Browse the corpus

420 SECTION 7: Cardiovascular Disease Arterial Occlusion David Carr Anna K. Nowacki INTRODUCTION AND EPIDEMIOLOGY Limb ischemia occurs when blood flow—and by extension, tissue perfusion—is limited enough to create symptoms; acute limb ischemia denotes rapid new event or a progression of a flow deficit, requiring recognition and rapid therapy for limb salvage. Critical limb ischemia is one end of the spectrum of peripheral arterial disease, when pain at rest, ulceration, or gangrene exists. Smoking and diabetes are the most important risk factors for peripheral arterial disease. 1 Additional risk factors include hyperlipidemia, hypertension, elevated blood homocys teine, and an elevated C-reactive protein level.2 The severity of peripheral arterial disease is linked to the risk of myocardial infarction, ischemic stroke, and death from vascular dis ease.3 The most frequently diseased arteries leading to limb ischemia are, in order of occurrence, the femoropopliteal, tibial, aortoiliac, and brachiocephalic vessels. Despite improvements in the management of peripheral arterial disease, current 1-year mortality after the onset of critical limb ischemia is 25%, and up to one quarter of survivors require amputation. 4,5 Over 200 million people are living with peripheral artery disease globally, with 70% of those in low- and middle-income countries. Between 2000 and 2010, the number of individuals with peripheral artery disease increased by nearly 30% in low- and middle-income countries and by 13% in high-income countries. 6 Data from the Global Burden of Disease projects show that on a global scale, there has been a significant increase in both disability and mortality associated with peripheral arterial dis ease, with a greater increase among women than among men. 7 In the United States, it is estimated that critical limb ischemia has an annual incidence of 0.35% and an average prevalence of 1.33%. This exceeds previous estimates and parallels the incremental increase in cardiovas cular risk factors. PATHOPHYSIOLOGY Acute limb ischemia results from a sudden decrease in blood supply to a limb, leading to tissue hypoperfusion and threatening limb viability. As time proceeds, cell death or irreversible tissue damage occurs. Without the presence of collateral vessels, peripheral nerves and skeletal muscle may suffer irreversible changes within 4 to 6 hours of vessel occlusion. Following restoration of blood flow, reperfusion injury can occur and may manifest as compartment syndrome, rhabdomyolysis, or metabolic derangements. Often, hyperkalemia, myoglobinemia, metabolic acidosis, and an elevation in creatine kinase level exist. The extent of reperfusion injury depends on the duration and location of the arte rial blockage, the amount of collateral flow, and the previous health of the involved limb. Approximately one third of all deaths from occlu sive arterial disease are secondary to metabolic complications after revascularization. Disorders that can lead to arterial occlusion are listed in Table 61-1.  THROMBOSIS Thrombotic occlusion is the most common cause of acute limb ischemia and can occur in native vessels and bypass grafts. In the lower limbs, thrombotic occlusion accounts for >80% of cases. 15 In the upper limbs, about half of all cases of acute limb ischemia are due to thrombosis, while about one third are due to embolism. 16 The clinical distinction between thrombosis and embolism in any given patient is not always clear.

