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Concurrent systemic and pulmonary septic emboli from isolated right-sided infective endocarditis are rare. One mechanism described is that of intrapulmonary shunting. We describe a case of widespread pulmonary and systemic septic embolization with sequelae in an intravenous drug user with concomitant chronic hepatitis C infection and discuss possible mechanisms involved in the pathogenesis., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Unlabelled: The blue (or purple) toe syndrome consists of the development of blue or violaceous discoloration of one or more toes in the absence of obvious trauma, serious cold-induced injury, or disorders producing generalized cyanosis. The major general categories are: (1) decreased arterial flow, (2) impaired venous outflow, and (3) abnormal circulating blood. Depending on its pathogenesis, the discoloration may be blanching or nonblanching. An accurate diagnosis is critical, because many of the causes threaten life and limb, but the patient's medical history, accompanying nondermatologic findings on physical examination, and a discriminating use of laboratory tests are usually more important than the nature of the cutaneous abnormalities in determining the cause., Learning Objectives: After completing this learning activity, participants should be able to define the blue (or purple) toe syndrome, categorize the causes, and recognize the important historical, clinical, and laboratory findings that differentiate the causes and lead to the correct diagnosis.

We report the case of a 58-year-old woman who developed acute onset of bilateral lower-extremity numbness and difficulty ambulating at home. On presentation to the emergency department, however, the patient's symptoms essentially had resolved. An aortic saddle embolus was suspected based on the patient's cardiac history and the absence of distal pulses in the lower extremities. This case illustrates that even with vague or resolving complaints, a high index of suspicion should be maintained for the diagnosis of aortic saddle embolus based on the patient's medical history and on physical examination.

Embolization of atheroma from the ascending aorta is a principal cause of stroke after cardiac operations. We have previously shown that intraoperative ultrasonographic scanning of the aorta rapidly, safely, and accurately identifies atheromatous disease in the ascending aorta. Intraoperative ultrasonography of the ascending aorta was performed in 500 of a consecutive series of 540 patients 50 years of age or older (mean 68 years) who underwent a variety of cardiac operations. Eighty-nine percent required bypass grafting. Sixty-eight patients (13.6% of the total) with a mean age of 72 years (range 55 to 85 years) had significant atheromatous disease in the ascending aorta and were considered to be at increased risk for embolization. Palpation identified the atheromatous disease in only 26 (38%) of these patients and underestimated its severity. A total of 168 modifications in the standard techniques for cannulation and clamping of the aorta were implemented in the 68 patients (mean 2.5 per patient) and included alterations in the sites of aortic cannulation (50 patients), aortic clamping (54 patients), attachment of the vein grafts (35 patients), and cannulation for infusion of cardioplegic solution (29 patients). Ten patients with severe diffuse atheromatous disease underwent graft replacement of the ascending aorta with hypothermic circulatory arrest without aortic clamping. Fourteen patients with symptoms or with high-grade carotid artery occlusive disease were treated by concomitant carotid endarterectomy. Thirty-day mortality for the entire group was 3.4% (17 patients). Permanent neurologic deficits occurred in five (1.0%) of the patients in the entire group but in none of the 68 patients with significant atheromatous disease in whom modifications in technique were used. One patient in the latter group had a reversible ischemic neurologic deficit. Modification of standard cannulation and clamping techniques based on ultrasonography may reduce the frequency of stroke related to atheromatous embolization.

The return of atrial mechanical function and its relationship to embolic events following cardioversion of atrial arrhythmias is controversial. Fourteen patients with atrial arrhythmias were evaluated with pulsed Doppler echocardiography before and after direct current (DC) cardioversion. The atrial filling fraction increased significantly: 1.14 +/- 4.3% at baseline versus 14.9 +/- 13.3%, 13.4 +/- 11.4%, and 21.9 +/- 13.5% at 5 minutes, 30 minutes, and 24 hours, respectively, following cardioversion. Absent atrial mechanical activity was noted in four patients immediately after cardioversion. Mechanical activity resumed by 30 minutes in one patient and at 24 hours in two others. Those with delayed atrial function had lower stroke volumes and atrial filling fractions following cardioversion. An embolic event occurred in one patient who had immediate return of atrial mechanical activity. This patient also had the largest atrial filling fraction of any patient at 24 hours (41%). These data suggest that the degree of atrial mechanical activity following cardioversion is variable and that embolic episodes are not necessarily related to delayed return of atrial mechanical activity following cardioversion.

