1. Trauma department Hsinglin Lin
Head trauma
Trauma department
Hsinglin Lin

2. Introduction Adequate oxygenation
Maintenance of sufficient blood pressure
Avoid secondary brain damage
Early consultation
BCT in hospital cannot treat

3. 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)

4. 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

5. 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

6. 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

7. 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

8. 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

9. 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

10. 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

12. a) Subfalcial (cingulate) herniation ; b) uncal herniation ; c) downward (central, transtentorial) herniation ; d) external herniation ; e) tonsillar herniation.

13. 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 mmHg

14. 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.

15. 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.

16. Basilar skull fx are sometimes associated with CSF leakage from nose (rhinorrhea) or the ear (otorrhea). 7th nerve palsy.

17. 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

19. Mild concussion consciousness preserved with noticeable degree of temporary neurologic dysfunction
Classic cerebral concussion-loss of consciousness , reversible, posttraumatic amnesia

20. 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.

21. Management of mild injury(GCS14-15)
CT – a history loss of consciousness, amnesia, or severe headaches.
observation at H for 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

22. 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

23. 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

24. 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.

25. Hyperventilation with worsening GCS or pupil dilation
Hyperventilation with worsening GCS or pupil dilation. Pco2 keep 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

26. Volume replacement, DPL, ultrasound routinely in the hypotension comatose patient.
Hypotensive patient’s neurologic examination is unreliable.
B.Secondary survey
Multiple trauma

27. 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

28. 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.

29. D.Diagnostic procedures: CT within 30 mins
Midline shift of >5 mm usually indicates of surgery

30. 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

31. 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.

32. 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.

33. 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