Infective endocarditis acute

Ischemic stroke has numerous causes. Cerebral infarction may result from large artery atherosclerosis, cardiac embolism, small artery lipohyalinosis, cryptogenic embolism, or, more rarely, from other diverse conditions such as arterial dissection, infective endocarditis, and sickle cell disease. Arterial occlusion is the cause of at least 80% of acute cerebral infarctions. " ... 

Infective endocarditis Historically referred to as bacterial endocarditis, this is an infection, either acute or subacute, that primarily affects the heart valves, but may extend into other surrounding areas of the heart. 

Thrombotic thrombocytopenic purpura is a rare acute or subacute disease in adults, rather similar to the hemolytic uremic syndrome in children, in which there is systemic malaise, fever, skin purpura, renal failure, hematuria and proteinuria. Hemorrhagic infarcts caused by platelet microthrombi occur in many organs in the brain they may cause stroke-like episodes (Matijevic and Wu 2006) although more commonly there is global encephalopathy. The blood film shows thrombocytopenia, hemolytic anemia and fragmented red cells. The differential diagnosis includes infective endocarditis, idiopathic thrombocytopenia, heparin-induced thrombocytopenia with thrombosis, systemic lupus erythematosus, non-bacterial thrombotic endocarditis and disseminated intravascular coagulation. 

Kalashnikova LA, Nasonov EL, Stoyanovich LZ et al. (1994). Sneddon s syndrome and the primary antiphospholipid syndrome. Cerebrovascular Diseases 4 76-82 Kanter MC, Hart RG (1991). Neurologic complications of infective endocarditis. Neurology 41 1015-1020 Kaposzta Z, Young E, Bath PMW et al. (1999). Clinical application of asymptomatic embolic signal detection in acute stroke a prospective study. Stroke 30 1814-1818 Katzav A, Chapman J, Shoenfeld Y (2003). 

Ruby RJ, Burton JR (1977). Acute reversible hemiparesis and hyponatremia. Lancet i 1212 Sabolek M, Bachus-Banaschak K, Bachus R et al. (2005). Multiple cerebral aneurysms as delayed complication of left cardiac myxoma a case report and review. Acta Neurology Scandinavica 111 345-350 Sacco RL, Kargman DE, Gu Q et al. (1995). Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction. The Northern Manhattan Stroke Study. Stroke 26 14-20 Salgado AV (1991). Central nervous system complications of infective endocarditis. 

Continue therapy until apparent cure has been achieved most acute infections are treated for 5-10 days. There are many exceptions to this, such as typhoid fever, tuberculosis and infective endocarditis, in which relapse is possible long after apparent clinical cure and so the drugs are continued for a longer time, determined by comparative or observational trials. Otherwise, prolonged therapy is to be avoided because it increases costs and the risks of adverse drug reactions. 

Staphylococcal septicaemia may be suspected where there is an abscess, e.g. of bone or lung, or with acute infective endocarditis or infection of intravenous catheters high dose flucloxacillin is indicated (vancomycin). 

Acute and chronic osteomyelitis Septic arthritis/bursitis Prosthetic joint infections IV line infection Infective endocarditis... 

Prior to 1997, erythromycin was an alternative antibiotic choice to amoxicillin for prophylaxis prior to dental, oral, esophageal, and respiratory procedures to prevent infective endocarditis (IE). Erythromycin is an alternative choice for treating a recurrence of acute rheumatic fever in patients allergic to penicillin [12]. Recently updated recommendations by the American Heart Association for IE... 

Recent studies have shown that greater accuracy in the diagnosis of Q fever can be achieved by looking at specific levels of classes of antibodies other than IgG, namely IgA and IgM. Combined detection of IgM and IgA in addition to IgG improves the. specificity of the assays and provides better accuracy in diagnosis. IgM levels are helpful in the determination of a recent infection. In acute Q fever, patients will have IgG antibodies to phase II and IgM antibodies to phases I and II. Increased IgG and IgA antibodies to phase I are often indicative of Q fever endocarditis. 

Although used as a simulant, it can cause acute bacterial meningitis, pneumonia, intraabdominal infections, enteric infections, urinary tract infections, septic arthritis, endophthalmitis, suppurative thyroiditis, sinusitis, osteomyelitis, endocarditis, and skin and soft tissue infections. There are also strains of E. coli (C17-A015) that produce lethal cytotoxins (C16-A052). ... 

