Vascular Thrombosis and Aneurysm About the Wrist




BACKGROUND


Chronic post-traumatic thrombosis and aneurysms of the ulnar and radial arteries may affect 10% to 15% of laborers who use their hands as a “hammer,” and thus this condition is the source of a significant social burden. This chapter discusses the etiology, evaluation, and management of post-traumatic occlusive disease about the wrist. It does not address management of patients with primary vasospastic disease.




COMPONENTS AND CONTROL OF PERIPHERAL BLOOD FLOW


In normal states, 80% to 90% of total digit blood flow is thermoregulatory (non-nutritional), whereas the remainder consists of the nutritional flow that passes through nutritional capillaries, essential for providing cells with the nutrients required for their viability ( Fig. 60-1 ). Control of digit blood flow is governed by complex factors that are elucidated incompletely. Regional blood flow depends on centrally generated pressure and peripheral vascular resistance. Changes in the latter factor are controlled by the sympathetic system (vasoconstriction, alpha-adrenergic pathways) and the nitric oxide pathways (vasodilation).




FIGURE 60-1


Microvascular bed from the skin surface . Arteriovenous anastomoses (AVAs) are responsible for regulating the nutritional flow that occurs in the capillaries. Excessive shunting through AVAs may decrease or even prevent nutritional flow.

(From Koman LA [ed]: Bowman Gray School of Medicine Orthopaedic Manual. Winston-Salem, NC: Wake Forest University Orthopaedic Press, 1997, with permission.)




ANATOMY


The ulnar and radial arteries branch into the superficial and deep palmar arches, respectively; in 5% of extremities, a persistent median artery is present ( Fig. 60-2 ). Although myriad normal variations of the digital vessels exist, they all share the presence of three common volar digital arteries at the level of the metacarpophalangeal joint. An arch is defined as “complete” if it is directly connected to the other arch or to a named vessel or collateral greater than 1.5 to 2 mm in diameter. Approximately 80% of superficial arches and 97% of deep arches are complete.




FIGURE 60-2


An arterial arch is defined as complete when it connects with a branch from another independent artery. The superficial palmar arch (main vessel: ulnar artery) is complete in 78.5% of patients, whereas the deep palmar arch (main vessel: radial artery) is complete in 98.5% of patients.

(From Koman LA [ed]: Bowman Gray School of Medicine Orthopaedic Manual. Winston-Salem, NC: Wake Forest University Orthopaedic Press, 1997, with permission.)




CLINICAL CONSEQUENCES OF UPPER EXTREMITY VASCULAR DISEASE


Symptoms and signs related to the vascular system result from failure of (1) structural components (i.e., inadequate arteries to supply the tissues), (2) functional components (i.e., vasospastic disease), or (3) both. The common denominator in all cases is the lack of adequate nutritional flow to deliver oxygen and essential metabolites to cells and the failure to recycle metabolic waste effectively. A critical vascular event (or injury) results in tissue necrosis with gangrene when surgical intervention is not sufficient to restore the structural integrity of the vessels. However, symptomatic, noncritical events in which the collateral circulation or control presents adequate compensation also occur.




CLASSIFICATION AND MECHANISM OF INJURY


Occlusive Disease (Ulnar and Radial Artery Thrombosis and Aneurysms)


Symptoms and signs of occlusive disease depend on the extent and location of thrombosis, presence or absence of distal emboli, adequacy of collateral circulation, and presence or absence of vasospasm. Based on anatomic and physiologic considerations, the following three-group classification by Koman and Urbaniak is useful in the selection of appropriate treatment options. Group I includes patients with occlusive disease and secondary vasospasm who have existing adequate collateral circulation. These patients require minimal or no treatment, and frequently the diagnosis is a fortuitous finding during physician visits for unrelated pathologies. Group II is composed of patients with occlusive disease and adequate collateral circulation, but in contrast to group I they have refractory vasospasm. They may be managed conservatively with sympatholytic medications (e.g., calcium channel blockers) to control the vasospasm, or surgically by sympathectomy performed by resection of the thrombosed segment and ligation, or by periarterial sympathectomy. Group III patients have occlusive disease, vasospasm, and inadequate collateral circulation. They require restoration of arterial continuity, with either surgical reconstruction or thrombolysis.


The etiologies of thrombosis and aneurysm are similar ( Fig 60-3 ). Repetitive, or even acute, trauma may cause intimal damage leading to thrombosis and/or aneurysmal dilatation, or peri-adventitial fibrosis, which results in vessel constriction or even total occlusion.




