Tbi 100121072336-phpapp02
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Transcript of Tbi 100121072336-phpapp02
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Toh C J
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Classification
Severity Anatomic findings
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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
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Classification
Anatomic findings
Focal
Diffuse
Contusion
Coup
Countrecoup
Gliding Fracture
HematomaEpidural
Subdural
Intraparenchymal
Intermediary
Concussion DAI
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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%
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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
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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
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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
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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
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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
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Secondary survey for head trauma
GCS Pupillary size
Active bleeding scalp wound
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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
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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
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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
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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.
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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
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Other NeuroExam
• Signs of Skull Base fracture
– Raccoon eyes
– Battle sign (after 8-12 h)
– CSF rhinorrhea or otorrhea
– Hemotympanum
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Imaging of head injury
• Modalities– Skull X-ray– CT scan– MRI
• Areas– Skull, brain– Cervical spine– Chest– Pelvis
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Skull Fracture• Types
– Depressed / non-depressed
• Importance– Non-depressed per se:
minimal– Depressed– A/w low GCS– Compound fractures– Foreign body
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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
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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)
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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
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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
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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.
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Management of TBI
Detection &
MonitorTreatment
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Detection &
Monitor
GCS
Pupillary reflex
ICP Monitor
Symptoms & sign of herniation
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Methods of monitoring intracranial pressure..
Fiberoptic sensors (Camino), Microchips (internal strain-gauge devices)(Codman) Air pouch technologies (Spiegelberg)
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Methods of monitoring intracranial pressure..
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EVD, External Ventricular Drain
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Primary injury
Secondary injury
Herniation Mass lesion
ICP
ICP
ICP ICP
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Secondary injury
Hypoxia Hypovolemia
Cerebral edema
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≠
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Managing raise ICP
General measure
Medical management
Surgical intervention
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General measure
Head elevation
Maintain normal temperature
Neck vein compression?
? Chest Physio
Hyperventilation
Fluid management
Glucose monitor
Maintain normal Blod pressure
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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.
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Neck vein compression?
•Neck in neutral position•Collar is fixed properly•Arm sling is not compressing the neck vein
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Maintain normal temperature
Keep patient’s body temperature within normal limit
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? Chest Physio
To give sedation during chest physiotherapy
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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
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Fluid management
Fluid management should aim primarily at preventing hypotension while optimizing cerebral perfusion pressure.
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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.
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Medical management
Sedation
Muscle relaxant
Barbiturate & Propofol
analgesic
antipyretic
Mannitol & Frusemide
Hypertonic saline
antiepileptics
Neuroprotective agent
BP control
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Sedation
analgesic
Midazolam + Morphine
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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
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Muscle relaxant Increase incidence of aspiration pneumonia
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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.
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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
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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
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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.
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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
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Surgical intervention
Removal of the pathological lesion
CSF diversion procedure
Open the cranium “craniectomy”
Remove part of the non-eloquent brain“Lobectomy”
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Removal of the pathological lesion
CSF diversion procedure
Open the cranium “craniectomy”
Remove part of the non-eloquent brain“Lobectomy”
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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
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Brain swelling
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Bleeding
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CPP = MAP - ICP
Take Home Message:Take Home Message:
ICP keep < 20 mmHg
CPP keep 60 to 70 mmHg
“Biar lambat asalkan selamat”
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Summary:
• Classification of TBI:
• Management:– Prehospital.– In Hospital:
• Primary survey & secondary survey.• Imaging• Monitor • “cerebral protection”• Surgical intervention.