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The first anatomic descriptions of the thoracic outlet can be traced to 150 ad when Galen identified the presence of a cervical rib in human dissections. However, it was not until 1742 that Hunauld established the association between a cervical rib and upper extremity symptoms. In 1821 Cooper characterized the constellation of neurovascular symptoms involving the thoracic outlet. Ochsner called this the scalene santicus syndrome in 1936 and described the presence of muscle abnormalities secondary to repetitive trauma. 1 Peet and associates first applied the term thoracic outlet syndrome (TOS) in 1956, which is applied to primary arterial, venous, and neurogenic pathologies.
In 1861 Coote described the first operation to treat thoracic outlet pathology in a patient diagnosed as having an “exostosis” of the seventh cervical vertebra. Coote resected a portion of the transverse process, and the patient’s symptoms improved. In 1910 Murphy published the initial report describing first rib resection for the treatment of neurogenic TOS. Adson and Coffey subsequently performed an anterior scalenectomy in 1927 but without concomitant rib resection. Because of high recurrence rates, Claggett resurrected the notion of first rib resection for treatment of TOS in 1962, adopting a posterior approach. Because this was a morbid operation, Roos introduced the transaxillary approach to first rib resection and scalenectomy in 1966. Other techniques have emerged in the ensuing decades, including supraclavicular scalenectomy with or without first rib resection, a combined supraclavicular and infraclavicular approach, and combinations thereof. More recently, thoracoscopic rib resection has been reported. This chapter focuses on transaxillary first rib resection and partial scalenectomy for TOS.
Patients with a diagnosis of TOS who are appropriate surgical candidates should undergo surgical decompression of the thoracic outlet. TOS is subdivided into three discrete entities: neurogenic, venous, and arterial. The optimal approach should be individualized depending on the patient’s symptoms and anatomy and the surgeon’s experience. The transaxillary approach is preferred by many surgeons because of its relative ease, low risk profile, and documented improvement in patients’ quality of life. This approach effectively decompresses the thoracic outlet and is generally reserved for patients with neurogenic or venous TOS. If vessel reconstruction is anticipated, a different approach should be used because the transaxillary approach limits proximal arterial exposure.
Careful history and physical examination enable classification of TOS. The neurogenic form accounts for the majority of cases in modern series (>95%). Symptoms of neurogenic TOS, which is more prevalent in women, include paresthesia, pain, and impaired strength in the affected shoulder, arm, or hand, along with occipital headaches and neck discomfort. There is commonly an antecedent history of hyperextension neck injury or repetitive neck trauma. Patients frequently present with tenderness on palpation of the shoulder, mastoid region, or supraclavicular fossa or over the anterior scalene muscle. Three physical examination maneuvers support the diagnosis of neurogenic TOS:
Rotation of the neck and tilting of the head to the opposite side to elicit pain in the affected arm.
The upper limb tension test in which the patient first abducts both arms to 90 degrees with the elbows in a locked position, dorsiflexes the wrists, and finally tilts the head to the side. Each subsequent step imparts greater traction on the brachial plexus, with the first two positions causing discomfort on the ipsilateral side and the head tilt position causing pain on the contralateral side.
The elevated arm stress test during which the patient raises both arms directly above the head and repeatedly opens and closes the fists. Characteristic upper extremity symptoms arise within 60 seconds in patients with neurogenic TOS.
A cold hand with discoloration may be present in neurogenic TOS. Vasospastic in nature, it should not be confused with the presentation of digital or forearm microemboli found in arterial TOS. A careful vascular physical examination should confirm the presence of normal circulation.
Patients with venous TOS typically present with acute onset of dull aching pain of the upper extremity, associated with arm edema and cyanosis. Paresthesias may be present but are because of hand swelling rather than thoracic outlet nerve involvement. A history of strenuous and repetitive work or athletics involving the affected extremity is common, and most patients are young. This specific condition is known as Paget-Schroetter syndrome or effort vein thrombosis, because the entrapped subclavian vein has progressed to thrombosis. Some patients present less acutely with nonthrombotic subclavian vein occlusion or stenosis manifested by intermittent swelling with activity. Regardless, the etiology of venous TOS is mechanical and treatment is ultimately aimed at eliminating not only the venous obstruction but also the muscular bands that have entrapped and damaged the vein.
