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• W1979638609 abstract "A 71-year-old man had painful blue toes after an episode of protracted vomiting. Abdominal, cardiac, and transesophageal ultrasound studies were performed before angiography was considered. A large mobile mass in the proximal descending thoracic aorta, which suggested thrombus, was identified by transesophageal echocardiography. With no further evaluation, anticoagulant therapy with heparin and warfarin was initiated. Three months later, repeated transesophageal echocardiography demonstrated only a tiny vestige of the plaque-related mass. The pain and discoloration of the toes resolved completely. The advantages and disadvantages of the various diagnostic and therapeutic approaches to peripheral embolization are discussed. A 71-year-old man had painful blue toes after an episode of protracted vomiting. Abdominal, cardiac, and transesophageal ultrasound studies were performed before angiography was considered. A large mobile mass in the proximal descending thoracic aorta, which suggested thrombus, was identified by transesophageal echocardiography. With no further evaluation, anticoagulant therapy with heparin and warfarin was initiated. Three months later, repeated transesophageal echocardiography demonstrated only a tiny vestige of the plaque-related mass. The pain and discoloration of the toes resolved completely. The advantages and disadvantages of the various diagnostic and therapeutic approaches to peripheral embolization are discussed. Current management of patients with digital embolization is often empiric and nonuniform. Angiographic determination of a presumed source of embolic material followed by surgical excision of that source has been the preferred approach.1Crane C Atherothrombotic embolism to lower extremities in arteriosclerosis.Arch Surg. 1967; 94: 96-101Crossref PubMed Scopus (23) Google Scholar, 2Lord Jr, JW Rossi G Daliana M Drago JR Schwartz AM Unsuspected abdominal aortic aneurysms as the cause of peripheral arterial occlusive disease.Ann Surg. 1973; 177: 767-771Crossref PubMed Scopus (31) Google Scholar, 3Kwaan JHM Vander Molen R Stemmer EA Connolly JE Peripheral embolism resulting from unsuspected atheromatous aortic plaques.Surgery. 1975; 78: 583-588PubMed Google Scholar, 4Heiskell CA Conn Jr, J Aortoarterial emboli.Am J Surg. 1976; 132: 4-7Abstract Full Text PDF PubMed Scopus (32) Google Scholar, 5Mehigan JT Stoney RJ Lower extremity atheromatous embolization.Am J Surg. 1976; 132: 163-166Abstract Full Text PDF PubMed Scopus (34) Google Scholar, 6Kempczinski RF Lower-extremity arterial emboli from ulcerating atherosclerotic plaques.JAMA. 1979; 241: 807-810Crossref PubMed Scopus (66) Google Scholar, 7Karmody AM Powers SR Monaco VJ Leather RP “Blue toe” syndrome: an indication for limb salvage surgery.Arch Surg. 1976; 111: 1263-1266Crossref PubMed Scopus (116) Google Scholar, 8Lee BY Brancato RF Thoden WR Madden JL Blue digit syndrome: urgent indication for digital salvage.Am J Surg. 1984; 147: 418-422Abstract Full Text PDF PubMed Scopus (19) Google Scholar Anticoagulation, which is standard therapy for thromboembolic arterial occlusion,9Abbott WM Maloney RD McCabe CC Lee CE Wirthlin LS Arterial embolism: a 44 year perspective.Am J Surg. 1982; 143: 460-464Abstract Full Text PDF PubMed Scopus (210) Google Scholar, 10Dale WA Differential management of acute peripheral arterial ischemia.J Vasc Surg. 1984; 1: 269-275Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar has not been advocated in microembolization because it is ineffective in eliminating the source of embolism and may also exacerbate cholesterol crystal embolization.3Kwaan JHM Vander Molen R Stemmer EA Connolly JE Peripheral embolism resulting from unsuspected atheromatous aortic plaques.Surgery. 