Types Of Thoracic Outlet Syndrome Research Articles

How I do it. Thoracic outlet syndrome and the transaxillary approach

Thoracic outlet syndrome (TOS) is a disease pattern that involves compression of neurologic venous or arterial structures as they pass through the thoracic outlet. TOS was first described as a vascular complication arising from the presence of a cervical rib. Over time, a better understanding of TOS has led to its wide range of presenting symptoms being divided into three distinct groups: arterial, venous, and neurogenic. Of the known cases, the current estimates of the incidence of neurogenic TOS, venous TOS, and arterial TOS are 95%, 3%, and 1%, respectively. The different types of TOS have completely different presentations, requiring expertise in the diagnosis, management, and treatment unique to each. We present our evaluation, diagnosis, and management method of TOS patients, with specific attention paid to the transaxillary approach.

Thoracic outlet syndrome: Its complexity is not disputed

Thoracic Outlet Syndrome (TOS) has a complex history that has led to misunderstanding and confusion from physicians. We review the history of TOS to better understand where this confusion comes from. We explain the etiology of TOS to give improved recommendations for treatment of this unique patient population. We present the case of a patient with two types of TOS to further examine the workup and treatment of a TOS patient.

Performance of First Rib Resection by Vascular Surgeons for Thoracic Outlet Syndrome Minimizes Hemorrhagic Complications

Thoracic outlet syndrome (TOS) takes on heterogeneous upper extremity manifestations depending on whether the artery, vein, or brachial plexus is primarily compressed. Despite sharing a common mechanism, the operative and perioperative management of these distinct types of TOS is disparate. As a result of these variable vascular and neurogenic symptoms, patients present to surgeons of various training backgrounds for surgical decompression. Surgeon specialty is known to correlate with outcomes for numerous vascular procedures, but its role in TOS is unclear. In this work, we examine the impact of surgeon specialty on short-term outcomes of first rib resection (FRR) for TOS. Using the American College of Surgeons National Surgical Quality Improvement Program database, 3070 patients were identified who underwent FRR for TOS during 2006 to 2017. Arterial, venous, and neurogenic TOS types were distinguished with International Classification of Diseases, Ninth Revision and Tenth Revision codes; patient characteristics, provider specialty, and postoperative outcomes were classified through a combination of standard National Surgical Quality Improvement Program variables and International Classification of Diseases data. Data analysis was performed with Stata version 14.2 (StataCorp LP, College Station, Tex). Most FRRs were performed by vascular surgeons (87.9%), general surgeons (6.9%), and thoracic surgeons (4.4%). The practice patterns between the specialties were significantly different (P < .001), with non-vascular surgeons operating on a significantly more undifferentiated TOS than vascular surgeons (16.9% vs 4.4%) but not less arterial or venous TOS (1.1% vs 2.4% and 8.6% vs 9.1%, respectively). Patients who underwent FRR with non-vascular surgeons experienced more frequent rate of postoperative transfusion (3.2% vs 1.2%; P = .001) and wound infection (1.9% vs 0.8%; P = .04). On multivariate regression, patients receiving FRR for venous TOS were more likely to experience an episode of postoperative hemorrhage requiring transfusion (odds ratio, 3.63; 95% confidence interval [CI], 1.43-9.25). Patients operated on by surgeons whose specialty was not among the top three most common specialties performing FRR had a 40% longer length operative time (incidence rate ratio, 1.42; 95% CI, 1.15-1.74) as well as a significantly increased odds of requiring a transfusion (odds ratio, 9.87; 95% CI, 2.28-42.68). These results suggest that despite the fact that vascular surgeons have a TOS practice with equivalent increased vascular complexity compared with non-vascular surgeons, their postoperative hemorrhage rates are decreased. This is likely due to the independent association between venous TOS and postoperative hemorrhage and pertains to familiarity with perioperative anticoagulation management as well as operative factors. The significantly increased operative times and transfusion requirements independently associated with specialties that uncommonly perform FRR raise further questions about the role of surgeon experience and volume in this procedure.

