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Lower Extremity Acute Ischemia Clinical Manifestations Acute lower extremity ischemia manifests with the "five Ps":

pain, pallor (Fig. 22-61), paresthesias, paralysis, and pulselessness, to which some add a sixth "P"poikilothermia or "perishing cold." Pain, however, is what causes a patient to present to the emergency room. The most common location for an embolus to lodge in the leg is at the common femoral bifurcation. Typically a patient will complain of foot and calf pain. In addition to absent pulses, there is a variable diminution of sensation, which varies from a mild reduction in sensation compared to the contralateral side to being completely insensate. Inability to move the affected muscle group is a sign of very severe ischemia and necessitates urgent revascularization. During evaluation of the affected extremity it is important to compare findings with the contralateral limb. Clinical evaluation is extremely important in determining the etiology and location of the obstruction. One of the most important pieces of information to obtain is whether the patient has had prior vascular procedures or if there is a history of lower extremity claudication. Either of these features suggests pre-existing vascular disease, renders revascularization more complicated, and usually mandates angiography to permit surgical planning. On the contrary, in a patient with no history suggestive of prior vascular disease, the etiology is most likely embolic and simple thrombectomy is more likely to be successful. FIG. 22-61.

Typical pallor in an acutely ischemic limb. Absent bilateral femoral pulses in a patient with bilateral lower extremity ischemia is most likely due to saddle embolus to the aortic bifurcation. A palpable femoral pulse and absent popliteal and distal pulses may either be due to distal common femoral embolus (the pulse being palpable above the level of occlusion) or embolus to the superficial femoral or popliteal arteries. Typically, emboli lodge at bifurcations where there are sudden changes in arterial diameter. A popliteal trifurcation embolus will present with calf ischemia and absent pedal pulses, possibly with a popliteal pulse present. The finding of palpable contralateral pulses in the absence of ipsilateral pulses in the ischemic leg is suggestive of an embolus, even if Doppler signals are present. Arteriography is not necessary in the patient with no history suggestive of vascular disease; nevertheless, all patients should be positioned on the operating room table in such a way that fluoroscopic access to the entire inflow and outflow tract is achievable if necessary. In an era when most vascular surgeons have endovascular capability, it is unacceptable to be unable to easily switch to a catheter-based approach should it become necessary. Medical Therapy

In the absence of any significant contraindication, the patient with an ischemic lower extremity should be immediately anticoagulated. This will prevent propagation of the clot into unaffected vascular beds. Intravenous fluid should be started and a Foley catheter inserted to monitor urine output. Baseline labs should be obtained and creatinine levels noted. Surgery The abdomen, contralateral groin, and entire lower extremity are prepped in the field. The groin is opened through a vertical incision, exposing the common femoral artery and its bifurcation. Frequently, the location of the embolus at the femoral bifurcation is readily apparent by the presence of a palpable proximal femoral pulse, which disappears distally. The artery is clamped and opened transversely over the bifurcation. Thrombus is extracted by passing a Fogarty balloon embolectomy catheter (Fig. 22-62). Good back-bleeding and antegrade bleeding suggest that the entire clot has been removed (Fig. 22-63). Embolic material often forms a cast of the vessel and is sent for culture and histologic examination. Completion angiography is advisable. The artery is then closed and the patient fully anticoagulated. FIG. 22-62.

Fogarty balloon embolectomy catheter. FIG. 22-63.

Technique for removal of thrombus using balloon catheter. When an embolus lodges in the popliteal artery, in most cases it can be extracted via a femoral incision using the techniques previously described. A femoral approach is preferred because the larger arterial size results in a lessened likelihood of arterial compromise when the artery is closed. The disadvantage is that the embolectomy catheter cannot be specifically directed into each of the infrapopliteal arteries. This can be achieved from the groin using fluoroscopic imaging and an over-the-wire thrombectomy catheter, which can be specifically directed into each of the infrapopliteal vessels. Otherwise, a separate incision exposing the popliteal bifurcation may be necessary to ensure completeness of thrombectomy. In the postoperative period it is important to seek the source of the embolus using echocardiography and CT scanning of the descending thoracic and abdominal aorta. A transthoracic or transesophageal echocardiogram should be performed looking for a cardiac source. An electrocardiogram (ECG) will diagnose atrial fibrillation. More unusual sources