1975; 78: 583-588PubMed Google Scholar, 6Kempczinski RF Lower-extremity arterial emboli from ulcerating atherosclerotic plaques.JAMA. 1979; 241: 807-810Crossref PubMed Scopus (66) Google Scholar, 11Jennings WC Corder CN Jarolim DR Blackwell J Cherian J Chen D Atheromatous embolism: varied clinical presentation and prognosis.South Med J. 1989; 82: 849-852Crossref PubMed Scopus (7) Google Scholar, 12Bruns FJ Segel DP Adler S Control of cholesterol embolization by discontinuation of anticoagulant therapy.Am J Med Sci. 1978; 275: 105-108Crossref PubMed Scopus (147) Google Scholar, 13Hyman BT Landas SK Ashman RF Schelper RL Robinson RA Warfarin-related purple toes syndrome and cholesterol microembolization.Am J Med. 1987; 82: 1233-1237Abstract Full Text PDF PubMed Scopus (161) Google Scholar, 14Dahlberg PJ Frecentese DF Cogbill TH Cholesterol embolism: experience with 22 histologically proven cases.Surgery. 1989; 105: 737-746PubMed Google Scholar Angiography is associated with risks of reembolization because of catheter-related trauma or atheroembolism and renal insufficiency, and sometimes it fails to detect a resectable source of embolic material.15Gaines PA Cumberland DC Kennedy A Welsh CL Moorhead P Rutley MS Cholesterol embolisation: a lethal complication of vascular catheterisation.Lancet. 1988; 1: 168-170Abstract PubMed Scopus (72) Google Scholar, 16Colt HG Begg RJ Saporito JJ Cooper WM Shapiro AP Cholesterol emboli after cardiac catheterization: eight cases and a review of the literature.Medicine. 1988; 67: 389-400Crossref PubMed Scopus (136) Google Scholar, 17Rosman HS Davis TP Reddy D Goldstein S Cholesterol embolization: clinical findings and implications.J Am Coll Cardiol. 1990; 15: 1296-1299Abstract Full Text PDF PubMed Scopus (53) Google Scholar Improved localization and characterization of the source of digital embolization might lead to better selection of patients for anticoagulant therapy, angiography, surgical intervention, or observation. Ultrasound modalities are now capable of demonstrating real-time images of vegetations, aneurysms, atheroma, and thrombi in the heart,18Pop G Sutherland GR Koudstaal PJ Sit TW de Jong G Roelandt JRTC Transesophageal echocardiography in the detection of intracardiac embolic sources in patients with transient ischemic attacks.Stroke. 1990; 21: 560-565Crossref PubMed Scopus (201) Google Scholar, 19Pearson AC Labovitz AJ Tatineni S Gomez CR Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology.J Am Coll Cardiol. 1991; 17: 66-72Abstract Full Text PDF PubMed Scopus (502) Google Scholar most segments of the aorta,20Tunick PA Kronzon I Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography.Am Heart J. 1990; 120: 658-660Abstract Full Text PDF PubMed Scopus (221) Google Scholar, 21Karalis DG Chandrasekaran K Victor MF Ross Jr, JJ Mintz GS Recognition and embolic potential of intraaortic atherosclerotic debris.J Am Coll Cardiol. 1991; 17: 73-78Abstract Full Text PDF PubMed Scopus (388) Google Scholar, 22Lewis BD James EM Current applications of duplex and color Doppler ultrasound imaging: abdomen.Mayo Clin Proc. 1989; 64: 1158-1169Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar and the carotid, femoral, and popliteal arteries.23Lewis BD James EM Welch TJ Current applications of duplex and color Doppler ultrasound imaging: carotid and peripheral vascular system.Mayo Clin Proc. 1989; 64: 1147-1157Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar Herein we describe a patient with microembolization of the lower extremities, in whom a clinical diagnosis of cholesterol embolization was suspected. Complete cardiovascular ultrasound imaging was performed before angiography was considered. Visualization of a large mobile mass, which was suggestive of plaque-related thrombus in the thoracic aorta, prompted the use of only anticoagulant therapy; the clinical outcome was good. A 71-year-old man was brought to the emergency department because of painful blue toes. On the day before admission, he had had four to five vigorous episodes of vomiting. Twelve hours after these episodes, he was awakened from sleep because of throbbing pain