On hundred fifty-four patients who underwent open mitral valvotomy in the years of 1968 to 1976 were reviewed 1 to 112 months (mean 48) postoperatively. There was one hospital death and there were 14 late deaths (nine cardiac), and 16 patients required reoperation during the follow-up period. Preoperative factors were examined to assess their association with an unsatisfactory postoperative course. End points included unsatisfactory symptomatic status, the need for reoperation, and postoperative death. Maori race and atrial fibrillation (AF) were associated with all three end points. Other preoperative factors associated with at least one unfavorable end point were female sex, unfavorable preoperative symptomatic status, the presence of mild associated mitral incompetence (MI), a previous operation, and the presence of calcification in the mitral valve. The degree of subvalvular fusion and the adequacy of valvotomy assessed at operation were also related to outcome. A binary regression program was developed to assist in the prediction of outcome from an assessment of preoperative factors. Preoperative embolism occurred in 31 patients and postoperative embolism in 13. Postoperative embolism occurred in 35% of patients with a preoperative embolic episode and AF. Open mitral valvotomy carries a low operative risk, but unfavorable preoperative factors militate against a satisfactory long-term result and protection from recurrent embolism is only partial.

Analysis of 99 M-mode echocardiograms recorded during and up to 144 months after healing of active bacterial endocarditis limited to the mitral valve in 27 patients disclosed the following: (1) Little to no change occurred in the echocardiographic size of the vegetations during the first 6 weeks after diagnosis and institution of appropriate antibiotic therapy unless a major systemic embolus occurred. (2) The echocardiographic size of the vegetations did not determine the amount of cardiac damage or dysfunction produced by the valvular infection. (3) The larger the vegetations by echocardiogram, the greater was the likelihood of a clinical event compatible with a systemic embolus. (4) The gravest prognostic sign yielded by the echocardiogram was evidence of rupture of chordae tendineae. (5) Although a useful adjunct to diagnosis before appropriate antibiotic therapy was instituted, once bacteriologic cure was achieved, the echocardiogram was of limited value in delineating an active from a heated vegetation. (6) The echocardiographic appearance of the vegetations was not determined by the type of infecting bacterium.

Analysis of 37 M-mode echocardiograms recorded during the period of active bacterial endocarditis (ABE) involving the aortic valve (AV) in 17 patients disclosed one or more echocardiographic abnormalities involving the aortic valve cusps or their immediate vicinity in 15 (88%), including "shaggy" echoes indicative of vegetations in 12 (71%). Of the 12 patients with echocardiographic evidence of AV vegetation, 11 developed overt congestive heart failure (CHF) and either died or had AV replacement, and seven had clinical events compatible with systemic emboli; of the five patients without echo-demonstrated vegetations, only one had CHF, none had AV replacement, two died, and one had a systemic embolus. In comparison to our previously reported echocardiographic observations in patients with ABE involving either the mitral (29 patients) or tricuspid valve (23 patients), infection involving the AV was far more liable to produce overt CHF and systemic emboli, to necessitate valve replacement, and to cause death during the period of active infection.

Sixty-nine patients receiving atrioventricular sequential (DVI) pacemakers are compared to 67 patients receiving ventricular demand (VVI) pacemakers for control of the symptoms of sinus node dysfunction. The populations were similar with comparable preparing incidences of each assayed symptom and number of symptoms per patient (symptom density). Syncope was well controlled by both DVI and VVI pacing. DVI pacing was better than VVI pacing for control of all other symptoms. Symptom density response: DVI pre, 3.3 +/- 0.95; post, 0.43 +/- 0.63; VVI pre, 3.2 +/- 0.97; post 1.75 +/- 1.44 (p less than 0.000). Atrial electrode problems were encountered in five (7.3%) of the DVI patients and one (0.74%) ventricular electrode required repositioning.

