introduction to neurosurgery & traumasmore common with ich, depressed #, severe head injury at...
TRANSCRIPT
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Introduction to neurosurgery
& traumas
Dr Waleed DabbasNeurosurgery Department
College of Medicine Al Balqa University
Al Salt- Jordan
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Neurosurgery
Specialty in brain and spine
Subspecialties:
Neurotrauma
Neurooncology
Cerebrovascular
Functional
Skull base
Neuroendocraniology
and spinal surgery
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Neurotraumas
Head injuries
Spinal injuries
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Just keep your head away and contemplate
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We do not like to see this????
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introduction
300/100 000/y
Of these 9/100 000 die
Some are inevitable others are potentially preventable
Causes:
MVA most common in young males. Contributes 60% of deaths from head injuries
Falls
Assaults
Domestic accidents
Sport injury
Gun shot
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continued
Primary impact is un preventable
Aim of management is to:
- minimise further brain damage from secondary complications
-Maintain adequate CPP
- Lower ICP
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Cerebral perfusion pressure
Normal ICP is less than 10 mm Hg, around 135 mm H2O, High ICP if >15
Best measured by EVD that is connected to ICP monitor
Cerebral perfusion pressure is :MAP-ICP
CPP ranging between 60-100 mm hg
MAP= diastolic+1/3 systolic
Cerebral blood flow CBF= CPP
CVR
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CPP= MAP-ICP
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Aetiology
Brain injury occurs at the time of impact and as a result development of secondary complications
Primary involves the initial mechanical injury due to local deformation and energy transformation.
Secondary encompass a cascade of biochemical and cellular processes which are initiated by primary process which may cause ongoing cellular damage or even death
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Primary damage
1- brain contusion and laceration
Coup and counter coup
Frontal and temporal
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continued
2-diffuse axonal injury This type occurs as a result of shearing
injury Causing tearing of axons Mild to severe
Mild :Concussion Severe usually causes corpus callosum, mid
brain, and SCP contusions. CT may be normal but patient in moribund
condition
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Secondary brain damage
May be preventableOccurs at any time after
initial impact
1-Intracranial haematomas
Epiduarl haematomas:from MMA, less likely from
venous source or fracture site
Takes biconvex shape. Mortality rate 10%. If deteriorates 40-50%
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continued
Sub dural haematomas
Classified to
Acute:
from rupture bridging veins.
concavo-convex shape.
high mortality rate 60%.
Usually associated with
intracerebral contusions and
shearing injury that
increases the morbidity and
mortality rate
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continued
subacute :Iso dense on CT scan, Symptoms appear within 4-21
days.
Chronic:More than 3 wUsually in infants and oldsHypo dense on CT scan
.
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continued
2- brain oedemaVery common after head injurymay be fatal if left untreatedVasogenic type.increases ICP.
3-CONING OR BRAIN HERNIATION
Central and lateral. Subfalcine transtentorial or diencephalic
,tonsillar.Due to increase in ICP from brain swelling or supratentorial
haematomas as a result of space occupyinglesion.
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Brain herniation syndromes
The shift of brain structures goes through weak points which are the orifices inside the skull which is a rigid box that does not expand in a response to this shift
Classified to:
Central or rostro-caudal
Lateral
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TYPES
Subfalcine or cingulate herniation:which is the mid line shift: due to space occupying lesion that shifts the ipsilateral structure to opposite underneath the interhemispheric falx.
If continues it ends with transtentorial herniation
Trans tentorial herniation: Lateral or uncal: common The uncus of the temporal lobe herniates
through the tentorial opening. Causing mid brain compression
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S&S
Earliest sign is decline in GCS. If proceeds it causes 3rd CN palsy then contralateral hemiplegia. At this stage brain herniation might be reversible but if it continues it end with pontine or medullary syndromes which are irreversible
Central or diencephalon as in mid line structure lesions or bilateral hemispheric lesions.
It causes rapid decline in GCS rather than causing the classic syndrome before it
Takes the same stages
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Tonsillar herniation
Posterior fossa lesions that cause herniation of the cerebellar tonsils via the foramen magnum
Causing significant medullary compression and sudden death
Up ward herniation may also occur at the same time through the tentorial herniation
Other types :Transcraniotomy herniation
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END RESULT
4-cerebral ischemia
Caused by progressive rise in ICP, hypoxia or hypotension
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OTHERS
5- infection
2-5%
as seen in compound depressed #, or basal skull #
6-Epilepsy
immediate after trauma
early within a week in 5%
late after a week in 5%
more common with ICH, depressed #, severe head injury
at 20-25%
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Classifications of head injury
1-According to severity
Mild GCS13-15 Moderate 9-12 Severe <9
2-According to morphology.Scalp injuries Cut and lacerated wounds Degloving wounds
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.skullVault: Linear: a crack within
the bone without displacement
Depressed: displacement of bone fragment inwards
Either compound or simple
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Comminuted: fragmented bone without displacement
Base: Anterior fossa Middle fossa Posterior fossa
.IntracranialExtra-axial EDHSDHSAH
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continued
Intra-axialBrain contusions and lacerationsBrain haematomasIntra ventricular haemorrhage
Head injuries may also be closed or openOpen:Basal skull factures and compound depressed fracturesOr as seen in penetrating injuries mainly in war time
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Management
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That includes
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Concepts of Initial assessment for traumas
1-Rapid primary survey
2-Resuscitation
3- Adjunct to primary survey /resuscitation
4-Detailed secondary survey
5-Adjuncts to secondary survey
6-Re evaluation
7-Definite care
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Primary survey
Get IV access, send bloods
A: airway check for obstruction. ETT
B: breathing
oxygenate, check respiratory movements. ?ventilation
C: circulation
BP, pulse. Control bleeding, restore volume
D: disability
GCS, Pupillary response, focal deficits
E: exposure
Completely undress patient, protect from hypothermia
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Resuscitation
GOALS Achieve normovolemia and hemodynamic
stability Compensate for the internal fluid fluxes
from the interstitial and intracellular compartment
Improve the microvascular blood flow Normalise oxygen delivery to cells Parameters: BP,PR,RR,O2 sat, urine output, pulse
pressure, perfusion.
