**5. Abdomen and retroperitoneum**

#### **5.1. The spleen**

Septic embolism to the spleen is well described as a complication of IE [10]. In fact, after SE to the central nervous system (>50%), spleen appears to be the second most commonly involved organ in terms of frequency (approximately 30%), with some variability across sources of reported data [18, 28, 89]. One of most common presentations of SE to the spleen is the appearance of single or multiple abscesses [90], including microscopic lesions that were difficult-to-detect until the advent of advanced CT imaging [89]. Abdominal CT and MRI are the gold standard for diagnosing splenic abscesses [8]. Infected splenic artery aneurysms attributed to embolic sequelae of IE have also been reported [91]. Clinical management involves splenectomy in about 50% of cases, with percutaneous drainage indicated for large isolated abscesses and patients who are poor surgical candidates [29]. In cases of splenic arterial aneurysm and infarction, prompt surgical intervention is recommended. Patients should undergo drainage of the abscess or splenectomy prior to any cardiac surgery. This may help prevent further propagation and/or distant spread of the systemic infectious process [8, 91]. An example of splenic SE is shown in **Figure 3** [92].

usually characterized by leukocytosis, elevated pancreatic enzymes, peri-pancreatic "stranding" on CT scan, and acute abdominal pain [29]. Most often, pancreatic involvement in the setting of IE and SE tends to be self-limited [10]. At times, the finding of pseudoaneurysms involving adjacent arterial structures may provide a hint that the origin of the observed clini-

**Figure 3.** An example of septic embolus to the spleen. In this particular case, the embolus originated from *Corynebacterium diphtheriae* endocarditis (source: Ref. [92]. Image used under the terms of Creative commons Attribution-Noncommercial-

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Similar to the pancreas, SE to the kidneys is most often described in the setting of multi-visceral involvement [29]. Overall, renal SE are relatively frequent in the setting of IE, and their manifestations include infarcts in 31% of cases and glomerulonephritis in 26% [98]. Of interest, glomerulonephritis seen in association with IE has been shown not to feature immune complex deposition [98]. The co-occurrence of SE to other organs with arterial "high-flow" characteristics is exemplified by cases involving simultaneous cerebral, splenic, renal, and intestinal emboli [96]. Clinically, patients with renal SE may be found to have hematuria, glomerulonephritis, and evidence of renal failure [10]. Management focuses on preservation of renal function and is generally supportive, including antibiotic treatment, end-organ support (if required), and percutaneous or open interventions (in cases where abscess drainage is indicated) [98–100]. Etiology of renal injury in patients with IE is not always obvious, especially given the combined effect of cardiac dysfunction, sepsis, and concurrent treatment with potentially nephrotoxic antibiotics [98, 101]. Systemic infection can lead to acute tubular necrosis, while antibiotic treatment can lead to acute interstitial nephritis [102]. It is important to differentiate these conditions from the glomerulonephritis that is seen in IE, with an outline of important

Given its large surface area and rich vasculature, the bowel receives a significant amount of cardiac output and is highly susceptible to SE originating from IE [10, 29]. Fortunately, when compared to other organs and organ systems outlined above, arterial distribution to the

cal syndrome is a result of SE [97].

differentiating factors provided in **Table 2**.

**5.5. The intestines including mesenteric involvement**

**5.4. The kidneys**

NoDerivs Unported license).

#### **5.2. The liver**

Septic emboli to the liver are relatively common, occurring in >10% of cases of IE [10]. Similar to SE to the spleen, SE to the liver have the potential to evolve over time, coalescing from smaller "micro-abscesses" into larger collections [10]. Hepatic abscesses can be present in association with either right-sided or left-sided endocarditis [93, 94]; however, it may be difficult to determine whether the origin of the infection is cardiac or extra-cardiac, especially when the involved microorganism has known affinity for both locations [94]. Clinical management should follow established guidelines and practices for the treatment of IE and hepatic abscesses [29]. Similar to splenic abscess management, hepatic abscess should be drained as soon as possible in order to prevent worsening and/or further spread of the systemic infectious process [95].

