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Traumatic  Head Injury Toh C J
No patient  want to be this ........ No Neurosurgeon  like to plant .......
 
Classification Severity  Anatomic  findings
Classification Severity  Minimal : GCS 15, no LOC or amnesia Mild : GCS 14, or 15 + LOC or amnesia  impaired alertness or memory Moderate : 9-13 or LOC  ≥ 5 min or  focal neurological deficit Severe : GCS 5 - 8  Critical : GCS 3 - 4
Classification Anatomic  findings Focal  Diffuse Contusion Coup Countrecoup Gliding Fracture Hematoma Epidural  Subdural  Intraparenchymal Intermediary Concussion DAI
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%
Classification Primary Secondary ,[object Object],[object Object],[object Object],Injury sustained by the  brain after the impact Causes:  Hypoxia, Hypoperfusion Examples: cerebral edema,  herniation
Prehospital management ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Head injury management in A&E room ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Head injury management in A&E room ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
A B C D  E
Secondary survey in trauma patients ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Secondary survey for head trauma GCS Pupillary  size Active   bleeding scalp wound
GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = incomprehensive  sound 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
GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries  3 = vocal sounds  4 = 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
GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries  3 = vocal sounds  4 = words Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain Pediatric age upto 6  months
Pupillary response : ,[object Object]
Other NeuroExam ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Other NeuroExam ,[object Object],[object Object],[object Object],[object Object],[object Object]
Imaging of head injury ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Skull Fracture ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute ExtraDural Hemorrhage ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute SubDural Hemorrhage ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Brain contusion (LEBAM) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Diffuse brain injury ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Management of TBI
Monro-Kellie hypothesis ,[object Object]
 
Management of  TBI Detection  & Monitor Treatment
Detection  & Monitor GCS Pupillary reflex ICP Monitor Symptoms & sign of herniation
Methods of monitoring intracranial pressure . Fiberoptic sensors (Camino),  Microchips (internal strain-gauge devices)(Codman)  Air pouch technologies (Spiegelberg)
Methods of monitoring intracranial pressure .
EVD, External Ventricular Drain
Primary  injury Secondary injury Herniation  Mass  lesion ICP   ICP   ICP   ICP  
Secondary injury Hypoxia Hypovolemia Cerebral  edema
How  to manage  raise ICP?
Cerebral  Protection ≠ Sedation
Managing raise  ICP General  measure Medical  management Surgical  intervention
General  measure Head elevation Maintain normal temperature Neck vein compression? ? Chest Physio Hyperventilation Fluid management Glucose monitor Maintain normal Blod pressure
Head elevation ,[object Object],[object Object]
Neck vein compression? ,[object Object],[object Object],[object Object]
Maintain  normal temperature Keep patient’s  body temperature  within normal limit
? Chest Physio To give sedation during chest physiotherapy
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
Fluid management ,[object Object]
Glucose monitor ,[object Object],[object Object]
Medical  management Sedation  Muscle relaxant   Barbiturate & Propofol analgesic antipyretic Mannitol & Frusemide   Hypertonic saline antiepileptics Neuroprotective  agent BP control
Sedation  analgesic Midazolam + Morphine
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
Muscle relaxant   Increase incidence of  aspiration pneumonia
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 blood–brain barrier impedes the penetration of the osmotic agent into the brain maintaining an osmotic diffusion gradient.  This osmotic effect of mannitol is delayed for 15–30 min. Mannitol consistently decreases ICP for 1–6 h.
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 3–4 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
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
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.
antipyretic antiepileptics Neuroprotective  agent it is evident that hyperthermia should be avoided Is not for reduce ICP. But to prevent fit which  will cause raise ICP Still under experimental stage
Surgical  intervention Removal of the  pathological lesion CSF diversion procedure Open the cranium  “ craniectomy” Remove part of the non-eloquent brain “ Lobectomy”
Removal of the  pathological lesion CSF diversion procedure Open the cranium  “ craniectomy”  Remove part of the non-eloquent brain “ Lobectomy”
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<90mmHg) Prevent hypoxia – edema Control hypertension Avoid transmission of pressure to ICP Avoid hypoxia (PaCO2 < 60mmHg) Prevent vasodilatation Control ventilation, aims PaCO2 35-40 mmHg Avoid  vasoconstriction / -dilatation Adequate sedation To reduce brain metabolism Do CT brain Ascertain intracranial pathology rapidly
Brain swelling
Bleeding
 
