american society of neuroimaging 34th annual meeting

1/8/2012

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American Society of Neuroimaging 35th Annual Meeting


Neurosonology Value in the Neuro-

Critical Care Unit (NCCU)

Alex Razumovsky, PhD, FAHA

Director

Sentient NeuroCare Services, Inc.



DISCLOSURES

FTE, Private Practice for profit


Daily TCD

Continuous EEG

ICP monitoring

Pb02

CBF


Multimodal Monitoring:

Vasospasm/Ischemia/high ICP Detection

• MAP

• SaO2

• ECG

• Et-CO2

• CVP

• Urine output

• ICP

• CBFV/TCD PbO2

cEEG

CT/MR Perfusion

The primary goal of

management for

TBI is the

prevention of

secondary damage

due to neuronal

hypoxia and

hypoperfusion

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Specific TCD Applications for NCCU

• Vasospasm diagnosis after SAH

• Vasospasm monitoring after SAH

• Vasospasm treatment effect after SAH

• Vasospasm diagnosis and monitoring after tumor resection

• Acute stroke diagnosis/monitoring

• PFO screening in acute stroke patients

• Evaluation of patients after CEA

• Neuroradiology test-occlusion (pre, during and post)

• Neuroradiology stenting (pre, during and post)

• Pre- and Post-treatment AVM evaluation

• Intracranial Hypertension and Brain Death


Multimodality Monitoring

• Clinical (Neurological)

• Anatomical (Angiography, MRI/MRA,

CT/CTA)

• Neurophysiological (EEG, EP, BAER)

• Hemodynamic Neuromonitoring (MAP,

ICP, CPP, CBF/CBFV)

• Metabolic (EtCO2, PaCO2, SaO2, SjO2)


Multimodality Monitoring

Classical parameters

• MAP

• ICP

• CPP

• SjvO2

• PtiO2

• PaCO2

• CBF/CBFV

New exp. parameters

• Parenchymal glucose,

lactate, glycerol, and

glutamate

• Brain temperature

• S-100B protein and NSE

• CtiBF (Thermodilution)

• Local CBF (LDF)

• rSO2 (NIRS)

• Interstitial local pH&pCO2


TCD AND VASOSPASM AFTER SAH

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Pathophysiological Alterations

following Aneurysmal SAH

• Intracerebral & Intraventricular Hemorrhage

• Hydrocephalus

• Cerebral edema

• Seizures & Seizure-like Activity

• Alteration in Respiratory Function

• Effect on the Heart

• Fluid and Electrolyte Disturbance

• Cerebral ischemia


Vasospasm and Cerebral Ischemia

• Although there are medical therapies for

vasospasm after SAH, early detection of

vasospasm and initiation of aggressive medical

therapy is of utmost importance to avoid

delayed neurological ischemia, morbidity, and

mortality


CEREBRAL VASOSPASM AND

ITS CLINICAL SIGNIFICANCE


Cerebral Vasospasm

• Some substances (numerous neurotransmitters, blood constituents or breakdown products, and autocoids) released at the time of SAH acts on smooth muscle wall to cause vasoconstriction

• Morphological changes of the arterial wall consistent with vasonecrosis or vasculopathy

• Mechanical compression may also result in vessels constriction

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Vasospasm mechanisms Leung, Stroke, 2002

Macdonald, NeurosurgRev, 2006

Blood breakdown products:

• ApolipoproteinE genotype

Immunomodulatory, neurotoxic, oxidative effects

APOE4 less effective than APOE3 in suppressing neurotoxicity

• Endothelin1 release from CSF leukocytes

Potent vasoconsrictor

Synergistic effect in vasoconstriction between

• APOE and Endothelin1


Double-hit model of delayed ischemic neurological deficits after SAH

based on Dreier et al. The two hits on the brain parenchyma consist of

acutely triggered microvascular spasm in response to spreading

depolarizations, superimposed on chronic vasospasm


Early Brain Injury Sehba F, 2011


Early Brain Injury and Potential Therapy Sehba F, 2011

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Clinical Features of Symptomatic

Vasospasm

• Variable clinical course

• Usually peaks at 7-10 days following SAH

• Usually gradually evolves with waxing and

waning symptoms

• New HA, seizures, or decreased alertness

• New focal neurological signs -

MCA/ACA/border zone


Cerebral Vasospasm and Delayed Ischemic Deficit

Dorsch et al., 1994

• Literature review of more than 30 000 cases

• Angiographic vasospasm occurred in 43.3% (range

19% - 97%)

• DID occurred in 32.3% (range 5%-90%)

• Outcome of DID:

- Death in 30.3%

- Permanent deficit in 34%

- Good outcome in 35.7%


A clinical review of cerebral vasospasm and delayed

ischaemia following aneurysm rupture Dorsch N, 2011

• Online and physical searches have been made of the relevant literature.

