AbstractA 54 year-old man had symptoms of acute right hemispheric cerebral ischemia. He was initially considered for participation in a trial of early thrombolysis in stroke, but an innominate artery embolus was found with no apparent arterial source. The embolus was removed by means of a combined brachial and carotid bifurcation approach to protect the cerebral vasculature from embolic fragmentation during extraction. Further investigation revealed deep venous thrombosis, evidence of pulmonary emboli, and a patent foramen ovale, supporting a diagnosis of paradoxic embolus. Additional treatment included anticoagulation and placement of an inferior vena caval filter. The unusual condition of paradoxic embolus is reviewed, and the management of this patient is discussed. (J Vasc Surg 1998;28:742-5.

Salvian, Anthony J.

Teal, Philip A.

Tsang, Victor T.

Turnbull, Robert G.

Elsevier - Publisher Connector 

742
Paradoxic embolus involves passage of a venous
embolus into the arterial system. Although the exis-
tence of this clinical event has been established for
many years, advances in our ability to diagnose
intracardiac right-to-left shunts has increased recog-
nition of the potential for paradoxic emboli to occur.
Still, management and prevention of this problem
are controversial. An unusual case is presented in
which the embolus lodged in the innominate artery
with a small fragment proceeding further into the
cerebral circulation, resulting in stroke. Surgical
intervention was necessary to prevent both impend-
ing brachial emboli and further cerebral embolism.
CASE REPORT
A 54-year-old man with a 1-hour history of headache
and collapse was referred to the Vancouver General
Hospital. His history included hypertension, hypercholes-
terolemia, and myocardial infarction 10 years earlier. He
did not have diabetes and had stopped smoking after the
myocardial infarction. At examination the Glasgow Coma
Score was 15, but he exhibited left hemiparesis and left-
sided neglect, and the eyes deviated to the right. Further
examination revealed left-sided sensory loss, increased
tone, visual field deficit, and hyperreflexia in keeping with
a right-hemispheric stroke. The patient also had a cold,
pulseless right arm. Cuff blood pressure was obtainable
only from the left arm, which was normal to examination.
There also was no right carotid impulse.
An electrocardiogram showed normal sinus rhythm
with old nonspecific anteroinferior T-wave changes. A
computed tomographic scan of the head showed no evi-
dence of intracerebral hemorrhage. Angiography revealed
a large embolus in the innominate artery that extended
into the proximal right common carotid artery (Fig 1).
Right subclavian flow was established in a retrograde man-
ner through the vertebral artery, and the carotid bifurca-
tion could not be clearly visualized. A distal embolus was
present in the superior division of the right middle cere-
bral artery bifurcation, accounting for the neurologic
symptoms.
The patient was taken urgently to the operating room,
where a standard carotid bifurcation exposure was per-
formed as was dissection of the brachial artery at the ante-
cubital fossa. With electroencephalographic monitoring,
the external and internal carotid arteries were clamped,
and a Fogarty balloon-tipped catheter was used to remove
a portion of the thrombus from the innominate and prox-
imal common carotid arteries. The rest of the thrombus
was extracted with a Fogarty catheter passed up from the
brachial artery. During this second part of the procedure,
the internal carotid artery was kept clamped, and the com-
mon carotid artery was flushed out before the arteriotomy
was closed. The common and internal carotid arteries
were free of atheromatous disease. Normal carotid and
brachial circulation was restored. The procedure was com-
pleted within 6 hours of the onset of symptoms.
A postoperative transthoracic echocardiogram did not
demonstrate an intracardiac source of thrombus, mechan-
ical defect, or right-to-left shunt. A paradoxic embolus was
Successful innominate
thromboembolectomy of a paradoxic
