INTENSIVE CARE INTENSIVE CARE AFTER ACUTE HEAD AFTER ACUTE HEAD

INJURYINJURY

ModeratorModerator : : Dr Anand Dr Anand KulkarniKulkarni

PresenterPresenter: : Dr Nikhil M.PDr Nikhil M.P

IntroductionIntroduction

• One third of all trauma deathsOne third of all trauma deaths

• 15-45 years of age15-45 years of age

• 49%-road traffic accidents,28%-falls,23%-49%-road traffic accidents,28%-falls,23%-gun shot injuries and other causesgun shot injuries and other causes

• Inpatient case fatality rates Inpatient case fatality rates

all head injuries- 2.6%to6.5%all head injuries- 2.6%to6.5%

severe injuries - 15 to 50%severe injuries - 15 to 50%

• Good outcome-Glasgow outcome scale of Good outcome-Glasgow outcome scale of 1or1or22

Glasgow outcome Glasgow outcome scalescale

1= good recovery.1= good recovery.

2= moderate disability.2= moderate disability.

3= severe disability.3= severe disability.

4= vegetative state.4= vegetative state.

5= dead.5= dead.

Determinants of outcome in Determinants of outcome in acute head injuryacute head injury

Primary vs. secondary insults Primary vs. secondary insults

Little can be done about the primaryLittle can be done about the primary injury to brain injury to brain Presence and severity of secondary Presence and severity of secondary

neuronal neuronal injury injury

Physiological insults are additive in their Physiological insults are additive in their effects on outcomeeffects on outcome

Opportunity on avoiding, identifying & Opportunity on avoiding, identifying & treating-physiological derangements treating-physiological derangements

Insult Insult Mortality Mortality Significant relation Significant relation to grades within to grades within GOSGOS

Duration of Duration of hypotension hypotension (SBP< 90mm (SBP< 90mm Hg)Hg)

yesyes No No

Hypoxia (spOHypoxia (spO2 2

<90%)<90%) yesyes No No

Pyrexia>38deg Pyrexia>38deg CelsiusCelsius

yesyes No No

Intracranial Intracranial hypertension> hypertension> 30mm Hg30mm Hg

yesyes No No

Cerebral Cerebral perfusion perfusion pressure(pressure(CPP<5OmCPP<5Om

mHmHg)g)

yesyes No No

Monitoring Monitoring

A rational approach to select A rational approach to select monitoring modalities monitoring modalities

maintaining cerebral blood flow maintaining cerebral blood flow and oxygenationand oxygenation

Ischemia a consistent finding in head Ischemia a consistent finding in head injury injury

Monitoring systemic Monitoring systemic physiologyphysiology

ABP with measurement of ICPABP with measurement of ICP Placement of right atrial or Placement of right atrial or

pulmonary artery catheterpulmonary artery catheter Pulse oximetryPulse oximetry ABGABG Core temperatureCore temperature Blood sugar Blood sugar

Intracranial pressure Intracranial pressure monitoringmonitoring Normal resting ICP is 0 to 15 mm HgNormal resting ICP is 0 to 15 mm Hg Transient elevation (straining, coughing Transient elevation (straining, coughing

and and trendelenburg position) trendelenburg position)

>20 mm Hg >20 mm Hg moderate moderate >40 mm Hg >40 mm Hg severe severe

Intracranial HTN develops in 50% of Intracranial HTN develops in 50% of patients in coma patients in coma caused by severe head injury.caused by severe head injury.

50-75% after evacuation of an 50-75% after evacuation of an intracranial haematomaintracranial haematoma

postoperative haematomapostoperative haematoma

progressive swelling of focalprogressive swelling of focal

contusionscontusions

diffuse brain swellingdiffuse brain swelling

• Severe intracranial HTN can Severe intracranial HTN can result in result in

secondary injury to the brain, secondary injury to the brain, due to due to

ischemia produced by reducing ischemia produced by reducing CPP and it can also distort and CPP and it can also distort and compress the brainstem.compress the brainstem.

Measurement of Measurement of intracranial pressure in ICUintracranial pressure in ICU

• To treat intracranial HTN effectively.To treat intracranial HTN effectively.

• No reliable clinical indicators in No reliable clinical indicators in patients with head injury.patients with head injury.

• Symptoms of raised ICP are Symptoms of raised ICP are impossible to elicit in a comatose impossible to elicit in a comatose patients.patients.

• Papilledema is uncommon after head Papilledema is uncommon after head injury even in patients with injury even in patients with intracranial HTN. intracranial HTN.

