Neurologic and Neurosurgical Emergencies in the ICU Division of Critical Care Medicine University of...

Neurologic and Neurologic and Neurosurgical Emergencies Neurosurgical Emergencies

in the ICUin the ICU

Division of Critical Care Division of Critical Care MedicineMedicine

University of AlbertaUniversity of Alberta

OverviewOverview

• Altered consciousness and comaAltered consciousness and coma• Increased intracranial pressureIncreased intracranial pressure• Neurogenic respiratory failureNeurogenic respiratory failure• Status epilepticusStatus epilepticus• Acute stroke interventionAcute stroke intervention• Intracerebral hemorrhageIntracerebral hemorrhage• Subarachnoid hemorrhageSubarachnoid hemorrhage• Head traumaHead trauma• Spinal cord injurySpinal cord injury

Altered Consciousness and ComaAltered Consciousness and Coma

• Consciousness requires arousal (coming from the Consciousness requires arousal (coming from the brainstem reticular formation) and content (the brainstem reticular formation) and content (the cerebral hemispheres)cerebral hemispheres)

• Alterations in consciousness stem from:Alterations in consciousness stem from:• Disorders affecting the reticular formationDisorders affecting the reticular formation• Disorders affecting both cerebral hemispheresDisorders affecting both cerebral hemispheres• Disorders affecting the connections between the brainstem Disorders affecting the connections between the brainstem

and the hemispheresand the hemispheres


• DefinitionsDefinitions• DeliriumDelirium: classically, altered awareness with motor and : classically, altered awareness with motor and

sympathetic hyperactivity, often with sleeplessness, sympathetic hyperactivity, often with sleeplessness, hallucinations, and delusionshallucinations, and delusions

• More recently used to describe any acute change in More recently used to describe any acute change in consciousness short of coma, as a synonym for consciousness short of coma, as a synonym for encephalopathyencephalopathy

• ObtundationObtundation: the patient appears to sleep much of the : the patient appears to sleep much of the day but has some spontaneous arousalsday but has some spontaneous arousals

• StuporStupor: the patient lies motionless unless aroused but : the patient lies motionless unless aroused but will awaken with stimulation; localizes or withdraws from will awaken with stimulation; localizes or withdraws from noxious stimulinoxious stimuli

• ComaComa: the patient makes no understandable response to : the patient makes no understandable response to stimulation but may display abnormal flexor stimulation but may display abnormal flexor (decorticate) or extensor (decerebrate) posturing.(decorticate) or extensor (decerebrate) posturing.


• Examining the patient with altered consciousness:Examining the patient with altered consciousness:• ABCs - insure adequate oxygenation and blood pressure before ABCs - insure adequate oxygenation and blood pressure before

proceedingproceeding• Be certain that the blood glucose is at least normalBe certain that the blood glucose is at least normal• If there is any reason to suspect thiamine deficiency, If there is any reason to suspect thiamine deficiency,

administer 100 mg thiamine IV administer 100 mg thiamine IV • The purpose of the coma examination is to determine The purpose of the coma examination is to determine

whether the upper brainstem is functioning.whether the upper brainstem is functioning.• Brainstem dysfunction means immediate imaging.Brainstem dysfunction means immediate imaging.• Bilateral hemispheral dysfunction leads initially to metabolic or Bilateral hemispheral dysfunction leads initially to metabolic or

toxic diagnoses.toxic diagnoses.

• Four domains to examine:Four domains to examine:• Pupillary responsesPupillary responses• Extraocular movementsExtraocular movements• Respiratory patternRespiratory pattern• Motor responsesMotor responses

Parasympatheticcontrol of pupil size

Sympatheticcontrol of pupil size

III III

VI VI

VIII VIII

MLF

Neck stretch receptors

-+

Control of Horizontal Eye MovementsControl of Horizontal Eye Movements

Assessing Eye MovementsAssessing Eye Movements

• Spontaneous horizontal conjugate eye movements Spontaneous horizontal conjugate eye movements prove that the brainstem centers for eye prove that the brainstem centers for eye movement are intact.movement are intact.• These overlap the portion of the reticular formation These overlap the portion of the reticular formation

necessary for consciousness.necessary for consciousness.• Therefore, coma in a patient with roving horizontal Therefore, coma in a patient with roving horizontal

conjugate eye movements is not due to brainstem conjugate eye movements is not due to brainstem dysfunction. If there are no spontaneous eye dysfunction. If there are no spontaneous eye movements, attempt to trigger them.movements, attempt to trigger them.

• In the absence of cervical spine disease, test In the absence of cervical spine disease, test cervico-ocular reflexes (“dolls’ eyes”):cervico-ocular reflexes (“dolls’ eyes”):• Turning the head to the right should cause the eyes to go Turning the head to the right should cause the eyes to go

left, and vice versa.left, and vice versa.• Same meaning as spontaneous movements regarding Same meaning as spontaneous movements regarding

the brain stemthe brain stem• Partial responses mean a problem involving the Partial responses mean a problem involving the

brainstem or cranial nerves.brainstem or cranial nerves.

