Head Injury• Scalp injury• Skull injury • Meningeal injury• Traumatic Brain Injury

WHAT IS THE DEFINITION OF A TRAUMATIC BRAIN INJURY

(TBI)?

Congenital brain injury

Pre-birth During birth

Acquired Brain Injury

After birth process

Traumatic Brain Injury(external physical force)

Closed Head Injury

Open Head

Injury

Non-traumatic Brain Injury

an acquired injury to the brain caused by an external physical force resulting in total or partial functional disability or psychosocial impairment or both that adversely affects a child’s educational performance.

StrokeBrain InfectionTumorAnoxia Exposure to Toxic Substances

Important note:Important note:

Brain injuries Brain injuries

that result from either an that result from either an

external external

or internal forceor internal force

may have similar effects.may have similar effects.

Epidemic in Indonesia Major cause of death and permanent

disability 70% of all road fatalities 50% of trauma death 10-20% of head injury: death on arrival Degree 10% mild head injury

10% moderate head injury80% severe head injury

Severity of primary injury Intracranial complications Hypoxaemia Hypercarbia Hypotension Anaemia Multiple injuries, proportional to Injury

Severity Score (ISS) Age

Prolonged prehospital time Admission to inappropriate hospital Delayed or inappropriate interhospital

transfer/retrieval Delay in definitive surgical treatment

Traumatic Brain Injury

Blunt(Closed) Penetrating

Explosion Fall GSW Stab Blast Fragment

Motor vehicle crashes (MVC)

Injury forces applied to particular anatomical areas produce a pattern of injury for the individual, e.g. Acceleration/deceleration

Appiled to the entire head, evident as disordered consciousness from the time of impact resulting from concussion, often with diffuse axonal injury and/or cerebral contusions (coup or contreceup) Local impact

Coup injuries to scalp, skull, meninges, brain Penetrating

Pathway of injury velocity and nature of projectile Crush injury

Scalp, skull and cranial nerve injuries

Coup-Contra Coup

Diffuse Axonal InjuryDiffuse Axonal Injury

Rotational forces onthe brain cause the

stretching and snappingof axons

Axon

1. Headache2. Vomiting3. Papilloedema occur in chronic condition4. Cushing response

› Bradicardia› Hipertension› Alteration of ventilatory pattern

5. Herniation › Uncal - ipsilateral dilated pupil

- contralateral hemiparesis- ipsilateral hemiparesis (Kernohan’s notch

phenomenom)› Central - rostrocaudal sign› Subfalcine› Tonsiller herniation

Mild – GCS 14-15Patient typically mildly lethargic, disoriented

Moderate – GCS 9-13Patient typically sleepy or obtunded, able to

follow commands with arousal.Confused.

Severe – GCS 3-8Patient comatose, unable to follow command or perform purposeful motor activity.Range of motor activity: localizes, withdraws,

decorticate posturing, decerebrate posturing, nil.

Severity GCS LOC PTAMild 14–15 <20 min-1 hr <24 hr

Moderate 9–13 1 – 24 hrs. > 24 hrs. - <7days

Severe 3–8 >24 hrs. >7 days

GCS = Glasgow Coma ScaleLOC = Loss of consciousnessPTA = Posttraumatic amnesia

Primary Injury: Function of energy transmitted to brain

◦ Very little can be done by health care providers to influence

◦ Cerebral concussion, contusion and degeneration, Diffuse Axonal Injury (DAI)

Secondary Injury: Function of damage to brain from systemic physiology

◦ Systemic Hypotension: Acute and easily treatable Hypoxia: Acute and easily treatable Fever and Electrolyte Imbalances

◦ Seizures

◦ Intracranial Pressure Can Lead to Herniation

PrimaryScalp

contusion, abrasion, laceration

Skull fracture

open, closed (note-compound base of skull fracture without a scalp laceration), linier, depressed

Meningeal injury

dural tear

Brain injury

concussion

contussion

diffuse axonalfocal – contusionlaceration and penetration

SecondaryIntracranial haemorrhage

Cerebral swellingcerebral hypoxiaCSF leakage and pneumocephalusmethabolic disordersinfectionepilepsy

Dorsolateral prefrontal cortex(executive function, including sustained and complex attention, memory retrieval, abstraction, judgement, insight, problem solving)

Amygdala (emotional learning and

conditioning, including fear/anxiety)

Anterior temporal cortex(memory retrieval, sensory-limbic integration)

Ventral brainstem (arousal, ascending activation of diencephalic, subcortical, and cortical structures)

Hippocampal-Entorhinal Complex (declarative memory)

Viewed on coronal MRI

Orbitofrontal cortex(emotional and social responding)

(

Postconcussion Symptoms (PCS)

