adding the analysis of waveforms obtained before and after ulnar and/or radial artery occlusion at the

wrist. Duplex ultrasound is useful when an obstructive lesion is localized by physical examination,

waveform analysis, or segmental pressure recordings. B-mode imaging and color Doppler can further

define the characteristics of the lesion and its hemodynamic severity. Finally, measurement of digital

PPG tracings can be obtained with and without manual pressure causing temporary occlusion of

hemodialysis grafts and fistulae when evaluating arterial steal in patients with renal failure.

ANGIOGRAPHY

Accurate delineation of the arterial anatomy of both arms, from the aortic arch to the digital arteries is

mandatory when obstructive lesions are suspected on clinical evaluation or by noninvasive testing.

Although conventional angiography remains the gold standard, modern computed tomography

angiography (CTA) and magnetic resonance angiography (MRA) has replaced this modality in many

practices (Fig. 90-8). In order to obtain comparison, both upper extremities should be imaged. If TOS is

suspected, provocative maneuvers are used while obtaining arterial images (Fig. 90-9). Of particular

importance is obtaining clear images of the hand circulation. Typically, the deep palmar arch arises

from the terminal part of the radial artery and the superficial arch by the ulnar artery. Nevertheless,

several variations exist (Fig. 90-10).

MANAGEMENT

5 The specific mode for revascularization used to treat upper extremity ischemia depends on the

location of the lesion, its etiology, and the available local resources and expertise. Atherosclerotic

lesions affecting the origin of the subclavian or innominate arteries are most frequently treated with

percutaneous transluminal angioplasty and stenting. This is more often achieved via a femoral approach

but can also be performed using a retrograde brachial or even a carotid approach. Despite its popularity

due to being minimally invasive, well tolerated by patients, widely available in the armamentarium of

multiple disciplines and having immediate angiographic results that are usually excellent, several

disadvantages should be considered when choosing this form of therapy. First, deployment of

intravascular devices across the origin of the vertebral artery, across an internal mammary previously

used as a coronary bypass and under the clavicle should be avoided due to the obvious possibility of

catastrophic results. Second, the long-term durability of intravascular stents in the ostia of the aortic

arch is not clearly established. Finally, we have seen an elevated rate of stent fractures in this

position.10 This is likely due to the extreme motion of the aortic arch and the supra-aortic trunks around

the cardiac cycle. Alternatively, open surgical bypasses and transpositions can be performed via small

incisions in the neck with excellent long-term results. For example, the subclavian artery can be

transposed to the common carotid artery using a small transverse neck incision. This procedure allows

for preservation of the vertebral artery and its long-term patency rate is virtually 100%.11 A short

carotid to subclavian bypass using prosthetic material can also be used with excellent long-term results

(Fig. 90-11). Finally, in some patients the best option resides in single or multiple-branched bypasses

arising from the aortic arch. A ministernotomy is used to expose the ascending arch and the bypass can

be anastomosed to the aorta using a side-biting clamp thus obviating the need for cardiopulmonary

bypass (Fig. 90-12).

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Figure 90-9. Selective digital subtraction angiography of the right arm in a patient with suspected arterial thoracic outlet

syndrome. Subclavian artery stenosis is not seen when injecting contrast with the arm in neutral (A) and moderate abduction (B),

but is evident when the arm is hyperabducted (C).

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Figure 90-10. Different types of complex superficial palmar arch found on 500 hand arteriograms.

Intervention during the acute inflammatory phase of Takayasu arteritis should be avoided. Steroid

and immunosuppressive therapy should be used instead and any intervention should be delayed until the

acute, active phase of the disease undergoes remission.12 This is often indicated by normalization of

serologic inflammatory markers. Antiplatelet therapies may lower the frequency of ischemic events.

During the chronic phase, reconstruction is carried out using similar techniques as those used for the

management of atherosclerotic occlusion (Fig. 90-13).

There is little controversy about the management of patients with arterial TOS. Untreated arterial

injury due to repetitive torsion and compression leads to stenosis, poststenotic aneurysmal dilation, and

distal embolism. In the majority of cases, evidence of distal embolism with compromise of the arteries

of the hand is already present by the time of presentation. Thus, thoracic outlet decompression and/or

arterial reconstruction is mandatory. Since the subclavian artery can be compressed at any point from

the root of the neck to the pectoralis minor tendon, the decompressive approach depends on the specific

anatomy of the patient. The surgical plan depends on the details obtained by imaging studies and the

experience of the surgeon. In the absence of anatomic anomalies and with compression demonstrated

only during arm abduction and elevation, first rib resection via the supraclavicular approach appears to

be the best choice. If chronic compression has caused arterial damage, revascularization is necessary.