Assessing Eye MovementsAssessing Eye Movements

• Vestibulo-ocular testing (“cold calorics”)Vestibulo-ocular testing (“cold calorics”)• Check for tympanic membrane perforation firstCheck for tympanic membrane perforation first• 50 - 60 mL ice water in one extra-ocular canal using soft tubing (e.g., from a 50 - 60 mL ice water in one extra-ocular canal using soft tubing (e.g., from a

butterfly; do not use an IV catheter, which can penetrate the tympanic butterfly; do not use an IV catheter, which can penetrate the tympanic membrane)membrane)

• Tonic deviation of both eyes toward cold ear indicates intact brainstem Tonic deviation of both eyes toward cold ear indicates intact brainstem function.function.

• Wait for one ear to warm up before testing the other ear.Wait for one ear to warm up before testing the other ear.• Nystagmus away from the cold ear is due to cortical correction of the Nystagmus away from the cold ear is due to cortical correction of the

brainstem-induced eye movement and means the patient is not comatose.brainstem-induced eye movement and means the patient is not comatose.

Respiratory Patterns in ComaRespiratory Patterns in Coma

• Cheyne – Stokes respiration: bilateral hemispheral dysfunction Cheyne – Stokes respiration: bilateral hemispheral dysfunction or congestive heart failureor congestive heart failure

• Central reflex hyperpnea: midbrain dysfunction causing Central reflex hyperpnea: midbrain dysfunction causing neurogenic pulmonary edemaneurogenic pulmonary edema• rarely see true central neurogenic hyperventilation with this lesion; central rarely see true central neurogenic hyperventilation with this lesion; central

hyperventilation is common with increased ICPhyperventilation is common with increased ICP

• Apneustic respiration (inspiratory cramp lasting up to 30 sec): Apneustic respiration (inspiratory cramp lasting up to 30 sec): pontine lesionpontine lesion

• Cluster breathing (Biot breathing): pontine lesionCluster breathing (Biot breathing): pontine lesion• Ataxic respiration: pontomedullary junction lesionAtaxic respiration: pontomedullary junction lesion

Motor ResponsesMotor Responses

• Defensive, avoidance, or withdrawal - indicative of cortical Defensive, avoidance, or withdrawal - indicative of cortical function (the patient is not comatose)function (the patient is not comatose)

• Flexor (decorticate) posturing - the cortex is not in control Flexor (decorticate) posturing - the cortex is not in control of the spinal cord, but the midbrain (red nucleus) isof the spinal cord, but the midbrain (red nucleus) is

• Extensor (decerebrate) posturing - the midbrain is not in Extensor (decerebrate) posturing - the midbrain is not in control but the pontomedullary region (vestibular nuclei) iscontrol but the pontomedullary region (vestibular nuclei) is

• Going from flexion to extension indicates worsening; Going from flexion to extension indicates worsening; extension to flexion, improvementextension to flexion, improvement

Increased Intracranial PressureIncreased Intracranial Pressure

• The volume of the skull is a constant (Monro-Kellie The volume of the skull is a constant (Monro-Kellie hypothesis) which contains:hypothesis) which contains:• BrainBrain• BloodBlood• CSFCSF

• An increase in the volume of any of these or the An increase in the volume of any of these or the introduction of alien tissue (e.g., tumor) will raise ICP.introduction of alien tissue (e.g., tumor) will raise ICP.

• Initially, the ICP rises slowly as volume is added (CSF and Initially, the ICP rises slowly as volume is added (CSF and then blood exits the skull) then blood exits the skull)

• But as the volume increases to rise, compliance worsens But as the volume increases to rise, compliance worsens and the pressure rises rapidly:and the pressure rises rapidly:• This impairs arterial blood flow, producing ischemiaThis impairs arterial blood flow, producing ischemia• Focal increases in volume also cause herniation from Focal increases in volume also cause herniation from

high pressure compartments to lower pressure oneshigh pressure compartments to lower pressure ones

Rosner View of Cerebral Blood FlowRosner View of Cerebral Blood Flow

Intact Auto-regulationIntact Auto-regulation

Defective Auto-regulationDefective Auto-regulation


• The standard theory of coma due to rostro-caudal The standard theory of coma due to rostro-caudal brainstem movement has been supplanted by brainstem movement has been supplanted by Ropper’s lateral shift theory.Ropper’s lateral shift theory.

• Shift is often heralded by a third cranial nerve palsy Shift is often heralded by a third cranial nerve palsy (usually causing a dilated pupil before failure of extra-(usually causing a dilated pupil before failure of extra-ocular movements).ocular movements).

HerniationHerniation

Standard ModelStandard Model

diencephalon

midbrain

ponstemporal lobe

uncus

midline

Inferred force vectorcausing transtentorial

herniation

Standard ModelStandard Model

midbrain

temporal lobe

uncus

thirdcranialnerves

cavernous sinuses

third nerve palsyfrom compression

cistern obliterated

Current ModelCurrent Model

diencephalon

midbrain

pons

temporal lobe

uncus

midline

Force vector displacingdiencephalon laterally

cistern widened

Current ModelCurrent Model

temporal lobe

uncus

thirdcranialnerves

cavernous sinuses

third nerve palsyfrom stretch

cistern widened

midline

Glasgow Coma ScaleGlasgow Coma Scale

• Best Eye Response. (4) Best Eye Response. (4) 1.1. No eye opening. No eye opening. 2.2. Eye opening to pain. Eye opening to pain. 3.3. Eye opening to verbal command. Eye opening to verbal command. 4.4. Eyes open spontaneously.Eyes open spontaneously.

