Myths vs facts in head injury

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Lots of myths about head injury are present in general public mind, trying to show light in this darkness with facts.

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Myths vs facts in head injury

  1. 1. Dr. Shailendra D. Anjankar
  2. 2. “No head iNjury is so trivial that it can be ignored, and none so serious that the life must be despaired of” ~ Hippocrates Sri Ganeshaya namaha!
  3. 3. Head Injury patient have poor prognosis and most of them die
  4. 4. Prognosis of patient is dependent on: 1. Initial GCS 2. Age of the Patient 3. Pupils size and reaction to light 4. Hypotension, Hypoxia and Anemia 5. Individual CT characteristics a. Status of basal cisterns b. Traumatic SAH c. Presence and degree of midline shift d. Presence and type of intracranial lesions
  5. 5. GCS GOS 1 (Death) 3 65% 4 45% 5 35% 6 24% 7-13 10-15% Fearnside et al in 315 pt Reference : 1. Fearnside MR, Cook RJ, McDougall P, et al.: The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical, and CT variables. Br J Neurosurg 7:267-279, 1993. 2. Braakman R, Gelpke GJ, Habbema JD, et al.: Systematic selection of prognostic features in patients with severe head injury. Neurosurg 6:362-370, 1980. GCS GOS 1 (Death) 3 100% 4 80% 5 68% 6 51% 7 27% 8 22% 9-15 15% Braakman et al in 305 pt Mortality in patients and its correlation with Admission GCS.
  6. 6. Mortality in patients and Age of Patient correlation
  7. 7. Prognosis of patients and its correlation with Pupils size and reactivity to light
  8. 8. Reference : Chesnut RM, Marshall SB, Piek J, et al.: Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochirurgica (Suppl) 59:121-5, 1993 Reference :Miller JD, Becker DP: Secondary insults to the injured brain. J Royal Coll Surg (Edinburgh) 27:292-298, 1982 Prognosis of patients with Hypoxia & Hypotension
  9. 9. References: 1. Marshall LF, Gantille T, Klauber MR, et al.: The outcome of severe closed head injury. J Neurosurg (Suppl) 75: 28-36, 1991. 2. Van Dongen KJ, Braakman R , Gelpke GJ: The prognostic value of computerized tomography in comatose head injured patients. J Neurosurg 59:951-957, 1983. 3. Kakarieka A: Traumatic subarachnoid hemorrhage. Springer-Verlag, Berlin, 1997. Prognosis of patients with CT characteristics
  10. 10. Marshall et al. Traumatic Coma Data Bank (TCDB). Presence of mass lesions carries a PPV of 78% to unfavorable outcome. Mortality is higher in acute subdural hematoma than in extradural hematoma. Reference: Marshall LF, Gautille T, Klauber MR, et al.: The outcome of severe closed head injury. J Neurosurg (Suppl) 75:28-36, 1991.
  11. 11. If we cant CURE the patient; but definitely can CARE for the patient.
  12. 12. Managing head injury patient is difficult.
  13. 13. Managing a Head Injury patient is simple if proper monitoring and timely interventions are undertaken. ICP should be vigilantly monitored and kept under normal limit by specific interventions. Need to have Good Neurointensive care units and strict adherence to protocols.
  14. 14. Airway Breathing Circulation (C - is not CT scan Brain) Disability Exposure
  15. 15. Handle Neck With Caution: Assume C-spine Injury Use Jaw Thrust Avoid Obstruction of Venous Drainage Intubate If GCS < 8 May Need to Protect Airway Due to Seizures or Trauma Intubation Should Be Oral
  16. 16. Even a Small Rise in PaCO2 Causes a Significant Rise in ICP “Adequate” Breathing may not be enough- Aim for PaCO2 of 35-40 mmHg Hyperventilation Is the Quickest Way to Lower ICP if there are signs of Herniation
  17. 17. Blood Pressure Must Be Optimized to Help Maintain Adequate CPP Only Use Isotonic Fluids for Volume Expansion May Need Inotropic or Pressor Support Control Bleeding
  18. 18. Primary Cellular Injury “Neurotransmitter Storm” Massive Depolarization of Brain Cells Glutamate Calcium NMDA Disruption of normal cellular processes: Protein Phosphorylation Microtubule Construction Enzyme Production Membrane and Cytoskeleton Breakdown Cell Death Oxygen Free Radical Pathway Activation Lipid Peroxidation Cell Membrane Dysfunction Cell Lysis Nitric Oxide Synthase High Nitric Oxide Levels Intracellular Signaling Processes
  19. 19. Systemic Insults Hypoxia (PaO2 < 60 mmHg) Hypotension (SBP < 90 mmHg) Anemia +/- Blood Loss (↓Oxygen Carrying Capacity) Hypo/Hypercapnia Secondary Systemic Insults Seizures Electrolyte Abnormalities Coagulopathy Infection Hyperthermia Iatrogenic (Under- resuscitation) Intracranial Insults Intracranial Hypertension Extra-axial Lesions Cerebral Edema (Peaks at 24-48 hrs post injury) Secondary Brain Injury
  20. 20. Surgery “to do or not to do” for head injury patient depends on Neurosurgeons wish.
