Download - Head Injury
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Head Injury• Scalp injury• Skull injury • Meningeal injury• Traumatic Brain Injury
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WHAT IS THE DEFINITION OF A TRAUMATIC BRAIN INJURY
(TBI)?
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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
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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.
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StrokeBrain InfectionTumorAnoxia Exposure to Toxic Substances
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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.
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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
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Severity of primary injury Intracranial complications Hypoxaemia Hypercarbia Hypotension Anaemia Multiple injuries, proportional to Injury
Severity Score (ISS) Age
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Prolonged prehospital time Admission to inappropriate hospital Delayed or inappropriate interhospital
transfer/retrieval Delay in definitive surgical treatment
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Traumatic Brain Injury
Blunt(Closed) Penetrating
Explosion Fall GSW Stab Blast Fragment
Motor vehicle crashes (MVC)
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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
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Coup-Contra Coup
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Diffuse Axonal InjuryDiffuse Axonal Injury
Rotational forces onthe brain cause the
stretching and snappingof axons
Axon
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1. Headache2. Vomiting3. Papilloedema occur in chronic condition4. Cushing response
› Bradicardia› Hipertension› Alteration of ventilatory pattern
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5. Herniation › Uncal - ipsilateral dilated pupil
- contralateral hemiparesis- ipsilateral hemiparesis (Kernohan’s notch
phenomenom)› Central - rostrocaudal sign› Subfalcine› Tonsiller herniation
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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.
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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
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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
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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
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SecondaryIntracranial haemorrhage
Cerebral swellingcerebral hypoxiaCSF leakage and pneumocephalusmethabolic disordersinfectionepilepsy
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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)
(
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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
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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)
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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
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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
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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
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The indication: › Airway is inadequate› GCS ≤ 8› Herniation› Rapid deteriorationShould be performed only by a competent
medical practitioner
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Gambar COB dgn ETT
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Early management of severe traumaThe management plan is based on:1. Primary survey2. Resuscitation3. Secondary survey4. Definitive care
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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
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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
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› 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
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› 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
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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
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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
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› 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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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%
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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
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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
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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
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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
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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
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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
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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.
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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
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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
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