head injury and role of anaesthesiologist in management
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Head injury and role of
anaesthesiologist inmanagement
DR.DEEPAK SOLANKI
M.D.
ANAESTHESIOLOGY
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Important physiology
Human brain receives ~ 15% of the resting cardiacoutput
20% of the bodys oxygen consumption
Mean cerebral blood flow ~ 50 ml/100g/min
CMRO2- 3.2 ml/100g/min
Glucose- main substrate (60 mg/100g/min)
CPP= MAP- ICP- VP
Normal ICP - 0-15 mm Hg in adults; in children 10mm Hg
Regulation of cerebral blood flow
Auto regulation- 60-160 mm Hg
Flow-metabolism coupling
CO2 & O2 reactivity
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Monro-Kellie doctrine
The total ICV is fixed because of inelastic nature ofthe skull & only small increases in its volume
can be tolerated before pressure within thecompartment rises dramatically
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Pathophysiology of Head injury
PrimaryThe initial,
irreversiblemechanical injury:
Lacerations
Intracerebralhaemorrhage
Contusions
Avulsion
DAI
Secondary- Further insultsthat ultimately lead toischemia: systemic
Hypotension
Hypoxemia Excessive hypocapnia
Anaemia
Hyperthermia
Hyper or hypoglycemia Sepsis & coagulopathy
Hypertension
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Intracranial causes of secondary braininjury
Factors causing elevation of ICP Hypercapnia HypoxemiaJugular venous obstruction
Increase in central venous pressure Cerebral edema Cerebral vasospasm Intracranial infection Cerebral hypoxemia Posttraumatic epilepsy
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Systemic effects of Head injury
Impaired gas exchange Associated chest & abdominal injuries
Impaired reflexes aspiration ARDS
Fat embolism syndrome
Cerebral hemisphere or basal ganglia damageapnea & hypoventilation; cheyne stoke,apneustic breathing
Neurogenic alterations in FRC & V/Q matching
Acute neurogenic pulmonary edema Severe hypertension
Cardiac dysrhythmias or M.I. & ECG abnormalities
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Systemic effects of Head injury
Hypotension in young children due to blood loss Coagulation disturbances- due to release of tissue
thromboplastin, hypothermia & large bloodtransfusion
Electrolyte abnormalities Hypokalemia- stress induced B adrenergic
stimulation, respiratory alkalosis fromhyperventilation & diuretic therapy
Hyponatremia- SIADH
Hypernatremia- Diabetes insipidus, repeatedadministration of mannitol
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Prehospital management
Prehospital management & faster transport andadmission important keys to survival
J. Neurosurgery 71:202-207, 1989
Primary survey
Airway management Breathing Circulation and Control of haemorrhage Disablilty AVPU, GCS, Cervical spine injury
Exposure and
Environment
control
Others Foley catheter, Gastric tube
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Airway management
Open airway-clear the mouth of vomitus etc; look forforeign bodies, soft tissue swellings
A jaw thrust is used instead of a head tilt chin lift to open the airway
Manual in line axial stabilization/ rigid collar for C-spine
Observe for hypoxemia as or when possible and giveO2 su lementation when re uired
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Indications for intubation andventilation
Immediately Coma (GCS
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Endotracheal intubation
Nasotracheal tube in the spontaneously breathingpatient, and orotracheal intubation in theapnoeic patient.
Nasal intubation best avoided in the basal skullfracture- risk passing the ETT through the skull
defect & infection Rapid sequence induction
Suppression of intubation response- lignocaine 1mg/kg
Ketamine contrindicated; propofol with caution;Thiopentone, etomidate ideal
Succinylcholine can be used hyperkalemia is aconsideration in >48 h after injury not in acutesettings
Precurarization
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Circulation
Look for breathing, movement, level ofconsciousness, skin colour and pulse
External haemorrhage should be identified andcontrolled with manual pressure
Hypotension is the most important predictor ofthe outcome
Hypotension is defined as < 90 mm of Hg inadults and less than the 5th percentile for theyounger age group
Pneumatic splint can be used
At least two large bore lines for fluid resuscitation
Keep the patient warm
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Fluid resuscitation
Isotonic fluid- Ringer lactate OR normal saline
Uncrossmatched O negative PRBC should beavailable for early use in patients with significantblood loss
The use of glucose containing solutions is
discouraged unless hypoglycemia is suspected Judicial use of fluids cerebral edema &
haemodilution to be avoided- ATLS instructors manual: AmericanCollege of surgeons, Chicago 1996
Adequacy of resuscitation reflected by the serum
lactate levels- Scalea etal Crit Care Med:22;1610-1615,1994 Hypertonic saline/ dextran infusion@ 4 ml/kg as a
10-20 minutes improves microcirculation andcerebral perfusion
Crystalloid versus colloids - debated
The ideal pre-hospital fluid regimen may be a
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Glasgow coma scale
Eye OpeningEye Opening
ScoreScore >>1 Year1 Year 0-1 Year0-1 Year
44 SpontaneouslySpontaneously SpontaneouslySpontaneously
33 To verbal commandTo verbal command To shoutTo shout
22 To painTo pain To painTo pain
11 No responseNo response No responseNo response
Best Motor ResponseBest Motor Response
66 Obeys commandObeys command
55 Localizes painLocalizes pain Localizes painLocalizes pain
44 Flexion withdrawalFlexion withdrawal Flexion withdrawalFlexion withdrawal
33 Flexion abnormal (decorticate)Flexion abnormal (decorticate) Flexion abnormal (decorticate)Flexion abnormal (decorticate)
