eMedicine Specialties > Orthopedic Surgery > Hand & Upper Extremity

Vascular Occlusive Syndromes of the Upper Extremity

Arian Mowlavi, MD, FACS, Consulting Staff, Department of Plastic Surgery, Cosmetic Surgery Clinics of Laguna Beach
Bradon J Wilhelmi, MD, Professor and Endowed Leonard J Weiner, MD, Chair of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine

Updated: Jan 19, 2010

Introduction

Background

Although upper extremity vascular disorders are less common than lower extremity disorders, upper extremity vascular disorders affect approximately 10% of the population. Causes of vascular compromise include acute trauma; chronic conditions, such as repetitive microtrauma; and systemic diseases involving metabolic processes, autoimmune processes, or both. General symptoms following vascular compromise include dysesthesias, paresthesias, pallor, cold intolerance, and ulceration that is associated with necrosis. The vascular system plays the critical role of delivering nutrients and clearing metabolic waste products from peripheral tissues, as well as maintaining systemic core temperature. Vascular flow is controlled by various processes, including vessel anatomy; vascular tone, which is controlled by neuroendocrine hormones along with autonomic nervous influence; and end-organ metabolic requirements. Unfortunately, vascular competence can often become compromised, leading to various disease pathologies.

Recent studies

Jones et al measured the resolution rates and factors associated with upper extremity catheter-associated deep venous thrombosis (DVT). They found that more than 50% of the DVTs resolved within 113 days when the catheter was removed 48 hours or less after diagnosis. Thrombosis resolved in only 25% of patients when the catheter was not removed. In multivariate analysis, only catheter removal predicted the likelihood of thrombus resolution (odds ratio, 3.25; 95% confidence interval, 1.16-9.09; P = .025). They noted that new-site catheter placement has a high rate of new associated DVT and that anticoagulation does not seem to increase resolution of catheter-related DVT in the upper extremities.^{[1 ]}

Kim et al reported on traumatic brachial artery injuries and risk factors for the development of upper extremity compartment syndrome. The investigators found that the risk of compartment syndrome was increased in cases of combined arterial injuries, combined nerve injuries, motor deficits, fractures, and increased intraoperative blood loss. Multivariate logistic regression showed that elevated intraoperative blood loss, combined arterial injury, and open fracture were independent risk factors for the development of compartment syndrome (OR 1.12, 5.79, and 2.68, respectively).^{[2 ]}

White et al reviewed the use of multidetector computed tomographic angiography (MDCTA) in the evaluation of combat casualties with vascular injuries. They found that MDCTA yielded high-resolution images useful in delayed evaluation of vascular injuries and that the presence of metallic fragments or orthopedic hardware did not significantly interfere with MDCTA. Fifteen studies were of the lower extremities, 4 of the upper extremities, and 2 of the neck. The investigators concluded that MDCTA is a reliable and promising alternative to traditional arteriography for evaluating clinically occult vascular trauma.^{[3 ]}

Pathophysiology

Multiple factors determine vascular flow. These include environmental events, metabolic demands, sympathetic nervous tone, and local and circulating humoral mediators. Vasoconstriction can result from increased sympathetic tone or alpha-adrenergic–stimulating humoral mediators, such as norepinephrine. In contrast, vasodilation may be prompted by parasympathetic tone (inhibiting the sympathetic tone), release of nitric oxide by endothelial cells, or myogenic autoregulatory mediators arising from increased cellular waste products, such as adenosine.

Investigators' most recent interest has surrounded the effect of endothelium on vascular tone, because of its capacity to produce 2 competing molecules: nitric oxide, a vasodilatory, endothelium-derived relaxing factor, and endothelin, a potent vasoconstrictor. Sympathetic nerves typically penetrate the arterial and venous walls, affecting the muscularis component at frequent intervals. These nerves travel variable distances in peripheral nerves prior to entering the perivascular adventitia.

In vasospastic disorders, abnormal vascular control can arise from abnormal receptor expression or from response to agonists, abnormal levels of local humoral mediators, aberrant myogenic and metabolic control mechanisms, and overwhelming sympathetic tone. In contrast, vascular insufficiency may result from physical trauma to vessels, with resulting transection or thrombotic or embolic sequelae.

Ultimate interstitial flow is determined by the pressure gradient across a single vascular lumen, as well as the total (potential) capacity of the arteriolar-capillary-venular bed. Vasospasm, which is observed in hypothenar hammer syndrome and Raynaud disease, may cause pressure gradients to fall below critical levels without affecting the total capacity of the vascular bed. In contrast, peripheral occlusive diseases, such as those seen in scleroderma, impede the pressure gradient as well as the total potential capacity of the vascular bed. This distinction is important because it affects indications for treatment and prognosis after surgery or other interventions.
 
Environmental factors, such as external toxins and ambient temperatures, affect vascular patency. This is of interest because the interaction between the external environment and the internal autonomic system has dynamic interplay. For example, for a period following digit replantation, the external temperature may affect inflow pressures at the amputation site but will not affect the vessels of the amputated part, since the sympathetic system of the adventitia will have been disrupted.

Relevant anatomy

In most patients, the dominant blood supply to the hand is provided by the superficial palmar arch, a continuation of the ulnar artery, and less so by the deep palmar arch, a continuation of the radial artery. Minor blood supply to the hand is provided for by intraosseous channels via the radial and ulnar bones, as well as by the median artery, which is present in a minority of patients. In approximately 80% of patients, the deep and superficial palmar arches are connected and are referred to as complete. This results in a dual perfusion supply to the common and proper digital vessels. This is an important attribute of hand vascular architecture, providing collateral blood flow in the event of vascular pathology affecting one of these palmar arches.

The vascular supply to the thumb is unique and includes sources directly from the radial artery and from the deep and superficial arch. In addition to its direct supply, the radial artery gives rise to a large dorsal artery, which passes distally to supply the thumb. The palmar blood supply to the thumb is provided by the princeps pollicis artery, which is derived from the first palmar metacarpal artery, the deep arch, the wrist dorsal metacarpal artery, or a terminal branch of the superficial palmar arch. The 4 terminal arteries to the thumb are the ulnar and radial palmar arteries and the ulnar and radial dorsal arteries. Vessels have been categorized arbitrarily based on their diameter and include macrovessels measuring 100 micrometers or greater in diameter versus microvessels measuring less than 100 micrometers.

Human skin provides the termination of the microcirculation, composed of nutritional papillary capillary beds, as well as nonnutritional thermoregulatory vessels. Interestingly, in normal physiology, 80-90% of microcirculation passes only through thermoregulatory vessels.

Frequency

United States

Upper extremity vascular disorders affect approximately 10% of the population.

