Adult Chest Surgery

Chapter 124. Thoracoscopic First Rib Resection with Dorsal Sympathectomy 

Thoracic outlet syndrome (TOS), a term coined by Rob and Standeven,refers to compression of the subclavian vessels and brachial plexus at the superior aperture of the chest. It was previously designated as scalenus anticus, costoclavicular, hyperabduction, cervical rib, and first thoracic rib syndromes according to presumed etiologies. The various syndromes are similar, and the compression mechanism is often difficult to identify. Most compressive factors operate against the first rib.2,3

SURGICAL ANATOMY

At the superior aperture of the thorax, the subclavian vessels and the brachial plexus traverse the cervicoaxillary canal to reach the upper extremity. The cervicoaxillary canal is divided into two sections by the first rib: the proximal division, composed of the scalene triangle and the costoclavicular space, and the distal division, composed of the axilla (Fig. 124-1). The proximal division is important to achieve acceptable neurovascular decompression. It is bounded superiorly by the clavicle, inferiorly by the first rib, anteromedially by the costoclavicular ligament, and posterolaterally by the scalenus medius (middle scalene) muscle and the long thoracic nerve. The scalenus anticus (anterior scalene) muscle, which inserts on the scalene tubercle of the first rib, divides the costoclavicular space into two compartments: The anteromedial compartment contains the subclavian vein, and the posterolateral compartment contains the subclavian artery and the brachial plexus. The latter compartment, which is bounded by the scalenus anticus (anterior scalene) muscle anteriorly, the scalenus medius (middle scalene) muscle posteriorly, and the first rib inferiorly, is called the scalene triangle.

Figure 124-1.

 

The cervicoaxillary canal has a proximal division consisting of the scalene triangle and costoclavicular space and a distal division composed of the axilla. The proximal division is more susceptible to neurovascular compression.

FUNCTIONAL ANATOMY

The cervicoaxillary canal, particularly its proximal division, also termed the costoclavicular area, normally has ample space for the passage of the neurovascular bundle without compression. Narrowing of this space occurs during functional maneuvers. It narrows during abduction of the arm because the clavicle rotates backward toward the first rib and the insertion of the scalenus anticus (anterior scalene) muscle. In hyperabduction, the neurovascular bundle is pulled around the pectoralis minor tendon, the coracoid process, and the head of the humerus. During this maneuver, the coracoid process tilts downward and thus exaggerates the tension on the bundle. The sternoclavicular joint, which ordinarily forms an angle of 15–20 degrees, forms a smaller angle when the outer end of the clavicle descends (as in drooping of the shoulders in poor posture), and narrowing of the costoclavicular space may occur. Normally, during inspiration, the scalenus anticus muscle raises the first rib and thus narrows the costoclavicular space. This muscle may cause an abnormal lift of the first rib, as in cases of severe emphysema or excessive muscular development, which is seen in young adults.

The scalene triangle, which normally occurs between the scalenus anticus anteriorly, the scalenus medius posteriorly, and first rib inferiorly, permits passage of the subclavian artery and the brachial plexus, which are in direct contact with the first rib. The space of the triangle is 1.2 cm at its base and approximately 6.7 cm in height. There is a close-fitting relationship between the neurovascular bundle and this triangular space. Anatomic variations may narrow the superior angle of the triangle, cause impingement on the upper components of the brachial plexus, and produce the upper type of TOS that involves the trunk containing elements of C5 and C6. If the base of the triangle is raised, compression of the subclavian artery and the trunk containing components of C7, C8, and T1 results in the lower type of thoracic outlet syndrome(Fig. 124-2).

Figure 124-2.

 

Components of the brachial plexus in the scalene triangle.

COMPRESSION FACTORS

Many factors may cause compression of the neurovascular bundle at the thoracic outlet, but the basic factor is deranged anatomy, to which congenital, traumatic, and occasionally, atherosclerotic factors may contribute5(Table 124-1). Bony abnormalities are present in approximately 30% of patients, either as cervical rib, bifid first rib and fusion of first and second ribs, clavicular deformities, or previous thoracoplasties.These abnormalities can be visualized on the plain posteroanterior chest film, but special x-ray views of the lower cervical spine may be required in some cases of cervical ribs.