of the left fifth toe. He noted bluish discoloration of his left fifth toe and throbbing and discoloration of his right great toe. He denied having chest pain, dyspnea, chills, sweats, or symptoms suggestive of transient upper extremity or cerebral ischemia. He had not recently undergone surgical intervention or angiography, nor had he experienced trauma. He took atenolol (100 mg/day) for hypertension and stable angina pectoris. He denied use of aspirin, tobacco, or alcohol. Past medical history included myocardial infarction, partial gastrectomy, and transurethral prostatic resection. The patient's blood pressure was 150/78 mm Hg in both arms. The heart rate was 90 beats/min, and the cardiac rhythm was regular. He was afebrile. A grade 1 (on the basis of 1 to 6) systolic ejection murmur at the lower left sternal border was audible. A cutaneous examination suggested faint livedo reticularis and mottling of the plantar lateral aspect of the left foot. The left fifth toe was tender and had bluish discoloration (Fig. 1 A and B). The right great toe had slight bluish discoloration over the plantar aspect, was tender, and blanched with pressure. No pallor on elevation or dependent rubor was noted. The peripheral pulses and the results of the rest of the general and neurologic examinations were unremarkable. Laboratory tests yielded a blood urea nitrogen level of 27 mg/dl and a serum creatinine concentration of 1.6 mg/dl. The erythrocyte sedimentation rate was 6 mm in 1 hour (Westergren). The cholesterol level was 110 mg/dl, and the triglycerides were 133 mg/dl. The following laboratory studies yielded normal results: aspartate aminotransferase, alkaline phosphatase, creatine kinase, lactate dehydrogenase, bilirubin, uric acid, hemoglobin, leukocytes, platelets, prothrombin time, activated partial thromboplastin time, rheumatoid factor, antinuclear antibody, and urinalysis. An electrocardiogram demonstrated sinus rhythm and evidence of an inferior infarction of undetermined duration. Chest roentgenography revealed a prominent left ventricular shadow. Abdominal and pelvic ultrasound images of the aorta and iliac vessels were unremarkable. Transthoracic echocardiography, with extended interrogation of the upper abdominal aorta from the subcostal window and the aortic arch from the suprasternal window, demonstrated no definite abnormalities. Biplanar transesophageal echocardiography disclosed no intracardiac source of embolism; however, 26 cm from the incisors, a mobile bilobed mass (1.5 by 2 cm) was detected affixed to the anterior lateral wall of the proximal descending thoracic aorta, in an area of increased mural echo density (Fig. 2). No additional investigative studies were done; anticoagulant therapy—intravenously administered heparin and orally administered warfarin—was initiated. After the patient had received heparin for 4 days, the prothrombin time international normalized ratio was 2.8. The serum creatinine concentration remained stable; values were between 1.5 and 1.7 mg/dl. No recurrent distal embolization was clinically evident. The pain in the left fifth toe was controlled with analgesics. Nifedipine and metoprolol were added, and atenolol therapy was discontinued. The patient was dismissed, and the warfarin therapy (5 mg/day) was continued. During the 3-month period between the initial transesophageal study and the follow-up examination, the patient's prothrombin time was determined twice per month. The prothrombin time ratios varied between 1.7 and 2.0, and the serum creatinine concentration remained stable. Three months after the patient was dismissed, the discoloration and discomfort of his left fifth toe had completely resolved (Fig. 1 C). Biplanar transesophageal echocardiography, which was repeated 3 months and 2 days after the initial study, revealed that a 2-mm mobile structure was the lone remnant attached to the thickened area of the proximal descending thoracic aorta (Fig. 3). Plaque-related thrombus in the thoracic aorta was a rarely identified cause of peripheral emboli in past decades; it was diagnosed in only 2 of 260 cases in the series reported by Darling and associates.24Darling RC Austen WG Linton RR Arterial embolism.Surg Gynecol Obstet. 