Neurotrauma.Dr NG NeuroEdu

1,096 views

Published on

0 Comments
5 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
1,096
On SlideShare
0
From Embeds
0
Number of Embeds
18
Actions
Shares
0
Downloads
0
Comments
0
Likes
5
Embeds 0
No embeds

No notes for slide

Neurotrauma.Dr NG NeuroEdu

  1. 1. NEUROTRAUMA Nishantha Gunasekera MBBS MS MRCS Consultant Neurosurgeon
  2. 2.  36 year old male presented to a District Hospital ED He was arrested for intoxication and fighting at 0530hrs ? Head injury He was found to be difficult to rouse at 0800hrs CT scan of head Initial examination (at District Hospital) GCS 15/15; PEARL 3mm
  3. 3. Natasha Richardson autopsy: internal brain bleed caused death The official word from the New York City medical examiners office is that actress Natasha Richardson died from a blunt impact to the head. Her death was ruled an accident Thursday after an autopsy was performed. The blunt impact caused internal brain bleeding (an epidural hematoma), which is what killed her, the M.E.s office reports, but it is still not clear exactly how she injured her head. Monday afternoon, during a private ski lesson on a beginner hill at Mont Tremblant in Quebec, Richardson fell in the middle of the ski run and did not appear to hit any object aside from the snow on the ground. Afterward, 45-year-old Richardson initially appeared fine and was “lucid”, talking, even making jokes.
  4. 4. Why is Neurotrauma management so important? Injuries to the brain, spinal cord and its associated structures – VITAL ORGANS Most patients are healthy, young and the productive people of society (MVA, accidents, assaults, war) Very good outcome if managed correctly Very poor outcome if managed incorrectly
  5. 5. Role of Nursing in Neurotrauma Correct handling of neurotrauma victims In-ward care is critical for good patient outcome Knowledge of possible injuries and their effects vital for good management and nursing care Understanding the long term problems of neurotrauma helps plan rehabilitation Education in prevention of neurotrauma Compassion for whom you care for and passion for what you do
  6. 6. Introduction Head injury Spinal injury Mixed head and spinal trauma Initial assessment (ABCDE) Transport Primary survey (ABCDE) Secondary survey Treatment Rehabilitation
  7. 7. Head Injury Mechanism Forces Patterns of injury Prevention Primary assessment
  8. 8. Mechanism and forces
  9. 9. Transport Stabilize the spine Airway Oxygen Fluids Inform casualty neurosurgical unit
  10. 10. Head injury Primary brain damage Secondary brain damage Prevention of primary and secondary brain damage
  11. 11. Head injuryPrimary brain damage Brain damage at the time of injurySecondary brain damage Damage due to effects of primary brain damage and other physiological changes that resultMain aim of management is limitation and reversal of secondary brain damage
  12. 12. Secondary brain damage Oedema Hypoxia Hypovolaemia Hypoglycaemia / Hyperglycaemia Hyperthermia Seizures Electrolytes Cytokines
  13. 13. Head injury Intracranial pressure (ICP) Cerebral perfusion pressure (CPP) Mean arterial pressure (MAP) How does it alter Monitoring of pressures
  14. 14. Head injury Mechanisms of controlling ICP  Non surgical  Surgical
  15. 15. Head injury Effects of raised ICP  Cardiovascular  Respiratory  Cushings reflex  Decerebration
  16. 16. Herniation syndromes a) Cingulate (subfalcine) b) Uncal c) Central (transtentorial) d) Thru’ defects f e) Tonsillar f ) Upward (cerebellar)
  17. 17. Clinical Stages of Central herniation STAGE Consciousness Respiration Pupils Occulomotor MotorDiencephalic Altered alertness, Sighs, yawns, Small congugate, Appropriate, lethargy, agitation later Cheyne- (1-3mm) Parinaud’s Babinski (some), stupor, Stokes slow Geganhalten(resists) comaMidbrain stupor Cheyne- Mod. Dolls eyes, Decorticate, Stokes, dilatation, Dyscongugate Decerebrate Tachypnoea (3-5mm) FixedLower pons coma Regular, Mid Dolls eyes Flaccid, Babinski shallow, position, rapid (20- Fixed 40/min)Medullary Coma 3/15 Slow, Widely irregular, dilated, gasps, apnea fixed
