|Year : 2020 | Volume
| Issue : 4 | Page : 420-428
Defining the factors leading to stroke due to retrograde embolism in arterial thoracic outlet syndrome by literature search and report of two cases
Aneesh Mohimen1, Ajay Kumar Dabas2, Jitesh Goel3, Ravi K Anadure4
1 Department of Radiology, Intervention Division, Command Hospital Air Force, Bengaluru, Karnataka, India
2 Department of Surgery, Vascular Division, Command Hospital Air Force, Bengaluru, Karnataka, India
3 Department of Medicine, Neurology Division, Command Hospital Air Force, Bengaluru, Karnataka, India
4 Department of Medicine, Neurology Division, Command Hospital Air Force, Bengaluru, Karnataka; Department of Neurology, Army Hospital (R&R), Delhi, India
|Date of Submission||14-Apr-2020|
|Date of Decision||15-Jun-2020|
|Date of Acceptance||23-Jun-2020|
|Date of Web Publication||24-Dec-2020|
Ajay Kumar Dabas
Department of Surgery, Vascular Division, Command Hospital Air Force, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
Context: Stroke due to retrograde embolization in a case of arterial thoracic outlet syndrome (aTOS) is rare, and little is known about predisposing factors. Objective: The aim of this study is to analyze the predisposing factors and mechanisms of stroke in aTOS based on literature survey and experience with two cases. Materials and Methods: – Data Sources and Selection: Databases MEDLINE, PubMed, Scopus, and Cochrane Library were searched, supplemented by scanning of reference lists of relevant publications. All publications with subclavian artery/axillary artery stenosis/occlusion, either due to bony and/or muscular abnormality, in the thoracic outlet, with stroke, till January 2020 were included. Data Extraction: The clinical and anatomical details such as gender, age, side affected the type of stroke (anterior/posterior), bony/skeleton abnormality, upper limb symptoms, and their duration, were noted and analyzed. Data Synthesis: A systematic analysis of the accessed reports was performed. Statistical Analysis: The measure of the significance of the association of various factors was calculated with z-test. Results: Forty-eight articles describing 58 patients were identified. Fifty-five patients were analyzed. The involvement of the right upper limb (P = 0.00001), age <40 years (P = 0.00001), and the presence of upper limb ischemic symptoms (P = 0.00001) significantly predispose to the development of stroke in aTOS. Twenty-seven percent had a recurrent stroke. Conclusions: Stroke is a rare complication of aTOS. A possible explanation exists for retrograde embolism; however, validation is required by further studies. Stroke in young with upper limb ischemia or absent pulses merits a search for aTOS.
Keywords: Arterial thoracic outlet syndrome, retrograde embolism, stroke
|How to cite this article:|
Mohimen A, Dabas AK, Goel J, Anadure RK. Defining the factors leading to stroke due to retrograde embolism in arterial thoracic outlet syndrome by literature search and report of two cases. Indian J Vasc Endovasc Surg 2020;7:420-8
|How to cite this URL:|
Mohimen A, Dabas AK, Goel J, Anadure RK. Defining the factors leading to stroke due to retrograde embolism in arterial thoracic outlet syndrome by literature search and report of two cases. Indian J Vasc Endovasc Surg [serial online] 2020 [cited 2021 Jan 28];7:420-8. Available from: https://www.indjvascsurg.org/text.asp?2020/7/4/420/304634
| Introduction|| |
Arterial thoracic outlet syndrome (aTOS) is uncommon. Still rare is stroke resulting from retrograde embolization due to aTOS.,
Two cases of aTOS resulting in stroke due to retrograde embolism to the brain are presented. The literature available on the subject is reviewed to expand the knowledge base on this rare entity and systemically analyzed.
| Subjects and Methods|| |
Two cases of aTOS presenting with stroke are presented. The stroke resulted due to retrograde embolization of thrombus from the subclavian artery (SCA) aneurysm.
A literature search was done using the databases MEDLINE, PubMed, SCOPUS, and Cochrane Library in Feb–March 2020. The fields chosen were “title, keywords, abstracts.”
The Medical Sub Heading (MeSH) terms used for the search were: aTOS, stroke, retrograde embolism, rib synostosis, SCA, axillary artery (AxA), cervical rib, musculoskeletal abnormalities, brain embolism and thrombosis, intracranial embolism and thrombosis, and case report.
