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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with infective endocarditis are frequently first evaluated in an emergency department at a time when clinical data are insufficient for a conclusive diagnosis. The records of 22 patients with proven bacterial endocarditis first seen in our emergency department were reviewed. The most common feature of the initial history was the presence of fever in 11 (50%). The most common physical finding was a heart murmur in 18 (82%). All patients had positive blood cultures. The most frequently isolated organism was Staphylococcus aureus. Pertinent clinical and laboratory data available on admission that enabled the emergency physician to suspect infective endocarditis were systemic manifestations of fever, malaise and arthralgias together with anemia, leukocytosis and hematuria.
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PMID:The recognition of infective endocarditis. 47 Feb 74

Bacterial endocarditis is an elusive disease that challenges clinicians' diagnostic capabilities. Because it can present with various combinations of extravalvular signs and symptoms, the underlying primary disease can go unnoticed.A review of the various extracardiac manifestations of bacterial endocarditis suggests three main patterns by which the valvular infection can be obscured. (1) A major clinical event may be so dramatic that subtle evidence of endocarditis is overlooked. The rupture of a mycotic aneurysm may simulate a subarachnoid hemorrhage from a congenital aneurysm. (2) The symptoms of bacterial endocarditis may be constitutional complaints easily attributable to a routine, trivial illness. Symptoms of low-grade fever, myalgias, back pain and anorexia may mimic a viral syndrome. (3) Endocarditis poses a difficult diagnostic dilemma when it generates constellations of findings that are classic for other disorders. Complaints of arthritis and arthralgias accompanied by hematuria and antinuclear antibody may suggest systemic lupus erythematosus; a renal biopsy study showing diffuse proliferative glomerulonephritis may support this diagnosis. The combination of fever, petechiae, altered mental status, thrombocytopenia, azotemia and anemia may promote the diagnosis of thrombotic thrombocytopenic purpura. When the protean guises of bacterial endocarditis create these clinical difficulties, errors in diagnosis occur and appropriate therapy is delayed. Keen awareness of the varied disease presentations will improve success in managing endocarditis by fostering rapid diagnosis and prompt therapy.
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PMID:Extracardiac manifestations of bacterial endocarditis. 51 15

In this paper demographic characteristics, etiology, pathology and clinical features of infective endocarditis are reviewed simultaneous presentation of the data from our series of 50 cases with infective endocarditis. The peak incidence of infective endocarditis is between 11 and 15 years. Both sexes are equally affected. Patients with congenital or acquired heart disease tend to have hemodynamic trauma to the endocardium and vascular endothelium. These sites form the nidus for circulating bacteria of either spontaneous origin or the result of any oro-dental, genitourinary or other surgery or procedures and produce vegetations characteristic of infective endocarditis. The location of the vegetation is dependent upon the predisposing cardiac lesion. Embolic phenomenon is another cardinal feature of endocarditis and may occur in any organ system. Although a large variety of microbes have been known to cause endocarditis, streptococci and staphylococci remain the most frequent offenders. Clinical diagnosis of infective endocarditis is difficult because of the insidious onset and varied clinical features. A high degree of suspicion is essential for early diagnosis. Any patient with known heart disease and unexplained fever should be suspect for endocarditis. Splenomegaly, petechiae and embolic phenomena support this diagnosis. New or changing murmurs, splinter hemorrhages, Osler's nodes. Janeway's lesions and Roth's spots may be present. Elevated sedimentation rate, microscopic hematuria, leukocytosis with a shift-to-the-left and anemia may further support the diagnosis. Congenital or acquired heart disease and fever are all that will be present in many cases. Only isolation of the causative agent from the blood can confirm the diagnosis.
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PMID:Infective endocarditis: a review. I. Incidence, etiology, pathology and clinical features. 72 71

The clinical, laboratory, and histopathological features of seven cases of Aspergillus fumigatus prosthetic valve endocarditis are presented. The exact nature of the lesion, a combination of infective fungal endocarditis and thrombosis on the prosthetic valve, is discussed and the difficulties in clinical diagnosis are emphasized. Helpful indications were sudden unexplained heart failure with the appearance of new murmurs, and emboli to large or medium-sized systemic arteries. Fever and anaemia were inconstant, and in no case was blood culture or precipitin investigation helpful. Spore contamination of operating theatre air was the likely source of infection, and measures taken to overcome this and other predisposing factors are discussed. Since medical diagnosis is usually late and the few reported cures in this condition have included replacement of the prosthesis, early surgical intervention combined with antifungal chemotherapy is advised.
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PMID:Aspergillus prosthetic valve endocarditis. 78 18

Rabits with Streptococcus viridans aortic valve endocarditis develop anaemia and reticulocytosis which increase with the duration of infection. Mean red cell counts decreased from 6.05 +/- 0.29 X 10(6) per mul before infection to 4.10 +/- 0.18 X 10(6) per mul after 11 to 20 days of endocarditis and reticulocytes increased from 1.16 +/- 0.14 X 10(5) per mul to 4.91 +/- 0.83 X 10(5) per mul after more than 20 days of endocarditis. The anaemia could not be explained by intravascular haemolysis. Anti-erythrocyte antibodies were not detected. Splenomegaly was a consistent finding and also increased with the duration of infection. Red cell half life (T1/2) was shortened to 4.7 +/- 0.3 days in rabbits with endocarditis compared with normal T1/2 of 11.1 +/- 0.5 days. The T1/2 of red cells from infected animals was prolonged when measured in noninfected rabbits and splenectomized animals had a mean red cell T1/2 of 9.25 days after three weeks of infection. These studies suggest that splenic enlargement associated with infection results in red cell sequestration, a mechanism not well recognized as contributing to the anaemia of endocarditis.
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PMID:Mechanism of anaemia in experimental bacterial endocarditis. 119 67