• Best Verbal Response. (5) Best Verbal Response. (5) 1.1. No verbal response No verbal response 2.2. Incomprehensible sounds. Incomprehensible sounds. 3.3. Inappropriate words. Inappropriate words. 4.4. Confused Confused 5.5. Orientated Orientated

• Best Motor Response. (6)Best Motor Response. (6) 1.1. No motor response. No motor response. 2.2. Extension to pain. Extension to pain. 3.3. Flexion to pain. Flexion to pain. 4.4. Withdrawal from pain. Withdrawal from pain. 5.5. Localizing pain. Localizing pain. 6.6. Obeys CommandsObeys Commands


• PlanningPlanning• Make plans to correct the underlying pathophysiology if Make plans to correct the underlying pathophysiology if

possible.possible.• Airway control and prevention of hypercapnea are Airway control and prevention of hypercapnea are

crucial:crucial:• When intubating patients with elevated ICP use thiopental, When intubating patients with elevated ICP use thiopental,

etomidate, or intravenous lidocaine to blunt the increase in etomidate, or intravenous lidocaine to blunt the increase in ICP associated with laryngoscopy and tube passage.ICP associated with laryngoscopy and tube passage.

• ICP monitoring usually needed to guide therapyICP monitoring usually needed to guide therapy• Posture and head positionPosture and head position

• Avoid jugular vein compressionAvoid jugular vein compression• Head should be in neutral positionHead should be in neutral position• Cervical collars should not be too tightCervical collars should not be too tight

• Elevation of the head and trunk may improve jugular Elevation of the head and trunk may improve jugular venous return.venous return.

• Zero the arterial pressure transducer at the ear, rather than Zero the arterial pressure transducer at the ear, rather than the heart, to measure the true cerebral perfusion pressure the heart, to measure the true cerebral perfusion pressure when the head is above the heart.when the head is above the heart.


• HyperventilationHyperventilation• PaCOPaCO22 < 35 mmHg works by decreasing blood flow < 35 mmHg works by decreasing blood flow

and should be reserved for emergency treatment and should be reserved for emergency treatment and only for brief periods.and only for brief periods.

• The major determinant of arteriolar caliber is the The major determinant of arteriolar caliber is the extracellular pH, not actually the PaCOextracellular pH, not actually the PaCO22, but this is the , but this is the parameter we can control.parameter we can control.

• Pharmacologic optionsPharmacologic options• Mannitol 0.25 gm/kg q4h (may need to increase dose Mannitol 0.25 gm/kg q4h (may need to increase dose

over time)over time)• Hypertonic saline (requires central line)Hypertonic saline (requires central line)

• -- 3%3%• -- 7.5%7.5%• -- 23.4% (30 mL over 10 min)23.4% (30 mL over 10 min)

• Steroids only for edema around tumors or abscesses Steroids only for edema around tumors or abscesses (not for use in trauma or cerebrovascular disease)(not for use in trauma or cerebrovascular disease)


• SedationSedation• Benzodiazepines and Propofol works by Benzodiazepines and Propofol works by

decreasing cerebral metabolic rate, which is decreasing cerebral metabolic rate, which is coupled to blood flowcoupled to blood flow

• Requires autoregulation, which often fails in Requires autoregulation, which often fails in patients with elevated ICPpatients with elevated ICP

• Often causes a drop in MAP, impairing cerebral Often causes a drop in MAP, impairing cerebral perfusion and thus requiring vasopressors perfusion and thus requiring vasopressors (e.g., norepinephrine)(e.g., norepinephrine)

• Neuromuscular junction blockadeNeuromuscular junction blockade• Titrate with train-of-four stimulator to 1 or 2 Titrate with train-of-four stimulator to 1 or 2

twitchestwitches• High-dose barbituratesHigh-dose barbiturates

• E.g., pentobarbital 5 – 12 mg/kg load followed E.g., pentobarbital 5 – 12 mg/kg load followed by infusion to control ICPby infusion to control ICP


• Surgical optionsSurgical options• Resect mass lesions if possibleResect mass lesions if possible• CraniectomyCraniectomy

• Lateral for focal lesionsLateral for focal lesions• Bifrontal (Kjellberg) for diffuse swellingBifrontal (Kjellberg) for diffuse swelling

Classification of Classification of Neurogenic Respiratory FailureNeurogenic Respiratory Failure

• Oxygenation failure (low PaOOxygenation failure (low PaO22))• primary difficulty with gas transportprimary difficulty with gas transport• usually reflects pulmonary parenchymal disease, V/Q usually reflects pulmonary parenchymal disease, V/Q

mismatch, or shuntingmismatch, or shunting

• Primary neurologic cause is neurogenic Primary neurologic cause is neurogenic pulmonary edema.pulmonary edema.• A state of increased lung water (interstitial and A state of increased lung water (interstitial and

sometimes alveolar):sometimes alveolar):• as a consequence of acute nervous system diseaseas a consequence of acute nervous system disease• in the absence of in the absence of