Interposition grafts from the ipsilateral common carotid to the axillary artery are commonly used. This

can best be achieved by a combination of supra- and infraclavicular exposure. Eight-millimeter PTFE

grafts tunneled underneath the clavicle or subcutaneously have excellent patency rates. Excision of a

cervical rib is usually done whereas full thoracic outlet decompression with scalenectomy is only

necessary if concomitant neurogenic TOS exists.13

Other occlusive lesions of the subclavian, axillary, and brachial artery are best treated with surgical

revascularization. Due to potential compression at the costoclavicular space, the high mobility of the

shoulder joint and the caliber of the brachial artery, endovascular approaches are rarely indicated in this

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segment of the circulation. The conduit of choice for bypasses in the upper extremity is the saphenous

vein. Many different configurations are available. The supraclavicular subclavian artery can be exposed

by an incision at the base of the neck and used as inflow for bypasses tunneled subcutaneously over the

clavicle and into the brachial artery. Alternatively, an excellent source of inflow is the common carotid

artery. The outflow anastomosis can be created in the distal brachial artery, the radial or ulnar arteries

in the proximal forearm (Fig. 90-14), or at the wrist and even in the arteries of the hand (Fig. 90-15).

Figure 90-11. A: Right carotid to subclavian bypass performed via a supraclavicular incision using a prosthetic 10-mm conduit. B:

CT scan showing patency of the bypass.

Figure 90-12. Aorto to inominate bypass. A ministernotomy is done and a side-biting clamp is used for creation of the proximal

anastomosis in the ascending aorta. The distal anastomosis is created at the bifurcation of the innominate artery.

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Figure 90-13. Arterial reconstruction on the patient with Takayasu arteritis shown in Figure 90-3. A median sternotomy with

bilateral neck incisions was used. The proximal anastomosis was done in the ascending aorta. One branch was anastomosed in an

end-to-end fashion to the right subclavian. A second branch was anastomosed to the right carotid (side-to-end) and then tunneled

via the prevertebral space and anastomosed end-to-end to the left carotid bifurcation. Finally, a side arm was used to revascularize

the left subclavian artery.

Figure 90-14. Large aneurysm of the distal brachial artery treated with a bifurcated bypass created with great saphenous vein. The

distal anastomosis (arrows) were created into the radial and ulnar arteries just distal to the elbow.

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Figure 90-15. Completion angiograms of two different saphenous vein bypasses with distal anastomosis to the palmar arch (A) and

radial artery at the snuffbox segment (B).

Figure 90-16. Ulnar artery aneurysm treated with arterial conduit (profunda femoris branch harvested from the thigh) in a patient

with hypothenar hammer syndrome.

Patients suffering from hypothenar hammer syndrome with mild symptoms and without an aneurysm

can be treated nonoperatively. Padded hand protection, avoidance of further repetitive trauma, tobacco

cessation (if applicable), and the use of calcium channel blockers, antiplatelet agents, and/or

anticoagulation all have been tried with some degree of success. Surgical intervention can include

simple ligation of the aneurysm if there is adequate collateral circulation; typically resection of the

affected segment with reconstruction is required (Fig. 90-16).

The management of Raynaud syndrome consists on the use of calcium channel blockers and

vasodilators.13

CONCLUSIONS

Although atherosclerosis is still the most common cause of upper extremity arterial disease, a myriad of

conditions associated with occupational and social risk factors are often the cause of arm and hand

ischemia. A complete history and physical examination often discloses a potential etiology and usually

points to the anatomic location of the culprit lesion. Bilateral hand ischemia is often associated with

systemic conditions, whereas unilaterality more commonly occurs with obstructive lesions. Accurate

delineation of the anatomy by the use of imaging modalities is necessary in order to plan

revascularization. Multiple endovascular and open surgical options are available for the management of

upper extremity arterial disorders.

