3 Upper Extremity
Authors: Kush Sharma and Ashraf Mansour
Contributors: Hattan Alghamdi
3.1 Overview
3.1.1 Anatomy
What are the zones of the upper extremity?(Illig 2019)
Division of the upper extremity into three zones:
Intrathoracic Zone: Inclusive of the aortic arch and its branches, innominate artery (dividing into right subclavian and right common carotid), left subclavian artery and left common carotid artery, as well as the innominate veins, and SVC.
- Arch classification helps determine difficulty of accessing the right innominate from a femoral approach. Type 1 innominate does not break the plane of the outer curve, Type 2 it is between the outer curve and inner curve and Type 3 it falls below the inner curve of the aortic arch.
Thoracic Outlet: Extends from the base of neck to the axilla. Includes the subclavian, proximal vertebral, and proximal axillary arteries, as well as the corresponding veins).
Axilla to Fingers: The arm.
What are some common exposures for major upper extremity arteries?(Illig 2019; Gary G Wind and R. James Valentine 2013)
Proximal Right Subclavian Artery: Access through a median sternotomy.
Proximal Left Subclavian Artery: An anterolateral thoracotomy is required in emergent settings for proximal left subclavian artery control.
- For proximal, mid and distal exposure is required a “trap door” exposure is used which is a combined anterolateral thoracotomy, third space sternotomy, and left supraclavicular incision.
Mid and Distal Subclavian Artery: Access through a supraclavicular Incision. After division of the platysma and clavicular head of the SCM, a fat pat of varying thickness is encountered which contains the omohyoid muscle.
This should be divided and placed supero-laterally. At this point, the anterior scalene muscle is exposed medially with the phrenic nerve running in a lateral to medial direction, which should be identified and preserved.
In a carotid/subclavian bypass division of the anterior scalene should be performed as close to the first rib as possible. Once divided the subclavian artery is exposed.
Axillary Artery: Exposure is gained through an infraclavicular incision, below the middle third of the clavicle.
Pectoralis major is divided and pectoralis minor is freed at the lateral margin of the wound. The axillary vein should be identified and followed supero-deeply to identify and expose the artery. Anatomically bound by the first rib proximally and the lateral edge of the teres major muscle distally.
For exposure of the first part of the axillary artery, the ipsilateral arm is abducted approximately 90 degrees and a horizontal skin incision 2 cm below the middle third of the clavicle should be made. The underlying pectoralis major is split by bluntly separating the fibers, exposing the tough clavipectoral fascia. At the lateral wound margin, the pectoralis minor can be freed and laterally retracted.
The axillary vein is the first structure to be encountered in the fascia and the artery lies just superior and deep to the vein. Make sure to protect the nerves of the brachial plexus which lie deep to the first part of axillary artery and are at risk of injury during blind placement of occluding arterial clamps.
Brachial Artery, Upper Arm: The brachial artery’s superficial location makes it vulnerable to injury and accounts for most vascular injuries of the upper extremities.
Brachial artery exposure involves a 5-8 cm longitudinal incision in the groove between the biceps/triceps muscles on the medial aspect of the arm. In the lower half of the arm, take care to avoid basilic vein damage as it runs in the subcutaneous tissue.
The neurovascular bundle is exposed by incising the deep fascia at the medial border of the biceps muscle, which then should be retracted anteriorly. The basilic vein should be identified and retracted into the posterior wound.
On opening the brachial sheath the median nerve is the most superficial structure and should be identified, protected and retracted. The brachial artery lies deep to the median nerve and is flanked by two brachial veins. Be mindful that the ulnar nerve lies posteriorly.
Brachial Artery, Antecubital Fossa: Exposure of the brachial artery in the antecubital fossa requires a transverse skin incision 1 cm distal to the midpoint of the antecubital crease.
After deepening, mobilize the basilic vein medially to avoid injury. The medial antebrachial cutaneous nerve should be identified and protected. The bicipital aponeurosis should be divided to exposure the brachial artery, which is flanked by two deep veins crossing tributaries.
To isolate the brachial artery ligation and division of these tributaries is required. The brachial artery bifurcates at the radial tuberosity into its radial and ulnar branches.
Immediately after the ulnar artery arises from the bifurcation origin, it gives off a short common interosseous branch, which bifurcates at the hiatus in the proximal interosseous membrane.
Radial Artery at the Wrist: This requires a 2-3 cm longitudinal incision generally between the palpable radial artery and cephalic vein.
Incision of the antebrachial fascia medially to the radius should expose the radial artery. Two veins accompany the artery and should be dissected away to isolate the artery.
The superficial radial nerve and its medial/lateral branches course between the cephalic vein and radial artery in this area.
Ulnar Artery: The ulnar artery courses beneath the superficial flexor muscles of the proximal forearm, emerging near the ulnar border at the midpoint between the elbow and the wrist.
In the distal forearm, the ulnar artery runs just deep to the antebrachial fascia and is easily exposed through a longitudinal incision placed radially to the flexor carpi ulnaris.
