**4. The thorax**

Given the pathophysiologic factors discussed earlier in the chapter, SE of cardiac origin tend to follow the pattern of "cardiac output." Consequently, a generalization can be made that the higher the blood flow to a specific organ or anatomic region, the higher the chance of SE traveling there. Within the thorax, there are two commonly described types of septic emboli those originating on the "left side" of the heart and involving the coronary arterial circulation or thoracic aorta [56, 57], and those originating from the "right side" and involving the pulmonary arterial circuit [58–60].

#### **4.1. Coronary circulation**

First described in the 1910s and 1920s, septic coronary embolism continues to be under-recognized as a cause of acute coronary ischemia [56]. These types of emboli predominantly originate from bacterial valvular vegetations [61]. A high index of clinical suspicion is required because electrocardiographic (ECG) and laboratory changes characteristic of myocardial ischemia can easily be misinterpreted as being due to more typical coronary artery thrombosis [29]. The diagnosis is established through the performance of a comprehensive work-up, including trans-thoracic and trans-esophageal echocardiography (TEE), with subsequent angiography as indicated [62, 63]. Management may include a variety of both non-interventional and interventional procedures, up to and including surgical cardiac revascularization at the time of valve replacement [29].

#### **4.2. Thoracic aorta**

of severe ischemic stroke, it is recommended to delay surgery by at least 4 weeks, and with hemorrhagic stroke (usually a more severe complication) at least 4 weeks are recommended

Septic embolization involving ocular and facial structures is extremely rare. There is, however, fragmentary case-based evidence for such occurrences. In one example, Dadu et al. [52], described SE involving the ophthalmic artery and the inferior muscular artery, resulting in diplopia due to medial rectus muscle paralysis. In that particular case, IE of the mitral valve was causative. In another rare occurrence, Cumurcu et al. [53], describe a case of a septic

The possibility of SE to the thyroid has been proposed in 1959 by Richie while describing acute suppurative thyroiditis in a child [54]. Cabizuca et al. [55], reported an unusual case of IE leading to acute thyroiditis, presumably due to septic embolization. Although undoubtedly uncommon, the paucity of literature reports in this area is likely due to limited aware-

Given the pathophysiologic factors discussed earlier in the chapter, SE of cardiac origin tend to follow the pattern of "cardiac output." Consequently, a generalization can be made that the higher the blood flow to a specific organ or anatomic region, the higher the chance of SE traveling there. Within the thorax, there are two commonly described types of septic emboli those originating on the "left side" of the heart and involving the coronary arterial circulation or thoracic aorta [56, 57], and those originating from the "right side" and involving the pul-

First described in the 1910s and 1920s, septic coronary embolism continues to be under-recognized as a cause of acute coronary ischemia [56]. These types of emboli predominantly originate from bacterial valvular vegetations [61]. A high index of clinical suspicion is required because electrocardiographic (ECG) and laboratory changes characteristic of myocardial ischemia can easily be misinterpreted as being due to more typical coronary artery thrombosis [29]. The diagnosis is established through the performance of a comprehensive work-up, including trans-thoracic and trans-esophageal echocardiography (TEE), with subsequent angiography as indicated [62, 63]. Management may include a variety of both non-interventional and interventional procedures, up

to and including surgical cardiac revascularization at the time of valve replacement [29].

prior to proceeding with cardiac surgery [50].

metastasis to the iris, resulting in iris abscess and endophthalmitis.

ness and under-recognition of similar clinical presentations.

**3.2. Eyes**

154 Advanced Concepts in Endocarditis

**3.3. Thyroid**

**4. The thorax**

monary arterial circuit [58–60].

**4.1. Coronary circulation**

Mycotic aneurysms of the aorta have been described as a consequence of septic emboli from infective endocarditis [64]. Clinical management of these lesions is challenging, partly due to the presence of active infection within the aneurysm itself, and partly due to the associated inflammatory changes and altered (e.g., diminished) structural integrity of the involved aorta [65]. Mycotic aortic aneurysms are associated with significant mortality and complications, including the potential for the development of aortoesophageal or aortotracheobronchial fistula [66, 67].

#### **4.3. Pulmonary artery**

Pulmonary artery aneurysms (PAA) of infectious etiology are among less frequently seen complications of endocarditis [68, 69]. They are similar to mycotic aneurysms, with the main difference being the location of occurrence [70]. PAAs (also referred to as Rasmussen's aneurysms) can be seen in patients with tuberculosis. However, there have been recent cases with PAAs being associated with endocarditis [70, 71]. These aneurysms require prompt surgical treatment given published mortality rates of approximately 50% [72]. Patients with aneurysms that are symptomatic or >6 centimeters in size are candidates for surgery [73]. Data regarding surgical treatment are limited; however, recent studies have shown that steel coil embolization may be applicable in this setting [70, 74–76]. While PAAs are uncommon in endocarditis, they should be considered in patients with IE that present with pulmonary symptoms.

#### **4.4. Pulmonary circulation**

Pulmonary SE are relatively common complications of right-sided IE (RSIE). As outlined in previous sections, any areas through which large volume of blood transits will be inherently susceptible to SE. The pulmonary arterial circuit is no exception in this regard. From an anatomic standpoint, evidence suggests that septic pulmonary emboli (SPE) involve both upper and lower lobes, with bilateral upper lobes involved in >70% of patients, and peripheral or subpleural zones involved in >90% of cases [58]. Centrally located lesions were noted in only about 25% of instances [58]. SPE are distinct from other types of pulmonary emboli because of their tendency to form cavitary lesions with air-fluid levels [77]. A significant proportion of patients with RSIE are intravenous drug users [78, 79], although there is an increasing number of patients with SPE who present with IE due to implanted cardiac devices [80, 81]. SPE in intravenous drug users can manifest with empyema, and is most likely to be associated with endocarditis due to *S. aureus* infection [82]. Other common complications of SPE include pulmonary abscess and pulmonary nodules [77]. If patients with either empyema or a pulmonary abscess are identified, it is crucial to continue intravenous antibiotics and preform an incision and drainage prior to any required valve surgery [83]. Waiting is not recommended as a strategy in these patients, mainly because of the risk of further complications associated with therapeutic delays [83, 84]. Pulmonary and perivalvular abscess should be suspected in intravenous drug users who fail to respond to antibiotic administration [84].

As with any other type of pulmonary embolism (PE), SPE can be life threatening [85–87]. It is important to note that it may be initially difficult to differentiate between the two types of PE. Consequently, diagnosis and management requires high levels of clinical suspicion, appropriate diagnostics (e.g., TEE), and immediate treatment (antibiotics, with surgery if indicated). Most SPE patients present with constitutional symptoms, dyspnea, chest pain, and cough (including hemoptysis) [58]. CT imaging may show the presence of cavitary lesions with an associated "feeding vessel sign," representing a pulmonary artery coursing directly into the infected area [88].