include mural thrombus from an aortic aneurysm; occasionally idiopathic arterial-to-arterial thrombus occurs, usually from thrombus that has formed on a grossly normal descending thoracic aorta. The aortic arch may also be a source of embolus from severe atheroma. The presence of mobile plaque on transesophageal echocardiography (TEE) is suggestive of this source. Paradoxical embolus occurs when a patient has a patent foramen ovale and an embolus from a deep venous thrombosis (DVT) crosses through the atrial defect into the left side of the heart and passes into the peripheral circulation. This is diagnosed using a technique termed bubble echocardiography, in which air bubbles introduced into the venous circulation can be seen traversing the septal defect. A more complex situation arises when a patient has pre-existing peripheral vascular disease and in situ thrombosis on top of pre-existing atheroma; frequently embolectomy catheters will not pass through these occlusions. Similarly, when a bypass graft fails, it is usually either due to progression of atheroma proximal or distal to the graft, or to intrinsic stenoses that develop within a vein graft. These are the more complex situations in which to revascularize the limb. There are essentially two options: surgical bypass or catheter-based lytic therapy. Angiography is necessary in both situations to determine the extent of the occlusion and to search for inflow and distal outflow vessels to which a bypass graft could be attached. Although the surgeon's preference tends to predominate in the approach to the ischemic limb, both approaches have been demonstrated to be fairly equivalent in terms of limb salvage. Criteria for selecting the appropriate approach are based on the presence or absence of good target vessels and availability of a suitable bypass conduit. If there are good distal vesselsusually inflow vessels are adequate or can be made adequateand a good saphenous vein is available, surgical bypass is recommended, as it is fast and reliable. In the absence of a good distal target, absent saphenous vein, or in a patient at high risk for surgery, lysis is recommended. Lysis Prior to lysis, a wire traversal test is performed by puncturing the contralateral femoral artery and advancing a wire over the bifurcation and down the native vessels or occluded graft in the contralateral limb. The degree of ease with which the wire is passed suggests fresh thrombus and is predictive of good results from lysis. A special catheter that allows a lytic agent to be sprayed into the clot along the length of the occlusion is inserted over the wire and lysis is begun. The agents most commonly used are urokinase and tissue plasminogen activator (t-PA). Lysis times are variable, ranging from 12 to 36 hours, and generally, the longer the lysis, the greater the risk of bleeding complications. Once the clot has been dissolved, underlying stenoses, which are predisposed to secondary thrombosis, are treated with balloon angioplasty, stenting, or bypass, as appropriate. The principal risk of lysis is bleeding. Lytic agents are absolutely contraindicated in patients with intracranial surgery, intracranial hemorrhage within the last 3 months, or in the presence of any active bleeding. Most bleeding complications occur at the arterial puncture sites, but concealed retroperitoneal bleeding is possible. Rarely, patients can sustain intracerebral hemorrhage, which can be fatal or disabling. Complications of Reperfusion of the Ischemic Limb

Reperfusion of the ischemic limb is variable in its physiologic effects, which directly relates to the severity and extent of the ischemia. Patients with a saddle embolus of the aortic bifurcation and severely ischemic limbs may sustain the full-blown "reperfusion syndrome." At the other end of the spectrum, patients with minimal muscle ischemia who are rapidly reperfused may have essentially no effects. However, many of these patients have severe underlying cardiac disease and poorly tolerate even short ischemic periods. Complications occurring after revascularization of the lower extremity and causes of recurrent thrombosis are listed in Tables 22-9 and 22-10. Therapy is directed toward forced alkaline diuresis by adding bicarbonate to the intravenous fluid. Alkalinization increases the solubility of myoglobin in the urine, preventing it from crystallizing in the tubules, which is what promotes acute renal failure. Table 22-9 Complications of Revascularization

Reperfusion syndrome Hypotension Hyperkalemia Myoglobinuria Renal failure Compartment syndrome Ischemic neuropathy Muscle necrosis Recurrent thrombosis Table 22-10 Causes of Recurrent Thrombosis

