VSITE - Upper Extremity Disease


Kush Sharma, MD and M Ashraf Mansour, MD 

Spectrum Health/Michigan State University College of Human Medicine, 

Grand Rapids, Michigan 

Kush Sharma is a 4th year integrated vascular surgery resident at Spectrum health-Michigan State University College of Human Medicine in Grand Rapids Michigan and Dr. Mansour is a vascular and endovascular surgeon.  He is academic chair, Spectrum Health Medical Group Department of Surgical Specialties.  He obtained his medical degree from Cairo University school of medicine followed by general surgery training at University of Colorado health sciences center in Denver Colorado. After serving in the United States Army as a major in the Medical Corps, he completed a fellowship in vascular and endovascular surgery at the Southern Illinois University School of Medicine.  Welcome Drs Sharma and Mansour

Anatomy/ Exposure of Vessels (Rutherford Chapter 57, Anatomic Exposures in Vascular Surgery)

What are the zones of the upper extremity?


Division of the upper extremity into three zones: 

  1. Intrathoracic zone including aortic arch, innominate artery, subclavian artery bilaterally, innominate veins, and SVC 

  2. Thoracic outlet (base of neck to the axilla including the subclavian, proximal vertebral, proximal axillary arteries/veins)

  3. Axilla to fingers (the arm)  


What are some common exposures for major upper extremity arteries?   

Right Subclavian Artery: Medial sternotomy (proximal) or right supraclavicular area (mid/distal)

Left Subclavian Artery: Anterolateral thoracotomy in emergent setting for proximal left subclavian artery control. When third space sternotomy, supraclavicular incision with thoracotomy🡪 “trap door” exposure 


Supraclavicular incision: After division of the platysma and clavicular head of the SCM, fat pat of varying thickness contains the omohyoid muscle. This should be divided and placed superiorly/laterally. At this point, the anterior scalene muscle is exposed medially with phrenic nerve running in lateral to medial direction. Division of anterior scalene for carotid/subclavian bypass should be performed as close to the first rib as possible. After this is performed, the subclavian artery is exposed. 


Axillary Artery: Infraclavicular exposure below middle 1/3rd of clavicle. Pec major split and pec minor freed at lateral wound. Axillary vein followed by deep and superior to get to 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 horizontal skin incision 2 cm below the middle third of the clavicle. Underlying pec major is split by bluntly separating the fibers and followed by exposing the tough clavipectoral fascia. At the lateral wound, the pec minor can be freed and laterally retracted. The axillary vein is first structure encountered in the sheath and the artery lies just superior and deep to the vein. Make sure to avoid nerves of brachial plexus that lie deep to first part of axillary artery and are at risk for injury during blind placement of occluding arterial clamps. (Wind et al)


What steps are involved for brachial artery exposure? 

Brachial artery: incision between biceps/triceps on medial arm (avoid basilic vein damage in subcutaneous and deep to the fasia at medial biceps. Median nerve seen and retracted. Two brachial vein are paired adjacent to artery. 


Superficial location makes it vulnerable to injury and accounts for most vascular injuries of 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 in the subcutaneous tissue. Neurovascular bundle exposed by incising the deep fascia at the medial border of the biceps muscle, which is retracted anteriorly. After retracting basilic vein into posterior wound ,brachial sheath is opened and median nerve is most superficial structure and retracted. The artery lies deep to the nerve and surrounded by two brachial veins. Posteriorly, is the presence of the ulnar nerve.  


Brachial Artery bifurcates at the radial tuberosity into radial/ulnar branches. After the bifurcation and immediately after its origin, the ulnar artery gives off a short common interosseous branch, which bifurcates at the hiatus in the proximal interosseous membrane. Exposure of brachial artery in the antecubital fossa requires a transverse skin incision 1 cm distal to the midpoint of the antecubital crease. After deepening, avoid injury to subcutaneous veins and mobilize the basilic vein medially. Medial antebrachial cutaneous nerve should be protected. Divide the bicipital aponeurosis and after division, exposure of the brachial artery is present, which is flanked by two deep veins and crossing branches. Isolation of brachial artery requires ligation and division of these crossing vein branches. 