#### **5.3. The pancreas**

Due to its vague clinical presentation, SE to the pancreas has the potential to go unrecognized. This is partially because SE to the pancreas often co-occurs with SE to other organs, potentially leading to "clinical masking" of organ-specific symptoms and/or signs [96]. Clinically, septic emboli to the pancreas may result in a picture resembling acute pancreatitis, and are

**Figure 3.** An example of septic embolus to the spleen. In this particular case, the embolus originated from *Corynebacterium diphtheriae* endocarditis (source: Ref. [92]. Image used under the terms of Creative commons Attribution-Noncommercial-NoDerivs Unported license).

usually characterized by leukocytosis, elevated pancreatic enzymes, peri-pancreatic "stranding" on CT scan, and acute abdominal pain [29]. Most often, pancreatic involvement in the setting of IE and SE tends to be self-limited [10]. At times, the finding of pseudoaneurysms involving adjacent arterial structures may provide a hint that the origin of the observed clinical syndrome is a result of SE [97].

#### **5.4. The kidneys**

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].

Septic embolism to the spleen is well described as a complication of IE [10]. In fact, after SE to the central nervous system (>50%), spleen appears to be the second most commonly involved organ in terms of frequency (approximately 30%), with some variability across sources of reported data [18, 28, 89]. One of most common presentations of SE to the spleen is the appearance of single or multiple abscesses [90], including microscopic lesions that were difficult-to-detect until the advent of advanced CT imaging [89]. Abdominal CT and MRI are the gold standard for diagnosing splenic abscesses [8]. Infected splenic artery aneurysms attributed to embolic sequelae of IE have also been reported [91]. Clinical management involves splenectomy in about 50% of cases, with percutaneous drainage indicated for large isolated abscesses and patients who are poor surgical candidates [29]. In cases of splenic arterial aneurysm and infarction, prompt surgical intervention is recommended. Patients should undergo drainage of the abscess or splenectomy prior to any cardiac surgery. This may help prevent further propagation and/or distant spread of the systemic infectious process [8, 91]. An example of splenic SE is shown in **Figure 3** [92].

Septic emboli to the liver are relatively common, occurring in >10% of cases of IE [10]. Similar to SE to the spleen, SE to the liver have the potential to evolve over time, coalescing from smaller "micro-abscesses" into larger collections [10]. Hepatic abscesses can be present in association with either right-sided or left-sided endocarditis [93, 94]; however, it may be difficult to determine whether the origin of the infection is cardiac or extra-cardiac, especially when the involved microorganism has known affinity for both locations [94]. Clinical management should follow established guidelines and practices for the treatment of IE and hepatic abscesses [29]. Similar to splenic abscess management, hepatic abscess should be drained as soon as possible in order to prevent worsening and/or further spread of the systemic infec-

Due to its vague clinical presentation, SE to the pancreas has the potential to go unrecognized. This is partially because SE to the pancreas often co-occurs with SE to other organs, potentially leading to "clinical masking" of organ-specific symptoms and/or signs [96]. Clinically, septic emboli to the pancreas may result in a picture resembling acute pancreatitis, and are

**5. Abdomen and retroperitoneum**

**5.1. The spleen**

156 Advanced Concepts in Endocarditis

**5.2. The liver**

tious process [95].

**5.3. The pancreas**

Similar to the pancreas, SE to the kidneys is most often described in the setting of multi-visceral involvement [29]. Overall, renal SE are relatively frequent in the setting of IE, and their manifestations include infarcts in 31% of cases and glomerulonephritis in 26% [98]. Of interest, glomerulonephritis seen in association with IE has been shown not to feature immune complex deposition [98]. The co-occurrence of SE to other organs with arterial "high-flow" characteristics is exemplified by cases involving simultaneous cerebral, splenic, renal, and intestinal emboli [96]. Clinically, patients with renal SE may be found to have hematuria, glomerulonephritis, and evidence of renal failure [10]. Management focuses on preservation of renal function and is generally supportive, including antibiotic treatment, end-organ support (if required), and percutaneous or open interventions (in cases where abscess drainage is indicated) [98–100].