Evaluation and treatment of thoracic outlet syndrome during the global pandemic due to SARS-CoV-2 and COVID-19

The global SARS-CoV-2/COVID-19 pandemic has required a reduction in nonemergency treatment for a variety of disorders. This report summarizes conclusions of an international multidisciplinary consensus group assembled to address evaluation and treatment of patients with thoracic outlet syndrome (TOS), a group of conditions characterized by extrinsic compression of the neurovascular structures serving the upper extremity. The following recommendations were developed in relation to the three defined types of TOS (neurogenic, venous, and arterial) and three phases of pandemic response (preparatory, urgent with limited resources, and emergency with complete diversion of resources).• In-person evaluation and treatment for neurogenic TOS (interventional or surgical) are generally postponed during all pandemic phases, with telephone/telemedicine visits and at-home physical therapy exercises recommended when feasible.• Venous TOS presenting with acute upper extremity deep venous thrombosis (Paget-Schroetter syndrome) is managed primarily with anticoagulation, with percutaneous interventions for venous TOS (thrombolysis) considered in early phases (I and II) and surgical treatment delayed until pandemic conditions resolve. Catheter-based interventions may also be considered for selected patients with central subclavian vein obstruction and threatened hemodialysis access in all pandemic phases, with definitive surgical treatment postponed.• Evaluation and surgical treatment for arterial TOS should be reserved for limb-threatening situations, such as acute upper extremity ischemia or acute digital embolization, in all phases of pandemic response. In late pandemic phases, surgery should be restricted to thrombolysis or brachial artery thromboembolectomy, with more definitive treatment delayed until pandemic conditions resolve.

Novel Surgical Approach for Decompression of the Scalene Triangle in Neurogenic Thoracic Outlet Syndrome.

Thoracic outlet syndrome (TOS) is a cause of upper extremity and shoulder dysfunction. TOS can present with a wide range of symptoms due to compression of the brachial plexus or its branches during their passage through the cervicothoracobrachial region or scalene triangle. There are three types of TOS: arterial, venous, and neurogenic. Neurogenic TOS (nTOS) is by far the most frequent type and represents more than 95% of all cases. Historically, surgical intervention for all types of TOS has evolved based on the treatment for a vascular etiology and has typically included a first rib resection. Despite nTOS being by far the more common type, most previous interventions have not considered treatment via peripheral nerve decompression.We describe surgical treatment of nTOS, performed on an outpatient basis, which focuses on the surgical decompression of the structures associated with the scalene triangle in conjunction with release of the pectoralis minor insertion through limited incisions. The procedure avoids the morbidity associated with first rib resection and is successful in ameliorating nTOS symptoms. Further, we propose a nomenclature shift to scalene triangle syndrome (STS) to reflect the nerve and arterial compressions needing to be addressed.

Neurogenic Thoracic Outlet Syndrome Caused by Vascular Compression of the Brachial Plexus: A Report of Two Cases.

Thoracic outlet syndrome (TOS) is caused by compression of the brachial plexus and/or subclavian vessels as they pass through the cervicothoracobrachial region, exiting the chest. There are three main types of TOS: neurogenic TOS, arterial TOS, and venous TOS. Neurogenic TOS accounts for approximately 95% of all cases, and it is usually caused by physical trauma (posttraumatic etiology), chronic repetitive motion (functional etiology), or bone or muscle anomalies (congenital etiology). We present two cases in which neurogenic TOS was elicited by vascular compression of the inferior portion of the brachial plexus.

Thoracic Outlet Syndrome

Thoracic outlet syndrome (TOS) is a condition caused by compression of the neurovascular structures leading to the arm passing through the thoracic outlet. The incidence of TOS is reported as 0.3 to 2% in the general population. There are three distinct types of TOS: neurogenic (95%), venous (4%), and arterial (1%). Treatment algorithms depend on the type of TOS. Arterial and venous TOS often present urgently with arterial or venous thrombosis, which is fairly easily identified by thorough history taking and a physical examination. Diagnosis is also aided by duplex ultrasonography. Restoration of arterial or venous flow can often be readily accomplished by thrombolysis. More important, however, is the diagnosis of the underlying structural component involved in the development of symptoms. Although statistically the most common, neurogenic TOS is often the most difficult to diagnose and treat. There are good data indicating that appropriately selected patients benefit from surgical therapy for neurogenic TOS as well. To prevent recurrence of symptoms, patients must undergo first rib resection and anterior scalenectomy, as well as resection of any rudimentary or cervical ribs. Regardless of the type of TOS encountered, proper therapy requires a thorough diagnostic evaluation and multimodal treatment. Keywords: thoracic outlet syndrome, arterial thoracic outlet syndrome, neurogenic thoracic outlet syndrome, venous thoracic outlet syndrome, TOS, effort thrombosis, thoracic outlet decompression

The Diagnostic Accuracy of Clinical Diagnostic Tests for Thoracic Outlet Syndrome