Recurrent embolization Inadequate thrombus removal Arterial injury from thrombectomy catheter Failure to treat critical lesion-causing thrombosis Extensive muscle edema precluding distal flow Underlying hypercoagulable state Technical problem with bypass graft/arteriotomy closure Buerger's Disease (Thromboangiitis Obliterans) Buerger's disease, also known as thromboangiitis obliterans, is a progressive nonatherosclerotic segmental inflammatory disease that most often affects small and medium-sized arteries, veins,

and nerves of the upper and lower extremities. 197 The clinical and pathologic findings of this disease entity were published in 1908 by Leo Buerger in a description of 11 amputated limbs. 198 The typical age range for occurrence is 20 to 50 years, and the disorder is more frequently found in males who smoke. The upper extremities may be involved, and a migratory superficial phlebitis may be present in up to 16% of patients, thus indicating a systemic inflammatory response. 199 In young adults presenting to the Mayo Clinic (19531981) with lower limb ischemia, Buerger's disease was diagnosed in 24%. 200 Conversely, the diagnosis was made in 9% of patients with ischemic finger ulcerations. The cause of thromboangiitis obliterans is unknown; however, use of or exposure to tobacco is essential to both the diagnosis and progression of the disease. Pathologically, thrombosis occurs in small to medium size arteries and veins with associated dense polymorphonuclear leukocyte aggregation, microabscesses, and multinucleated giant cells. The chronic phase of the disease shows a decrease in the hypercellularity and frequent recanalization of the vessel lumen. 201 End-stage lesions demonstrate organized thrombus and blood vessel fibrosis. Although the disease is common in Asia, North American males do not appear to have any particular predisposition, as the diagnosis is made in less than 1% of patients with severe limb ischemia. Buerger's disease typically presents in young male smokers, with symptoms beginning prior to age 40. Patients initially present with foot, leg, arm, or hand claudication, which may be mistaken for joint or neuromuscular problems. Progression of the disease leads to calf claudication and eventually ischemic rest pain and ulcerations on the toes, feet, or fingers. A complete history should exclude diabetes, hyperlipidemia, or autoimmune disease as possible etiologies for the occlusive lesions. Because it is likely that multiple limbs are involved, angiography should be performed of all four limbs. Even if symptoms are not yet present in a limb, angiographic findings may be demonstrated. Characteristic angiographic findings show disease confinement to the distal circulation, usually infrapopliteal and distal to the brachial artery. The occlusions are segmental and show "skip" lesions with extensive collateralization, the so-called "corkscrew collaterals." The treatment of thromboangiitis obliterans revolves around strict smoking cessation. In patients who are able to abstain, disease remission is impressive and amputation avoidance is increased. In the experience reported from Oregon Health Sciences Center, no disease progression with associated tissue loss occurred after discontinuation of tobacco. The role of surgical intervention is minimal in Buerger's disease, as there is often no acceptable target vessel for bypass. Furthermore, autogenous vein conduits are limited secondary to coexisting migratory thrombophlebitis. Mills and associates reported their results of 31% limb loss in 26 patients over 15 years, thus authenticating the virulence of Buerger's disease involving the lower extremities. 202 In addition, others have described a significant discrepancy in limb loss in patients that continued to smoke versus those who discontinued tobacco use (35 versus 67%). 203

Thromboangiitis obliterans
From Wikipedia, the free encyclopedia

Buerger's disease

Classification and external resources

Complete occlusion of the right and stenosis of the left femoral artery as seen in a case of thromboangiitis obliterans

ICD-10

I73.1

ICD-9

443.1

OMIM

211480

DiseasesDB

1762

MedlinePlus

000172

eMedicine

med/253

MeSH

C14.907.137.870

Not to be confused with Berger's disease (IgA nephropathy) Thromboangiitis obliterans (also known as Buerger's disease) is a recurring progressiveinflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet. It is strongly associated with use of tobacco products,[1] primarily from smoking, but also from smokeless tobacco.
Contents
[hide]

1 Signs and symptoms 2 Diagnosis 3 Pathophysiology 4 Prevention 5 Treatment 6 Prognosis 7 Epidemiology 8 History 9 Notes 10 References 11 External links

[edit]Signs

and symptoms

There is a recurrent acute and chronic inflammation and thrombosis of arteries and veins of the hands and feet. The main symptom is pain in the affected areas. Ulcerations andgangrene in the extremities are common complications, often resulting in the need foramputation of the involved extremity. This disease was first reported by Leo Buerger in 1908, who described a disease in which the characteristic pathologic findings acute inflammation and thrombosis (clotting) of arteries and veins affected the hands and feet. Another name for Buergers disease is thromboangiitis obliterans.

