Vascular disorders of the upper limb

Introduction

Arterial diseases of the upper limb are relatively rare in comparison with those involving the lower extremity. The good collateral supply around the shoulder and elbow explains why chronic occlusive disease is commonly asymptomatic, but acute occlusion caused by embolism can result in limb-threatening ischaemia. In addition, thoracic outlet syndrome, subclavian–axillary vein thrombosis and occupational vascular problems need to be considered. In this chapter, we do not review vasospastic disorders, connective tissue disease, vasculitis and Raynaud’s disease, as these are covered in Chapter 12, nor vascular trauma, which is covered in Chapter 9. The main causes of upper limb vascular disease are summarised in Box 11.1 .

Clinical examination

Vascular assessment of the upper limb should include the thoracic outlet. Palpation and auscultation of the supra-clavicular region may help to detect a cervical rib, a subclavian artery stenosis or aneurysm. The arm pulses should be examined with the arm placed in the neutral position and then in abduction and external rotation (surrender position) to detect arterial thoracic outlet compression. Pulse palpation is important and must include the axillary, brachial, radial and ulnar pulses. The nail folds should be examined for infarcts and splinter haemorrhages. The blood pressure should be measured in both arms, preferably using a hand-held Doppler. A difference of more than 15% is abnormal.

Examination in cases of hand ischaemia is not complete unless Allen’s test is performed. The examiner compresses the radial and ulnar arteries at the wrist. The examiner then asks the subject to clench the fist to empty the hand of blood. The radial artery is then released, and the hand is observed for return of colour. The test is then repeated for the ulnar artery. The test is normal if refilling of the hand is complete within less than 10 seconds from either side. Any portion of the hand that does not blush is an indication of incomplete continuity of the palmar arch.

Occlusive disease

Occlusive lesions of the brachiocephalic and subclavian arteries occur in relatively young patients with mean ages ranging from 50 to 60 years. These lesions are less frequent than those involving the carotid bifurcation. Atherosclerosis is the predominant cause in Europe, with Buerger’s disease and Takayasu’s arteritis rarely seen. The symptoms of occlusive disease of the upper extremities include muscle fatigue and ischaemic rest pain. Digital necrosis or atheroembolisation is less common than in the lower extremities, accounting for no more than 5% of patients with limb ischaemia.

Brachiocephalic artery

Stenotic lesions of the brachiocephalic artery are uncommon and may be asymptomatic in 13–22% of patients. ^, Symptomatic patients may present with ischaemia of the right upper extremity, carotid territory symptoms or vertebrobasilar symptoms. The diagnosis is suspected by physical examination (i.e., right supra-clavicular/cervical bruit, absent right subclavian or axillary pulse) and confirmed by duplex scanning, conventional angiography, or computed tomographic angiography (CTA) or magnetic resonance angiography (MRA). Most patients (61–84%) with brachiocephalic artery occlusion have multiple lesions of the aortic arch vessels. Symptomatic stenotic lesions of the brachiocephalic artery may be treated surgically or radiologically. Surgically, this can be approached by median sternotomy with direct bypass grafting from the aortic arch, or indirectly by extra-anatomical bypass such as subclavian–subclavian, contralateral carotid–carotid or subclavian–carotid bypass.

Aorto-brachiocephalic bypass

Extra-anatomical bypasses have a lower morbidity and mortality but direct bypasses from the aortic arch are more durable. In total, the combined post-operative death and stroke rate for direct reconstruction of the supra-aortic trunks ranges from 2.6–16% ( Table 11.1 ). The primary patency is about 90% with a 72% survival rate at 10 years.

Table 11.1

Direct reconstruction of the supra-aortic vessels: complications and late patency

Authors, year	No. patients	Mean follow-up (month) [range]	Complications (%)	Primary patency (%)
Takach et al., 2005	113	61.2 ± 6	Death: 2.7	10 years: ∗ 94.4 ± ± 4
		[3–264]	Stroke: 2.7
			MI: ∗ 1.8
Berguer et al., 1998	100	51 ± 4.8	Stroke + death: 16	5 years: † 94 ± 3
		[1–184]	Morbidity: 27
Uurto et al., 2002	76	158 [6–136]	Death: 2.6 Morbidity: 19.7	1 year: 95 5 years: ‡ 91 15 years: ‡ 89

MI , myocardial infarction.

∗ 22 patients were followed at 10 years.

† 34 patients followed at 5 years.

‡ 54 patients followed at 5 years and 25 at 15 years.

A median sternotomy is used with extension into the neck. The left brachiocephalic vein is identified ( Fig. 11.1a ). A partial occluding clamp is applied to the ascending aorta proximal to the brachiocephalic artery to avoid the risk of fracturing atheromatous plaque ( Fig. 11.1b ). An 8–10-mm prosthetic graft is anastomosed at this site with deep suture placement in the aortic wall ( Fig. 11.1c ). Once the anastomosis is completed, a clamp is applied across the graft and systemic heparin is given. The brachiocephalic artery is clamped, sectioned and the proximal stump oversewn. The patent distal artery is spatulated and the graft attached in an end-to-end fashion ( Fig. 11.1d ). Air is evacuated from the graft by back-bleeding the subclavian artery, then flow is released into the arm and then into the carotid artery. The mortality of direct bypass ranges from 5.8–8% in Kieffer’s and Berguer’s series, ^, with a primary patency rate at 5 years of 94% in both series.

Brachiocephalic endarterectomy

The proximal location of the disease with extension into the aortic arch makes this technique hazardous. Attempts to remove an orifice lesion may initiate an aortic dissection or distal embolisation. For this reason, bypass or endovascular therapy are preferred for all brachiocephalic lesions where treatment is indicated, except perhaps for those located in the distal segment.

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