ypass grafts. In the lower limbs, thrombotic occlusion accounts for >80% of cases. 15 In the upper limbs, about half of all cases of acute limb ischemia are due to thrombosis, while about one third are due to embolism. 16 The clinical distinction between thrombosis and embolism in any given patient is not always clear. Thrombosis most often occurs in the presence of atherosclero sis; due to the presence of collateral vasculature, thrombotic ischemia presents more gradually than an acute embolic event. However, it is also possible for plaque to embolize directly or to foster thrombus formation that embolizes and creates an acute high grade. Other than plaque rupture, progression of ischemic injury can occur by: (1) propagation of clot to occlude collateral vessels, (2) ischemiarelated distal edema leading to high compartment pressures (compart ment syndrome), (3) fragmentation of clot into the microcirculation, and (4) edema of the microvasculature cells. Large-vessel reperfusion may not resolve obstruction of the microvasculature. Uncommonly, arterial thrombosis develops in an apparently normal vessel without plaque; these patients should be evaluated for an under lying hypercoagulable condition. Subclinical vessel injury (from injec tions, catheters, or other mechanical events) or early atherosclerosis may still exist in these patients.  EMBOLISM Occlusion from embolism is less common than occlusion from thrombosis. The heart is the predominant source of peripheral emboli, with atrial fibrillation being responsible for most cases. Another cardiac source is a mural thrombus in the ventricle after recent myocardial infarction. Both atrial fibrillation and acute myocardial infarction predispose to poor cardiac wall motion and stagnant blood flow that promote clot formation. Patients with an acute myocardial infarction may develop a left ventricular thrombus as early as 24 hours and as late as 3 months after the event, with overall rates reported as about 3%, with anterior infarct thrombi rates as high as 9%. 17 Less common causes include emboli from mechanical valves, tumor emboli from atrial myxomas, vegetations from valve leaflets, and parts of prosthetic cardiac devices. Noncardiac sources of arterial emboli include thrombi from aneu rysms and atheromatous plaques. Mural thrombi in aneurysms of aor toiliac, femoral, popliteal, and subclavian arteries are the most notable sources. Atheroemboli consist of cholesterol-laden debris and platelet aggregates and result from plaque fragmentation that causes obstruction of the microcirculation, producing symptoms in the hands, feet (blue toe syndrome), or cerebral circulation (transient ischemic attack). Paradoxical embolization occurs when a venous clot passes from the right to the left side of the heart through an intracardiac shunt, most commonly a patent foramen ovale. An embolus may fragment and embolize distally, or it may propagate locally and create a larger clot. Emboli tend to lodge in places where vessels taper or branch, with the most common location in the leg being the bifurcation of the common femoral artery, followed by the popliteal artery. In the upper limb, the brachial artery is most commonly affected by an embolism.  OTHER CAUSES Intentional or accidental intra-arterial drug injections can result in local vasospasm, infectious arteritis, thrombosis, pseudoaneurysm, endocarditis, and mycotic aneurysm. Inert particles or drug crystals can embolize to obstruct end arteries, which can lead to gangrene of the digits. The prolonged use of vasopressor medications may result in arterial ischemia; when using these agents, observe closely for adequate extremity perfusion, particularly in patients with known preexisting vascular disease.

les or drug crystals can embolize to obstruct end arteries, which can lead to gangrene of the digits. The prolonged use of vasopressor medications may result in arterial ischemia; when using these agents, observe closely for adequate extremity perfusion, particularly in patients with known preexisting vascular disease. An aortic dissection can propagate into the subclavian or iliofemoral systems and present with neurologic dysfunction and/or extremity ischemia findings. The false lumen created by the dissection occludes flow in the involved artery. CLINICAL FEATURES Patients with acute limb ischemia exhibit one or more of the “six Ps”: pain, pallor, paralysis, pulselessness, paresthesias, and poikilother mia (for cold). A lack of one or more of these findings does not exclude ischemia. Pain alone may be the earliest symptom of ischemia, localized in the limb distal to the site of obstruction. Skin changes include pallor first, followed by blotchy and mottled areas of cyanosis, and then associated petechiae and blisters. Late find ings consist of skin and fat necrosis. CHAPTER Tintinalli_Sec07_p0329-0424.indd 420 8/2/19 6:43 PM