Table 124-1. Etiologic Factors of Neurovascular Compression Syndromes

Anatomic

Potential sites of neurovascular compression

   Interscalene triangle

   Costoclavicular space

   Subcoracoid area

Congenital

Cervical rib and its fascial remnants

Rudimentary first thoracic rib

Scalene muscles

   Anterior

   Middle

   Minimus

Adventitious fibrous bands

Bifid clavicle

Exostosis of first thoracic rib

Enlarged transverse process of C7

Omohyoid muscle

Anomalous course of transverse cervical artery

Brachial plexus postfixed

Flat clavicle

Traumatic

Fracture of clavicle

Dislocation of head of humerus

Crushing injury to upper thorax

Sudden, unaccustomed muscular efforts involving shoulder girdle muscles

Cervical spondylosis and injuries to cervical spine

Atherosclerosis

 

SYMPTOMS AND SIGNS

The symptoms of TOS depend on whether the nerves or blood vessels or both are compressed in the cervicoaxillary canal. Neurogenic manifestations are observed more frequently than vascular ones. Symptoms of pain and paresthesias are present in approximately 95% of patients. Motor weakness and occasionally atrophy of hypothenar and interosseous muscles, which is the ulnar type of atrophy, are present in approximately 10%. The symptoms occur most commonly in areas supplied by the ulnar nerve, which include the medial aspects of the arm and hand, the fifth finger, and the lateral aspects of the fourth finger. The onset of pain is usually insidious and commonly involves the neck, shoulder, arm, and hand. The pain and paresthesias may be precipitated by strenuous physical exercise or sustained physical effort with the arm in abduction and the neck in hyperextension. Symptoms may be initiated by sleeping with the arms abducted and the hands clasped behind the neck. In other cases, trauma to the upper extremities or the cervical spine is a precipitating factor. Physical examination may be noncontributory. When present, objective physical findings usually consist of hypesthesia along the medial aspects of the forearm and hand. Atrophy, when evident, is usually described in the hypothenar and interosseous muscles with clawing of the fourth and fifth fingers. In the upper type of TOS, in which components of C5 and C6 are involved in the compression (see Fig. 124-2), pain is usually in the deltoid area and the lateral aspects of the arm. The presence of this pain should induce action to exclude a herniated cervical disk. Entrapment of C7 and C8 components that contribute to the median nerve produces symptoms in the index and sometimes middle fingers. Compression of components of C5, C6, C7, C8, and T1 can occur at the thoracic outlet by a cervical rib and produce symptoms of various degrees in the distribution of these nerves.

In some patients, the pain is atypical, involving the anterior chest wall or parascapular area, and is termed pseudoangina because it simulates angina pectoris. These patients may have normal coronary arteriograms and ulnar nerve conduction velocities decreased to values of 48 m/s and less, which strongly suggests the diagnosis of thoracic outlet syndrome. The shoulder, arm, and hand symptoms that usually provide clues for the diagnosis of TOS may be absent or minimal initially compared with the severity of the chest pain. The diagnosis of TOS frequently is overlooked; many of these patients are committed to becoming "cardiac cripples" without an appropriate diagnosis or to developing severe psychological depression when told that their coronary arteries are normal and that they have no significant cause for their pain.6

Symptoms of arterial compression include coldness, weakness, easy fatigability of the arm and hand, and pain that is usually diffuse.3,7 Raynaud's phenomenon is noted in approximately 7.5% of patients with thoracic outlet syndrome.Unlike Raynaud's disease, which is usually bilateral and symmetric and elicited by cold or emotion, Raynaud's phenomenon in neurovascular compression usually is unilateral and is more likely to be precipitated by hyperabduction of the involved arm, turning of the head, or carrying heavy objects. Sensitivity to cold also may be present. Symptoms include sudden onset of cold and blanching of one or more fingers, followed slowly by cyanosis and persistent rubor. Vascular symptoms in neurovascular compression may be precursors of permanent arterial thrombosis.When present, arterial occlusion, usually of the subclavian artery, is manifest by persistent coldness, cyanosis or pallor of the fingers, and in some instances ulceration or gangrene. Palpation in the parascapular area may reveal prominent pulsation, which indicates poststenotic dilatation or aneurysm of the subclavian artery.8