Mortality/Morbidity

General symptoms following vascular compromise include dysesthesias, paresthesias, pallor, cold intolerance, ulceration, and tissue necrosis. Vascular competence can often become compromised, leading to various disease pathologies.

Race

No current findings identify any one race as having a particular propensity for developing vascular occlusive syndromes.

Sex

See Treatment, Medical Care. The onset of vascular occlusive disorders is affected by the sex of the patient. For example, Raynaud disease affects women aged 30-50 years. In contrast, males are affected in a bimodal fashion. Acute traumatic vascular disorders are more common in younger males because of the high incidence of motor vehicle accidents in this age group. In contrast, repetitive traumatic vascular disorders occur most often in middle-aged males who are employed in manual-type labor. In the latter case, the labor engaged in usually involves handheld vibrating tools that cause chronic trauma.

Age

See Treatment, Medical Care. Patient age also determines propensity for vascular occlusive disorders. As mentioned above, Raynaud disease affects women aged 30-50 years. Males have a bimodal affliction, with young males (because of the high incidence of motor vehicle accidents among them) most often suffering acute traumatic vascular disorders and middle-aged males (specifically, those involved in manual-type work) being most frequently affected by repetitive traumatic vascular disorders.

Clinical

History

Patient evaluation for suspected vascular pathology should include the eliciting of detailed descriptions of the trauma mechanism (penetrating or nonpenetrating), exposure to repetitive insults, the history of familial or blood disorders, drug or tobacco use, and any concurrent illness.

• Patients with insidious vascular compromise may initially report numbness, increased pain, or cold sensitivity.
• As vascular insufficiency progresses, patients may report weakness or even present with frank gangrene resulting from tissue necrosis.

Physical

A complete physical examination of the entire upper extremity and neck is warranted.

• The following must be documented: capillary refill; skin turgor; signs of infection; tissue compromise, such as ulceration or gangrene; and quality of pulses.
• Presence of masses, bruits, or both masses and bruits should be noted.
• An Allen test should be performed to differentially evaluate the patency of the ulnar and radial arteries at the distal forearm. Documenting time-to-refilling is valuable for serial examinations.
• Additionally, several diagnostic evaluations may be completed to confirm suspected diagnoses (see Workup, Imaging Studies).

Causes

Causes of vascular compromise include acute trauma; chronic modalities, such as repetitive microtrauma; and systemic disease processes involving metabolic and/or autoimmune processes. See Treatment, Medical Care for a more in-depth discussion.

Differential Diagnoses

Thromboembolism

Other Problems to Be Considered

Arteriovenous Fistulas
Buerger Disease (Thromboangiitis Obliterans)
Churg-Strauss Disease
Churg-Strauss Syndrome (Allergic Granulomatosis)
CREST Syndrome
Giant Cell Arteritis
Raynaud Phenomenon
Scleroderma
Takayasu Arteritis
Thoracic Outlet Syndrome
Upper Extremity Occlusive Disease
Wegener Granulomatosis

Workup

Imaging Studies

• Handheld Doppler ultrasound is used to analyze variation in the pulse waveform by reflections of sound generated by intraluminal moving red blood cells. The loudness and pitch of the audible signal is determined by the intraluminal flow. This modality allows for delineation of venous versus arterial pulses.
  • B-mode Doppler ultrasound allows for evaluation of pulsatile flow, which is depicted by a triphasic flow, involving an initial systolic upstroke followed immediately by a transient downstroke flow reversal and finally a minor upstroke elastic recoil.
  • Various monophasic patterns allow differentiation of stenosis versus occlusion of vessels.
• Digital plethysmography allows for assessment of digital volume changes over time. Serial patterns of digital volume changes can be used to differentiate vasospastic from vaso-occlusive disease. Qualified vascular technicians are required for these discriminating analyses. Segmental arterial pressures are obtained by comparing the digital brachial index (DBI) and/or radial brachial index (RBI)–ulnar brachial index (UBI) pressures to the brachial artery pressure. Specifically, DBI or RBI ratios less than 0.7 indicate inadequate blood perfusion of end organs and encourage intervention. Digital plethysmography is a valuable and reliable tool to assess the severity of vasospasm, isolated or as part of a combined occlusive/vasospastic disorder, such as in scleroderma. The technique is also particularly valuable as a tool to objectify cold-induced vasospasm in vibration-induced white finger syndrome (VWFS) secondary to chronic hand vibrations.
• Color duplex images are useful for evaluation of masses and used for differentiating ganglia, aneurysms, and pseudoaneurysms.
• Radionuclide imaging can be used to obtain a 2-dimensional assessment of the vascular anatomy, as well as to ascertain temporal patterns of perfusion.
  • A radionuclide, such as technetium-99m pertechnetate, is injected intravenously, and 3 serial images are taken. The first image is similar to an angiogram, the second image involves serial pictures obtained over a 1.5-minute period that are used to assess blood pooling and flow dynamics, and finally, the third phase mimics a bone scan.
  • This modality allows for evaluation of vaso-occlusive diseases, such as aneurysms, as well as vasospastic diseases.
  • Recently, this modality has been used as a prognostic test for determining extent of frostbite injury or even degree of tissue viability following electrical injury. Absence or presence, including delay, of radiotracer in zones distal to occluded vessels allows for evaluation of the severity of the occlusion.
• Vital capillaroscopy is a noninvasive modality used to assess integrity of nutritional papillary capillaries.
  • Using epillumination microscopic technique and specialized computer manipulations, qualitative and quantitative information can be obtained about the status of these terminal vessels.
  • Currently, no other diagnostic tool is capable of providing assessment of these microvessels.^{[4,5 ]}
• High-resolution magnetic resonance angiography (MRA) allows for visualization of arterial and venous structures. The advantage of MRA is that it allows for vivid images without need for arterial vascular access and without patient exposure to ionizing radiation or potentially allergy-inducing contrast dyes.
• Finally, contrast angiography remains the criterion standard, most accurately revealing detailed vascular anatomic information. With computer manipulation, it is possible to evaluate flow direction, source of collateral flow, degree of retrograde filling, and even venous outflow. Relative indications for arteriography include suspicion of partial arterial injury resulting in an intimal flap, proximal traction injury, distal vessel occlusion caused by embolic showering, and pseudoaneurysm formation.
  • Despite its obvious advantages, this modality is used sparingly because it is costly and associated with various complications.
  • Complications can include arterial wall injury, local vasospasm, distal embolic showering, and contrast-induced allergic reaction.
• In general, the various discussed modalities provide the clinician with further evidence of vascular pathology, especially when patients are evaluated with and without vascular stressors. In fact, most clinicians recommend completion of vascular studies before, during, and after controlled exposure to stressors, such as thermal variation, induced anoxia, or emotional lability.

