Traumatic Brain Injury

Introduction• Adequate oxygenation • Maintenance of sufficient blood pressure• Avoid secondary brain damage

• 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