embolus
Robert G. Turnbull, MD, Victor T. Tsang, MD, Philip A. Teal, MD, and
Anthony J. Salvian, MD, Vancouver, British Columbia, Canada
A 54 year-old man had symptoms of acute right hemispheric cerebral ischemia. He was
initially considered for participation in a trial of early thrombolysis in stroke, but an
innominate artery embolus was found with no apparent arterial source. The embolus
was removed by means of a combined brachial and carotid bifurcation approach to pro-
tect the cerebral vasculature from embolic fragmentation during extraction. Further
investigation revealed deep venous thrombosis, evidence of pulmonary emboli, and a
patent foramen ovale, supporting a diagnosis of paradoxic embolus. Additional treat-
ment included anticoagulation and placement of an inferior vena caval filter. The unusu-
al condition of paradoxic embolus is reviewed, and the management of this patient is dis-
cussed. (J Vasc Surg 1998;28:742-5.)
From the Division of Vascular Surgery, Department of Surgery,
and Division of Neurology, Department of Medicine (Dr.
Teal), University of British Columbia, Vancouver General
Hospital.
Reprint requests: Dr. A.J. Salvian, 708-750 West Broadway,
Vancouver, British Columbia, Canada V5Z 1H6.
Copyright © 1998 by The Society for Vascular Surgery and
International Society for Cardiovascular Surgery, North
American Chapter.
0741-5214/98/$5.00 + 0 24/4/92216
JOURNAL OF VASCULAR SURGERY
Volume 28, Number 4 Turnbull et al 743
suspected, and on further questioning, the patient admit-
ted to increasing right leg pain with mild swelling and pro-
gressive dyspnea over the 2-week period before admission.
Duplex ultrasonography of the right leg revealed throm-
bus involving the common femoral vein and extending
into the popliteal and calf veins. A ventilation-perfusion
scan demonstrated evidence of bilateral pulmonary
emboli. A search was made for a venous-arterial commu-
nication. Transesophageal echocardiography was per-
formed and demonstrated a patent foramen ovale with
marked right-to-left shunting during respiration and
coughing.
The patient’s neurologic status showed steady
improvement, and he quickly regained much of his left-
sided motor and sensory function. A computed tomo-
graphic scan obtained on the first postoperative day con-
firmed a 4.5-cm region of effacement in the right tempo-
ral region (Fig 2). The dyspnea resolved, and leg swelling
responded to rest and elevation. A Greenfield filter was
placed in the inferior vena cava on the fifth postoperative
day, and the patient was discharged later that day. Three
months after the operation he still had a left visual field
deficit, a slight left pronator drift, decreased fine sensation
in the left hand and arm, slowed fine finger movements,
and a decreased left arm swing. The patient continued to
be observed for resolution of the cerebral insult and for
deep venous thrombosis and pulmonary embolism.
DISCUSSION
This case report demonstrates the unusual situa-
tion of a massive paradoxic embolism lodged in the
innominate artery. A smaller embolic fragment had
already made its way into the middle cerebral artery
circulation and caused neurologic symptoms. A por-
tion of the innominate embolus would likely have
traveled down the brachial circulation.
The patient was treated with emergency surgical
removal of the innominate embolus to restore com-
promised cerebral and brachial circulation and to
prevent further embolization of debris. Access was
gained through both the right neck and right
brachial sites. This allowed effective restoration of
both carotid and brachial circulation and protected
the cerebral vasculature from embolic debris, which
might be dislodged during brachial embolectomy. A
more direct approach to the innominate artery
through a sternotomy was not favored because of a
higher morbidity associated with sternotomy and a
need to explore the carotid bifurcation for emboli,
because this area was not well visualized on the pre-
operative angiogram. It was also felt that direct sur-
gical manipulation of the innominate artery might
dislodge embolic debris, resulting in further cerebral
