head injury and role of anaesthesiologist in management

8/6/2019 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 !

head injury and role of anaesthesiologist in management

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