  21. 21. 1. Penetrating injuries or blunt injuries with breach of the calvarium/skull 2. Presence of expanding intracranial hematoma a) Epidural Hematoma b) Subdural Hematoma 3. Malignant cerebral edema Decompressive Craniotomy - Decreases ICP, improves cerebral perfusion, prevents ischemia
  22. 22. Epidural Hematoma • Middle Meningeal Artery (36%) • Head Injury without LOC + Lucid Interval followed by deterioration (Classic presentation = 47% of cases) • Lenticular Shape on CT • Surgery is Indicated – If volume > 30 cm3 EDH
  23. 23. Subdural Hematoma • Injury to Bridging Veins • Blood accumulation between dura mater and pia arachinoid mater • Increased risk in elderly and alcoholics due to decreased brain volume • Hyperdense crescent shaped lesion on CT • Surgery is Indicated – If size > 10 mm on CT or if 5 mm shift SDH
  24. 24. Surgery should be done only after pupils start dilating.
  25. 25. * Reactive: ICP increasing * Nonreactive (altered LOC): increased ICP * Nonreactive (normal LOC): not from head injury Pupils Both dilated * Nonreactive: brainstem * Reactive: often reversible Unilaterally dilated
  26. 26. Right side bleed will only cause left hemiparesis
  27. 27. Patient with E2 (eye opening to pain) response can be M6 (following commands).
  28. 28. There are few combinations with are possible and some which are not. E2 is compatible with M1, M2, M3, M4, M5 (pain response) E3 or E4 patient should be M6 (command response) V1, V2, V3 cannot be with M6
  29. 29. Neurological Posturing Decorticate Posturing (M3) = Upper extremity flexion with lower extremity extension (Cortical Injury above the midbrain) Decerebrate Posturing (M2) = Arm extension and internal rotation with wrist flexion (Indicative of brainstem injury, Very Poor predictor of outcome)
  30. 30. All trauma patient requires CT scan Head.
  31. 31. New Orleans Criteria CT imaging is required for patients with minor head injury with any one of the following findings. The Criteria only apply to patients who have a GCS of 15. 1.Headache 2.Vomiting 3.Age > 60 years 4.Drug or Alcohol Intoxication 5.Persistent anterograde amnesia 6.Visible trauma above the clavicle 7.Seizure Canadian CT Head Rule CT Imaging is only required for patients with minor head injury with any one of the following findings. The criteria apply to patients with minor head injury who present with GCS of 13-15 after witnessed LOC, amnesia or confusion. High Risk for Neurosurgical Intervention 1.GCS < 15 at two hours after injury 2.Suspected open or depressed skull fracture 3.Any sign of basilar skull fracture (Hemotympanum, Peri-orbital Eccymosis, Otorrhea or Rhinorrhea, Battle sign) 4.Two or more episodes of vomiting 5.Age > 65 years Medium risk for Brain Injury Detection by CT Imaging 1.Amnesia before impact of 30 or more minutes 2.Dangerous mechanism (E.g. Pedestrican vs. Motor vehicle, Ejection from motor vehicle or fall from an elevation of 3 or more feet or 5 stairs)
  32. 32. Head CT Clinical Rules New Orleans Criteria  Sensitivity and Specificity of detecting a clinically significant CT finding  Sensitivity = 100%  Specificity = 24.5 %  Estimated to decrease CT imaging by 23% Canadian Head CT Rule  Sensitivity and Specificity for need for neurosurgical intervention and clinically significant finding on CT imaging  Sensitivity = 100%  Specificity = 68%  Proposed to reduce CT scanning by 46%
  33. 33. Sub arachnoid hemorrhage in brain means aneurysmal bleed.