The palmar branch of the ulnar nerve courses superficially to the antebrachial fascia and should be preserved during arterial exposure to avoid injury.
What common aberrant upper extremity/arch anatomy is important to be aware of?
Bovine Arch: Where the innominate and left common carotid arteries share a common origin.(Layton et al. 2006)
Aberrant Vertebral Artery: Where the vertebral artery arises directly from the aortic arch.
Aberrant Right Subclavian Artery: Where there is no innominate artery and instead the right common carotid arises directly from the aorta.
Confusingly the right subclavian artery, then originates from the aortic arch distal to the left subclavian artery.
To supply the right arm it therefore, needs to pass behind the esophagus and anterior to the spine.
Of note, thoracic aortic disease is associated with aberrant anatomy, with high rates of bovine arch (25%), isolated L vertebral (6-8%), and aberrant R subclavian (1-2%).(Dumfarth et al. 2015)
3.1.2 Etiology
How does evaluation of upper extremity ischemia differentiate from lower extremity ischemia?
Upper extremity ischemia <5% of patients with limb ischemia are a result of underlying atherosclerosis, which is in contrast to lower extremity.(Shuja 2019)
Vast majority of cases caused by embolic, autoimmune, or connective tissue disorders.
How can upper extremity disease be classified?
Anatomic Location:
- Large vs. Small Vessel
Disease Process:
- Vaso-occlusive disease often requires endovascular/surgical management.
- Vasospastic disease is more responsive to pharmacological management.
3.1.3 Evaluation
How should patients be evaluated who have concern for upper extremity disease?
Detailed H+P evaluation (pulse palpation, auscultation at supraclavicular/infraclavicular fossa may reveal a bruit concerning for subclavian artery stenosis, upper extremity neurovascular/skin exam)
Brachial/forearm blood pressures and if suspected claudication, measured at rest and 2-5 minutes after exercise. Look for a gradient of >20 mmHg is considered significant
Some or all of 6 P’s of acute limb ischemia with symptoms occurring within 14 days are deemed acute
Doppler insonation of radial, ulnar, palmar, and digital arteries
Vascular Lab Evaluation
Segmental Pressure Measurements
Duplex Ultrasound (look for large vessel occlusive disease)
Other Imaging
- CTA/MRA
Clinical Lab tests
Inflammatory disorders-CBC, ESR, CRP, ANA, RF
Hypercoagulable screening
3.2 Vaso-occlusive Disease
3.2.1 Demographics
What are causes and symptoms associated with subclavian/axillary occlusive disease? (Jack L Cronenwett, Alik Farber, and Erica L. Mitchell 2020)
Etiology: Atherosclerosis is the most common cause of subclavian/axillary occlusive disease. Left SCA > Right involvement. Less common causes include Takayasu disease, giant cell arteritis, or arterial TOS
Symptoms: Upper extremity arm/hand ischemia or neurologic symptoms due to subclavian-vertebral steal.
Because significant collaterals, minimal pain on exertion even with subclavian occlusion.
Innominate disease can present with complex steal syndrome from the vertebral artery.(Rodriguez 2016)
What are causes and symptoms associated with brachial/forearm occlusive disease?
Etiology: MCC of brachial artery occlusion is cardiac origin embolus.
Atherosclerosis RARELY affects the brachial artery. Forearm occlusive disease can be seen in advanced ESRD or DM where calcific atherosclerosis of radial/ulnar arteries is present.
Distal axillary/proximal brachial stenosis can be from repetitive trauma from crutch use.
Radiation arteritis - may be seen with radiation after breast cancer therapy. Lesions characteristically tapered with smooth border. May occur alongside a brachial plexopathy.(Goldstein et al. 2010; Modrall and Sadjadi 2003)
Less common causes include Buerger’s disease or Raynaud Phenomenon
3.2.2 Management
3.2.2.1 Chronic Limb Threatening Ischemia
How/when is upper extremity occlusive disease treated?
Indications for treatment
70% stenosis and associated symptoms or deficit
Lesion with ipsilateral ICA requiring treatment
Pre-occlusive lesion in a good surgical candidate (>5y life expectancy)
Innominate or SCA Occlusive Disease
Endovascular with balloon expandable stent via femoral or ipsilateral brachial artery. (Chatterjee et al. 2013; Bradaric et al. 2015; Saha et al. 2017; Palchik et al. 2008; Mordasini et al. 2011) Preferred in:
Short segment or ostial disease with adequate distance to the vertebral artery origin.
History of neck surgery or radiation.
Surgery:
Bypass from aortic arch through median sternotomy - Most durable option, particularly for dense R innominate disease, so preferred in patients who can tolerate.
Endarterectomy not appropriate if disease involves the origin.(Aiello and Morrissey 2011; Mansukhani et al. 2018; Berguer, Morasch, and Kline 1998; Daniel et al. 2014; Reul et al. 1991; Berguer et al. 1999; Byrne et al. 2007)
Complications include compression of the graft on sternal closure, so proximal anastomosis should be placed to the side of the aorta.