Less frequently, the symptoms are those of venous obstruction or occlusion, commonly recognized as effort thrombosis, or Paget-Schroetter syndrome (see Chap. 125). The condition characteristically results in edema, discoloration of the arm, distention of the superficial veins of the limb and shoulder, and some degree of aches and pains. In some patients, the condition is observed on waking; in others, it follows sustained efforts with the arm in abduction. Sudden backward and downward bracing of the shoulders, heavy lifting, or strenuous physical activity involving the arm may constrict the vein and initiate venospasm, with or without subsequent thrombosis. On examination, in patients with definite venous thrombosis, there is usually moderate tenderness over the axillary vein, and a cordlike structure may be felt that corresponds to the course of the vein. The acute symptoms may subside in a few weeks or days as the collateral circulation develops. Recurrence follows with inadequacy of the collateral circulation.

Objective physical findings are more common in patients with primarily vascular as opposed to neural compression. Loss or diminution of radial pulse and reproduction of symptoms can be elicited by the three classic clinical maneuvers (described below)—the Adson or scalene test,the costoclavicular test, and the hyperabduction test.10

DIAGNOSIS

The diagnosis of TOS includes history, physical and neurologic examinations, films of the chest and cervical spine, electromyogram, and ulnar nerve conduction velocity (UNCV). In some patients with atypical manifestations, other diagnostic procedures, such as cervical myelography, peripheral or coronary arteriography, and phlebography should be considered. A detailed history and physical examination, together with neurologic examination, often can result in a tentative diagnosis of neurovascular compression. This diagnosis is strengthened when one or more of the classic clinical maneuvers is positive and is confirmed by the finding of decreased UNCV.7

Clinical Maneuvers

The clinical evaluation is best based on the physical findings of loss or decrease of radial pulses and reproduction of symptoms that can be elicited by the three classic maneuvers.

ADSON OR SCALENE TEST9

This maneuver tightens the anterior and middle scalene muscles and thus decreases the interspace and magnifies any preexisting compression of the subclavian artery and brachial plexus. The patient is instructed to take and hold a deep breath, extend the neck fully, and turn the head toward the side. Obliteration or decrease of the radial pulse suggests compression.5,10

COSTOCLAVICULAR TEST (MILITARY POSITION)

This maneuver narrows the costoclavicular space by approximating the clavicle to the first rib and thus tends to compress the neurovascular bundle. Changes in the radial pulse with production of symptoms indicate compression. The shoulders are drawn downward and backward.5,10

HYPERABDUCTION TEST

When the arm is hyperabducted to 180 degrees, the components of the neurovascular bundle are pulled around the pectoralis minor tendon, the coracoid process, and the head of the humerus. If the radial pulse is decreased, compression should be suspected. 5,10

Radiographic Findings

Films of the chest and cervical spine are helpful in revealing bony abnormalities, particularly cervical ribs and bony degenerative changes. If osteophytic changes and intervertebral disk space narrowing are present on plain cervical films, a cervical CT scan should be performed to rule out bony encroachment and narrowing of the spinal canal and the intervertebral foramina.

