From the Department of Neurology, New York Medical College, Valhalla
(M.I.W.), and the Department of Neuroradiology, Phelps Memorial Hospital,
Sleepy Hollow, NY (A.K.).
Methods—One hundred sixty consecutive patients with suspected
cerebral vascular disease or pending surgery underwent MR angiography
with flow analysis. Simulated TI position was maintained for 3
to 4 minutes per acquisition.
Results—The cohort consisted of 89 females (56%) and 71 males
(44%) with a mean age of 66 years (range, 17 to 89 years).
Hypoplastic vertebral arteries with flow less than 50 mL/s were
present in 40 patients (25%). Profound alteration in basilar
artery flow was noted in this group with increased frequency of
microinfarctions on MRI (77% versus 38%). Unsuspected carotid
occlusion (n=6) and vertebral artery occlusion (n=2) were associated
with significant basilar artery flow changes. Flow reversal was
present in five cases. Carotid arterial changes were
not significant with simulated TI. No overt ischemic symptoms
developed during these maneuvers.
Conclusions—Simulated TI is safe yet induces distinct and
potentially detrimental flow abnormalities. Individuals identified with
the biological markers of hypoplasia, carotid and vertebral occlusion,
severe stenosis, or prior ischemic vascular disease
should receive special attention to neck position not only during
surgery but also in the postoperative period. Sustained neck
hyperextension greater than 12 minutes appears to be a neglected
potential hemodynamic factor that may play a pivotal
role in the pathogenesis of perioperative stroke.
It has been assumed that POS and ischemic syndromes result from
embolism, vasospasm, bleeding, hypoxia, or thrombosis during
the surgical procedure.6 7 A relatively
overlooked hypothesis is that tracheal intubation (TI) significantly
induces hemodynamic and perfusional changes and may be
a major link to the occurrence of this
syndrome.8 9 10
On the basis of previous studies11 12 and the
unique anatomy of the vertebral arteries passing through the
foramen transversarium of the transverse processes of the vertebral
column, we speculate that neck angulation induces mechanical
compression with secondary luminal changes producing
hemodynamic changes.
Study Design
DMRA and flow analysis offer the opportunity to measure
qualitative and quantitative hemodynamic changes in
vivo (real time) that may arise with simulated intubation. Thus, the
primary outcome measure was to determine whether simulated TI induces
significant hemodynamic changes that would be important
in risk stratification and assessment of clinical status.
Materials
Hypoplasia
Statistical Analysis
Table 2
HVAs with flow less than 50 mL/min were present in 40 patients
(25%) (Figure 2
There were six cases of unsuspected carotid artery occlusion
(three right and three left). One individual also had HVAs. Two
vertebral artery occlusions were identified, but not in the HVA cohort.
There was no evidence of dissection. Flow reversal was identified in
five cases (Figure 2D
Table 3
Anterior circulation changes were seen equally in the HVA cohort
(25/34; 74%) and in the non-HVA group (74/99; 75%). This was not
significant. Basilar artery flow reduction occurred in one third (33%)
of the HVA cohort compared with less than 20% of the non-HVA cohort.
This was an interesting trend but was not statistically significant
(P=0.08). We have previously used a basilar artery perfusion
index formulation12 that has not been validated.
This ratio of posterior blood flow [Basilar Artery/(Basilar Artery+2
Internal Carotid Arteries)] revealed that the basilar artery
quotient was disproportionately reduced in 24 patients with HVA (60%),
whereas this occurred in only 45 patients in the non-HVA cohort
(38%) (Figure 2E
The HVA cohort displays a unique vulnerability to simulated TI,
with significant mechanical compression at the atlanto-axial and
atlanto-occipital junctions. This is not influenced by age or
medication.12 The presence of an HVA imposes
specific physiological stresses, ie, changes in
regional hypovolemia, slow flow, reversible flow, and altered perfusion
in the absence of neurological symptoms. The high incidence of
posterior circulation silent infarctions and absence of
ischemic symptomatology during simulated TI suggest that a
threshold exists and portend that an "in vivo" accident is imminent
if this position is maintained too long or if neck position during the
operation and during the postoperative period is neglected.
Investigators have previously demonstrated that intimal injuries as
well as atherosclerotic changes can have a dynamic pathophysiology
leading to tears,17 rupture,
vasoconstriction, local thrombosis, or occlusion. Local areas of
injured intima may attract granulocytes that lead to local inflammatory
reactions and subsequent platelet clumping, resulting in luminal
constriction and even thrombosis. While the emergence of neurological
symptoms such as seizures, hemiparesis, and aphasia after surgery is
often attributed to intraoperative embolism or a local complication of
surgery, ie, hypoxia, we speculate on the basis of our data
that a significant number of POS are due to neck angulation
difficulties. This suggests that the prior slow flow or reversible flow
could develop into irreversible flow. However, our study is limited to
the immediate real-time period with no long-term follow-up. Thus, in
the setting of general anesthesia, physicians and nurses
should be aware that neck positioning is crucial and should be
monitored not only in the operating room but also in the recovery
room.
