Toh C J

Classification

Severity Anatomic findings

Classification

Severity

Minimal: GCS 15, no LOC or amnesia

Mild: GCS 14, or 15 + LOC or amnesia impaired alertness or memory

Moderate: 9-13 or LOC ≥ 5 min or focal neurological deficit

Severe: GCS 5 - 8

Critical: GCS 3 - 4

Classification

Anatomic findings

Focal

Diffuse

Contusion

Coup

Countrecoup

Gliding Fracture

HematomaEpidural

Subdural

Intraparenchymal

Intermediary

Concussion DAI

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%

Classification

Primary Secondary

Injury sustained by the brain at the time of impact

Examples: Brain laceration Brain contusion

Injury sustained by the brain after the impact

Causes: Hypoxia, Hypoperfusion

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:1 = no response2 = to pain3 = to call4 = spontaneous

Verbal response:1 = no response2 = incomprehensive sound3 = inappropriate words4 = confuse5 = alert

Motor response:1 = no response2 = extension (decerebrate)3 = flexion (decorticate)4 = withdrawal5 = localizing pain6 = obey command

EYE Response:1 = no response2 = to pain3 = to call4 = spontaneous

Verbal response:1 = no response2 = cries 3 = vocal sounds 4 = words5 = orientated to face

Motor response:1 = no response2 = extension (decerebrate)3 = flexion (decorticate)4 = withdrawal5 = localizing pain6 = obey command

Pediatric age 1- 5 yrs

EYE Response:1 = no response2 = to pain3 = to call4 = spontaneous

Verbal response:1 = no response2 = cries 3 = vocal sounds 4 = words

Motor response:1 = no response2 = extension (decerebrate)3 = flexion (decorticate)4 = withdrawal5 = localizing pain

Pediatric age upto 6 months

Pupillary Pupillary

responseresponse::

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

Skull Fracture• Types

– Depressed / non-depressed

• Importance– Non-depressed per se:

minimal– Depressed– A/w low GCS– Compound fractures– Foreign body

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.

Management of TBI

Detection &

MonitorTreatment

Detection &

Monitor

GCS

Pupillary reflex

ICP Monitor

Symptoms & sign of herniation

Methods of monitoring intracranial pressure..

Fiberoptic sensors (Camino), Microchips (internal strain-gauge devices)(Codman) Air pouch technologies (Spiegelberg)

Methods of monitoring intracranial pressure..

EVD, External Ventricular Drain

Primary injury

Secondary injury

Herniation Mass lesion

ICP

ICP

ICP ICP

Secondary injury

Hypoxia Hypovolemia

Cerebral edema

≠

Managing raise ICP

General measure

Medical management

Surgical intervention

General measure

Head elevation

Maintain normal temperature

Neck vein compression?

? Chest Physio

Hyperventilation

Fluid management

Glucose monitor

Maintain normal Blod pressure

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.

Neck vein compression?

•Neck in neutral position•Collar is fixed properly•Arm sling is not compressing the neck vein

Maintain normal temperature

Keep patient’s body temperature within normal limit

? Chest Physio

To give sedation during chest physiotherapy

Hyperventilation

NO HYPERVENTILATION !!!!Keep patient at the lower limit of normocapnia (32mmHg)

Optimal Oxygenation !!!

Increased CO2 = Vasoconstriction and Decreased ICPDecreased CO2 = Vasodilatation and Increased ICP

Fluid management

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

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.

Medical management

Sedation

Muscle relaxant

Barbiturate & Propofol

analgesic

antipyretic

Mannitol & Frusemide

Hypertonic saline

antiepileptics

Neuroprotective agent

BP control

Sedation

analgesic

Midazolam + Morphine

Barbiturate & Propofol

Barbiturates appear to exert their ICP-lowering effectsthrough 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 & Frusemide

The administration of mannitol has become the firstchoice 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 blood–brain barrier impedes the penetration of the osmotic agent into the brain 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 & Frusemide

An ultra-early single-shot administration of high-dose mannitol (1.4 g/kg) in the emergency room significantlyimproves 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 3–4 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

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

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 traumapatients 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.

antipyretic

antiepileptics

Neuroprotective agent

it is evident that hyperthermia should be avoided

Is not for reduce ICP.But to prevent fit which will cause raise ICP

Still under experimental stage

Surgical intervention

Removal of the pathological lesion

CSF diversion procedure

Open the cranium “craniectomy”

Remove part of the non-eloquent brain“Lobectomy”

Removal of the pathological lesion

CSF diversion procedure

Open the cranium “craniectomy”

Remove part of the non-eloquent brain“Lobectomy”

Steps RationaleRespiratory 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<90mmHg) Prevent hypoxia – edema

Control hypertension Avoid transmission of pressure to ICP

Avoid hypoxia (PaCO2 < 60mmHg) Prevent vasodilatation

Control ventilation, aims PaCO2 35-40 mmHg

Avoid vasoconstriction / -dilatation

Adequate sedation To reduce brain metabolism

Do CT brain Ascertain intracranial pathology rapidly

Summary of TBI management

Brain swelling

Bleeding

CPP = MAP - ICP

Take Home Message:Take Home Message:

ICP keep < 20 mmHg

CPP keep 60 to 70 mmHg

“Biar lambat asalkan selamat”

Summary:

• Classification of TBI:

• Management:– Prehospital.– In Hospital:

• Primary survey & secondary survey.• Imaging• Monitor • “cerebral protection”• Surgical intervention.