Head Trauma Head trauma Trauma

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Head Trauma Head trauma Trauma Powered By Docstoc
					Head trauma
 Trauma department
    Hsinglin Lin
•   Adequate oxygenation
•   Maintenance of sufficient blood pressure
•   Avoid secondary brain damage
•   Early consultation
•   BCT in hospital cannot treat
• Consulting neurosurgeon
 1.age and mechanism
 2.Respiratory and cardiovascular status (BP)
 3.Minineurologic ex., GCS( Motor
 response), pupillary reactions
 4.associated injuries
 5.Result of diagnostic studies (CT)
        Eye Opening Response

• Spontaneous--open with blinking at baseline 4

• To verbal stimuli, command, speech 3 points
• To pain only (not applied to face) 2 points
• No response 1 point
             Verbal Response

• Oriented 5 points
• Confused conversation, but able to answer
  questions 4 points

• Inappropriate words 3 points
• Incomprehensible speech 2 points
• No response 1 point
              Motor Response
• Obeys commands for movement 6 points
• Purposeful movement to painful stimulus 5 points
• Withdraws in response to pain 4 points
• Flexion in response to pain (decorticate posturing)
  3 points

• Extension response in response to pain
  (decerebrate posturing) 2 points

• No response 1 point
  Computed tomographic done in a
   patient has any of the following
• The patient is eye opening only to pain or does not
  converse (Glasgow Coma Score 12/15 or less)
• A deteriorating level of consciousness or
  progressive focal neurological signs
• Confusion or drowsiness (Glasgow Coma Score
  13 or 14/15) followed by failure to improve within
  at most four hours of clinical observation
• Radiological/clinical evidence of a fracture,
  whatever the level of consciousness
• New focal neurological signs which are not
  getting worse
• Full consciousness (Glasgow Coma Score 15/15)
  with no fracture but other features, such as:
   • severe and persistent headache
   • nausea and vomiting
   • irritability or altered behaviour
   • a seizure
• A: Scalp, 2.connective tissure,
  3.apponeurosis, 4.losse tissue,
• B:Skull : cranial vault and base
• C:Meninges: dura mater, arachnoid and pia
  mater. Most common injury: Middle
  meningeal a. in epidural space, Subdural
  space : bridge vein
• D:Brain:cerebrum, cerebellum, brainstem
• E: CSF
• F: Tentorium:Oculomotor nerve runs along the
 edge of tentorium. Parasympathetic fibers lie on
 surface –dilation. Down and out with further
 Uncal herniation: compression of the corticospinal
 tract in the midbrain - weakness of opposite side
 Kenohan’s notch syndrome: Same side
a) Subfalcial (cingulate)
       herniation ;
  b) uncal herniation ;
 c) downward (central,
       herniation ;
 d) external herniation ;
e) tonsillar herniation.
• A: ICP: normal 10 mmHg, >20 mmHg:
  clear abnormal >40 mmHg: severe
• B: Cerebral perfusion pressure: <70
  mmHg – poor outcome, CPP=MAP-ICP
• C: cerebral blood flow: 50ml/100g of
  brain/min, <5ml/100g/min cell death,
  autoregulation : MAP 50-160 mmHg
• A:Mechanism, 1.blunt:automobile
  collisions, fall, blunt assault, 2.penetrating:
  gunshot, stab w’d
• B:Severity of injury: severe:GCS
  <8 ,moderate:9-13,mild:14-15.
• C:Morphology and Injury: 1.Skull Fx,
  2.Intracranial lesion.
              Skull fracture
• Signs of Skull base fx: periobital
  ecchymosis (raccoon eyes), retroauricular
  ecchymosis (Battle’s sign), CSF leakage, 7th
  nerve palsy
• Fragments depressed more than the
  thickness of the skull require surgical repair.
• Skull Fx increases the likelihood of
  intracrainal hematoma.
• Basilar skull fx are sometimes associated
  with CSF leakage from nose (rhinorrhea) or
  the ear (otorrhea). 7th nerve palsy.
           Intracranial lesions
• Focal lesions:
• 1.EDH, often from middle meningeal a., relatively
  uncommon, treated early prognosis excellent,
  lucid interval, talk and die
• 2.SDH, tearing of bridging vein, brain damage
  much sever and prognosis worse than EDH
• 3.Contusion and intracerebral hematomas,