Two cases of disseminated histoplasmosis caused by H. capsulatum in Nigerian children are reported. This is a rare infection in this part of the world. The main clinical features were fever, weight loss, lassitude, lymphadenopathy, hepatosplenomegaly and severe anaemia, features indistinguishable from those of tuberculosis, Hodgkins and other reticuloses. Recognition of this infection in this environment is possible if it is considered in the differential diagnosis of pyrexia of undetermined origin and appropriate laboratory tests carried out on suitable specimens such as bone marrow, splenic aspirate or biopsy material. Treatment of choice is amphotericin B given intravenously, starting with 0-25 mg/kg. and increasing slowly to 1 mg/kg. Other useful drugs are Septrin and rifampicin which can be given concurrently. Subcutaneous abscesses and multiple bone lesions occurred in both our cases presumably as a result of blood stream infection, or embolisation from endocarditis.
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PMID:Disseminated histoplasmosis due to histoplasma capsulatum in two Nigerian children. 122 26

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

The authors investigated the cause of cerebral infarctions in elderly patients with anemia. Among 411 patients with acute cerebral infarctions, eight patients showed anemia (Hb < 10 g/dl) at the time of stroke. Only 2 patients had strokes during hospitalization were aware of their anemias before stroke. They were classified into two groups. One was the sudden onset group (4 patients) of whom 3 had malignant tumors, and 2 showed disseminated intravascular coagulations (DIC). There were no patients with atrial fibrillation or cardiac disease. All patients showed cortical infarction, and two died soon after stroke. Autopsy revealed verruca formation of the mitral valve in one patient and thrombus in the right ventricle in another. We thought that non-bacterial thrombotic endocarditis (NBTE) was the major cause of cerebral infarctions in this group. The other group consisted of 4 cases of thrombotic stroke. Their neurological symptoms appeared to be progressive. They also showed cortical infarctions except for one case of pontine infarction. Severe stenosis of the cerebral arteries was revealed by angiography in two patients and by autopsy in one. We concluded that cerebral infarctions in elderly patients with anemia can be important signs of underlying malignant tumors in sudden onset strokes or cases of severe cerebral artery stenosis with thrombotic strokes.
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PMID:[Cerebral infarctions in elderly patients with anemia]. 149 44

A 50-year-old man complained of lumbar pains, lack of energy, dysarthria and ataxic gait. Investigation revealed progressive anaemia (haemoglobin initially 10.5 g/dl, later 6.8 g/dl) and thrombocytopenia (initially 67,000/microliters, later 25,000/microliters). In addition he had unexplained pyrexia of up to 39.8 degrees C. Lactate dehydrogenase was 780 U/l and fragmented red cells were noted in the blood film. Because of suspicion of thrombotic thrombocytopenic purpura, treatment with fresh plasma by infusion was immediately initiated. On the third day of treatment he developed left ventricular failure; auscultation revealed a blowing early diastolic murmur over Erb's point together with a spindle-shaped early diastolic murmur over the right second intercostal space. Computed tomography of the skull showed recent haemorrhage into the left half of the cerebellum and an older right posterior infarct. The abdominal ultrasound scan suggested a haemorrhagic spleen infarct. In view of these findings the diagnosis was revised to embolizing aortic endocarditis with aortic reflux (confirmed by colour Doppler echo-cardiography). Aortic valve replacement was performed immediately, and the patient was treated with gentamycin 80 mg/d and teicoplanin 400 mg/d for four weeks. Postoperatively he was given 12 units of platelet concentrate and the platelet count remained stable thereafter (greater than 100,000/microliters). Splenectomy became necessary because the splenic haematoma increased in size during oral anticoagulant therapy. After a 6 week hospital stay the patient was discharged in good condition.
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PMID:[Embolizing aortic valve endocarditis in the differential diagnosis of thrombotic thrombocytopenic purpura]. 153 83

A total of 99 cases of viridans streptococcal endocarditis encountered during the period of 1973 and 1990 at the Veterans General Hospital-Taipei were reviewed to evaluate its prognostic factors. Applying strict clinical and laboratory criteria, 24 cases were categorized as definite, 44 probable, 23 possible and 8 likely. The symptoms were frequently subtle and atypical but initial laboratory tests gave useful indications: 69.1% with leukocytosis, 78% with anemia, 58.5% with elevation of LDH level, 88.9% with elevation of ESR value and 100% with elevation of CRP level. Furthermore, 32.4% of the cases demonstrated proteinuria and 67.4% microscopic hematuria. Seventy-three of the subjects had a history of underlying heart disease, predominantly rheumatic heart disease. Histological examination and echocardiography revealed that 51 patients suffered from vegetative endocarditis, 7 (13.7%) of whom were found to have anatomically confirmed vegetations without initial echocardiographic evidence, Vascular events were seen in 61 cases (61.6%): peripheral stigmata (32 cases), cerebral vascular accidents (17 cases), pulmonary embolism (10 cases) and others (2 cases). The overall mortality rate was 18.2%. Congestive heart failure with embolization was the most common cause of death in this group. The presence of vegetation was not well correlated with embolic events. There was no statistically significant association between the mortality and the following characteristics: age, sex, underlying heart disease, evidence of echocardiographically detected vegetations, major surgical intervention and recurrent cases except for embolic events (p less than 0.01). In conclusion, viridans streptococcal endocarditis complicated embolic events usually presented with a fulminant course and a grave outcome.
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PMID:Overview of viridans streptococcal endocarditis: clinical analysis of 99 cases. 165 35


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