• The incidence of delayed ischemic deficit (DID) or symptomatic vasospasm

reported in 1994 was 32.5% in over 30,000 reported cases. In recent years, 1994-

2009, it was 6,775/23,806, or 28.5%.

• Many of the recent reports did not specify whether a calcium antagonist was used

routinely, and when this was stated (usually nimodipine or nicardipine), DID was

noted in 22.0% of 10,739 reported patients.

• The outcome of DID in the earlier survey was a death rate of 31.6%, with

favorable outcomes in 36.2%. In recent reports, though with fewer than 1,000

patients, the outcome is possibly better, with death in 25.6% and good outcome in

54.1%.

• It thus appears likely that delayed vasospasm is still common but less so, and that

the overall outcome has improved. This may be due to the more widespread use of

calcium antagonists and more effective fluid management.


TCD DIAGNOSIS OF

VASOSPASM

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CBF vs. CBFV

• 133Xe

• Stable xenon-enhanced CT

• MRI/MRA

• CT/CTA

• PET

• SPECT

• The time, expense, and complexity of these

techniques still limits its use in routine clinical

practice American Society of Neuroimaging 35th Annual Meeting

TCD Diagnosis of Vasospasm

Newell et al., 1993


Diagnosis and Monitoring of

Vasospasm: ANGIOGRAPHY

• Degree of angiographic vasospasm does not

always correlate with the clinical condition.

Some patients remain asymptomatic with

severe vasospasm demonstrated by

angiography

• Incidence of angiographic vasospasm is nearly

twice that of DID


Diagnosis and Monitoring of

Vasospasm: TCD

• High CBFV can identify patients at higher risk

for developing DID, but also may occur in

asymptomatic patients

• Neurologist/Neurointensivist must determine

whether the severity and location of the vessel

narrowing/high CBFV are appropriate to cause

the clinical deficit

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Transcranial Doppler in cerebral vasospasm Newell et al., 1990

MCA CBFV ≥ 120 cm/s 25% narrowing

MCA CBFV ≥ 140 cm/s 25-50% narrowing

MCA CBFV ≥ 200 cm/s 50% narrowing

TCD DSA


TCD Criteria for diagnosis of vasospasm

Mean CBFV MCA/ICA ratio Interpretation

(cm/s) (Lindegaard Ratio)

<100 < 3 Nonspecific

100-139 3-6 Mild

140-199 3-6 Moderate

>200 >6 Severe


TCD and vasospasm after SAH

• Currently, the gold standard for VSP diagnosis is cerebral angiography, replaceable by CTA, only when angiography is not available. Obviously, it is not feasible to perform such investigation as frequently as bedside clinical assessment.

• Repeated clinical assessments of a patient's neurological status carry the problem of detecting the clinical signs and symptoms of VSP, which occur only after VSP has already manifested its deleterious effects on the cerebral parenchyma.

• TCD is a non-invasive, non-expensive and sensitive modality allowing for bedside monitoring to determine CBFV’s indicative of changes in vascular diameter


TCD and vasospasm after SAH

• TCD can be useful pre-, intra- and post-operatively, while helping to recognize the development of cerebral VSP before the onset of its clinical effects

• VSP following SAH is a very important source of morbidity and mortality. Too often, the first sign is a neurologic deficit, which may be too late to reverse

• TCD assists in the clinical decision-making regarding further diagnostic evaluation and therapeutic interventions.

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Guidelines for the Management of

Aneurysmal SAH Stroke Council, AHA, 1994

• Summary and Recommendations: 1. SAH is a medical emergency…

2. CT scanning for suspected SAH is strongly

recommended…

3. Selective cerebral angiography to document...

4. TCD is recommended for the diagnosis and

monitoring of VSP, although the cerebral

angiography may be required for definitive

diagnosis


Prediction of symptomatic VSP after

SAH with TCD

• An early CBFV increase

(Seiler et al., 1988)

• A rapid CBFV increase in

the first 6 days (Grote et

al., 1988)

• A CBFV increase of at

least 50 cm/sec during 24

hours (Grosset et al.,

1993)