Ipsilateral CCA to subclavian artery (bypass or transposition) - Recent NSQIP study showed no difference in stroke and death for CS bypass vs transposition, therefore procedure should be determined by anatomic constraints.(Cinà et al. 2002; Vliet et al. 1995) Small studies and systematic reviews have shown that patency of carotid subclavian bypass is better with synthetic graft than with autologous vein.(AbuRahma, Robinson, and Jennings 2000; Illuminati et al. 2018; Ziomek et al. 1986)
An additional indication for carotid subclavian bypass is as a staged revascularization prior to TEVAR for aneurysmal disease requiring coverage of the LSA
How does the exposure differentiate in transposition vs bypass?
Arterial transposition via a short, transverse cervical incision above the clavicle between two heads of SCM (bypass is lateral to entire SCM)
Sub-platysmal flaps created and avoid EJ vein damage
Omohypoid divided between heads of SCM and IJ mobilized laterally (bypass IJ is mobilized medially to expose CCA and care must be taken to avoid phrenic nerve in more lateral approach)
CCA is reflected medially with vagus nerve
On the left side, the thoracic duct is identifiable and divided followed by dividing the vertebral vein
Subclavian artery and proximal branches identified (anterior scalene is in lateral dissection)
What are some common complications after carotid subclavian bypass in order of highest to lowest incidence?
Phrenic nerve palsy (most common) - most often managed conservatively.
Recurrent laryngeal palsy
Lymphatic leak, seen more on the L with thoracic duct injury
Neck hematoma(Voigt et al. 2019)
When carotid-subclavian bypass compared to transposition?
Vertebral artery takes origin from the subclavian artery in a very proximal position or is dominant over the contralateral side, then bypass preferred. (Morasch 2009)
For coronary-subclavian steal with patent internal mammary artery to coronary artery bypass graft, then bypass (a carotid-subclavian transposition requires a more proximal clamp with occlusion of inline antegrade flow to the coronary bypass during the procedure) (Cua et al. 2017)
Contralateral CCA bypass with anterior or retropharyngeal tunneling.
Brachial/forearm Occlusive disease
Endovascular: PTA evidence is anecdotal with stents for lesions unresponsive to PTA or dissection following angioplasty.(Cheun et al. 2019; Nasser et al. 2014; Dineen, Smith, and Arko 2007)
Surgery: GSV vein bypass remains standard for revascularization with bypasses to superficial or deep palmar arch have good patency rates. Tunneling is subcutaneous if to distal ulnar or superficial palmar arch whereas anatomical to distal radial artery over the anatomic snuffbox.(Chang et al. 2003; Masden, Seruya, and Higgins 2012; Spinelli et al. 2010)
3.2.2.2 Acute Limb Ischemia
What is the procedure of choice in acute limb ischemia of the upper extremity?
With acute presentation of upper limb ischemia and a localizing examination, may be reasonable to proceed directly to OR for embolectomy to minimize ischemia time.(Wahlberg, Goldstone, and Olofsson 2006; Henke 2009)
What are some postoperative complications of an embolectomy for acute limb ischemia?
Brachial sheath hematoma - parasthesias and weakness in the median nerve distribution require emergent re-exploration and decompression. Even small hematomas that are not readily identifiable on clinical exam, can cause compression on the median nerve and are a surgical emergency.(D. D. Tran and Andersen 2011)
Compartment Syndrome - If prolonged ischemia or no hematoma found, and forearm compartments appear tense, then should proceed with fasciotomies to treat forearm compartment syndrome. Rarely performed prophylactically due to significant morbidity.(Gelberman et al. 1981; Kistler, Ilyas, and Thoder 2018; Leversedge et al. 2011)
Three compartments - forearm volar (flexor, superficial, and deep), mobile wad (lateral), and dorsal (extensor, superficial, and deep). Volar compartments most susceptible to ischemia and compartment syndrome, most vulnerable muscle are flexor digitorum profundas and flexor pollicus longus.(Ronel, Mtui, and Nolan 2004)
Volar/Henry approach decompresses lateral and volar compartments with a single incision, includes carpal tunnel release.
3.3 Vasospastic Disorders
3.3.1 Iatrogenic or Vasopressor Induced Ischemia
You are called to the intensive care unit for a septic patient with acute bilateral upper limb ischemia, what is the management strategy?
Critically ill patients on vasopressors with bilateral upper extremity ischemia are often managed best with supportive measures and attempts to wean vasopressors (especially norepinephrine).(Gregory J. Landry et al. 2018)
Limited role for radial artery embolectomy, only in clear ischemia isolated to the distribution of an occluded radial artery, often secondary to line placement.(Valentine, Modrall, and Clagett 2005)
3.3.2 Raynaud’s Phenomenon
What is Raynaud’s and what causes it?