A search string was created using Boolean logic and proximity operators.
The original articles, case reports, case series, posters (e-posters), clinical images were identified. As a next step, similar articles/related articles/citing articles were searched for.
The reference list of the identified studies was also searched. An effort was made to access the article from authors through E-mail when the articles could not be accessed. Google translation service was used to translate the non-English language articles into English.
The articles included were from which it could be deciphered clearly (1) the phenomenon of SCA or AxA thrombosis/occlusion, resulted in stroke due to retrograde embolism and that (2) SCA/AxA thrombosis occurred due to bony and/or muscular abnormality in thoracic outlet location.
The articles excluded were those due to thrombosis of the brachiocephalic trunk, embolism due to thrombosis of vertebral artery (VA)/carotid arteries (CA) where the source of embolism was either ascending aorta, arch of aorta, common carotid artery (CCA), or SCA proximal to the origin of VA.
The flow chart for the selection of the study and cases is given in [Figure 1].
Description of the cases
A 20-year-old right-handed male presented with three episodes of the right hemispheric complex partial seizures with secondary generalization. He was started on antiepileptics. On recovery from the postictal state, he had left hemiparesis. He was transferred to our center approximately 6 h after the initial ictus. Initial evaluation revealed a Glasgow Coma Scale of 9/15 (E2V3M4) with left hemiparesis. Only other positive clinical findings were absent right brachial and weak right radial pulse, with a pressure difference of 30 mmHg between the two upper limbs.
Noncontrast computed tomography (CT) and magnetic resonance imaging (MRI) showed a right middle cerebral territory infarct [Figure 2]. There was complete occlusion of the M1 segment of the right middle cerebral artery on magnetic resonance angiography (MRA). Both CCA, internal carotids artery, VA, and arch of the aorta were normal. He was managed with anti-edema measures and required mechanical ventilation. Decompressive craniectomy was required on the 3rd day due to mass effect. He was weaned off the ventilator after 2 weeks. Subsequent CT angiogram (CTA) showed bilateral cervical rib with thrombus in the right SCA causing near-total luminal occlusion and poststenotic dilatation [Figure 3]. He subsequently underwent right cervical rib excision, excision of one cm of damaged artery and end-to-end anastomosis [Figure 4], [Figure 5], [Figure 6]. However, there was no pulse palpable at the wrist. An attempt at thrombectomy through radial and ulnar radial artery was unsuccessful, pointing toward the chronic embolic phenomenon. On recovery, he gave a history of the right upper limb claudication (forearm and hand) of 6 months duration. He was managed as a case of musculoskeletal pain.
|Figure 2: NCCT and magnetic resonance imaging brain showing acute right middle cerebral artery infarct|
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|Figure 3: Computed tomography angio showing subclavian artery narrowed and lined by thrombus with post stenotic dilatation|
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|Figure 4: Subclavian artery normal proximal segment and distal dilated segment|
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The history and workup were negative for vasculitis, prothrombotic state, and cardioembolic source (normal trans-esophageal and transthoracic ECHO).
At present, he is ambulant and independent for activities of daily living with residual left side spastic hemiparesis. The right brachial artery is palpable with a feeble radial pulse.
During follow-up, the left side showed no evidence of arterial TOS on CTA and color doppler and hence was not operated. However, he has been advised regular follow-up.