Radial artery at the wrist with 2-3 cm longitudinal incision generally between radial artery and cephalic vein. Radial artery was exposed by incising the antebrachial fascia just medial to the radius. Two veins accompany the artery and should be dissected away during arterial isolation. The superficial radial nerve and its medial/lateral branches course between the cephalic vein and radial artery in the area. 

Exposure of the ulnar artery is by coursing beneath the superficial flexor muscles in the proximal forearm, emerging near the ulnar border at the point midway between the elbow and the wrist. In the distal forearm, the ulnar artery course just beneath the antebrachial fascia and is easily exposed through a longitudinal incision placed radial to the flexor carbi ulnaris. The palmar branch of the ulnar nerve courses the superficial to the antebrachial fascia and should be preserved during arterial exposure 


What common aberrant upper extremity/arch anatomy is important to be aware of?    

  • Bovine arch with left common carotid/left subclavian have common origin 

  • Vertebral artery directly off the aortic arch 

  • Aberrant right subclavian where innominate becomes right CCA and right subclavian distal to last branch on left side passing behind esophagus to supply the right arm  


Epidemiology, etiology, and diagnostic evaluation (Rutherford Chapter 117, Vascular Decision Making: Upper Extremity Disease) 


How does evaluation of upper extremity ischemia differentiate from lower extremity ischemia?

  • Upper extremity ischemia <5% of patients with limb ischemia and in contrast to lower extremity, atherosclerosis is not a major contributor to upper extremity ischemia 

  • Vast majority of cases caused by autoimmune/connective tissue disorders 


How can upper extremity disease be classified? 

Anatomic Location

  • Large vs. Small Vessel


Disease Process: 

  • Vasospastic or occlusive. Vasospastic disease is more responsive to pharmacologic management while occlusive requiring endovascular/surgical management.  


How should patients be evaluated who have concern for upper extremity disease? 

Diagnostic Evaluation

  1. Detailed H+P evaluation (pulse palpation, auscultation at supraclavicular/infraclavicular fossa may reaveal a bruit concerning for subclavian artery stenosis, upper extremity neurovascular/skin exam)

  2. 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

  3. Some or all of 6 P’s of acute limb ischemia with symptoms occurring within 14 days are deemed acute  

  4. Doppler insonation of radial, ulnar, palmar, and digital arteries 

  5. Vascular Lab Evaluation

    1. Segmental Pressure Measurements 

    2. Duplex Ultrasound (look for large vessel occlusive disease)

  6. Other Imaging

    1. CTA/MRA

  7. Clinical Lab tests 

    1. Inflammatory disorders-CBC, ESR, ANA, RF

    2. Hypercoagulable screening


Vaso-occlusive disease (Vascular Decision Making: Upper Extremity Disease) 

What are causes and symptoms associated with subclavian/axillary occlusive disease? 

  • 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 


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. Distal axillary/proximal brachial stenosis can be from repetitive trauma from crutch use. 

  • Forearm occlusive disease can be seen in advanced ESRD/DM where calcific atherosclerosis of radial/ulnar arteries is present. Less common causes include Beurger disease or Raynaud Phenomenon 


How/when is upper extremity occlusive disease treated? 

  • SCA Occlusive Disease

    • Endovascular: treated with stenting if they are short segment and not close to the vertebral artery origin. Balloon expandable stents favorable for ostial lesions and access can be via the femoral or ipsilateral brachial artery 

    • Surgery:

      • Bypass from aortic arch through median sternotomy 

      • Ipsilateral CCA to subclavian artery (bypass or transposition) 

      • Contralateral CCA (anterior or retropharyngeal)

  • Brachial/forearm Occlusive disease 

    • Endovascular: PTA evidence is anecdotal with stents for lesions unresponsive to PTA or dissection following angioplasty 

    • 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 


Vasospastic Disorders (Rutherford Chapter 117, 141) 

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. 