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References

1. Lally EV. Raynaud’s phenomenon. Curr Opin Rheumatol 1992;4(6):825–836.

2. Bowling JC, Dowd PM. Raynaud’s disease. Lancet 2003;361(9374):2078–2080.

3. Kreienberg Paul B, Chang BB, Roddy SP, et al. Hand ischemia in end stage renal disease. In:

Rodriguez HE, Pearce WH, Yao JST, eds. “The Ischemic Extremity.” Shelton Connecticut. United

States: People’s Medical Publishing House USA; 2010:525–531.

4. Wu W, Chaer RA. Nonarteriosclerotic vascular disease. Surg Clin North Am 2013;93(4):833–875.

5. Ayarragaray JE. Ergotism: a change of persepective. Ann Vasc Surg 2014; 28(1):265–268.

6. Kee ST, Dake MD, Wolfe-Johnson B, et al. Ischemia of the throwing hand in major league baseball

pitchers: embolic occlusion from aneurysms of axillary artery branches. J Vasc Interv Radiol

1995;6(6):979–982.

7. Kumar HR, Rodriguez HE. Thenar and hypothenar hammer syndrome. In: Gilbert R, Upchurch GR

Jr, Henke PK, eds. Clinical Scenarios in Vascular Surgery. 2nd ed. Philadelphia, PA: Wolters Kluwer

Health; 2015.

8. Sumner DS. Non-invasive assessment of upper extremity ischemia. In: Bergan JJ, Yao JST, eds.

Evaluation and Treatment of Upper and Lower Extremity Circulatory Disorders. Orlando, FL: Grune &

Stratton; 1984:75–95.

9. Karwowski JK, Johnson B, Dalman RL. Upper extremity ischemia: diagnostic techniques and clinical

applications. In: Mansour MA, Labropoulos N. eds. Vascular Diagnosis. Philadelphia, PA: Elsevier

Saunders; 2005:325–330.

10. Usman AA, Resnick SA, Benzuly KH, et al. Late stent fractures after endoluminal treatment of ostial

supraaortic trunk arterial occlusive lesions. J Vasc Interv Radiol 2010;21(9):1364–1369.

11. Morasch MD. Technique for subclavian to carotid transposition, tips, and tricks. J Vasc Surg

2009;49(1):251–254.

12. Keser G, Direskeneli H, Aksu K. Management of Takayasu arteritis: a systematic review.

Rheumatology (Oxford) 2014;53(5):793–801.

13. Miller D, Rodriguez HE. Management of vascular thoracic outlet syndrome. In: Eskandari MK,

Morasch MD, Pearce WH, et al., eds, Contemporary Vascular Surgery. United States: People’s Medical

Publishing House-USA; 2011:469–476.

14. Caglayan E, Axmann S, Hellmich M, et al. Vardenafil for the treatment of Raynaud phenomenon: a

randomized, double-blind, placebo-controlled crossover study. Arch Intern Med 2012;172(15):1182–

1184.

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Chapter 91

Renal and Splanchnic Vascular Disease

Dawn M. Coleman, John E. Rectenwald, and Gilbert R. Upchurch, Jr.

Key Points

1 Splanchnic vascular disease is uncommon across the spectrum of vascular surgery practice, but

remains central to the specialty.

2 Intestinal ischemia may result from presplanchnic conditions that decrease total mesenteric blood

flow (i.e., heart failure and hypovolemia), splanchnic conditions that decrease regional blood flow

through the mesenteric circulation (i.e., thromboembolism) or postsplanchnic venous congestion

(i.e., mesenteric vein thrombosis and cirrhosis).

3 The most common causes of AMI include: embolization (40% to 50%), arterial thrombosis (25% to

30%), nonocclusive mesenteric ischemia (15% to 20%), and mesenteric venous thrombosis (5% to

15%).

4 Patients with AMI warrant immediate medical management that includes the establishment of

adequate intravenous access and hemodynamic monitoring, systemic anticoagulation with heparin,

fluid resuscitation, correction of electrolyte abnormalities, and administration of broad-spectrum

antibiotics.

5 The progression from minor symptoms to AMI and intestinal infarction is unpredictable; almost half

of patients presenting with AMI describe previous symptoms of CMI.

6 Distribution of splanchnic artery aneurysms is as follows: Splenic artery (60%) > hepatic arteries

(20%) > superior mesenteric artery (5.5%) > celiac artery (4%) and gastric and gastroepiploic

arteries (4%) > ileocolic arteries (3%) > pancreaticoduodenal arteries (2%) > gastroduodenal

artery (1.5%) > inferior mesenteric artery (<1%).