Nerve Conduction Velocity and Electromyography

This test is used widely in the differential diagnosis of the causes of arm pain, tingling, and numbness with or without motor weakness of the hand. Such symptoms may result from compression at various sites: in the spine; at the thoracic outlet; around the elbow, where it causes tardy ulnar nerve palsy; or on the flexor aspects of the wrist, where it produces carpal tunnel syndrome. For diagnosis and localization of the site of compression, cathodal stimulation is applied at various points along the course of the nerve. Motor conduction velocities of the ulnar, median, radial, and musculocutaneous nerves can be measured reliably. Caldwell and colleagues have improved the technique of measuring UNCV for evaluation of patients with thoracic outlet compression.11 Conduction velocities over proximal and distal segments of the ulnar nerve are determined by recording the action potentials generated in the hypothenar or first dorsal interosseous muscles. The points of stimulation are the supraclavicular fossa, middle upper arm, below the elbow, and at the wrist.7

EQUIPMENT

Electromyographic examination of each upper extremity and determination of the conduction velocities are done with the Meditron 201 AD or 312 or the TECA-3 electromyograph; coaxial cable with three needles or surface electrodes is used to record muscle potentials, which appear on the fluorescent screen.

TECHNIQUE

The conduction velocity is determined by the Krusen-Caldwell technique.12 The patient is placed on the examination table with the arm fully extended at the elbow and in about 20 degrees of abduction at the shoulder to facilitate stimulation over the course of the ulnar nerve. The ulnar nerve is stimulated at the four points by a special stimulation unit that imparts an electrical stimulus with strength of 350 V with the patient's load, which is approximately equal to 300 V, with a skin resistance of 5000 . Supramaximal stimulation is used at all points to obtain maximal response. The duration of the stimulation is 0.2 ms, except for muscular individuals, for whom it is 0.5 ms. Time of stimulation, conduction delay, and muscle response appear on the TECA screen; time markers occur each millisecond on the sweep. The latency period to stimulation from the four points of stimulation to the recording electrode is obtained from the TECA digital recorder or calculated from the tracing on the screen.

NORMAL UNCVS

The normal values of the UNCVs according to the Krusen-Caldwell technique11 are 72 m/s or above across the outlet, 55 m/s or above around the elbow, and 59 m/s or above in the forearm. Wrist delay is 2.5–3.5 ms. Decreased velocity in a segment or increased delay at the wrist indicates either compression, injury, neuropathy, or neurologic disorders. Decreased velocity across the outlet is consistent with TOS. Decreased velocity around the elbow signifies ulnar nerve entrapment or neuropathy. Increased delay at the wrist is encountered in carpal tunnel syndrome.

GRADING OF COMPRESSION

The clinical picture of TOS correlates fairly well with the conduction velocity across the outlet. Any value less than 70 m/s indicates neurovascular compression. The severity is graded according to the decrease in velocity across the thoracic outlet: Compression is considered slight when the velocity is 66–69 m/s, mild when the velocity is 60–65 m/s, moderate when the velocity is 55–59 m/s, and severe when the velocity is 54 m/s and below.

Angiography

Simple clinical observations usually suffice to determine the degree of vascular impairment in the upper extremity. Peripheral angiography8,13 is indicated in some patients, as in the presence of a paraclavicular pulsating mass, the absence of a radial pulse, or the presence of supraclavicular or infraclavicular bruits. Retrograde or antegrade arteriograms of the subclavian and brachial arteries to demonstrate or localize the pathology should be obtained. In cases of venous stenosis or obstruction, as in Paget-Schroetter syndrome (see Chap. 125), phlebograms are used to determine the extent of thrombosis and the status of the collateral circulation.

