Eur Radiol (2008) 18: 2433–2445 DOI 10.1007/s00330-008-1037-3

Teran W. Colen Martin Gunn Erin Cook Theodore Dubinsky

Received: 17 November 2007 Revised: 6 March 2008 Accepted: 6 April 2008 Published online: 4 June 2008 # European Society of Radiology 2008

T. W. Colen (*) . M. Gunn . E. Cook . T. Dubinsky Department of Radiology, University of Washington Medical Center, 1959 NE Pacific Ave, Box 357115 Seattle, WA, 98195, USA e-mail: [email protected] Tel.: +1-510-3871644

CARD IAC

Radiologic manifestations of extra-cardiac complications of infective endocarditis

Abstract Infective endocarditis (IE) is a disease with high morbidity and a mortality rate of 9–30%, even with appropriate diagnosis and therapy. Septic emboli, caused by IE, can affect any organ or tissue in the body with an arterial supply and occur in 12–40% of IE cases. The most common extracardiac organ system involved in IE is the central nervous system. Other organs frequently involved are the lungs (especially in right-sided IE), spleen, kidneys, liver, and the musculoskeletal system. In addition, the

Introduction Infective endocarditis (IE) is a disease with high morbidity and mortality. Even with appropriate diagnosis and therapy, the mortality rate is 9–30% [1]. The overall incidence of native valve endocarditis is estimated to be 1.5–11.6 per 100,000 persons per year. [2]. However, in people with cardiac-valve abnormalities, such as mitral valve prolapse, degenerative valve disease, rheumatic heart disease, or prosthetic valves, the incidence is higher [3]. In intravenous drug abusers (IVDAs), the incidence of IE is estimated at 150–2,000 per 100,000 persons per year [4]. However, in IVDAs, it is associated with a lower mortality, as the majority of these cases involve the right side of the heart and consequently these patients do not suffer devastating neurologic complications or heart failure as frequently. Non-cardiac predisposing conditions include poor dental hygiene, long-term hemodialysis, diabetes mellitus, and human immunodeficiency virus (HIV) infection [3]. With the increased use of permanent pacemakers (PPM) and implantable cardioverter defibrillators (ICD), the incidence of both lead- and valve-related vegetations has risen [5].

arterial system itself is susceptible to the development of potentially fatal mycotic aneurysms. As extra-cardiac complications often antedate the clinical diagnosis of IE, it is important that the diagnosis is suggested when characteristic findings are encountered during imaging. In addition, imaging is often used to monitor the extent of complications in patients with a known diagnosis of IE. Keywords Endocarditis . Infective . Septic emboli

The most common organism in IE is Staphylococcus aureus, which has been more prevalent than viridans streptococci in recent series [3]. Less frequent organisms include Streptococcus bovis, coagulase-negative staphylococci, enterococci [6], Coxiella burnetii (Q fever) [7], fungi (especially Candida [8]), and the HACEK group microorganisms [Haemophilus species (H. parainfluenzae, H. aphrophilus, and H. paraphrophilus), Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species) [9]. Fever, anorexia, weight loss, malaise, night sweats, and heart murmur are common, but non-specific, symptoms. The diagnosis of IE can be difficult to make in patients with few or absent classic peripheral stigmata [9], so standardized criteria, and the use of adequate valve imaging, have been developed to assess patients suspected of IE. The modified Duke criteria (Table 1) include several major and minor clinical criteria used in making the diagnosis of IE. The most serious complications of IE, and those with the greatest influence on prognosis, are congestive heart disease and neurological insults. Most commonly, congestive heart disease is caused by mechanical valvular damage due to the infection. Valvular vegetations are a result of

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Table 1 Modified Duke clinical criteria for diagnosis of infective endocarditisa Criterion level

