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• W2051288341 abstract "HomeCirculationVol. 115, No. 6Pulmonary Embolism and Fever Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBPulmonary Embolism and FeverWhen Should Right-Sided Infective Endocarditis Be Considered? Gaetano Nucifora, MD, Luigi Badano, MD, Fjoralba Hysko, MD, Giuseppe Allocca, MD, Pasquale Gianfagna, MD and Paolo Fioretti, MD Gaetano NuciforaGaetano Nucifora From the Departments of Cardiopulmonary Science (G.N., L.B., G.A., P.G., P.F.) and Radiological Science (F.H.), Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. Search for more papers by this author , Luigi BadanoLuigi Badano From the Departments of Cardiopulmonary Science (G.N., L.B., G.A., P.G., P.F.) and Radiological Science (F.H.), Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. Search for more papers by this author , Fjoralba HyskoFjoralba Hysko From the Departments of Cardiopulmonary Science (G.N., L.B., G.A., P.G., P.F.) and Radiological Science (F.H.), Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. Search for more papers by this author , Giuseppe AlloccaGiuseppe Allocca From the Departments of Cardiopulmonary Science (G.N., L.B., G.A., P.G., P.F.) and Radiological Science (F.H.), Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. Search for more papers by this author , Pasquale GianfagnaPasquale Gianfagna From the Departments of Cardiopulmonary Science (G.N., L.B., G.A., P.G., P.F.) and Radiological Science (F.H.), Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. Search for more papers by this author and Paolo FiorettiPaolo Fioretti From the Departments of Cardiopulmonary Science (G.N., L.B., G.A., P.G., P.F.) and Radiological Science (F.H.), Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. Search for more papers by this author Originally published13 Feb 2007https://doi.org/10.1161/CIRCULATIONAHA.106.674358Circulation. 2007;115:e173–e176Case presentation: A 39-year-old woman with chronic alcoholism became febrile (38.8°C) and markedly dyspneic on the fourth postoperative day of gastric surgery. Laboratory evaluation revealed anemia (hemoglobin 8.5 g/dL), thrombocytopenia (platelet count 30 000/mm3), and elevation of inflammatory markers (white blood cell count 18 000/mm3, C-reactive protein 187 mg/dL, and erythrocyte sedimentation rate 50 mm/s). Limb venous ultrasonography was negative for deep vein thrombosis, but pulmonary embolism (PE) was diagnosed on the basis of contrast-enhanced multidetector-row spiral computed tomography (MSCT; Figure 1A). Anticoagulation therapy was considered to be contraindicated because of recent surgery and thrombocytopenia, and a retrievable inferior vena cava filter was placed. With persistent high-grade fever and dyspnea and with the finding of Streptococcus agalactiae bacteremia, the patient underwent a transthoracic echocardiography examination on the sixth postoperative day that showed a large, mobile vegetation attached to the pulmonary valve (Figure 1B). A diagnosis of infective endocarditis (IE) of the pulmonary valve complicated by septic PE was then made, and the patient was referred for vena cava filter removal and pulmonary valve replacement. During vena cava filter removal, an acute thromboembolic stroke occurred, and transesophageal echocardiography documented a patent foramen ovale with right-to-left shunt. Ten days later, the patient underwent successful pulmonary valve replacement and surgical closure of the patent foramen ovale. Download figureDownload PowerPointFigure 1. A, MSCT shows a large filling defect in the main pulmonary artery, above the pulmonary valve (black arrow), and a filling defect in the terminal part of the right pulmonary artery (white arrow). B, 2D transthoracic echocardiography performed a few days later shows a large vegetation attached to the arterial surface of the medial cusp of the pulmonary valve. Ao indicates ascending aorta; LA, left atrium; PA, pulmonary artery; and Veg, vegetation.Clinical Significance of Fever During PEFever has long been recognized as commonly accompanying PE. Stein et al1 reported a temperature >37.5°C in 50% of patients with acute PE, but whether the fever was caused by the PE or an associated disease was not clarified. Murray et al2 encountered fever >38°C attributed solely to acute PE in 57.1% of patients, whereas fever without any other