22 Extension (decerebrate)Extension (decerebrate) Extension (decerebrate)Extension (decerebrate)
11 No responseNo response No responseNo response
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Glasgow coma scale
Best verbal responseBest verbal response
ScoreScore >5 Years>5 Years 2-5 Years2-5 Years 0-2 Years0-2 Years
55 Oriented and conversesOriented and converses Appropriate wordsAppropriate words Cries appropriatelyCries appropriately
44 Disoriented and conversesDisoriented and converses Inappropriate wordsInappropriate words CriesCries
33 Inappropriate words; criesInappropriate words; cries ScreamsScreams Inappropriate crying/screamingInappropriate crying/screaming
22 Incomprehensible soundsIncomprehensible sounds GruntsGrunts GruntsGrunts
11 No responseNo response No responseNo response No responseNo response
Patients who are intubated are unable to speak are evaluated only with eye openingand motor scores, and the suffix T is added to the their score to indicate that thepatient is intubated. In intubated patients, the maximal GCS score is 10T and theminimum score is 2T
If eyes closed by swelling suffix C GCS 13-15- mild head injury; 9-12- moderate head injury, < 8- severe head injury.
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Secondary survey
History AMPLE -Allergies, Medications, Past medical
history/ Pregnancy, Last meal, Events relating tothe injury
Examination
Head- palpation for fractures and lacerations Eyes- visual acuity, pupillary size & reactivity,
ocular motility & haemorrhage and to removecontact lens
Face- ecchymosis or leakage of CSF from ears/nose
Neck- midline trachea, edema, JVP distension
Spine- pain or a step off through the entire column
Chest, Abdomen, Pelvis & perineum
Detailed neurological examination repeat
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Pupillary examination
Should be performed after resuscitation & beforeadministration of sedatives or paralytics
Pupil reactivity to light - positive reaction - > 1mm constriction
Pupil asymmetry - > 1mm difference
Fixed/Dilated Pupils - >4mm and react < 1mm
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Indications of CT scan
GCS less than 13 at any point since the injury GCS equal to 13 or 14 at 2 hours after the injury Suspected open or depressed skull fracture Any sign of basal skull fracture Post-traumatic seizure Focal neurological deficit More than one episode of vomiting Amnesia for greater than 30 minutes of events
before impact If LOC in patients older then 65 years,
coagulopathy or dangerous mechanism ofinjury
I di i f f l
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Indications for referral to
neurosurgeon
Persistent coma (GCS
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Transfer
Key to a successful and safe transfer
Adequate resuscitation & stabilization of the patientprior to transfer
Adequate monitoring, apt. resuscitation equipment &drugs
Accompanied by experienced, skilleddoctor/paramedics
Good communication b/w referring & receiving centresand efficient handover
What the receiving centre need to know
Patients age and medical history, if known Neurological status
Cardiorespiratory state
Injuries and imaging findings
Management and care given
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Intensive care
after Head injury
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Early indicators of prognosis
Glasgow coma scale score
Glasgow outcome scale
Age - >60 years
Pupillary diameter & light reflex Hypotension
CT scan features
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Glasgow outcome scale
Glasgow outcomescale
1= Dead2= persistent vegetative
state3= Severe Disability4= Moderate disability5= Good recovery
Extended Glasgowoutcome scale
1= Dead2= persistent vegetative
state3= Lower severe
disability4= Upper severe
disability5= Lower moderate
Disability6= Upper moderate
Disability
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Marshall classification
Diffuse injuriesDiffuse injuries CT FeaturesCT Features Mortality rate (%)Mortality rate (%)
Type IType I No visible pathologyNo visible pathology 1010
Type IIType II Diffuse injuries withDiffuse injuries with
cisterns present & < 5cisterns present & < 5
mm shiftmm shift
1414
Type IIIType III Diffuse injuries withDiffuse injuries with
compressed or absentcompressed or absentcisterns & < 5 mm shiftcisterns & < 5 mm shift
3434
Type IVType IV Diffuse injuries with > 5Diffuse injuries with > 5
mm shiftmm shift5656
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Monitoring
Monitoring systemic physiology- Direct arterial blood pressure
CVP line
Continuous pulse oximetry
Core temperature monitoring Regular measurement of blood sugar
Global CNS monitoring
Transcranial Doppler Ultrasound - for non invasive
estimation of CBFJugular venous monitoring
Monitoring of brain electrical activity - EEG ,MLAEP
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Jugular venous oximetry
As long as haemoglobin and arterial saturationremain constant, the SjVO2 is an indicator ofcerebral oxygen demand
Based on Ficks principle- CMRO2=CBFx(SaO2-
SjvO2)
Retrograde cannulation of the internal jugularvein in the cephaloid direction
Serial sampling or fibreoptic catheters for continuous monitoring
Normal value 55- 71% Useful in monitoring interventions such as hyperventilation therapy
Newer techniques for brain oximetry-NIRS, direct
tissue oximetry, cerebral micro dialysis
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Brain targeted therapy
PaO2 >60 mm Hg or Oxygen saturation >90%
PaCO2 35-40 mm Hg
MAP>90 mm Hg
ICP treatment at upper threshold of 20-25 mm Hg
CPP >60 mm Hg* SjVO2 >55%
Blood sugar- 70-130 mg/dl
Avoid & correct electrolyte imbalance
Temperature < 37o
c Seizure control*In the absence of cerebral ischemia, aggressive attempts to maintain CPP
above 70 mm Hg withfluids and pressors should be avoided because of the risk of adult respiratory
distress syndrome.