Description

Major criteria

Positive blood culture (BC) Two separate positive BCs consistent with IE (V. streptococci, Streptococcus bovis, HACEKb group, S. aureus, and enterococci) in the absence of a primary focus Two positive BCs drawn >12 h apart or four positive BCs irrespective of the timing One positive BC for C. brunetii or antiphase-I immunoglobulin G antibody titer >1:800 Evidence of endocardial involvement Positive echocardiogram (transesophageal echo recommended in prosthetic valves rated at least possible IE by clinical criteria, or complicated IE; or transthoracic echo as the first test in other patients] Vegetation on valve or supporting structure Abscess New partial dehiscence of prosthetic valve New valvular regurgitation Predisposition (predisposing heart conditionc or intravenous drug use) Fever Vascular phenomena (major arterial emboli, intracranial or conjunctival hemorrhage, or Janeway’s lesions) Immunologic phenomena (glomerulonephritis, Osler’s node, Roth’s spots, or rheumatoid factor) Microbiological evidence: positive BC that does not meet major criteria or serological evidence of infection

Minor criteria

a Cases are defined as clinically definite if they fulfill two major criteria, one major criterion plus three minor criteria, or five minor criteria. Cases are defined as possible if they fulfill one major and one minor criterion, or three minor criteria b HACEK denotes Haemophilus species (H. parainfluenzae, H. aphrophilus, and H. paraphrophilus), Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species c High risk conditions include previous infective endocarditis, aortic-valve disease, rheumatic heart disease, prosthetic heart valve, coarctation of the aorta, and complex cyanotic congenital heart diseases. Moderate risk conditions include mitral valve prolapse with valvular regurgitation or leaf thickening, isolated mitral stenosis, tricuspid valve disease, pulmonary stenosis, and hypertrophic cardiomyopathy. Low or no-risk conditions include secundum atrial septal defect, ischemic heart disease, previous coronary bypass graft surgery, and mitral valve prolapse with thin leaflets in the absence of regurgitation

platelet and fibrin aggregation, bacterial adherence and proliferation, leading to thrombus formation [10]. The size and mobility of valvular vegetations are important predictors of whether or not the patient will develop septic emboli, the main causative factor for the extra-cardiac complications of IE [1]. Septic emboli can affect any organ or tissue in the body and occur in 12–40% of IE cases [11]. The most common extra-cardiac organ system involved in IE is the central nervous system. Other organs often involved are the lungs (especially in right-sided IE), spleen, kidneys, liver, and musculoskeletal system. In addition, the arterial system itself is susceptible to the development of potentially fatal mycotic aneurysms (Table 2). Apart from echocardiography, the utility of radiological imaging is not well established for the diagnosis of IE. Nevertheless, many case series describing the radiologic appearance of complications have been published [12–19]. Although transthoracic echocardiography can be used to effectively assess the presence of valvular vegetations and evaluate cardiac function [19], transesophageal echocardiography (TEE) is recommended as the first-line of investigation in patients with prosthetic valves, complicated IE, and in those rated as at least possible candidates for IE by the modified Duke criteria [20].

Although an increasing number of case reports are appearing in the literature that suggest that MRI [21] and multi-detector-row CT (MDCT) [22, 23] can be used to detect valvular vegetations (Fig. 1), the main role of these techniques is in monitoring the complications. The role of MRI in the assessment of valve function is well established, and a number of recent studies utilizing ECG-gated MDCT have shown promising results for morphological [24] and functional [25, 26] analysis of valves. It is likely that these techniques will play a greater role in the diagnosis of endocarditis in the future. This pictorial essay reviews the radiologic findings in the common extra-cardiac complications of IE. Complications are grouped by neurological, thoracic, abdominal, and musculoskeletal complications. Familiarity with these lesions in cases where IE is suspected as a possible etiology allow the radiologist to play an important role in this patient population that is often clinically challenging.

Neurologic complications Neurological complications are the most common extracardiac manifestations in IE and occur in approximately

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Table 2 Extra-cardiac complications of IE System

Complication

Central nervous system Thoracic Abdominal Musculoskeletal Vascular

Embolic stroke, intracranial hemorrhage, intracranial mycotic aneurysm, brain abscess, meningitis Septic pulmonary emboli, pulmonary edema, pulmonary abscess, pleural effusion/empyema, pneumothorax Renal infarction, renal failure, splenic infarction, hepatic infarction, mesenteric ischemia Spondylodiscitis, osteomyelitis, septic arthritis, peripheral soft tissue abscess Major arterial emboli, mycotic aneurysm (including aortic aneurysm), vasculitis (including aortits)

20–40% of cases [27]. Patients with neurological complications are also the group most associated with an increased mortality rate. CT, MRI, and angiography are useful in evaluating neurological complications [19].

ysms are seen in 2–10% of IE cases [10]. They are the result of septic embolization to the arterial vasa vasorum and spread of infection through the intima and destruction of the vessel wall. The most common organism involved is Streptococcus.