definite or possible explanatory cause was observed in 14% of 311 patients in the PIOPED (Prospective Investigation Of Pulmonary Embolism Diagnosis) study.3 PE-related fever is usually low-grade, rarely exceeding 38.3°C, and short-lived, reaching its peak the same day on which the PE occurs and gradually disappearing within 1 week.2–4The pathogenesis of PE-related fever has not yet been fully clarified. It has been suggested that 1 or a combination of a variety of potential pyrogenic mechanisms occurs: infarction and tissue necrosis, hemorrhage, local vascular irritation or inflammation, atelectasis, or self-limited occult superinfections.2,5 The presence of a slight inflammatory response is indirectly confirmed by the concomitant increase of serum markers of inflammation.4,6 The presence of a modest leucocytosis (rarely exceedingly 20 000/mm3) during the first hospital week is not uncommon, being described in up to 20% of patients with PE who have no other possible or defined cause of leucocytosis.2,7 The differential white blood cell count usually remains normal, only rarely showing a slight neutrophilia.7 Similarly, a slight increase in erythrocyte sedimentation rate and in C-reactive protein can also be observed.4,8True PE-related fever is not associated with the extension of vascular obstruction and does not have any prognostic role4,6; its presence should not dissuade the clinician from diagnosing PE and initiating appropriate therapy. Furthermore, PE-related fever usually subsides after anticoagulant treatment, whereas the addition of antibiotics does not provide any additional benefit.4,9The features of PE-related fever are similar to postoperative fever. Most early postoperative fevers (within the first 48 hours after surgery) have no clearly defined infectious cause and resolve without therapy. Therefore, among patients with onset of PE in the early postoperative period, fever could be also ascribed to the surgical procedure.10 Conversely, high-grade fever, especially if long-lasting or remittent and associated with a marked increase of serum markers of inflammation, could indicate advanced malignancy or pneumonia or other infections, or it could be the expression of septic embolic phenomena; it should prompt an exhaustive search for its cause, because management could be strongly affected (Figure 2; Table 1).2–4,6,11Download figureDownload PowerPointFigure 2. PE and fever: a clinical diagnostic algorithm. TEE indicates transesophageal echocardiography; TTE, transthoracic echocardiography; PM, pacemaker; and post-op, postoperative.TABLE 1. Other Possible Causes of Fever Among Patients With PECause% of CasesData derived from Stein et al.3Advanced malignancy33Other infection with or without septic embolic phenomena22Recent operation13Trauma or multiple fractures11Pneumonia9Intracerebral bleed or acute stroke4Endotracheal tube2Delirium tremens2Polymyositis2Intraperitoneal catheter2Diagnostic Role of Computed Tomography and EchocardiographyThe introduction of MSCT has greatly improved the visualization of peripheral pulmonary arteries and detection of small emboli compared with spiral computed tomography (CT) angiography.12,13 Because of its better spatial resolution, MSCT is becoming the new standard of reference for imaging nonmassive PE, and it is frequently used as the first-line imaging modality, alone or in combination with lung scintigaphy and inferior limb venous ultrasonography.12,13MSCT allows diagnosis of PE by disclosing vascular abnormalities (intravascular filling defects, total cutoff of vascular enhancement, or enlargement of an occluded vessel) and ancillary findings (pleura-based, wedge-shaped areas of increased attenuation with no contrast enhancement, linear atelectasis; Figure 3).12 CT can also evaluate the presence of deep venous thrombosis in the abdomen, pelvis, thighs, and calves without additional intravenous injection of contrast material by scanning the lower limbs 3 to 4 minutes after scanning of the pulmonary vessels.12Download figureDownload PowerPointFigure 3. A, MSCT shows filling defects at the bifurcation of the left and right pulmonary arteries (white arrow) and multifocal filling defects in the segmental level of the left pulmonary artery (white arrowhead). B, MSCT (lung window) of the same patient shows focal peripheral confluent opacities in the anterior segment of