[edit]Diagnosis A concrete diagnosis of thromboangiitis obliterans is often difficult as it relies heavily on exclusion of other conditions. The commonly followed diagnostic criteria are outlined below although the criteria tend to differ slightly from author to author. Olin (2000) proposes the following criteria: [2]

1.

Typically between 2040 years old and male, although recently females have been diagnosed.

2. 3.

Current (or recent) history of tobacco use Presence of distal extremity ischemia (indicated by claudication, pain at rest, ischemic ulcers or gangrene) documented by noninvasive vascular testing such as ultrasound

4.

Exclusion of other autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory tests.

5.

Exclusion of a proximal source of emboli by echocardiography and arteriography

6.

Consistent arteriographic findings in the clinically involved and noninvolved limbs.

Buergers disease can be mimicked by a wide variety of other diseases that cause diminished blood flow to the extremities. These other disorders must be ruled out with an aggressive evaluation, because their treatments differ substantially from that of Buergers disease. For Buergers there is no treatment known to be effective. Diseases with which Buergers disease may be confused include atherosclerosis (build-up of cholesterol plaques in the arteries), endocarditis (an infection of the lining of the heart), other types of vasculitis, severe Raynauds phenomenon associated with connective tissue disorders (e.g., lupus or scleroderma), clotting disorders of the blood, and others. Angiograms of the upper and lower extremities can be helpful in making the diagnosis of Buergers disease. In the proper clinical setting, certain angiographic findings are diagnostic of Buergers. These findings include a corkscrew appearance of arteries that result from vascular damage, particularly the arteries in the region of the wrists and ankles. Angiograms may also show occlusions (blockages) or stenosis (narrowings) in multiple areas of both the arms and legs. The changes are particularly

apparent in the blood vessels in the lower right hand portion of the picture (the ulnar artery distribution). To rule out other forms of vasculitis (by excluding involvement of vascular regions atypical for Buergers), it is sometimes necessary to perform angiograms of other body regions (e.g., a mesenteric angiogram). Skin biopsies of affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well. [edit]Pathophysiology There are characteristic pathologic findings of acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet (the lower limbs being more common). The mechanisms underlying Buerger's disease are still largely unknown. It is suspected thatimmunological reactions play a role. The association of Buergers disease with tobacco use, particularly cigarette smoking, cannot be overemphasized. Most patients with Buergers are regular smokers, but some cases occur in patients who only smoke moderately; others have been reported in users of smokeless tobacco. It has been postulated that Buergers disease is an autoimmune reaction (one in which the bodys immune system attacks the bodys own tissues) triggered by some constituent of tobacco. [edit]Prevention The cause of the disease is unknown but thought to be autoimmune in nature and heavily linked to tobacco use in patients with Buerger's as primary disease. There have also been links to persons with digestive disorders. [edit] Treatment Smoking cessation has shown to slow the progression of the disease and decrease the severity of amputation in most patients, but does not halt the progression. Vascular surgery can sometimes be helpful in treating limbs with poor perfusion secondary to this disease. Use of vascular growth factor and stem cell injections have been showing promise in clinical studies. Streptokinase has been proposed as adjuvant therapy in some cases.[3]

In addition Limaprost, an oral PGE1 derivative, has shown efficacy in one published randomized trial.[4] [edit]Prognosis Buerger's is not immediately fatal, but it is life-shortening. Amputation is common and major amputations (of limbs rather than fingers/toes) are almost twice as common in patients who continue to smoke. Death rate has not been consistently shown as higher in patients who do not cease smoking but for this and other health concerns quitting is highly recommended. Female patients tend to show much higher longevity rates than men. Despite the clear presence of inflammation in this disorder, anti-inflammatory agents such as corticosteroids have not been shown to be beneficial in healing, but do have significant anti-inflammatory and pain relief qualities in low dosage intermittent form. Similarly, strategies of anticoagulation (thinning of the blood with aspirin or other agents to prevent clots) have not proven effective. The only way to slow the progression of the disease is to abstain from all tobacco products. [edit]Epidemiology Buerger's is more common among men than women. It is more common in , Japan, India, and Manipur along the "old silk route" than in the United States and Europe. The disease is most common among South Asians. [edit]History Buerger's disease was first reported by Felix von Winiwarter in 1879 in Austria. [5] It wasn't until 1908, however, that the disease was given its first accurate pathological description, by Leo Buerger at Mount Sinai Hospital in New York City.[6] Buerger called it "presenile spontaneous gangrene" after studying amputations in 11 patients. As reported by Alan Michie in God Save The Queen, published in 1952 (see pages 194 and following), King George VI was diagnosed with the disease in late 1948 and early 1949. Both legs were affected, the right more seriously than the left. The King's doctors prescribed complete rest and electric treatment to stimulate circulation, but either unaware of the connection between the disease and smoking (the King was a heavy smoker) or unable to persuade the King to stop smoking, the disease failed to respond to their treatment. On March 12, 1949, the King underwent a lumbar sympathectomy, performed at Buckingham Palace by Dr. James R.