Exaggeration of normal physiologic response with episodic pallor or cyanosis of the fingers caused by small digital artery vasoconstriction occurring in response to cold or emotional stress. There is an abnormality with sympathetic nervous system, resulting in a multifactorial problem involving a combination of vascular, neural, and humoral factors.(Shuja 2019; Gregory J. Landry 2019)
What are the subtypes of Raynaud’s phenomenon and what is the underlying pathology?
Primary: Raynaud’s disease-idiopathic form that is a benign process not associated with structural vascular change. Triggers include (cold, emotional stress, caffeine) resulting in digital smooth muscle contraction and temporary digital hypoperfusion.
Secondary: Fixed vascular obstruction to blood flow decreasing threshold for cold induced vasospasm or progress to tissue loss. Diseases associated include mixed connective tissue disease, SLE, and rheumatoid arthritis, and scleroderma (accounts for 80-90% of cases). In setting of lower digital blood pressure, symptomatic digital ischemia or tissue loss under low stress conditions. With cold/emotional stress, vasoconstrictive response of digital artery smooth muscle further causes arterial closure and resultant symptoms
What are diagnostic criteria for Raynaud’s?
Clinical (Progression of ischemia with white -> blue -> red finger discoloration. Episodes can be self-limited and may last from less than a minute, but generally not longer than 10-20 minutes
Qualitative testing for severity of cold sensitivity in Raynaud’s syndrome can be useful. Most basic test is cold sensitivity and recovery after ice water immersion. >10 minutes return to baseline pressure concerning for Raynaud’s
Segmental pressures with finger systolic blood pressure can differentiate purely vasospastic vs occlusive disease. Difference of more than 15 mm Hg between fingers or absolute finger pressure <70 mm Hg may indicate occlusive disease
Serologic evaluation (ANA/RF)
What are appropriate treatments for Raynaud’s phenomenon?
Medical-cold/tobacco avoidance lead to improvement in around half of patients. Calcium channel blocker (nifedipine ER 30mg qday) and losartan (50mg BID) have been shown to be most effective.(Gregory J. Landry 2013; Wigley and Flavahan 2016) Other drugs include alpha blocker, sildenafil, fluoxetine (SSRI), reserpine, cilostazol, captopril.
- OUTCOMES ARE POOR IN PATIENTS WITH ARTERIAL OBSTRUCTION. If there is an asymmetric vascular examination, then further non-invasive vascular imaging is needed.
Surgical-thoracic sympathectomy (used for treatment of digital artery vasospasm/digital ischemic ulceration). For vasospasm, thoracic sympathectomy is initially successful, but symptoms return generally within 3-6 months.
Immunosuppression/immunomodulation for connective tissue disorders associated with secondary Raynaud phenomenon
See Landry’s Review in JVS for a good treatment algorithm.(Gregory J. Landry 2013)
3.3.3 Ergotism
What is Ergotism?
Ergot is a parasitic fungal disease that has a particular prevalence for infecting rye plants and ergot alkaloids have been linked to epidemic poisonings that manifested as ergotism from consumption of rye. Modern day is rare.(Stanley, Veith, and Wakefield 2014)
What causes Ergotism and how do patients present?
Ergotamine is chemically like endogenous catecholamines/indolamines and when applied clinically, it behaves as an agonist to alpha-adrenergic, sertoninergic, and dopaminergic receptors. Can be seen with ergot alkaloid migraine medications. Despite limited bioavailability, vasocontrictive effects have been reported to last for 24 hours or longer
Gangrenous-mild limb pain followed by burning pain/shooting and
Convulsive-heaviness in limbs and head associated with diarrhea. Could result in tonic-clonic spasms
How can you diagnose Ergotism and what is the process for treating this disease?
Upper extremity ischemia (i.e. digital ulceration) in the setting of ergot alkaloid use (typically for migraines). The treatment includes:
Volume expansion and IV heparin as anticoagulation
IV infusion of nitroprusside, nitroglycerin, iloprost or combination
Infusion of Ca 2+ channel blockers
Surgical: for thrombosis, consider thrombolysis. Avoid or delay amputations as much as possible to maximize amount of tissue recovery.
3.3.4 Buerger’s Disease
How is Buerger’s disease categorized?
Non-atherosclerotic, segmental, inflammatory disease of small/medium sized arteries in distal extremities (upper and lower) of tobacco users distinct from either atherosclerosis of immune arteritis(Jack L Cronenwett, Alik Farber, and Erica L. Mitchell 2020; Le Joncour et al. 2018)
What clinical criteria can help diagnose Buerger’s?
Diagnosis of Buerger’s disease requires 5 criteria(Akar 2019)
Smoking history
Onset before age 45 or 50
Distal extremity ischemia with infrapopliteal arterial occlusions and often upper limb involvement
Classic angiographic findings of segmental occlusions of distal arteries with corkscrew collaterals
Absence of atherosclerotic risk factors (besides smoking, of course), autoimmune disease, diabetes or proximal embolic source.
