PIVOTAL ROLE IN CRITICAL CARE PIVOTAL ROLE IN CRITICAL CARE MANAGEMENTMANAGEMENT

RAISED INTRACRANIAL RAISED INTRACRANIAL PRESSUREPRESSURE

INTRODUCTIONINTRODUCTION What is intracranial pressure?What is intracranial pressure?

Pressure within the cranial cavity (within a Pressure within the cranial cavity (within a rigid structure) Skull /cranialvault exerted rigid structure) Skull /cranialvault exerted by the intracranial contentsby the intracranial contents.

Normal Intracranial PressureNormal Intracranial Pressure 5 – 15 mmHg in adult at rest5 – 15 mmHg in adult at rest <20mmHg usually in most In recumbent posture – 8mmHg or 110

mmH20 Zero in standing posture due to Zero in standing posture due to

transmission of CSF column to the lumbar transmission of CSF column to the lumbar region.region.

A View of CSFA View of CSF 110 0 function of CSF in mechanical one – water function of CSF in mechanical one – water

jacket.(1500gm of brain tissue jacket.(1500gm of brain tissue 50gm in 50gm in CSF)CSF)

Average intracranial volume is 1700ml Volume of brain is 1200-1400ml CSF Volume 70 – 160ml (104ml-mean) Spinal subarachanoid space 10-20ml of CSFSpinal subarachanoid space 10-20ml of CSF Average rate of CSF formation is

◦ 21-22 ml/hr ◦ 0.35ml/min◦ 500ml/day ◦ renewed 4 or 5 times daily

Main site of formation of CSF – choroid Main site of formation of CSF – choroid plexure floor of the lateral, third, fourth plexure floor of the lateral, third, fourth ventricleventricle

Blood brain barrier – is formed byBlood brain barrier – is formed by◦ Endothelium of the choroidal, brain capillaries ◦ Plasma membrane, adventitia of these vessels, Plasma membrane, adventitia of these vessels,

pericapillary foot processes of astrocytespericapillary foot processes of astrocytes◦ CSF has “sink action” Davson’s term◦ CSF third circulation by “WILLIAM HARVEY” CSF third circulation by “WILLIAM HARVEY”

(Blood, Lymph)(Blood, Lymph)

Raised ICPRaised ICP Part of compartmental syndrome Persistent elevation of > 20mmHg for Persistent elevation of > 20mmHg for

> 10min is raised ICP > 10min is raised ICP > 30mmHg – poor prognosis> 30mmHg – poor prognosis..

MONRO – KELLIE DOCTRINEMONRO – KELLIE DOCTRINE An increase in the volume of any one of

the three components brain, blood, CSF must be at the expense of the other two beyond the autoregulation.

Brain is least compressible among the Brain is least compressible among the three.three.

Cerebral blood flow is autoregulatedCerebral blood flow is autoregulated Autoregulation persist until cerebral Autoregulation persist until cerebral

prefusion pressure is in range of 60-160 prefusion pressure is in range of 60-160 mmHgmmHg

If CPP <60mmHg -- If CPP <60mmHg -- CBFCBF

CUSHING TRIADCUSHING TRIAD HypertensionHypertension BradycardiaBradycardia Irregular respirationIrregular respiration Later phenomenon of raised ICTLater phenomenon of raised ICT

Intracranial Pressure causesIntracranial Pressure causes Intracranial MassesIntracranial Masses Blockage of CSFBlockage of CSF HaemorrhageHaemorrhage Hypertensive encephalopahtyHypertensive encephalopahty Venous Sinus thrombosisVenous Sinus thrombosis HyperadrenalismHyperadrenalism Attitude sicknessAttitude sickness TetracyclineTetracycline Vit-A intoxicationVit-A intoxication

Cerebral or Extracerebral massCerebral or Extracerebral mass ◦ Tumor◦ Massive infraction with edema◦ Contusion◦ Parenchymal◦ SDH : EDH◦ Abscess

General Brain Swelling General Brain Swelling ◦ Anoxia, Acute hyponatremia◦ A hepatic failure◦ Hypertensive encephalopathy◦ Reye syndrome

Venous PressureVenous Pressure◦ Heart Failure◦ Obs. Of superior mediastinum Jugular veins◦ Cerebral vein thrombosis

Obstruction to flow and absorption of CSFObstruction to flow and absorption of CSF◦ Hydrocephalus◦ Meningitis – usual cause◦ If at absorption surface – the ventricles remain

normal in size. Volume of CSFVolume of CSF

◦ Meningits ; SAH CSF production CSF production

◦ Choroid plexus tumors◦ In children hydrocephalus

TYPES OF CEREBRAL EDEMATYPES OF CEREBRAL EDEMA CytotoxicCytotoxic

◦ Cerebral swelling cellular engorgement neuron, glia

◦ Is due to ischemia Vasogenic edemaVasogenic edema

◦ Accumalation of extracellular fluid◦ Defective BBB◦ Leaky capillaries◦ Seen in metastases, gliomas, meningiomas

Changes in CRANIUMChanges in CRANIUM Sub falcine hermation Sub falcine hermation

◦ Shift of cingulate gyrus of one hemisphere under the falxcerebri to contra lateral side.