Attention is called to a poorly recognized syndrome of neonatal renal arterial embolism, presumably from the ductus arteriosum, resulting in malignant hypertension, congestive heart failure, respiratory distress, and increased renin secretion. Radiographic studies revealed a ductus diverticulum and multiple narrowed arteries including the lower pole branches of the right renal artery. Renal scan showed poor imaging of the lower pole of the right kidney. Nephrectomy resulted in a prompt return of the blood pressure into the normal range. Eight cases recorded in the literature resemble the one reported here, and six of the eight had an associated thrombosis of the ductus arteriosum. Our patient appears to be the first case recognized by modern techniques followed by nephrectomy and clinical cure.

A review of 494 myocardial lesions at least 3 cm. in one dimension reveal 418 (85 per cent) related to atherosclerotic coronary lesions, 55 (11 per cent) related to coronary emboli of various types, 18(3.5 per cent) without specific coronary lesions but related to clinical events associated with coronary hypoperfusion, and 3 (0.5 per cent) associated with miscellaneous coronary lesions. In 399 of 418 (96 per cent) atherosclerotic coronary lesions of all ages complete occlusion (remote of fresh) or histological evidence of lumenal recanalization was present. These coronary lesions were situated within extramural coronary artery segments one to several centimeters proximal to the myocardial lesions which were confined to the distribution of the respective partially or totally occluded coronary segments. In the atherosclerotic cornary lesions less than 2 weeks of age partially or totally occlusive thrombus was found in 67 of 69 (97 per cent) cases and a underlying plaque ulceration, erosion, or rupture was present in 64 of 69 (93 per cent) instances. These endothelial and intimal injuries were generally focal in nature, often extending over a length of only 100 to 200 mu. In no instance could it be stated with certainty that the oldest portion of the atherosclerotic ulceration-thrombus complex was younger in age than its associated myocardial lesion. On the contrary, in 10 of 69 (14 per cent) of the cases portion of the coronary thrombus, usually at the site of plaque ulceration, were histologically older than the myocardial lesion. In addition, the presence of thrombus and plaque debris admixtures further suggested the antecedent nature of the coronary lesion in relation to the myocardial lesion. Atherosclerotic coronary lesions associated with myocardial lesions of 2 to 8 weeks of age had identifiable thromboses in all instances and underlying plaque ulceration, erosions, or ruptures in 17 of 21 (80 per cent). Endothelial injuries were more difficult to assess due to the obscuring features of organizing lumenal thrombus. Interface i.e., plaque ulceration, erosions, or ruptures, were reliably detectable up to approximately on month of age. Coronary arter thromboemboli accounted for a significant percentage of myocardial lesions, were usually associated with normal or minimal coronary artery disease, and frequently involved smaller intramural coronary vessels of the heart. Organization and recanalization of thromboemboemboli tended to be rapid and complete so that in the late stages the residual intimal plaque was sometimes difficult to identify. Myocardial lesions related to clinical events associated with coronary artery hypoperfusion centric, and not confined to the distribution of a single coronary artery. They were unassociated with acute coronary lesions and histologically displayed contraction band necrosis more frequently than the embolic and atherosclerotic related lesions. An explanation was found for the overwhelming majority of myocardial lesions...

It is generally appreciated in the cardiovascular literature that calcium emboli to a central retinal artery or its branches may be the presenting feature of otherwise uncomplicated calcific aortic stenosis. The ophthalmologic literature provides good evidence for this point. Over a 7-month period, four such cases have come to our attention. Other potential sources of emboli were excluded by standard noninvasive and invasive diagnostic techniques, and two patients underwent successful aortic valve replacement. Previous studies of calcific aortic stenosis have demonstrated postmortem histologic evidence of calcium emboli to various organs, for example, heart, kidney, or brain. Since these emboli are small, their occurrence is clinically silent. The retinal circulation is unique in that its occlusion by a calcium microembolus results in loss of vision, and this symptom may be a clue to the presence of calcific aortic stenosis.

