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Splenic infarction is a common complication of left-sided IE (40 per cent of cases). Only 5 per cent of patients with splenic infarction will develop splenic abscess. This infection develops via 1 of 2 mechanisms Bacteremic seeding of a bland infarction, created via splenic artery occlusion by embolized vegetations, or direct seeding of the spleen by an infected embolus also originating from an infected valvular vegetation. Viridans streptococci and S aureus each account for 40 per cent of cases in which splenic abscess cultures are positive, whereas the enterococci account for 15 per cent of cases. Aerobic Gram-negative bacilli and fungi are isolated in, 5 per cent of cases. Clinical splenomegaly, present in up to 30 per cent of cases of IE, is not a reliable sign of splenic infarction or abscess. Splenic infarction delineated by imaging techniques is often asymptomatic Back, left-flank, or left-upper-quadrant pain or abdominal tenderness, when present, may be associated with either splenic infarction or abscess. Splenic rupture with hemorrhage is a rare complication of infarction. Persistent or recurrent bacteremia, persistent fever, or other signs of sepsis are suggestive of splenic abscess, Abdominal CT or MRI appear to be the best tests for diagnosis of splenic abscess, with sensitivities and specificities of 90 per cent to 95 per cent. On ultrasonography, a sonolucent lesion suggests abscess. Infarcts are generally associated with clinical and radiographic improvement during appropriate antibiotic therapy. Ongoing sepsis, recurrent positive blood cultures, and persistence or enlargement of splenic defects CT or MRI suggest splenic abscess, which responds poorly to antibiotic therapy alone. Definitive treatment is splenectomy with appropriate antibiotics. Percutaneous drainage or aspiration of splenic abscess is an alternative to splenectomy for the patient who is a poor surgical candidate. Splenectomy should be performed before valve-replacement surgery because of the risk of infection of the valve prosthesis as a result of the bacteremia from abscess.
As heart failure sets in, there is activation of RAS (Fig 2.1). Adrenergic stimulation of beta-1 receptors in juxtaglomerular apparatus of the kidneys results in release of renin.
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