  18. 18. Clinical stages of Uncal Herniation (Trauma) STAGE CONSCIOUSNESS RESPIRATION PUPILS OCCULOMOTOR MOTOREarly 3rd Alert, Normal Ipsilateral Doll’s (-), Appropriate, Maybe Babinskinerve oriented, dilatation dysconjugate obeysLate 3rd Stuporous, Sustained Fully EOO Ipsilateral hyper-nerve comatose ventilation dilates (External weakness occulomotor Kernohan’s ophthalmoplegia) phenomenon rarelyMidbrain Comatose Sustained Contralateral Absent Decerebrate hyperpnea dilates, both fixed (7mm)
  19. 19. Herniated Right Uncus
  20. 20. Head injury Monitoring ICP  Clinical  Invasive  ICU (Nursing)
  21. 21. Head injury Management of specific injuries  Minor 12-15 Observation only  Moderate 8-11 Observation/ treatment  Severe <8 Most need treatment  Based on GCS  Mechanism  Anatomy
  22. 22. Glasgow Coma ScaleGlasgow Coma Score
  23. 23. Head Injury Investigations  Skull x ray AP/lateral  CT scan, bone window  CT reconstruction  MRI When to do what investigation?
  24. 24. Head Injury Compound fractures Extra dural haemorrhage (EDH) Acute Subdural Haemorrhage (SDH) Chronic SDH Intracerebral Haemorrhage (ICH) Traumatic subarachnoid haemorrhage (SAH) Intraventricular haemorrhage (IVH) Contre-coupe injury DIFFUSE AXONAL INJURY (DAI)
  25. 25. NORMAL CT
  26. 26. Compound fracture
  27. 27. Compound fractures cntd.
  28. 28. Compoundfractures cntd.
  29. 29. Compound fractures cntd.
  30. 30. Comp. fractures Complications
  31. 31. EDH
  32. 32. EDH
  33. 33. EDH (MRI)
  34. 34. EDH (MRI) cntd.
  35. 35. EDH (MRI) cntd.
  36. 36. ASDH
  37. 37. CSDH
  38. 38. CSDH
  39. 39. ICH
  40. 40. ICH -trauma
  41. 41. Traumatic SAH
  42. 42. IVH
  43. 43. DAI
  44. 44. Contre coup injury Injury directly opposite the site of impact Maybe an EDH with SDH on the other side Both have to be managed May need surgery for both Outcome may be poorer
  45. 45. Modalities of Treatment  Mechanical  Medical  Surgical
  46. 46. Management Trauma Systems Guides: Regionalized trauma systems Option: Neurosurgeons need to have a responsive system in place Option: In rural setting, where no neurosurgeon: know how to Rx extra- dural haematoma in deteriorating pt
  47. 47. Primary surveyCLINICAL ASSESSMENT!!  ABCDE  GCS  Resuscitate  History  Image  Specific Treatment
  48. 48. Initial Assessment ATLS Airway Breathing Circulation Disability Exposure
  49. 49. Treatment Initial Management Options Rapid physiologic resuscitation No intracranial HTN Rx unless herniation or rapid neurologic deterioration Cautious hyperventilation Mannitol if adequate volume established Sedation as desired with careful monitoring (GCS) Short-acting neuromuscular blockade prn
  50. 50. Treatment Resus: Blood Pressure Guides: Achieve SBP > 90 mm Hg Options: MAP > 90 mm Hg CPP > 70 mm Hg Use fluid infusion to achieve above
  51. 51. Treatment Resuscitation: Hypoxia Guides: PaO2 > 60 mmHg, O2 sat > 90% Options: Endotracheal intubation for  GCS < 9  Unable to maintain airway  Persistent hypoxia
  52. 52. Secondary survey CLICAL ASSESSMENT!! All injuries From head to toe Treat on priority basis Chest-abdomen-c spine-head- limbs Refer to appropriate speciality surgeon
  53. 53. Treatment Hyperventilation Standards: Normal ICP, avoid sustained pCO2 < 25 mm Hg in severe TBI Guides: Avoid early prophylactic hyperventilation (pCO2 < 35 mm Hg)  Note: During first 24 hours, cerebral perfusion can be compromised due to low cerebral blood flow
  54. 54. Treatment Hyperventilation Options Option: Hyperventilation useful briefly  Acute neurologic deterioration  Longer use if intracranial HTN persists despite other medical therapies (sedation, paralysis, mannitol, CSF drainage) Option: Test for cerebral ischaemia  Jugular venous O2 sat, AV O2 sat diff  If sustained pCO2 < 30 mm Hg needed