Other Tests

• Skin surface temperatures can be used to estimate digital perfusion. This modality, however, is only reliable within physiologic temperatures ranging from 20-30°C. Its primary value is to assess the efficacy of stellate ganglion block to enhance digital perfusion as a preoperative indication of the potential value of digital sympathectomy. An increase of more than 1 or 2°C suggests an ischemia-related condition, as seen with scleroderma and Raynaud disease, that could potentially be improved.

Treatment

Medical Care

Chronic vascular occlusive diseases

Chronic vascular occlusive diseases occur secondary to repetitive trauma; atherosclerosis; proximal embolic events; systemic diseases, such as collagen vascular disease and vasculitis; and/or hypercoagulable states. Symptoms include pain, pallor, cold intolerance, paresthesias, and ulcerations. Such symptoms may present suddenly in workers who perform repetitive maneuvers involving a hammerlike device. Referred to as hypothenar hammer syndrome, this syndrome presents with pain in the region of the hook of hamate along with paresthesia and decreased temperatures in the ring and little fingers. This syndrome is caused by disruption of the internal elastic lamina, resulting in aneurysmal dilatation and mural thrombosis of the ulnar artery in the Guyon canal. Diagnosis is made based on history and pulsatile mass present in 10% of patients or on findings from Doppler ultrasound or angiography of the upper extremity.

Treatment for chronic vascular occlusive diseases involves thrombolytic agents acutely and, if these are unsuccessful, surgery. Because of the pathophysiology of thrombus formation and maturation, it is important to note that thrombolytic agents are not typically successful. In hypothenar hammer syndrome, surgical intervention includes resection of the ulnar artery locally, since the thrombosed vessel causes focal inflammation and swelling and sympathetic hyperstimulation of the adjacent ulnar nerve segment. Ulnar artery bypass graft with a vein conduit is recommended if patients complain of persistent pain and cold intolerance of the involved digits and if the segmental digital-brachial pressure ratio is less than 0.7. Otherwise, segmental resection is appropriate if the collateral circulation is sufficient. Despite these guidelines, adequacy of vascular flow distally into the digits cannot be confirmed until the vascular segment has been resected intraoperatively.

Thoracic outlet syndrome

Thoracic outlet syndrome follows compression of the subclavian artery and lower brachial trunk of the brachial plexus. Patients typically present with reports of ulnar dermatome paresthesia, especially of the small finger. Systemic symptoms may include occipital headaches. Diagnosis can be made based on a positive result on an Adson test, a costoclavicular maneuver, a Wright hyperabduction external rotation test, or a Russe overhead exercise test. Chest radiography with lordotic views may demonstrate an accessory cervical rib, which can be the source of compression on neurovascular bundles. Finally, diagnostic infiltration of local anesthetic solution into the anterior scalene muscle (diagnostic anterior scalene block) can be used to diagnose thoracic outlet syndrome.

Treatment of thoracic outlet syndrome involves physical therapy to allow for muscle rebalancing, scalene muscle lengthening, and improved brachial plexus gliding. Physical therapy may also result in postural correction and strengthening of shoulder girdle muscles. If physical therapy is not successful, then anterior scalenotomy, brachial plexus neurolysis, and first-rib resection have been described with variable efficacy.^{[6 ]}

Embolism

Embolism to distal vessels results in acute pain and pallor in previously noncompromised tissue. Patients present with the classic bluish finger and demonstrate petechiae of the digital tip and nail beds. As many as 70% of upper extremity emboli arise from the heart, but the subclavian artery (as part of thoracic outlet syndrome) and superficial palmar arch also are common sources. Cardiac sources produce mural thrombi that develop in the setting of atrial fibrillation; subclavian arterial thrombi are caused by compression from thoracic outlet syndrome.

Embolism treatment consists of immediate anticoagulation with heparin followed by 3 months of warfarin therapy. Thrombolytic therapy has been advocated as being more efficacious. Local treatment of acute small-vessel occlusion through infusion via a catheter floated down the radial or ulnar artery is often preferable for reasons of efficiency. This also reduces the risk of systemic complications, particularly in the case of tissue plasminogen activator (t-PA), which has the additional advantage of an extremely short half-life. Embolectomy can be attempted if emboli are embedded in vessels proximal to the superficial arch.

Aneurysm

An aneurysm may form in the vessel wall following intraluminal injury that leads to uniform and gradual dilatation of the vessel wall. This is in contrast to a pseudoaneurysm, which develops following penetrating injury of the vessel wall, leading to a saclike out-patching without an endothelial lining. Aneurysms present as expanding, palpable, painless masses. Symptoms may develop only following external compression of neighboring sensory nerves. The natural course of these lesions involves slow progression to thrombus formation and production of emboli. Diagnosis can be confirmed based on Doppler ultrasonography, angiography, or both. Treatment involves resection of the lesion and repair with a patch graft or interposition graft.

Raynaud disease and Raynaud phenomenon

Raynaud disease is a purely vasospastic condition without underlying cause, sometimes leading to acral necrosis. It is defined in Dorland's Illustrated Medical Dictionary as "a primary or idiopathic vascular disorder characterized by bilateral attacks of Raynaud phenomenon." Raynaud disease usually occurs in persons aged 30-50 years. Prevalence is greater in females than in males, and symptoms last more than 2 years. Patients demonstrate bilateral hand involvement, with pallor of digits secondary to cold exposure or psychologic stressors. Patients report dysesthesia of involved digits. Diagnosis of Raynaud disease is made on the basis of demonstration of triphasic color change of the overlying digit skin.

In contrast to Raynaud disease, Raynaud phenomenon presents concurrently with CREST syndrome (see CREST Syndrome), in which tissue necrosis results from spastic and occlusive disease. CREST syndrome refers to disease processes involving symptoms of generalized calcinosis, Raynaud phenomenon, esophageal dysfunction, scleroderma, and telangiectasia. Symptoms specific to Raynaud phenomenon include digital ischemic pain, nonhealing ulcers, and development of gangrene. Moreover, patients present with progressive joint contractures, including adduction contracture of the thumb and fixed flexion contractures of proximal interphalangeal joints with secondary extension contracture of the metacarpophalangeal joints. Ulcers develop over the proximal interphalangeal joints secondary to ischemia, pressure, minor trauma, or a combination of factors.^{[7 ]}

Initial treatment of both Raynaud disease and Raynaud phenomenon involves inhibition of vasospasms, thus improving microvascular flow and maximizing capillary perfusion. Treatment initially consists of cessation of smoking, biofeedback therapies (temperature control), and calcium channel blockers.^{[8 ]}Avoiding exposure to cold by wearing protective garments, including hand warmers, are important first-line measures. Raynaud disease is most effectively treated with these conservative measures.