Although rarely are biopsy sent, pathology will show panvasculitis within small and medium-sized arteries, highly cellular intraluminal thrombus (contains CD68, Cd3, Cd8 inflammatory cells), preserved elastic lamina structure, unlike atherosclerotic lesions.(Akar 2019; Kobayashi et al. 1999)
What is important about diagnosing Buerger’s
Typically a diagnosis of exclusion
Must rule out proximal embolic source, trauma, local lesions (e.g. pop entrapment or cystic adventitial disease), autoimmune disease, hypercoagulable status, atherosclerosis
What physical exam and non-invasive/invasive imaging findings of Buerger’s?
Distal, but not proximal arterial disease (palpable brachial/popliteal but absent/reduced at ankle or wrist)
Digital brachial index (DBI) <0.6 and flat/reduced digital waveforms
CTA/MRA/DSA or duplex - characteristic findings of serpiginous/corkscrew collaterals, occlusion of distal calf/pedal arteries, and normal proximal arteries.(Busch 2011; Fujii et al. 2011)
What is the mainstay treatment in Buerger’s disease?
Smoking cessation! Only treatment to improve symptoms and reduce amputation risk if achieved before onset of gangrene or tissue loss. May even require inpatient admission for intensive smoking cessation therapy.(Hooten, Bruns, and Hays 1998) It is important to remember following treatments will likely fail without smoking cessation.(J. W. Olin 2000)
If smoking cessation does not improve, medical management with antiplatelet agents, immunomodulators, vasodilators (Calcium channel blockers and cilostazol(Dean and Satiani 2001)), anticoagulants(Kubota et al. 1997), and IPC.(Montori et al. 2002)
Endovascular-distal small vessel intervention
Surgical-upper extremity autogenous vein bypass-limited success due to poor outflow
Sometimes can consider upper extremity sympathectomy, but unproven benefit
Amputation-reported in 30-40% who are followed longer than 5 years(Jeffrey W. Olin 2018)
3.3.5 Large Artery Vasculitis
What are common characteristics for patients who are suspected to have a large vessel vasculitis? (Shanmugam 2019; Weyand and Goronzy 2003)
Affect aorta and major branches
Present with non-specific heterogenous symptoms making the diagnosis challenging. Most commonly, they present with systemic or constitutional symptoms (fatigue, fever, weight loss, arthralgias)
Frequently, diagnosis made with presence of constitutional symptoms, elevated inflammatory markers (ESR/CRP), and dedicated imaging (MRA, CTA, DUS, or PET)
How can you differentiate Takayasu arteritis vs giant cell arteritis?
3.3.5.1 Takayasu arteritis
Involves aorta and major arch branches(Ehlert and Abularrage 2019)
Young patients (20-40 years) and female in 80-90% of cases, Asian populations
American College of Rheumatology (ACR) Criteria(Maz et al. 2021)
Onset <40 years
Claudication of an upper extremity
Decreased brachial pulse
>10 mmHg SBP between arms
Bruit over subclavian arteries or aorta
Arteriographic evidence of narrowing/occlusion in aorta/primary branches/or large upper/lower extremity arteries
3.3.5.2 Giant cell arteritis
Aorta and main branches, but predilection for carotid artery branches(Bongartz and Matteson 2006)
Diagnosis:
Age at disease onset > 50 years
New headache
Temporal artery abnormality
Elevated ESR (>50) - can be normal in up to a quarter of cases.
Abnormal (temporal) artery biopsy (gold standard test)
Other symptoms include jaw pain with mastication or visual changes
Associated with Polymyalgia rheumatic, characterized by morning stiffness in shoulders/hips occurring in 40-50% of patients.(Weyand and Goronzy 2014)
Arteriography/MRA/CTA/PET may be used to assess large vessel involvement - classic finding is smooth, tapering stenosis.
3.3.5.3 Management
What is the medical treatment for GCA and when do you consider surgical treatment?
Medical-steroid therapy - In as many as 50% of patients who have a large vessel vasculitis refractory to glucocorticoid therapy alone, patients will trial immunomodulators or cytotoxic trugs (i.e. methotrexate, azathioprine, mycophenolate, tocilizumab, or leflunomide)
Intervention - Avoid intervention in the acute setting. Once in remission, treatment of symptomatic arterial lesions or those at aneurysm size threshold should be considered and as many as 50-70% with large vessel vasculitis will require intervention.
Endovascular - angioplasty/stent/stent graft for large vessel vasculitis have all been described, however higher restenosis in endovascular compared to open treatment
Open Surgery (gold standard) - lesions are long, fibrotic and therefore less amenable to endovascular treatment. Bypass grafts from aorta-CCA are the most common (CEA should be avoid due to pathology involved)
Upper extremity bypass with autogenous vein to the brachial artery
Aortic aneurysms should be managed with open surgery(Janssen et al. 2008)
Mid aortic syndrome likely needs open repair from uninvolved aorta-usually thoracic aorta-to bifurcation bypass with jump graft to involved visceral vessels.(Ehlert and Abularrage 2019)
3.3.5.4 Surveillance
How should patients be monitored with active large artery vasculitis?
