Annals of Vascular Surgery
Volume 24, Issue 4 , Pages 554.e7-554.e12, May 2010

Recurrent Upper Extremity Embolism Due to a Crutch-Induced Arterial Injury: A Different Cause of Upper Extremity Embolism

Department of Surgery, Seoul St. Mary's Hospital, The Catholic University of Korea, College of Medicine, Seoul, Korea

published online 25 January 2010.

Article Outline

Acute embolism of the upper extremity is a relatively infrequent event compared to the lower extremity, but it will affect the function of the limb involved and may occasionally lead to amputation. Most upper extremity emboli are of cardiac origin, with the remainder arising from subclavian aneurysm, occlusive disease, or iatrogenic causes. Rarely, crutch-induced repetitive trauma of an upper extremity can produce recurrent embolic events. Frequently, this process is initially diagnosed and treated as a brachial artery embolism; such a misdiagnosis is associated with recurrent embolism. We report herein two uncommon cases of axillobrachial arterial injuries secondary to crutch trauma as a source of recurrent emboli to an upper extremity.

 

Many patients with physical disabilities of the hips and legs are required to use assistive devices for mobility. With the increasing use of lower limb prosthetic devices and the associated increase in the temporary use of axillary crutches, it is anticipated that crutch-induced arterial injury (CAI) will be on the rise. Damage to the axillobrachial artery is a well-known but rarely reported complication of chronic use of axillary crutches.1, 2, 3, 4, 5, 6 Excessive weight-bearing on the axillary piece of the crutch can result in a sevenfold increase in the force on the axilla,7 and this increased force causes repetitive trauma to the axillobrachial artery, leading to stenosis, formation of an aneurysm, and secondary thromboembolic events.8 We present two cases of recurrent embolism involving the upper extremity (UE) due to incorrect use of axillary crutches and offer a comprehensive review of the English literature regarding the types of lesions, duration of crutch use, treatment modalities, results, and incidence of recurrent embolic attacks.

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Case 1 

A 42-year-old man visited our clinic for evaluation of pallor, decreased sensation, and weakness in his left forearm of 8hr duration. The patient had marked shortening and a flexion deformity of the left leg caused by poliomyelitis in childhood and had used one axillary crutch since 6 years of age. During the 7-year period prior to this admission, the patient underwent left brachial artery (BA) embolectomy three times due to recurrent BA embolism. The patient had no history of heart disease or diabetes and did not smoke. On physical examination, hyperpigmentation caused by repeated trauma was noted 4cm distal to the axillary crease. The left arm was cold below the elbow. The BA was palpated just above the elbow, but no other pulses were detected in the left arm. An electrocardiogram and an echocardiogram were normal. There was no evidence of thoracic outlet syndrome on radiologic studies. With apparent signs and symptoms of arterial ischemia, an emergency angiographic examination was carried out through the femoral route. The angiogram showed a 70% diameter-reducing short-segment stenosis at the axillobrachial junction. Complete occlusion of the BA at the level of the elbow and multiple small filling defects in the radial and ulnar arteries were noted (Fig. 1). The focal luminal narrowing of the proximal BA was treated with endarterectomy and vein patch angioplasty, and distal BA occlusion was treated with a balloon thromboembolectomy (Fig. 2). Postoperatively, the forearm became warm and pink, with palpable radial, ulnar, and BA pulses. The patient was instructed to change the crutch to the forearm type to prevent further injuries to the axillobrachial artery. On follow-up examination 9 months postoperatively, the patient was doing well and had good pulse in the forearm but with mild numbness and pain in the hand during exercise.

  • View full-size image.
  • Fig. 1 

    Left upper extremity angiogram. The angiogram demonstrates a focal axillary artery stenosis with embolic occlusion of the brachia, distal ulnar, and radial arteries.

