Classification Minimal: GCS 15, no LOC or amnesia Mild: GCS 14, or 15 + LOC or amnesiaSeverity impaired alertness or memory Moderate: 9-13 or LOC ≥ 5 min or focal neurological deficit Severe: GCS 5 - 8 Critical: GCS 3 - 4
Marshall CT Grading of Brain TraumaDiffuse Injury CT appearance Mortality Grade I Normal CT scan 9.6% II Cisterns present. Shift < 13.5% 5mm III Cisterns 34% compressed/absent. Shift < 5mm. IV Shift > 5mm 56.2%
Classification Primary SecondaryInjury sustained by the Injury sustained by thebrain at the time of brain after the impactimpact Causes: Hypoxia, Examples: Brain laceration Hypoperfusion Brain contusion Examples: cerebral edema, herniation
Prehospital managementHow 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
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
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
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
Secondary survey for head trauma GCS Pupillary size Active bleeding scalp wound
EYE Response: Verbal response: Motor response:1 = no response 1 = no response 1 = no response2 = to pain 2 = incomprehensive 2 = extension3 = to call sound (decerebrate)4 = spontaneous 3 = inappropriate 3 = flexion words (decorticate) 4 = confuse 4 = withdrawal 5 = alert 5 = localizing pain 6 = obey command
Pediatric age 1- 5 yrsEYE Response: Verbal response: Motor response:1 = no response 1 = no response 1 = no response2 = to pain 2 = cries 2 = extension3 = to call 3 = vocal sounds (decerebrate)4 = spontaneous 4 = words 3 = flexion 5 = orientated to face (decorticate) 4 = withdrawal 5 = localizing pain 6 = obey command
Pediatric age upto 6 monthsEYE Response: Verbal response: Motor response:1 = no response 1 = no response 1 = no response2 = to pain 2 = cries 2 = extension3 = to call 3 = vocal sounds (decerebrate)4 = spontaneous 4 = words 3 = flexion (decorticate) 4 = withdrawal 5 = localizing pain
Pupillaryresponse:• Pupillary response can determine the level of nervous system dysfunction in a comatose patient.
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
Other NeuroExam• Signs of Skull Base fracture – Raccoon eyes – Battle sign (after 8-12 h) – CSF rhinorrhea or otorrhea – Hemotympanum
Imaging of head injury• Modalities – Skull X-ray – CT scan – MRI• Areas – Skull, brain – Cervical spine – Chest – Pelvis
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
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)
Brain contusion (LEBAM)• Young• Direct brain injury• Size: small → large• If multiple – means severe diffuse brain injury• Surgery if – Large – Easily accessible (senang buang)• Prognosis: moderate
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
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.
Managing raise ICPGeneral Medical Surgicalmeasure management intervention
Head elevation Neck vein compression? Maintain normal Blod pressure Maintain normal temperature ? Chest Physio HyperventilationGeneralmeasure Fluid management Glucose monitor
Head elevationHead is raised 30 to 45 degreesabove the level of the heart. This will enhance the venous drainage and thus reducing the intracranial blood volume and ICP.
Neck vein compression?•Neck in neutral position•Collar is fixed properly•Arm sling is not compressing the neck vein
Keep patient’s Maintainbody temperature normal temperaturewithin normal limit
To give sedation during chest physiotherapy ? Chest Physio
Increased CO2 = Vasoconstriction and Decreased ICPDecreased CO2 = Vasodilatation and Increased ICP NO HYPERVENTILATION !!!! Keep patient at the lower limit of normocapnia (32mmHg) Optimal Oxygenation !!! Hyperventilation
Patient with injuries to the brainare often hyperglycaemic.High level of serum glucose levelsmay aggravate cerebral edemathrough an osmotic mechanismand may be responsible forincreased anaerobic glycolysisleading to lactic acidosis. Glucose monitor
Mannitol & Frusemide BP control analgesic Hypertonic salineBarbiturate & Propofol antipyreticMuscle relaxant antiepileptics Neuroprotective Sedation agent Medical management
analgesic Midazolam + MorphineSedation
Barbiturates appear to exert their ICP-lowering effectsBarbiturate & Propofol through vasoconstriction, which results in a reduction in CBF and CBV secondary to the suppression of cerebral metabolism
Muscle relaxant Increase incidence of aspiration pneumonia
Mannitol & FrusemideThe administration of mannitol has become the firstchoice for pharmacological ICP reduction,Mannitol has an immediate plasma-expanding effect thatreduces haematocrit and blood viscosity and increasesCBF and cerebral oxygenation delivery.Hyperosmotic agents remove more water from the brainthan from other organs because the blood–brain barrierimpedes the penetration of the osmotic agent into thebrain maintaining an osmotic diffusion gradient.This osmotic effect of mannitol is delayed for 15–30 min.Mannitol consistently decreases ICP for 1–6 h.
Mannitol & FrusemideAn ultra-early single-shot administration of high-dosemannitol (1.4 g/kg) in the emergency room significantlyimproves the 6-month clinical outcome after head injuryOne risk of hyperosmotic agents is the rebound effect, whichmight increase ICP. To reduce this risk it is recommendedthat mannitol should be administrated as repeated bolusesrather than continuously, only in patients with increased ICPand not longer than 3–4 daysAs mannitol is entirely excreted in the urine there is a risk ofacute tubular necrosis, particularly if serum osmolarityexceeds 320 mOsmol/l
Mannitol & FrusemideAlthough furosemide itself has only a minimal effect onICP, in combination with mannitol it enhances the effectsof mannitol on plasma osmolality, resulting in a greaterreduction of brain water content
Hypertonic salineSeveral studies have shown that hypertonicsaline is equal or even superior to mannitol inreducing ICP.Vialet et al. suggested that hypertonic saline(2 ml/kg, 7.5%) is an effective and safe initialtreatment for intracranial hypertensionepisodes in head traumapatients when osmotherapy is indicated.Even very high concentrated hypertonicsaline solutions (23.5%) can be used andcan reduce ICP in poor grade patients withsubarachnoid haemorrhage.
it is evident that hyperthermia should be avoided antipyreticIs not for reduce ICP.But to prevent fit whichwill cause raise ICP antiepileptics Neuroprotective agent Still under experimental stage
Remove part of the non-eloquent brain “Lobectomy” Open the cranium “craniectomy”CSF diversion procedure Removal of thepathological lesion Surgical intervention
Remove part of the non-eloquent brain “Lobectomy” Open the cranium “craniectomy”CSF diversion procedure Removal of thepathological lesion
Summary of TBI management Steps RationaleRespiratory support (intubation & Comatose, unable to protect airwaysventilation)Elevate head 30-45° Facilitate venous drainageStraighten neck, no tape encircling the Facilitate venous drainageneckAvoid hypotension (SBP<90mmHg) Prevent hypoxia – edemaControl hypertension Avoid transmission of pressure to ICPAvoid hypoxia (PaCO2 < 60mmHg) Prevent vasodilatationControl ventilation, aims PaCO2 35-40 Avoid vasoconstriction / -dilatationmmHgAdequate sedation To reduce brain metabolismDo CT brain Ascertain intracranial pathology rapidly
Take Home Message: CPP = MAP - ICP ICP keep < 20 mmHg CPP keep 60 to 70 mmHg“Biar lambat asalkan selamat”