Embolic stroke Embolic stroke is the most common neurologic complication of IE and occur in 15–20% of IE cases [10]. In as many as 75% of IE cases complicated by stroke, the embolic stroke precedes the diagnosis of IE [2]. Staphylococcus aureus is by far the most common organism involved. Embolic strokes are seen most commonly in left-sided IE cases, especially affecting the mitral valve. The rate of symptomatic cerebral aneurysms is higher with vegetations >10 mm [6]. More than 90% of cases are in the middle cerebral artery vascular territory (MCA) [9]. They are typically located in a subsegmental distribution, at the corticomedullary junction, extending into the grey matter (Fig. 2). Embolic strokes are often multiple, can cause vasogenic edema, and can enhance in their subacute phase [28]. Most cases occur within 2–4 weeks after the initiation of microbial therapy [9]. Rarely, septic emboli can lead to meningitis and the formation of brain abscesses (Fig. 3). Computed tomography and MRI are highly sensitive and provide useful information on the distribution and extent of the embolic stroke and for determining if hemorrhage is present. This is useful clinical information because middlecerebral-artery cardioembolic stroke carries a much lower chance of neurological recovery than strokes in other sites [29], and surgery for hemorrhagic strokes should be delayed for 2–3 weeks [30]. Recent evidence [29] suggests that early cardiac surgery for uncomplicated embolic strokes carries a low risk of secondary cerebral hemorrhage and shows favorable short- and long-term survival [6]. Intracranial hemorrhage and intracranial mycotic aneurysm Intracranial hemorrhage is seen in 5% of IE cases [10]. It can be due to mycotic aneurysm rupture, hemorrhage transformation of embolic stroke, or secondary arteritis caused by vessel occlusion. Intracranial mycotic aneur-

Fig. 1 Mitral valve vegetation. Staphylococcus aureus mitral valve endocarditis in a 31-year-old male intravenous drug user with a 1month history of chills, fevers, and palpitations. a Transesophageal echo (TEE) demonstrates an echogenic mass on the posterior leaflet of the mitral valve (white arrow). b Non-gated CT scan of the abdomen with intravenous contrast, performed 2 days later, shows the vegetation as a hypodensity in the region of the posterior leaflet of the mitral valve

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Fig. 2 Embolic stroke. Mitral valve Staphylococcus aureus endocarditis with embolic cerebral infarctions in a 31-year-old male with history of IVDA, fevers, chills, and vomiting. a Noncontrast CT demonstrates a vague hypodensity in the right parietal region. b FLAIR, c diffusion, and d ADC mapping from MRI reveal multiple bilateral foci of signal abnormality at the corticomedullary junction. Findings are characteristic of, and represent, embolic infarctions

Intracranial mycotic aneurysms most commonly occur at the distal branch points of the MCA (Fig. 4) and are multiple in up to 29% of cases [2]. If present, they are associated with an overall mortality of 60%, and as high as 80% if ruptured [9]. They may present with a headache, focal neurological deficits, or altered mental status. Some intracranial mycotic aneurysms are thought to leak slowly, causing meningeal irritation. In this case, the lumbar puncture will often be sterile but have evidence of hemorrhage [9]. Although mycotic aneurysms can be seen with CT angiography and MRI/MRA, conventional angiography is more sensitive for aneurysm detection [2]. However, screening for mycotic aneurysms with conventional angi-

ography in IE cases is not warranted as most frequently septic emboli precede aneurysm formation [9]. Treatment of mycotic aneurysms remains an area of controversy due to their unpredictable nature. With antimicrobial therapy alone, some aneurysms regress, while others enlarge. Also, some patients develop new aneurysms and/or experience rupture while on treatment. The critical decision of whether to forego surgical treatment of an intracranial mycotic aneurysm until after valve replacement surgery can have disastrous consequences if the patient is to be placed on anticoagulation. Alternatively, if the patient undergoes craniotomy for aneurysmal clipping, the risk of congestive heart failure is increased. Endovascular therapy has been developed as a safe alternative to surgery and should be

