Systemic Pathology of Infective Endocarditis Table

Systemic manifestations of IE may be due to generalized sepsis, immune reactions—including immune complex disease—or related to emboli or ischemia with organ atrophy, ischemia, or infarction. Classic peripheral stigmata of IE may not be evident with right-sided IE or with infections due to HACEK organisms [22]. Similar to all disseminated infections, IE related sepsis may present with fever (or fever of unknown origin), leukocytosis, disseminated intravascular coagulation (diC), adult respiratory distress syndrome (diffuse alveolar damage), jaundice, and other sequelae of hypotension including multiorgan failure.

Table 2.3. Pathology of Systemic Sequelae of Infective Endocarditis Sepsis

Diffuse alveolar damage Cholestasis Systemic emboli Infarct / atrophy Abscess Roth spots Osler nodes Janeway lesions Splenic infarct or rupture Mycotic aneurysms Pulmonary emboli Infarct Abscess Empyema Immune complex phenomena Vasculitis


Renal manifestations include interstitial nephritis and pyelonephritis. There may be immune complex formation between bacterial antigens and antibodies, which deposits in the glomeruli leading to glomerular damage [47]. Focal necrotizing and diffuse proliferative glomerulonephritis may manifest as acute nephritis and renal failure. Type 1 membra-noproliferative glomerulonephritis may lead to nephrotic syndrome. Crescentic glomeru-lonephritis with rapidly progressive glome-rulonephritis can also occur. Emboli to the kidney may cause infarction, hematuria, flank pain, and renal abscesses.

Emboli may occur in right- and left-sided IE [48]. Emboli can occur before therapy, during therapy, or even after therapy [22]. Emboli from left-sided valve or cardiac lesions may affect any systemic organ leading to visceral infarction, ischemia, or organ atrophy. Either bland fibrin platelet material of the vegetation or infected components containing microorganisms may embolize. The propensity for embolization may be related to the size and mobility of the vegetation, as seen on echocardiogram [48].

The effect of the embolic material depends upon the size of the embolus, whether it contains microbes, the size of the occluded blood vessel, the degree of collaterals in the organ, and the metabolic demand of the organ. Vascular spasm may also contribute. If there are prominent numbers of organisms in the embolic material, the organ may form an abscess, in addition to an infarct, which is referred to as a septic infarct. Coronary arterial emboli may lead to angina, myocardial infarction or sudden death. Embolic myocardial infarcts are usually large, and myocardial abscesses may develop.

The central nervous system is the most common site involved by IE and neurologic deficits may be due to many different causes [22,48]. Cerebrovascular embolism may manifest as transient ischemic attacks or stroke. Cerebral infarcts may be hemorrhagic and non-hemorrhagic [49]. Mycotic aneurysms of infected cerebral arteries may thrombose or rupture (Figures 2.19, 2.20).

Figure 2.19. Gross photograph of the base of the brain with adherent blood clot. Subarachnoid hemorrhage occurred due to a ruptured mycotic cerebral artery aneurysm. The mitral valve was infected with bacteria. Ruler = 1 cm.
Splenic Infarct Pathology

Other serious neurological complications are cerebral abscesses and meningitis.

Splenic infarcts may cause abdominal, back, or flank pain. Splenic infarcts may be bland ischemic infarcts or septic infarcts both of which may lead to abscess formation [22]. Rarely the spleen may rupture, leading to intra-peritoneal bleeding. Gut ischemia and infarction may occur if the mesenteric circulation is embolized. Emboli to the limbs may cause acute ischemia or gangrene. When a vascular surgeon performs a thrombectomy or embolectomy in a patient with acute limb ischemia the removed material should be examined for infection with bacterial and fungal stains.

Right-sided endocarditis may lead to infected pulmonary emboli, pulmonary infarction, abscesses, and empyema. If large, these pulmonary emboli may cause sudden death. If there is an intracardiac shunt, either preexisting or developed due to IE, paradoxical embolism is possible with vegetation fragments embolizing into the systemic circulation bypassing the lung.

Osler nodes (tender subcutaneous nodules on the digits), Janeway lesions (red or hemorrhagic nontender lesion on the palms or soles), and Roth spots (retinal hemorrhages) are due to emboli to small blood vessels. These are now rarely encountered with modern medical care. Petechiae and subungual hemorrhages may be seen on the skin. Small-vessel vasculitis may be due to an infected embolus (a mycotic aneurysm) or immune complexes [50].

Mycotic aneurysms may occur in any circulation, but are most common in the central nervous system circulation [22,51]. Cerebral vessels are commonly involved, followed by visceral arteries and arteries of the extremities. Branch points are usually affected. They may develop in the aortic wall adjacent to the valve or distant to it. These aneurysms weaken the vessel wall and may rupture and hemorrhage even after the infection has been treated (Figures 2.19, 2.20]. Subclinical rupture may lead to pseudoa-neurysm formation. They also may thrombose. Surgical intervention is usually required [22].

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