DIFFERENTIAL DIAGNOSIS

TOS should be differentiated from various neurologic, vascular, cardiac, pulmonary, and esophageal conditions5,6,10 (Table 124-2). Neurologic causes of pain in the shoulder and arm are more difficult to recognize and may arise from involvement of the nervous system in the spine, the brachial plexus, or the peripheral nerves. A common neurologic cause of pain in the upper extremities is a herniated cervical intervertebral disk. The herniation almost invariably occurs at the interspace between the fifth and the sixth or the sixth and the seventh cervical vertebrae and produces characteristic symptoms. Onset of pain and stiffness of the neck is manifested with varying frequency. The pain radiates along the medial border of the scapula into the shoulder, occasionally into the anterior chest wall, and down the lateral aspect of the arm, at times into the fingers. Numbness and paresthesias in the fingers may be present. The segmental distribution of pain is a prominent feature. A herniated disk between the C5 and C6 vertebrae that compresses the C6 nerve root causes pain or numbness primarily in the thumb and to a lesser extent in the index finger. The biceps muscle and the radial wrist extensor are weak, and the reflex of the biceps muscle is reduced or abolished. A herniated disk between the C6 and C7 vertebrae that compresses the C7 nerve root produces pain or numbness in the index finger and weakness of index finger flexion and ulnar wrist extension; the triceps muscle is weak, and its reflex is reduced or abolished. Any of these herniated disks may cause numbness along the ulnar border of the arm and hand owing to spasm of the anterior scalene muscle. Rarely, pain and paresthesias in the ulnar distribution may be related to herniation between the C7 and the Tl vertebrae, which causes compression of the C8 nerve root. Compression of the latter nerve root produces weakness of intrinsic hand muscles.5,12 Although rupture of the fifth and sixth disks produces hypesthesia in this area, only rupture of the seventh disk produces pain down the medial aspect of the arm.The diagnosis of a ruptured cervical disk is based primarily on the history and physical findings; lateral films of the cervical spine reveal loss or reversal of cervical curvature, with the apex of the reversal of curvature located at the level of the disk involved. Electromyography can localize the site and extent of the nerve root irritation. When a herniated disk is suspected, cervical myelography should be done to confirm the diagnosis.5,12

Table 124-2. Differential Diagnosis of TOS Nerve Compression

Cervical spine

Ruptured intervertebral disc

Degenerative disease

Osteoarthritis

Spinal cord tumors

Brachial plexus

Superior sulcus tumors

Trauma-postural palsy

Peripheral nerves

Entrapment neuropathy

   Carpal tunnel—median nerve

   Ulnar nerve—elbow

   Radial nerve

   Suprascapular nerve

Medical neuropathies

Trauma

Tumor

Vascular phenomena

Arterial

   Arteriosclerosis-aneurysm

Occlusive

   Thromboangiitis obliterans

   Embolism

Functional

Raynaud's disease

Reflex vasomotor dystrophy

Causalgia

Vasculitis, collagen disease, panniculitis

Venous thrombophlebitis

Mediastinal venous obstruction

Malignant

Benign

Other diseases

Angina pectoris

Esophageal

Pulmonary

 

Another condition that causes upper extremity pain is cervical spondylosis, a degenerative disease of the intervertebral disk and the adjacent vertebral margin that causes spur formation and the production of ridges into the spinal canal or intervertebral foramina. Films and a CT scan of the cervical spine and electromyography help in making the diagnosis of this condition.

Several arterial and venous conditions can be confused with TOS (see Table 124-2); the differentiation often can be made clinically. In atypical patients who present with chest pain alone, it is important to suspect the TOS in addition to angina pectoris. Exercise stress testing and coronary angiography may exclude coronary artery disease when there is a high index of suspicion of angina pectoris.6,10

THERAPY

Patients with TOS should be given physiotherapy when the diagnosis is made. Proper physiotherapy includes heat massages, active neck exercises, stretching of the scalenus muscles, strengthening of the upper trapezius muscle, and posture instruction. Because sagging of the shoulder girdle, which is common among the middle-aged, is a major cause in this syndrome, many patients with less severe cases are improved by strengthening the shoulder girdle and by improving posture.6,10,12

Most patients with TOS who have UNCVs of more than 60 m/s improve with conservative management. If the conduction velocity is below that level, most patients, despite physiotherapy, may remain symptomatic, and surgical resection of the first rib and correction of other bony abnormalities may be needed to provide relief of symptoms.3,10

If symptoms of neurovascular compression continue after physiotherapy, and the conduction velocity shows slight or no improvement or regression, surgical resection of the first rib and cervical rib, when present, should be considered.3,10 Clagettpopularized the high posterior thoracoplasty approach for first rib resection, Falconer and Li14 emphasized the anterior approach, and Roos and Owens15 introduced the transaxillary route.