embolism.
A postoperative search was made for the source
of this patient’s unusual thrombus. When the
echocardiogram was found to be normal, a paradox-
ic embolus was suspected, and the patient was ques-
tioned specifically for signs and symptoms of venous
thromboembolism. The shortness of breath and leg
swelling were quite mild and had not been brought
to light in the preoperative assessment. A trans-
esophageal electrocardiogram was obtained and
revealed a patent foramen ovale, supporting the
diagnosis. It was chosen not to repair this lesion
because of the added morbidity of the procedure. A
Greenfield filter was placed to prevent possible fur-
ther pulmonary and paradoxic emboli from deep
venous thrombosis of the right leg. There have been
reports of subsequent paradoxic emboli despite
insertion of a Greenfield filter,1,2 and future surgical
closure of the patent foramen ovale remains under
consideration for this patient. Meanwhile, the
patient is receiving anticoagulation therapy to pro-
Fig 1. Digital subtraction angiogram demonstrates an
embolic filling defect in the innominate artery. Flow into
the right subclavian, carotid, and vertebral arteries is
markedly impaired. The right carotid bifurcation was not
visualized.
JOURNAL OF VASCULAR SURGERY
744 Turnbull et al October 1998
tect him from further thromboembolism. An under-
lying cause of the venous thrombosis could not be
elucidated.
Paradoxic embolism was first described by
Cohnheim in 18773 and is an infrequent event,
accounting for fewer than 2% of all arterial emboli.4
It may be defined as passage of a venous thrombus
through a right-to-left shunt resulting in systemic
arterial embolization. Diagnosis is typically based on
the presence of an arterial embolism without a cor-
responding source in the left heart or the proximal
arterial tree, an embolic source within the venous
system with or without pulmonary embolism, an
abnormal intracardiac or intrapulmonary communi-
cation between right and left circulations, and a
pressure gradient that promotes right-to-left shunt-
ing at some point in the cardiac cycle.5 Although
most of these emboli are venous thrombus from
branches of the inferior vena cava,6,7 reports exist of
paradoxic embolization of fat,8 tumor,9 amniotic
fluid,5 and air.10,11
Sites of paradoxic arterial embolization usually
involve the cerebral vasculature or the extremi-
ties,1,12 although coronary, renal, and splenic arteri-
al emboli have been described.13 The site for right-
to-left shunting among such patients usually is a
patent foramen ovale; however, other atrial septal
defects, ventricular septal defects, and aortocaval and
pulmonary arteriovenous fistulas have been implicat-
ed.13-15 Patent foramen ovale has been found to be
present in 20% to 30% of the healthy popula-
tion.16,17 The actual overall risk for paradoxic embo-
lus in the presence of a patent foramen ovale is
unknown12 but likely correlates with the size and
hemodynamic features of the defect.
Treatment of patients with paradoxic emboli is
controversial and must be individualized. The acute
ischemic event must be addressed, and further
embolism must be prevented. In general anticoagu-
lation is indicated1 and is continued for 3 to 6
months or indefinitely if the patient has a patent
foramen ovale or chronic obstructive pulmonary dis-
ease–induced pulmonary hypertension, which would
enhance right-to-left flow.5,13 If deep venous throm-
Fig 2. Computed tomographic scan obtained 24 hours after the onset of symptom shows
early evidence of ischemic brain injury in the distribution of the left middle cerebral artery.
There is cortical effacement of the right temporal region.
JOURNAL OF VASCULAR SURGERY
Volume 28, Number 4 Turnbull et al 745
bosis is present, a vena caval filter should be consid-
ered, especially if pulmonary embolism is present or
if anticoagulation is contraindicated. Peripheral
emboli should be extracted when possible or man-
aged with thrombolysis. Surgical closure of a patent
foramen ovale, transcatheter closure, fibrinolysis,
and anticoagulation and antiplatelet therapy all have