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Fig. 3 Multiple brain abscesses. A 41-year-old male with aortic valve endocarditis and a history of IVDA presented with headaches and fevers. a Noncontrast CT demonstrates a large right temporal mass with hemorrhage and surrounding edema. b Contrast CT shows rim enhancement surrounding the mass. c Axial FLAIR shows the lesion to be hyperintense with vasogenic edema. d Coronal post-gadolinium T1 shows rim enhancement surrounding the lesion, a second rim enhancing lesion in the left frontal lobe (arrowhead), and enhancement of the meningeal layers adjacent to the larger lesion (long arrow), consistent with meningeal inflammation. Brain abscesses and meningitis are rare complications of IE

considered at the time the intracranial mycotic aneurysm is detected [31].

Thoracic complications Extra-cardiac thoracic complications typically occur as a consequence of right-sided IE and include septic pulmonary emboli, pulmonary infarction, pneumonia, pulmonary abscesses, pleural effusions, empyema, pneumothorax, and mycotic aneurysms of the pulmonary arteries [32].

Septic pulmonary emboli Septic pulmonary emboli occur in approximately 65–75% of patients with right-sided endocarditis [10]. Intravenous drug abusers account for approximately 75% of patients with septic pulmonary emboli [33]. The typical radiographic pattern is peripheral, poorly marginated bilateral lung nodules that often demonstrate cavitary changes and moderately thick irregular walls [34] (Fig. 5). Computed tomography is superior to radiography in showing the presence and extent of septic pulmonary emboli [34]. On CT, the nodules typically measure 5–35 mm [16], have a

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Fig. 4 Ruptured intracranial mycotic aneurysm. A 48-yearold immunosuppressed female with multiple medical problems including prior VSD repair, who presented with headache, nausea, and vomiting. TEE showed mitral valve endocarditis and blood cultures grew alpha hemolytic Streptococcus. a Noncontrast CT demonstrates a large left frontoparietal intraparenchymal hemorrhage with surrounding edema and mass effect on the left lateral ventricle. There is also intraventricular hemorrhage. b Gradient echo MRI demonstrates decreased signal intensity in the intraparenchymal and intraventricular hemorrhages, consistent with blood degradation products. c Oblique and d lateral views of a cerebral angiogram demonstrate a large mycotic aneurysm in a peripheral branch of the left middle cerebral artery

Fig. 5 Septic pulmonary emboli and empyema. A 47-yearold intravenous drug user with fever and cough and Staphylococcus aureus tricuspid valve endocarditis. a AP chest radiograph demonstrates bilateral pleural effusions. There are vague bilateral opacities in the lung apicies. b On CT there are multiple, bilateral peripheral cavitary lesions, typical of septic pulmonary emboli. c Inferiorly, there are bilateral pleural fluid collections

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peripheral and basilar predominance, and may demonstrate air-bronchograms. A “feeding vessel sign” has also been described [16], but a recent MDCT study [12] shows that most of these vessels either course around the nodule or represent a pulmonary vein [12], and that the condition is therefore nonspecific. Nodules may increase in number and change from day to day [34]. Empyema Empyemas are frequently associated with Staphylococcal infection [34]. Radiographs may show a pleural collection, which is immobile on decubitus views, or may be in a nondependent area if the collection is loculated. CT features include pleural effusion, thickening and enhancement of the visceral and parietal pleurae, and inflammation of the extrapleural fat (Fig. 5). Pulmonary edema Fifteen to 65% of patients with IE have associated heart failure [35] (Fig. 6), which is the most common cause of mortality in patients with IE [2]. Usually, heart failure develops with involvement of either the aortic valve or mitral valve [35]. The predominant cause is aortic or mitral valvular insufficiency from destruction, although less commonly it can be due to rupture of the chordae tendinae,

Fig. 7 Renal infarction. a A 46-year-old male with abdominal pain, acute renal failure, and HACEK endocarditis. Renal ultrasound demonstrates a hypoechoic region in the interpolar region of the right kidney (thick arrow). There is also a small amount of perinephric fluid (arrowhead). b Abdominal CT with intravenous contrast shows a wedge-shaped hypodensity in the right kidney (arrow)

vegetative embolization into the coronary arteries, or functional stenosis [2]. Damage to the valve can take only days, and acute heart failure may ensue rapidly [35]. Clinical and radiographic features of heart failure of IE may be subtle but are identical to those one would expect in acute heart failure of other etiologies [2].