Can clinical diagnostic tests accurately diagnose patients presenting with symptoms of thoracic outlet syndrome? Summary of Key Findings: A thorough literature search returned 6 possible studies; 3 studies met the inclusion criteria and were included. Two studies supported the use of clinical diagnostic tests for the diagnosis of thoracic outlet syndrome. One study reported high false-positive rates among clinical diagnostic tests for thoracic outlet syndrome. One study reported that clinical diagnostic test findings correlate to provocative positioned magnetic resonance imaging findings. Clinical Bottom Line: There is moderate evidence to support the use of the Halstead maneuver (also known as the costoclavicular maneuver or exaggerated military brace test), Wright's test, Cyriax Release test, and supraclavicular pressure test to have good diagnostic accuracy for the provocation of symptoms in patients presenting with upper extremity pathology. However, these clinical diagnostic tests do not appear to allow for the differential diagnosis of thoracic outlet syndrome exclusively. The use of the Adson's test and Roos test should be discontinued for the differential diagnosis of thoracic outlet syndrome. Strength of Recommendation: Grade B evidence exists to support the accuracy of the Halstead maneuver, Wright's test, Cyriax Release test, and supraclavicular pressure test for the diagnosis of upper extremity pathology in general. Grade C evidence exists for the use of these clinical diagnostic tests to exclusively diagnose thoracic outlet syndrome.

Outcomes of Surgical Paraclavicular Thoracic Outlet Decompression

Thoracic outlet syndrome (TOS) is a constellation of signs and symptoms caused by compression of the neurovascular structures in the thoracic outlet. These structures include the brachial plexus, the subclavian vein, and the subclavian artery, resulting in neurogenic (NTOS), venous (VTOS), and arterial (ATOS) types of TOS, respectively. The purpose of this study was to evaluate the outcomes of paraclavicular surgical decompression for TOS. A prospective analysis of patients who underwent surgical decompression for TOS at a newly established center was performed. Diagnosis of TOS was based on clinical history, a physical examination, and additional diagnostic studies. The indication for surgery in patients diagnosed with NTOS was the presence of persistent symptoms after a trial of physical therapy. Primary outcomes were assessed according to Derkash's classification as excellent, good, fair, and poor. Secondary outcomes included mortality, complications, and duration of hospital stay. Between August 2004 and June 2011, 40 paraclavicular decompression procedures were performed on 36 patients (16 men) with TOS. The mean age was 36.5 years (range: 15-68). Bilateral decompression was performed on 4 patients. The types were NTOS (n = 19; 48%), VTOS (n = 16; 40%), and ATOS (n = 5; 12%). In addition to pain, the most common presenting symptom was numbness in NTOS, swelling in VTOS, and coolness in ATOS. A history of trauma was present in 22.2%. Two patients suffered from recurrent symptoms after previous transaxillary first rib resection for VTOS at another institution. Diagnostic tests performed included nerve conduction studies (43%), venogram (40%), and arteriogram (20%). All patients underwent paraclavicular decompression, which included radical anterior and partial middle scalenectomy, brachial plexus neurolysis, and first rib resection. The first rib resection was partial, through a supraclavicular only approach in NTOS and ATOS patients (60%) or complete, through a supra- and infraclavicular approach for VTOS patients (40%). Functional outcomes were excellent, good, fair, and poor in 74.4%, 15.4%, 10.3%, and 0% of cases, respectively. One patient was lost to follow-up. Two patients with incomplete relief of symptoms after paraclavicular decompression for NTOS underwent pectoralis minor decompression. There were no deaths. Complications included pleural effusion requiring evacuation (n = 4), neuropraxia (n = 1), and lymph leak (n = 1) treated with tube thoracostomy. No patients experienced injury to the long thoracic or phrenic nerves. The mean duration of hospital stay was 4.4 days. The mean follow-up was 10.3 months. In our experience, surgical paraclavicular decompression can provide safe and effective relief of NTOS, VTOS, and ATOS symptoms. Functional outcomes were excellent or good in the majority of patients, with minimal complications.

