Transcript Head trauma - 高雄醫學大學附設中和紀念醫院

Head trauma
Trauma department
Hsinglin Lin
Introduction
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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
points
• 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
features:
• 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
Anatomy
• A: Scalp 1.skin, 2.connective tissure,
3.apponeurosis, 4.losse tissue,
5.pericranium.
• 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
compression.
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,
transtentorial)
herniation ;
d) external herniation ;
e) tonsillar herniation.
Physiology
• A: ICP: normal 10 mmHg, >20 mmHg:
clear abnormal >40 mmHg: severe
elevation
• 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
Classication
• 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
injury
• Mild concussion consciousness preserved
with noticeable degree of temporary
neurologic dysfunction
• Classic cerebral concussion-loss of
consciousness , reversible, posttraumatic
amnesia
• Post-concussion syndrome- long-lasting
neurologic deficits, include memory
difficulties, dizziness, nausea, anosmia and
depression.
• Diffuse axonal injury- prolonged
posttraumatic coma not due to mass lesion
or ischemia insults. Decortication and
decerebration with autonomic dysfunction.
Management of mild
injury(GCS14-15)
• 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
body
• 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
pneumpthorax
• Volume replacement, DPL, ultrasound
routinely in the hypotension comatose
patient.
• 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
responses
• 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
mins
• Midline shift of >5 mm usually indicates of
surgery
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
hypotension.
• 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