This study follows the clinical course of 22 patients in the active phase of infective endocarditis who inderwent valve replacement at North Carolina Memorial Hospital between March, 1966, and March, 1976. At the time of operation, there was gross valve tissue destruction in 16 patients, verrucae in nine, ruptured chordae tendineae in five, and myocardial or annular abscess formation in five. Four patients survived less than 6 months after the initial operation. One survived almost 3 years before dying of recurrent carcinoma of the lung. The remaining 17 patients have been followed an average of 4.6 years. Major postoperative complications were as follows: paravalvular problem, five patients; congestive heart failure, seven patients; complete heart block, three patients; systemic arterial emboli, four patients. These complications often were associated with the preoperative presence of annular or myocardial abscess. Thus it appears that postoperative complications often result from annular structural deficiencies rather than being directly related to active infection.

The use of electrical energy for the immediate treatment of atrial and ventricular arrhythmias is practical and easily applied. The method, though simple, is the most effective method for terminating cardiac arrhythmias and is associated with only a low risk if properly employed. In symptomatic patients, the utilization of cardioversion reduces patient discomfort and complications which may occur while awaiting pharmacologic reversion of arrhythmia. At present, transthoracic defibrillation is the only practical method for terminating VF. Despite the safety of electrical reversion, proper precautions are necessary to prevent complications. In particular, the discharge of excessive energies, especially in the presence of digitalis toxicity, promises grave and life-threatening consequences. The use of antiarrhythmic medications is not supplanted by cardioversion and defibrillation. Rather, ongoing drug therapy is frequently necessary to prevent recurrence of arrhythmia.

We have demonstrated a phenomenon occurring during coronary artery bypass grafting (CABG) which has not been previously described. Thirteen instances of fatal perioperative myocardial infarction following CABG were associated with intraoperative atheromatous embolization in the coronary microcirculation. In five cases the emboli originated from ulcerative atherosclerotic lesions in the aortic root at the site of the vein graft ostia; in two cases they likely emanated from coronary endarterectomy sites; and in two cases from mechanical disruption of plaques in the major epicardial coronary arteries during the operation. These nine cases occurred during initial revascularization procedures. We have performed 4,095 initial CABG procedures, and the nine cases represent a risk of 0.22%. A further four cases occurred during repeat CABG procedures and resulted from manipulative disruption of atheroma in old vein grafts. Our total number of repeat CABGs is 175, and the risk at reoperation is 2.29%; this represents a tenfold increase in risk for this complication at reoperation. Inadequate histologic sampling of the myocardium at autopsy will necessarily result in underestimation of the incidence of this phenomenon. Analysis of angiograms prior to repeat CABG can identify patients at increased risk who have severe graft atherosclerosis as opposed to myointimal hyperplasia. To reduce the incidence of atheroembolism at reoperation, we advocate ligation of the vein graft at the level of the distal anastomosis as early as possible during dissection on reopening the chest.

The effects of transfusion of whole blood clot emboli and aged citrated platelet-poor plasma on pulmonary capillary permeability were investigated in anesthetized sheep by continuous collection of pulmonary lymph. Changes in lymph flow and lymph-to-plasma ratios (CL/CP) for albumin and globulin were utilized to detect changes in permeability. Infusion of 0.5 cc/kg of finely (less than or equal to 1 mm) diced autologous whole blood clot resulted in a 170% increase in lymph flow over control with no change in CL/CP for albumin or globulin. Infusion of 1 cc/kg of autologous clot increased lymph flow 180% over control and increased CL/CP for albumin and globulin. Infusion of homologous platelet-poor plasma caused greater increases in lymph flow without changes in CL/CP. Changes in each of these three groups were consistent with increased permeability. Balloon occlusion of one main pulmonary artery was induced without a fall in cardiac output and resulted in no change in lymph flow of CL/CP despite a rise in pulmonary vascular resistance (PVR). Femoral arteriovenous fistulas were created to increase cardiac output, but no change in lymph flow or CL/CP occurred. The results in these latter two experiments suggest that increased perfusion per unit lung capillary bed or increased PVR were not primarily responsible for the changes observed in the emboli-treated and plasma-infused animals. Since both emboli and aged platelet-poor plasma increased pulmonary capillary permeability, the permeability increasing factor appears to be humoral in origin. Similar humoral factors may be important in the pathogenesis of the adult respiratory distress syndrome in man.