In conclusion, sustained hyperextension simulating TI for up to
12 minutes appears to be safe and unaccompanied by ischemic
symptoms. The use of DMRA as a novel surveillance technique indicates
that significant blood flow abnormalities occur in a cohort with HVA.
This group demonstrated a higher incidence of silent posterior
circulation infarctions, suggesting that they are at disproportionate
risk for future ischemic insults. Subjects with a high degree
of carotid stenosis or occlusion with hypoplasia are also at
increased risk. The presence of these biological markers for augmented
stroke risk should result in special attention focused on neck position
during intubation, surgery, and the postoperative period and should
also provide a future strategy for modifying neck positions during
activities of daily living.
Presented at the 49th Annual Meeting, American Academy of Neurology, April 16, 1997, Boston, Mass.
Received February 24, 1998;
revision received May 5, 1998;
accepted May 5, 1998.
2.
Nosan DK, Gomez CR, Maves MD.
Perioperative stroke in patients undergoing head and
neck surgery. Ann Otol Rhinol Laryngol. 1993;102:717–723.[Medline]
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Landercasper J, Merz BJ, Cogbill TH, Srutt PJ,
Cochrane RH, Olson RAM, Hutter RD. Perioperative stroke
risk in 173 consecutive patients with a past history of stroke.
Arch Surg. 1990;125:986–989.
4.
Turnipseed WD, Berkoff HA, Belzer FO. Post-operative
stroke in cardiac and peripheral vascular disease.
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Kim J, Gelb AW. Predicting
perioperative stroke. J Neurosurg
Anesth. 1995;7:211–215.[Medline]
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6.
Duke BJ, Moore EE, Brega KE. Posterior circulation
cerebral infarcts associated with repair of thoracic aortic disruption
using partial left heart bypass. J Trauma. 1997;42:1135–1139.[Medline]
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7.
Libman RB, Wirkowski E, Neystat N, Barr W, Gelb S,
Graver M. Stroke associated with cardiac surgery: determinants, timing,
and stroke sub-types. Arch Neurol. 1997;54:83–87.
8.
Gould DB, Cunningham K. Internal carotid artery
dissection after remote surgery. Stroke. 1994;25:1276–1278.[Abstract]
9.
Tettenborn B, Caplan LR, Sloan NA, Estol MD, Pessin
MS, DeWitt LD, Haley C, Price TR. Post-operative brainstem and
cerebellar infarcts. Neurology. 1993;43:471–477.
10.
Fisher CM. Basilar artery embolism after surgery under
general anesthesia: a case report. Neurology. 1993;43:1856–1857.
11.
Weintraub MI. Beauty parlor stroke syndrome: report of
five cases. JAMA. 1993;269:2085–2086.
12.
Weintraub MI, Khoury A. Critical neck positioning as an
independent risk factor for posterior circulation stroke. J
Neuroimaging. 1995;5:16–22.[Medline]
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Pulsinelli W. Pathophysiology of acute ischemic
stroke. Lancet. 1992;339:533–536.[Medline]
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Hart R, Hindman B. Mechanisms of
perioperative cerebral infarction. Stroke. 1982;13:766–773.
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Arnold V, Lerhmann R, Kursarve HK, et al.
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© 1998 American Heart Association, Inc.
Original Contributions
Cerebral Hemodynamic Changes Induced by Simulated Tracheal Intubation: A Possible Role in Perioperative Stroke?
Magnetic Resonance Angiography and Flow Analysis in 160 Cases
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and
Purpose—Perioperative stroke is a rare
complication of generalized surgery (1% to 6%). Unexpected
difficulties with tracheal intubation (TI), as well as the
hyperextended position, may predispose a patient to or play a role in
stroke. We sought to identify blood flow changes in carotid and
vertebral arterial circulation during simulated TI and
develop profile models for stroke risk before possible generalized
surgery.