A 19-year-old young right handed athlete presented with acute-onset diplopia. Examination revealed the left 6th cranial nerve palsy. The patient gradually developed right hemiparesis and altered sensorium, at which time he was referred to our hospital. On arrival, he had left 6th nerve palsy and left hemiparesis and absent left upper limb pulses. MRI brain showed infarcts in the pons and lower midbrain (left side) and right cerebellar hemisphere. No medullary, upper brainstem or posterior cerebral artery (PCA) territory infarcts were noted. MRA revealed complete occlusion of the mid and distal basilar artery. Good opacification of bilateral PCA was noted from the posterior communicating artery. Because of stable neurological deficits, and 18 h after onset and good PCA opacification, mechanical thrombectomy (MT) was not considered initially due to the risk of distal PCA embolization. However, after approximately 4 h, the patient developed upper brainstem signs in the form of ptosis and obtundation of the sensorium, at which time he was taken up for MT. MT was performed with a 4 mm x 25 mm Revive retrievable stent (Raynham, MA, USA, Codman Neuro/DePuy Synthes, Johnson and Johnson) achieving TICI 3 (thrombolysis in cerebral infarction) recanalization [Figure 7] and [Figure 8]. Postprocedure, patients had gradual recovery with residual left hemiparesis. Subsequent CTA revealed bilateral cervical ribs with aneurysmal dilatation of the left SCA just distal to the first rib. Left AxA and brachial artery were thrombosed 3 weeks later, he underwent left cervical rib resection and excision of the aneurysmal arterial segment with end-to-end anastomosis through the supraclavicular approach. Thrombectomy of AxA and brachial artery was also attempted but failed. Fogarty catheter could not be passed beyond axilla. The brachial artery at the elbow was thick and cord-like on exploration, and the trans-brachial embolectomy attempt was abandoned. The above findings pointed to the chronic embolic phenomenon.
|Figure 7: Digital subtraction angiography: Occluded basilar artery prior to mechanical thrombectomy|
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Currently, the patient is ambulant with residual right hemiparesis and has mild residual ptosis and warm limb but absent radial and ulnar pulses.
On recovery, the patient denied any history of upper limb ischemic symptoms. The operative findings were a suggestive chronic embolic phenomenon.
In both cases, workup and history were negative for any vasculitis, prothrombotic state, or cardioembolic source. The reason for stroke in both cases was retrograde embolism to the brain due to aTOS. In both cases, clinical and operative findings suggested a long-standing condition leading to recurrent episodes of embolization.
| Results|| |
The literature search resulted in a total of 48 articles out of which three were original articles, 43 case reports/series and one each an e-posters and a clinical image. The search did not yield any meta-analysis/systemic reviews. Forty-four were in English, and one each was in Spanish, French, Dutch, and Japanese.
A total of 58 cases have been described, including the present two cases. The number of reported cases has increased in the last two decades. Twenty-nine cases have been reported in this century (2000–2020) compared to 29 cases reported in more than a century, i.e., from the first reported case in 1887 till 1999.
The demographic and clinical details are depicted in [Table 1] (cases reported from 1887 to 1999) and [Table 2] (cases reported from 2000 till 2020).
Fifty-five cases were included for analysis as three cases were excluded due to the lack of adequate clinical details.
The measure of the significance of proportions was calculated with z-test for age, side of aTOS, and the presence of upper limb symptoms.
Stroke occurred in anterior circulatory territory alone in 34 and posterior circulation territory alone in 18, and in three cases, both anterior and posterior circulatory territories were involved. In fifteen cases [14/55], i.e., 27% of cases the stroke was recurrent.
In 36, i.e., 68% (36/53) of patients, stroke was preceded by features of upper limb ischemia (claudication/pallor/digital ulcers) by weeks to years. In seventeen cases, there was no history of upper limb ischemia, and in two cases, the presence or absence of upper limb ischemic symptoms was not mentioned.
The anatomical anomaly/abnormality at the thoracic outlet was cervical rib in 38 cases, fracture (clavicle/first rib) in four cases, and in three cases, it was an abnormal first rib. In nine cases, there was no bony abnormality at the thoracic outlet. In one case, the anomaly was not outlined.
Right upper limb involvement, i. e., right aTOS occurred in 46 cases and left only in nine cases.
Age ranged from 8 to 91 years. Forty-three cases were 40 years or younger and 12 were older than 40 years.
The measure of significance of proportions was calculated with z-test for age, side of aTOS and the presence of upper limb symptoms. The presence of upper limb ischemic symptoms [(P = 0.00001) with confidence interval (0.5536,0.8048)], right side aTOS [(P = 0.00001) and confidence interval (0.7368, 0.9360)] and age >40 years [(P = 0.00001), and confidence interval (0.66055,0.867450)] had significant association with the development of stroke.
| Discussion|| |
Arterial TOS is the least common among all types of TOS. Poststenotic dilatation (PSD)/aneurysm formation of SCA and adjoining AxA, resulting in thrombosis and distal embolization, is a usual and well-documented phenomenon in aTOS., It is both logical and intuitive.