Learmonth. The operation, as such, was successful, but the King was warned that it was a pallative, not a cure, and that there could be no assurance that the disease would not grow worse. From all accounts, the King continued to smoke.

y y y y Background
Buerger disease, a nonatherosclerotic vascular disease also known as thromboangiitis obliterans (TAO), is characterized by the absence or minimal presence of atheromas, segmental vascular inflammation, vasoocclusive phenomenon, and involvement of small- and medium-sized arteries and veins of the upper and lower extremities. The condition is strongly associated with heavy tobacco use, and progression of the disease is closely linked to continued use. The typical presentations are rest pain, unremitting ischemic ulcerations, and gangrene of the digits of hands and feet, and as the disease evolves, the patients may require several surgical amputations.[1, 2] The first reported case of thromboangiitis obliterans was described in Germany by von Winiwarter in an 1879 article titled "A strange form of endarteritis and endophlebitis with gangrene of the feet."[3] A little more than a quarter of a century later, in Brookline, NY, Leo Buerger published a detailed description of the disease in which he referred to the clinical presentation of thromboangiitis obliterans as "presenile spontaneous gangrene."[4] The paper discussed the pathological findings in 11 limbs amputated from Jewish patients with the disease.

The feet of a patient with Buerger disease. Note the ischemic ulcers on the distal portion of the left great, second, and fifth toes. Though the patient's right foot is normal in gross appearance, angiography demonstrated compromised arterial flow to both feet.

y Pathophysiology

Next Section: Pathophy

While the etiology of Buerger disease is unknown, exposure to tobacco is essential for both initiation and progression of the disease. The notion that the condition is linked to tobacco exposure is supported by the fact that the disease is more common in countries with heavy use of tobacco and is perhaps most common among natives of Bangladesh who smoke a specific type of cigarettes, homemade from raw tobacco, called "bidi." While the overwhelming majority of patients with Buerger disease smoke, a few cases have been reported in nonsmokers that have been attributed to the use of chewing tobacco. The disease mechanism underlying Buerger disease remains unclear, but a few observations have led investigators to implicate an immunologic phenomenon that leads to vasodysfunction and inflammatory thrombi. Patients with the disease show hypersensitivity to intradermally injected tobacco extracts, have increased cellular sensitivity to types I and III collagen, have elevated serum antiendothelial cell antibody titers, and have impaired peripheral vasculature endothelium-dependent vasorelaxation. Increased prevalence of HLA-A9, HLA-A54, and HLA-B5 is observed in these patients, which suggests a genetic component to the disease.

Epidemiology
Frequency
United States The prevalence of Buerger disease has decreased over the past half decade, partly because the prevalence of smoking has decreased, but also because the diagnostic criteria have become more stringent. In 1947, the prevalence of the disease in the United States was 104 cases per 100,000 population. More recently, prevalence has been estimated at 12.6-20 cases per 100,000 population.

Mortality/Morbidity
Death from Buerger disease is rare, but in patients with the disease who continue to smoke, 43% require 1 or more amputations in 7.6 years. Most recently, in a December 2004 CDC publication, the 2002 deaths report in the United States

divided by cause of death, month, race, and sex (based on the International Classification of Diseases, Tenth Revision, 1992), reported a total of 9 deaths related to TAO, depicting male to female gender ratio of 2:1 and white to black ethnicity ratio of 8:1.

Race
Buerger disease is relatively less common in people of northern European descent. Natives of India, Korea, and Japan, and Israeli Jews of Ashkenazi descent, have the highest incidence of the disease.[5]

Sex
Though Buerger disease is more common in males (male-to-female ratio, 3:1), incidence is believed to be increasing among women, and this trend is postulated to be due to the increased prevalence of smoking among women.

Age
Most patients with Buerger disease are aged 20-45 year