◦ Septum pellucidum may shift from midline. Uncal HerniationUncal Herniation Tentorial – Mid brainTentorial – Mid brain Tonsillar – Foramen magnumTonsillar – Foramen magnum

CLINICAL FEATURESCLINICAL FEATURESHeadacheHeadache

Worse in early morning, lying down

Increased on coughing, straining, bending

Improves through the day, ambulation

Associated with vomiting

Relieved by analgesia

Dull acheOften mild

Reason : Reason : ◦ relative hypercarbic, hypoxia state during relative hypercarbic, hypoxia state during

sleep may be responsible for exacerbation sleep may be responsible for exacerbation on waking upon waking up

◦ Compression of pain sensitive vascular Compression of pain sensitive vascular structuresstructures

Clinical Signs of herniationBrain stem compression

Loss of pupillary activityImpairment of eye movementsHyperventilation Motor posturing flexion or extension

Herniation is often is rapidly fatal

Vomiting with / without NauseaVomiting with / without Nausea◦ Projectile◦ Due to irritation of the vagal nuclei in the floor

of fourth ventricle by the ICP◦ Relieves headache Temporarily

Double vision, Blurred visionDouble vision, Blurred vision◦ Due to III, VI CN palsies

Frontal Lobe Frontal Lobe ◦ Personality changes◦ Unsteadiness of gait◦ Incontinence of urine

Right side hemiplegia, garbled speech – Right side hemiplegia, garbled speech – dominant temporal lobedominant temporal lobe.

Lethargy, drowsiness Unconsciousness – COMAUnconsciousness – COMA Papilloedema – due to CSF shunted into

optic nerve sheaths, may be the only sign of increased CSF / increased ICP

Arterial hypertensionArterial hypertension FeverFever

InvestigationsInvestigations CT Scan with Contrast MRI with ContrastMRI with Contrast

◦ Except cerebral abscess Technetium brain scan – destructive skull Technetium brain scan – destructive skull

vault, skull base lesionsvault, skull base lesions EEG – Cerebral abscess, focal slow waves seenEEG – Cerebral abscess, focal slow waves seen Skull Film- not useful in hemispherical tumors Routine tests Routine tests Angiography, volumetric MRI Lumbarpuncture only after imaging Biopsy

SPECIFIC INVESTIGATIONSSPECIFIC INVESTIGATIONSInvasive intracranial pressure

monitoring Extradural <1%, baseline drift Subdural Intraparenchymal, accurate 1%, breakage Intraventricular can also be used for

drainage, increased inflammation rateCisternographyTransfontametryTranscranial doppler flow velocity

IMMEDIATE MEASURES IMMEDIATE MEASURES Rapidly effective areRapidly effective are

Elevate head end by 30-45Elevate head end by 30-4500 – straight – straight head position head position ◦ Head elevation - Head elevation - JVP, JVP, venous outflowvenous outflow◦ Sharp head angulation - avoidedSharp head angulation - avoided

Hyperventilation – Acute lowering of ICPHyperventilation – Acute lowering of ICP◦ 16-20 cycles / min (ventilated) / Ambu bag by 16-20 cycles / min (ventilated) / Ambu bag by

face maskface mask◦ Action < 30minAction < 30min◦ Diminishes in 1-3 hrDiminishes in 1-3 hr◦ Tapered over 6-12 hrTapered over 6-12 hr◦ Sudden cessationSudden cessation leads to increased ICPleads to increased ICP

Hyperventilation should be such that Hyperventilation should be such that PCoPCo22 < < 30mmHg30mmHg

If < 25mmHg – exacerbate cerebral If < 25mmHg – exacerbate cerebral ischemia by causing excessive ischemia by causing excessive vasoconstrictionvasoconstriction..