SOMATIC• Headache• Dizziness• Fatigue – for

physical and mental

• Visual Disturbances

• Sensitivity to Noise and Light

COGNITIVE• Decreased Concentration• Memory ProblemsNEUROPSYCHIATRIC• Anxiety• Depression• Irritability• Mood Swings• Sleep Disturbances

Natural history is recovery within weeks/months (Levin 1987)

A small percentage will have persistent symptoms (Alexander, Neurology 1995)

Repeat concussions – more morbidity (Collins, et al, Neurosurgery 2002)

Educational interventions effective in reducing symptoms (Ponsford, et al. 2002)

Attention/Concentration

Speed of Mental Processing

Learning/Information Retrieval

Executive Functions (e. g., Planning, Problem Solving, Self Monitoring) May see judgment problems, apathy, inappropriate behaviors

Factors influencing outcome- airway

- breathing- control of haemorrhage- prevention and shock treatment- avoidance of factors ↑ ICP

• head down position• hypoxia• hypercarbia

• vomiting

- recognition of serious associated injury

- effective communication and transport

Lateral position for airway controlin Px with susp spinal injury

The face in turned slightly down wordsthe tongue to fall forwards saliva and vomit will drain out

The indication: › Airway is inadequate› GCS ≤ 8› Herniation› Rapid deteriorationShould be performed only by a competent

medical practitioner

Gambar COB dgn ETT

Early management of severe traumaThe management plan is based on:1. Primary survey2. Resuscitation3. Secondary survey4. Definitive care

Primary survey› Airway with cervical spine immobilized in neutral

position› Breathing pattern and adequacy› Circulation and haemorrhage› Disability, minineurological examination:

GCS Pupils Motor deficit

› Exposure: completely expose the patient for an adequate examination but protect against hypothermia

Resuscitation› Airway

Ensure patient airway Unconscious patient: intubated if skilled Note: maintain cervical spine immobilization

until radiological examination excludes spinal injury

› Breathing and oxygenation Ensure adequate ventilation Mechanically ventilate if intubated Give supplemental oxygen initially

› Circulation support and control haemorrhage Treat shock aggressively to improve tissue

perfusion Control external haemorrhage

› Assess response to resuscitation using physiological parameters: pulse, blood pressure, skin colour, capilary refill and urine output

› Nasogastric tube and urinary catheter unless contraindicated

› Head injury alone, without scalp injury, does not cause hypotension. If hypotension is present, identify the cause, e.g.:• Hypovolaemic shock, • spinal injury.• Rarely, may be due to medulallary failure.• Blood loss from a scalp or head injury may

cause hypotension (hypovolaemic shock) in children

Secondary survey› Special neurosurgical assessment including

Glasgow Coma Score (GCS) and external sign of injury to the head

› Record the pulse, blood pressure, respiratory rate and temperature

› Systematically examine each region of the body, i.e. head-to-toe examination

› Connect to monitors as available› Re-evaluate the GCS› Radiological examination-lateral X-ray spine,

chest, pelvis, other areas as indicated, skull X-ray and CT head scan

History› Cause of injury. This will help in determining

the mechanism and pattern of head injury› Loss of consciousness at the injury site› Has the patient talked before becoming

unconscious? If so, there is some secondary cause of a poor neurological state, e.g. Hypoxia, hypotension, intracranial haematoma

› Pupillary response

› Were the pupils equal or unequal at the scene of the injury? Initial equality with change to inequality suggest a lateralised mass lession

› Cardiorespiratory status at the injury site and response to resuscitation

› History of drugs or alcohol, both prior to and at the time of injury

› Other medical disease, previous head injury and ocular conditions

CNS examination› Glasglow Coma Scale (GCS)› Pupillary responses

are they equal or unequal? Were the pupils equal at the time of the incident (report from ambulance officer) and have they the same response now?

› Motor patternhemiparesis, quadriparesisflexion or extension to pain (from supraorbital, trapezius or tendo achilles pressure)

› Inspection of the face and scalp› Palpation of the face and scalp and any laceration

for a depressed fracture› Palpation of the spine for the tenderness and

deformity

Glasgow Coma Scale (GCS)This scale examines three areas of behaviour: eye

opening, response to voice and motor responses. The score can be quantitative with 3 being the lowest score and 15 normal

Eye opening› Spontaneous E4 › To speech 3› To pain 2› Nil 1

Verbal response› Orientated V5› Confused conversation 4› Inappropriate words 3› Incomprehensible sound 2› Nil 1

Best motor response› Obeys M 6› Localizes 5› Withdraws 4› Abnormal flexion 3› Extension 2› Nil 1

Coma Score (E+V+M) = 3-15

CT head scan guidelines› GCS < 15 after resuscitation› Neurological deterioration, i.e 2 point or more on

the GCS, hemiparesis, squint› Drowsiness or confusion (GCS 9-14 persisting>2 h)› Persistent headache, vomiting› Focal neurological signs› Fracture – known or suspected› Penetrating injury – known or suspected› Age – over 50 years of age › Post-operative assessment

Comment A CT scan is the investigation of choice where available. Except for an uncomplicated minor head injury, all patients ideally should have a CT scan.