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Case 2 

A 49-year-old man was hospitalized because of right UE numbness, coldness, and claudication. The patient had been using one crutch for the past 40 years due to poliomyelitis involving the right lower extremity (LE). Seven months previously, the patient had an embolic occlusion of the right BA and was treated with thrombolytic therapy. On examination, the right UE was pale, cyanotic, cold, and pulseless. We did not find any other embolic source such as atrial fibrillation, thoracic outlet obstruction, or a hypercoagulable state. An angiogram showed complete occlusion of the axillary artery (AA) with emboli occluding the right brachial, radial, and ulnar arteries (Fig. 3). Surgical thrombectomy through an antecubital incision was attempted, but the thrombus was so hard it could not be retrieved. Bypass grafting of the polytetrafluoroethylene graft from the proximal AA to the BA was carried out because of inadequate quality of the saphenous vein, and a distal balloon thromboembolectomy was performed. After surgery, good pulses were restored in the right UE. The patient was trained in the use of elbow-supporting crutches. At a 14-month follow-up examination, the right UE remained well perfused with palpable pulses.

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Literature Review 

Crutch-induced AA stenosis and thrombosis was first reported in 1930,8 and a crutch-induced AA aneurysm was first reported in the English literature in 1953.9 Since then, 29 cases of CAI have been reported in the English literature.1, 2, 3, 4, 5, 6, 9, 10, 11, 12, 13, 14 We have reviewed the 29 reported cases in addition to the two cases presented herein (Table I).

Table I. Summary of published cases of crutch-induced axillobrachial artery injuries
ReferenceAge (years)SexSiteDuration of crutch usePresenting symptomRecurrent embolismType of lesionTreatment modalitiesResulta
Platt (1930)838MLeftSince early infancyIschemic symptomYesThrombotic occlusionElbow crutchFair
41MRightSince early childhoodIschemic symptom Thrombotic occlusionElbow crutchGood
Rob and Standeven (1956)956MLeft47 yearsIschemic symptom Thrombotic occlusionSympathectomyFair
54MRightSince early childhoodIschemic symptom Thrombotic occlusionSympathectomyGood
57MRightSince early childhoodIschemic symptom Thrombotic occlusionSympathectomyFair
58FRight55 yearsIschemic symptom AneurysmSympathectomyFair
Brooks and Fowler (1964)248MRight43 yearsIschemic symptom Thrombotic occlusionSympathetic blockFair
50MRightSince childhoodIschemic symptomYesThrombotic occlusionSympathectomyPoor
65MRight60 yearsIschemic symptom Thrombotic occlusionSympathetic blockPoor
Danese et al. (1969)1065MRight59 yearsIschemic symptomYesAneurysmSurgeryGood
Abbott and Darling (1973)184MLeftSince childhoodIschemic symptom AneurysmSurgeryGood
71MRightSince childhoodIschemic symptomYesAneurysmSurgeryFair
67MLeftSince adolescenceIschemic symptomYesAneurysmSurgeryFair
68FRight47 yearsIschemic symptom AneurysmSurgeryGood
65bFRight9 yearsIschemic symptom AneurysmSurgeryGood
65bFLeft10 yearsPulsating mass AneurysmSurgeryGood
76FLeft25 yearsIschemic symptom AneurysmSurgeryGood
59MLeftSince childhoodNo symptom AneurysmObservation
Thomas and Deshmukh (1973)1376MLeft63 yearsIschemic symptomYesAneurysmSurgeryGood
Schramek et al. (1974)567MLeft50 yearsIschemic symptomYesThrombotic occlusionSurgeryGood
54MLeft31 yearsIschemic symptom AneurysmSurgeryGood
Ettien (1980)377FLeft40 yearsIschemic symptom AneurysmSurgeryGood
Lee et al. (1987)461MLeft56 yearsIschemic symptomYesAneurysmSurgeryGood
Feldman et al. (1995)1162MLeftSince childhoodIschemic symptomYesAneurysmSurgeryFair
66MLeft2 monthsIschemic symptom Thrombotic occlusionPTAGood
64MRight56 yearsIschemic symptomYesThrombotic occlusionPTAPoor
Tripp and Cook (1998)654MLeftIntermittent usePulsating mass AneurysmSurgeryGood
Oran et al. (2000)1239MRight33 yearsIschemic symptom Thrombotic occlusionPTA with stentGood
McFall et al. (2004)1453FRight10 yearsIschemic symptom Thrombotic occlusionSurgeryGood
Present case42MLeft36 yearsIschemic symptomYesThrombotic occlusionSurgeryFair
49MRight40 yearsIschemic symptomYesThrombotic occlusionSurgeryGood

aGood, no ischemic symptoms; fair, some residual ischemic symptoms; poor, amputation.

bSame patient.