MannitolMannitol◦ Biphasic actionBiphasic action◦ ICP by cerebral dehydrating effectICP by cerebral dehydrating effect◦ RAPID infusion is imp.RAPID infusion is imp.◦ Brain volume – by osmotic gradientBrain volume – by osmotic gradient◦ Osmotic diuretic – free water clearanceOsmotic diuretic – free water clearance

20% mannitol 1g/kg loading dose20% mannitol 1g/kg loading dose Every 4-6hrs @ 0.25 – 0.5g/kgEvery 4-6hrs @ 0.25 – 0.5g/kg It should be given over 10minIt should be given over 10min Action in 10-20min lasts for 3-6 hrsAction in 10-20min lasts for 3-6 hrs

◦ Disadvantages:Disadvantages: Congestive cardiac failure – due to volume Congestive cardiac failure – due to volume

contractioncontraction Hypokalemia– serum electrolytes every 6hrsHypokalemia– serum electrolytes every 6hrs HyperosmolarityHyperosmolarity ATN ATN Sudden rebound increased ICPSudden rebound increased ICP Normal saline (0.9%) should be givenNormal saline (0.9%) should be given No action if > 315m osm/kg , maintain <300 or <280No action if > 315m osm/kg , maintain <300 or <280

Drainage of CSF Drainage of CSF ◦ 5-10ml of CSF to be removed5-10ml of CSF to be removed

Use of steroids Use of steroids ◦ Dexamethasone 4-6mg 6Dexamethasone 4-6mg 6thth Hrly Hrly

Neurosurgical proceduresCraniotomyVentriculostomyPlacement of ICP monitor

ICP monitorsVentricular monitors

External drainage can be doneHigh infection rateIncreased after 5 days

IntraparenchymalIt is fibroptic , acurate, 1% infectgion,

inflexible, BreakageEpiudural Transudes

Superficial to dura<1% infectionBaseline drift (>5-10mmHg)

Normal Intracranial Pressure 50-

200cmH2O (4-15mmHg)Jugular venous pressure is normally

principle determinant of ICP

Initially as volume is added to the intracranial space, minimal increase in pressure occurs – Highly compliant nature of intra cranial contents

As intracranial volume increases CSF is displaced

through foramen magnum blood is displaced from compressed brain tissue

Loss of compliance

Further increase in intracranial volume leads to

dramatic elevation of ICP

CEREBRL PERFUSION PRESSURE

Important determinant of CBFCPP = MABP – ICPIn presence of auto regulation, CBF is maintained

at a constant level across a wide range of CPP ( 50-150mmHg)

In presence of injury auto regulation impairedCBF directly proportional to CPPCPP should be maintain 70-120mmHg<70mmHg secondary hypoxic ischemic damage> 120mmHg break through hyperperfusion

ICP WAVEFORMSEffects of systemic arterial, venous

pressure on intracranial contentsInitial offered deflection systemic arterial

pressure wave two types

Lundberg A wavesPlateau waves – Dangerous elevation of ICP

20-80mmHg

Global HypokinesiaLundberg B waves

Less amplitude 20mmHg 1-5minutes Less Dangerous Marker of abnormal auto regulation

Respiration patternNo localizing value

Depressed inspiration - Severe ComaCheyne stokes respiration – Hyperventilation

& Apnea, Bihemispheric lesions, Metabolic encephalopathy, stable breathing pattern,

Doesnot imply impending respiratory arrest Hyperventilation – Systemic diseases ,

Meatabolic acidosi, Hepatic encephalopathy, Central neurogenic hyperventilation, CNS

Lymphoma, Brain stem damage

Localizing valueApneustic breathing – Prolonged inspirtory

phase, apnea – pontine damage Cluster breathing , shallow

hyperventilation, cerebellar damageAtaxic (biot’s ) breathing – irregular

choatic , medullary respiratory centre, apnea

What is Kernohans notch?What is lymphatic blood supply of brain?What is Queckenstedt test?Where is megalencephaly seen?What are late signs of late intracranial

pressure?Where is hyperventilation useful?

GENERALIZED TREATMENTGENERALIZED TREATMENT Sedation, Paralysis – needs intubation

◦ Morphine IV 2.5mg every hrlyMorphine IV 2.5mg every hrly◦ Fenatanyl IV 50mg/mlFenatanyl IV 50mg/ml

25-100mg IVP –rapid control25-100mg IVP –rapid control Infusion 4mg/250ml NS @ 5ml /hrInfusion 4mg/250ml NS @ 5ml /hr

◦ Propofol IV 10mg/ml – reversiblePropofol IV 10mg/ml – reversible 5-50mcg/kg/min5-50mcg/kg/min

BP management BP management ◦ if CPP > 120mmHgif CPP > 120mmHg◦ if ICP > 20mmHgif ICP > 20mmHg◦maintainmaintain CPP > 70mmHg by treatment of CPP > 70mmHg by treatment of

hypertensionhypertension◦ Labetalol IV 5mg/ml - Labetalol IV 5mg/ml - 1 1 1 blocker 20 – 80 1 blocker 20 – 80

mg every 10-20minutesmg every 10-20minutes◦ Nicardpine IV 25mg / 250 ml Ns @5ml /HrNicardpine IV 25mg / 250 ml Ns @5ml /Hr◦ Increase BP by Dopamine 800mg/500ml NS Increase BP by Dopamine 800mg/500ml NS