est symptom of ischemia, localized in the limb distal to the site of obstruction. Skin changes include pallor first, followed by blotchy and mottled areas of cyanosis, and then associated petechiae and blisters. Late find ings consist of skin and fat necrosis. CHAPTER Tintinalli_Sec07_p0329-0424.indd 420 8/2/19 6:43 PM CHAPTER 61: Arterial Occlusion 421 With vessel occlusion, severe and steady pain in the involved extremity associated with decreased skin temperature is common. Hypoesthe sia or hyperesthesia due to ischemic neuropathy is typically an early finding, as is muscle weakness. Two-point discrimination, vibratory sensation, and proprioception are often diminished prior to the loss of deep sensation. Absence of a palpable distal pulse is not a particularly helpful sign in a patient with long-standing vascular disease unless accompanied by skin changes compatible with acute arterial obstruc tion. An abrupt loss of a previously strong pulse is suggestive of acute embolization. Atheroemboli present clinically with several different areas of involvement, with pain and cyanosis in the involved digit, petechiae, and local muscle pain and tenderness at the site of infarction ( blue toe syndrome). Pulses are generally preserved, assuming they were present prior to the event. Table 61-1 notes symptoms of other related disorders. As ischemic injury progresses, anesthesia and paralysis become evi dent and foreshadow impending gangrene and the loss of limb viability. Preservation of light touch on skin testing is a good guide to tissue viability. A patient with an acute ischemic limb with signs of muscle paralysis, sensory loss, and prolonged ischemia has a limb that is likely nonviable. The Rutherford criteria (Table 61-2) provide a more formal prognostic stratification of the clinical stages of acute limb ischemia. Limb viability is dependent on the effectiveness of collateral circula tion, and no arbitrary time period can exclude treatment options despite the common belief that “treatment must occur in 4 to 6 hours. ”  ACUTE VERSUS CHRONIC ARTERIAL DISEASE Acute limb ischemia is defined as symptoms starting within a 2-week period. Pain over the distal forefoot waking the patient at night or TABLE 61-1 Disorders Associated With Acute Arterial Occlusion Disorder Cause Symptoms/Signs Management Thrombus Atherosclerosis or thrombosis of bypass grafts Intermittent claudication Medical first, then consider interventional Embolism Cardiac source: atrial fibrillation, rheumatic heart disease, mechanical valves, post–myocardial infarction thrombus, atrial myxomas, and leaflet vegetations/ endocarditis Sudden onset of territorial arterial symptoms Preventive anticoagulation, embolectomy Catheterization complication (brachial or femoral) Can occur during standard angioplasty, angiography, or arterial blood gas Expanding hematoma, pain, temperature and pulse changes Conservative vs.

nd leaflet vegetations/ endocarditis Sudden onset of territorial arterial symptoms Preventive anticoagulation, embolectomy Catheterization complication (brachial or femoral) Can occur during standard angioplasty, angiography, or arterial blood gas Expanding hematoma, pain, temperature and pulse changes Conservative vs. operative repair Trash foot or blue toe syndrome Cholesterol/platelet aggregate emboli Painful cyanotic discoloration of isolated portion of foot; remainder of the foot is warm Conservative therapy Vasculitis: rheumatoid arthritis, lupus, polyarteritis nodosa Autoimmune inflammation of small arteries Systemic symptoms and multiorgan ischemia Steroids, immunosuppressive agents Raynaud’s disease Vasospasm in small arteries or arterioles provoked by cold or stressors Local pain, pallor, cyanosis, numbness, paresthesias in hands usually resolving in 30–60 min Rewarming, medications: calcium channel blockers, α-blockers, vasodilators Takayasu’s arteritis Autoimmune vasculitis of aortic arch and branches Young Asian women: peripheral ischemia and necrosis leading to pulseless phase; may have fever, rash, muscle aches, arthritis Steroids, immunosuppressive agents Thromboangiitis obliterans (Buerger’s disease) Nonatherosclerotic segmental inflammation of small/medium vessels; typically, seen only in smokers Painful nodules, ulceration, and gangrenous digits in young adults (age 20–40 y) Smoking cessation HIV arteritis 10 Chronic inflammation of arteries associated with low CD4 counts Intermittent claudication Optimization of HIV management, angioplasty, or vein graft Hypothenar hammer syndrome Repeated trauma to the hypothenar area with hammering in laborers, as well as those using vibrational tools, causing narrowing of ulnar artery or aneurysmal degeneration Painful discoloration of one or more ulnar fingers with sparing of thumb Aspirin, nifedipine, intra-arterial fibrinolysis, interposition vein graft Popliteal artery entrapment (young males) and popliteal aneurysms (older males) Anatomic crowding of popliteal fossa with anomalous relationships between