1967; 124: 106-114PubMed Google Scholar Additional single cases have been described. In three cases of plaque-related thrombus diagnosed by aortography, one was fatal,25Mestres C-A Campistol JM Margarit LC Almirall J Condom E Mulet J Acute thrombosis of the thoracic aorta diagnosed during life: a rare entity [letter].J Thorac Cardiovasc Surg. 1989; 98: 1149PubMed Google Scholar another was successfully managed with anticoagulant therapy,26Goebel N Maire R Streuli R Flottierende Thromben in der Aorta ascendens.Vasa. 1983; 12: 397-399PubMed Google Scholar and a third was surgically resected.27Sadony V Walz M Löhr E Rimpel J Richter H-J Unusual cause of recurrent arterial embolism: floating thrombus in the aortic arch surgically removed under hypothermic cardiocirculatory arrest.Eur J Cardiothorac Surg. 1988; 2: 469-471Crossref PubMed Scopus (31) Google Scholar An additional case of multiple emboli was diagnosed by transesophageal echocardiography. Plaque-related thrombus was found in the aortic arch during surgical repair.28Tunick PA Culliford AT Lamparello PJ Kronzon I Atheromatosis of the aortic arch as an occult source of multiple systemic emboli.Ann Intern Med. 1991; 114: 391-392Crossref PubMed Scopus (127) Google Scholar To our knowledge, our case is the first reported instance in which both a nonangiographic diagnosis and nonsurgical therapy were used. This approach departs from prior practice. We used anticoagulant therapy for our patient because the suspected thrombus was prominent and apparently distinct sonographically from the underlying atheroma. In addition, his cardiac status suggested that surgical intervention might increase morbidity and mortality. Resolution of the mass without symptoms or worsening of renal function suggests that the detected mass was thrombus that dissolved with usual heparin and warfarin therapy. Silent reembolization cannot be excluded. The decision to use anticoagulant therapy for small but mobile “aortic debris,” as has been detected in the thoracic aorta by transesophageal echocardiography,18Pop G Sutherland GR Koudstaal PJ Sit TW de Jong G Roelandt JRTC Transesophageal echocardiography in the detection of intracardiac embolic sources in patients with transient ischemic attacks.Stroke. 1990; 21: 560-565Crossref PubMed Scopus (201) Google Scholar, 19Pearson AC Labovitz AJ Tatineni S Gomez CR Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology.J Am Coll Cardiol. 1991; 17: 66-72Abstract Full Text PDF PubMed Scopus (502) Google Scholar, 20Tunick PA Kronzon I Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography.Am Heart J. 1990; 120: 658-660Abstract Full Text PDF PubMed Scopus (221) Google Scholar, 21Karalis DG Chandrasekaran K Victor MF Ross Jr, JJ Mintz GS Recognition and embolic potential of intraaortic atherosclerotic debris.J Am Coll Cardiol. 1991; 17: 73-78Abstract Full Text PDF PubMed Scopus (388) Google Scholar is difficult for three reasons. First, aortic debris may represent multiple pathologic processes; pathologic correlations of structures detected by transesophageal echocardiography are rare. As depicted in other publications, these debris are smaller and more echo-reflective than the mass identified in our patient, which had ultrasound characteristics similar to thombi in the heart. Second, warfarin therapy may exacerbate atheromatous embolization, which is known to occur in the diffusely “shaggy” atherosclerotic aorta. Finally, by clinical evaluation the distinction among thromboembolic occlusion of a major artery, thromboembolic microembolization, and atheromatous microembolization is often ambiguous.1Crane C Atherothrombotic embolism to lower extremities in arteriosclerosis.Arch Surg. 1967; 94: 96-101Crossref PubMed Scopus (23) Google Scholar, 3Kwaan JHM Vander Molen R Stemmer EA Connolly JE Peripheral embolism resulting from unsuspected atheromatous aortic plaques.Surgery. 