Relevance of Bone Anomalies in Patients with Thoracic Outlet Syndrome

Skeletal anomalies are recognized as potential causes of thoracic outlet syndrome (TOS); however, there is a paucity of information regarding the specific bone anomalies associated with TOS and their relative incidence among the different clinical types of TOS. This study describes the prevalence of bone anomalies in a population with TOS. A retrospective chart review of the clinical records and imaging studies of all patients who were surgically treated at our institution for TOS between 1991-2011 was conducted. A descriptive analysis of the cohort of patients with associated bone anomalies was performed and compared with the cohort of patients without bone anomalies. During the study period, 400 patients underwent operative procedures for TOS. Of these, 115 (29%) harbored a bone anomaly and the remaining 285 did not. The bone anomalies included 80 (69%) cervical ribs, 25 (22%) clavicular anomalies, and 10 (9%) isolated first rib aberrations. Ninety (78%) of the bone anomalies were congenital, while 25 (22%) were posttraumatic. The bone anomaly cohort was predominantly female (76%), with an average age of 36 years. The distribution of neurogenic, arterial, and venous types of TOS in the cohort with bone anomalies was 63%, 33%, and 4%, respectively, while it was 51% neurogenic, 11% arterial, and 38% venous in the cohort without bone anomalies. These distributions were significantly different (chi-squared: 56.75; P < 0.0001). The likelihood of neurogenic compression was roughly equivalent between the 2 cohorts (odds ratio [OR]: 1.6; P = 0.03), while the likelihood of arterial compression was much higher in the presence of a bone anomaly (OR: 4.0; P < 0.001) and the likelihood of venous compression was much lower in the presence of bone anomaly (OR: 0.07; P < 0.001). Conversely, 33% of all neurogenic TOS cases, 54% of all arterial TOS cases, and 4% of all venous TOS cases were associated with a bone anomaly. In our experience, the incidence of bone anomalies among patients treated for TOS was 29%, which is higher than previously reported. Cervical ribs were present in 20% of our patients with TOS, an estimated 40 times higher prevalence than that in the general population. However, acquired clavicular deformities and isolated abnormal first ribs were found in 9% of our patients, accounting for almost one-third of all bone anomalies present in this TOS population. The incidence of bone anomalies is rather different among the subtypes of TOS. The strongest association with the presence of a bone anomaly occurs in patients with arterial TOS, although 46% of all our arterial TOS cases did not have a bone anomaly. The presence of bone anomalies does not seem to influence the occurrence of neurogenic TOS, while venous TOS likely has no association with congenital bone anomalies, but occasionally mid and medial clavicular fracture calluses may cause venous TOS.

Thoracic Outlet Syndrome—Postural Type: Ultrasound Imaging of Pectoralis Minor and Brachial Plexus Abnormalities

Thoracic outlet syndrome (TOS) is a controversial diagnosis that sometimes is referred to as disputed or nonspecific neurogenic TOS because diagnostic test results typically are negative or inconclusive [1-10]. A review of the pathomechanics and associated dysfuncional body habitus suggests that use of the term “postural TOS” is more appropriate for this ommon type of presentation [10]. Postural TOS is thus recommended in cases without bjectifiable neurologic or vascular abnormality. In contrast, the less-common type of TOS nvolves compromise of the neurovascular bundle (NVB), which includes the brachial lexus (BP), the axillary or subclavian artery, and the axillary or subclavian vein [1-8,10]. Compression in all types of TOS may occur superiorly at the interscalene space, the costoclavicular space, or beneath the pectoralis minor muscle (PMM). The PMM location is recognized as a common and important site of compression in both the postural and nonpostural types of TOS [1-3,9-13]. The findings on an electrodiagnostic examination (EDX) typically are normal in patients with postural TOS because there is no axonal damage and no significant conduction block or demyelination [1,8,10]. Results of blood-flow studies usually are normal as well, and although they may reveal mild vascular compromise during stress maneuvers [1,2], this finding may not be clinically significant because it also can be seen in asymptomatic persons [1,7-9]. In addition, it is important to consider differential diagnoses and rule out the following conditions: cervical radiculopathy, peripheral nerve entrapment (median or ulnar), peripheral polyneuropathy, cervical cord lesion, or superior sulcus (Pancoast) tumor. The EDX may reveal the first 3 categories, but cervical magnetic resonance imaging (MRI) and a chest radiograph will be needed if the other conditions are considered. Neuromuscular ultrasound (NMUS) is a new imaging modality for examining nerve structures within the thoracic outlet area [14,15]. NMUS has unique applications for the postural type of TOS; as some researchers have noted, “evaluation of proximal nerves is often problematic when using electrodiagnostic techniques and may be more easily studied with ultrasound” [16]. My experience with this type of postural TOS [1,2,9,12,17,18] suggests that the PMM is contributory, and NMUS now appears to support these prior clinical impressions. Palpation of increased tension and trigger points in the PMM, combined with shoulder protraction, suggests that the PMM has shortened. The hypothesis herein is that the effects of a tight PMM can be observed to affect the NVB and explain the symptoms. The goal of this article is to present and analyze imaging findings in patients with TOS who were examined with NMUS while in neutral and stress positions, while monitoring for symptoms.