popliteal artery and surrounding muscle and fascia or luminal narrowing and thrombosis of aneurysm Pain in anterior aspect of lower one third of leg with exercise, reproducible with active ankle plantar flexion or passive dorsiflexion Surgical repair of popliteal fossa or aneurysm and grafting External iliac artery endofibrosis 12 External iliac artery fibrosis secondary to prolonged hip flexion Thigh pain and numbness in cyclists and triathletes: measure pre- and postcycling ankle-brachial indexes Surgical management or catheter dilatation Local arterial trauma 13,14 Penetrating or blunt damage to vessel Suspect in patients with knee dislocation or penetrating extremity trauma Surgical repair Shock-related arterial ischemia Low cardiac output states: congestive heart failure, sepsis, cardiogenic or hypovolemic shock Generalized hypoperfusion Resuscitation with fluids, blood products, vasopressors, inotropes; treat infection Thoracic aortic dissection False lumen of dissection occludes arteries Chest or back pain Surgical repair Abbreviation: HIV = human immunodeficiency virus (infection). Tintinalli_Sec07_p0329-0424.indd 421 8/2/19 6:43 PM

ed hypoperfusion Resuscitation with fluids, blood products, vasopressors, inotropes; treat infection Thoracic aortic dissection False lumen of dissection occludes arteries Chest or back pain Surgical repair Abbreviation: HIV = human immunodeficiency virus (infection). Tintinalli_Sec07_p0329-0424.indd 421 8/2/19 6:43 PM 422 SECTION 7: Cardiovascular Disease requiring the patient to hang his or her feet over the bed is suggestive of severe arterial occlusion and requires prompt consultation and treatment. In contrast to acute disease, chronic peripheral arterial disease has intermittent claudication, which may progress to intermittent ischemic pain at rest. Claudication is a cramp-like pain, ache, or tiredness that is brought on by exercise and relieved by rest, similarly to angina in the heart. It is reproducible, resolves within 2 to 5 minutes of rest, and recurs at consistent walking distances. Unlike claudication, the pain of acute limb ischemia is not relieved by rest or gravity, is not well localized, and can present as marked worsening of chronic pain. Classical teaching suggests that single-vessel disease in one of the segments noted in Table 61-3 may result in localized claudication, whereas multivessel disease results in less focal rest pain or tissue loss. Table 61-3 lists symptom sites of commonly compromised arteries.  OTHER DIAGNOSES THAT MIMIC ARTERIAL ISCHEMIA The pain of intermittent vascular claudication can be confused with other triggers ( Table 61-4) including spinal stenosis or lumbosacral radiculopathy. Other causes of extremity pains include chronic com partment syndrome, venous claudication, nerve root compression, Baker’s cyst, or foot, hip, or ankle arthritis. It is important to consider the following three steps in the differential diagnosis of acute limb ischemia: 1. Look for conditions mimicking acute limb ischemia. 2. Consider nonatherosclerotic causes of arterial occlusion. 3. If neither of the above exists, determine if the ischemia is caused by an arterial thrombus or embolus. DIAGNOSIS Obtain an adequate history, focusing on the timing and acuity of symptom onset, pattern of claudication, any previous revascularization or diagnosis of ischemia, and assessment of risk factors. Patients with known peripheral arterial disease or previous revascularization may have subacute symptoms due to the development of collateral vessels. A history of an abruptly ischemic limb in a patient with atrial fibrillation or recent myocardial infarction strongly suggests an embolus. Acute ischemia in the limb of a patient known to have advanced peripheral arterial disease is more likely due to thrombosis or a low cardiac output state. In patients without antecedent claudication and a normal uninvolved limb, embolic occlusion is likely (Table 61-5). On physical examination, look at the skin and palpate peripheral pulses of both extremities, comparing the less or unaffected and the affected limbs. Shiny, hyperpigmented skin with hair loss and ulceration, muscle atrophy, and poor pulses are the hallmarks of chronic peripheral arterial disease. Listen to the heart and abdomen, seeking bruits and murmurs. POCUS helps detect an abdominal aortic aneurysm. Use a hand-held Doppler US device over pulse areas to detect presence or absence of blood flow and the amplitude. Approximately 10% of patients have only one pedal or ankle pulse present secondary to an anatomic variation. If Doppler-detected blood flow is in the affected limb, measure the ankle-brachial index to assist in risk-stratifying the patient. The anklebrachial index is the ratio of the systolic blood pressure with the cuff just above the malleolus (with the Doppler probe over the posterior tibial or dorsalis pedis artery) to the highest brachial pressure in either arm.