INDICATIONS OF ICP INDICATIONS OF ICP MONITORINGMONITORING GCS<8 and abnormal CT scan GCS<8 and abnormal CT scan oror GCS<8 and normal CT scan but with adverse GCS<8 and normal CT scan but with adverse

featuresfeatures age>40yrsage>40yrs hypotensionhypotension decerebratedecerebrate Inability to monitor serial neurological Inability to monitor serial neurological

examinationsexaminations Treatment that increase ICP (PEEP)Treatment that increase ICP (PEEP)

ModalitiesModalities

Ventriculostomy cathetersVentriculostomy catheters

remains the preferred choice.remains the preferred choice.

allows treatment of elevated allows treatment of elevated ICP by intermittent drainage of CSF. ICP by intermittent drainage of CSF.

Microsensor transducerMicrosensor transducer

Fiberoptic transducerFiberoptic transducer

How long ?How long ?

As long as ICP remains elevatedAs long as ICP remains elevated

Active management of ICP Active management of ICP

For 3 days in the absence of For 3 days in the absence of significant significant

ICP elevationICP elevation

ComplicationsComplications

VentriculitisVentriculitis

Intracerebral hemorrhagesIntracerebral hemorrhages

contraindicationscontraindications severe coagulopathiessevere coagulopathies

Cerebral perfusion Cerebral perfusion monitoringmonitoringNormal cerebral blood flow is 54+12 Normal cerebral blood flow is 54+12

ml/100 g/min in adults and 1.06+0.03 ml/100 g/min in adults and 1.06+0.03 ml/100g/min in children.ml/100g/min in children.

Normal cerebral metabolic Normal cerebral metabolic rate(CMRO2) of oxygen is 1.5micro rate(CMRO2) of oxygen is 1.5micro mol/g/min.mol/g/min.

After head injury CMRO2 is reduced After head injury CMRO2 is reduced by approx 50% by approx 50%

Measurement of cerebral perfusion in the ICUCerebral perfusion pressureCerebral perfusion pressure simplest measuresimplest measure

MAP minus ICPMAP minus ICP

Normal lower limit of Normal lower limit of autoregulation for CPP is 50mm Hgautoregulation for CPP is 50mm Hg

Ability to auto regulate may be Ability to auto regulate may be impaired, CBF may decrease with CPP impaired, CBF may decrease with CPP values<50mm Hgvalues<50mm Hg

Assess only ischemia caused by Assess only ischemia caused by increased ICP or decreased BP increased ICP or decreased BP

•Transcranial Doppler Transcranial Doppler ultrasonography (TCD)ultrasonography (TCD)

Reduction in middle cerebral artery flow velocity-a useful marker

As ICP increases CPP decreases and highly pulsatile flow velocity pattern is seen.

Pulsatality index-describes waveform pattern

Cerebral vasospasm- TCD velocity.

•Cerebral blood flowCerebral blood flow Kety - Schmidt technique.Kety - Schmidt technique.

Inhaled Xenon techniqueInhaled Xenon technique

Both these methods are intermittent Both these methods are intermittent technique and requires the patient to be technique and requires the patient to be haemodynamically stablehaemodynamically stable

Thermal diffusion method Thermal diffusion method Laser doppler method Laser doppler method

•Jugular venous saturationJugular venous saturation

To monitor cerebral hypoxia and To monitor cerebral hypoxia and ischemiaischemia

Right jugular venous oximetry -to assess Right jugular venous oximetry -to assess the adequacy of CBF in head injurythe adequacy of CBF in head injury

Reductions in sjvo2 provide an useful Reductions in sjvo2 provide an useful marker of inadequate CBFmarker of inadequate CBF

Measured with a fiberoptic oxygen Measured with a fiberoptic oxygen saturation cathetersaturation catheter

Near infrared Near infrared spectroscopyspectroscopy

Measures cerebral oxygen Measures cerebral oxygen saturation.saturation.

Reflects changes in oxygenated, Reflects changes in oxygenated, deoxygenated and total hemoglobin.deoxygenated and total hemoglobin.

Absorbance of NIRS light by extra Absorbance of NIRS light by extra vascular blood vascular blood used to identify used to identify intracranial hematomasintracranial hematomas

Medical management of Medical management of head injuryhead injury

Surgical lesion should be ruled out Surgical lesion should be ruled out by CT scan wheneverby CT scan whenever

Unexpected severe intra cranial Unexpected severe intra cranial hypertension develops.hypertension develops.

When it is accompanied by When it is accompanied by neurological deterioration.neurological deterioration.

Refractory to medical management.Refractory to medical management.