Although the occurrence of an arterial embolus is usually a cataclysmic event prompting emergency presentationand early diagnosis, we have managed 22 patients who presented more than 48 hours after the onset of symptoms. The diagnosis was apparent in only six patients. The remainder had subacute limb ischemia, and arteriography was used to help delineate the diagnosis in 14 of these patients. In most instances arteriograms were atypical of chronic occlusive disease, rather than diagnostic of arterial emboli. Embolectomy was performed a mean of 13 days after the onset of symptoms, with retrieval of thromboembolic material in all instances. Two patients died (mortality rate of 9%), and the limb salvage rate for the 25 limbs explored was 88%. Among 22 lower extremity embolectomies, foot pulses were restored in 13 patients (59%), and four patients (18%) had viable extremities without pulses. Adjunctive arterial reconstruction was required in three patients.

Despite a general impression to the contrary, a recent survey showed that the current mortality rate for acute arterial ischemia approximates 25%. Much of this apparently relates to toxins and procoagulants released from the dying limb, a tendency which may be enhanced further by attempts at revascularization. Based on these observations, we have utilized selective management of acute arterial ischemia in an attempt to minimize deaths and to salvage the maximum number of limbs. If the patient presents within 6 to 8 hours of the onset of acute arterial occlusion and if paralysis or anesthesia is present, then ultimate limb loss is likely. The therapeutic choices are high-dose heparin therapy, operative removal of the clot, or amputation of the limb--the ultimate choice being dependent upon the particular status of the patient. But if sensation and motor function are present, viability of the limb is not threatened, and good results can be obtained by utilizing anticoagulation and delayed elective revascularization, if the latter is indicated. But revascularization attempts after 10 to 12 hours of severe ischemia often are unsuccessful, and ischemia is followed by either recurrent thrombosis and ultimate limb loss, or by death from the systemic effects of reperfusion of ischemic tissue. This type of limb is managed best by using high-dose heparin therapy if viable, or by amputation if it is not. Employing the above criteria, 54 patients with acute arterial ischemia averaging 59 years of age, were treated. Seventeen had immediate thrombectomy, yielding two deaths and four subsequent amputations. Twenty-nine received anticoagulation treatment, resulting in one death and five amputations, and six had immediate amputation, yielding one death. Three had no specific treatment, with one poor result. There were four deaths in the entire series--a mortality rate of 7.5%--and two thirds of the limbs were salvaged. We have concluded that selective management, as prescribed above, was responsible for a significant decrease in mortality rate with no corresponding increase in limb loss, and that high-dose heparin therapy ultimately may prove the initial treatment of choice in all cases of acute arterial ischemia.

The late results of isolated mitral valve replacement were retrospectively evaluated in 357 patients receiving a Björk-Shiley (B-S) tilting disc prosthesis and 96 patients receiving a porcine bioprosthesis (PB) (Vascor or Carpentier-Edwards) between March, 1973, and July, 1978. The groups were comparable with regard to age, sex, New York Heart Association functional class, preoperative cardiac rhythm (sinus or atrial fibrillation), left atrial size (normal or enlarged), and presence of thrombus in the left atrium at operation. All of the B-S and 14 of the PB patients received long-term anticoagulant therapy. The median duration of follow-up was 46 months in the B-S group and 32 months in the PB group. At 5 years, survival was 70% for the B-S and 68% for the PB groups (NS). The percentage of patients free of thromboembolic episodes was 77% for the B-S and 78% for the PB groups (NS). Fifty-six percent of the B-S and 49% of the PB patients were alive and free of thromboembolism, complications related to anticoagulant therapy, or other valve-related complications (dehiscence, degeneration, or endocarditis) (NS). The presence of atrial fibrillation, enlarged left atrium, preoperative thromboembolic episodes, and left atrial thrombus had no effect on the incidence of thromboembolic complications with either prosthesis. From this analysis, it appears that the major advantage of the PB over the B-S prosthesis is its use in patients in whom long-term anticoagulation is contraindicated.