In one patient, the CAI developed bilaterally. The range of CAI patient ages was 38-84 years (mean 60±10), occurring most commonly in the 50s and 60s. There were 24 males and six females. The left side was involved in 16 cases, and the right side was involved in 15 cases, with no statistical differences. With respect to the lesion associated with the CAI, there were aneurysms in 16 cases and stenoses or occlusions in 15 cases. Twenty-four patients used crutches for >30 years, and one patient used a crutch for 2 months. Among 31 lesions, 28 were associated with ischemic symptoms due to arterial occlusion, two were pulsating masses, and one was detected incidentally during another diagnostic test. Twelve of the 28 ischemia-associated cases had postsurgical recurrences, suggesting a recurrent embolic event or chronic arterial insufficiency preexisting the deterioration of symptoms; and in 43% of the patients, recurrent emboli developed prior to establishing an accurate diagnosis. Nine patients were initially diagnosed erroneously and treated for a BA thromboembolism. Recurrent embolic attacks due to aneurysms and stenoses occurred in six patients each. Among the 16 patients with aneurysms, intraluminal thrombi occurred in eight. With respect to treatment, with the exception of one lesion in an untreated terminal cancer patient, outcomes were good in 18 cases and fair in nine cases and amputation was performed in three cases. The latter had stenoses or occlusions.

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Discussion 

With an increasing number of patients with permanent physical disabilities or using LE prosthetic devices, the use of axillary crutches has also increased. Axillary crutches are designed to help the individual walk with reduced weight-bearing on the LE. The purpose of the horizontal axillary bar on the crutch is to provide lateral stability with pressure against the chest wall. However, when crutches are used incorrectly, 34% of the body weight is transferred to the axilla,15 resulting in up to a sevenfold increase in the force on the axilla.7 This force caused by the incorrect use of an axillary crutch is well established as a cause of axillobrachial arterial injuries.

Repetitive trauma due to the use of axillary crutches causes disruption and degeneration of the tunica intima and tunica media, leading to stenosis or the formation of an aneurysm and subsequent distal embolization of the thrombus, which gradually occludes distal vessels and may compromise the results of revascularization during later ischemic episodes.1, 4, 5, 9, 13, 16, 17 Injury to the intimal layer is likely to lead to thrombosis, while progressive damage to the intimal and medial layers and eventual fragmentation of both the arterial intima and the lamina elastica may cause formation of an aneurysm.5 Formation of an aneurysm is relatively rare compared to stenotic or thrombotic occlusions, possibly because it takes several decades to weaken the wall of the artery and cause the formation of an aneurysm.13 However, review of the available case literature shows that the incidence rates of aneurysms and stenotic or occlusive lesions are similar, developing in cases in which crutches have been used for just a few months; the duration of use of crutches does not differ between patients with aneurysms and stenotic or occlusive lesions. Thus, it appears that the magnitude of force delivered by the crutch, rather than the duration of use, is more important for the formation of an aneurysm.