General measuresGeneral measures

• Head elevation-Head elevation- elevating the head & elevating the head & keeping the head in neutral position keeping the head in neutral position have been standard practice for have been standard practice for management of ICP in past. management of ICP in past.

• Treatment of systemic Treatment of systemic hypertensionhypertension

common with head injury.common with head injury. SBP>DBP SBP>DBP Hyperdynamic state including Hyperdynamic state including

tachycardia & increased cardiac output.tachycardia & increased cardiac output. Autoregulation is impaired in Autoregulation is impaired in

severe head injury, systemic severe head injury, systemic hypertension may increase CBP & ICP hypertension may increase CBP & ICP and may exacerbate cerebral edemaand may exacerbate cerebral edema..

• Often resolves with sedation Often resolves with sedation

• Hydralazine & nitroprussideHydralazine & nitroprusside

• Beta & alpha blockers.Beta & alpha blockers.

Fever Fever common during recovery common during recovery

from head injury.from head injury.

potent cerebral vasodilator potent cerebral vasodilator & increase ICP and cerebral & increase ICP and cerebral metabolic requirements.metabolic requirements.

Prevention of seizures

Occurs early (<7 days) or late (>7 days) after head injury.

More common after 7 days.

Phenytoin & carbamazepine.

•Specific measuresSpecific measures

Target CPP values >60-70mmHgTarget CPP values >60-70mmHg..

Ventilatory support & use of Ventilatory support & use of hypocapnia for ICP reductionhypocapnia for ICP reduction

Patients with GCS<8Patients with GCS<8

HyperventilationHyperventilation Constricts cerebral blood vesselsConstricts cerebral blood vessels

Decreases CBV Decreases CBV

Decreases ICPDecreases ICP

• Accompanied by reduction in Accompanied by reduction in global cerebral blood flow.global cerebral blood flow.

• Hyperventilation has only short Hyperventilation has only short lived effectiveness in decreasing lived effectiveness in decreasing ICPICP

Neuromuscular blockade & Neuromuscular blockade & sedationsedation

Currently the subject is of debate.Currently the subject is of debate.Prevents rise in ICP produced by Prevents rise in ICP produced by

coughing & bucking on the tube.coughing & bucking on the tube.Increased respiratory Increased respiratory

complications.complications.Long term neuromuscular blockadeLong term neuromuscular blockade Continued paralysis.Continued paralysis. Acute myopathy.Acute myopathy.

Intravenous anesthetic agent preserve pressure auto regulation & cerebrovascular response to CO2

Barbiturates less commonly used now.

Propofol

Midazolam in combination with propofol & fentanyl.

Fluid therapy & feedingFluid therapy & feeding

Accurate fluid management may be complicated by continuing or concealed hemorrhage but every effort must be made to restore normovolemia & prevent hypertension.

By clinical & laboratory assessment of volume status and invasive hemodynamic monitoring.

30-40ml/ kg of maintenance 30-40ml/ kg of maintenance fluid per day.fluid per day.

Hypotonic & dextrose Hypotonic & dextrose containing fluids should be containing fluids should be avoided.avoided.

Increase in plasma oncotic Increase in plasma oncotic pressure in blood brain barrier pressure in blood brain barrier disruption.disruption.

Colloids effective.Colloids effective.

High nutritional requirements High nutritional requirements and feeding should be instituted and feeding should be instituted early (<24hrs)early (<24hrs)

Hyper osmolar therapyHyper osmolar therapy Mannitol traditionally used Mannitol traditionally used

to elevate plasma osmolarity & to to elevate plasma osmolarity & to decrease brain edema ( 20% decrease brain edema ( 20% solution)solution)

Reduces ICP by improving Reduces ICP by improving CPP & microcirculatory dynamics.CPP & microcirculatory dynamics.

Secondary increase in ICP Secondary increase in ICP when BBB is disrupted, fluid when BBB is disrupted, fluid overload and renal toxicity.overload and renal toxicity.

Cerebral metabolic Cerebral metabolic suppressantssuppressants

IV barbituratesIV barbiturates

cardiovascular cardiovascular depression depression

prolonged ICU stay prolonged ICU stay

pulmonary infectionpulmonary infection Excitatory amino acid antagonist Calcium channel blockers( Nimodipine) Antioxidants Corticosteroids Hypothermia

ReferencesReferences

• Text book of Neuroanaesthesia & Text book of Neuroanaesthesia & critical care, 1critical care, 1stst edition. edition.

• Anaesthesia & neurosurgery, Anaesthesia & neurosurgery, Cotrel, 2005 edition.Cotrel, 2005 edition.