Arterial TOS typically manifests in one of three ways: asymptomatic, arm claudication, or critical ischemia of the hand. The majority of these patients have a cervical rib that may or may not be fused to the first rib, which most commonly is posterior to the subclavian artery. The etiology is chronic repetitive injury to the subclavian artery as it exits the thoracic outlet. This injury may cause subclavian artery stenosis but more commonly leads to ectasia or a true aneurysm. In asymptomatic patients a pulsatile mass or supraclavicular bruit can be detected on physical examination. Arm claudication is caused by areas of stenosis, which may be fixed, because of longstanding injury, or dynamic and occur with the arm abducted or extended only. Critical ischemia is because of emboli of fibrin-enriched platelet aggregates that originate from an ulcerated mural thrombus in the aneurysmal segment. The aneurysm is typically small, may be subtle on imaging studies, and may be prone to embolize related to its position rather than its size.
Preoperative physical therapy should be attempted for at least 8 weeks in patients with a diagnosis of neurogenic TOS. The aims of therapy are to improve posture and achieve greater range of motion. Patients with persistent symptoms of neurogenic TOS despite 8 weeks of physical therapy merit surgical intervention. At least 60% of patients improve with physical therapy and lifestyle alterations.
A radiographically guided anterior scalene block with local anesthetic (lidocaine) injection may provide a few hours of symptomatic relief. Patients with suspected neurogenic TOS often present with a constellation of physical complaints, not all of which are directly attributable to the disorder. A scalene block not only helps confirm the diagnosis but also simulates the expected postoperative result. This provides the patient and the surgeon with reassurance that surgical intervention will be beneficial and demonstrates which symptoms can be reliably expected to improve. As an alternative to surgical therapy patients can then opt for a onabotulinum toxin A (Botox, Allergan, Irvine, Calif.) injection. The Botox takes an average of 2 weeks to work and can be repeated once. This may provide symptomatic relief for 2 to 3 months, allowing participation in physical therapy. However, not all TOS patients respond to Botox. After two injections, the anterior scalene muscle becomes fibrotic and scarred and no longer responds as well to the Botox. This practice is especially helpful in patients who have had cervical spine fusions or shoulder operations, because they can strengthen the muscles of their neck and back, which may alleviate the TOS symptoms.
Plain-film chest radiograph is recommended for all patients undergoing surgical intervention for TOS to rule out supernumerary cervical ribs.
In young patients (<40 years of age) with a classic presentation of neurogenic TOS, there is no need for extensive preoperative testing. Older patients and those with a history of neck trauma should undergo magnetic resonance imaging to rule out cervical disc pathology.
Nerve conduction studies are typically normal in neurogenic TOS but may be useful in ruling out nerve compression such as carpal tunnel or cubital compression syndrome.
Duplex ultrasonography is the initial diagnostic modality to confirm pathology in patients with arterial TOS. Although useful to confirm axillosubclavian vein thrombosis in patients with suspected venous TOS, it is frequently unnecessary. Patients presenting acutely with classic signs and symptoms of venous TOS should undergo prompt venography for both diagnosis and therapeutic intervention. Patients with venous TOS should ultimately undergo imaging of the contralateral extremity with and without abduction, because the rate of bilateral venous compression ranges from 3% to 21%.
Therapeutic systemic anticoagulation with warfarin is initiated preoperatively only in patients with evidence of chronic venous TOS. Before surgery these patients are bridged from warfarin therapy to subcutaneous low-molecular-weight heparin.
Prophylactic antibiotics are administered perioperatively. A first-generation cephalosporin is preferred. In patients with penicillin allergy, clindamycin or vancomycin is used.
Incorrect diagnosis. A successful operation hinges on an accurate preoperative diagnosis. A thorough history and physical examination and an anterior scalene block help to identify the correct neurogenic patients for an operation.
Brachial plexus injury. Proper positioning and careful retraction help prevent excessive traction and injury to the brachial plexus.
Misidentification of the first rib. Proper identification of the first rib requires careful attention on the part of the surgeon, because its anatomic position is more cephalad than is frequently expected.
Incomplete first rib resection. Incomplete first rib resection has been associated with greater rates of recurrent TOS.
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