• cardiac disorders (CHF),cardiac disorders (CHF),• pulmonary disorders (ARDS), orpulmonary disorders (ARDS), or• hypervolemiahypervolemia

Causes of Neurogenic Pulmonary Causes of Neurogenic Pulmonary EdemaEdema

• CommonCommon

1.1. SAHSAH

2.2. head traumahead trauma

3.3. intracerebral intracerebral hemorrhagehemorrhage

4.4. seizures or status seizures or status epilepticusepilepticus

• RareRare1.1. medullary tumorsmedullary tumors

2.2. multiple sclerosismultiple sclerosis

3.3. spinal cord infarctionspinal cord infarction

4.4. Guillain-Barré Guillain-Barré syndromesyndrome

5.5. miscellaneous miscellaneous conditions causing conditions causing

6.6. intracranial intracranial hypertensionhypertension

7.7. many case reports of many case reports of other conditionsother conditions

Classification of Classification of Neurogenic Respiratory Failure Neurogenic Respiratory Failure

• Ventilatory failure (inadequate minute Ventilatory failure (inadequate minute ventilation [VE] for the volume of COventilation [VE] for the volume of CO22 produced):produced):• In central respiratory failure, the brainstem response to In central respiratory failure, the brainstem response to

COCO22 is inadequate, and the PaCO is inadequate, and the PaCO22 begins to rise early. begins to rise early.• In neuromuscular ventilatory failure, the tidal volume In neuromuscular ventilatory failure, the tidal volume

begins to fall, and the PaCObegins to fall, and the PaCO2 2 is initially normal (or low).is initially normal (or low).

• Most common causes are:Most common causes are:• Myasthenia gravisMyasthenia gravis• Guillain-Barré syndromeGuillain-Barré syndrome• Critical illness polyneuropathy, myopathyCritical illness polyneuropathy, myopathy• Cervical spine diseaseCervical spine disease

Management of Neurogenic Management of Neurogenic Ventilatory FailureVentilatory Failure

• Airway protection and mechanical ventilationAirway protection and mechanical ventilation• Don’t wait for the PaCODon’t wait for the PaCO22 to rise to rise

• Specific therapiesSpecific therapies• Myasthenia: IgIV, plasma exchangeMyasthenia: IgIV, plasma exchange• Guillain-Barré: plasma exchange, IgIVGuillain-Barré: plasma exchange, IgIV• Critical illness polyneuropathy, myopathy: timeCritical illness polyneuropathy, myopathy: time

Status EpilepticusStatus Epilepticus


• DefinitionDefinition• Typically diagnosed after 30 min of either:Typically diagnosed after 30 min of either:

• Continuous seizure activity Continuous seizure activity • Intermittent seizures without recovery betweenIntermittent seizures without recovery between

• Don’t wait for 30 min to treat:Don’t wait for 30 min to treat:• Seizures become more difficult to treat the longer they last.Seizures become more difficult to treat the longer they last.• More systemic complications occur (e.g., aspiration).More systemic complications occur (e.g., aspiration).• Most seizures end spontaneously within 7 min in adults and Most seizures end spontaneously within 7 min in adults and

12 min in children:12 min in children:• These are reasonable points to start treating to These are reasonable points to start treating to

terminate seizures in order to prevent the establishment terminate seizures in order to prevent the establishment of status.of status.

• Types of status epilepticus:Types of status epilepticus:• ConvulsiveConvulsive• NonconvulsiveNonconvulsive


• Initial treatmentInitial treatment• Lorazepam IV 0.1 mg/kgLorazepam IV 0.1 mg/kg• AlternativesAlternatives::

• Phenobarbital IV 20 mg/kgPhenobarbital IV 20 mg/kg• Valproate IV 20 - 30 mg/kgValproate IV 20 - 30 mg/kg

• If IV access cannot be establishedIf IV access cannot be established,,• Midazolam (buccal, nasal, IM)Midazolam (buccal, nasal, IM)

• Failure of the first drug given in adequate dosage Failure of the first drug given in adequate dosage constitutes refractory status.constitutes refractory status.


• Treatment of refractory status (RSE)Treatment of refractory status (RSE)• Midazolam 0.2 mg/kg loading dose with immediate Midazolam 0.2 mg/kg loading dose with immediate

infusion 0.1 – 2.0 mg/kg/hrinfusion 0.1 – 2.0 mg/kg/hr• Must have EEG monitoring and demonstrate seizure Must have EEG monitoring and demonstrate seizure

suppressionsuppression• After 12 hours free of seizures attempt to taperAfter 12 hours free of seizures attempt to taper• May need other drugs (e.g., phenytoin, phenobarbital ) to May need other drugs (e.g., phenytoin, phenobarbital ) to

prevent recurrenceprevent recurrence• Other options for RSEOther options for RSE

• PropofolPropofol• PentobarbitalPentobarbital

Acute StrokeAcute Stroke

Acute Stroke InterventionAcute Stroke Intervention

• Intravenous thrombolysis is indicated for patients with:Intravenous thrombolysis is indicated for patients with:• A clinical diagnosis of ischemic strokeA clinical diagnosis of ischemic stroke• A CT scan excluding intracerebral hemorrhageA CT scan excluding intracerebral hemorrhage• Onset of symptoms less than 3 hours before starting Onset of symptoms less than 3 hours before starting

treatmenttreatment• No contraindications (see ACLS text for list)No contraindications (see ACLS text for list)

