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Wayne Triner, DO, MPH, FACEP
Professor, Emergency Medicine
     Albany Medical College &
     State University at Albany
   All TBI                     790
    / 100,000 py
    Mod to Severe 41
    / 100,000 py
     1.2 x risk Maori
     2-5 x risk in rural
the incidence of TBI per 100 000 people
per year (790 cases), especially mild TBI
(749 cases), in New Zealand was
substantially greater than in other high-
income countries. in Europe (47–453
cases) and North America (51–618
cases).
   Primary
     Direct tissue injury
   Secondary
       Cerebral perfusion/edema
       Vasoregulation
       Tissue ischemia
       Herniation
   Cerebral Blood Flow
            CBF ~ CPP – CVP

   Cerebral Perfusion Pressure
            CPP = MAP – ICP

            CBF ~ (MAP – ICP) - CVP
   Mild
     GCS > 12
   Moderate
     GCS 12-8
   Severe
     GCS < 8
Eye Opening                        Mild
 4=Spontaneous
                                     GCS > 12
 3=To voice
 2=To pain                        Moderate
 1=None                             GCS 12-8
                                   Severe
Verbal                               GCS < 8
 5=Normal conversation
 4=Disoriented conversation
 3=Words, but not coherent
 2=No words......only sounds
 1=None

Motor
 6=Normal
 5=Localizes to pain
 4=Withdraws to pain
 3=Decorticate posture
 2=Decerebrate
 1=None
   GCS 13-15
   < 30 minute LOC
   Non-focal exam
   Short term                 Long term
     Mood and cognitive         Depression
      disturbances               Dementia
     Validation                 Parkinson’s
     Variable rate of CT        Cognitive deficits
      abnormalities
The goal being identification of significant
  conditions amenable to intervention
LEVEL I RECOMMENDATION                             LEVEL II RECOMMENDATION
A noncontrast head CT is indicated                 A noncontrast head CT should be
in head trauma patients with loss of               considered in head trauma patients
consciousness or pos- traumatic                    with no loss of consciousness or
amnesia only if one of the                         post-traumatic amnesia if there is
following is present:                              focal deficit, vomiting, severe
headache, vomiting, age > 60                       headache, age > 65 years, signs of
years, drug or alcohol                             basilar skull Fx, GCS < 15,
intoxication, deficits in short-term               coagulopathy or dangerous
memory, physical evidence of                       mechanism (ejection from vehicle,
trauma above the                                   pedestrian struck, fall of more than
clavicle, posttraumatic seizure, GCS               3 ft or 5 stairs)
< 15, focal deficit or coagulopathy.