  34. 34. Trauma is leading cause. Rx – maintain intravascular volume to prevent ischemia from vasospasm. Mortality 39% { national traumatic coma databank}
  35. 35. Patient with poly trauma, head injury is always a priority.
  36. 36. We have to treat a patient as a whole, and not only a specific organ. PRIMARY BRAIN INJURY DOES NOT CAUSE SHOCK, BUT SHOCK DOES CAUSE SECONDARY BRAIN INJURY
  37. 37. *THE BRAIN NEEDS OXYGEN *OXYGEN IS CARRIED IN BLOOD NO BLOOD, NO OXYGEN, … …BRAIN CELLS DIE Principles of Trauma Management 1. Organized team approach 2. Assumption of most serious injury 3. Treatment along with diagnosis 4. Thorough examination 5. Frequent assessment
  38. 38. Head injury patient having hypotension.
  39. 39. Vital Sign Change with Increasing ICP Respiration Increase, decrease, irregular Pulse Decrease BP Increase, widening pulse pressure • Cushing’s response classically explained as – - Hypertension - Bradycardia - Altered Respiratory pattern in a setting of Increased ICP
  40. 40. carotid baroreceptors respond with parasympathetic stimulation resulting in bradycardia sympathetic stimulation causes hypertension sympathetic stimulation of the heart to correct poor perfusion. ischemia to hypothalamus Poor perfusion to the brain, If hypotension develops
  41. 41. Neurosurgery clearance required for operating on poly trauma patient with associated head injury.
  42. 42. “Clearance given” is itself a myth. No one can guarantee further deterioration if patient is stable at that point. Only, few precautions can be taken to avoid aggravation of the problem- Example- 1.Avoid Nitous oxide during anestheisa in pneumocephalus. 2. Avoid Spinal anesthesia/ Lumbar puncture in patient with intracranial mass lesion
  43. 43. Patient with altered sensorium and poly trauma, should always have concomitant Head injury.
  44. 44. A – Alcohol E – Endocrine/ Electrolyte I – Insulin O – Opiate/Oxygen U – Uremia T – Toxin/Trauma/Temprature I – Infections P – Psychiatric/ porphyria S – SAH, Stroke, SOL, Shock, E- Endocrine/Electrolyte • Hypothyroidism/ Hyperthyroidism • Hyperparathyroidism • Adrenal Hypofunction • Diabetes Mellitus • Hyponatremia (<120Meq/dL) • Hepatic coma • Serum Osmollity (<240, >330mOsm/l) • Hypercalcemia (>19mg/dL) “AEIOU TIPS” – for altered sensorium
  45. 45. If SpO2 is maintained, intubation can be avoided in severe head injury patient in emergency.
  46. 46. Indications for intubation in traumatic brain injury 1. GCS <8 2. Loss of airway reflexes or presence of signs/ symptoms of an airway injury 3. Ventilatory insufficiency (PaO2 < 80 mmHg on room air or a PaCO2 > 50mmHg) 4. Severe facial injuries (La Forte fracture, mandibular fracture) 5. Seizures  Severe head injury patient or the patient in altered sensorium who have risk of aspiration and hypoxia, it is advisable to intubate the patient to protect airway and maintain blood oxygen saturation.
  47. 47. No Loss of consciousness means no Head injury.
  48. 48. *The diagnosis of a Mild Traumatic Brain Injury does not require a LOC. *The most famous and striking example of a severe TBI with no LOC is the case of Phineas Gage, in 1848. *Phineas Gage never lost consciousness. He was reported to be sitting up and talking with the iron bar protruding from his left temporal and frontal lobes
  49. 49. Post Traumatic Amnesia (PTA) *Amnesia for even a few minutes after a blow to the head is evidence of diffuse brain damage. *PTA continues to be “the primary and most specific diagnostic indicator of injury”. Reference: Brown AW et al., “Predictive utility of weekly post-traumatic amnesia assessments after brain injury: a multicentre analysis” (2010) 24:3 Brain Injury 472-478. Less than 5 minutes very mild 5 to 60 minutes mild 1 to 24 hours moderate 1 to 7 days severe 1 to 4 weeks very severe More than 4 weeks extremely severe
  50. 50. Mild head injury patient, with normal scan recovers completely.