• A CBFV increase of 50 cm/sec during 48 hours (Wardlow et al., 1998)

• Relative changes in CBFV’s (two or threefold CBFV increase) in patients with aneurysmal SAH correlated better with clinically significant VSP than absolute CBFV’s (Naval et al,

2005)


SAH Pt 1

Day 1

Rt MCA (M1 segm); 60 cm/s Lt MCA (M1 segm); 64 cm/s

Day 3

Rt MCA; 100 cm/s Lt MCA; 110 cm/s


SAH Pt 1

Day 8

Rt MCA (M1 segm); 212 cm/s Lt MCA (M1 segm); 230 cm/s

Day 15


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SAH. Pt 2

Day 5

Lt MCA; 126 cm/s Rt MCA; 88 cm/s

Day 6



SAH. Pt 2

Day 7



SAH. Pt. 3

Day 3


Day 4



SAH. Pt 3

Day 5


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Role of TCD: VSP Diagnosis

• Elevated CBFV’s in asymptomatic patients warrant

meticulous observation in some closely supervised

setting until CBFV’s begin trend downward

• Elevated CBFV’s in a particular vascular territory can

focus subsequent neurologic examinations to detect

subtle changes earlier in their clinical course


Role of TCD: VSP Diagnosis

• In symptomatic patients, elevated CBFV’s most

likely represent significant vessel narrowing and

may obviate the need for cerebral angiography. At

this point, triple-H therapy can be initiated or

advanced

• Asymptomatic patients without elevated CBFV’s

probably can avoid additional angiography.

However, we need to consider patient’s age

because elderly patient’s could develop VSP in

normal or slightly abnormal CBFV range


2011 AHA/ASA Metrics for Measuring

Quality of Care in Comprehensive Stroke

Centers

• Among different measures for Comprehensive

Stroke Centers is:

Median frequency of noninvasive monitoring

for surveillance for vasospasm in patients with

aneurysmal SAH during the period between

three and 14 days after SAH


TCD AND VASOSPASM AFTER TBI

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TBI

• Every 21 seconds, one person

in the US sustains traumatic

brain injury (TBI)

• An estimated 5.3 million

Americans – little more than

2% of the US population –

currently live with disabilities

resulting from brain injury

• Each year, 80,000 Americans

experience the onset of long-

term disability following TBI

• Okie, NEJM, 2005: Among

surviving soldiers wounded in

combat in Iraq and Afghanistan,

TBI appears to account for a

larger proportion of casualties

than it has in other recent U.S.

wars. According to the Joint

Theater Trauma Registry, 22%

had injuries to the head, face, or

neck.

Armonda et al, 2006: 47.4% had

traumatic cerebral vasospasm.

Majority were blast related injury

Civilian

Battlefield


Blast TBI

• Blast injuries historically

seen by providers as

limited to military concern

Peacetime terrorism over

the last decade has

reminded us otherwise

•


Why we need talk about blast TBI?

• Mortality:

– Oklahoma City 167

– US Embassy 223

– World Trade Center 2,801

– Madrid train bombings 191

– London 56

– Domodedovo 37

– Minsk metro 12

Large number of injured…


TBI PATHOPHYSIOLOGY

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Balancing Multisystem Interactions

TBI


TBI: Pathophysiology

Primary Injury:

- Contusions/Hemorrhages

- Diffuse Axonal Injury (DAI)

Secondary Injury (Intracranial) occurs hours to weeks after injury:

- Blood Flow and Metabolic Changes

- Traumatic Hematomas

- Cerebral Edema

- Hydrocephalus

- Increased Intracranial Pressure - PTSD?!


Decrease in CBF

BRAIN

EDEMA

More Brain Ischemic Blood Vessels

Edema brain cells Dilate

Increased ICP

Cell Injury


TBI and vasospasm

• Cerebral posttraumatic VSP (PTV) was first described by Lorn in 1936

• The incidence of CT documented traumatic SAH has been identified in 4% to 63% of pts after TBI

• Study from the University of Mississippi Medical Center indicated that traumatic SAH complicate course of TBI in 69% of the patients due to the presence of PTV

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WARTIME TRAUMATIC CEREBRAL VASOSPASM:

RECENT REVIEW OF COMBAT CASUALTIES

Armonda et al., Neurosurgery, 2006

• The first study to analyze the effects of

blast-related injury on the cerebral

vasculature

• This study showed that TCV occurred in a

substantial number of patients with severe

neurotrauma, and clinical outcomes were

worse for those with this condition


25 yo, severe concussion (IED)

no hemorrhage (Courtesy of Dr. Armonda)

CBFV

(cm/sec)

Calendar

TLA

TLA TLA


Mild TBI


Transcranial Doppler to screen on admission patients with

mild to moderate traumatic brain injury.