ffected limb, measure the ankle-brachial index to assist in risk-stratifying the patient. The anklebrachial index is the ratio of the systolic blood pressure with the cuff just above the malleolus (with the Doppler probe over the posterior tibial or dorsalis pedis artery) to the highest brachial pressure in either arm. Patients with chronic peripheral arterial disease have an ankle-brachial index of <0.9, while values of <0.4 suggest severe disease. An anklebrachial index of >1.3 is likely secondary to a noncompressible vessel. In TABLE 61-2 Rutherford Criteria for Acute Limb Ischemia Findings Doppler Signals Category Description/Prognosis Sensory Loss Muscle Weakness Arterial Venous I. Viable Not immediately threatened None None Audible Audible II. Threatened a. Marginally b. Immediately Salvageable if promptly treated Salvageable with immediate revascularization Minimal (toes) or none More than toes, associated with rest pain None Mild, moderate Inaudible Inaudible Audible Audible III. Irreversible Major tissue loss or permanent nerve damage inevitable Profound, anesthetic Profound, paralysis (rigor) Inaudible Inaudible Source: Reproduced with permission from Rutherford RB, Baker JD, Ernst C, et al: Recommended standards for reports dealing with lower extremity ischemia: revised edition. J Vasc Surg 26: 517, 1997. TABLE 61-3 Artery-Specific Claudication Sites Artery Involved Claudication Site Iliac artery Buttocks, thigh, and sometimes calf (if bilateral, may cause impotence in men) Common femoral artery Thigh Superficial femoral artery Upper two thirds of calf Popliteal artery Lower one third of calf Infrapopliteal (tibial and peroneal) artery Foot TABLE 61-4 Differential Diagnosis of Acute Limb Ischemia *Conditions mimicking acute limb ischemia •  Systemic  shock (especially if associated with chronic occlusive disease) •  Phlegmasia  cerulea dolens •  Acute  compressive neuropathy Differential diagnosis for acute limb ischemia (other than acute peripheral arterial disease) •  Arterial  trauma •  Aortic/arterial  dissection •  Arteritis  with thrombosis (e.g., giant cell arteritis, thromboangiitis obliterans) •  HIV  arteriopathy •  Spontaneous  thrombosis associated with a hypercoagulable state •  Popliteal  adventitial cyst with thrombosis •  Popliteal  entrapment with thrombosis •  Vasospasm  with thrombosis (e.g., ergotism) •  Compartment  syndrome Acute Peripheral Arterial Disease •  Thrombosis  of an atherosclerotic stenosed artery •  Thrombosis  of an arterial bypass graft •   Embolism from heart, aneurysm, plaque or critical stenosis upstream (including cholesterol or atherothrombotic emboli secondary to endovascular procedures) •  Thrombosed  aneurysm with or without embolization *Two of the three conditions (deep vein thrombosis, neuropathy) that may mimic arterial occlusion should be expected to have arterial pulses, except if occult chronic peripheral arterial disease existed prior to the acute event. Low cardiac output makes the chronic arterial ischemia more manifest in terms of symptoms and physical findings. Source: Reproduced with permission from Norgren L, Hiatt WR, Dormandy JA, et al: Inter-society consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg 45: S5A, 2007. Abbreviation: HIV = human immunodeficiency virus. Tintinalli_Sec07_p0329-0424.indd 422 8/2/19 6:43 PM