• rt-PA 0.9 mg/kg (up to 90 mg)rt-PA 0.9 mg/kg (up to 90 mg)• 10% bolus, remainder over 60 min10% bolus, remainder over 60 min

• Between 3 and 6 hours, intra-arterial therapy may be Between 3 and 6 hours, intra-arterial therapy may be an optionan option

• No role for acute heparin in evolving or completed No role for acute heparin in evolving or completed strokestroke• May be needed later for secondary prevention in patients with May be needed later for secondary prevention in patients with

atrial fibrillationatrial fibrillation

Intracerebral HemorrhageIntracerebral Hemorrhage


• Hypertensive hemorrhages occur in the:Hypertensive hemorrhages occur in the:• PutamenPutamen• ThalamusThalamus• PonsPons• CerebellumCerebellum

• Patients with hemorrhages elsewhere, or without Patients with hemorrhages elsewhere, or without a history of hypertension, need to be worked up a history of hypertension, need to be worked up for underlying vascular lesions or a bleeding for underlying vascular lesions or a bleeding diathesis.diathesis.

• For supratentorial hemorrhage, the major For supratentorial hemorrhage, the major determinant of survival is hemorrhage volume:determinant of survival is hemorrhage volume:• < 30 mL usually survive< 30 mL usually survive• > 60 mL frequently die> 60 mL frequently die

• Patients with cerebellar hemorrhages often Patients with cerebellar hemorrhages often benefit from surgical evacuationbenefit from surgical evacuation• Proceed before cranial nerve findings develop.Proceed before cranial nerve findings develop.


• Management remains controversialManagement remains controversial• Airway controlAirway control• Lowering mean arterial pressure may limit hemorrhage Lowering mean arterial pressure may limit hemorrhage

growthgrowth• Correct coagulopathyCorrect coagulopathy• Recombinant factor VIIa under studyRecombinant factor VIIa under study• Surgical intervention not routinely usefulSurgical intervention not routinely useful

• May be helpful with superficial lesionsMay be helpful with superficial lesions

Subarachnoid HemorrhageSubarachnoid Hemorrhage

Subarachnoid HemorrhageSubarachnoid Hemorrhage

• Most commonly due to ruptured aneurysmMost commonly due to ruptured aneurysm

• Present with sudden headache, often diminished Present with sudden headache, often diminished consciousnessconsciousness• Focal findings suggest intracerebral hemorrhage, which Focal findings suggest intracerebral hemorrhage, which

may occur due to dissection of blood from the bleeding may occur due to dissection of blood from the bleeding aneurysm into the cortex.aneurysm into the cortex.

Current Management Strategies for Current Management Strategies for SAHSAH

• Early definitive aneurysm obliteration Early definitive aneurysm obliteration

• Induce hypertension and increase cardiac output Induce hypertension and increase cardiac output to treat vasospasmto treat vasospasm

• Nimodipine or nicardipine to relieve or Nimodipine or nicardipine to relieve or ameliorate the effects of vasospasmameliorate the effects of vasospasm

• Interventional neuroradiologic techniques (e.g., Interventional neuroradiologic techniques (e.g., angioplasty and intra-arterial verapamil or angioplasty and intra-arterial verapamil or nicardipine infusion) to treat vasospasm nicardipine infusion) to treat vasospasm

• Ventricular drainage to treat hydrocephalusVentricular drainage to treat hydrocephalus

Complications of Aneurysmal SAHComplications of Aneurysmal SAH

• RebleedingRebleeding

• Cerebral vasospasmCerebral vasospasm

• Volume disturbancesVolume disturbances

• Osmolar disturbancesOsmolar disturbances

• SeizuresSeizures

• Arrhythmias and other Arrhythmias and other cardiovascular cardiovascular complicationscomplications

• CNS infectionsCNS infections

• Other complications of Other complications of critical illnesscritical illness

Aneurysmal RebleedingAneurysmal Rebleeding

• Risk of rebleeding from unsecured aneurysms:Risk of rebleeding from unsecured aneurysms:• about 4% on the first post-bleed day about 4% on the first post-bleed day • about 1.5% per day up to day 28about 1.5% per day up to day 28

• Mortality of rebleeding following the diagnosis of Mortality of rebleeding following the diagnosis of SAH exceeds 75%. SAH exceeds 75%.

• Rebleeding is more frequent in:Rebleeding is more frequent in: • patients with higher grades of SAH patients with higher grades of SAH • womenwomen• those with systolic blood pressures over 170 mmHgthose with systolic blood pressures over 170 mmHg

Volume and Osmolar DisturbancesVolume and Osmolar Disturbances

• Reported in about 30% of SAH patients Reported in about 30% of SAH patients • Most common problem is cerebral salt wastingMost common problem is cerebral salt wasting

• SIADH should not be diagnosed in the period of risk for SIADH should not be diagnosed in the period of risk for vasospasm.vasospasm.