7 Renal artery occlusive disease is the most common cause of correctable HTN in adults and the third

most common cause of HTN in children and should be considered in the clinical context of: (1)

childhood HTN, (2) severe HTN in women <45 years of age, (3) acute and rapid escalation of mild

HTN in older patients (>50 years), (4) initial diastolic BP >115 mm Hg, and (5) rapid deterioration

in renal function following the administration of antihypertensive therapy (especially with ACE

inhibition).

8 Medical therapy remains the mainstay of treatment for RVH with comprehensive goals of care that

should encompass glycemic control, cholesterol reduction, smoking cessation, blood pressure

reduction, and antiplatelet therapy with aspirin for primary prevention. ACC/AHA guidelines

support the use of ACE inhibitors (ACE-I), angiotensin receptor blockers (ARBs), calcium channel

blockers, and beta blockers with a class I indication.

9 Several recent clinical trials comparing renal artery stenting to best medical management for renal

artery stenosis have failed to demonstrate a conclusive clinical benefit to the endovascular treatment

of renal artery stenosis.

SPLANCHNIC VASCULAR OCCLUSIVE AND ANEURYSMAL DISEASE

INTRODUCTION

1 Splanchnic vascular disease is uncommon across the spectrum of vascular surgery practice, but

remains central to the specialty. Patients often seek medical attention from alternative specialists,

emphasizing the importance of cross-disciplinary awareness. Acute mesenteric ischemia (AMI) remains

associated with delayed diagnosis and dismal mortality despite notable progress in the diagnosis and

treatment of patients with vascular disease. This section elaborates on the current treatment standards

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for both splanchnic vascular occlusive disease and aneurysms.

ANATOMY AND PHYSIOLOGY

Three branches of the abdominal aorta perfuse the gastrointestinal tract. The celiac artery originates at

the level of T12 and branches into the left gastric, common hepatic, and splenic arteries in a classic

pattern in 65% to 75% of cases.1 Variations are noted in Table 91-1 and may include a true trifurcation

of these vessels (25% of the population), replaced and accessory hepatic vasculature, a common

celiacomesenteric trunk (<1% of the population), and a persistent ventral anastomosis between the

proper hepatic, and a replaced right hepatic artery (off the SMA) denoted as an “arch of Buhler” (<4%

of the population). Additionally, the splenic artery can be found to originate directly off the aorta, SMA,

left gastric or hepatic arteries. The celiac axis supplies primarily the stomach, duodenum, spleen, liver,

and pancreas. The SMA originates approximately 1 to 2 cm caudad to the celiac artery and branches into

the inferior pancreaticoduodenal artery, 4 to 6 jejunal and 9 to 13 ileal branches, the middle colic

artery, the right colic artery, and terminates as the iliocolic artery. The SMA supplies primarily the

lower portion of the pancreas gland, jejunum, ileum, ascending colon, and the proximal half of the

transverse colon. The inferior mesenteric artery (IMA) originates off the terminal aorta at the level of

L3 and divides into the left colic artery, sigmoid branches and continues as the superior hemorrhoidal

artery.1 This small and most distal mesenteric branch artery supplies primarily the large bowel from the

level of the midtransverse colon to the rectum.

Collateralization is a crucial concept when considering the mesenteric circulation. On the grounds of

redundancy, given multiple potential sources of collateral flow, at least two of the three major branch

vessels must be occluded or have a critical stenosis for mesenteric ischemia to manifest. While arterial

collaterals may be small in the physiologic circulation, they have the potential to hypertrophy

dramatically when increased flow is required. Figure 91-1 demonstrates several important collateral

pathways. The gastroduodenal artery (GDA) and pancreaticoduodenal arcade make up the primary

potential pathway for collateral flow between the celiac axis and the SMA. In addition to the

aforementioned arc of Buhler, the arc of Barkow consists of arteries in the omentum (SMA branches)

that connect to the right and left gastroepiploic arteries (celiac branches). The marginal artery of

Drummond is the major collateral route between the SMA and IMA; it lies within the colon mesentery

giving rise to the vasa recta. The arc of Riolan lies within a more central portion of the mesentery

connecting the middle and left colic arteries. Finally, the IMA may also receive collateral flow from

lumbar branches of the aorta, hemorrhoidal branches of the internal iliac artery, and the middle sacral

artery.

Table 91-1 Normal and Variant Mesenteric Arterial Anatomy

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