FIGURE 60-3


Acute or repeated trauma may cause direct intimal damage, leading to stasis and thus predisposing to thrombosis. Chronic low-grade trauma initially may be responsible for periadventitial thickening resulting in constriction and stenosis, which may resolve spontaneously, be treated by surgical stripping of the adventitia, or lead to subsequent intimal damage with thrombosis.

(From Koman LA [ed]: Bowman Gray School of Medicine Orthopaedic Manual. Winston-Salem, NC: Wake Forest University Orthopaedic Press, 1997, with permission.)




DIAGNOSIS AND EVALUATION


History


Taking a meticulous and detailed history is important and should emphasize (1) the presence or absence of trauma (e.g., using the hand as a hammer); (2) environmental factors (e.g., profession, current medications, drug exposure, and smoking); and (3) congenital factors, such as personal and family history of collagen vascular disease, clotting abnormalities (or previous clotting episodes), and heart problems.


Symptoms and Signs


Pain, numbness, cold intolerance, nail bed changes, and/or the presence of a mass are the hallmarks of arterial compromise. In addition, color changes (the white, blue, and red of Raynaud’s phenomenon), pulsating or throbbing masses, ulcers, and/or gangrene also may be accompanying phenomena. A precise history of the frequency of attacks, digit distribution, and duration of color changes is critical. The presence of unilateral Raynaud’s phenomenon represents occlusive disease, unless proven otherwise .


The patient should be evaluated with standardized, validated outcome instruments (questionnaires) that provide an objective and reproducible assessment of his or her current status and allow valid comparisons following the effects of intervention. Common instruments include the visual analog pain scale (VAS), the pain portion of the Rand Corporation Short Form 36 (SF 36), the McGill Short Form Pain Questionnaire, and self-administered questionnaires designed to assess upper extremity symptoms/function. Cold intolerance may be assessed by using the McCabe Cold Sensitivity Severity Scale.


Physical Examination


Physical examination should address the entire upper extremity from the neck to the fingertips. It includes inspection, palpation, range of motion, evaluation of motor power, sensibility, and status of the vascular system. Thoracic outlet syndrome should be included in the differential diagnosis. The vascular status should include an evaluation of skin color, texture, temperature, and autonomic function, and the presence of atrophy, hair loss, ulcers, and petechiae should be documented.


Patencies of the ulnar and radial arterial systems are evaluated by palpating the pulses and performing the timed Allen test ( Fig. 60-4 ). The Allen test is performed by asking the patient to close the hand as tightly as possible for 1 minute or until blanching of all fingers occurs. Then the radial and ulnar arteries are occluded by the examiner and released sequentially. The examiner releases the compression over one of the two arteries while maintaining a pressure of 11 pounds on the other. The return of color to the hand indicates a patent vessel. The timed version of the Allen test was devised by Gelberman and Blasingame in 1981. Evaluation of 800 hands in 400 controls showed that 91% of hands were considered “normal” when uniform refill occurred in less than 6 seconds. In our experience, delayed refill of longer than 3 seconds warrants careful analysis.




FIGURE 60-4


The Allen test is represented schematically . Blood is exsanguinated from the hand, and both the radial and ulnar arteries are compressed ( left ). After release of the ulnar artery ( middle ), no blood flow passes through the occluded artery, and the palm remains pale. With release of the radial artery ( right ), the entire hand fills rapidly through the radial artery if the arch is complete. The order of the testing maneuvers can be reversed to test the radial artery in a similar fashion. The test is best described as demonstrating flow or no flow through a specific artery.

(From Koman LA [ed]: Bowman Gray School of Medicine Orthopaedic Manual. Winston-Salem, NC: Wake Forest University Orthopaedic Press, 1997, with permission.)


Finally, a digital Allen test may be performed for assessment of occlusion of a digital artery at or distal to the metacarpophalangeal joint. Both digital arteries at the base of the finger are compressed, and then the patient elevates and fully flexes the finger several times, or the finger is “milked” to obtain blanching. Subsequently, the hand is lowered, and the examiner releases compression from one of the arteries. If blanching disappears and color returns, the artery is patent.