• Acute SAH patients should Acute SAH patients should nevernever be allowed to become be allowed to become volume depleted.volume depleted.

• The primary problem is excess of natriuretic factors, The primary problem is excess of natriuretic factors, with secondary water retention to attempt to maintain with secondary water retention to attempt to maintain volume (converse of SIADH).volume (converse of SIADH).

• Prophylaxis: maintain adequate salt intakeProphylaxis: maintain adequate salt intake• (e.g., 3L+ saline/d)(e.g., 3L+ saline/d)• some use mineralocorticoid supplementationsome use mineralocorticoid supplementation

• If hypo-osmolality occurs, need to increase the If hypo-osmolality occurs, need to increase the osmolality of the fluids administered to exceed osmolality of the fluids administered to exceed that of the urine excretedthat of the urine excreted• hypertonic saline (1.8% - 3%) as neededhypertonic saline (1.8% - 3%) as needed• some also give supplemental salt enterallysome also give supplemental salt enterally

Head TraumaHead Trauma

Secondary Injury in Head TraumaSecondary Injury in Head Trauma

• Hypoxia and hypotension are the 2 major causes of Hypoxia and hypotension are the 2 major causes of secondary CNS injury following head trauma.secondary CNS injury following head trauma.

• Even in the best intensive care units, these complications Even in the best intensive care units, these complications occur frequently.occur frequently.

• Preventing hypoxia and hypotension could have the Preventing hypoxia and hypotension could have the greatest effect of any currently available treatment for greatest effect of any currently available treatment for head trauma.head trauma.

Fluid Thresholds and Outcome from Fluid Thresholds and Outcome from Severe Brain InjurySevere Brain Injury

• Retrospective study (from the NIH multicenter Retrospective study (from the NIH multicenter hypothermia trial data) of the effect on GOS of ICP, hypothermia trial data) of the effect on GOS of ICP, MAP, CPP, and fluid balance at 6 months after injury MAP, CPP, and fluid balance at 6 months after injury

• Univariate predictors of poor outcome:Univariate predictors of poor outcome: • ICP > 25 mm HgICP > 25 mm Hg• MAP < 70 mm Hg or MAP < 70 mm Hg or • CPP < 60 mm Hg CPP < 60 mm Hg andand fluid balance < -594 mL fluid balance < -594 mL

• Conclusions: Conclusions: Exceeding thresholds of ICP, MAP, CPP, Exceeding thresholds of ICP, MAP, CPP, and fluid volume may be detrimental to severe and fluid volume may be detrimental to severe brain injury outcome.brain injury outcome.

• Fluid balance lower than -594 mL was associated Fluid balance lower than -594 mL was associated with an adverse effect on outcome, independent of with an adverse effect on outcome, independent of its relationship to intracranial pressure, mean its relationship to intracranial pressure, mean arterial pressure, or cerebral perfusion pressure.arterial pressure, or cerebral perfusion pressure.

Diffuse Axonal InjuryDiffuse Axonal Injury

• An active process triggered by the injury that An active process triggered by the injury that takes about 24 hours to develop in humanstakes about 24 hours to develop in humans

• May occur without any radiographic abnormalityMay occur without any radiographic abnormality

• Frequently seen in areas of radiographically Frequently seen in areas of radiographically apparent “shear injuryapparent “shear injury””• this latter finding usually occurs at the grey-white this latter finding usually occurs at the grey-white

junctionjunction

• Is a major cause of long-term disabilityIs a major cause of long-term disability

Management Management • Resuscitation and airway managementResuscitation and airway management

• avoid hypoxia and hypotensionavoid hypoxia and hypotension• concomitant cervical spine lesionsconcomitant cervical spine lesions• methods of intubationmethods of intubation

• orotracheal with inline stabilizationorotracheal with inline stabilization• no nasal tubes (tracheal or gastric)no nasal tubes (tracheal or gastric)

• fiberopticfiberoptic• posture and head positionposture and head position

• effects on ICP and CPPeffects on ICP and CPP

• Antiseizure drugsAntiseizure drugs• phenytoin 20 mg/kg phenytoin 20 mg/kg • only for the first week for patients without seizuresonly for the first week for patients without seizures

• Free radical scavengersFree radical scavengers• potential future therapiespotential future therapies

• Nutrition and GI bleeding prophylaxisNutrition and GI bleeding prophylaxis• Thromboembolism prophylaxisThromboembolism prophylaxis

Spinal Cord InjurySpinal Cord Injury

• Complete SCIComplete SCI• Loss of all function below the level of the lesionLoss of all function below the level of the lesion

• Typically associated with spinal shockTypically associated with spinal shock

• Incomplete SCIIncomplete SCI• Central cord syndromeCentral cord syndrome• Anterior cord syndromeAnterior cord syndrome• Brown-Sequard syndromeBrown-Sequard syndrome• Spinal cord injury without radiologic abnormality Spinal cord injury without radiologic abnormality

