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TexasOrtho -> RE: TOS differential diagnosis (May 31, 2008 11:26:13 AM)
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I just started my first class at Texas Tech's doctoral program. The class is called advanced clinical practice for the cervicothoracic joint and thoracic outlet. I just finished a big writeup on pathoanatomy, pathophysiology, and biomechanics of TOS as an assignment. It hasn't been graded, so you'll have to consider the source (me), but it might help a little. There are some really good articles I used to get this stuff from. I'm learning more about the thoracic outlet than I ever thought possible.
Module I: Pathoanatomy, Pathophysiology, Biomechanics of TOS
1a.
1. Is “thoracic outlet” a clinically appropriate term? Which terminology might better encompass the clinical entity “thoracic outlet syndrome”?
The use of the term “thoracic outlet” may not be the most clinically appropriate term for a number of reasons. One of its most significant drawbacks is the lack of consensus between basic and clinical scientists as to what the thoracic outlet actually is. While clinicians have often associated the thoracic outlet as the scalene triangle, anatomists associate the term thoracic outlet with the inferior thoracic aperture. The lack of a clearly defined operational definition may limit the degree of continuity between basic and clinical science, impeding investigations as the most appropriate means of diagnosing and treating clinical “thoracic outlet syndrome”.
The Ranney article proposes a refinement of the term “thoracic outlet syndrome” based on both anatomical and clinical grounds. According to Ranney, these refinements would result in terminology both more precise and useful for the clinician. The proposed anatomic change would be to divide area previously known as the thoracic outlet into cervical and thoracic outlets. The cervical outlet would be a more precise description of the upper roots of the brachial plexus (C5-C7) as they exit the cervical spine into the thorax. The thoracic outlet would describe the exit of structures truly exiting the thorax such as the subclavian artery and lower roots of the brachial plexus.
The clinical diagnosis of “thoracic outlet syndrome” could be modified to be known as “cervicoaxillary syndrome”. As the exact nature of the symptoms becomes known, a more precise clinical diagnosis could be made to reflect the tissues involved. For example, neurogenic signs of the upper brachial plexus without evidence of vascular compromise could be termed cervical outlet syndrome. By extension signs of vascular compromise and/or lower brachial plexus signs might be referred to as true thoracic outlet syndrome.
2. Based on the other readings in this section, and your knowledge of the anatomy in this area, discuss the possible clinical presentation that one could expect at any given site in the “thoracic outlet”.
Given the variety of tissues passing through the cervical and thoracic outlet, we could expect a range of upper-quarter signs including arterial insufficiency, venous insufficiency, neurogenic, and possibly sympathetic signs.
Arterial signs:
· Postural or activity induced claudication of the extremity
· Worsening of symptoms during exposure to cold and improvement with heat
o Patient may report a seasonal variation in symptoms
· Poorly localized upper extremity pain and possibly a “glove” distribution
· Post-traumatic thrombotic or embolic event causing tissue necrosis, ulceration, and even gangrene of the digits (severe cases)
o Most commonly localized in the radial hand
· Positive Adson, Hyperabduction, and 90 degree abduction external rotation test
o These tests have questionable specificity however
Venous signs:
· Affected limb feels weak, swollen, cyanotic after activity
· Deep chest, shoulder, arm pain
· Tingling paresthesias are common
· Positional provocation is possible
Neurogenic signs (most common):
· Most commonly the lower brachial plexus (C8-TI roots)
· Sensory symptoms
o Pain
o Supraclavicular, axillary, cervical (most common)
o Retrosternal or parascapular (less common)
o Poorly localized and often nondermatomal
o Paresthesias
o Generally more localized to C8 through TI dermatomes
o Sensory symptoms often relieved by discontinuing activity or resting arm on a table
· Motor symptoms
o Grip and hand dexterity may be involved
o Intrinsic hand muscle weakness in chronic cases
o Thenar muscle atrophy in chronic cases
· Sympathetic Involvement
o Vasomotor disruption
o Cyanosis during cold or emotional disturbance
o Trophic changes
o Thin skin, nail thickening, loss of hair
1b.
1. Discuss the extrinsic factors that can lead to symptoms of thoracic outlet syndrome.
Extrinsic factors may be thought of as occurring as a result of adaptations from injury or adaptation to repetitive loading. As such, trauma to cervical, thoracic, and upper extremity could be extrinsic causes of thoracic outlet syndrome. Symptoms of thoracic outlet syndrome could be the direct result of the trauma or secondary to injuries to adjacent structures.