As lesions may develop after an initial normal scan, serial CT scans may be required if neurosurgical deterioration occur

Skull X-ray guidelinesIn rural area where a CT scan is not available or readily accessible, a plan skull X-ray can provide useful information. The pictures required are AP, lateral, Towne’s view and tangential to the point of impact for demonstrating a depressed fracture

Indications› Loss of consciousness, amnesia› Persisting headache› Focal neurological signs› Scalp injury› Suspected penetrating injury› CSF or blood from nose or ear› Palpable or visible skull deformity› Difficulty in clinical assessment› Patient with GCS 15, essntially asymptomatic

but “at risk” bacause of a defect blow or fall onto a hard surface, etc, especially in a patient over 50 years of age

CommentThe presence of a skull fracture may influence treatment, i.e.›A skull fracture is associated with an increased risk of intracranial haemorrhage and a CT scan is indicated

›A compound fracture, including base of skull can be associated with an increased risk of infection and a depressed fracture with an increased risk of epilepsy especially if associated with dural penetration

›A fracture indicates the site for surgery particularly in a rapidly deteriorating patient in whom an extradural haematoma is suspected

›Pneumocephalus – presence and volume is a consideration in aerial transport

Criteria for admission to hospital with head injury:• Confusion or any other decreased level of consciousness• Neurological symtoms or sign – including persistent

headache, vomiting• Difficulty in clinical assessment, e.g. alcohol, epilepsy• Other medical condition, e.g. coagulation defects, diabetes

mellitus• Skull fracture• Abnormal CT brain scan• Responsible observation not available outside the hospital• Age – patients over 50 years of age• Children under 5 years of age

Minor head injury› A minor head injury is defined as one where the

Glasgow Coma Score is 14-15› Admit and observe the patient if: a). There has been loss of consciousness or a period of

post-traumatic amnesiab). The patient remains confused

c). The patient is under 5 years of age or over 50 years of age

d). Presence or development of focal neurological signs e). Severe headache with or without vomiting

Discharge of minor head injury patient› Orientated in time and place› No focal neurological signs› No skull fracture› A responsible person is available to continue

observation of the patient› Discharge check list – advise to report back to hospital

immediately if there is:a) Vomiting b) Complains of severe headache or dizzinessc) Becomes restless, drowsy or unconsciousd) Had a convulsion or fit

Definitive management of traumatic brain injury› Immediate surgery for evacuation of

hematoma, if necessary› Monitor ICP with implanted pressure gauge› Medically manage cerebral edema to maintain

cerebral perfusion pressure > 70 mmHg› Perform serial head CT Scans

20% of cerebral contusions may enlarge to surgical hematoma

Concussion› Brief loss of consciousness with normal

head CT Scan, normal neuro exam › Patient may have mild lethargy and/or

confusion › Treatment: observation› In sport, avoid any risk of reinjury until any

sxs have completely resolvedSecond impact before full recovery

may be fatal

Skull fracture› May or not have associated underlying brain injury› Linier or non-depressed-observe› Open or compound-irrigate, close, antibiotic coverage› Depressed-require surgical repair

Any associated dural tear or brain laceration requires surgical repair

› Basilliar skull fracture-fracture around orbital roof, sphenoid bone, or petrous or mastoid portion of temporal bone.

Signs:Battle’s or Racoon’s eye signs May be associates with injury to cranial nerves 2,7 or 8 or CSF leak into nose (rhinorhea) or ear (otorhea)- these require special attention. Seldom life threatening

Cerebral contusion / intracranial hematoma› Area of focal tissue injury. Neurological

deficit depends on area injured.› Commonly occur in coupe / contra coupe

pattern eg. Frontal / occipital› 20% of contusions may expand into

surgical hematoma› Observe patients in ICU, repeat head CT-

Scan within 24 hours

Epidural Hematoma – EDH› Lens shaped hematoma between dura and skull› Associated with skull fracture and laceration of

dural artery (e.g. Middle meningeal artery)› Urderlying brain is ussually not injured› Arterialized bleeding result in rapid expansion

of hematoma and neurological decline› Often present with brief loss consciousness,

followed by lucid interval of minute to hours, before rapid neurological decline into coma