(SCIWORA)(SCIWORA)

Central Cord SyndromeCentral Cord Syndrome

• Typically results from an extension injuryTypically results from an extension injury• Greater impairment of upper than lower Greater impairment of upper than lower

extremity functionextremity function• Urinary retentionUrinary retention• Sparing of sacral sensationSparing of sacral sensation

Moderate

Marked

Anterior Cord SyndromeAnterior Cord Syndrome

• Due either toDue either to: : • Compression of the anterior portion of the cord by a Compression of the anterior portion of the cord by a

vertebral bodyvertebral body• Anterior spinal artery occlusionAnterior spinal artery occlusion

• Presents with preservation of dorsal column Presents with preservation of dorsal column function (vibration and position sense)function (vibration and position sense)

Brown-Sequard SyndromeBrown-Sequard Syndrome

• Hemisection of the cordHemisection of the cord

• Usually due to penetrating injuryUsually due to penetrating injury

Spinal Cord Injury Without Radiologic Spinal Cord Injury Without Radiologic Abnormality (SCIWORA)Abnormality (SCIWORA)

• No bony abnormalities on plain film or CTNo bony abnormalities on plain film or CT• MRI may show abnormalitiesMRI may show abnormalities

• Usually in children; symptoms may be transient Usually in children; symptoms may be transient at firstat first

• Should probably lead to immobilization to prevent Should probably lead to immobilization to prevent subsequent development of cord damagesubsequent development of cord damage

Secondary InjurySecondary Injury

• After the initial macroscopic injury, secondary After the initial macroscopic injury, secondary injuries are an important cause of disability:injuries are an important cause of disability:• Movement of unstable spineMovement of unstable spine• Vascular insufficiencyVascular insufficiency• Free radical induced damageFree radical induced damage

Neural Control of Blood Pressure and Neural Control of Blood Pressure and

Blood FlowBlood Flow

• Complete lesions above T1 will therefore eliminate all Complete lesions above T1 will therefore eliminate all sympathetic outflow.sympathetic outflow.

• Lesions between T1 and T6 will preserve sympathetic Lesions between T1 and T6 will preserve sympathetic tone in the head and upper extremities but deny it to tone in the head and upper extremities but deny it to the adrenals and the lower extremities.the adrenals and the lower extremities.

• Lesions between T6 and the lumbar cord will preserve Lesions between T6 and the lumbar cord will preserve adrenal innervation but denervate the lower adrenal innervation but denervate the lower extremities.extremities.

CNS Disturbances Affecting the CNS Disturbances Affecting the Cardiovascular SystemCardiovascular System

• ““Spinal” shockSpinal” shock• Actually refers to the acute loss of tendon reflexes and Actually refers to the acute loss of tendon reflexes and

muscle tone below the level of a spinal cord lesionmuscle tone below the level of a spinal cord lesion• However, neurogenic hypotension is very common and However, neurogenic hypotension is very common and

can be profound with spinal cord lesions above T1:can be profound with spinal cord lesions above T1:• In the series of Vale In the series of Vale et alet al, 40% of patients with complete , 40% of patients with complete

cervical spinal cord lesions were in neurogenic shock on cervical spinal cord lesions were in neurogenic shock on presentation.presentation.

• Hypotension in spinal shock is typically accompanied by Hypotension in spinal shock is typically accompanied by bradycardia, reflecting loss of cardiac sympathetic bradycardia, reflecting loss of cardiac sympathetic efferents and unopposed vagal tone:efferents and unopposed vagal tone:

• These patients are unable to mount a tachycardic response These patients are unable to mount a tachycardic response to volume depletion.to volume depletion.

• Because of their vasodilation they are warm, but may still Because of their vasodilation they are warm, but may still have elevated venous lactate concentrations.have elevated venous lactate concentrations.


• It is tempting to treat this hypotension with volume It is tempting to treat this hypotension with volume expansion, even if the patient is not volume depleted.expansion, even if the patient is not volume depleted.• Initially this is appropriate as venous return is frequently Initially this is appropriate as venous return is frequently

reduced. reduced. • However, this must be pursued cautiously.However, this must be pursued cautiously.

• If the patient is conscious, making urine, and the If the patient is conscious, making urine, and the venous lactate is decreasing, the MAP is probably venous lactate is decreasing, the MAP is probably adequate.adequate.

• Neurogenic pulmonary edema is common in patients Neurogenic pulmonary edema is common in patients with cervical spinal cord lesions, complicating their with cervical spinal cord lesions, complicating their management.management.