LABORATORY BLOOD TESTS


The initial laboratory evaluation should include an evaluation for a possible autoimmune disease or hypercoagulable state. The latter has a major negative causal effect on occlusive diseases. The presence of an underlying disorder affects the natural history, management, and prognosis. Testing should include a complete blood count with differential, erythrocyte sedimentation rate, C-reactive protein, factor V Leiden, abnormal protein C or S, antithrombin III, and antiphospholipid antibodies ( Table 60-1 ).



TABLE 60-1

Laboratory Studies in the Evaluation of a Patient with Upper Extremity Vascular Disorder

































Basic inflammatory indices Erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
Connective tissue diseases Antinuclear antibody (ANA)
Antiphospholipid antibodies
Antineutrophil cytoplasmic antibodies (ANCAs)
Rheumatoid factor (RF)
Serum protein electrophoresis
Complement C3 and C4
Cryoglobulins
Coagulopathies Prothrombin time and partial thromboplastin time
Protein C and protein S
Factor V Leiden
Other Homocysteine levels

From Koman LA (ed): Bowman Gray School of Medicine Orthopaedic Manual. Winston-Salem, NC: Wake Forest University Orthopaedic Press, 2007, with permission.




LABORATORY EVALUATION AND TESTING


Upper extremity integrity of structure and function is evaluated at rest and under the application of a stressor. The combined use of the following modalities permits physiologic-specific and patient-oriented management:



  • 1.

    Doppler ultrasonography


  • 2.

    Digital plethysmography (pulse volume recording) ( Fig. 60-5 )




    FIGURE 60-5


    ( Top ) Normal triphasic arterial wave pattern is schematically depicted. ( Bottom ) The changes that occur with stenosis and occlusion are demonstrated.

    (From Koman LA [ed]: Bowman Gray School of Medicine Orthopaedic Manual. Winston-Salem, NC: Wake Forest University Orthopaedic Press, 1997, with permission.)


  • 3.

    Segmental arterial pressures (SAPs). Measurement of digital brachial indexes (DBIs) also guides the treatment decision. The DBI is the ratio of the brachial blood pressure to the digital blood pressure. If the DBI is greater than or equal to 0.7, there is adequate collateral circulation, and resection may be performed. If the DBI is less than 0.7, collateral circulation is adequate, and arterial reconstruction is warranted.


  • 4.

    Color duplex imaging


  • 5.

    Laser Doppler perfusion imaging (LDPI)


  • 6.

    Laser Doppler fluxmetry (LDF) cutaneous perfusion measurements


  • 7.

    Skin surface temperature recordings


  • 8.

    Nailfold vital capillaroscopy, which is the only means of directly estimating nutritional flow


  • 9.

    Isolated cold stress testing (ICST). This uses LDF and cutaneous digital temperature measurements before, during, and after the application of stress (in the form of cold temperature) and is invaluable in assessing the capability of a vascular bed to respond to and recover from physiologic stress. ICST yields reproducible data to facilitate physiologic staging and monitor the effects of management.


  • 10.

    Technetium-99m three-phase bone scanning (TPBS)


  • 11.

    Magnetic resonance angiography (MR angiography), including the use of gadolinium contrast, and computed tomography angiography (CT angiography), are promising less invasive techniques.


  • 12.

    Arteriography, the gold standard for providing structural “anatomic” information. However, symptoms may not necessarily correlate with arteriographic findings. In this case, the additional studies previously mentioned will help to evaluate both macrovascular and microvascular flow. “Cut-film” arteriograms using subtraction techniques when performed with newer contrast agents and vasodilators provide optimal structural information.





MANAGEMENT


The goal of management is to restore pulsatile digital flow. A restoration of flow improves symptoms, function, and health-related quality of life significantly. To obtain optimal function of the vascular system, restoration of pulsatile flow into nutritional channels under stressed and unstressed conditions is critical. Depending on the functional stage (described in the previous text), initial management is nonoperative, operative, or a combination of both. Management options include (1) environmental and behavioral modifications, such as elimination of smoking; (2) oral pharmacologic intervention; (3) biofeedback; (4) cervicothoracic sympathectomy; (5) thrombolytic therapy; and (6) surgical intervention, such as resection and ligation of involved segment(s) (Leriche-type sympathectomy), peripheral sympathectomy, embolectomy, and arterial reconstruction ( Table 60-2 ). The potential risks and benefits of treatment must be considered for each case and tailored to the needs and expectations of the patient.


Jul 10, 2019 | Posted by in ORTHOPEDIC | Comments Off on Vascular Thrombosis and Aneurysm About the Wrist

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