Lab data tracked at least monthly for 6 months with close follow-up to ensure appropriate response to medical treatment and enable physicians to assess for adverse effects of medical treatment
Repeat tests after remission reached and imaging choice to evaluate large vessels (DUS/CTA/MRA)
3.3.6 Other Vasculitis syndromes
Polyarteritis Nodosum - Focal necrotizing lesions primarily affecting medium-sized muscular arteries, peak incidence in 40s. Multiple saccular aneurysms secondary to inflammatory destruction of vessel media.(Shanmugam 2019; Weyand and Goronzy 2003)
Behçet Disease - recurrent oral pathos ulcers, genital ulcers and uveitis.(Shanmugam 2019; Weyand and Goronzy 2003)
3.4 Aneurysmal Disease
3.4.1 Subclavian Artery Aneurysms
How are subclavian aneurysms caused and how can they present? (Baig and Timaran 2019)
Etiology
Degenerative - atherosclerotic or due to aberrant right subclavian with degenerative changes in proximal subclavian known as “Kommerell diverticulum”(Tanaka, Milner, and Ota 2015)
Traumatic - blunt, penetrating, iatrogenic with attempted catheter placement
Radiation induced, sometimes seen after radiation for breast cancer.(Mohan et al. 2016)
Thoracic outlet obstruction - no need to investigate for aTOS if there is another plausible cause.
Presentation
- Rare, comprises 1% of peripheral aneurysms.
- Exam-pulsatile supraclavicular mass or bruit, absent/diminished pulses, signs of microembolization (“blue finger”)
- Most discovered incidentally, however referred chest, neck, shoulder pain, upper extremity ischemia due to thrombosis or distal embolism, brachial plexus compression, hoarseness from right recurrent laryngeal nerve compression
- Dysphagia from esophageal compression in aberrant right subclavian artery.(Tanaka, Milner, and Ota 2015)
- Rarely rupture
Evaluation
What are diagnostic studies and treatment modalities for subclavian aneurysms?
CXR-mediastinal mass may suggest neoplasm
MRA/CTA important to delineate extent of aneurysm and proximity to ipsilateral vertebral artery
Management
Open Repair-resection/endoaneurysmorrhaphy with end to end (small aneurysms) or interposition prosthetic graft(Vierhout et al. 2010)
Proximal-median sternotomy with supraclavicular fossa extension for adequate proximal control for right side, however supraclavicular with left anterolateral thoracotomy for left subclavian aneurysm
Mid-Distal-supraclavicular/infraclavicular generally adequate for control where again resection of the clavicle may be needed
Endovascular Repair-transbrachial/transfemoral approach with covered stent(Maskanakis et al. 2018)
- Must consider vertebral artery origin. Can cover vertebral artery if contralateral vertebral artery is patent and of adequate size, however posterior circulation stroke may occur when the contralateral vertebral artery is highly stenotic, hypoplastic or occluded.
Hybrid Repair-embolization/coils of proximal subclavian artery combined with subclavian transposition or carotid-subclavian bypass
For aberrant subclavian artery aneurysm, resection or exclusion of the aneurysmal artery with vascular reconstruction of the subclavian artery is recommended. Especially in the setting of dysphagia lusoria, subclavian artery reconstructed by interposition graft where proximal anastomosis is on ascending aorta. Alternatively, left posterolateral thoracotomy for proximal aneurysm resection and right supraclavicular incision for reconstruction of subclavian artery by end to side to the right CCA has been reported.(Tanaka, Milner, and Ota 2015)
3.4.2 Axillary Artery Aneurysms
How are axillary aneurysms caused and how can they present?
Etiology
Blunt/penetrating trauma
Congenital (infrequently reported)
Post-traumatic axillary aneurysms (repeated abduction/external rotation downward toward humeral head in baseball pitchers)
Presentation
- Exam-pulsatile supraclavicular mass or bruit, absent/diminished pulses, signs of microembolization (“blue finger”)
What are diagnostic studies and treatment modalities for axillary aneurysms?
Evaluation
Ultrasound
CTA/MRA of upper extremity
Management
Open Repair-resection with interposition vein grafting or prosthetic if inadequate vein is present.
Endovascular repair-covered stent graft can be placed with occasional embolization with micro coils to isolate sac and prevent retrograde endoleaks
3.4.3 Brachial Artery Aneurysms
How are brachial aneurysms caused and how can they present?
Etiology
False aneurysms secondary to repetitive trauma
Iatrogenic complications - Seen in 1-3% of brachial artery access - increased risk in older age, female patients, and larger sheaths.(Treitl et al. 2015) More on appropriate access technique can be found in Chapter 22
IV drug abuse - infected pseudoaneurysms in antecubital fossa.