The transaxillary route is an expedient approach for complete removal of the first rib with decompression of the seventh and eighth cervical and first thoracic nerve roots and the lower trunks of the brachial plexus. First rib resection can be performed without the need for major muscle division, as in the posterior approach; without the need for retraction of the brachial plexus, as in the anterior supraclavicular approach14 ; and without the difficulty of removing the posterior segment of the rib, as in the infraclavicular approach. In addition, first rib resection shortens the postoperative disability and provides better cosmetic results than the anterior and posterior approaches, particularly because 80% of patients are female.3

INDICATIONS FOR DORSAL SYMPATHECTOMY WITH FIRST RIB RESECTION/MANAGEMENT WITH VIDEO-ASSISTED THORACIC SURGERY

Dorsal sympathectomy and the management of TOS are significantly improved with video assistance through magnification and an improved light system. Video-assisted thoracic surgery (VATS) offers better visualization of anatomic structures in a "deep hole," with an additional bonus of excellent visualization for other members of the team, particularly surgical residents. In addition, for sympathectomy alone, it produces less pain for the patient and a shorter hospitalization.

Video assistance is used in two techniques. One involves sympathectomy through three ports with standard video-assisted thoracic surgery. The second technique involves a transaxillary incision with removal of the first rib using video-assistance magnification and light; the surgeon operates either directly or secondarily while visualizing the image through the television set. This second technique was popularized by Martinez.16

Major indications for dorsal sympathectomy include hyperhidrosis, Raynaud's phenomenon and Raynaud's disease, causalgia, reflex sympathetic dystrophy, and vascular insufficiency of the upper extremity. Except for hyperhidrosis (see Chap. 121), all the other indications require the usual diagnostic techniques, including cervical sympathetic block to assess whether the symptoms are relieved by temporary blockade of the sympathetic ganglia. When Raynaud' s phenomenon of a minor to moderate degree is associated with thoracic outlet syndrome, the simple removal of the first rib (and cervical rib, if one is found) and stripping of the axillary-subclavian artery (neurectomy) will relieve most symptoms after the initial operation.3

It is rarely necessary to perform a sympathectomy unless the Raynaud's is of a very severe type, in which case a dorsal sympathectomy is carried out with first rib resection. In contrast, with recurrent TOS and causalgia, it has been found that the dorsal sympathectomy should be performed with the initial reoperation procedure.17,18

PATHOPHYSIOLOGY

The principal physiologic effect expected of sympathectomy is the release of vasomotor control and hyperactive tone of the arterioles and smaller arteries that have a muscular element in the vessel wall. Circulation to the skin, peripheral extremity, and bone receives major improvement, but the effect on skeletal muscle of the arm is minimal. The other known function is the control of cutaneous sweating, which is profuse and undesirable. Sympathectomy eliminates perspiration in that quadrant of the body but increases perspiration elsewhere. Reflex sympathetic dystrophy is associated with pain, neuroesthenia, cutaneous atrophy (Sudeck-Leriche syndrome), and posttraumatic limb. These patients also benefit from a sympathectomy if a diagnostic block is effective. Sympathectomy is not recommended in diabetic neuropathy. Nor should it be performed in any of the vascular vasospastic syndromes until after conservative management, including cessation of tobacco products and institution of beta blockers, peripheral vasodilators, and calcium channel blockers, has been tried.19

Preganglionic sympathetic nerves derived from the spinal cord do not follow a corresponding relationship to the accompanying somatic nerves. The cervical ganglia of C1 to C4 are fused into a superior cervical ganglion, C5 and C6 into the middle cervical ganglion, and C7 and C8 into the inferior ganglion, which combines with the ganglion from T1 to the larger stellate ganglion. Cervical ganglionectomy is not used for denervation of the upper extremity because the preganglionic sympathetic outflow from the spinal cord to the arm is usually from T2 through T9, mostly from T2 through T4. In about 10% of cases, T1 preganglionic fibers also supply the upper extremity. To remove the preganglionic fibers to the upper extremity in most patients, removal of paravertebral ganglia T2 and T3 with the interconnecting chain is sufficient. Postganglionic fibers from these two segments often join, and branches then follow the nerves of the brachial plexus. The joined T2 and T3 fibers that bypass the stellate ganglion are known as the nerve of Kuntz.20 To ensure that all the remaining patients who have a T1 connection through the stellate ganglion obtain adequate sympathetic denervation, the lower third of the stellate ganglion also should be removed, as recommended by Palumbo.21