• These patients commonly develop pulmonary These patients commonly develop pulmonary vascular redistribution, interstitial edema, increased vascular redistribution, interstitial edema, increased AaDOAaDO22, and on occasional alveolar edema at PCWPs in , and on occasional alveolar edema at PCWPs in the 18 - 20 mmHg range:the 18 - 20 mmHg range:• May provide important clues to the mechanisms of NPEMay provide important clues to the mechanisms of NPE

Management of Cardiovascular Shock Management of Cardiovascular Shock After Spinal Cord InjuryAfter Spinal Cord Injury

• Always suspect associated injuries:Always suspect associated injuries:• Usual symptoms and physical findings may be absent Usual symptoms and physical findings may be absent

due to the spinal cord injury.due to the spinal cord injury.• Volume resuscitation cannot be guided solely by Volume resuscitation cannot be guided solely by

physical findings:physical findings:• Hypotension and bradycardia will persist regardless of Hypotension and bradycardia will persist regardless of

the volume of saline or colloid administered.the volume of saline or colloid administered.• Replace the missing adrenergic tone with Replace the missing adrenergic tone with --

agonists (phenylephrine or norepinephrine agonists (phenylephrine or norepinephrine depending on heart rate).depending on heart rate).

Spinal Perfusion Pressure Spinal Perfusion Pressure ManagementManagement

• Developed by analogy to cerebral perfusion Developed by analogy to cerebral perfusion pressure managementpressure management• Attempt to prevent cord ischemia by raising blood Attempt to prevent cord ischemia by raising blood

pressure.pressure.• Assumes that the same secondary injury mechanisms Assumes that the same secondary injury mechanisms

(hypotension and hypoxia) worsen the outcome from spinal (hypotension and hypoxia) worsen the outcome from spinal cord injury as in head injurycord injury as in head injury

• NASCIS II and III provide an inference that oxygen-derives NASCIS II and III provide an inference that oxygen-derives free radicals worsen outcome after spinal cord injury.free radicals worsen outcome after spinal cord injury.

• Maintained MAP > 85 mmHg using fluids, colloids, and Maintained MAP > 85 mmHg using fluids, colloids, and vasopressorsvasopressors

• 30% of patients with complete cervical injuries were able to 30% of patients with complete cervical injuries were able to walk at 1 year and 20% had regained bladder functionwalk at 1 year and 20% had regained bladder function


• Autonomic dysreflexia:Autonomic dysreflexia:• Patients with lesions above T5 may develop Patients with lesions above T5 may develop

hypertension and profuse sweating in response to a hypertension and profuse sweating in response to a distended viscus (usually the bladder).distended viscus (usually the bladder).

• Presumably represents adrenal release of Presumably represents adrenal release of catecholamines via spinal cord pathways not being catecholamines via spinal cord pathways not being controlled by brainstem centerscontrolled by brainstem centers

Neurogenic Ventilatory Disturbance Neurogenic Ventilatory Disturbance Syndromes: Spinal Cord DisordersSyndromes: Spinal Cord Disorders

• Lesions above or at C4Lesions above or at C4• Phrenic nerve failurePhrenic nerve failure

• Lesions between C4 – T6Lesions between C4 – T6• Loss of parasternal intercostal contraction causes chest Loss of parasternal intercostal contraction causes chest

wall to sink during inspiration, decreasing the tidal wall to sink during inspiration, decreasing the tidal volumevolume

• Loss of sympathetic innervation to the lungs can also Loss of sympathetic innervation to the lungs can also prompt bronchospasm (imbalance of parasympathetic prompt bronchospasm (imbalance of parasympathetic and sympathetic tone).and sympathetic tone).

ManagementManagement

• ABCsABCs• If intubation needed, use in-line stabilizationIf intubation needed, use in-line stabilization

• Direct laryngoscopy vs. fiberopticDirect laryngoscopy vs. fiberoptic• Maintain blood pressure with volume, packed RBCs, Maintain blood pressure with volume, packed RBCs,

vasopressors as neededvasopressors as needed

• Prevent secondary injuryPrevent secondary injury• Log-rollingLog-rolling

• Consider concomitant head injuryConsider concomitant head injury

DVT ProphylaxisDVT Prophylaxis

• StandardsStandards• Either:Either:

• LMW heparin, rotating bed, adjusted dose heparin LMW heparin, rotating bed, adjusted dose heparin (1.5 x control aPTT), or a combination of these, or(1.5 x control aPTT), or a combination of these, or

• Low-dose unfractionated heparin plus sequential Low-dose unfractionated heparin plus sequential compression devices or electrical stimulationcompression devices or electrical stimulation

• GuidelinesGuidelines• Low-dose unfractionated heparin alone is insufficient.Low-dose unfractionated heparin alone is insufficient.• Oral anticoagulation alone probably not indicatedOral anticoagulation alone probably not indicated

• OptionsOptions• 3-month duration of prophylaxis3-month duration of prophylaxis• Use IVC filters for patients failing anticoagulation or intolerant Use IVC filters for patients failing anticoagulation or intolerant

of itof it

SummarySummary

• Altered consciousness and comaAltered consciousness and coma• Increased intracranial pressureIncreased intracranial pressure• Neurogenic respiratory failureNeurogenic respiratory failure• Status epilepticusStatus epilepticus• Acute stroke interventionAcute stroke intervention• Intracerebral hemorrhageIntracerebral hemorrhage• Subarachnoid hemorrhageSubarachnoid hemorrhage• Head traumaHead trauma• Spinal cord injurySpinal cord injury

Neurologic and Neurosurgical Emergencies in the ICU Division of Critical Care Medicine University of...

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Transcript of Neurologic and Neurosurgical Emergencies in the ICU Division of Critical Care Medicine University of...