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Hyperventilation
Chronic prolonged hyperventilation (PaCO2 < 25mm Hg ) should be avoided in absence ofincreased ICP
Prophylactic hyperventilation (PaCO2 < 35 mm
Hg ) during first 24 hours of injury to beavoided
May be needed for brief period when there isacute neurological deterioration
For longer period in intracranial hypertensionrefractory to sedation, CSF drainage & osmoticdiuretics
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Sedation
Aim to decrease CBF, cerebral metabolism & ICPwhile preserving pressure autoregulation andthe cerebrovascular response to CO2
Propofol good agent, but risk of hypotension and
CPP Continuous infusion- lipid overload, should be
taken into account for daily caloric intake
Midazolam + opioids
Fentanyl, sufentanil & alfentanil can increase ICPin patients with head injury due to changes inPaCO2 (in spontaneously breathing pts) and
reflex cerebral vasodilatation
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Neuromuscular blockade
Used to synchronise ventilation, manipulatePaCO2 and minimise increases in ICP caused by
coughing and bucking over the ETT
Atracurium commonly used, tolerated well
hemodynamically Laudanosine epileptogenic, not a clinical
problem in humans
Pancuronium boluses or Vecuronium infusion also
used
Long term use assocoated with continuedparalysis after drug discontinuation & acutemyopathy dpecially with steroid based agents
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Fluid therapy
Guided by clinical and lab assessment & byinvasive haemodynamic monitoring
Target serum osmolality 290-300 mOsm
Hypotonic fluids and dextrose containingsolutions are avoided
Hypertonic saline small volume resuscitation
Albumin or plasma can be used for maintenanceof plasma oncotic pressure Lund protocol
Pentastarch may be effective in reducing thecerebral edema associated with cerebralischemic and reperfusion injury
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Nutrition
Metabolic rate ~140% of resting metabolic rate Increase largely abolished by neuromuscular
blockade or barbiturate coma 15% Of calories - protein Negative nitrogen balance for approximately first
3 weeks after injury Early (
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General Measures
Head position 15-30
o
c elevation of the head ofthe bed
Prophylaxis
Thomboembolism
Stress ulcerTreatment of coagulopthies
Physiotherapy
Moderate Hypothermia (32-33oc) improvesoutcome by reducing
vCMRO2,vNeurotransmission
v Frequency of energy depleting ischemicdepolarizations
v Free radical production
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Osmotic therapy
Mannitol is effective for control of ICP Effective dose- 0.25 mg/kg -1 mg/kg body weight
Also used in case of transtentorial herniation orprogressive neurological deterioration notattributable to extracranial causes
Serum osmolality to be kept
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Antiepileptic therapy
Early- 7days Factors associated with increased risk: GCS
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Cerebral metabolic suppressants
Decrease ICP
High dose barbiturate (Barbiturate coma) inhaemodynamically stable patients withrefractory intracranial hypertension
Titrate dose to achieve EEG burst suppression
Propofol, etomidate, ketamine, opioids can alsobe used
S/E prolonged recovery, increased chestinfections
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Novel neuroprotective intervention
Anaesthetic agents - High dose barbiturate(Barbiturate coma), Propofol, etomidate,
ketamine, opioids
Excitatory amino acid antagonist dizoclipine
Calcium channel blockers Nimodipine
Antioxidants pegorgetin, tirilazad
Steroids
Sodium channel blockers phenytoin,
lamotrigine, lubelozole, riluzole NSAIDS - indomethecin
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No Head injury is so serious that it
should be despaired or not so trivial
that it can be ignored
-HippocratesThank you !
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