Raynaud phenomenon, unlike Raynaud disease, is an intermittent bilateral attack of ischemia of the fingers or toes, as well as sometimes of the ears or nose. It is marked by severe pallor and is often accompanied by paresthesia and pain. The condition is brought on by cold or emotional stimuli, and the symptoms are relieved by heat. Raynaud phenomenon may be idiopathic, often afflicting young females of slender stature, or it may be secondary to an underlying, identifiable disease, such as scleroderma. The diagnostic term Raynaud phenomenon refers solely to the signs and symptoms consistent with the vasospastic episodes. Raynaud phenomenon does not lead to ischemic ulcers, whereas the underlying condition may lead to ulceration.

Management eventually requires surgical intervention with peripheral/periarterial sympathectomy. This includes dissection of adventitia from arterial trunks and transection of neural connections between involved arteries and paired peripheral nerves. Other surgical modalities include vascular bypass and/or cervicothoracic sympathectomy, each of which results in a 50% recurrence of symptoms. Treatment for contractures is dependent on disease severity. If contractures are mild, physical therapy is employed; if contractures are severe or dorsal skin ulcers are present, arthrodesis of proximal interphalangeal joints into a functional position is performed, which promotes primary wound closure. Maintenance of the digital cascade is pursued.

Advanced peripheral vasculitis conditions

Advanced peripheral vasculitis conditions include Wegener granulomatosis, Churg-Strauss syndrome, Takayasu arteritis, Buerger disease, and giant cell arteritis. Takayasu arteritis is referred to as the pulseless disease. It occurs in females aged 10-30 years and involves stenosis of the aortic arch, carotid arteries, and, less often, upper extremity vessels. Giant cell arteritis involves the subclavian vessels and affects women older than 50 years. It is associated with increased erythrocyte sedimentation rate values. Treatment involves systemic steroids. Buerger disease, referred to as a thromboangiitis obliterans, involves vasculitis of medium-size and small vessels. It is associated with smoking and affects the lower extremities more than it does the upper extremities. Treatment is focused on behavior modification, such as avoidance of coldexposure and cessation of smoking.

Anticoagulation and thrombolysis are rarely effective in these disease processes. Therefore, vascular reconstruction with venous or arterial grafting is generally necessary for definitive treatment. Bypass grafting following complete occlusion of involved vessels is inevitable because anticoagulation and thrombolytic therapy have not proven to be efficacious.

When one considers digital-vessel bypass surgery, considering digital-vessel diameters is important. In general, the proper digital vessels are smaller than the common digital vessels. Additionally, the diameters of the ulnar proper digital vessels of the thumb, as well as of the index and long fingers, are greater than those of their corresponding radial proper digital vessels. In contrast, the radial proper digital vessels of the ring and small fingers are larger than their corresponding ulnar proper digital vessels. Preoperative arteriography may demonstrate an incomplete arch or thrombosis of the radial or ulnar arteries, especially in women smokers.

Surgical Care

Traumatic, acute arterial injury is common and may occur after penetrating or blunt trauma. Most isolated vascular injuries do not require immediate attention, since collateral perfusion prevents tissue compromise. Critical injuries following penetrating trauma that require immediate revascularization typically occur if the brachial artery or both the radial and ulnar arteries have been severed. Infrequently, vascular repair of a single ulnar or radial injury is necessary because of inadequate collateral flow from the remaining intact artery. Brachial injuries occurring proximal to the origin of the profunda brachii are most susceptible to distal tissue perfusion compromise.

Critical injuries following blunt trauma involve either a closed brachial artery laceration due to a supracondylar humerus fracture or development of compartment syndrome after a crushing or penetrating injury that causes arterial injury. If treated promptly with immediate wide fasciotomy, increased pressures leading to tissue death and functional deficit may be avoided. If left untreated, the patient develops an intrinsic plus position hand deformity associated with intrinsic muscle contraction. Signs of intrinsic contracture include metacarpophalangeal joint flexion and interphalangeal joint extension; passive hyperextension of the metacarpophalangeal joint decreases active and passive flexion capacity of the interphalangeal joints. The Bunnell intrinsic tightness test confirms only contracture of intrinsic muscles. This syndrome results in increased intracompartmental pressures, typically greater than 30 mm Hg, which result in necrosis of the deepest muscles.

If hypoperfusion is suspected, the DBI may be obtained to assess perfusion following arterial injury, and a Striker needle can be used to monitor intracompartmental pressures following crush injuries. Digital pulse oximetry is helpful as well. In all suspected vascular injuries that are treated conservatively, close monitoring is necessary. For example, following high-energy gunshot wounds with arterial contusion, thrombosis and progressive ischemia are not uncommon after prolonged delays. In contrast, some clinical suspicion of a forearm compartment syndrome is a sufficient indication for fasciotomy, particularly because pressure measurements and other laboratory tests may be unreliable and user dependent and will inevitably delay definitive treatment.

Traumatic, noncritical vascular injuries involve cases in which tissue perfusion is not compromised, despite vascular injury. Although not absolutely indicated, revascularization can be undertaken in some of these situations. The clinician may choose to repair vascular injuries intraoperatively if exploration of the injury must be undertaken to repair the injury and to rule out injury to other vital structures, such as tendons and nerves. Arterial repair may restore enhanced parallel flow in case of future injury, prophylaxis against future cold intolerance symptoms, and enhanced tissue healing. Thrombosis rate following radial or ulnar artery repair at the wrist is high and may negate this endeavor.

Iatrogenic arterial injuries involve procedures requiring arterial cannulation or injection. Brachial artery injury is observed in approximately 0.5% of patients following cannulation for cardiac catheterization. Similarly, injury to the radial artery is observed in 23% of patients following repeated measurement of arterial blood gasses. Such injuries may result in pseudoaneurysm formation, creation of an arteriovenous fistula, or acute thrombosis with distal embolization.

The most routine diagnostic test involves use of handheld Doppler imaging to evaluate pulses distal to the gross injury while compressing any sources of collateral flow. Alternatively, color duplex Doppler ultrasonography can be used to evaluate vessel structural integrity. Although arteriography is the criterion standard test for vascular integrity, its use is not routine.

Surgical reconstruction must be undertaken under tourniquet control in the operating room and with the aid of loupe or microscopic magnification. Surgical exposure is necessary and is provided for by extension of the traumatic laceration both proximally and distally. Following debridement of necrotic tissue, vital structures must be identified and tagged both proximally and distally prior to any repairs. In particular, vessels are trimmed to healthy intimal tissue and clamped with atraumatic vascular clamps.