Bouzat et a, Neurosurgery, 2011

• In patients with no severe brain lesions on

CT following mild to moderate TBI, TCD

on admission, in complement with brain CT

scan, could accurately screen patients at risk

for secondary neurological deterioration

(edema, herniation, hydrocephalus) within

first week after TBI

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Patient with GSW. The CBFV and PI asymmetry

Right MCA

Left MCA


Role of TCD: Traumatic Brain Injury

• CBFV’s often increased in patients with TBI due to the vasospasm

• TCD waveform changes can signal significant ICP changes

• Sudden onset of the asymmetric pattern of the CBFV’s and PI’s could indicate midline shift

• TCD ultrasonography is valid in predicting the patient’s outcome


TCD AND VASOSPASM AFTER

TUMOR RESECTION


Tumor Resection and Vasospasm

• The occurrence of vasospasm and delayed

cerebral ischemia after resection of

intracranial tumor has not received

extensive attention clinically, and is often

misdiagnosed and improperly treated as

surgical brain damage or brain swelling

• However, DID from vasospasm after tumor

resection is a complication that is being

reported in increasing numbers

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Tumor Resection and Vasospasm: Literature

review

• Reports are sparse and mainly case series

• Vasospasm was found in 2% to 49% patients. No

significant difference among age, sex, surgical

approaches, pathological diagnosis, duration of

surgery, amount of blood loss and transfusion

during surgery were found, but significant

difference was seen in cisternal hemorrhage on CT

scan and the amount of blood in cerebrospinal

fluid


Tumor Resection and Vasospasm: Probable

Mechanism

• It is suggested that accumulation of blood in the basal cisterns may have been responsible for this unusual condition, and it is therefore important to consider vasospasm as a probable etiological cause of clinical deterioration in patients undergoing the surgical removal of a cerebral tumor.

• For this reason, whenever any neurological deterioration occurs in such patients, it is advisable to perform TCD in order to verify the presence of any vasospasm and promptly commence suitable treatment.


Suprasellar tumor resection.

The CBFV's and Trends of the Systemic

Hemodynamic

RIGHT LEFT

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10/3010/3111/111/211/311/411/511/611/711/811/911/10 10/3010/3111/111/211/311/411/511/611/711/811/911/10

Calendar

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MCA M1

MCA M2

ACA

ICA C1

VA

BA

MAP

ICP

Hct

PaCO2

Temp


Factors influencing TCD data

interpretation

• Patient age

• The presence of moderate to severe anemia

(Hct <27)

• Impaired CBF autoregulation (passive CBFV

variation with MAP changes)

• Hyperemia induced by triple-H therapy

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Role of TCD: Vasospasm Monitoring

• It is useful to perform TCD test on admission (or

ASAP after surgery) and perform daily TCD

studies when patient is in the ICU

• The frequency with which TCD should be

performed may be guided by patient clinical

presentation, knowledge of risk factors for VSP,

early clinical course

• TCD studies should be performed after

endovascular treatment to identify patients with

recurrent VSP American Society of Neuroimaging 35th Annual Meeting

Role of TCD: Vasospasm Monitoring

• The presence and temporal profile of CBFV’s in all available vessels must be detected and serially monitored

• The pattern of CBFV’s elevation may indicate the need to follow patient carefully for evidence of deficits related to specific vascular territory

• Waveform appearance either regionally, or globally may be clinically significant


CEA/STENTING EFFECT

EVALUATION


Role of TCD: CEA/Stenting

• TCD evaluation of CVR (CO2 induced response)

allows selection and quantification of patients with

true cerebrovascular insufficiency

• TCD can directly insonate the intracranial arteries

to evaluate collateral circulation around the circle

of Willis and to select those patients who most and

least likely to benefit from i/o shunt insertion

during CEA

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• TCD provides continuous noninvasive

monitoring of the right and left MCA CBFV’s

and immediately detects changes in cerebral

perfusion during CEA manipulation (cross-

clamping)/stenting

• Malfunction of the shunt (twisting or

compression) can be promptly detected by

TCD and corrected



• TCD monitoring provides the opportunity to

assess the rate of microemboli to the brain in

patients before, during or after CEA/stenting to

verify whether these phenomena have ceased after

procedure. If not, the pharmacological

intervention can be instituted

• If CBFV is markedly decreased from the baseline

level after CEA/stenting, intraluminal

complications can be suspected and exploration of

the arteriotomy can be immediately carried out



• Patients with a relative hyperemia after shunt

insertion/CEA/stenting (100% or greater

increase in CBFV MCA) can be identified and

pharmacological intervention can be instituted

if necessary


TCD AND NEURORADIOLOGY

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Neuroradiology (Test-Occlusion)