Seizures Seizures ◦ Iv.Phenytoin 25mg/min slowlyIv.Phenytoin 25mg/min slowly◦ Iv. Diazepam resp.depressionIv. Diazepam resp.depression◦ Iv.LorazepamIv.Lorazepam◦ TheopentalTheopental

FeverFever◦ Acetaminophem 650mg every 4hrlyAcetaminophem 650mg every 4hrly◦ Indomethacin 25 mg every 6hrlyIndomethacin 25 mg every 6hrly

Blood glucose – Between 70-140mg/dlBlood glucose – Between 70-140mg/dl NaNa++ > 140mmol/L > 140mmol/L Avoid fluid overload, dehydrationAvoid fluid overload, dehydration High caloric feeds High caloric feeds Hyperosmolar isovolemia neededHyperosmolar isovolemia needed Foley’s catheterFoley’s catheter

SPECIFIC TREATMENTSPECIFIC TREATMENT Decompressive surgeryDecompressive surgery

◦ Removal of temporal bone on non dominent side Removal of temporal bone on non dominent side acouste neuromaacouste neuroma

ChemotherapyChemotherapy DiureticsDiuretics Pentobarbital coma – refractory casesPentobarbital coma – refractory cases

- may cause - may cause hypotension hypotension

- 10 -20mg /kg flaccid - 10 -20mg /kg flaccid comacoma

- EEG every 24-48hrs- EEG every 24-48hrs HemicraniectomyHemicraniectomy

PROGNOSISPROGNOSIS

◦ Poor Prognosis – CPP < 60mmHg > 20minPoor Prognosis – CPP < 60mmHg > 20min◦ Refractory to Pentobarbital coma◦ Motor response – to pain is imp prognostic Motor response – to pain is imp prognostic

sign flexor responsesign flexor response

Idiopathic Intracranial HypertensionIdiopathic Intracranial Hypertension

Pseudo tumor cerebriPseudo tumor cerebri Marked papilloedemaMarked papilloedema No increased ventricular sizeNo increased ventricular size Obese young womenObese young women Headache, visual blurringHeadache, visual blurring VI cranial nerve palsyVI cranial nerve palsy CSF Pressure increasedCSF Pressure increased Imaging is normalImaging is normal It is due to decreased absorption of CSFIt is due to decreased absorption of CSF Treatment Treatment

◦ Steroids , Acetazolamide, shuntingSteroids , Acetazolamide, shunting

Normal Pressure HydrocephalusEnlarged cerebral ventriclesNo cortical atrophyDementiaUrinary incontinence gait apraxiaCSF pressure NormalTreatment

LumbarpunctureSudden increase in pressure on infusion of

normal saline shunt

ICP WAVES Lundberg A waves (Plateau waves)

Dangerous elevation of ICP20 – 80 mmHg5min -1hr in durationAssociated with 60mmHg CPP

Lundberg B waves 10 – 20 mmHg1 – 5 minLess dangerousIntracranial compliance

A – PathologicB – ArterialC - Respiratory

Step wise approachICP Monitor ventriculostomy versus

parenchymalGoals

ICP < 20mmHgCPP > 60mmHg

ICP > 20-25mmHg for > 5minDrain CSF via ventriculostomy (If in

place)Elevate head end of bed –midline head

position

Maintain (serum osmolality < 320mosml)GlucocorticoidsSedationParalysisHyperventilationPressor therapy

Refractory Cases

Phentobarb comaHypothermiaHyperventilationHemicraniectomy

Headings Defination Normal Values Brief descripation of CSF Autoregulation of CBF Evaluation of raised ICP Monas Kellie Doctrine Cushing Traid Changes in ICP Changes in Cranium Types of Cerebral Edema Causes Clinical features Investigations Teatment ProtocolN.Pressure hydrocephalus Idiopathic intracranial HTN Prognosis

References Harrison's Principles of Internal Medicine 18th edi. Adam and Uietor’s Principles of Neurology 7th edi. Cecil text book of Medicine 22nd edi. On call neurology – Marshall , meych Neurology investigations – Hugher Kumar and clarck clinical medicine – 5th edi. Oxford prionciples of critical card API text book of medicine – 8th edi. Davidson & Principles , practice of Medicine 20th edi. Bailey and Love – 25th edi. Klashmigton manual of clinical therapeutics Youtube.com Newscience.com

Thanks to Dr.John Israel Prof & Head of Medicine

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