Key Words: basilar artery • vertebral artery • stroke, perioperative • intubation, intratracheal
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Despite advances in
surgical and anesthetic techniques, perioperative
stroke (POS) remains a significant problem. Estimates of its prevalence
suggest a range from 1% to 6%,1 2 3 4 with a
mortality rate approaching 60% in certain individuals with prior
stroke.5 Preoperative risk assessment has proven
to be unreliable and in fact is an imprecise science. Thus, clinicians
and patients face an uncertain dilemma without definitive biological
markers.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
We designed a prospective community-based study to determine
whether dynamic MR angiography (DMRA) would serve as a useful screening
test to predict risk of stroke. Specifically, the issue of changes
induced by simulated TI through hyperextension was addressed. We used
standard neck angulation techniques simulating the "sniffing"
position demonstrated by a board-certified anesthesiologist. Thus, our
observations and conclusions will be limited to the immediate period of
induction and extubation. Subjects were followed for periods of up to 2
to 3 weeks to determine clinical status.
From June 1994 through December 1996, 160 consecutive patients
were screened for the effects of simulated TI by DMRA and flow
analysis with the use of a technique previously
described.12 Among the 160 subjects screened were
individuals who were scheduled for surgery and others who were future
surgical candidates, eg, coronary artery bypass graft, cataract
surgery, or cholecystectomy candidates. However, the majority of the
individuals were considered high risk and were studied in relation to
suspected cerebral vascular disease and symptomatology. The ages ranged
from 17 to 89 years, with 44% males and 56% females (Table 1
). Phelps
Memorial Hospital Investigational Review Board approved the protocol,
and informed consent was provided.
View this table:
[in a new window]
Table 1. Demographics
All patients were examined with a 1.5-T superconductive magnet
(General Electric Signa; x5). MR angiography was performed in the
axial plane, in a neutral position, and during hyperextension, with the
two-dimensional time of flight technique (repetition time, 37
milliseconds; minimum echo time flip angle, 65o;
RB, 16 kHz; field of view, 24 cm; slice thickness, 1.9 mm;
matrix, 256x128; number of excitations, 1). A volume neck coil
at the origins of the vertebral and common carotid arteries and the
distal portion of the basilar arteries was included. The images
were analyzed for stenosis and dissection, and the size
of the vertebral arteries was assessed for hypoplasia. Flow
analysis was also performed with a volume neck coil, in a
neutral position and during hyperextension, with the use of the cine
phase-contrast technique with peripheral gating and flow
compensation (flow direction, S/I; flip angle,
20o; repetition time, 22 milliseconds; field of
view, 24 cm; slice thickness, 5 mm; multiple locations; velocity
encoding, 60 cm/s; matrix, 256x128; number of excitations, 2;
frequency direction, anteroposterior). Three measurements were
performed in one acquisition: the first below the carotid bifurcations,
the second above the bifurcations, and the third in the mid aspect of
the basilar artery (Figure 1). Scan time
was 3 to 4 minutes per acquisition. Image analysis was then
performed by choosing the region of interest of the specific artery and
downloading the images into the computer. In all cases, flow
analysis was performed at the same level with the subject in a
neutral position and during hyperextension with the same physical
parameters, and the processing was done by the same
operator. The error in the differences measured between hyperextension
and the neutral position is very low. For each region of interest,
computerized data were generated: volume flow rate (milliliters per
minute) and velocity (centimeters per second) were charted and graphed
(Figure 1C and 1D). Patients were advised to report any new symptoms
produced by this positioning.
View larger version (42K):
[in a new window]
Figure 1. A and B, Site of flow analysis
measurements (dotted lines), below and above the carotid bifurcations
and in the mid basilar artery (perpendicular to the vessels). RV
indicates right vertebral artery; LV, left vertebral artery; RCCA,
right common carotid artery; LCCA, left common carotid artery; RICA,
right internal carotid artery; LICA, left internal carotid artery; and
B, basilar artery. C and D, Normal MR angiography and flow
analysis with vertebral arteries of equal size. Avg indicates
average; Pek, peak.
Asymmetry in the size of the vertebral arteries is well
documented, yet hypoplasia is not clearly defined. Consequently, we
defined hypoplasia by two parameters: (1) when the
vertebral diameter was two thirds less than the opposite artery and (2)
when the flow was less than 50 mL/min (normal vertebral artery blood
flow=61 to 115 mL/min).
Each subject served as his or her own control. Student's
t test (two tailed) was used to measure continuous
variables, and the 
2 test for independence
was used to assess the relationship between hypoplasia and MRI
outcomes. Values are reported as mean±SD. A value of
P<0.05 was regarded as statistically significant.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The cohort consisted of 89 females (56%) and 71 males (44%)
(Table 1
). Age ranged from 17 to
89 years (mean age, 66 years). Hypoplastic vertebral arteries
(HVAs) with flow less than 50 mL/min were present in 40 subjects
(25%). Hypertension was present in 31 of 120 subjects (26%) and
was present in the HVA cohort in 11 of 40 (28%). Diabetes mellitus
was present in 5 of 120 subjects (4%) and in the HVA cohort in 2
of 40 (5%). A history of prior stroke was present in 30 of 120
subjects (25%) and in the HVA cohort in 10 of 40 (25%). identifies infarctions observed
on MRI. The overall majority of these events were clinically silent.