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? 

  1. Medical-cold/tobacco avoidance. Calcium channel blocker (nifedipine) has been the most effective and losartan has also been beneficial. Fluoxetine (SSRI). Other drugs include alpha blocker, sildenafil, reserpine, cilostazol, captopril. NOT GOOD OUTCOMES IN PATIENTS WITH ARTERIAL OBSTRUCTION 

  2. Surgical-thoracic sympathectomy (used for treatment of digital artery vasospasm/digital ischemic ulceration). For vasospasm, thoracic sympathetcomy is initially successful, but symptoms return generally within 3-6 months. 

  3. Immunosuppression/immunomodulation for connective tissue disorders associated with secondary Raynaud phenomenon

Ergotism (Chapter 64, Current Therapy in Vascular in Endovascular Therapy) 

What is Ergotism?

  • Etiology: 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 


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. 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) 



  • Volume expansion and IV heparin as anticoagulation 

  • IV infusion of nitroprusside, nitroglycerin, ilioprost or combination

  • Infusion of Ca 2+ channel blockers 

  • Surgical: for thrombosis, consider thrombolysis 


Buerger’s Disease (Thromboangiitis Obliterans) (Vascular Decision Making: Buerger Disease) 

How is Buerger’s disease categorized?

  • Non-atherosclerotic, segmental, inflammatory disease of small/medium sized arteries in distal extremities of tobacco users distinct from either atherosclerosis of immune arteritis 

What clinical criteria can help diagnose Buerger’s?

  • Smoking history, onset before 50 years, infrapopliteal arterial occlusions, upper limb involvement, absence of atherosclerotic risk factors besides smoking 


What is important about diagnosing Buerger’s 

  • Typically a diagnosis of exclusion

  • Must rule out proximal embolic source, trauma, local lesions (eg 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)

  • DBI<0.6 and flat/reduced digital waveforms 

  • CTA/MRA/DSA-characteristic corkscrew collateral 


What is the mainstay treatment in Buerger’s disease?

  1. Smoking cessation! Only treatment to improve symptoms and reduce amputation risk if achieved before onset of gangrene or tissue loss. Important to remember following treatments will likely fail without smoking cessation. 

  2. If smoking cessation does not improve, medical management with antiplatelet agents, immunomodulators, vasodilators, anticoagulants 

  3. Endovascular-distal small vessel intervention

  4. Surgical-upper extremity autogenous vein bypass-limited success due to poor outflow 

  5. Sometimes can consider upper extremity sympathectomy, but unproven benefit 

  6. Amputation-reported in 30-40% who are followed longer than 5 years 

Large Artery Vasculitis (Vascular Decision: Making Large Artery Vasculitis, Rutherford Chapter 137) 

What are common characteristics for patients who are suspected to have a large vessel vasculitis? 

  • 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, and dedicated imaging (MRA, CTA, DUS, or PET)


How can you differentiate takayasu arteritis vs giant cell arteritis? 

  1. Takayasu arteritis 

    1. Aorta and primary 

    2. Young patients <20 years and female in 80-90% of cases, Asian populations

    3. Criteria (ACR)

      1. Onset <40 years

      2. Claudication of an extremity 

      3. Decreased brachial pulse 

      4. >10 mmHg SBP between arms

      5. Bruit over subclavian arteries or aorta

      6. Arteriographic evidence of narrowing/occlusion in aorta/primary branches/or large upper/lower extremity arteries

  2. Giant cell arteritis 

    1. Aorta and main branches, but pre-dilection for carotid artery branches

    2. Diagnosis: 

      1. Age at disease onset > 50 years 

      2. New headache

      3. Temporal artery abnormality 

      4. Elevated ESR (>50) 

      5. Abnormal artery biopsy (gold standard test)

    3. Other symptoms include jaw pain with mastication or visual changes

    4. Associated with Polymyalgia rheumatic, characterized by morning stiffness in shoulders/hips occurring in 40-50% of patients 

    5. Arteriography/MRA/CTA/PET may be used to assess large vessel involvement


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)

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 truxs (ie methotrexate, azathioprine, mycophenolate, tocilizumab, or leflunomide) 

  • Intervention-once remission, treatment of symptomatic arterial lesions 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 


Aneurysmal Disease (Rutherford Chapter 84) 


How are subclavian aneurysms caused and how can they present?