Connective tissue disorders (ex. type IV Ehlers Danlos)
Presentation
Exam: pulsatile mass
Local pain or symptoms of median nerve compression
Hand/digital ischemia from thrombosis/distal embolization
What are diagnostic studies and treatment modalities for brachial aneurysms?
Evaluation
Duplex Ultrasound
CTA/MRA of upper extremity may be needed to delineate extent of aneurysm
Management
Open Repair (preferred)-resection with patch or interposition vein grafting
Endovascular repair-rare and generally in a traumatic setting
Iatrogenic injuries-due to access and nonoperative treatment for small/asymptomatic pseudoaneurysms that are likely to thrombose spontaneously. Direct suture repair with evacuation of hematoma is possible. Thrombin injection is less favorable due to location and short neck.
Neurological symptoms from median nerve compression require an urgent repair, open surgery best for decompression.
3.4.4 Radial Artery Pseudoaneurysm
How do you manage a patient who presents with a radial artery pseudoaneurysm after a coronary angiogram on year ago?
Small pseudoaneurysms <3cm have a high rate of spontaneous thrombosis. However, larger psuedoaneurysms or those with symptoms require treatment. Often best managed with open excision and primary repair or interposition graft.(Tosti et al. 2017)
Can also be seen as a result of trauma.(Bagir, Sayit, and Tanrivermis Sayit 2017)
3.5 Occupational Vascular Disease
There are some occupational vascular disorders than contribute to vascular disease in the upper extremity. Hand arm vibration syndrome and hypothenar hammer are of particular importance.(Eskandari and Morgan 2020)
3.5.1 Hand-Arm Vibration Syndrome
Etiology
Vibrating handheld machines (i.e. pneumatic hammers and drills, grinders, and chain saws)
Linear relationship between exposure over years and onset of this syndrome
Exact mechanism unknown, but thought that endothelial damage with sympathetic hyperactivity -> finger blanching attack
Presentation
Various stages seen where early results in slight tingling/numbness and lateral, the tips of one or more fingers experience attacks of blanching that is usually precipitated by cold
Blanching typically lasts 1 hour and terminates with reactive hyperemia, but prolonged exposure can cause bluish black cyanosis of fingers
Evaluation
Detailed history with use of vibrating tools/symptoms of Raynaud phenomenon
Objectively: cold induced ischemia with recording time until digital temperature recovers
Digital occlusion with noninvasive digit pressures or duplex scanning
Management
Avoidance of vibratory tools
Nifedipine (Ca2+ channel blocker) in advanced cases
IV prostanoid (i.e. prostacyclin) for digital gangrene
Surgery-cervical sympathetectomy or digital sympathectomy rarely needed
3.5.2 Hypothenar hammer syndrome
Etiology
Repetitive use of palm of hand in activities that involve pushing, pounding, twisting - particularly to the ulnar artery as it exits guyots canal and crosses the hook of the hamate.(Ferris et al. 2000)
Name comes from reports of mechanics, factory workers, carpenters or laborers who habitually use there hands as a hammer are ad risk for disease
Repetitive trauma leads to thrombotic occlusion, aneurysm formation or both
Presentation
Asymmetrical distribution involving dominant upper extremity where cyanosis and pallor can occur and digits affected are ulnar distribution in nature
Cool/mottled digits or severe cases with ischemic ulcers
Evaluation
Duplex ultrasound
CTA or MRA
Arteriography (gold standard) with corkscrew pattern typically in affected vessels
Management
Conservative-smoking cessation/hand protection/cold avoidance.(Carr et al. 2019)
Medical-calcium channel blockers/antiplatelet
Surgical (severe digital ischemia/aneurysm)-ligation if adequate collateral or interposition vein graft has good long term patency.
3.5.3 Environmental Exposures
Exposure to what environmental agents can result in upper extremity ischemia?
Acrosteolysis
Exposure to polyvinyl chloride can result in ischemic hand symptoms similar to those of Raynaud syndrome
Angiography-damage to digital arteries with multiple stenosis/occlusions or hyper vascularity adjacent to areas of bone resorption
Treatment-supportive
Electrical burns
<1000 V cause injuries limited to immediate skin/soft tissue, however >1000 V cause damage from entry to exit point
Results in arterial necrosis with thrombus or bleeding and gangrene of digits develop
Initially can be occlusion/thrombosis or spasm, however later damage can cause aneurysmal degeneration
Treatment-dependent on soft tissue/bone injuries as well. Can have reconstruction with free flap due to local vascular damage or occlusion of major artery requiring bypass grafting
Extreme thermal injuries
Workers at risk with chronic exposure to cold (slaughterhouse, canning factory, and fisheries)
Raynaud syndrome symptoms due to vasomotor disturbances in the hands when exposed to extreme chronic thermal trauma
Treatment-Supportive
3.6 Sports Medicine
How can athletes specifically be affected by upper extremity ischemia?
Athletes who engage in strenuous or exaggerated hand/shoulder activity may be susceptible to upper extremity ischemia from arterial injury manifested by Raynaud syndrome, symptoms of sudden arterial occlusion or digital embolization.