Endocarditis is often referred to as either acute or subacute depending on the clinical presentation. Acute bacterial endocarditis is a fulminating infection associated with high fevers, systemic toxicity, and death within days to weeks if untreated. Subacute infectious endocarditis is a more indolent infection, usually occurring in a setting of prior valvular heart disease. 

Fig. 16. Acute endocarditis in virus A/PR/8/34(HlNl) infected animal, the third day. Hematoxilin-eosin staining, magnification X 200.

Clinical improvement, especially the disappearance of fever or defervescence, is the best parameter to judge the response to therapy. However, clinical improvement can be difficult to monitor objectively in critically ill patients with multi-system disease. Also, clinical improvement can be very slow for certain infections, e.g. tuberculosis. The peripheral blood leukocyte count including the presence of early stages in leucocyte differention and the level of serum C-Reactive Protein (CRP, an acute phase protein) are parameters that can be sequentially determined to monitor improvement. For monitoring the effect of treatment of chronic infections such as endocarditis or osteomyelitis, weekly determination of the erythrocyte sedimentation rate has been proven useful. 

Cautions Recent major surgery (Coronary artery bypass graft, OB delivery, organ biopsy), cerebrovascular disease, recent GI or GU bleeding, hypertension, mitral stenosis with atrial fibrillation, acute pericarditis, bacterial endocarditis, hepatic/renal impairment, diabetic retinopathy, ophthalmic hemorrhaging, septic thrombophlebitis, occluded AV cannula at an infected site, advanced age, those receiving oral anticoagulants... 

Other causes of acute nephritis are reactions to drugs, acute infection of the kidneys, systemic diseases with immune complexes such as SLE, bacterial endocarditis, and finally disease in which the antigen is unknown but possibly related to antecedent viral infections. 

There are a number of nonspecific laboratory tests that are useful to support the diagnosis of infection. The inflammatory process initiated by an infection sets up a complex of host responses. Activation of complements, such as C3a and C5a, initiates inflammation and sets off a cascade of changes and the subsequent release of mediators, all of which can be measured and monitored. Serum complement concentrations, particularly C3, usually are consumed as part of the host defense mechanism and subsequently are reduced during the early stages of an acute infectious process. Acute-phase reactants, such as the erythrocyte sedimentation rate (ESR) and the C-reactive protein concentration, are elevated in the presence of an inflammatory process but do not confirm the presence of infection because they are often elevated in noninfectious conditions, such as collagen-vascular diseases and arthritis. Large elevations in ESR are associated with infections such as endocarditis, osteomyelitis, and intraabdominal infections. ... 

Blood cultures usually should be performed in the acutely ill febrile patient. Blood culture collection should coincide with sharp elevations in temperature, suggesting the possibility of microorganisms or microbial antigens in the bloodstream. Ideally, blood should be obtained from peripheral sites as two sets (one set consists of an aerobic bottle and one set an anaerobic bottle) from two different sites approximately 1 hour apart. In selected infections, bacteremia is qualitatively continuous (e.g., endocarditis), so cultures may be obtained at any time. ... 

The mitral and aortic valves are affected most commonly in cases involving a single valve. Subacute endocarditis tends to involve the mitral valve, whereas acute disease often involves the aortic valve. Up to 35% of cases involve concomitant infections of both the aortic and the mitral valves. Infection of the tricuspid valve is less common, with a majority of these cases occurring in patients with a history of IVDA. It is rare for the pulmonary valve to be infected. ... 

Patients with IE typically have laboratory abnormalities however, none of these changes is specific for the disease. Anemia (normocytic, normochromic), leukocytosis, and thrombocytopenia may be present. The white blood cell (WBC) count is often normal or only shghtly elevated, sometimes with a mild left shift. Acute bacterial endocarditis, however, may present with an elevated WBC count, consistent with a fulminant infection. The erythrocyte sedimentation rate (ESR) is elevated in 90% to 100% of patients, and the level of C-reactive protein also may be elevated. Often the urinary analysis is abnormal, with proteinuria and microscopic hematuria occurring in approximately 50% of individuals. 

---