effect on ICP, in combination with mannitol it enhances the effects of mannitol on plasma osmolality, resulting in a greater reduction of brain water content 56. Hypertonic saline Several studies have shown that hypertonic saline is equal or even superior to mannitol in reducing ICP. Vialet et al. suggested that hypertonic saline (2 ml/kg, 7.5%) is an effective and safe initial treatment for intracranial hypertension episodes in head trauma patients when osmotherapy is indicated. Even very high concentrated hypertonic saline solutions (23.5%) can be used and can reduce ICP in poor grade patients with subarachnoid haemorrhage. 57. antipyretic antiepileptics Neuroprotectiveagent it is evident that hyperthermia should be avoided Is not for reduce ICP. But to prevent fit whichwill cause raise ICP Still under experimental stage 58. Surgicalintervention Removal of thepathological lesion CSF diversion procedure Open the cranium craniectomy Remove part of the non-eloquent brain Lobectomy 59. Removal of thepathological lesion CSF diversion procedure Open the cranium craniectomyRemove part of the non-eloquent brain Lobectomy 60. Summary of TBI management Steps Rationale Respiratory support (intubation & ventilation) Comatose, unable to protect airways Elevate head 30-45 Facilitate venous drainage Straighten neck, no tape encircling the neck Facilitate venous drainage Avoid hypotension (SBP