                                                                                         Clinical Policy:
              Neuroimaging and Decisionmaking in Adult Mild Traumatic Brain Injury in the Acute Setting
                                                                                             ACEP 2008
   Understand the risk factors
     Age
     Small brains
     Inability to fully evaluate
     Propensity for bleeding
     Mechanism and evidence of trauma
   Recognize neurological abnormalities
     HA, vomiting, focal deficits
   Recommendations
     “Neuro rest”
   Proven
     ?????
   ABCs
   Limit secondary brain injury
   Preservation of CBF
   Issues of coagulation
     Reversal of coagulopathies
      ▪ F VIIa
      ▪ Prothrombin complex concentrate
      ▪ Vit K and FFP
   “Evidence based”
   Standards, Guidelines and Options
    • Preserve oxygenation
      (at all costs)
    • Avoidance of hypotension
      (SBP < 90)
    • Euventilation
Rapid reduction in ICP
   3 compartment
    model
   Below pCO2 < 23,
    CBF < 20
    ml/100g/min
   Preserve oxygenation (at all costs)
     Issues of airway management
      ▪ Pre-hospital ETT
      ▪ Neuro-protective RSI
       ▪ Laryngeal manipulation
       ▪ Hypotension
       ▪ ICP management
   Avoidance of hypotension (SBP < 90)
     Preserve CBF
     Control of cerebral edema
      ▪ Brief hyperventilation
     Hyperosmolar therapy
   Recommendations;
     Level II
       ▪ Mannitol is effective for the control of raised
         intracranial pressure at doses of 0.25 to 1 g/kg.
         Hypotension (SBP < 90) should be avoided
     Level III
       ▪ Restrict mannitol use prior to ICP monitoring to
         patients with signs of transtentorial herniation or
         deteriorating mental status not attributable to other
         causes
   Mechanism of Action
     Blood rheology
       ▪ immediate plasma volume expansion
     Osmotic redistribution
   Hypertonic Saline
     23.4% 50 ml
   Typically uncus herniating across tentorum
     CN III compression
      ▪ pupillary dilitation
        ▪ 80% ipsilateral to side of structural lesion
     Pyramidal tract compression
      ▪ Contralateral weakness
        ▪ 80% contralateral to side of structural lesion
     Rapid deterioration of mental status
     Cushing’s reflex
   No Level I or II recommendations
   Level III:
     No change in all-cause mortality
     46% improved chance of favorable outcome (GOS
      4-5)
     Some evidence of improved outcome with > 48
      hours of cooling
   Most common CT finding
    in TBI
   Often occurs in concert
    with other imaging
    abnormalities
   Neuro deficits reflect
    parenchymal injury and
    generally not a vascular
    insult
   High Mortality Rate
   Association with Skull Fracture
   Acute
   Higher Mortality Rate
    Than EDH
     underlying brain injury
     co-morbidity
   Chronic
   Subacute
   Presence of
    contusion does not
    independently
    predict outcome
• Cisterns
• Gray – White
  Interface
   Decompressable lesion with neuro findings
     SDH, EDH, very few contusions
     Traumatic SAH is not decompressable and not an
     indication for aneurysm screening
   Indications of increasing ICP
     Deteriorating mental status
     Herniation syndromes
   Decompressive craniectomy
   Cerebral edema              ICP determination
   Monitoring                    early detection of mass
     GCS < 8 and Abnormal         lesions
      Head CT                     limit potentially harmful
     GCS < 8 and Normal           therapies
      Head CT with...             determination of
      ▪ age > 40                   prognosis
      ▪ posturing                 CSF drainage*
      ▪ hypotension
   All about GCS
   GSW injury reflect patterns of ballistics
   Issues in
    management
     Hearing
     Antibiotics
     Disposition
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: Interactions between factors determining prognosis in populations of patients with severe head injury. In Frowein RA, Wilcke O,
Karimi-Nejad A, et al. Advances in Neurosurgery: Head Injuries-Tumors of the Cerebellar Region. Springer-Verlag, Berlin: 12-15, 1978.
3 Phuenpathom N, Choomuang M, Ratanalert S: Outcome and outcome prediction in acute subdural hematoma. Surg Neurol 40:22-25, 1993
   Strong factor in determining outcome from
    severe TBI
   This holds true even after correcting for co-
    morbid conditions.
   TBI Biomarkers
     Need for imaging
     Validation
     Prognostication
   Intervention
     Hypothermia
     Progesterone
     Reduction of oxidative stress
Head injury