Abdominal complications of IE Fig. 6 Congestive heart failure. A 41-year-old male presented with shortness of breath and right toe pain (due to common iliac artery occlusion). TEE showed mitral valve endocarditis with regurgitation, confirmed with positive cultures for Streptococcus viridans. Portable AP chest radiograph demonstrates acute alveolar pulmonary edema and cardiomegaly

Common sites for abdominal complications of IE include the kidneys and spleen and, in the majority of cases, the complications are due to septic emboli, leading to infarction. Rarely, the formation of abscesses can occur following infarction. Renal failure is also sometimes seen. Liver and bowel complications are uncommon.

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Renal emboli

Renal failure

Renal involvement in IE is a common extra-cardiac manifestation of IE. Renal embolic infarctions occur in up to 66% of cases [36]. Clinically, patients may present with flank pain or hematuria. Gray-scale ultrasound is insensitive for detecting acute renal infarction, and detection of renal perfusion defects with Doppler techniques is limited, although contrast-enhanced ultrasonography appears promising [37]. Perinephric fluid may be seen as an indirect sign of infarction. On gray-scale ultrasound, lesions may appear hypoechoic (Fig. 7). Renal infarcts are often demonstrated on contrast-enhanced CT as multiple wedge-shaped hypoperfusion defects. The “cortical rim sign” is seen in half of renal infarctions owing to the early branching and collateral flow of the capsular arteries, leading to preserved cortical perfusion adjacent to a wedge-shaped area of hypoperfusion (Fig. 7b). Interestingly, renal emboli/infarction can occur several months after blood cultures are cleared of infection. Rarely, renal infarctions can progress to abscess [36, 38].

Renal insufficiency is observed in 15–33% of IE cases [4]. Most commonly, this is as a result of ischemia and nephrotoxic therapy. Decreased perfusion to the kidney can be detected on contrast-enhanced CT as a relative decrease in attenuation to the affected kidney or kidneys. Less commonly, renal insufficiency is seen as a result of renal emboli or glomerulonephritis. Splenic emboli Splenic emboli are seen in as many as 55% of IE cases, especially in cases where Staphylococcus is the pathogen. Clinically, patients may present with left upper quadrant pain or referred pain to the left shoulder. In the early stages, splenic infarctions are hemorrhagic and will often appear as wedge-shaped hypodensities, predominately peripherally, compared to the unaffected spleen parenchyma (Fig. 8). Typically, this is seen on non-contrast CT as well as contrast-enhanced CT. Later, they become smaller in size, fibrose, and more dense. Rarely, as with renal infarcts, splenic infarcts can progress to splenic abscesses. As these lesions are associated with high mortality, percutaneous drainage is required, and if inadequate, splenectomy is often required. Mesenteric ischemia Mesenteric ischemia, leading to bowel infarction, is an uncommon complication of IE. However, it is associated with a high mortality, approaching 70%. If bowel ischemia does occur in IE, it is most often the result of embolic phenomenon, hypoperfusion due to cardiac insufficiency, or secondary to mycotic aneurysm formation (Fig. 9). These patients often present with abdominal pain, guiacpositive stools, and/or ileus.

Musculoskeletal complications

Fig. 8 Splenic infarction. Same patient as Fig. 2. a Abdominal CT with intravenous contrast shows a wedge-shaped hypodensity in the periphery of the spleen. b Coronal reformat from the abdominal CT shows the extent of the splenic infarction

Musculoskeletal manifestations of IE occur frequently and are present in up to 44% of cases [39]. However, the majority of cases are self-limiting and consist of arthralgia, myalgia, low back pain, and aseptic peripheral arthritis. Other peripheral musculoskeletal complications due to embolic events include spondylodiscitis, osteomyelitis, septic arthritis, sacroiliitis, muscular infarcts, and peripheral abscesses. The presence of osteoarticular complications puts the patient at a higher risk of having major embolic events to the CNS or lungs [17].