Vessel repair must be performed without tension, thus necessitating use of reversed interposition vein grafting if the vessel stumps cannot be juxtaposed following mobilization. Vessel mobilization can be optimized by ligation of nonessential branches. Donor-site venous grafts depend on the caliber of the injured vessel and can include superficial veins of the dorsum of the hand; superficial veins of the arm, such as the cephalic and basilic veins or their terminal branches; or harvests taken from the lower leg, such as the distal saphenous vein or its terminal branches.

Following surgical repair and before release of vascular clamps, systemic heparin (3000-5000 U) is administered. Postoperatively, only aspirin (325 mg/d PO) administration is recommended unless intraoperative anastomosis complications are confronted, in which case postoperative heparin infusion is continued.

Various other surgical interventions have been described for management of vascular injuries. In the setting of bony injuries or more critical injuries that require immediate attention, prolonged extremity ischemia can be avoided with temporary silastic catheter shunting. Fasciotomy is indicated in the setting of overt or impending compartment syndrome. Although not regularly required, venous repair is indicated in the setting of circumferential soft-tissue injuries or amputation injuries with compromise of all venous outflow. Adequate venous drainage of the upper extremity requires a minimum of 1 draining vein (although 2 veins are preferred) and can be provided with reconstruction of a combination of the following: cephalic vein, basilic vein, and vena comitantes.

Venous insufficiency can be detected following appropriate arterial inflow and presents with gradual distention and a bluish appearance of the distal extremity. Following iatrogenic injuries, acute thrombolytic therapy has been advocated as first-line therapy, especially for cases involving embolic showering to distal nutrient microvessels. However, thrombolytic therapy is contraindicated in the presence of pseudoaneurysm. For cases of thrombosis and emboli to large vessels, embolectomy using arteriotomy with a Fogarty balloon catheter has been advocated. Finally, suture ligation of arteriovenous fistulas and patch graft using venous tissue for pseudoaneurysm or intimal flap repair may be required.

Medication

Upon surgical repair of traumatic vascular injury and before the release of vascular clamps to allow return of blood perfusion, systemic heparin (3000-5000 U) is administered. Postoperatively, only aspirin (325 mg/d PO) administration is recommended unless intraoperative anastomosis complications are confronted. If such complications do occur, postoperative therapeutic heparin infusion is continued (titrated to keep activated partial thromboplastin time [aPTT] between 50 and 80 s). Persantine (dipyridamole) is an appropriate alternative to aspirin and has a similar platelet mode of action.

Following iatrogenic vascular injuries, acute thrombolytic therapy has been advocated as first-line therapy, especially for cases involving embolic showering to distal nutrient microvessels. Thrombolytic medication options include either tissue plasminogen activator (t-PA), given at a dose of 100 mg IV over 2 hours, or streptokinase, given at a dose of 1.5 million U IV over 1 hour. However, thrombolytic therapy is contraindicated in the presence of a pseudoaneurysm, in which case, surgical intervention is preferred.

Hypothenar hammer syndrome, which presents with pain in the region of the hook of hamate along with paresthesia and decreased temperatures in the ring and little fingers, follows disruption of the internal elastic lamina. The condition results in aneurysmal dilatation and mural thrombosis of the ulnar artery in the Guyon canal. Diagnosis is made based on history, a positive result on an Allen test, and, in a minority of cases (10%), a pulsatile mass. Doppler ultrasound or angiography of the upper extremity will confirm the diagnosis. Treatment involves thrombolytic agents (t-PA, given at a dose of 100 mg IV over 2 h, or streptokinase, given at a dose of 1.5 million U IV over 1 h) acutely and, if this treatment is unsuccessful, surgery. In fact, most cases of hypothenar hammer syndrome are diagnosed at a time when successful thrombolysis is no longer possible.

Vaso-occlusive disease of the terminal vessels may arise from proximal showering of emboli from either vascular or cardiac thrombi. Treatment consists of immediate anticoagulation with heparin (3000-5000 U IV bolus followed by titrated infusion to keep aPTT between 50 and 80 s) followed by 3 months of warfarin (Coumadin) PO therapy (titrated to keep prothrombin time [PT] between 2 and 3 s). Thrombolytic therapy can be attempted if anticoagulation does not improve symptoms acutely (t-PA, given at a dose of 100 mg IV over 2 h, or streptokinase, given at a dose of 1.5 million U IV over 1 h). Embolectomy can be attempted if emboli are embedded in vessels proximal to the superficial arch and anticoagulant therapy has proven ineffective.

Initial treatment of both Raynaud disease and Raynaud phenomenon involves inhibition of vasospasms, thus improving microvascular flow and maximizing capillary perfusion. Treatment initially consists of smoking cessation, biofeedback therapies (temperature control), and calcium channel blockers. Calcium channel blockers include diltiazem (Cardizem SR), 60 mg PO every 12 hours, or verapamil, 150 mg PO at bedtime.

Anticoagulants

Prevent recurrent or ongoing thromboembolic occlusion of the vertebrobasilar circulation. Used for treatment and prevention of deep vein thrombosis (DVT), pulmonary embolism (PE), unstable angina, atrial fibrillation with emboli formation, and acute arterial occlusion.

Heparin

Acts with antithrombin III to inactivate thrombin and inhibit thromboplastin formation.

Dosing

Adult

Prophylaxis: 3000-5000 U SC q8-12h
Thrombosis treatment: Loading dose 50 U/kg IV, then 10-20 U/kg/h IV (adjust based on PTT)

Pediatric

Infants: Loading dose 50 U/kg IV bolus, then 20 U/kg/h IV by continuous infusion
Children: Loading dose 50 U/kg IV, then 15-25 U/kg continuous infusion or 100 U/kg/dose q4h IV intermittent bolus

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis, active bleeding, history of heparin-induced thrombocytopenia

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

In neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) from benzyl alcohol, which is used as preservative; caution in severe hypotension and shock; monitor for bleeding in peptic ulcer disease, menstruation, and increased capillary permeability and when giving IM injections; uncontrolled bleeding/anticoagulation disorders may occur (follow PTT, thrombin time, or activated clotting time to assess effectiveness)

Warfarin (Coumadin)

Interferes with hepatic synthesis of vitamin K–dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.
Tailor dose to maintain an INR in the range of 2-3.