Patients with reflex sympathetic dystrophy or sympathetic maintained pain syndrome (SMPS) must complain of pain outside a peripheral nerve distribution.22 Although the injury itself may have been minor, the pain appears out of proportion to the injury. We have seen two types of reflex sympathetic dystrophy or SMPS; one involves the hand or even a majority of the upper extremity, and a second is localized to one or more digits. In no instance can the patient's pain be completely accounted for by an injury to a specific nerve, although injury to a specific nerve may cause the more diffuse symptoms. The patient also demonstrates diminished hand function. Several patients have been referred with a diagnosis of SMPS, and on examination, it is quite apparent that although they may complain of diffuse pain, the hand functions normally with a full range of movement, and motor power is demonstrated. These patients, of course, do not have SMPS. The patient also must demonstrate some joint stiffness. The skin and soft tissue trophic changes demonstrate varying amounts of vasomotor instability, depending on the stage of SMPS.

According to Mackinnon and Dellon,22 there are early, intermediate, and late stages of SMPS. In the early stages, vasomotor instability is noted, with very dramatic sympathetic overactivity apparent in the hand or digit involved. Instability, with symptoms varying between redness and warmth and cyanosis and sweating, is noted in this early stage. Edema is also a classic finding in the early stage. In the intermediate stage of SMPS, pain is a less dramatic component and is usually elicited by attempts to move the joints. At rest, the patient may be quite comfortable. The edema and vasomotor changes have settled by this time, and the hand has the appearance of a "burned out," dystrophic hand, with marked stiffness and atrophy of the soft tissue noted. The normal wrinkles on the dorsum of the hand are no longer apparent. The fingertips may have a tapered appearance. The nail growth is usually more exaggerated than in the normal hand, and the hand is often cool and pale. The intermediate stage will extend over a number of months. During the late stage, all the superimposed problems of disuse atrophy may take effect. During this stage, problems with the elbow and shoulder are very common, even though the initial SMPS involved only the hand or one or more digits. The degree of pain experienced during the late phase is variable and is often the result of disuse and stiffness. SMPS can affect other areas of the body and has been observed in the foot, face, and penis.

TECHNIQUE OF TRANSAXILLARY THORACOSCOPIC FIRST RIB RESECTION WITH DORSAL SYMPATHECTOMY

The operated arm is held or suspended over an ether screen. After prepping and draping the axilla, an incision is made below the axillary hairline, between the pectoralis major and latissimus dorsi muscles (Fig. 124-3). The incision is made through the skin and subcutaneous tissue down to the chest wall, and dissection is carried up to the first rib. Care is taken not to injure the intercostal brachial nerve. The videothoracoscope is inserted, andwhile watching the screen, the scalenus anticus muscle is divided at the scalene tubercle.

Figure 124-3.

 

Video-assisted thoracic surgery incision and port placement for transaxillary first rib resection with dorsal sympathectomy.

 

After collapsing the lung on the operated side, a triangular portion of the first rib is removed, with the vertex of the triangle at the scalene tubercle (Fig. 124-4). The costoclavicular ligament is divided medially, and the medial segment of the first rib is removed back to the costal cartilage of the sternum. The posterior segment of the first rib is dissected, with attention to the neurovascular structures, and divided near the transverse process.

Figure 124-4.

 

A triangular portion of the first rib is removed, with the vertex of the triangle at the scalene tubercle.

 

The head and neck of the first rib are carefully removed with special, reinforced, Urschel pituitary and Urschel-Leksell rongeurs. Care is taken not to injure the C8 and T1 nerve roots. The parietal pleura is dissected inferiorly from the T1 nerve root, and the dorsal sympathectomy chain is exposed (Fig. 124-5). T1, T2, and T3 ganglia with the sympathetic chain are removed after clipping the gray and white afferent and efferent rami communicantes. The area is cauterized to minimize sprouting and regeneration. A no. 20 chest tube is used to expand the lung after closing the incision.

