1. TraumaticHead Injury Toh C J

2. No patientwant to be this ........ No Neurosurgeonlike to plant ....... 3. 4. Classification SeverityAnatomicfindings 5. Classification SeverityMinimal : GCS 15, no LOC or amnesia Mild : GCS 14, or 15 + LOC or amnesiaimpaired alertness or memory Moderate : 9-13 or LOC 5 min orfocal neurological deficit Severe : GCS 5 - 8Critical : GCS 3 - 4 6. Classification Anatomicfindings FocalDiffuse Contusion Coup Countrecoup Gliding Fracture Hematoma EpiduralSubduralIntraparenchymal Intermediary Concussion DAI 7. Marshall CT Grading of Brain Trauma Diffuse Injury Grade CT appearance Mortality I Normal CT scan 9.6% II Cisterns present. Shift < 5mm 13.5% III Cisterns compressed/absent. Shift < 5mm.34% IV Shift > 5mm 56.2% 8. Classification Primary Secondary

• Injury sustained by the brain at the time of impact

• Examples: Brain laceration

• Brain contusion

Injury sustained by thebrain after the impact Causes:Hypoxia, Hypoperfusion Examples: cerebral edema,herniation 9. Prehospital management

How to transfer head injury patient:

Stabilize patient at trauma scene

Do not move patient unnecessarily

Maintain ABC, ABC, ABC, ABC

Protect cervical spine

Stop active bleeding

Relay information to receiving doctors

• ABC status

• GCS & pupil size

• Suspected injuries

Transfer patient only if it is SAFE

10. Head injury management in A&E room

General aims

• Stabilization

• Prevention of secondary brain injury

Specific aims

• Protect the airway & oxygenate

• Ventilate to normocapnia

• Correct hypovolaemia and hypotension

• CT Scan when appropriate

• Neurosurgery if indicated

• Intensive Care for further monitoring and management

11. Head injury management in A&E room

Means of stabilization RESUSCITATION

Primary Survey & Resuscitation (ABC)

• To detect and treat immediately life-threatening conditions

• Idea: to keep the patient alive

Secondary surgery

• To detect injury that can kill patient in few hours

• Idea: to keep the patient alive longer

Definitive treatment

• Managing above injury urgently

12. A B C DE 13. Secondary survey in trauma patients

To detect life-threatening injury

• can kill in few hours if not treated

Head-to-toe examination

Injuries

• Intracranial hematomas

• Pneumo- or hemo-thorax

• Intra-abdominal organ injury

• Pelvic fracture

• Actively bleeding wound

In head trauma

• Basically to detect increased ICP

14. Secondary survey for head trauma GCS Pupillarysize Active bleeding scalp wound 15. GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = incomprehensivesound 3 = inappropriate words 4 = confuse 5 = alert Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command 16. GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries3 = vocal sounds4 = words 5 = orientated to face Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command Pediatric age 1- 5 yrs 17. GCS EYE Response: 1 = no response 2 = to pain 3 = to call 4 = spontaneous Verbal response: 1 = no response 2 = cries3 = vocal sounds4 = words Motor response: 1 = no response 2 = extension (decerebrate) 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain Pediatric age upto 6months 18. Pupillary response :

Pupillary response can determine the level of nervous system dysfunction in a comatose patient.

19. Other NeuroExam

Full exam

• Visual acuity in an alert patient

• Pupillary light reflexes, both direct and consensual

• Retinal detachment or hemorrhages or papilledema

• Spinal tenderness and, if the patient is cooperative, limb movements

• Motor weaknesses, if possible, and gross sensory deficits

• Reflexes, plantar response

20. Other NeuroExam

Signs of Skull Base fracture

• Raccoon eyes

• Battle sign (after 8-12 h)

• CSF rhinorrhea or otorrhea

• Hemotympanum

21. Imaging of head injury

Modalities

• Skull X-ray

• CT scan

• MRI

Areas

• Skull, brain

• Cervical spine

• Chest

• Pelvis

22. Skull Fracture

Types

• Depressed / non-depressed

Importance

• Non-depressed per se: minimal

• Depressed

• A/w low GCS

• Compound fractures

• Foreign body

23. Acute ExtraDural Hemorrhage

Young patient

Between skull & dura

No direct injury to brain

Blood clot from torn blood vessel of dura (artery)

Trauma okay slowly deteriorating coma death

EDH patient should NOT die

If patient die we better die too

24. Acute SubDural Hemorrhage

Young patient

Clot between dura & brain surface

From damaged brain surface

• Brain laceration (otak koyak)

• Burst lobe (otak pecah)

• DIRECT brain injury

Hematoma usually thin

Major problem damaged brain

Outcome worse than EDH

Usually need surgery, to remove

• Hematoma

• Skull bone (open the box)

25. Brain contusion (LEBAM)

Young

Direct brain injury

Size: smalllarge

If multiple means severe diffuse brain injury

Surgery if

• Large

• Easily accessible (senang buang)

Prognosis: moderate

26. Diffuse brain injury

Young

CT scan normal

Very small white dots

Acceleration decerelation

Shearing force

Poor GCS with normal CT scan

Treatment based on GCS, ICP & CPP

Important to repeat CT after 24-48 hours

• Edema

• Delayed hematoma

27. 28. Management of TBI 29. Monro-Kellie hypothesis

The sum of the intracranial volumes of blood, brain, CSF is constant, and that an increase in any one of these must be offset by an equal decrease in another, or else pressure will rise.