Dosing

Adult

5-15 mg/d PO qd for 2-5 d; adjust dose according to desired INR (2-3 for most patients; mechanical heart valves, desired INR is 2.5-3.5)
ACCP guidelines: 5 mg initially unless rapid attainment of therapeutic INR is necessary; use 7.5-10 mg if patient is elderly or has other bleeding risk factors

Pediatric

0.05-0.34 mg/kg/d PO/IV/IM

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate; medications that may increase anticoagulant effects of warfarin include oral antibiotics, capecitabine, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Severe hepatic or renal disease, bleeding, peptic ulcer

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Must monitor closely; INR preferred test rather than PT, to adjust dose; monitor vitamin K intake; consider decreasing doses in hepatic impairment and elderly persons
Monitor INR; bleeding caused by overanticoagulation; to rapidly correct overcoumadinization, use either vitamin K, fresh frozen plasma, or both

Thrombolytics

Used for acute myocardial infarction (AMI), pulmonary emboli (PE), and acute ischemic stroke.

Alteplase (Activase)

t-PA and fibrin-specific agent with brief half-life of 5 min. Initiates local fibrinolysis by binding to fibrin in the thrombus. Used in management of AMI, acute ischemic stroke, and PE.
Adjunctive therapy with IV heparin necessary to maintain patency of arteries recanalized by t-PA, especially during first 24-48 h.

Dosing

Adult

AMI and PE: 15 mg IV initial bolus, followed by 50 mg IV over next 30 min and then 35 mg IV over next h; total dose not to exceed 100 mg Stroke: 0.9 mg/kg (do not exceed 90 mg) IV over 60 min, with 10% of total dose administered as initial IV bolus over 1 min

Pediatric

Not established

Interactions

Anticoagulants and antiplatelets may increase risk of bleeding; may give heparin with and after alteplase infusions to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications

Contraindications

Documented hypersensitivity; active internal bleeding, cerebrovascular accident or stroke within last 2 mo, intracranial or intraspinal surgery or trauma, intracranial hemorrhage on pretreatment evaluation, suspicion of subarachnoid hemorrhage, intracranial neoplasm, arteriovenous malformation or aneurysm, bleeding diathesis, or severe, uncontrolled hypertension

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH

Streptokinase (Kabikinase, Streptase)

Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. Increase in fibrinolytic activity that degrades fibrinogen levels for 24-36 h takes place with intravenous infusion of streptokinase.

Dosing

Adult

PE: Loading dose of 250,000 IU IV through a peripheral vein over 30 min
DVT or arterial embolism: Load as with PE, then 100,000 IU/h IV for 24-72h
Coronary artery thrombosis: 1.5 MU IV over 60 min

Pediatric

3500-4000 U/kg over 30 min, followed by 1000-1500 U/kg/h

Interactions

Antifibrinolytic agents may decrease effects of streptokinase; heparin, warfarin, and aspirin may increase risk of bleeding

Contraindications

Documented hypersensitivity; active internal bleeding, intracranial neoplasm, aneurysm, diathesis, severe uncontrolled arterial hypertension

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in severe hypertension, intramuscular administration of medications, trauma or surgery in the previous 10 days; measure hematocrit, platelet count, aPTT, TT, PT or fibrinogen levels before therapy is implemented; either TT or aPTT should be less than twice the normal control value following infusion of streptokinase and before (re)instituting heparin; do not take blood pressure in the lower extremities, as it may dislodge a possible deep vein thrombus; PT, aPTT, TT, or fibrinogen should be monitored 4 h after initiation of therapy; if maintenance infusion inadequate to maintain thrombin clotting time 2-5 times control, refer to the package insert, Physicians' Desk Reference, or the drug information service of the American Hospital Formulary Service (AHFS) for adjustments; antibodies remain 3-6 months following dose; adverse effects include bleeding, hypotension, fever, bruising, rash, GI upset, hemorrhage, anaphylaxis

Antiarrhythmics

Used for angina, prevention of reinfarction, hypertension, atrial fibrillation or flutter, and paroxysmal atrial tachycardia (PAT).

Diltiazem (Cardizem CD, Dilacor, Tiamate, Tiazac, Cardizem LA)

During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.
Calcium channel blockers also inhibit movement of calcium ions across cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Dosing

Adult

30 mg PO qid initially; increase to 180-360 mg/d in 3-4 divided doses prn
SR: 60-120 mg PO bid; increase to 360 mg/d maximum
CD: 120-360 mg/d (maximum 480 mg/d)
IV: 0.25 mg/kg IV over 2 min, then 0.35 mg/kg over 2 min, then 5-15 mg/h drip; then switch to 120-360 mg/d PO

Pediatric

Not established

Interactions

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when given with beta-blockers, may increase cardiac depression; cimetidine may increase diltiazem levels

Contraindications

Documented hypersensitivity; severe CHF, sick sinus syndrome, second- or third-degree AV block, and hypotension (< 90 mm Hg systolic); bradycardia, ECG abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur

Verapamil (Calan, Calan SR, Covera-HS, Verelan)

Calcium channel blocker. Only the nondihydropyridines are effective for rate control. During depolarization, inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Dosing

Adult

Arrhythmias: Second line for paroxysmal supraventricular tachycardia (PSVT) with narrow QRS complex and adequate BP 2.5-5 mg IV over 1-2 min; repeat 5-10 mg in 15-30 min prn (30 mg maximum)
Angina: 80-120 mg PO tid, increase to 480 mg/d maximum
HTN: 80-180 mg PO tid or SR tabs 120-240 mg/d PO to 240 mg bid

Pediatric

<1 year: 0.1-0.2 mg/kg IV bolus over 2 min; if no response, repeat in 30 min
1-15 years: 0.1-0.3 mg/kg (ie, 2-5 mg) IV bolus over 2 min; single dose not to exceed 5 mg; if no response, repeat in 30 min; not to exceed total dose of 10 mg
>15 years: Administer as in adults

Interactions

Verapamil may increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone, can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta blockers, may increase cardiac depression; cimetidine may increase verapamil levels; verapamil may increase theophylline levels

Contraindications

Documented hypersensitivity; severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment); monitor liver function periodically

Antiplatelet agents

Used for prophylaxis and treatment of PE and DVT, and AF with embolization, as well as other postoperative indications.

Dipyridamole (Persantine)

To complement usual warfarin therapy. Platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased cyclic-3', 5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.

Dosing

Adult

75-100 mg PO qid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Theophylline may decrease hypotensive effects; antiplatelet activity of dipyridamole may increase heparin toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in hypotension; medication has peripheral vasodilating effects

Salicylates

Used to manage mild pain, headache, fever, and inflammation, as well as for prevention of emboli and myocardial infarction (MI).

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

Benefits adults. Inhibits prostaglandin synthesis preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.