  51. 51. Post Concussive Syndrome •Constellation of symptoms that develops within 4 weeks of the injury and may persist for months •Treatment is with analgesia, anti-depressents and anti-emetics Concussion (Latin “Concutere” = shake violently) (In technical language – its SOFTWARE not a HARDWARE problem.)
  52. 52. Another concussion during this period can lead to irreparable damage to Brain tissue.
  53. 53. Mean arterial pressure monitoring not required if ICP is normal in head injury patient.
  54. 54. Maintenance of Cerebral perfusion pressure is more important in treating increased ICP patients. *Our Goal  to maintain CPP by 1) Reducing ICP, +/- 2) Increasing MAP Management aimed at maintaining CPP (70 mmHg) improves outcomes. (Formulas) CPP = MAP- ICP MAP = 2xDP+SP/3 Reference: Rosner et al. (1995) Journal of Neurosurgery, 83(6)
  55. 55. Outside of the limits of autoregulation, raising MAP raises CPP and raising ICP lowers CPP.
  56. 56. Mannitol should be given in all patients with head injury.
  57. 57. Mannitol Osmotic agent Mechanism of action – works as osmotic diuretic  extract extra and intra cellular edema fluid from brain Free radical scavenger Reduces ICP within 30 minutes, last 6-8 hours Dosage 0.25-1 gm/kg bolus Additional mechanism Reduces blood viscosity ( by hemodilution) and improves Rheology Increases CBF vasoconstriction decreases volume reduces ICP. Risks 1. Repeated dose reduced osmotic gradient 2. Hyperosmolar state ( serum osm>320 mOsm) renal failure, rhabdomyolysis, hemolysis 3. Increase size of EDH
  58. 58. ICP and cerebral edema can not be decreased by measures except Mannitol or surgery.
  59. 59. ICP can be decreased by 1. Head elevation to 30 degree 2. Medication – Furosemide, Acetazolamide, 3% saline, Glycerol 3. Hypothermia – by decreasing cerebral metabolism 4. CSF drainage 5. Barbiturate coma
  60. 60. Keep neck mid-line and elevate head of bed …. To what degree? Reference: Feldman et al. (1992) Journal of Neurosurgery, 76 Head Elevation
  61. 61. *Decreased CSF formation *Decreased systemic and cerebral blood volume (impairs sodium and water movement across blood brain barrier) *May have best affect in conjunction with mannitol Loop Diuretic - Furosemide: Reference: Pollay et al. (1983) Journal of Neurosurgery, 59. Hypertonic saline Causes – reduction in mean ICP, is effective within 12 hours of continuous infusion of 3% saline solution. Little continued benefit after 72 hours of treatment Reference: Qureshi et al. (1998) Critical Care Medicine, 26(3)
  62. 62. Reference: Qureshi et al. (1998) Critical Care Medicine, 26(3) Goal: Sodium 145-155 mmol/L Hyperosmolar Therapy • Sodium: square • ICP: circle
  63. 63. *32.5 degree C body temp., reduced cerebral metabolic rate for oxygen (CMRO2) by 45% without change in CBF *Also, the intracranial pressure decreased significantl (p < 0.01) *Side-effects: • Potassium flux • Coagulopathy • Shivering • Skin Breakdown Hypothermia Reference: Metz et al. (1996) Journal of Neurosurgery, 85(4)
  64. 64. CSF drainage- * It is effective and safe. *Provides gradient for bulk flow of edema fluid from parenchyma of brain to ventricles. *Ex- Continuous (EVD) or Intermittent (tapping) can be done. Barbiturate Coma *Lowers ICP, cerebral metabolic O2 demand *Not indicated in the Emergency
  65. 65. Hyperventilation can be increased if ICP is not decreasing.