Etiology of renal injury in patients with IE is not always obvious, especially given the combined effect of cardiac dysfunction, sepsis, and concurrent treatment with potentially nephrotoxic antibiotics [98, 101]. Systemic infection can lead to acute tubular necrosis, while antibiotic treatment can lead to acute interstitial nephritis [102]. It is important to differentiate these conditions from the glomerulonephritis that is seen in IE, with an outline of important differentiating factors provided in **Table 2**.

#### **5.5. The intestines including mesenteric involvement**

Given its large surface area and rich vasculature, the bowel receives a significant amount of cardiac output and is highly susceptible to SE originating from IE [10, 29]. Fortunately, when compared to other organs and organ systems outlined above, arterial distribution to the


**Table 2.** Types of kidney injury, including their associated differentiating characteristics [102].

bowel appears to be less commonly affected (e.g., superior mesenteric artery in 3%, inferior mesenteric in <1%) [103]. This may be, at least in part, due to the presence of some degree of redundancy within the mesenteric vasculature, as opposed to a lack of such redundancy in the kidney or spleen. Occlusion of the superior mesenteric artery by SE is relatively well described in the setting of mitral valve endocarditis [104]. Mesenteric pseudoaneurysm attributable to SE has also been described [105]. In cases of acute arterial occlusion, bowel infarction may follow without prompt restoration of adequate blood flow to the involved segment(s) of bowel [106].

and Janeway lesions are rare (2.7 and 1.6% cases, respectively) but highly suggestive of endocarditis [111]. **Figure 4A** shows an example of an Osler node, while **Figure 4B** demonstrates a

**Figure 4.** (A, left) An example of an Osler node in a patient with infective endocarditis (source: Ref. [112], image used in accordance with the terms of the CC BY 4.0 License); (B, right) Janeway lesions (see arrows) in a patient with aortic valve vegetation (source: Ref. [113], image used under the terms of the Creative Commons Attribution-NonCommercial

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This potentially devastating presentation has been reported in the setting of more severe cases of IE, often involving valve replacement [114–116], with some patients experience multiple/ recurring embolic events [114, 115]. In terms of clinical presentation, patients may exhibit a broad spectrum of complaints including pain, pallor, poikilothermia, and paresthesias with extreme cases threatening the viability of the limb itself [114]. Both surgical and thrombolytic management options have been reported [117, 118]. Prompt recognition of the cardiac source

Due to their non-specific nature and general commonality, joint-related complaints can be challenging to diagnose and easily misinterpreted. Not infrequently, multiple diagnostic tools must be utilized to successfully identify the cardiac source of the patient's original symptoms (and thus the proximal source of infection) [119]. In one case, it was the complaint of septic arthritis which led to the ultimate diagnosis of streptococcal endocarditis [120]. Similar to other embolic phenomena associated with IE, septic arthritis tends to be a manifestation of

This section will discuss a heterogeneous group of less common manifestations of SE affecting the CNS, including extracranial involvement. The paucity of published literature in this broad

Janeway lesion [112, 113].

4.0 International License).

**6.2. Septic arthritis**

**6.1. Acute extremity ischemia**

of SE is critical in preventing further embolic events.

multi-focal metastases of infectious material [119, 121].

**7. Uncommon neurologic presentations**

#### **5.6. Reproductive organs**

The involvement of reproductive organs in septic embolic complications is very uncommon. However, the authors believe that at least a brief overview of this under-recognized topic is warranted. In terms of testicular involvement, symptomatic presentation, including swelling, has been reported in conjunction with right-sided endocarditis [107]. It is thought that the this unusual clinical picture may result from SE [52, 107]. In another case, pneumococcal pulmonary valve endocarditis has been circumstantially linked to epididymo-orchitis and a scrotal abscess [108], although the directionality of causation may be difficult to prove except for the fact that *Streptococcus pneumoniae* isolated from the epididymo-orchitis is seldom a primary cause of scrotal infection. Equally uncommon, ovarian involvement has also been reported. In an exceedingly rare case, a female patient presented with a giant pyomyoma suggestive of ovarian neoplasm [109]. The origin of this presentation, however, was traced to *Streptococcus agalactiae* endocarditis and deep vein thrombosis of the right external iliac and femoral veins [109].