  • Degenerative (atherosclerotic or due to aberrant right subclavian with degenerative changes in proximal subclavian known as “Kommerell diverticulum”)

  • Traumatic (blunt, penetrating, iatrogenic with attempted catheter placement) 

  • Thoracic outlet obstruction



  • 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 thromboembolic phenomenon, brachial plexus compression, hoarseness from right recurrent laryngeal nerve compression

  • Dysphagia from esophageal compression in aberrant right subclavian artery


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 


  • Open Repair-resection/endoaneurysmorrhaphy with end to end (small aneurysms) or interposition prosthetic graft 

    • 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 

    • 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. 


How are axillary aneurysms caused and how can they present?


  • Blunt/penetrating trauma

  • Congenital (infrequently reported)

  • Post-traumatic axillary aneurysms (repeated abduction/external rotation downward toward humeral head in baseball pitchers) 


  • Exam-pulsatile supraclavicular mass or bruit, absent/diminished pulses, signs of microembolization (“blue finger”)


What are diagnostic studies and treatment modalities for axillary aneurysms? 


  • Ultrasound

  • CTA/MRA of upper extremity


  • 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

How are brachial aneurysms caused and how can they present?


  • False aneurysms secondary to repetitive trauma

  • Iatrogenic complications 

  • IV drug abuse (infected pseudoaneurysms in antecubital fossa) 

  • Connective tissue disorders (ex. type IV Ehlers danlos)


  • Exam: pulsatile mass 

  • Local pain or symptoms of median nerve compressions

  • Hand/digital ischemia from thrombosis/distal embolization 


What are diagnostic studies and treatment modalities for brachial aneurysms? 


  • Duplex Ultrasound

  • CTA/MRA of upper extremity may be needed to delineate extent of aneurysm 


  • 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. 


Occupational Vascular Disease (Rutherford Chapter 185) 


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. Can you talk to us about the key information from these syndromes?

Hand-Arm Vibration Syndrome 


  • Vibrating handheld machines (eg 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 


  • 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 


  • 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 



  • Avoidance of vibratory tools

  • Nifedipine (Ca2+ channel blocker) in advanced cases 

  • IV prostanoid (ie prostacyclin) for digital gangrene 

  • Surgery-cervical sympathetectomy or digital sympathectomy rarely needed


Hypothenar hammer syndrome


  • Repetitive use of palm of hand in activities that involve pushing, pounding, twisting

  • 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 



  • 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 



  • Duplex ultrasound 

  • CTA or MRA 

  • Arteriography (gold standard) with corkscrew pattern typically in affected vessels 



  • Conservative-smoking cessation/hand protection/cold avoidance 

  • Medical-calcium channel blockers/antiplatelet

  • Surgical (severe digital ischemia/aneurysm)-ligation if adequate collateral or interposition vein graft


Exposure to what environmental agents can result in upper extremity ischemia? 


  • 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 


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


The main syndromes are quadrilateral space syndrome and humeral compression of the axillary artery. What important information here do our listeners need to know? 