During the present study no overt ischemic symptoms
developed during these maneuvers or in the follow-up periods.
View this table:
[in a new window]
Table 2. Infarctions Observed on
MRI ). Males and females were
equally represented. Left side (n=16), right side (n=17),
and bilateral (n=7) involvement were noted. Compensatory increased
blood flow in the contralateral vertebral artery was usually seen with
hypertension. Nine of these individuals displayed severe or occluded
carotids, whereas 31 had mild carotid atherosclerosis.
This difference approached statistical significance in relation to MRI
infarctional changes (t8=1.42,
P=0.194). With a larger sample size, this would be
significant.
View larger version (34K):
[in a new window]
Figure 2. A and B, Hypoplastic right vertebral artery. C and
D, Slow flow and reversal of flow. E and F, Basilar artery flow
reduction. Abbreviations are as in Figure 1 .). identifies flow abnormalities
detected on DMRA, which were significant only in the HVA group (77%
versus 38%) (P<0.01). The proximal posterior circulation
demonstrated cerebellar infarction (n=13), the middle circulation
revealed pontine infarction (n=14), and the distal posterior
circulation revealed thalamic (n=15), occipital (n=13), and basal
ganglionic (n=13) infarctions. Anterior cortical infarctions
(frontal/parietal) were also noted (n=25). Six individuals in
the HVA cohort did not have brain MRI. Of the 99 non-HVA subjects, 36
(36%) displayed posterior circulation infarcts. Of the 34 HVA
patients, 23 (68%) displayed both posterior and anterior infarctions
on MRI, whereas 37 of the 99 non-HVA subjects displayed evidence of
both infarctions (37%). This difference was statistically significant
(21=9.37,
P<0.01).
View this table:
[in a new window]
Table 3. Flow
Abnormalities and 2F). This difference is statistically
significant (21=6.19,
P<0.05).
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Risk stratification relying solely on history of
hypertension, diabetes, cardiac disease,
hypercholesterolemia, prior stroke, or heart
attack is insensitive and insufficient to predict in vivo events.
Transient changes in blood flow during hyperextension have been
identified in a specific cohort that displays a higher incidence of
infarction of the posterior circulation. Despite the absence of acute
ischemia or stroke, the aforementioned association with
hyperextension for 12 minutes raises many questions. It is well known
that individuals are placed in the hyperextended position with various
other procedures during surgery; consequently, if this position is
maintained for more than 12 minutes, could this induce a POS? Perhaps
it is worthwhile to abandon surrogate markers that relate to the status
and degree of atherosclerosis. Our results argue that
DMRA represents a novel, in vivo challenge test that is more
sensitive than other techniques in demonstrating enhanced
susceptibility to TI. It is not known whether these reversible flow
changes become irreversible on the basis of duration of positioning or
local inflammation, but this may be a logical conclusion. The striking
vascular changes seen in the cohort with HVA raise the question of
whether the mechanism of injury may be acute, as noted in the figures,
as well as delayed, with intimal damage and secondary changes that
evolve over hours or days.13 The fact that
80% of POS is noted in the postoperative period at a mean of 10 days
after the operation2 14 may represent
this delayed effect. It is noteworthy that the HVA cohort displayed a
significantly higher incidence of posterior and combined infarctions,
suggesting that this is an independent harbinger of stroke. The
magnitude of these data, seen in only 25% of the study population,
suggests that this could be a public health concern since HVA has been
estimated to occur in 40% of the
population.6 15 Patients with prior stroke
merit special attention since investigators have documented that the
presence of preoperative findings of cerebral vascular disease augments
the risk 5- to 10-fold for stroke3 and myocardial
infarction.16
Acknowledgments
The authors gratefully acknowledge the statistical assistance of
Steven Cole, PhD (Research Designs, Decatur, Ga).
Footnotes
Reprint requests to Michael I. Weintraub, MD, Department of Neurology, Phelps Memorial Hospital, 325 S Highland Ave, Briarcliff Manor, NY 10510.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
1.
Roach GW, Kanchuger M, Mangano CM, Newman M,
Nussmeier N, Wolman R, Aggarwal A, Marschall K, Graham SH, Ley C,
Ozanne G, Mangano DT. Adverse cerebral outcomes after coronary
bypass surgery. N Engl J Med. 1996;335:1857–1863.
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