Contemporary management of thoracic outlet syndrome

The diagnosis and management of thoracic outlet syndrome (TOS) has been surrounded by controversy since this disorder was first recognized. Recent evidence from observational studies has helped us better understand the pathophysiology of different TOS subtypes and guide clinical decision making for this disorder. The identification of anatomic anomalies involved with the cause of different TOS subtypes has been made easier by contemporary diagnostic techniques. This includes the injection of neuromuscular blocking agents into anterior scalene muscles to help confirm the diagnosis of neurogenic TOS. Surgical intervention by means of first rib resection and anterior scalenectomy is an effective treatment for patients diagnosed with neurogenic and venous TOS, resulting in a significant increase in quality-of-life measures for the majority of patients. Patients with acute and chronic venous TOS should be maintained on anticoagulation during the perioperative period and may not need thrombolysis prior to surgery. Finally, patients with arterial TOS should undergo cervical or first rib resection with or without arterial reconstruction to alleviate and prevent recurrence of symptoms. The management of TOS requires a multidisciplinary approach with specific treatment algorithms for each TOS subtype. Appropriately selected patients with all different types of TOS may benefit from surgical intervention.

Current management of thoracic outlet syndrome

Thoracic outlet syndrome (TOS) is a condition caused by compression of the neurovascular structures leading to the arm passing through the thoracic outlet. There are three distinct types of TOS: neurogenic (95%), venous (4%-5%), and arterial (1%). Treatment algorithms depend on the type of TOS. Although statistically the most common type, neurogenic TOS can often be the most difficult to diagnose and treat. We have good follow-up data indicating that appropriately selected patients benefit from surgical intervention. Arterial and venous TOS often present more urgently with arterial or venous thrombosis. The thrombosis is typically recognized expeditiously by thorough history taking and physical examination, augmented by duplex ultrasonography. The restoration of blood flow, be it venous or arterial, often can be accomplished readily by thrombolysis. The key, however, comes in diagnosing the underlying structural component involved in the development of symptoms. To prevent recurrence, patients must undergo first rib resection and anterior scalenectomy, as well as resection of any rudimentary or cervical ribs. In the case of arterial TOS, the subclavian artery often requires reconstruction as well. Regardless of the type of TOS encountered, proper treatment requires a multidisciplinary approach.

Vascular thoracic outlet syndrome

In the methods section of the article on vascular thoracic outlet syndrome (TOS) by Geven et al. [1], the authors point out that their indication for the diagnosis of ‘vascular TOS’ was an abnormal PPG study indicating signs of vascular compression of the subclavian artery. I question the labeling of the patients described here as having ‘vascular’ TOS. As the authors point out in their opening paragraph, there are two types of vascular TOS, arterial and venous. Because these two types are totally different from each other, the terms arterial TOS and venous TOS should be employed and the term ‘vascular’ eliminated. Venous TOS is manifested by symptoms of swelling and cyanosis, while arterial TOS by symptoms of ischemic fingers and arm claudication. Neurogenic TOS is identified by symptoms of paresthesia, weakness, and pain, not only in the upper extremity, but usually in the neck as well. Further, arterial TOS is almost always associated with a cervical rib or anomalous first rib. The symptoms of arterial TOS are usually the result of emboli from subclavian artery thrombosis, either from subclavian artery stenosis or subclavian artery aneurysm with mural thrombus. Only 6 of the 32 patients in this study had cervical ribs. Unfortunately, the authors fail to describe their patients’ symptoms which would help define the type of TOS they were treating. However, since all operations were transaxillary rib resections and none were arterial repairs, it can be assumed that none of these patients had arterial TOS and probably the large majority, if not all, of the patients had neurogenic TOS. Confusion regarding the differentiation between arterial and neurogenic TOS is common because many patients with neurogenic TOS have symptoms of coldness and color changes in their hands along with their other symptoms. These symptoms do not establish a diagnosis of arterial or vascular TOS. They are the result arteriolar vasoconstriction brought on by sympathetic nerve stimulation from compression of the sympathetic nerve fibers that accompany the C7 and C8 nerve roots [2]. Thus, these symptoms are those of neurogenic TOS