Acute embolism of the UE is relatively infrequent and a less severe problem compared to the LE. The reported incidence of acute UE embolism is 7-36% of cases of acute embolism of the limbs,16, 17, 18, 19, 20 and amputation rates for UE embolism are much lower than those for LE embolism (0–4% vs. 9-24%, respectively).19, 20, 21, 22, 23, 24, 25 The presence of a rich collateral supply to the UE, particularly at the shoulder, elbow, and forearm, makes acute UE occlusions at this level better tolerated and limb loss far less than with LE emboli. A CAI in the UE has several distinct clinical characteristics compared with other causes of UE embolism. Recurrent embolism and amputation rates are much higher in patients with CAI. The incidence rates of recurrent embolic events in UE embolic patients are reported to be 2.6-7%,25, 26 but in the CAI group the incidence is 43%. The amputation rate associated with CAI is 10% compared with 0–4% of patients with UE emboli.23, 24, 25 The long-term prognosis is much poorer in patients with CAI compared with other causes of ischemia involving the UE. Complete recovery of normal UE function is achieved in 84% of patients with UE emboli who are treated,16 but only 60% of patients with CAI recover complete UE function, 30% of patients have some residual ischemic symptoms, and 10% of patients require amputation. The most important cause of these differences is recurrent emboli leading to small-vessel occlusion that might jeopardize the result of arterial reconstruction due to obliteration of arterial outflow and that can be erroneously diagnosed as a BA thromboembolism. The presenting symptoms of aneurysms are different between the two groups. The majority of patients with other causes of AA aneurysms have shoulder pain and pulsating masses; and only 25% of patients have ischemic symptoms.27 Among 16 cases of aneurysms caused by CAI, 81% of patients complained of acute ischemic symptoms. The incidence of distal embolic phenomena is fairly high compared with previous reports of emboli from subclavian or AA aneurysms.27 Aneurysms formed by a CAI have intraluminal thrombi much more frequently compared with other aneurysms (56% vs. 25%, respectively).27 Such loose thrombi may become dislodged on further trauma from crutches and may form acute, chronic, or repetitive emboli. The perioperative mortality rate is lower in patients with CAI than other embolic patients. The mortality rate of patients with UE emboli is reported to be 3.7-23%,23, 25, 26, 28, 29, 30 but in patients with a CAI there were no perioperative deaths. Since a limited duration of limb ischemia can be tolerated, when clinical findings strongly suggest an arterial embolism, the immediate initiation of treatment is mandatory. Sometimes misdiagnosis of the underlying lesion is made by incomplete studies due to the urgency of this situation. The most likely misdiagnosis is a BA embolus; this diagnosis occurred preoperatively in nine of the patients with a CAI. If a correct diagnosis is not made, secondary procedures may be necessary, with possibly poor long-term results. Suspicion should be aroused when a patient who has been using crutches with ischemic signs and symptoms of the UE does not have a valid source of peripheral emboli, such as valvular heart disease, cardiac arrhythmia, or thoracic outlet syndrome.12 By means of vascular imaging techniques, such as angiography, Doppler ultrasonography, magnetic resonance angiography (MRA), or computed tomography angiography (CTA), diagnosis of CAI is easy. Arteriography is necessary to clearly define the arterial anatomy and to identify areas of embolic occlusion more distally, but the arteriogram does not reveal the true dimension of the aneurysm. For an exact diagnosis of a CAI, arteriography and another radiologic modality, such as CTA or MRA, should be combined.

These lesions threaten the involved UE with the risk of thrombosis and embolic injuries. Treatment should be considered on discovery of these lesions, even if asymptomatic, to prevent limb loss and dysfunction. The mainstay of treatment for an aneurysm caused by a CAI consists of resection and reconstruction with a suitable graft whenever possible.1, 4, 6 Distal embolectomy should also be performed. Others have performed exclusion of the aneurysm with subsequent bypass grafting to optimize limb blood flow.31, 32, 33 However, exclusion of the aneurysm is prone to recurrence and rupture due to the rich collateral circulation of the shoulder, and indeed, recurrence with rupture of an AA aneurysm treated initially with exclusion and bypass has been reported from the Mayo Clinic.34 Surgical alternatives for management of arterial thrombosis or stenosis include thrombectomy, axillobrachial bypass, and primary vessel repair. Recently, this lesion was successfully treated by percutaneous transluminal angioplasty with or without a self-expandable stent.11, 12 After the ischemia has been controlled, all efforts should be made to eliminate axillary pressure. The patient should use Canadian or forearm crutches to avoid future trauma to the axillary region.

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Conclusion 

In conclusion, a CAI in the UE has been described rarely, and this has several distinct clinical characteristics compared with other causes of UE embolism. The main reason of poor outcome is progressive obliteration of small vessels caused by recurrent embolization that might jeopardize the results of arterial reconstruction. A high index of suspicion and early identification of the proximal arterial lesion is critical for good long-term therapeutic results.

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References 

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PII: S0890-5096(09)00345-8

doi:10.1016/j.avsg.2009.11.005

Annals of Vascular Surgery
Volume 24, Issue 4 , Pages 554.e7-554.e12, May 2010