ms and physical findings. Source: Reproduced with permission from Norgren L, Hiatt WR, Dormandy JA, et al: Inter-society consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg 45: S5A, 2007. Abbreviation: HIV = human immunodeficiency virus. Tintinalli_Sec07_p0329-0424.indd 422 8/2/19 6:43 PM CHAPTER 61: Arterial Occlusion 423 such cases, do more detailed pressure measurements like a toe-brachial pressure using specialized equipment. (See Video: Ankle Brachial Index)  LABORATORY EVALUATION Aside from seeking markers of cellular ischemia or injury (e.g., cre atine kinase, myoglobin, and serum lactate), assess the metabolic status (electrolytes and glucose), renal function (BUN and creatinine plus urinalysis), potential anemia and infection (CBC), and bleeding tendency (prothrombin and partial thromboplastin times). Levels of cardiac injury markers and ECG may identify triggers including infarction or rhythm change.  IMAGING Acute critical limb ischemia is a time-sensitive diagnosis; once sus pected, consult a surgeon as soon as possible, even while obtaining diagnostic imaging. Duplex US is very accurate for detecting complete or incomplete arterial obstruction. Sensitivity declines for localization of thromboembolic occlusion at or below the calf level. Emergency physi cian–performed POCUS focusing on the aorta, iliac vessels, and femoral artery bifurcation may localize emboli or thromboses, expediting diag nosis and management. 18 Transthoracic cardiac echocardiography can help detect embolic sources, and transesophageal approaches add the ability to detect aortic root pathology. Arteriography often occurs in the operating room or intervention lab just prior to direct therapy. CT with contrast is the most readily available study in the ED, and it has a sensitivity similar to that of conventional uniplanar contrast studies in large vessels. MRI has higher sensitivity and specificity than CT angiography but is less readily available. The selection of most timely and appropriate imaging technique is best a joint decision between the ED physician, vascular surgeon, and/or interventional radiologist. TREATMENT The objectives of therapy for acute arterial obstruction are restoration of blood flow to preserve limb and life and prevention of recurrent thrombosis or embolism (Table 61-6). In the ED, IV unfractionated heparin (weight-based 80 units/kg bolus followed by an infusion of 18 units/kg/h) is the initial therapy of choice. It prevents clot extension, recurrent embolization, venous thrombosis, microthrombi distal to the obstruction, and reocclusion after reperfusion. 19,20 Direct thrombin inhibitors, such as lepirudin or argatroban, are an alternative treatment option when heparin-induced thrombocytopenia with thrombosis is of concern. 19,21 Aspirin (325 milligrams in naive patients) may enhance clot reduction through antiplatelet actions. Pain management and optimization of limb perfusion by treating lowflow states such as heart failure are also important steps in care. Stratifying patients with acute limb ischemia by Rutherford criteria (Table 61-2) in conjunction with early surgical consultation guides ini tial care. Patients with stage I and stage IIa limb ischemia may undergo diagnostic imaging workup prior to more definitive treatments. Patients with stage IIb ischemia often require immediate revascularization without additional prior diagnostic imaging. Patients with stage III ischemia have irreversible damage and likely require amputation. The vascular surgeon will determine definitive treatment, which can include catheterdirected thrombolysis, percutaneous mechanical thromboembolectomy, revision of an occluded bypass graft, and revascularization with either percutaneous transluminal angioplasty or standard surgery.