  55. 55. Treatment Hyperventilation Rapidly lowers ICP via vasoconstriction, which reduces cerebral blood flow One RCT Considerable uncertainty Possible beneficial effect on mortality No proven neurologic outcome benefit
  56. 56. Treatment Mannitol Guides: Controls increased ICP  Severe TBI  0.25 to 1.0 gr/kg body weight  Renal problems  Electrolyte imbalance  Good drug in good hands
  57. 57. Treatment Mannitol Options Options: Use in herniation, rapid decline Avoid hypovolaemia Keep serum osmolarity below 320mOsm to avoid renal failure Achieve euvolaemia, use a Foley Use intermittent boluses, may be better
  58. 58. Treatment Mannitol May reverse brain swelling, lower ICP Few eligible RCTs Considerable uncertainty May be superior:  to pentobarbital for increased ICP  in setting of measured increased ICP
  59. 59. Treatment High Dose Barbiturates Guides: Controls increased ICP  May be useful when maximal therapies fail  Includes both medical and surgical Rx  Severe TBI, salvageable  Haemodynamically stable
  60. 60. Treatment Barbiturates Lower ICP via lower cerebral metabolism Few eligible RCTs Noted hypotension in 1 of 4 patients May offset any beneficial ICP effects
  61. 61. Treatment Cerebral Perfusion Pressure Guides: Maintain CPP at 70 mm Hg Reduce ICP by  Mechanical means (position, collar)  Medical means (mannitol, frusemide)  Ventilation  Surgery (drain, decompressive craniectomy)
  62. 62. Treatment ICP Rx Algorithm Insert ICP monitor, maintain CPP > 70 Ventricular drainage Repeat CT Hyperventilate to pCO2 30-35 mm hg Mannitol 0.25 to 1.0 gr/kg Second tier Rx: barbitruates, pCO2 < 30 CLINICALL ASSESSMENT!!
  63. 63. Treatment ICP Monitoring Guides Useful in severe TBI (GCS < 9) Guides: Abnormal initial head CT  Hematomas, contusions  Edema, compressed basal cisterns All other recommendations are options
  64. 64. Treatment ICP Monitoring: Normal CT Guides: ICP monitor with normal CT if two of three noted  Age > 40 years  Persistent BP < 90 mm Hg  Motor posturing
  65. 65. Treatment ICP Monitoring Not Indicated Guides: Not useful with GCS > 8 May be useful if traumatic mass lesion is evident on head CT
  66. 66. Treatment ICP Monitoring Technology Ventricular catheter (Camino catheter) External strain gauge Accurate, low-cost, reliable Parenchymal monitor: drifting values Subarachnoid, subdural, epidural:
  67. 67. Treatment Seizure Prophylaxis Guides: High risk: prevent early sz  Phenytoin, carbamazepine effective  Reduces spikes in ICP in theory  No difference in long-term outcome
  68. 68. Treatment Seizure Prophylaxis, Rx Reduced secondary damage due to increased metabolism, ICP, glutamate Six RCTs RR for early sz prophylaxis: 0.34 For every 100 patients treated, 10 would remain seizure-free for the first week No reduction in late seizures or outcome
  69. 69. Treatment Steroids Standards: Not recommended  No decrease in ICP  No improved outcome  Used with caution in our units for traumatic brain injury
  70. 70. Treatment Calcium Channel Blockers Prevent vasospasm, keep blood flow Four RCTs Considerable uncertainty Two RCTs, traumatic SAH, nimodipine  Pooled OR 0.59 for death (95% CI .37-.94)  Pooled OR 0.67 for death, disability
  71. 71. Treatment Surgical Craniotomy EDH, ASDH, ICH Craniotomy and removal of bone flap only Burr hole External drainage (EVD) Wound toilet (debridement)
  72. 72. EDH -surgery
  73. 73. EDH –surgery cntd.
  74. 74. CSDH surgery
  75. 75. CSDH surgery
  76. 76. REHABILITAION Starts in the ward Continues until the patient is back to his/her optimum Multidisciplinary (nurses, physiotherapists, relatives, doctors) Special equipment
  77. 77. IN WARD NURSING Care of the unconscious  MONITORING  Nutrition (oral, nasogastric, tpn)  Drugs  Bed sores  Eye, nose, mouth care  Bladder, bowel  Stimulation  Mobilization  Physiotherapy  Education
  78. 78. Physiotherapy Exercise Chest physio DVT prophylaxis Bed sores Walking training OT Cognitive Long term management – home care with regular supervision
  79. 79. Qs&As

×