the left upper lobe (white arrow), which suggests pulmonary infarction.However, among persistently high-grade febrile patients, the presence of signs of PE should not deter one from searching for other potential causes of fever. The same CT examination can provide alternative explanations of fever (ie, thoracic or abdominal cancer, pneumonia or other infections) and is a valuable tool to identify septic PE phenomena.11,12 Characteristic CT findings in septic PE consist of discrete nodules with varying degrees of cavitation and subpleural, wedge-shaped heterogeneous areas of increased attenuation with rimlike peripheral enhancement. The nodules tend to be most numerous in the lower lobes. In many cases, a vessel can be seen leading directly to the nodules (“feeding vessel sign”).11,12 Unfortunately, these hallmark CT signs of septic PE are not always present (especially in case of fresh or large embolization), nor is the cause of PE always identifiable by CT (Table 2).14TABLE 2. Possible Causes of Septic PELemierre syndrome (septic thrombophlebitis of the internal jugular vein secondary to acute oropharyngeal infection)Right-sided IEInfected central venous catheterDental abscessPerinephric abscessOsteomyelitisSoft tissue infectionsRight-sided IE, a common cause of septic PE, is particularly difficulty to diagnose by CT because of the low temporal resolution of the technique, its inability to evaluate motion, and the presence of motion artifacts.15 Occasionally, some features, such as a filling defect inside the main pulmonary artery close to the pulmonary valve rather than the classic saddle embolus at the level of the bifurcation of pulmonary trunk, could suggest pulmonary IE (Figure 1). It is therefore crucial to maintain a high clinical suspicion of right-sided IE among patients with fever that is not justified by PE alone and without CT findings that potentially explain fever or septic PE phenomena, especially if the patient has risk factors for right-sided IE (ie, intravenous drug use, congenital heart defects, pacemaker leads, central venous lines, chronic alcoholism, dermal infections, malignancies, or immunologic deficiency).16,17 In this clinical scenario, transthoracic and transesophageal echocardiography should be performed without delay, even if not recommended by current guidelines on PE.18–20 Echocardiography has a strong diagnostic and prognostic role, with crucial therapeutic implications. Transthoracic echocardiography is generally adequate to correctly diagnose tricuspid vegetations.21 Transesophageal echocardiography should also be performed, because it is more sensitive in the diagnosis of pulmonary valve IE and pacemaker lead infections.22,23 Transesophageal echocardiography is also more valuable in recognizing prosthetic valve endocarditis and unusual locations of right-sided endocarditis (ie, the Eustachian valve) and in detecting IE complications (right-sided valvular insufficiency or dehiscence, congestive heart failure, and paravalvular abscesses).15,24,25In this group of patients, early implementation of echocardiography in the diagnostic algorithm alerts the clinician to appropriate antimicrobial therapy, which is usually sufficient to achieve remission of the infective disease without complications.11 Persistent fever despite antimicrobial therapy, vegetations larger than 1 cm, multivalvular involvement, and right-sided heart failure identify patients at higher risk who may benefit from surgical treatment.16,26 Conversely, not performing echocardiography or performing it too late in these patients could expose them to potential complications that sometimes lead to death or significant morbidity, related not only to the progression of infection but also to an incorrect or even harmful treatment.ConclusionsMSCT is frequently the first-line imaging modality in patients with suspected nonmassive PE. The use of echocardiography is limited to patients who are hemodynamically unstable and those with suspected massive PE; echocardiography may also be used to identify patients who could benefit from thrombolytic therapy.18,19 In the clinical scenario of documented nonmassive PE associated with unexplained persistent fever, early implementation of echocardiography could be of stronger diagnostic value, because right-sided IE could be the cause of septic PE. Its correct diagnosis can avoid potential complications related to inappropriate or even harmful treatment and to progression of infection, and it can address the appropriate antimicrobial (and eventually, surgical) therapy.DisclosuresNone.FootnotesReprint requests to Gaetano Nucifora, MD, Cardiopulmonary Science Department, Azienda Ospedaliero-Universitaria di Udine, P. le S. Maria della Misericordia 15, 33100 Udine, Italy. E-mail [email protected] References 1 Stein PD, Willis PW III, DeMets DL. History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. Am J Cardiol. 