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Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
Head injury
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Head injury

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  • 1. Wayne Triner, DO, MPH, FACEPProfessor, 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 ruralthe incidence of TBI per 100 000 peopleper year (790 cases), especially mild TBI(749 cases), in New Zealand wassubstantially greater than in other high-income countries. in Europe (47–453cases) and North America (51–618cases).
  • 3.  Primary  Direct tissue injury Secondary  Cerebral perfusion/edema  Vasoregulation  Tissue ischemia  Herniation
  • 4.  Cerebral Blood Flow CBF ~ CPP – CVP Cerebral Perfusion Pressure CPP = MAP – ICP CBF ~ (MAP – ICP) - CVP
  • 5.  Mild  GCS > 12 Moderate  GCS 12-8 Severe  GCS < 8
  • 6. Eye Opening  Mild 4=Spontaneous  GCS > 12 3=To voice 2=To pain  Moderate 1=None  GCS 12-8  SevereVerbal  GCS < 8 5=Normal conversation 4=Disoriented conversation 3=Words, but not coherent 2=No words......only sounds 1=NoneMotor 6=Normal 5=Localizes to pain 4=Withdraws to pain 3=Decorticate posture 2=Decerebrate 1=None
  • 7.  GCS 13-15 < 30 minute LOC Non-focal exam
  • 8.  Short term  Long term  Mood and cognitive  Depression disturbances  Dementia  Validation  Parkinson’s  Variable rate of CT  Cognitive deficits abnormalities
  • 9. The goal being identification of significant conditions amenable to intervention
  • 10. LEVEL I RECOMMENDATION LEVEL II RECOMMENDATIONA noncontrast head CT is indicated A noncontrast head CT should bein head trauma patients with loss of considered in head trauma patientsconsciousness or pos- traumatic with no loss of consciousness oramnesia only if one of the post-traumatic amnesia if there isfollowing is present: focal deficit, vomiting, severeheadache, vomiting, age > 60 headache, age > 65 years, signs ofyears, drug or alcohol basilar skull Fx, GCS < 15,intoxication, deficits in short-term coagulopathy or dangerousmemory, physical evidence of mechanism (ejection from vehicle,trauma above the pedestrian struck, fall of more thanclavicle, 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
  • 11.  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
  • 12.  Recommendations  “Neuro rest” Proven  ?????
  • 13.  ABCs Limit secondary brain injury Preservation of CBF Issues of coagulation  Reversal of coagulopathies ▪ F VIIa ▪ Prothrombin complex concentrate ▪ Vit K and FFP
  • 14.  “Evidence based” Standards, Guidelines and Options • Preserve oxygenation (at all costs) • Avoidance of hypotension (SBP < 90) • Euventilation
  • 15. Rapid reduction in ICP  3 compartment model  Below pCO2 < 23, CBF < 20 ml/100g/min
  • 16.  Preserve oxygenation (at all costs)  Issues of airway management ▪ Pre-hospital ETT ▪ Neuro-protective RSI ▪ Laryngeal manipulation ▪ Hypotension ▪ ICP management
  • 17.  Avoidance of hypotension (SBP < 90)  Preserve CBF  Control of cerebral edema ▪ Brief hyperventilation  Hyperosmolar therapy
  • 18.  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
  • 19.  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
  • 20.  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
  • 21.  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
  • 22.  High Mortality Rate Association with Skull Fracture
  • 23.  Acute Higher Mortality Rate Than EDH  underlying brain injury  co-morbidity Chronic Subacute
  • 24.  Presence of contusion does not independently predict outcome
  • 25. • Cisterns• Gray – White Interface
  • 26.  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
  • 27.  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
  • 28.  All about GCS GSW injury reflect patterns of ballistics
  • 29.  Issues in management  Hearing  Antibiotics  Disposition
  • 30. 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
  • 31.  Strong factor in determining outcome from severe TBI This holds true even after correcting for co- morbid conditions.
  • 32.  TBI Biomarkers  Need for imaging  Validation  Prognostication Intervention  Hypothermia  Progesterone  Reduction of oxidative stress

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