Vascular Occlusive Syndromes of the Upper Extremity 

Updated: Oct 03, 2019
Author: Bradon J Wilhelmi, MD; Chief Editor: Harris Gellman, MD 

Overview

Background

Although upper-extremity vascular disorders are less common than lower-extremity disorders, they nonetheless affect approximately 10% of the population. Causes of vascular compromise include the following:

  • Acute trauma
  • Chronic conditions, such as repetitive microtrauma
  • Systemic diseases involving metabolic processes, autoimmune processes, or both

General symptoms following vascular compromise include the following:

  • Dysesthesias
  • Paresthesias
  • Pallor
  • Cold intolerance
  • 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.

It is of the 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.

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 to a lesser degree by the deep palmar arch, a continuation of the radial artery. Minor blood supply to the hand is provided 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 four terminal arteries to the thumb are the ulnar and radial palmar arteries and the ulnar and radial dorsal arteries. Vessels have been categorized arbitrarily on the basis of their diameter, with macrovessels measuring 100 μm or greater in diameter and microvessels measuring less than 100 μm.

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.

Pathophysiology

Multiple factors determine vascular flow, including the following:

  • Environmental events
  • Metabolic demands
  • Sympathetic nervous tone
  • 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.

Considerable interest has been focused on the effect of endothelium on vascular tone, because of its capacity to produce two 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, because the sympathetic system of the adventitia will have been disrupted.

Etiology

Causes of vascular compromise include the following:

  • Acute trauma
  • Chronic modalities, such as repetitive microtrauma
  • Systemic disease processes involving metabolic or autoimmune processes

Epidemiology

Patient age influences the propensity for vascular occlusive disorders. Raynaud disease affects women aged 30-50 years. Males are affected bimodally, with different disorders being prominent in young males as opposed to middle-aged men. 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 men who are employed in manual-type labor. In the latter case, the labor usually involves handheld vibrating tools that cause chronic trauma.

The onset of vascular occlusive disorders is affected by the sex of the patient. As noted, Raynaud disease affects women aged 30-50 years, whereas males are affected in a bimodal fashion. 

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

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. Thus, 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.

 

Presentation

History

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.

Patient evaluation for suspected vascular pathology should include eliciting detailed descriptions of the following:

  • Trauma mechanism (penetrating or nonpenetrating)
  • Exposure to repetitive insults
  • History of familial or blood disorders
  • Drug or tobacco use
  • 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 Examination

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
  • Quality of pulses
  • Presence of masses, bruits, or both

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).

Complications

Acute trauma with ensuing vascular compromise of distal extremity tissue must be treated on an emergency basis to minimize distal tissue loss. Partial vascular compromise left untreated may result in muscular fibrosis and contractures of varying severity. Without vascular supply, the involved limb may be lost within hours.

More often, partial vascular compromise is left untreated, in which case the patient may develop an intrinsic plus hand deformity associated with intrinsic muscle contraction. Signs of intrinsic contracture include metacarpophalangeal (MCP) joint flexion and interphalangeal (IP) joint extension; passive hyperextension of the MCP joint decreases active flexion capacity of IP 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 an 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 dysmotility, sclerodactyly, 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 IP (PIP) joints, with secondary extension contracture of MCP joints. Ulcers may develop over PIP joints, secondary to ischemia, pressure, minor trauma, or a combination of factors.

 

DDx

 

Workup

Imaging Studies

Handheld Doppler ultrasonography (US) 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 delineation of venous versus arterial pulses.

B-mode Doppler US allows 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.

Color duplex images are useful for evaluating masses and for differentiating ganglia, aneurysms, and pseudoaneurysms.

Radionuclide imaging can be used to obtain a two-dimensional (2D) 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 three serial images are taken. The first image is similar to an angiogram, the second involves serial pictures obtained over a 1.5-minute period that are used to assess blood pooling and flow dynamics, and the third mimics a bone scan.

This modality allows evaluation of vaso-occlusive diseases, such as aneurysms, as well as vasospastic diseases. It has also 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. With the aid of 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.[1, 2]

High-resolution magnetic resonance angiography (MRA) allows visualization of arterial and venous structures.[3, 4, 5] The advantage of MRA is that it provides vivid images without the need for arterial vascular access and without patient exposure to ionizing radiation or potentially allergy-inducing contrast dyes.

In a study reviewing the use of multidetector computed tomographic angiography (MDCTA) in the assessment of combat casualties with vascular injuries, White et al 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.[6] They concluded that MDCTA is a reliable and promising alternative to traditional arteriography for evaluating clinically occult vascular trauma.

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

Digital plethysmography allows assessment of digital volume changes over time. Serial volume-change patterns can be used to differentiate vasospastic from vaso-occlusive disease. Qualified vascular technicians are required for these 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 lower than 0.7 indicate inadequate blood perfusion of end organs and encourage intervention.

Digital plethysmography is a valuable and reliable tool for assessing the severity of vasospasm, either in isolation or as part of a combined occlusive/vasospastic disorder (eg, scleroderma). The technique is also particularly valuable as a tool for objectifying cold-induced vasospasm in vibration-induced white finger syndrome (VWFS) secondary to chronic hand vibrations.

