Distal radial artery lesion as a source of digital emboli
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1 Distal radial artery lesion as a source of digital emboli G. Matthew Longo, MD, Andrew C. Friedman, MD, Ronald R. Hollins, MD, Cary J. Buresh, MD, and B. Timothy Baxter, MD, Omaha, Neb Ischemic changes of the digits caused by emboli are rare. When they do occur, the typical sites of origin include the heart, the proximal subclavian artery, and the thoracic outlet. Dialysis access or iatrogenic injuries may be a more distal source of emboli. Two patients, each with embolization to the thumb and index finger from a lesion in the anatomical snuff-box, were studied. Neither patient had any other atherosclerotic occlusive disease, and both lesions occurred precisely where the extensor pollicis longus crossed the artery and would be expected to compress it against the proximal epiphysis of the first metacarpal when the hand was closed. These lesions were excised, and bypass was performed, with rapid resolution of symptoms. This is an unusual cause of digital embolization that should be considered in patients with emboli to the thumb and index finger. (J Vasc Surg 1998;28:710-4.) Ischemic changes of the digits caused by embolic phenomenon are rare. When they do occur, the nidus for emboli include the heart, proximal atherosclerotic occlusive and aneurysmal disease. 1 Occasionally, ischemic changes in the digits result from emboli originating from a more distal source after iatrogenic catheter placement, 2 complications associated with dialysis access, repetitive work-related trauma, 3,4 and hypothenar hammer syndrome. 5 Blunt and penetrating trauma and intravenous (IV) drug abuse 6 have also been documented as sources for digital emboli. Each patient was found to have a plaque in the radial artery within the anatomical snuff-box. These lesions were subtle and occurred where the artery passed between the extensor pollicis longus and the proximal epiphysis of the first metacarpal. Emboli originating from the plaque resulted in severe digital ischemia of the thumb and index finger. PATIENT PRESENTATION AND EVALUATION The first patient was a healthy 37-year-old woman referred to the University of Nebraska Medical Center (UNMC) by her family practitioner From the Department of Surgery, University of Nebraska Medical Center. Reprint requests: B.T. Baxter, MD, Department of Surgery, UNMC, 600 S 42nd Street, Omaha, NE Copyright 1998 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter /98/$ /4/93026 for evaluation of pain and discoloration of her left index finger. The patient noted a sudden onset of discoloration of her left index finger 4 months before she came to UNMC. This was associated with significant pain that was exacerbated by cold. There was no prior history of trauma to the hand, wrist, or upper extremity, and no history of Raynaud s syndrome. The patient worked as a checker in a department store and smoked packs of cigarettes per day for 20 years. She had no history of peripheral vascular disease and denied illicit drug use. Cyanosis of the left index finger and thumb was revealed by means of a physical examination. Both digits had sloughing of the skin at the distal fingertip. Radial and ulnar pulses were normal and equal. Sensation was decreased on the distal one third of the index finger and thumb and absent on the tip of the index finger. The findings of laboratory studies drawn to exclude vasculitis, including ANA (<1.4; normal < 1:40), cryoglobulins (negative), and an erythrocyte sedimentation rate (18 mm/h; normal <20), were normal. A work-up for a hypercoaguable state, including anticardiolipin antibody and protein C and protein S levels, was done by the referring physician. The findings from all these tests were normal. Digital pressures were significantly decreased in the thumb, with no obtainable signal in the second digit (Table I). Segmental pressures of the left upper extremity were normal. No significant dilatation or evidence of stenosis was found by means of duplex imaging of the subclavian artery. Healthy cardiac valves and wall motion without thrombus were 710
2 Volume 28, Number 4 Longo et al 711 shown by means of transthoracic echocardiogram, and there was no significant disease in the ascending aorta or of the arch. Occlusion of the proper digital arteries of the left thumb and index finger was shown and embolization to the artery of the ring finger was suggested by means of an arteriogram of the aortic arch, left arm, and hand. Additionally, there was an irregular, eccentric plaque of the left radial artery at the level of the first metacarpophalangeal joint (Fig 1). The second patient was a healthy 56-year-old woman who had a 6-week history of left index finger ischemia. The patient initially experienced acute swelling and pain in her left hand. The swelling resolved within 4 to 5 days, during which she had persistent pain in the index finger. This finger remained cyanotic, blue, and painful. The patient had no prior history of trauma to the left hand, and she had never used tobacco products. She was employed as a full-time nurse. Physical examination revealed normal ulnar and radial pulses. All 5 digits were cool to the touch, and the index finger was cyanotic, with sloughing of the skin at the