Quadrilateral space syndrome


  • 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



  • 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 



  • Muscle atrophy, paresthesias, poorly localized shoulder pain and pain in quadrilateral space



  • Medical: Oral anti-inflammatory medications, PT, limitation of activities

  • Surgery: decompression with neurolysis/excision of fibrous bands or other space occupying lesions 

Humeral head compression of axillary artery


  • 3rd portion of axillary artery compressed by head of humerus 



  • Arm is abducted and externally rotated with downward compression of humeral head to axillary artery



  • Arm fatigue, loss of pitch velocity, finger numbness, Raynaud, cutaneous embolization



  • Provocative maneuvers with impedance of flow through axillary artery on ultrasonography

  • Arteriography with rest and provocative position 



  • 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 pec minor


Thoracic Outlet Compression (this is covered in a separate segment of the Audible Bleeding podcast)


Vascular Trauma-Upper Extremity (Rutherford Chapter 184) 

We will next discuss Vascular surgery trauma. This is discussed in detail in a separate podcast so we will go over some important specifics for upper extremity vascular injury. 

What is the mechanism and management of upper extremity axillary artery trauma?

Mechanism and Pattern

  • Predominantly in penetrating trauma with equal incidence in proximal/middle/distal divisions and brachial plexus injury in >1/3rd of arterial injury

Diagnostic Considerations

  • 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 


Surgical Considerations 

  • Primary repair or treated with interposition graft 

  • If hemodynamically stable, can consider covered stent based on location to thoracic outlet via femoral/brachial approach


What is the mechanism and management of upper extremity brachial artery trauma?

Mechanism and Pattern

  • Frequently associated with humerus fractures/elbow dislocation

  • Penetrating trauma


Diagnostic Considerations

  • Pulse deficit in majority (>75% of cases)

  • Upper extremity Doppler of CTA 


Surgical Considerations 

  • Given course, can be extensively mobilized and repaired in end-to-end fashion in 50% of cases. Otherwise, treatment with an interposition graft 


What is the mechanism and management of upper extremity radial/ulnar artery trauma?

Mechanism and Pattern

  • Associated with significant soft tissue pattern 


Diagnostic Considerations

  • Pulse deficit in >80% of patients 

  • Doppler based Allen test-confirm radial/ulnar contribution to palmar arch 


Surgical Considerations 

  • 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



What are some indications for carotid-subclavian bypass?

  1. Atherosclerosis 

  2. Staged revascularization prior to TEVAR for aneurysmal disease requiring coverage of the LSA


How does the exposure differentiate in transposition vs bypass?

Exposure (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?

Complications (Long Term Outcomes after Carotid-Subclavian Bypass in Setting of TEVAR, Voigt et all, JVS, 2017)  

  1. Phrenic nerve palsy  

  2. Recurrent laryngeal palsy  

  3. Lymphatic leak  

  4. Neck hematoma  


When carotid-subclavian bypass compared to transposition?  

  1. Vertebral artery takes origin from the subclavian artery in a very proximal position🡪Bypass

  2. For coronary-subclavian steal with patent internal mammary artery to coronary artery bypass graft🡪Bypass (a carotid-subclavian transposition requires a more proximal clamp with occlusion of inline antegrade flow to the coronary bypass during the procedure) 


Cronenwett, Jack L., Alik Farber, and Erica L. Mitchell. Vascular Decision Making: Medical, Endovascular, Surgical, E-Book. Wolters Kluwer, 2020. 


Morasch, Mark D. "Technique for subclavian to carotid transposition, tips, and tricks." Journal of vascular surgery 49.1 (2009): 251-254.


Sidawy, Anton N., and Bruce A. Perler. Rutherford's Vascular Surgery and Endovascular Therapy, E-Book. Elsevier Health Sciences, 2018.


Stanley, James C., Frank Veith, and Thomas W. Wakefield. Current Therapy in Vascular and Endovascular Surgery E-Book. Elsevier Health Sciences, 2014.


Voigt, Soraya L., et al. "Outcomes of carotid-subclavian bypass performed in the setting of thoracic endovascular aortic repair." Journal of vascular surgery 69.3 (2019): 701-709.

Wind, Gary G., and R. James Valentine. Anatomic exposures in vascular surgery. Lippincott Williams & Wilkins, 2013.

Kush Sharma and Ash Mansour of Michigan State University sit down to discuss Upper extremity arterial pathology for the VSITE and board review.