Skin surface temperatures can be used to estimate digital perfusion.[7] This modality, however, is only reliable for physiologic temperatures within the range of 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 1-2°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 the following:

  • Repetitive trauma
  • Atherosclerosis
  • Proximal embolic events
  • Systemic diseases, such as collagen vascular disease and vasculitis

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 on the basis of the history and the presence of a pulsatile mass in 10% of patients or on the basis of findings from Doppler ultrasonography (US) or angiography of the upper extremity.

Treatment of chronic vascular occlusive diseases involves administration of thrombolytic agents 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. Good long-term results have been reported after surgical intervention for symptomatic hypothenar hammer syndrome.[8]

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.

The diagnosis can be 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 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.[9]

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 after intraluminal injury that leads to uniform and gradual dilatation of the vessel wall. This is in contrast to a pseudoaneurysm, which develops after penetrating injury of the vessel wall, leading to a saclike outpatching 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 by means of Doppler US, 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, 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 (PIP) joints with secondary extension contracture of the metacarpophalangeal (MCP) joints. Ulcers develop over the PIP joints secondary to ischemia, pressure, minor trauma, or a combination of factors.[10]

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.[11] Avoiding exposure to cold by wearing protective garments, including hand warmers, is an important first-line measure. 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. In 2014, a 12-member international committee developed a three-step approach for the diagnosis of this phenomenon, along with five additional criteria for the diagnosis of primary Raynaud phenomenon.[12]

Management of Raynaud phenomenon 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 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 PIP 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, thromboangiitis obliterans (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 (ESR) values. Treatment involves systemic steroids.

Thromboangiitis obliterans (Buerger disease) 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 cold exposure 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 proved efficacious.

In considering digital-vessel bypass surgery, it is important to take digital-vessel diameters into account. 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, whereas 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, because 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 MCP joint flexion and interphalangeal (IP) joint extension; passive hyperextension of the MCP joint decreases active and passive flexion capacity of the IP 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 digital brachial index (DBI) may be obtained to assess perfusion after arterial injury, and a Stryker needle can be used to monitor intracompartmental pressures after crush injuries. Digital pulse oximetry is helpful as well.

In all suspected vascular injuries that are treated conservatively, close monitoring is necessary. For example, after high-energy gunshot wounds with arterial contusion, thrombosis and progressive ischemia are not uncommon with 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 revascularization is not absolutely indicated, it 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. The thrombosis rate after 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. In the setting of such injury, the risk of compartment syndrome is increased in cases of combined arterial injuries, combined nerve injuries, motor deficits, fractures, and increased intraoperative blood loss.[13]

Similarly, injury to the radial artery is observed in 23% of patients after repeated measurement of arterial blood gases. Such injuries may result in pseudoaneurysm formation, creation of an arteriovenous fistula, or acute thrombosis with distal embolization. Because of the growth in the use of the transradial approach for catheter-based interventions, vascular complications involving the radial artery are becoming increasingly common.[14]  

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 US 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 achieved through extension of the traumatic laceration both proximally and distally. After débridement of necrotic tissue, vital structures must be identified and tagged both proximally and distally before 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 after mobilization. Vessel mobilization can be optimized by ligating nonessential branches. Donor-site venous grafts depend on the caliber of the injured vessel and can include the following:

  • Superficial veins of the dorsum of the hand
  • Superficial veins of the arm, such as the cephalic and basilic veins or their terminal branches
  • Harvests taken from the lower leg, such as the distal saphenous vein or its terminal branches

After surgical repair and before release of vascular clamps, systemic heparin (3000-5000 U) is administered. Postoperatively, only aspirin (325 mg/day PO) administration is recommended unless intraoperative anastomotic complications are encountered, 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.

Venous repair, though not regularly required, 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 one draining vein (though two are preferred) and can be provided with reconstruction of a combination of the following: cephalic vein, basilic vein, and venae comitantes.

Venous insufficiency can be detected following appropriate arterial inflow and presents with gradual distention and a bluish appearance of the distal extremity. For 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

Medication Summary

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/day 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] in the range of 50-80 s). Dipyridamole is an appropriate alternative to aspirin and has a similar platelet mode of action.

After 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), 100 mg IV over 2 hours, or streptokinase, 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 on the basis of 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, 100 mg IV over 2 hours, or streptokinase, 1.5 million U IV over 1 hour) 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 in the range of 50-80 s) followed by 3 months of warfarin PO therapy (titrated to keep prothrombin time [PT] in the range of 2-3 s).

Thrombolytic therapy can be attempted if anticoagulation does not improve symptoms acutely (t-PA, 100 mg IV over 2 hours, or streptokinase, 1.5 million U IV over 1 hour). 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, 60 mg PO every 12 hours, or verapamil, 150 mg PO at bedtime.

Anticoagulants

Class Summary

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.

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.

Thrombolytics

Class Summary

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.

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.

Antiarrhythmics

Class Summary

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.

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.

Antiplatelet agents

Class Summary

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.

Salicylates

Class Summary

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.