  66. 66. Cerebral Blood Flow Regulation of Cerebral Vascular Resistance PaCo2 (mmHg) Normal 30 - 50 mmHg Ref: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651 Hyperventilation *Not recommended as prophylactic intervention *Never lower than 25 mm Hg *Reduces ICP by vasoconstriction, may lead to cerebral ischemia *Used as a last resort measure *Aim is to - Maintain PaCO2 at 30-35 mm Hg
  67. 67. Routine Nursing activities have no effect on ICP.
  68. 68. 0 2 4 6 8 10 12 14 16 18 20 Before During After Turning Suctioning Bathing Nursing Activities and ICP Reference: Rising (1993) Journal of Neuroscience Nursing, 25(5) ICP
  69. 69. Relatives should not touch the Severe Head Injury patient in ICU.
  70. 70. Family Contact and ICP Reference: Treolar (1991) Journal of Neuroscience Nursing, 23(5) Presence, touch and voice of family / significant others has been demonstrated to decrease ICP Note: Visitors requires education and preparation before spending time at bedside ! Similarly, music therapy is also known for better recovery. It stimulate brain function controlling movement, cognition, speech, emotions and the senses. Reference: Bradt, J. et al. Music therapy for acquired brain injury. Cochrane Database of Systematic Reviews 2010 Jul 7;(7)
  71. 71. Healing Hand – Doctors Relatives
  72. 72. Treating patient with Head Injury is a TEAM WORK!
  73. 73. Neuroprotective drugs are fool proof in preventing further brain damage
  74. 74. Market is full of Hundreds of Neuroprotective drugs! And the evidence available for its efficacy are done by either pharmaceutical company or in their collaboration. So, how effective they are, is the matter of debate and doctors personal discretion.
  75. 75. Anticonvulsants prevents post traumatic seizures.
  76. 76. Prophylactic phenytoin reduces the incidence of seizure in the first week after injury but not thereafter in moderate to severe head injury. Brain Injury Foundation recommends anti-epileptic medications be administered to high risk patients for first 7 days post-injury *There are insufficient data to recommend routine PTS prophylaxis in patients with mild TBI.
  77. 77. Children recover better than adult after severe head injury.
  78. 78. *The developing brain may be at more risk. It will take longer to see the effects of the brain injury. *Even though a young child's brain has more plasticity and a greater ability for other neurons to take on new function, the brain is less developed overall. *Our data of 509 patient of head injury in pediatric population showed bad outcome for severe head injury
  79. 79. Sedation and paralysing medication can be continued for long time for head injury if patient on ventilator.
  80. 80. *Dictum  “Weaning process should start just after Intubation”. Ventilators are for respiratory support, not substitute! *Neuromuscular blockade is indicated for intubation; but long acting blocking agents should be avoided because they limit serial examinations *Longer term use can cause myopathy and dependence on ventilator.
  81. 81. “Recovery will take about a year”.
  82. 82. When a person has a brain injury, the concept of recovery may be misleading. For a person with a brain injury, although they may look the same the changes are most likely long-lasting and adjustment is an ongoing process. For Brain Injury, PREVENTION is always better than CURE; WEAR HELMET , if you are riding a bike, or sitting at rear.
  83. 83. Hyponatremia in Head injury is only due to SIADH.
  84. 84. Head injury have no effect on heart.
  85. 85. The pathophysiology of cardiovascular complications after brain injury. Refernce: Gregory T , and Smith M Contin Educ Anaesth Crit Care Pain 2011
  86. 86. Typical ECG changes after SAH showing deep T wave inversion and prolongation of the QTc interval.
  87. 87. Delayed quadriplegia in head injury patient is because of missed cervical spine injury.
  88. 88. Critical illness polyneuropathy (CIP) and myopathy (CIM) * are complications of critical illness that present with muscle weakness simulating quadriplegia. *Functional changes can cause electrical inexcitability of nerves and muscles with reversible muscle weakness. *Mechanism- Microvascular changes and cytopathic hypoxia might disrupt energy supply and use. An acquired sodium channelopathy causing reduced muscle membrane and nerve excitability is underlying cause of CIP and CIM. Reference: Latronico N et al. Critical illness polyneuropathy and myopathy: a major cause of muscle weakness and paralysis. Lancet Neurol. 2011 Oct;10(10):931-41.
  89. 89. Your questions..
  90. 90. Fact is more stranger than fiction! Thank you.

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