However, retrograde embolization from SCA to VA/CA is counterintuitive. It is not only a rare phenomenon but also difficult to explain.
Since it was first described by Gould,, it has been reported by others too.,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,
The incidence of retrograde embolism leading to stroke in cases of aTOS has been 0.8% in one series of 120 stroke cases in young patients and 5% (2/40) in other series.,
However, it is difficult to determine the real incidence of such a rare condition.
This rare condition was brought to the light, the first time by an astute surgeon Gould A P, who followed one patient for 3 years and not only accurately diagnosed but also correctly interpreted the findings., This was well before the invention of the X rays. A similar explanation was offered later by Symmonds in two cases; however, apart from X-ray proof of cervical ribs, SCA thrombosis, and retrograde embolism was still a clinical deduction. Yates and Smith, later, proved findings of SCA/AxA artery thrombosis and cerebral infarction on autopsy and lent further credence to the retrograde embolic pathway.,
Almost one and half-century has passed since this problem was first recognized. However, a correct scientific explanation and the precipitating anatomical factors remain elusive. A few plausible explanations have been put forward by some authors and merit a discussion.
Prior demonstrated the positional reversal of flow in SCA, proximal to the level of stenosis, on the affected side, which resolved completely after the surgery. Gooneratne et al. also demonstrated reversal of blood blow in SCA in a patient with right side aTOS and bilateral posterior circulation stroke. The reversal of blood flow was more prominent with the occlusion of SCA.
Chen et al. proposed that thrombus being lower in density compared to blood could result in upstream mobilization.
Jusufovic et al. further tried to delineate the process. They ruled out the vessel wall inflammation by a negative 18 FDG PET/CT and showed that the thrombi in CA were not anchored to the wall and hence propagated from the SCA. Saunders et al. also used PET scan to rule out any arteritis.
Kalita et al. proposed that a combination of SCA stenosis/occlusion, along with the existence of the Venturi effect at the origin of the right carotid artery, leads to retrograde embolism. Their proposed explanation is not substantiated by any scientific observation or color doppler observations in their study. Moreover, the retrograde embolic phenomenon occurs both on the right and left.
Another explanation proposed by Palmer and Weaver is based on the Bernoulli principle. The high flow in the carotid artery (CA)/vertebral arteries (VA) in the presence of occluded/stenosed SCA causes a low-pressure area that draws thrombi back and up into VA/CA. The thrombosis of SCA aneurysm is not mandatory, but a transient/positional SCA stenosis/occlusion would create conditions for the thrombus to be drawn into VA/CCA. This is supported by the fact that not in all cases, the SCA was completely thrombosed.
Retrograde flow has been well documented in descending aorta and now being evaluated as an etiologic factor in stroke.
Hence, probably, all three mechanisms work in combination. The thrombi being less dense float and are thrown back up and into VA/CA assisted by periods of retrograde flow and low pressure at the origin of these vessels. The thrombosis of SCA/Ax A is not mandatory. However, intimal damage due to external compression leading to the production of thrombi is essential.
However, additional factors must play a role in that only a very small percentage of aTOS presents with stroke. Whether there is a peculiar subset of anatomical factors or it is just a matter of time that leads to stroke in such cases is unknown and should be a subject of further study.
A glaring fact that emerges from this study is that there was a window of opportunity for intervention in 68% cases as these presented with upper limb ischemic features. This varied from weeks to a few years. Hence, prompt evaluation of determining the etiology of upper limb ischemic symptoms and treatment needs emphasis.
The reverse is also true. That is, in patients with stroke and upper limb ischemic symptoms,
aTOS should be looked for, as the etiologic factor.
In a scenario of aTOS along with TIA/stroke, aTOS should be addressed as soon as possible because stroke/TIA recurred in 27 % cases.
| Conclusion|| |
Stroke due to retrograde embolization of thrombus from aTOS though rare is a reality. The phenomenon can be explained. Further study is required to determine the role of anatomical and hemodynamic factors. While evaluating stroke in young, aTOS should be looked for as part of an etiological search. Moreover, the stroke should also be considered as a rare complication of aTOS.
We are thankful to Dr. Ramanathan Saranga Bharathi, MCh, and Dr. Akshay Pratap Singh Chauhan MCh for all the help rendered in the preparation of this manuscript.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
[Table 1], [Table 2]