1981; 47: 218–223.CrossrefMedlineGoogle Scholar2 Murray HW, Ellis GC, Blumenthal DS, Sos TA. Fever and pulmonary thromboembolism. Am J Med. 1979; 67: 232–235.CrossrefMedlineGoogle Scholar3 Stein PD, Afzal A, Henry JW, Villareal CG. Fever in acute pulmonary embolism. Chest. 2000; 117: 39–42.CrossrefMedlineGoogle Scholar4 Kokturk N, Demir N, Oguzulgen IK, Demirel K, Ekim N. Fever in pulmonary embolism. Blood Coagul Fibrinolysis. 2005; 16: 341–347.CrossrefMedlineGoogle Scholar5 Chirinos JA, Heresi GA, Velasquez H, Jy W, Jimenez JJ, Ahn E, Horstman LL, Soriano AO, Zambrano JP, Ahn YS. Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism. J Am Coll Cardiol. 2005; 45: 1467–1471.CrossrefMedlineGoogle Scholar6 Calvo-Romero JM, Lima-Rodriguez EM, Perez-Miranda M, Bureo-Dacal P. 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Chest. 2005; 128: 162–166.CrossrefMedlineGoogle Scholar12 Han D, Lee KS, Franquet T, Muller NL, Kim TS, Kim H, Kwon OJ, Byun HS. Thrombotic and nonthrombotic pulmonary arterial embolism: spectrum of imaging findings. Radiographics. 2003; 23: 1521–1539.CrossrefMedlineGoogle Scholar13 Schoepf UJ. Diagnosing pulmonary embolism: time to rewrite the textbooks. Int J Cardiovasc Imaging. 2005; 21: 155–163.CrossrefMedlineGoogle Scholar14 Iwasaki Y, Nagata K, Nakanishi M, Natuhara A, Harada H, Kubota Y, Yokomura I, Hashimoto S, Nakagawa M. Spiral CT findings in septic pulmonary emboli. Eur J Radiol. 2001; 37: 190–194.CrossrefMedlineGoogle Scholar15 Sachdev M, Peterson GE, Jollis JG. Imaging techniques for diagnosis of infective endocarditis. Cardiol Clin. 2003; 21: 185–195.CrossrefMedlineGoogle Scholar16 Panidis IP, Kotler MN, Mintz GS, Segal BL, Ross JJ. Right heart endocarditis: clinical and echocardiographic features. Am Heart J. 1984; 107: 759–764.CrossrefMedlineGoogle Scholar17 Laguno M, Miro O, Font C, de la SA. Pacemaker-related endocarditis: report of 7 cases and review of the literature. Cardiology. 1998; 90: 244–248.CrossrefMedlineGoogle Scholar18 Task Force on Pulmonary Embolism, European Society of Cardiology. Guidelines on diagnosis and management of acute pulmonary embolism. Eur Heart J. 2000; 21: 1301–1336.CrossrefMedlineGoogle Scholar19 British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development Group. British Thoracic Society guidelines for the management of suspected acute pulmonary embolism. Thorax. 2003; 58: 470–483.CrossrefMedlineGoogle Scholar20 American College of Emergency Physicians Clinical Policies Committee; Clinical Policies Committee Subcommittee on Suspected Pulmonary Embolism. Clinical policy: critical issues in the evaluation and management of adult patients presenting with suspected pulmonary embolism [published correction appears in Ann Emerg Med. 2003;42:288]. Ann Emerg Med. 2003; 41: 257–270.CrossrefMedlineGoogle Scholar21 San Roman JA, Vilacosta I, Zamorano JL, Almeria C, Sanchez-Harguindey L. Transesophageal echocardiography in right-sided endocarditis. J Am Coll Cardiol. 1993; 21: 1226–1230.CrossrefMedlineGoogle Scholar22 Herrera CJ, Mehlman DJ, Hartz RS, Talano JV, McPherson DD. Comparison of transesophageal and transthoracic echocardiography for diagnosis of right-sided cardiac lesions. Am J Cardiol. 1992; 70: 964–966.CrossrefMedlineGoogle Scholar23 Vilacosta I, Sarria C, San Roman JA, Jimenez J, Castillo JA, Iturralde E, Rollan MJ, Martinez EL. Usefulness of transesophageal echocardiography for diagnosis of infected transvenous permanent pacemakers. Circulation. 1994; 89: 2684–2687.CrossrefMedlineGoogle Scholar24 Bach DS. 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February 13, 2007Vol 115, Issue 6 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.106.674358PMID: 17296860 Originally publishedFebruary 13, 2007 PDF download Advertisement" @default.
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