fingertip. Noninvasive vascular studies revealed normal brachial, ulnar, and radial artery pressures, with triphasic waveforms bilaterally. Doppler signals were absent in the thumb and index finger. No obstructive or aneurysmal dilatation of the subclavian, axillary, brachial, or ulnar arteries was shown by means of duplex ultrasound scan. Laboratory evaluation results were negative for vasculitis and hypercoaguability. An irregular plaque narrowing of the lumen of the radial artery near the origins of the princeps pollicis and superficial palmar branches was shown by means of angiography. The digital arteries to the thumb and index finger were occluded (Fig 2). TREATMENT After completion of the clinical evaluation, the radial artery lesions that were presumed to be the source of the digital emboli were repaired surgically in both cases. The same operative approach was used in both cases. Under axillary block, an oblique incision was made over the course of the radial artery in the anatomical snuff-box. The radial artery was dissected proximal and distal to the atherosclerotic lesion. During the dissection, a branch of the cephalic vein of the appropriate size was identified. The lesion was palpable in both cases and was located directly beneath the extensor pollicis longus tendon. Proximal and distal control of the radial artery was obtained with vessel loops. The cephalic vein branch was excised and flushed. The patient received Fig 1. The site of the radial artery lesion (arrowhead) and the sites of embolic occlusion (arrows) shown by means of arteriogram units of IV heparin before clamping the radial artery. After longitudinal arteriotomy, the intimal lesion was identified, and the segment was excised. The cephalic vein branch was interposed with a spatulated end-to-end anastomosis done with a running 8-0 Prolene suture and 5 magnification. The interposition graft provided additional length, allowing the graft to be positioned to either side of the prominence of the base of the metacarpal head. An irregular surface covered with platelets and thrombus with intimal thickening and focal disruption of the internal elastic lamina was revealed in both patients by means of a histologic examination of specimens (Fig 3). On higher magnification, occasional macrophages were seen, but there was no evidence of a lymphocytic or neutrophilic cellular infiltrate. Granulomas and giant cells were not present. Both patients had complete resolution of ischemic symptoms within 1 month. Good flow within the radial artery graft was shown by means of Doppler examination with ulnar artery compression. Graft patency and improvement in digital pressures was shown after surgery by means of repeated vascular studies (Table I). At 2-year and 4-year followup examinations, both patients remained symptomfree, except for mild residual cold intolerance. DISCUSSION Two similar cases of hand ischemia associated with focal lesions in the radial artery, within the anatomical snuff-box, were studied. There are several important clinical features of these cases. First, before treatment there was progressive digital ischemia with neurosensory and tissue loss. It was
3 712 Longo et al October 1998 Fig 2. A, The site of the radial artery lesion (arrowhead) and the sites of embolic occlusion (arrows) shown by means of arteriogram. B, A magnified view of the radial artery lesion (arrowhead). Fig 3. Longitudinal section of radial artery (original magnification, 20). Histopathologic description: The section reveals a segment of artery with mild intimal thickening (area between the 2 arrows). Centrally, the intima is much thicker, consisting of smooth muscle cells, collagen, and ground substance. Underlying this area, there is disruption of the internal elastic lamina (arrowhead).
4 Volume 28, Number 4 Longo et al 713 Table I. Digital pressures Patient 1 Brachial 1st 2nd 3rd 4th 5th Preoperative Left Postoperative Left Patient 2 Preoperative Left Postoperative Left A comparison of the digital pressures in the 2 patients reveals a return to normal after revascularization. The elevated preoperative digital pressures of patient 1 reflect a hypertensive state at the time of the study. suggested by means of arteriography that this was caused by chronic embolization to the digital vessels perfused by the radial artery. Second, the radial artery lesion was focal and discrete and could have been missed without high-quality magnified angiographic images. Finally, surgical excision and bypass provided rapid and sustained resolution of symptoms. Anatomic variations in the course of the radial artery are well documented, with the common variants being the radial artery lying on the deep fascia and the radial artery lying on the extensor tendons of the thumb instead of beneath them. 7 However, it is rare for an abnormality to be seen with clinical symptoms. Most radial artery lesions that result in hand ischemia are caused by iatrogenic or traumatic injury. Although specific anatomic anomalies in the course of the radial artery were not identified in our patients, both lesions occurred precisely at the site where the radial artery was traversed by the extensor pollicis longus. This relationship suggests repeated arterial compression between the tendon and the base of the first metacarpal may play a role in the process. In a patient who has digital ischemia, often the differential diagnosis can be narrowed and further testing can be directed by means of a careful history and complete physical examination of the upper extremity. 