Dosing

Adult

Pain, fever: 325-650 mg PO/PR q4-6h
Rheumatoid arthritis (RA): 3-6 g/d PO in divided doses
Platelet inhibitory action: 81-325 mg/d PO Prevention of MI: 81-325 mg/d PO

Pediatric

Antipyretic: 10-15 mg/kg/dose PO/PR q4h up to 80 mg/kg/d RA: 60-100 mg/kg/d
PO divided q4-6h (monitor serum levels to maintain 15-30 mg/dL)

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; because of association of aspirin with Reye syndrome, do not use in children ( <16 y) with viral infection

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with a history of blood coagulation defects, or who are taking anticoagulants; use linked to Reye syndrome (avoid use with viral illness in children); avoid use with CrCl <10 mL/min and in severe liver disease; avoid or limit alcohol intake; allergies; GI upset and erosion are common adverse reactions

Follow-up

Complications

• Acute trauma with ensuing vascular compromise of distal extremity tissue must be treated emergently to minimize distal tissue loss. Partial vascular compromise left untreated may result in muscular fibrosis and contractures of varying severity. The patient may risk loss of the involved limb within hours without vascular supply. More often, partial vascular compromise is left untreated, in which case the patient may develop an intrinsic plus position hand deformity associated with intrinsic muscle contraction. Signs of intrinsic contracture include metacarpal phalangeal joint flexion and interphalangeal joint extension; passive hyperextension of the metacarpal phalangeal joint decreases active flexion capacity of interphalangeal joints (Bunnell sign).
• Noncritical arterial injury may lead to pseudoaneurysm, arteriovenous fistulation, or endothelial injury with mural thrombosis and seeding of emboli. Traumatic, noncritical vascular injuries involve cases in which tissue perfusion is not compromised, despite vascular injury. Such injuries may result in pseudoaneurysm formation, creation of an arteriovenous fistula, or acute thrombosis with distal embolization.
• Raynaud disease usually occurs in persons aged 30-50 years, with increased prevalence in women. Symptoms generally last longer than 2 years. Patients demonstrate bilateral hand involvement with pallor of digits secondary to cold exposure or psychologic stressors. Complications include intermittent complaints of dysesthesia of involved digits. In contrast, CREST syndrome represents disease processes involving symptoms of generalized calcinosis, esophageal dysfunction, scleroderma, telangiectasia, and Raynaud phenomenon. Symptoms specific to Raynaud phenomenon include digital ischemic pain, nonhealing ulcers, and the development of gangrene. Patients present with progressive joint contractures, including adduction contracture of the thumb and fixed flexion contractures of proximal interphalangeal joints, with secondary extension contracture of metacarpophalangeal joints. Ulcers may develop over proximal interphalangeal joints, secondary to ischemia, pressure, minor trauma, or a combination of factors.

Prognosis

• Vaso-occlusive diseases give rise to variable morbidity in patients, depending on the pathophysiology of the underlying condition. Vascular flow is determined by multiple factors, including environmental events, metabolic demands, sympathetic nervous tone, and local or circulating humoral mediators. When vascular flow is compromised, symptoms, including dysesthesias, paresthesias, pallor, cold intolerance, and ulceration associated with tissue necrosis, may be present. As such, vaso-occlusive diseases result in significant morbidity.
• Causes of vascular compromise include acute trauma or chronic modalities, such as repetitive microtrauma and systemic diseases involving metabolic processes, autoimmune processes, or both. Environmental factors as trivial as arsenic exposure may lead to severe, chronic peripheral vasospasm. Patient history and physical examination, as well as multiple diagnostic modalities, may be used to diagnose the cause of vascular compromise. Depending on the etiology of the vascular compromise, numerous conservative measures, as well as more aggressive surgical interventions, may be indicated.

Miscellaneous

Medicolegal Pitfalls

• It is of utmost importance to stress to patients with vaso-occlusive disease that their vascular pathology may or may not be curable. In general, generalized vaso-occlusive disorders cannot be cured, whereas focal vascular disorders often are curable. Therefore, any treatments provided, whether conservative or surgical, may only be temporizing measures.

References

1. Jones MA, Lee DY, Segall JA, Landry GJ, Liem TK, Mitchell EL, et al. Characterizing resolution of catheter-associated upper extremity deep venous thrombosis. J Vasc Surg. Oct 29 2009;[Medline].

2. Kim JY, Buck DW 2nd, Forte AJ, Subramanian VS, Birman MV, Schierle CF, et al. Risk factors for compartment syndrome in traumatic brachial artery injuries: an institutional experience in 139 patients. J Trauma. Dec 2009;67(6):1339-44. [Medline].

3. White PW, Gillespie DL, Feurstein I, Aidinian G, Phinney S, Cox MW, et al. Sixty-four slice multidetector computed tomographic angiography in the evaluation of vascular trauma. J Trauma. Jan 2010;68(1):96-102. [Medline].

4. Murray AK, Moore TL, Manning JB, Taylor C, Griffiths CE, Herrick AL. Noninvasive imaging techniques in the assessment of scleroderma spectrum disorders. Arthritis Rheum. Aug 15 2009;61(8):1103-11. [Medline].

5. O'Doherty J, McNamara P, Clancy NT, Enfield JG, Leahy MJ. Comparison of instruments for investigation of microcirculatory blood flow and red blood cell concentration. J Biomed Opt. May-Jun 2009;14(3):034025. [Medline].

6. Chang DC, Rotellini-Coltvet LA, Mukherjee D, De Leon R, Freischlag JA. Surgical intervention for thoracic outlet syndrome improves patient's quality of life. J Vasc Surg. Mar 2009;49(3):630-5; discussion 635-7. [Medline].

7. Steen V, Denton CP, Pope JE, Matucci-Cerinic M. Digital ulcers: overt vascular disease in systemic sclerosis. Rheumatology (Oxford). Jun 2009;48 Suppl 3:iii19-24. [Medline].

8. Kowal-Bielecka O, Landewé R, Avouac J, Chwiesko S, Miniati I, Czirjak L, et al. EULAR recommendations for the treatment of systemic sclerosis: a report from the EULAR Scleroderma Trials and Research group (EUSTAR). Ann Rheum Dis. May 2009;68(5):620-8. [Medline].

9. Dalinka MK, Meyer S, Kricun ME, et al. Magnetic resonance imaging of the wrist. Hand Clin. Feb 1991;7(1):87-98. [Medline].

10. Disa JJ, Chung KC, Gellad FE, et al. Efficacy of magnetic resonance angiography in the evaluation of vascular malformations of the hand. Plast Reconstr Surg. Jan 1997;99(1):136-44; discussion 145-7. [Medline].