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Head injury

  • 1. Wayne Triner, DO, MPH, FACEP Professor, Emergency Medicine Albany Medical College & State University at Albany
  • 2. All TBI 790 / 100,000 py  Mod to Severe 41 / 100,000 py  1.2 x risk Maori  2-5 x risk in rural the incidence of TBI per 100 000 people per year (790 cases), especially mild TBI (749 cases), in New Zealand was substantially greater than in other high- income countries. in Europe (47–453 cases) and North America (51–618 cases).
  • 3.
  • 4. Primary  Direct tissue injury  Secondary  Cerebral perfusion/edema  Vasoregulation  Tissue ischemia  Herniation
  • 5. Cerebral Blood Flow CBF ~ CPP – CVP  Cerebral Perfusion Pressure CPP = MAP – ICP CBF ~ (MAP – ICP) - CVP
  • 6. Mild  GCS > 12  Moderate  GCS 12-8  Severe  GCS < 8
  • 7. Eye Opening  Mild  4=Spontaneous  GCS > 12  3=To voice  2=To pain  Moderate  1=None  GCS 12-8  Severe Verbal  GCS < 8  5=Normal conversation  4=Disoriented conversation  3=Words, but not coherent  2=No words......only sounds  1=None Motor  6=Normal  5=Localizes to pain  4=Withdraws to pain  3=Decorticate posture  2=Decerebrate  1=None
  • 8. GCS 13-15  < 30 minute LOC  Non-focal exam
  • 9. Short term  Long term  Mood and cognitive  Depression disturbances  Dementia  Validation  Parkinson’s  Variable rate of CT  Cognitive deficits abnormalities
  • 10. The goal being identification of significant conditions amenable to intervention
  • 11. LEVEL I RECOMMENDATION LEVEL II RECOMMENDATION A noncontrast head CT is indicated A noncontrast head CT should be in head trauma patients with loss of considered in head trauma patients consciousness or pos- traumatic with no loss of consciousness or amnesia only if one of the post-traumatic amnesia if there is following is present: focal deficit, vomiting, severe headache, vomiting, age > 60 headache, age > 65 years, signs of years, drug or alcohol basilar skull Fx, GCS < 15, intoxication, deficits in short-term coagulopathy or dangerous memory, physical evidence of mechanism (ejection from vehicle, trauma above the pedestrian struck, fall of more than clavicle, posttraumatic seizure, GCS 3 ft or 5 stairs) < 15, focal deficit or coagulopathy. Clinical Policy: Neuroimaging and Decisionmaking in Adult Mild Traumatic Brain Injury in the Acute Setting ACEP 2008
  • 12. Understand the risk factors  Age  Small brains  Inability to fully evaluate  Propensity for bleeding  Mechanism and evidence of trauma  Recognize neurological abnormalities  HA, vomiting, focal deficits
  • 13. Recommendations  “Neuro rest”  Proven  ?????
  • 14.
  • 15. ABCs  Limit secondary brain injury  Preservation of CBF  Issues of coagulation  Reversal of coagulopathies ▪ F VIIa ▪ Prothrombin complex concentrate ▪ Vit K and FFP
  • 16. “Evidence based”  Standards, Guidelines and Options • Preserve oxygenation (at all costs) • Avoidance of hypotension (SBP < 90) • Euventilation
  • 17. Rapid reduction in ICP  3 compartment model  Below pCO2 < 23, CBF < 20 ml/100g/min
  • 18. Preserve oxygenation (at all costs)  Issues of airway management ▪ Pre-hospital ETT ▪ Neuro-protective RSI ▪ Laryngeal manipulation ▪ Hypotension ▪ ICP management
  • 19. Avoidance of hypotension (SBP < 90)  Preserve CBF  Control of cerebral edema ▪ Brief hyperventilation  Hyperosmolar therapy
  • 20. Recommendations;  Level II ▪ Mannitol is effective for the control of raised intracranial pressure at doses of 0.25 to 1 g/kg. Hypotension (SBP < 90) should be avoided  Level III ▪ Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or deteriorating mental status not attributable to other causes  Mechanism of Action  Blood rheology ▪ immediate plasma volume expansion  Osmotic redistribution  Hypertonic Saline  23.4% 50 ml
  • 21. Typically uncus herniating across tentorum  CN III compression ▪ pupillary dilitation ▪ 80% ipsilateral to side of structural lesion  Pyramidal tract compression ▪ Contralateral weakness ▪ 80% contralateral to side of structural lesion  Rapid deterioration of mental status  Cushing’s reflex
  • 22. No Level I or II recommendations  Level III:  No change in all-cause mortality  46% improved chance of favorable outcome (GOS 4-5)  Some evidence of improved outcome with > 48 hours of cooling
  • 23. Most common CT finding in TBI  Often occurs in concert with other imaging abnormalities  Neuro deficits reflect parenchymal injury and generally not a vascular insult
  • 24. High Mortality Rate  Association with Skull Fracture
  • 25. Acute  Higher Mortality Rate Than EDH  underlying brain injury  co-morbidity  Chronic  Subacute
  • 26. Presence of contusion does not independently predict outcome
  • 27. • Cisterns • Gray – White Interface
  • 28. Decompressable lesion with neuro findings  SDH, EDH, very few contusions  Traumatic SAH is not decompressable and not an indication for aneurysm screening  Indications of increasing ICP  Deteriorating mental status  Herniation syndromes  Decompressive craniectomy
  • 29. Cerebral edema  ICP determination  Monitoring  early detection of mass  GCS < 8 and Abnormal lesions Head CT  limit potentially harmful  GCS < 8 and Normal therapies Head CT with...  determination of ▪ age > 40 prognosis ▪ posturing  CSF drainage* ▪ hypotension
  • 30. All about GCS  GSW injury reflect patterns of ballistics
  • 31. Issues in management  Hearing  Antibiotics  Disposition
  • 32. 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: Interactions between factors determining prognosis in populations of patients with severe head injury. In Frowein RA, Wilcke O, Karimi-Nejad A, et al. Advances in Neurosurgery: Head Injuries-Tumors of the Cerebellar Region. Springer-Verlag, Berlin: 12-15, 1978. 3 Phuenpathom N, Choomuang M, Ratanalert S: Outcome and outcome prediction in acute subdural hematoma. Surg Neurol 40:22-25, 1993
  • 33. Strong factor in determining outcome from severe TBI  This holds true even after correcting for co- morbid conditions.
  • 34. TBI Biomarkers  Need for imaging  Validation  Prognostication  Intervention  Hypothermia  Progesterone  Reduction of oxidative stress