8,9 Bilateral symptoms suggest vasospastic disease or occlusive disease from systemic abnormalities, such as diabetes or connective tissue diseases. Noninvasive vascular laboratory evaluation complements the history and physical examination. Digital blood pressures and waveform analysis in the warm hand will localize the disease. Segmental pressures or duplex examination is useful in assessing inflow and identifying arterial lesions between the thoracic outlet and the wrist. For embolic disease, we have also found transesophageal echocardiography to be useful, not only as a means of excluding a cardiac source, but also as a means of identifying mobile plaque in the ascending aorta or near the subclavian orifice. We use arteriography when patients have large vessel occlusive disease or unilateral digital occlusive disease. High-quality magnified views of the hands were essential in identifying the lesions in both of the cases presented. These images provide multiple views of the vessels, minimizing the chance of missing a significant lesion because of vessel overlap. Magnification is important in viewing the lesions because they are subtle. Additionally, these images of the digital arteries usually distinguish between embolization and a local occlusive process. When an embolic source is identified, it should be excluded from the circulation and should be followed by local arterial reconstruction when possible. It is important in the repair to use the shortest possible conduit and to exclude the entire diseased segment of artery. 10 Because of the small size of the distal radial artery, we used a branch of the cephalic vein harvested through the same incision. Others have described using a distal saphenous vein or basilic vein for the bypass graft, although these would be much larger than the distal radial artery. 11 Digital ischemia is a diagnostic challenge to the primary care physician because it is so uncommon. It is usually attributed to local trauma on initial evaluation, and referral is prompted by progression, with obvious physical findings such as ulceration or cyanosis. Early identification of correctable vascular lesions is critical because short-term sensory loss, ulceration, and superficial necrosis are usually reversible. Our patients were symptomatic for several months before their referrals. Eliminating the embolic source typically reverses the process when significant tissue loss has not occurred. Both patients had improvement in the digital pressures, healing of skin lesions, and return of normal skin color. Although the unusual location of these lesions suggests local trauma, both patients denied trauma to the hand or wrist. Repetitive work-related activities that result in frequent blunt trauma to the
5 714 Longo et al October 1998 hypothenar eminence and the use of vibratory tools are known to be associated with arterial injuries to the hand. One of our patients worked as a checker in a department store, possibly using a repetitive activity that may have played some contributory role. The other patient had worked as a nurse. Although we did not identify a specific anatomic anomaly, the precise localization to the point where the artery would be compressed between the extensor pollicis longus and the base of the first metacarpal suggests a chronic vascular injury. No other atherosclerotic occlusive disease was seen on the angiograms. These cases highlight the importance of high-quality angiography in the evaluation of patients with digital occlusive disease. REFERENCES 1. Hunter GC, Hall KA. Subclavian and axillary artery aneurysm. In: Ernst CB, Stanley JC, editors. Current Therapy in Vascular Surgery. St. Louis: Mosby; p Lee KL, Miller JG, Laitung G. Hand ischaemia following radial artery cannulation. J Hand Surg [Br] 1995;20: Redfern AB, Zimmerman NB. Neurologic and ischemic complications of upper extremity vascular access for dialysis. J Hand Surg [Am] 1995;20: Spittell PC, Spittell JA. Occlusive arterial disease of the hand due to repetitive blunt trauma: A review with illustrative cases. Int J Cardiol 1993;38: Nehler MR, Taylor LM, Porter JM. Hypothenar Hammer Syndrome. In: Ernst CB, Stanley JC, editors. Current Therapy In Vascular Surgery. St. Louis: Mosby; p Yellim AE, Frankhouse JH, Weaver FA. Vascular injury secondary to drug abuse. In: Ernst CB, Stanley JC, editors. Current Therapy In Vascular Surgery. St. Louis: Mosby; p Ikeda A, Ugawa A, Kazihara Y. Arterial patterns in the hand based on a three-dimensional analysis of 220 cadaver hands. J Hand Surg [Am] 1988;13: McNamara MF, Takaki HS, Yao JST, et al. A systematic approach to severe hand ischemia. Surgery 1978;83: Wiglis EF. Evaluation and treatment of chronic digital ischemia. Ann Surg 1981;193: Mesh CL, McCarthy WJ, Pearce WH, Flinn WR, Shireman PK, Yao JST. Upper extremity bypass grafting. A 15-year experience. Arch Surg 1993;128: Dalman RL. Upper extremity arterial bypass distal to the wrist. Ann Vasc Surg 1997;11: Submitted Apr 20, 1998; accepted Jul 9, 1998.
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