1975; 78: 583-588PubMed Google Scholar, 28Tunick PA Culliford AT Lamparello PJ Kronzon I Atheromatosis of the aortic arch as an occult source of multiple systemic emboli.Ann Intern Med. 1991; 114: 391-392Crossref PubMed Scopus (127) Google Scholar, 29Flory CM Arterial occlusions produced by emboli from eroded aortic atheromatous plaques.Am J Pathol. 1945; 21: 549-565PubMed Google Scholar A clinical trial of anticoagulant therapy, aspirin, and observation based on ultrasound findings may be warranted in patients who have experienced peripheral embolization. Cardiac and vascular ultrasound techniques may detect a cardiac or vascular source of embolism and thus obviate angiography and its potentially deleterious effects. Nonetheless, these methods have disadvantages. Portions of the aortic arch, abdominal aorta, and iliac artery may be visualized suboptimally. Origins of visceral arteries and thrombi within them may be obscured. Unilateral pedal emboli may be due to second lesions distal to the aortic bifurcation or may reflect proximal thrombus that has fragmented en route. Ultrasound studies may be unable to define these multiple lesions optimally. In patients in whom clinical assessment suggests visceral ischemia, deficits in peripheral pulses, or involvement of the upper and lower extremities, angiography remains essential for determining the embolic source,5Mehigan JT Stoney RJ Lower extremity atheromatous embolization.Am J Surg. 1976; 132: 163-166Abstract Full Text PDF PubMed Scopus (34) Google Scholar the site of embolization, and the potential for corrective therapy. Management of patients with digital microembolization is a complicated process that necessitates clinical, laboratory, and structural assessment of the circulatory system and the clotting process. Anticoagulant therapy, angiography, and surgical intervention may be beneficial or deleterious, depending on the precise cause of embolization. In patients who have embolization from aneurysms, resection and repair prevent further embolization.2Lord Jr, JW Rossi G Daliana M Drago JR Schwartz AM Unsuspected abdominal aortic aneurysms as the cause of peripheral arterial occlusive disease.Ann Surg. 1973; 177: 767-771Crossref PubMed Scopus (31) Google Scholar Repair has also been advocated for patients with discrete ulcerations of the abdominal aorta or the iliac or femoral arteries.3Kwaan JHM Vander Molen R Stemmer EA Connolly JE Peripheral embolism resulting from unsuspected atheromatous aortic plaques.Surgery. 1975; 78: 583-588PubMed Google Scholar, 6Kempczinski RF Lower-extremity arterial emboli from ulcerating atherosclerotic plaques.JAMA. 1979; 241: 807-810Crossref PubMed Scopus (66) Google Scholar Patients with a diffusely “shaggy” aorta and atheromatous embolization may or may not benefit from a surgical approach.30Hollier LH Kazmier FJ Ochsner J Bowen JC Procter CD “Shaggy” aorta syndrome with atheromatous embolization to visceral vessels.Ann Vasc Surg. 1991; 5: 439-444Abstract Full Text PDF PubMed Scopus (74) Google Scholar Withholding angiography in such patients without a resectable lesion may prevent iatrogenic exacerbation of atheroembolism. Our report demonstrates that in patients with peripheral embolization, a strategy that involves a complete ultrasound evaluation before consideration of angiography and surgical treatment may lead to a successful outcome. Furthermore, anticoagulant therapy may be appropriate for acute lesions that are suggestive of plaque-related thrombus." @default.
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• W1979638609 title "Digital Embolization From Plaque-Related Thrombus in the Thoracic Aorta: Identification With Transesophageal Echocardiography and Resolution With Warfarin Therapy" @default.
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