been described5,12,13,18 with no prominent advan-
tage evident from a particular management strategy.
Hanna et al.19 observed no recurrences during a
mean follow-up period of 28 months among 15
patients with paradoxic cerebral embolus who
underwent treatment with aspirin, warfarin, open
heart closure, or a septal occlusion device.
Paradoxic embolism is a rare diagnosis that
should be entertained when a patient has arterial
embolism with no clear embolic source. A search
should be made for deep venous thrombosis and a
patent foramen ovale, both of which may be sub-
clinical. This case study illustrates a novel approach
to a large paradoxic embolus in an unusual location,
which if left untreated may have fragmented with
devastating consequences.
REFERENCES
1. Katz S, Andros G, Kohl R, Harris R, Dulawa L, Oblath R.
Arterial emboli of venous origin. Surg Gynecol Obstet
1992;174:17-21.
2. Dalman R, Kohler TR. Cerebrovascular accident after
Greenfield filter placement for paradoxical embolism. J Vasc
Surg 1989;9:452-4.
3. Cohnheim J. Thrombose und embolie. In: Vorlesungen uber
allgemeine pathologie. Vol 1. Berlin: Hirschwald, 1877:134.
4. Biller J, Johnson MR, Adams HP Jr, Kerber RE, Corbett JJ,
Bruno A, et al. Further observations on cerebral or retinal
ischemia in patients with right-left intracardiac shunts. Arch
Neurol 1987;44:740-3.
5. Ward R, Jones D, Haponik EF. Paradoxical embolism: an
underrecognized problem. Chest 1995;108:549-58.
6. Stollberger C, Slany J, Schuster I, Leitner H, Winkler W,
Karnik R. The prevalence of deep venous thrombosis in
patients with suspected paradoxical embolism. Ann Intern
Med 1993;119:461-5.
7. Jungbluth A, Erbel R, Darius H, Rumpelt H, Meyer J.
Paradoxical coronary embolism: case report and review of the
literature. Am Heart J 1988;116:879-85.
8. Pell ACH, Hughes D, Keating J, Christie J, Busuttil A,
Sutherland GR. Brief report: fulminating fat embolism syn-
drome caused by paradoxical embolism through a patent
foramen ovale. N Engl J Med 1993;329:926-9.
9. Dahl-Iverson E. Embolie paradoxale de l’artere iliaque
externe gauche-embolectomie. Lyon Cir 1930;1:39-42.
10. Marquez J, Sladen A, Gendaell H, Boehnke M, Mendelow
H. Paradoxical cerebral air embolism without an intracardiac
defect. J Neurosurg 1981;55:997-1000.
11. Gronert GA, Messick JM, Cucchiara RF, Michenfelder JD.
Paradoxical air embolism from a patent foramen ovale.
Anesthesiology 1979;50:548-9.
12. Chaikof EL, Campbell BE, Smith RB. Paradoxical embolism
and acute arterial occlusion: rare or unsuspected? J Vasc Surg
1994;20:377-84.
13. Loscalzo J. Paradoxical embolism: clinical presentation, diag-
nostic strategies, and therapeutic options. Am Heart J
1986;112:141-5.
14. Hunter DD. Pulmonary arteriovenous malformation: an
unusual case of cerebral embolism. Can Med Assoc J
1965;93:662-5.
15. Bridger JE. Aortocaval fistula: a rare cause of paradoxical pul-
monary embolism. Postgrad Med J 1994;70:122-3.
16. Wilmshurst PT, deBelder MA. Patent foramen ovale in adult
life. Br Heart J 1994;71:209-12.
17. Hagen PT, Scholz DG, Edwards WD. Incidence and size of
patent foramen ovale during the first 10 decades of life: an
autopsy study of 965 normal hearts. Mayo Clin Proc
1984;59:17-20.
18. Zeiro C, Canterin FA, Pavan D, Nicolosi GL. Spontaneous
closure of a patent foramen ovale and disappearance of
impending paradoxical embolism after fibrinolytic therapy in
the course of massive pulmonary embolism. Am J Cardiol
1995;76:422-4.
19. Hanna JP, Sun JP, Furlan AJ, Stewart WJ, Sila CA, Tan M.
Patent foramen ovale and brain infarct: echocardiographic
predictors, recurrence and prevention. Stroke 1994;25:
782-6.
Submitted Dec 10, 1997; accepted May 26, 1998.


Successful innominate thromboembolectomy of a paradoxic embolus 

file:///data/remote/core/dit/data/elsevier/pdf/4c5/aHR0cDovL2FwaS5lbHNldmllci5jb20vY29udGVudC9hcnRpY2xlL3BpaS9zMDc0MTUyMTQ5ODcwMTA2NQ==.pdf

Successful innominate thromboembolectomy of a paradoxic embolus

Abstract

Similar works

Full text

Available Versions

Elsevier - Publisher Connector

Elsevier - Publisher Connector