11. Edwards EA. Organization of the small arteries of the hand and digits. Am J Surg. Jun 1960;99:837-46. [Medline].

12. el-Gammal TA, Blair WF. Digital periarterial sympathectomy for ischaemic digital pain and ulcers. J Hand Surg [Br]. Nov 1991;16(4):382-5. [Medline].

13. Flatt AE. Digital artery sympathectomy. J Hand Surg [Am]. Nov 1980;5(6):550-6. [Medline].

14. Goldberg I, Bahar A, Yosipovitch Z. Gangrene of the upper extremity following intra-arterial injection of drugs. A case report and review of the literature. Clin Orthop Relat Res. Sep 1984;188:223-9. [Medline].

15. Greenfield AD, Shepherd JT, Whelan RF. The part played by the nervous system in the response to cold of the circulation through the finger tip. Clin Sci (Lond). Aug 1951;10(3):347-60. [Medline].

16. Ho PK, Weiland AJ, McClinton MA, et al. Aneurysms of the upper extremity. J Hand Surg [Am]. Jan 1987;12(1):39-46. [Medline].

17. Holder LE, Merine DS, Yang A. Nuclear medicine, contrast angiography, and magnetic resonance imaging for evaluating vascular problems in the hand. Hand Clin. Feb 1993;9(1):85-113. [Medline].

18. Ikeda A, Ugawa A, Kazihara Y, et al. Arterial patterns in the hand based on a three-dimensional analysis of 220 cadaver hands. J Hand Surg [Am]. Jul 1988;13(4):501-9. [Medline].

19. Joyce JW. Buerger's disease (thromboangiitis obliterans). Rheum Dis Clin North Am. May 1990;16(2):463-70. [Medline].

20. Kleinert HE, Burget GC, Morgan JA, et al. Aneurysms of the hand. Arch Surg. Apr 1973;106(4):554-7. [Medline].

21. Kleinert HE, Volianitis GJ. Thrombosis of the palmar arterial arch and its tributaries: etiology and newer concepts in treatment. J Trauma. Jul 1965;83:447-57. [Medline].

22. Koman LA, Bond MG, Carter RE, et al. Evaluation of upper extremity vasculature with high-resolution ultrasound. J Hand Surg [Am]. Mar 1985;10(2):249-55. [Medline].

23. Koman LA, Koman LA, et al. Diagnostic study of vascular lesions. Hand Clin. May 1985;1(2):217-31. [Medline].

24. Koman LA, Nunley JA, Goldner JL, et al. Isolated cold stress testing in the assessment of symptoms in the upper extremity: preliminary communication. J Hand Surg [Am]. May 1984;9(3):305-13. [Medline].

25. Koman LA, Smith BP, Pollock FE Jr, et al. The microcirculatory effects of peripheral sympathectomy. J Hand Surg [Am]. Sep 1995;20(5):709-17. [Medline].

26. Koman LA, Urbaniak JR. Ulnar artery insufficiency: a guide to treatment. J Hand Surg [Am]. Jan 1981;6(1):16-24. [Medline].

27. McClinton MA. Tumors and aneurysms of the upper extremity. Hand Clin. Feb 1993;9(1):151-69. [Medline].

28. McNamara TO, Bomberger RA. Factors affecting initial and 6 month patency rates after intraarterial thrombolysis with high dose urokinase. Am J Surg. Dec 1986;152(6):709-12. [Medline].

29. Merritt WH. Comprehensive management of Raynaud's syndrome. Clin Plast Surg. Jan 1997;24(1):133-59. [Medline].

30. Miller LM, Morgan RF. Vasospastic disorders. Etiology, recognition, and treatment. Hand Clin. Feb 1993;9(1):171-87. [Medline].

31. Rich NM, Hobson RW, Collins GJ. Traumatic arteriovenous fistulas and false aneurysms: a review of 558 lesions. Surgery. Dec 1975;78(6):817-28. [Medline].

32. Strandness DE, Schultz RD, Sumner DS, et al. Ultrasonic flow detection. A useful technique in the evaluation of peripheral vascular disease. Am J Surg. Mar 1967;113(3):311-20. [Medline].

33. Troum SJ, Smith TL, Koman LA, et al. Management of vasospastic disorders of the hand. Clin Plast Surg. Jan 1997;24(1):121-32. [Medline].

34. Wilgis EF. Digital sympathectomy for vascular insufficiency. Hand Clin. May 1985;1(2):361-7. [Medline].

35. Zimmerman NB. Occlusive vascular disorders of the upper extremity. Hand Clin. Feb 1993;9(1):139-50. [Medline].

36. Zimmerman NB, Zimmerman SI, McClinton MA, et al. Long-term recovery following surgical treatment for ulnar artery occlusion. J Hand Surg [Am]. Jan 1994;19(1):17-21. [Medline].

Keywords

vascular disorders, vascular compromise, vasospastic disorders, vascular insufficiency, hypothenar hammer syndrome, chronic vascular occlusive disease, thoracic outlet syndrome, embolism, Raynaud disease, Raynaud's disease, Raynaud syndrome, Raynaud's syndrome, Raynaud phenomenon, Raynaud's phenomenon, peripheral vasculitis, Wegener granulomatosis, Wegener's granulomatosis, Churg-Strauss syndrome, Takayasu vasculitis, Buerger disease, Buerger's disease, thromboangiitis obliterans, giant cell arteritis, aneurysm, pseudoaneurysm, CREST syndrome

Contributor Information and Disclosures

Author

Arian Mowlavi, MD, FACS, Consulting Staff, Department of Plastic Surgery, Cosmetic Surgery Clinics of Laguna Beach
Arian Mowlavi, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Bradon J Wilhelmi, MD, Professor and Endowed Leonard J Weiner, MD, Chair of Plastic Surgery, Residency Program Director, University of Louisville School of Medicine
Bradon J Wilhelmi, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Hand Surgery, American Association of Clinical Anatomists, American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Society for Aesthetic Plastic Surgery, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Plastic Surgeons, Association for Surgical Education, Plastic Surgery Research Council, and Wound Healing Society
Disclosure: Nothing to disclose.

Medical Editor

Joseph E Sheppard, MD, Associate Professor of Clinical Orthopedic Surgery, Chief of Hand and Upper Extremity Service, Department of Orthopedic Surgery, University of Arizona Health Sciences Center, University Physicians Healthcare
Joseph E Sheppard, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Society for Surgery of the Hand, Clinical Orthopaedic Society, and Western Orthopaedic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

N Ake Nystrom, MD, PhD, Associate Professor of Orthopedic Surgery and Plastic Surgery, University of Nebraska Medical Center
Disclosure: Nothing to disclose.

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Harris Gellman, MD, Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami School of Medicine
Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society
Disclosure: Nothing to disclose.

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