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ICP
Skull is a rigid contains:
brain: 1200-1600 ml +150 ml of ECF
CSF: 130- 150 ml
blood: 100-150
They are incompressible and in balance
Monro Kellie doctrine; pressure volume curve
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Monro- Kellie Doctrine
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Adjuncts Treatment
ECG
Urinary output
Catheters
Pulse oximeter and PCO2
ABGs
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Secondary survey
Proceed to secondary survey when
primary completed
ABCDEs are reassessed
Vital function returning to normal
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Key components to secondary survey
History: A M P L E Observational at scene, initial clinical observation, progress. Physical examination: head to toe Tubes and fingers in every orifice Complete Neuro exam,: palpate for spine tenderness Musculoskeletal checks Special diagnostic tests
Keep hard neck collar on Re evaluation to minimise missed injuries Pain killers as appropriate
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Points to get in head injuries
Mechanism of injury Circumstances of injury LOC PTA Headache and vomiting Seizures Weakness CSF leak Spine pain Other symptoms
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Examination
1- level of consciousness GCS (E4 V5 M6).
take the best response. Lowest score 3 highest 15, if intubated (ETT) give 1
2-Pupillary reaction:
unresponsive unilaterally implies pathology of ipsilateral 3ed N. herniation
Anisocoria may be physiological if mild
3-Focality:
asymmetric response implies intracranial event
4-Signs of head trauma
5-Signs of basal skull #: CSF leak, raccoon eyes, sub conjunctival bleed, battle’s sign .
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Imaging in trauma
Initial trauma series Lateral c- spine x-ray CXR Pelvis Abdominal U/S if handy CT Scan brain, c-spine as routine In multiple trauma chest, abdomen and
pelvis should be included Angiography in vascular injuries mainly in
pelvis MRI in spinal trauma
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Indications for CT and admission
LOC or PTA >5 minutes
Hx of epilepsy
GCS <15 or decline in GCS
Neurological deficits
CSF leak
Positive radiological findings
Social indication?
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Treatment
mild and moderate injuries, linear, comminutedObservation:Basal skull #:observation, antibiotics ?CSF leak ceases within 3-10d in 90-95%If continues drainage or dural repair may be needed
Compound depressed #:craniectomy and antibioticsEDH:needs craniotomy if thickness more the 1 cm. or if causing mass effect
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CONTINUED
SDH:
usually associated with other injuries that require craniotomy vs craniectomy + ICP monitor
Post traumatic epilepsy:
treatment is controversial
Anticonvulsants usually phenytoin loading and maintenance may be given to patients at risk.
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Management of severe head injury
Coma implies:
inadequate airway controlICP is usually elevatedHemodynamics are unstableAim to maintain adequate cerebral perfusionpressure to maintain the integrity of neurons
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What brain needs
Rest
Oxygen
Glucose
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Treatment
Intubate
Oxygenate
Keep head up at 30
EVD for ICP monitor and CSF drainage
Mannitol is effective bolus or infusion
Lasix may help
Steroids are controversial
Anticonvulsants in high risk patients
SBP must be >100
O2 sat >98%
PCO2 32-35
Temperature <37
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Continued
Barbiturates for refractory ICP in salvageable patients. Needs enough experience before getting used due to serious side effects
craniectomy:
Is an effective surgical method for ICP control in certain cases
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Consequences
Death
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How brain responds
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ICP=MAP= ZER0= DEATH
Any increase in intracranial constituents results in subsequent compensatory responses to maintain normal ICP
Failure of compensatory mechanisms results in rise of ICP and reduction in CPP and subsequent herniating syndromes and eventually brain death
CBF is zero when ICP = MAP
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ICP Waves
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Brain death: no blood flow
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So, do not run away or turn your back in this long battle??
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Vegetative state
Severe disability
Moderate to mild disability
Back to normal
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Other complications
Epilepsy
Infection
Normal pressure hydrocephalus
Post concussional syndrome
Medical complications: electrolyte disturbances, bed sores, DVT, PE…etc
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POST CONCUSSIONAL SYNDROME
Common after head injuries
Characterised by headache, poor memory and concentration, lack of interest, dizziness, depression.
Needs reassurance.
Pain relievers
antidepressants
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End