Static or repetitive loading could also predispose an individual to thoracic outlet syndrome. For example, the developmental descent of the scapula occurs to a greater degree in women and creates a greater traction on the neurovascular bundle. This process could be worsened in the presence of sloping shoulders or heavy breasts. Lastly, habitual posturing either through vocation or avocation may place greater traction or relative impingement of the neurovascular bundle.
2. How can each one of these extrinsic factors be assessed/uncovered in the clinic, and what is the impact that dysfunction in each joint-complex will have on the thoracic outlet passageways?
Acquiring basic demographic information may assist the clinician’s suspicion of these extrinsic factors. Age, gender, and vocational activities may provide valuable clues regarding the patient’s likelihood for thoracic outlet. The nature of onset could also raise the level of suspicion (traumatic vs. atraumatic).
It is possible that dysfunction of proximal and distal joint complexes could affect the passageways of the thoracic outlet. Injury or dysfunction of the cervical region could affect the size of the scalene triangle. Chronic cervical dysfunction could lead to fibrosis of the scalene and/or scalene triangle and affect the neurovascular bundle. Distally, injuries to the shoulder, elbow, wrist, and hand are likely to affect the neural and vascular trees of the extremity. Altered neurodynamics of these areas could lead to proximal involvement of the brachial plexus.
3. What are the intrinsic factors leading to thoracic outlet syndrome?
Intrinsic factors may be thought of as congenital or acquired. Congenital factors include the presence of a cervical rib. The incidence of cervical rib has been reported in only 1 in 200 individuals however. A more likely congenital anomaly would be the presence of a band of fibrous tissue that run through the thoracic outlet and elevate or kink the neurovascular tissues.
Acquired intrinsic factors may include space-occupying lesions in or around the thoracic outlet. These may include a large callus formation following a clavicular fracture, tumors of the first rib (rare), and a Pancoast tumor. Although rare, the presence of a primary spinal cord or brachial plexus tumor or even an inflammatory lymphadenopathy could encroach upon the neurovascular bundle of the thoracic outlet.
4. Is there a way for the clinician to determine whether any of these intrinsic factors are present in the patient with thoracic outlet syndrome and contributing to the symptoms? How so?
A detailed history could supply the clinician with useful information. However even the most thorough history may not have sufficient specificity to rule in a specific intrinsic cause of thoracic outlet syndrome.
Plain film radiographs would be a relatively simple way to identify a cervical rib or large subclavicular callus. Further diagnostic workup per lymphadenopathy may be indicated (blood panel, imaging, biopsy etc...). This testing would be under the discretion of the appropriate provider.
Clinical testing specific to intrinsic factors listed above is likely to be nonspecific.
1c.
1. What role do muscles play in the development of thoracic outlet syndrome?
The anterior/medial scalene and pectoralis minor have the most direct interaction with the neurovascular bundle. Hypertrophy of the anterior or medial scalene can narrow the outlet and compress the thoracic outlet to greater strain during postural or dynamic activity. Further distally, hypertrophy or tightness of the pectoralis minor could impede the function of the neurovascular bundle as it advances into the proximal upper extremity. Lastly the pectoralis major could exert compressive forces upon the thoracic outlet. The scalene and pectoralis minor can be assessed and treated clinically through manual, passive and active movements.
2. What happens during overhead arm activity that contributes to the pathomechanics of thoracic outlet syndrome?
As the arm is elevated, the neurovascular structures of the proximal and distal thoracic outlet are subjected to varying degrees of stress. Proximally, elevation could produce a narrowing of the subclavicular space in the presence of an elevated rib or previous clavicular fracture.
Distally, the subcoracoid space could provide either a compressive or traction event for the neurovascular bundle during overhead activity. Hyperabduction and external rotation approximates the pectoralis minor to the thorax and expose the nerves and vessels to compression. This event would seem more likely to occur in the presence of a tight pectoralis minor and major.
The more caudal tissues of the brachial plexus, such as the medial cord and ulnar nerve, are placed under greater amounts of tensile forces as the arm is elevated. This could predispose the ulnar nerve to a traction injury causing sensory or motor disturbances. It would seem reasonable that this could be exacerbated by underlying inferior glenohumeral laxity or instability.
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