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Fig. 9 Superior mesenteric artery mycotic aneuerysm and occlu-" sion. Same patient as Fig. 6. a Sagittal and b coronal 10-mm maximal intensity projection (MIP) images from a CTA of the chest abdomen and pelvis demonstrate a mycotic aneurysm with superior mesenteric artery (SMA) occlusion. The artifact from the balloon pump is visible on the sagittal MIP

Spondylodiscitis Spondylodiscitis occurs in 1.8–5% of IE cases [30]. Overall, in patients with spondylodiscitis, an underlying diagnosis of IE may be as high as 31% [40]. Patients with spondylodiscitis and a history of pre-existing heart disease or appropriate microbiologic patterns should be investigated for IE [41]. Some have also suggested that in patients with IE and back pain, pyogenic spondylodiscitis should be investigated [40]. Neurologic sequelae of spondylodiscitis, such as epidural abscess and paralysis, are less common in patients with IE [40] and have been more frequently observed in cases involving Staphylococcus. Patients with spondylodiscitis usually do not present until infection has spread across a disc and involves at least two vertebral body levels. MRI is highly sensitive and specific for diagnosing spondylodiscitis. Typical MRI findings include low signal marrow on T1-weighted images, high signal on T2weighted images and contrast enhancement of the marrow on post-gadolinium T1-weighted images with erosion destruction of at least one vertebral endplate (Fig. 10) [42]. The disc may also enhance if an abscess has not formed, and there is usually evidence of paraspinal or epidural enhancement. Nuclear scintigraphy, which is highly sensitive but only modestly specific for spondylodiscitis, will show a focal area of increased radiotracer uptake at the involved levels on bone scan [43] (Fig. 10). Osteomyelitis and septic arthritis Osteomyelitis and septic arthritis are reported to occur in up to 4.3% of cases of IE. These complications occur more frequently in IVDAs (17.8%) and in patients with tricuspid valve involvement [17]. Infections have a predilection for the large joints, including the hip, knee, ankle, shoulder, and sacroiliac joints (Fig. 11) [17]. MRI is highly sensitive for the diagnosis of osteomyelitis and septic arthritis. However, MRI diagnosis of septic arthritis is usually not specific and is similar to any inflammatory arthritis. If the diagnosis of septic arthritis is suspected clinically, the joint should be aspirated. On MRI, osteomyelitis typically demonstrates low signal intensity on T1-weighted images and high signal intensity on T2-weighted images and enhances on post-gadolinium T1-weighted images. Additional findings of an intra-osseous abscess, sequestrum, cortical destruction, or a cloaca may be present.

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developing IE [44], thus the two often occur in combination. Additionally, emboli to the extremities can cause mycotic aneurysms, peripheral muscular infarcts, and embolic abscesses. Although both ultrasound and CT are useful for the diagnosis of soft-tissue abscesses, MRI is the preferred imaging investigation. Typical MRI findings include low signal on T1-weighted sequences, high signal on T2-weighted sequences, and peripheral contrast enhancement on post-gadolinium T1-weighted sequences.

Vascular complications of IE Vascular complications are important in IE and are listed among the minor criteria for the modified Duke criteria [9]. They include major arterial emboli, septic pulmonary emboli, mycotic aneurysm, intracranial hemorrhage, and

Fig. 10 Spondylodiscitis with epidural abscess. A 46-year-old male IVDA who presented with fevers, back and right hip pain, aortic and tricuspid valve vegetations, and Staphylococcus aureus bacteremia. a Sagittal CT of the lumbar spine demonstrates grade 1 anterolisthesis of L5/S1 with increased density of the L5 and S1 vertebral bodies and increased density in the epidural space (thin arrows). b Sagittal T2 MRI shows increased signal intensity with destruction of the L5 and S1 vertebral bodies. c Axial T1 post-gadolinium with fat saturation demonstrates abnormal enhancement of L5/S1 region with extension into the epidural (thick arrow) and prevertebral space. d Sagittal and e axial SPECT from a technetium-99m methylene-diphosphonate bone scan demonstrate increased radiotracer uptake in the L5/S1 region, consistent with increased bone turnover