  associated SDH, frontal and temporal lobes
• 4.diffuse injury- most common type of brain
• Mild concussion consciousness preserved
  with noticeable degree of temporary
  neurologic dysfunction
• Classic cerebral concussion-loss of
  consciousness , reversible, posttraumatic
• Post-concussion syndrome- long-lasting
  neurologic deficits, include memory
  difficulties, dizziness, nausea, anosmia and
• Diffuse axonal injury- prolonged
  posttraumatic coma not due to mass lesion
  or ischemia insults. Decortication and
  decerebration with autonomic dysfunction.
         Management of mild
• CT – a history loss of consciousness,
  amnesia, or severe headaches.
• observation at H for 12-24 hours
• Skull X-ray – penetrating head injury,
  1.linear or compression fx, 2.midline
  postion of pineal grand, 3.Air-fluid levels
  4.pneumocephalus, 5.facial fx., 6.foreign
• Skull base fx.: racoon’s eye, CSF rhinorrhea
  or ottorhea, hemotympanum, or Battle’s
  sign – admission for observation
• C-spine X-ray – signs of tenderness or pain.
• Mild head-injury patient with normal CT
  sacn, can be brought back to H promptly,
  can be dischrged with reliable companion
 Manageemnt of moderate head
      injury (GCS 9-13)
• Able to follow simple commands, but
  confused or somnolent and have focal
  neurologic deficits such as hemiparesis
• CT scan
• Admission
    Management of severe head
        injury (GCS 3-8)
• Unable to follow simple commands even
  cardiopulmonary stabilization
• A. Primary survey and resuscitation
  hypotension, hypoxemia, and anemia
  1. Airway and breathing: transient
  respiratory arrest after head injury- death at
  scene. Early intubation with 100% O2.
• Hyperventilation with worsening GCS or
  pupil dilation. Pco2 keep 25-35 mmHg.
• 2.Circulation: hypotension usually not due
  to the brain injury itself except terminal
  medullary failure. Associated spinal cord
  injury (quadriplegia or paraplegia), cardiac
  contusion or temponade, and tension
• Volume replacement, DPL, ultrasound
  routinely in the hypotension comatose
• Hypotensive patient’s neurologic
  examination is unreliable.
• B.Secondary survey
  Multiple trauma
• C.Neurologic ex. :After cardiopulmonary
  stabilized, rapid and directed neurologic
  exam: GCS, pupillary light response, doll’s
  eye movement(oculocephalics),
  calorics(oculovestibulars), corneal
• Obtain a reliable minneurologic ex. Prior
  sedating or paralyzing P’t
• Bilaterally dilated and nonreactive pupils
  can be due to inadequate brain perfusion.
• Bilateral small pupils suggest drug
  effects(opiates), metabolic encephalopathies,
  destructive lesion of pons, Mild dilation of
  pupil and a sluggish pupillary response of
  the eye are early signs of temporal hernia.
• D.Diagnostic procedures: CT within 30
• Midline shift of >5 mm usually indicates of
           Medical therapies
• A. IV fluids: dehydration is more harmful
  than beneficial in these patients. Not use
  hypotonic fluids and glucose-containing
  fluids. Prevent hyponatremia.
• B. hyperventilation: aggressive and
  prolonged hyperventilation impaired
  cerebral perfusion with ischemia by
  vasoconstriction. Esp, Pco2 <25mmHg
• Keep Pco2 above 30 mmHg and 25-30
  mmHg with IICP.
• Mannitol: 1g/kg with bolus without
  hypotension comatose patient who initially
  normal, reactive pupils, but develop dilation
  or bilateral dilation and nonreactive pupil.
• Lasix: 0.3 to 0.5 mg/kg combined with mannitol.
• Steroids: not beneficial.
• Barbiturates: not indicated in the acute injury
  resusciative phase, effect reduce IICP but cause
• Anticonvulsants: phenytoin reduced the incidence
  of seizures in the first week but not thereafter.
        Surgical management
• A.Scalp W’d : shave the hair and clear the
  W’d before suturing. carefully inspect the
  W’d for fx and foreign material. Open and
  depression skull fx, consulted neurosurgeon
  before close.
• B.Depressed Skull Fx.: depressiom greater
  than the thickness of adjacent skull.
• Intracranial mass lesions