 
 
 
 
 
 
 
 
Take Home Message: CPP =  MAP - ICP ICP keep < 20 mmHg CPP keep 60 to 70 mmHg “ Biar lambat asalkan selamat”
 
Summary: ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]

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Traumatic Head Injury Guide

  • 1. Traumatic Head Injury Toh C J
  • 2. No patient want to be this ........ No Neurosurgeon like to plant .......
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  • 4. Classification Severity Anatomic findings
  • 5. Classification Severity Minimal : GCS 15, no LOC or amnesia Mild : GCS 14, or 15 + LOC or amnesia impaired alertness or memory Moderate : 9-13 or LOC ≥ 5 min or focal neurological deficit Severe : GCS 5 - 8 Critical : GCS 3 - 4
  • 6. Classification Anatomic findings Focal Diffuse Contusion Coup Countrecoup Gliding Fracture Hematoma Epidural Subdural Intraparenchymal 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%
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  • 12. A B C D E
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  • 14. Secondary survey for head trauma GCS Pupillary size 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 = incomprehensive sound 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 = cries 3 = vocal sounds 4 = 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 = cries 3 = vocal sounds 4 = words Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain Pediatric age upto 6 months
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  • 31. Management of TBI 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 .
  • 36. Primary injury Secondary injury Herniation Mass lesion ICP  ICP  ICP  ICP 
  • 37. Secondary injury Hypoxia Hypovolemia Cerebral edema
  • 38. How to manage raise ICP?
  • 39. Cerebral Protection ≠ Sedation
  • 40. Managing raise ICP General measure Medical management Surgical intervention
  • 41. General measure Head elevation Maintain normal temperature Neck vein compression? ? Chest Physio Hyperventilation Fluid management Glucose monitor Maintain normal Blod pressure
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  • 44. Maintain normal temperature Keep patient’s body temperature within 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
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  • 49. Medical management Sedation Muscle relaxant Barbiturate & Propofol analgesic antipyretic Mannitol & Frusemide Hypertonic saline antiepileptics Neuroprotective agent BP control
  • 50. Sedation analgesic 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 of aspiration 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 blood–brain barrier impedes the penetration of the osmotic agent into the brain maintaining an osmotic diffusion gradient. This osmotic effect of mannitol is delayed for 15–30 min. Mannitol consistently decreases ICP for 1–6 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 3–4 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 Neuroprotective agent it is evident that hyperthermia should be avoided Is not for reduce ICP. But to prevent fit which will cause raise ICP Still under experimental stage
  • 58. Surgical intervention Removal of the pathological lesion CSF diversion procedure Open the cranium “ craniectomy” Remove part of the non-eloquent brain “ Lobectomy”
  • 59. Removal of the pathological lesion CSF diversion procedure Open the cranium “ craniectomy” Remove 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<90mmHg) Prevent hypoxia – edema Control hypertension Avoid transmission of pressure to ICP Avoid hypoxia (PaCO2 < 60mmHg) Prevent vasodilatation Control ventilation, aims PaCO2 35-40 mmHg Avoid vasoconstriction / -dilatation Adequate sedation To reduce brain metabolism Do CT brain Ascertain intracranial pathology rapidly
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  • 72. Take Home Message: CPP = MAP - ICP ICP keep < 20 mmHg CPP keep 60 to 70 mmHg “ Biar lambat asalkan selamat”
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