damage and likely require amputation. The vascular surgeon will determine definitive treatment, which can include catheterdirected thrombolysis, percutaneous mechanical thromboembolectomy, revision of an occluded bypass graft, and revascularization with either percutaneous transluminal angioplasty or standard surgery. 2,18 Catheterdirected intra-arterial thrombolysis is more common now than systemic IV thrombolysis for peripheral artery embolic or thrombotic disease. 19,20 In a subacute thrombotic occlusion with a well-developed collateral blood supply, medical management is common. The longer-term nonsurgical management of peripheral arterial disease focuses on the combination of smoking cessation, structured exercise, and pharmacotherapy. Antiplatelet therapy with either aspirin (75 to 100 milligrams daily) or clopidogrel (75 milligrams daily) can reduce mortality from cardiovascular causes in patients with peripheral arterial disease. Dual antiplatelet therapy is not initially recommended. The American College of Cardiology/American Heart Association 2016 guidelines include cilostazol, a phosphodiesterase inhibitor, as a Class I recommendation for the treatment of intermittent claudication. Pentoxifylline is no longer recommended. 19,20 A multidisciplinary approach including a team of specialists, wound care experts, and nutritionists helps to decrease morbidity and improve long-term outcome. DISPOSITION AND FOLLOW-UP Patients with acute or worsening chronic ischemia require observation, hospital admission, or immediate transfer to a center with vascular surgery capability. Patients with chronic peripheral arterial disease without an immediate threat to limb viability absent other acute illness can be discharged home to follow up with a vascular surgeon or primary care physician. Instruct patients to return immediately for worsening of symptoms (especially pain) and to start aspirin (81 milligrams daily after first dose of 325 milligrams if there are no contraindications). SPECIAL CONSIDERATIONS  UPPER EXTREMITY ISCHEMIA Acute arterial occlusion in the upper extremities is much less common than in the lower limbs. Due to well-developed collateral circulation around the shoulder and elbow, ischemia here is better tolerated, with ischemic pain at rest and gangrene rare absent distal embolization. Causes of upper limb ischemia include vasospasm, arteritis, trauma, atherosclerotic plaque rupture, embolism, iatrogenic injury (e.g., dur ing brachial artery access for cardiac catheterization), thoracic out let syndromes, aneurysms, and hypercoagulable states. After clinical examination, investigate with segmental blood pressure measurements above and below the elbow, Doppler evaluation, duplex US, and arteriography. Treatment of acute limb-threatening ischemia of the hand and forearm includes heparin (Table 61-6) and emergent surgical thromboembolectomy. REFERENCES The complete reference list is available online at www.TintinalliEM.com.

ssure measurements above and below the elbow, Doppler evaluation, duplex US, and arteriography. Treatment of acute limb-threatening ischemia of the hand and forearm includes heparin (Table 61-6) and emergent surgical thromboembolectomy. REFERENCES The complete reference list is available online at www.TintinalliEM.com. TABLE 61-5 Embolic Versus Thrombotic Occlusion Factor Embolism Thrombosis History of claudication No Yes Physical examination Normal contralateral limb Marked signs of occlusive arterial disease bilaterally Source identified Often None Timing Sudden, exact time known More gradual Radiologic features Sudden abrupt cutoff in blood flow with no collateral circulation and minimal diseased vessel Widespread disease with collaterals present and gradual narrowing of blood flow seen TABLE 61-6 ED Medical Therapy for Acute Limb Ischemia Intervention Comments Unfractionated heparin19 80 units/kg IV bolus followed by infusion of 18 units/kg/h Antiplatelet therapy19 Aspirin 325 milligrams PO first dose or clopidogrel 75 milligrams if patient is allergic to aspirin Pain control As needed for patient comfort and cooperation Optimize perfusion Treat low-flow states and shock Place extremity in dependent position Environment protection Protect ischemic limb from temperature extremes Tintinalli_Sec07_p0329-0424.indd 423 8/2/19 6:43 PM Tintinalli_Sec07_p0329-0424.indd 424 8/2/19 6:43 PM