3.6.1 Quadrilateral space syndrome
Anatomy
Bordered by teres minor superiorly, humeral shaft laterally, and teres major inferiorly, and long head of triceps muscle medially
Posterior humeral circumflex artery and axillary nerve in space
Etiology
Compression of posterior humeral circumflex occurs with abduction/external rotation
Typically seen with chronic overhand motion athletes (pitchers/volleyball players)
Vascular-repetitive mechanical trauma to posterior circumflex humeral artery
Neurogenic-fixed structural impaction of quadrilateral space by fibrous bands or space-occupying lesions
Presentation
- Muscle atrophy, paresthesias, poorly localized shoulder pain and pain in quadrilateral space
Management
Medical: Oral anti-inflammatory medications, PT, limitation of activities
Surgery: decompression with neurolysis/excision of fibrous bands or other space occupying lesions
3.6.2 Humeral head compression of axillary artery
Anatomy
- 3rd portion of axillary artery compressed by head of humerus
Etiology
- Arm is abducted and externally rotated with downward compression of humeral head to axillary artery
Presentation
- Arm fatigue, loss of pitch velocity, finger numbness, Raynaud, cutaneous embolization
Evaluation
Provocative maneuvers with impedance of flow through axillary artery on ultrasonography
Arteriography with rest and provocative position
Management
Supportive with avoidance of throwing motion
Surgical-saphenous vein patch for no improvement or structural injury may require resection with saphenous vein bypass anatomically or extra-anatomic tunneling above pectoralis minor muscle
3.6.3 Thoracic Outlet Syndrome
Thoracic outlet syndrome and cervical rib abnormalities are covered extensively in another chapter. For more information see Chapter 4
3.7 Vascular Trauma-Upper Extremity
This is discussed in detail in Chapter 19, so we will go over some important specifics for upper extremity vascular injury. (Kauvar and Kraiss 2020)
3.7.1 Subclavian Artery Trauma
What is the management strategy for an iatrogenic placement of a subclavian artery catheter?
Critically ill patients can be treated effectively with the use of a closure device or covered stent placement.(Yoon et al. 2015; V. Tran et al. 2009; Cohen et al. 2014) Cut down in the mid subclavian artery is very difficult to perform and results in increased blood loss and worse outcomes.
Trauma to the proximal subclavian should be accessed on R through a median sternotomy or trapdoor incision. On the left, the proximal subclavian is accessed best through an anterolateral thoracotomy.
3.7.2 Axillary Artery Trauma
What is the mechanism and management of upper extremity axillary artery trauma?
Etiology
- Predominantly in penetrating trauma with equal incidence in proximal/middle/distal divisions and brachial plexus injury in >1/3rd of arterial injury
Evaluation
Physical exam with deficiencies in upper extremity pulses/ischemic changes, but may not be present given collateral flow from axillary artery to upper extremity
High index of suspicion with location of injury proximity to course of axillary artery
Upper extremity Doppler or CTA if patient is stable for diagnosis
Management
Primary repair or treated with interposition graft
If hemodynamically stable, can consider covered stent based on location to thoracic outlet via femoral/brachial approach. Discussed in more detail in Section 9.3
3.7.3 Brachial Artery Trauma
What is the mechanism and management of upper extremity brachial artery trauma?
Etiology
Frequently associated with humerus fractures/elbow dislocation. Seen often in children.
Penetrating trauma
Evaluation
Pulse deficit in majority (>75% of cases)
Upper extremity Doppler of CTA
Management
- Given course, can be extensively mobilized and repaired in end-to-end fashion in 50% of cases. Otherwise, treatment with an interposition graft
- Need to differentiate injury from spasm.
3.7.4 Radial/ulnar artery trauma
What is the mechanism and management of upper extremity radial/ulnar artery trauma?
Etiology
- Associated with significant soft tissue pattern
Evaluation
Pulse deficit in >80% of patients
Doppler based Allen test-confirm radial/ulnar contribution to palmar arch
Management
If Allen test reveals a patent palmar arch, the injured artery can be ligated
If palmar arch is not patent in the absence of contribution of the injured artery, it should be repaired
If both are damaged, preference to ulnar artery as dominant contribution to hand
Generally, repair can be done in an end to end fashion given mobility of the vessel
3.8 Upper Extremity Lymphedema
3.8.1 Etiology
Often due to breast cancer therapy and axillary lymph node dissection.(Morrell et al. 2005)
3.8.2 Management
Initial treatment includes decongestive therapy, such as daily massage for 2-4 weeks. Once the girth and symptoms stabilize, then can transition to long term management with compression sleeve.(Mondry, Riffenburgh, and Johnstone 2004)
Severe cases my require lymph node transfer.(Warren et al. 2007)
Lymphangiosarcoma in the setting of lymphedema (Stewart-Treves syndrome) without distant disease is best managed with wide local excision and adjuvant chemoradiation. Prognosis is poor.(Sharma and Schwartz 2012)