Figure 124-5.

 

T1, T2, and T3 ganglia with the sympathetic chain are removed after clipping the gray and white afferent and efferent rami communicantes.

COMPLICATIONS

Horner's Syndrome

If the fibers of C7 and C8 (the upper part of the stellate ganglion) are removed, Horner's syndrome results. This involves miosis, enophthalmos, drooping of the eyelid (ptosis), and flushing of that side of the face with loss of sweating in that area.23

Postsympathetic Neuralgia

The complication of postsympathectomy neuralgia is less common in the upper extremities than in the lower extremities. The pain usually occurs in the shoulder and upper arm on the lateral aspect. Clinical history usually substantiates this diagnosis if the symptoms occur within the first 3 months. The confirmation may be obtained by a test involving skin resistance of pseudomotor activity detection. Tests reveal increased sympathetic activity and suggest a rebound phenomenon from the nonsympathectomized adjacent dermatomes. Rebound may be a regeneration of nerve fibers or an increased response of peripheral nerves to catecholamines. Symptoms usually resolve in 3–6 weeks with conservative management. Phenytoin sodium (Dilantin), carbamazepine (Tegretol), and calcium channel blockers all are used in the medical management of these symptoms.24

Recurrent Symptoms

Occasionally, following an excellent sympathectomy, with a warm hand and good circulation, recurrent symptoms may recur as early as 3 months. These may be secondary to the regeneration or sprouting and rehooking of nerves or failure to strip the sympathetic nerves from the artery itself and the transfer of sympathetic tone through these nerves. Therefore, it is important to strip the axillary-subclavian artery of its local sympathetic nerves in each case at the initial operation.25 Also, during the initial procedure, cauterization of the bed of the sympathectomy area produces sympathetic effects that usually last at least 3 years.

RESULTS

In 926 patients, sympathectomy alone or in conjunction with first rib removal for TOS has been successful.26 In only six patients has sympathetic activity recurred in less than 6 months. All of these patients were treated conservatively initially. Three of the 6 required repeat sympathectomy. Postsympathectomy neuralgia occurred in only 2 of 926 patients. Both these patients were managed successfully in a conservative manner. In the patients in whom Horner's syndrome was not created deliberately, four developed the syndrome. All resolved spontaneously in several months. Forty-two cases of Raynaud's phenomena were treated successfully with first rib resection alone or with periarterial neurectomy without initial sympathectomy.25 The results of reoperation are good if an accurate diagnosis is made and the proper procedure is used.18 More than 1200 patients have been followed up for 6 months to 15 years. All patients improved initially after reoperation, and in 79%, the improvement was maintained for more than 5 years. In 14% of the patients, symptoms were managed with physiotherapy; 7% required a second reoperation, in every case because of rescarring. There were no deaths, and only two patients had infections that required drainage.26

SUMMARY

TOS is recognized in approximately 8% of the population. Its manifestations may be neurologic or vascular or both depending on the component of the neurovascular bundle predominantly compressed. The diagnosis is suspected from the clinical picture and usually is substantiated by determination of the UNCV. Treatment is conservative initially, but persistence of significant symptoms is an indication for first rib resection and occurs in approximately 5% of patients with diagnosed TOS. Primary resection is performed preferably through the thorascopic transaxillary approach. Symptoms of various degrees may recur after first rib resection in approximately 10% of patients. Most of the patients improve with physiotherapy, and only 1.6% require reoperation. Reoperation for recurrent symptoms is performed through a high posterior thoracoplasty incision.17,18,26

REFERENCES

1. Rob CG, Standeven A: Arterial occlusion complicating thoracic outlet compression syndrome. Br Med J 2:709–12, 1958. [PubMed: 13572875]

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3. Urschel HC Jr, Paulson DL, McNamara JJ: Thoracic outlet syndrome. Ann Thorac Surg 6:1–10, 1968. [PubMed: 5748008]

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