Peripheral soft-tissue infections Skin and subcutaneous abscesses occur commonly in IVDAs, usually at the site of injection rather than as embolic events from IE [44]. However, a history of skin abscesses does increase the probability of an IVDA

Fig. 11 Sacroiliac septic arthritis. A 28-year-old male active intravenous drug user with recurrent Streptococcus viridans and Streptococcus mitis endocarditis after aortic valve replacement for IE. a AP pelvic radiograph demonstrates asymmetrically increased density of the right sacroiliac joint. b T1 post-gadolinium with fatsaturation MRI demonstrates abnormal enhancement of the right sacroiliac joint with associated soft-tissue inflammation

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vasculitis. Given the pathophysiology, most of these entities can be seen in any organ [9]. Mycotic aneurysm Fifteen to 25% of IE patients develop mycotic aneurysms [35], which most often occur in subacute IE. They are often multiple and may involve any vessel, but they most frequently occur in the CNS, sinuses of Valsalva, abdominal aorta, superior mesenteric artery (Fig. 12), and splenic, pulmonary and coronary arteries. The pathogenesis is most commonly due to embolization to the vaso vasorum with subsequent spread of infection through the intima and vessel wall. The predilection of mycotic aneurysm for branch points likely reflects sites for impaction [3]. Aortitis, intra-aortic vegetations, or pseudoaneurysms may occur as a consequence of aortic root abscesses

associated with an infected native or prosthetic aortic valve [45]. Although mycotic aneurysms arising in the abdominal aorta and its mesenteric branches are frequent sites of mycotic aneurysm development, they are frequently not recognized until they rupture [35]. Some authors have recommended performing empiric angiographic surveys with elective repair of lesions in the mesenteric circulation [35]. However, with the advent of high-quality MDCT [13] and gadolinium-enhanced MRA, these non-invasive techniques are likely to surpass diagnostic catheter angiography as screening examinations. Major arterial emboli Systemic embolization can occur in 22–50% of cases of IE [9]. In pooled data and meta-analyses, systemic embolization was increased in patients with vegetations larger than 10 mm [46], in younger patients [47], and in those with mitral valve involvement [9]. It can precede diagnosis, occur during therapy or after therapy has been completed [9] (although the rate of embolization falls rapidly following initiation of antibiotic therapy). In extremities, emboli may produce pain or overt ischemia. Vasculitis Vasculitis is thought to be due to the deposition of circulating immune complexes on various endothelial locations, leading to complement activation and vascular injury [35]. This yields several of the classic cutaneous findings (Janeway lesions, petechiae, Osler’s nodes, and splinter hemorrhages), and is thought to play a role in the development of other organ complications in the kidney and CNS.

Conclusion

Fig. 12 Ruptured ileocolic mycotic aneurysm. A 73-year-old patient with abdominal pain and distention, vomiting, rash, murmur, and palpable right flank mass. TEE showed a 14-mm vegetation on aortic valve, and blood cultures were positive for Streptococcus anginosus. a Axial CTA demonstrates intraperitoneal fluid and fat stranding in the right abdomen with an abnormal central collection of contrast, consistent with a mycotic aneurysm. b A coronal reformation shows the mycotic aneurysm at a distal branch of the ileocolic artery

IE is a multi-system disease with a diverse range of cardiac and extra-cardiac manifestations with a potential for significant mortality and morbidity. It is important for radiologists to keep this disease entity in mind when encountering its complications because they often precede the diagnosis of IE. If a finding suggestive of infective endocarditis in encountered by the radiologist, auscultation of the heart, followed by transesophageal echocardiography should be considered. Routine screening of the CNS, lungs, abdomen, and pelvis has not been advocated in patients with IE. However, MRI/ MRA or CT/CTA of the brain and intracranial vessels should be performed prior to cardiac surgery and in patients with neurological symptoms. CT of the chest, abdomen, and pelvis should be considered when patients have pulmonary or abdominal symptoms. Additionally, for IE patients presenting with back pain, MRI has high sensitivity and specificity for the evaluation of spondylodiscitis.

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