Between 1969 and 1978 7,000 patients underwent cardiopulmonary bypass at Bellevue and University Hospitals. In seven of these patients, sudden loss of hearing in one ear developed immediately after the operation. Four of the seven patients showed improvement in hearing after the initial loss, although in no case did the hearing return completely to normal. None of the patients had vertigo but two were listless postoperatively. Two of the operations were for congenital heart disease; the remainder were coronary artery bypass procedures. All of the affected patients were male. There was no predilection as to which ear was affected. The most likely cause is particulate emboli generated by cardiopulmonary bypass. Other possible sources of emboli include air, antifoam, fat, and particulate matter from calcified valves and the aorta. Improvement in the kind of pump and the addition of various filters in the period between 1969 and 1978 did not eliminate unilateral hearing loss. The relationship between cerebral emboli and decreased consciousness after operations is also discussed.

This report describes the case of a 32-year-old woman with the sudden onset of chest pain and an evolving inferior wall infarction proved by the electrocardiogram and enzyme studies. The patient underwent embolectomy 2 months later for a thromboembolus in the right main coronary artery. An autologous patch graft was used to close the arteriotomy. Four years later, the patient is asymptomatic, having no activity limitations. The patch graft to the right coronary artery is patent. This case exemplifies and reaffirms the possibility of emboli being lodged in the coronary arteries in certain types of disease. It may be necessary to operate in order to re-establish proper coronary circulation.

Eighty eight cases of unilateral Raynaud's phenomenon of the hand were studied. The condition in most is progressive and should be treated early--before irreversible changes occur.

Our experience at the Cleveland Clinic and that in the literature with splenic infarction were reviewed to describe the natural history of splenic infarction and provide guidelines for management. Data for this review included 75 patients identified by clinical studies or at autopsy during a 10-year period and a review of 77 cases reported in the literature. The cause of the infarct varied with age; patients under 40 years old most often had an associated hematologic disorder, while those older than 41 years old most often had an embolic event. Other etiologic factors included splenic vascular disease, anatomic abnormalities, collagen vascular disease, pancreatic disease, and nonhematologic malignancy. Left upper quadrant pain was the predominant symptom. Changes in the blood count included anemia (53%), leukocytosis (49%), and thrombocytosis (7%). Liver-spleen scans were diagnostic in 90% of patients and computerized tomography identified the infarct in 75%. Initial management consisted of hydration, analgesics, and frequent monitoring, with resolution of symptoms in 7 to 14 days. Splenectomy was performed for persistent symptoms or a complication of the infarct (splenic pseudocyst, abscess, or hemorrhage). An uncomplicated splenic infarction can be managed safely with medical treatment, but early surgical intervention (splenectomy) is necessary to lower the mortality rate of a complication of the infarct.

One hundred and twenty-four patients treated by Fogarty balloon catheter embolectomy from 1964 through 1973 were reviewed and compared to an earlier series of 82 patients treated by direct extraction during the interval from 1948 to 1963. In patients undergoing embolectomy, the incidence of rheumatic heart disease (RHD) declined from 55 to 27 percent, and that of arteriosclerotic heart disease (ASHD) rose from 39 to 55 percent. The operative mortality rate of those with RHD was unchanged and that of patients with ASHD declined from 74 to 36 percent. This was attributed, in part, to the lesser degree of operative stress entailed by the Fogarty catheter and the local anesthesia. Limb salvage was 82 percent when ischemic symptoms were less than 24 hours in duration and 66 percent when such symptoms were more than 24 hours in duration. The amputation rate for the entire group was 22 percent. The low 2 year survival of patients with ASHD and of amputees was ascribed to the wide extent of their atherosclerotic cardiovascular disease. This was emphasized by the fact that 44 percent of late deaths were due to myocardial infarction.