30. 31. Management ofTBI Detection& Monitor Treatment 32. Detection& Monitor GCS Pupillary reflex ICP Monitor Symptoms & sign of herniation 33. Methods of monitoring intracranial pressure . Fiberoptic sensors (Camino),Microchips (internal strain-gauge devices)(Codman)Air pouch technologies (Spiegelberg) 34. Methods of monitoring intracranial pressure . 35. EVD, External Ventricular Drain 36. Primaryinjury Secondary injury HerniationMasslesion ICP ICP ICP ICP 37. Secondary injury Hypoxia Hypovolemia Cerebraledema 38. Howto manageraise ICP? 39. CerebralProtection Sedation 40. Managing raiseICP Generalmeasure Medicalmanagement Surgicalintervention 41. Generalmeasure Head elevation Maintain normal temperature Neck vein compression? ? Chest Physio Hyperventilation Fluid management Glucose monitor Maintain normal Blod pressure 42. Head elevation

Head is raised 30 to 45 degrees above the level of the heart.

• This will enhance the venous drainage and thus reducing the intracranial blood volume and ICP.

43. Neck vein compression?

Neck in neutral position

Collar is fixed properly

Arm sling is not compressing the neck vein

44. Maintainnormal temperature Keep patientsbody temperaturewithin normal limit 45. ? Chest Physio To give sedation during chest physiotherapy 46. Hyperventilation NO HYPERVENTILATION!!!! Keep patient at the lower limit of normocapnia (32mmHg) Optimal Oxygenation!!! Increased CO2 = Vasoconstriction and Decreased ICP Decreased CO2 = Vasodilatation and Increased ICP 47. Fluid management

• Fluid management should aim primarily at preventing hypotension while optimizing cerebral perfusion pressure.

48. Glucose monitor

• Patient with injuries to the brain are often hyperglycaemic.

• High level of serum glucose levels may aggravate cerebral edema through an osmotic mechanism and may be responsible for increased anaerobic glycolysis leading to lactic acidosis.

49. Medicalmanagement SedationMuscle relaxant Barbiturate & Propofol analgesic antipyretic Mannitol & Frusemide Hypertonic saline antiepileptics Neuroprotectiveagent BP control 50. Sedationanalgesic Midazolam + Morphine 51. Barbiturate & Propofol Barbiturates appear to exert their ICP-lowering effects through vasoconstriction, which results in a reduction in CBF and CBV secondary to the suppression of cerebral metabolism 52. Muscle relaxant Increase incidence ofaspiration pneumonia 53. Mannitol & Frusemide The administration of mannitol has become the first choice for pharmacological ICP reduction , Mannitol has an immediate plasma-expanding effect that reduces haematocrit and blood viscosity and increases CBF and cerebral oxygenation delivery. Hyperosmotic agents remove more water from the brain than from other organs because the bloodbrain barrier impedes the penetration of the osmotic agent into the brain maintaining an osmotic diffusion gradient.This osmotic effect of mannitol is delayed for 1530 min. Mannitol consistently decreases ICP for 16 h. 54. Mannitol & Frusemide An ultra-early single-shot administration of high-dose mannitol (1.4 g/kg) in the emergency room significantly improves the 6-month clinical outcome after head injury One risk of hyperosmotic agents is the rebound effect, which might increase ICP. To reduce this risk it is recommended that mannitol should be administrated as repeated boluses rather than continuously, only in patients with increased ICP and not longer than 34 days As mannitol is entirely excreted in the urine there is a risk of acute tubular necrosis, particularly if serum osmolarity exceeds 320 mOsmol/l 55. Mannitol & Frusemide Although furosemide itself has only a minimal effect on ICP, in combination with mannitol it enhances the effects of mannitol on plasma osmolality, resulting in a greater reduction of brain water content 56. Hypertonic saline Several studies have shown that hypertonic saline is equal or even superior to mannitol in reducing ICP. Vialet et al. suggested that hypertonic saline (2 ml/kg, 7.5%) is an effective and safe initial treatment for intracranial hypertension episodes in head trauma patients when osmotherapy is indicated. Even very high concentrated hypertonic saline solutions (23.5%) can be used and can reduce ICP in poor grade patients with subarachnoid haemorrhage. 57. antipyretic antiepileptics Neuroprotectiveagent it is evident that hyperthermia should be avoided Is not for reduce ICP. But to prevent fit whichwill cause raise ICP Still under experimental stage 58. Surgicalintervention Removal of thepathological lesion CSF diversion procedure Open the cranium craniectomy Remove part of the non-eloquent brain Lobectomy 59. Removal of thepathological lesion CSF diversion procedure Open the cranium craniectomyRemove part of the non-eloquent brain Lobectomy 60. Summary of TBI management Steps Rationale Respiratory support (intubation & ventilation) Comatose, unable to protect airways Elevate head 30-45 Facilitate venous drainage Straighten neck, no tape encircling the neck Facilitate venous drainage Avoid hypotension (SBP