• Patients with giant intracranial aneurysms

(not accessible with direct surgery/coiling)

and vascular tumors (cervical cancer) may

undergo temporary/permanent occlusion of

the internal carotid artery, to determine

brain tolerance to exclusion of that vessel if

it must be sacrificed


Neuroradiology: Test-Occlusion

Arteriogram of a giant

aneurysm of the ICA

MCA CBFV during test-occlusion


Predicting cerebral ischemia…

Eckert et al, AJNR, 1998


Role of TCD: Neuroradiology (Test-Occlusion)

• TCD Monitoring of the ipsilateral MCA CBFV during test-occlusion determines the percent change in CBFV during balloon inflation and documents the collateral pathways patency/absency

• This information compliments the balloon occlusion procedure and can help in identifying the patients who are at risk for hemodynamic stroke following ICA permanent occlusion

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AVM Treatment

PRE-EMBOLIZATION POSTEMBOLIZATION

TCD PRE-EMBOLIZATION TCD POST-EMBOLIZATION


Role of TCD: AVM

• TCD study can provide two different types of

clinical information: the diagnosis and anatomical

localization of AVM

• TCD can be useful addition to CT-scanning and

for planning the angiography

• TCD offers the prospect of reducing the number of

X-ray exposures required in follow up


TCD AND INTRACRANIAL

HYPERTENSION


TCD wave-form changes with

development of intracranial

hypertension

Normal ICP

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Patient with GSW Trend shows almost direct inverse relationship between

CBFV and PI

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CBFV ICP PI

CALENDAR

MCA CBFV

MCA PI

ICP

RIGHT LEFT


TCD role for intracranial

hypertension evaluation

• TCD wave-form changes indicates abnormally high ICP, especially after 30 to 35 mm Hg

• TCD changes may alarm Neuro-ICU personnel and may indicate malfunctioning of ICP probe

• Sudden onset of asymmetrical CBFV’s and PI’s changes may indicate potential mid-line shift

• TCD quantitative and qualitative analysis must be taken into account for evaluation of intracranial hypertension, however, MAP, PaCO2 and cardiac output must be within the normal limits


TCD in the management of

TBI/Intracranial Hypertension

Pulsatility Index (PI) measurements permit the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available

TCD is an excellent first-line examination to determine those patients who need urgent aggressive treatment and continuous invasive ICP monitoring

Preliminary study suggests that TCD could be used in pre-hospital care to detect patients whose CPP may be impaired


Role of TCD: Intracranial Hypertension

• TCD waveform changes can signal significant ICP changes, usually after 30 – 35 mm Hg

• TCD waveform changes can alarm NCCU personnel and indicate malfunctioning of ICP probe

• CBFV’s decreased in patients with suspected intracranial hypertension and decreased brain compliance

• Sudden onset of the asymmetric pattern of the CBFV’s and PI’s could indicate midline shift

• TCD quantitative and qualitative analysis is valid in predicting intracranial hypertension

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TCD AND BRAIN DEATH


TCD wave form progression from intact

CBFV to circulatory arrest

Hassler et al., 1988

C P P


TCD pattern in patient with brain

stem stroke


CPP = 0

TCD pattern in Brain Death

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Role of TCD: Brain Death

• Quickly detects dramatically elevated ICP

• Confirms brain death in comatose patients

• Reliably determines arrest of cerebral

circulation, which can shorten observation

time for organ retrieval in patient with brain

death


TODAY:

• The value of TCD in clinical practice is well

established, especially to measure and grade

vasospasm following SAH and TBI

• Based on AHA Guidelines and many years of clinical

practice TCD is a tool employed by the

Neurosurgeon, Neurointensivist and Neurologist in

the management with SAH, TBI, acute stroke, etc

TCD is Critical Tool in Critical Care


TCD as a Modality

• Will be very good, reliable and accurate , if:

• Dedicated Personnel

• Daily Monitoring of the Technical

Performance Quality

• Quality of Interpretation

american society of neuroimaging 34th annual meeting

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