› Extreme neurosurgical emergency. Timely diagnosis and surgery is often followed by excellent recovery

Subdural hematoma – SDH› Crescent shaped hematoma lying between brain and dura,

conforming to brain surface

› Indicative of high acceleration / deceleration injury with tearing of bridging veins or cortical arterioles

› Usually associated with severe diffuse injury, immediate deep coma from moment of impact

› Extreme neurosurgical emergency

› 30% mortality, 30% good outcome

DAI – diffuse axonal injury› Also known as shear injury or brain stem contusion

› High acceleration/deceleration injury with shock waves and momentary tissue distortion causing microscopic tearing of nerve fibers

› radiographically consist of small petechial hemorrhages in white matter tracts

› Cause immediate deep coma

› Often associated with severe cerebral edema and ICP elevation

› Mortality is 30-40%, good outcome 20-30%

Gunshot wound-GSW› Cause mixtures of skull fracture, DAI,

intracerebral hemorrhage, epidural and subdural hematomas, in addition to direct tissue injury. May also couse injury to major cerebral vessels.

› High velocity weapons cause extreme diffuse injury from tissue cavitation

Chronic subdural hematoma› Usually found in older patients with cerebral

atrophy› Minor trauma causes small, often minimally

symptomatic subdural hemorrhage. As clot liquifies over next 1-3 weeks, the hemorrhage

may expand into a significant mass.› CT apperance, hypodense crescent shaped mass

between dura and brain› Presenting symptoms: elevated ICP often

associated with hemiparesis. May also cause TIA-like episodes or seizures

› Treatment consists of surgical drainage of hematoma via burrholes and irrigation. Most patients make excellent recovery

Intubate & ventilate with GCS<9 the goal: PaO2=100mmHg, PaCO2 35mmHg, O2 sat

96%, hyperventilation (PaCO2< 30mmHg) should be

avoided Cerebral perfusion

the goal: CPP>70mmHg, MAP>90mmHg hypotension (systolic BP<90mmHg) must be avoided

Intravenous fluid electrolites normovolaemic is the goal, avoid dehydration on or ever hydration normal serum electrolyte should be maintaned Head posture: should be elevated to 20-30°

Corticosteroid: are not recommended Transfer to CT and / or neurosurgical unit

Active treatment of intracranial pressureOnly be under taken of there is evidence of - rapid neurological deterioration- signs of uncal herniation- ↑ ICP from the ICP monitoring- modality (should be decided by neurosurgeon)

• CSF drainage• intravenous mannitol• hyperventilation• barbiturate• mild hypothermia• decompressive craniectomy

Prevention of intracranial infectionThis can result from basal skull fracture or from a

penetrating craniocerebral injury. CSF rhinorrhoea or otorrhoea, intracranial aerocele or a known or suspected penetrating injury require careful assessment. The indication for prophylactic antibiotic therapy is controversial. A neurosurgical consultation is indicated.

1. CSF rhinorrhoea or otorrhoea – swab for culture and sensitivity and observe

2. Intracranial aerocele – antibiotic therapy3. Penetrating craniocerebral injury – surgical repair

and antibiotic therapy

Restlessness and analgesiao Before prescribing analgesia, it is important to determine the cause of restlestness, e.g.: cerebral hypoxia from airway inadequacy or poor ventilation or poor perfusion, raised intracranial pressure, pain, alcohol intoxication or a full bladder.

oDrugs other than paracetamol or codeine phosphate require neurosurgical consultation

Post traumatic epilepsy The risk factors for epilepsy are: intradural haematomas, dural laceration with cortical injury, depressed fractures, a post-traumatic amnesia period of 24 h early post traumatic

epilepsy

The indication for prophylactic anti-convulsant therapy is controversial. A neurosurgical consultation is indicated both for the cause of the epilepsy and for consideration for anti-convulsant therapy.

Scalp Wounds1. shave at least 3 cm around the wound

2. gently palpate the laceration with a gloved finger. This may provide information regarding an underlying fracture

3. if a fracture is found unexpectedly, do not remove bone fragments: contact your neurosurgeon at once.

4. Scalp wounds may bleed profusely and cause hypertension. Secure haemostasis by pressure or suturing early

5. if the wound edges are badly torn, excise non – viable scalp and where possible suture the scalp in two layers

Airway-protect cervical spine Breathing-oxygenation Treat shock-control haemorrhage Maintenance fluids after resuscitation Full neurological examination early and establish a working

diagnosis Prevent secondary brain injury Assess and treat non cerebral injuries X-ray (or CT-Scan if available) when cardiorespiratory

stability achieved Consult early with a neurosurgical unit and consider

transfer, particularly in the multiple injured patient (after stabilization of extracranial injuries)

Continually re-assess neurological status