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

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

A urinary tract infection with possible septicemia and endocarditis developed in a 36-year-old man. The illness was complicated by pulmonary embolism, thrombocytopenia, hematemesis, hepatic dysfunction, paralytic ileus and accelerated hypertension. The latter finding suggested pheochromocytoma. Treatment with antibiotics and phenoxybenzamine hydrochloride was associated with notable clinical improvement. A chromaffin cell tumor was surgically removed above the lift kidney. Conclusively, a pheochromocytoma may mimic and be present in association with infection.
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PMID:Infection and pheochromocytoma. 57 92

Twenty-four patients with infective endocarditis (IE) are described, fourteen with Staph. aureus and ten with other organisms. Despite the acute nature of the infection, ten of the fourteen with Staph. aureus IE were hypocomplementaemic; six of these ten had normal levels of C4 associated with low C3 levels, suggesting activation of the alternate complement pathway. Factor B (C3PA) was also low in three of these six cases. In the ten patients with non-Staph. IE, three had hypocomplementaemia with low levels of C4, C3, and Factor B, probably due to C1 (classical pathway) activation with feedback activation of the alternate pathway. In addition, thrombocytopenia was noted in nine of the twenty-four patients and was associated with hypocomplementaemia; the degree of renal insufficiency noted in these patients also correlated with hypocomplementaemia. In Staph. aureus IE thrombocytopenia and hypocomplementaemia, occurring early in the course of the disease, may be due to a non-immune interaction of Staph. cell wall products (Protein A) with immunoglobulin, complement components, and thrombocytes.
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PMID:Activation of the alternate complement pathway in Staph. aureus infective endocarditis and its relationship to thrombocytopenia, coagulation abnormalities, and acute glomerulonephritis. 73 1

Analysis of 182 patients with chronic disseminated intravascular coagulopathy and malignancy shows common features. Migratory thrombophlebitis occurred in 96 patients while at least a single episode of thrombophlebitis was noted in 113. Seventy-five of the patients bled and 45 had arterial emboli in various organs. Twelve patients had the triad of thrombophlebitis, hemorrhage, and arterial emboli, often sequentially. Hematologic data showed derangements associated with intravascular coagulation, the most prominent of which were hypofibrinogenemia and thrombocytopenia. Other abnormalities included prolonged prothrombin time, increased fibrinogen-fibrin degradation products, decreased levels of factors V and VIII, cryofibrinogenemia, and microangiopathic hemolytic anemia. Forty-one patients had lesions of non-bacterial thrombotic endocarditis at autopsy; 31 of these had arterial emboli during life. None of the lesions were infected. Mitral and aortic valves were most frequently involved. No single mechanism that causes the disseminated intravascular coagulopathy has been identified. However, cell products--secretions and enzymes--and the cells themselves have been proposed as the procoagulant(s) responsible for the syndrome. In addition to treatment of the underlying neoplasm, symptomatic disseminated intravascular coagulopathy should be controlled. Heparin is the drug of choice for treatment of this problem, very little benefit having been observed with warfarin therapy. Long-term use of anticoagulants is potentially feasible for control of chronic disseminated intravascular coagulopathy, but without effective control of the underlying tumor ultimately will be unsuccessful.
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PMID:Trousseau's syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features. 83 36

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

Total hydroxyproline excretion in 24-hour urine was determined in 20 cases of systemic lupus erythematosus (SLE) before and during treatment. Additionally the excretion of hydroxyproline was determined in 14 patients receiving steroids for various other diseases (endocarditis, thrombocytopenia, acute leukemia, apofocal polyarthritis, ischialgia, spastic bronchitis, pleuritis and Dressler's post-infarction syndrome). The normal hydroxyproline value was established in 40 healthy persons. The normalization of pathologically increased hydroxyproline excretion in patients with SLE during treatment with prednisone in doses from 1.0 to 1.35 mg/kg/daily was associated with remission of clinical symptoms. Large doses of prednisone in pathological processes not primarily affecting connective tissue increased the 24-hour excretion of hydroxyproline and small doses of prednisone had no effect on hydroxyprolinuria.
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PMID:Effect of antiphlogistic steroids on urinary hydroxyproline excretion in systemic lupus erythematosus. 95 50

Two clinical cases of female patients with hepatic cirrhosis and autoimmune multisystemic involvement with infectious intercurrent are reported. Case 1 presented infective endocarditis and erysipelas on the left thigh. In the course of the clinical picture a cutaneous vasculitis developed in the same place together with autoimmune thrombocytopenia, leukopenia and pulmonary restrictive picture with inflammatory pattern. There are also elevate immune complexes and complement consumption. Case 2 presented erysipelas on the left thigh cutaneous vasculitis and complement consumption. In Case 1 the infective endocarditis was treated with antibiotic therapy during 4 weeks followed by 1 mg/kg corticoid (Prednisone) with thrombocytopenia and leukopenia reversion. Case 2 presented an improvement with antibiotic only. The relation between chronic liver diseases and systemic autoimmune phenomena is commented, special attention being paid to the cutaneous, hematological and pulmonary affection.
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PMID:[Two cases of severe cutaneous vasculitis with thrombocytopenia associated with hepatic cirrhosis: autoimmune and infective-inflammatory component with endothelial lesion and restrictive pulmonary pattern in one case]. 130 15

We report a retrospective, clinicopathologic study of 139 patients who died during treatment of a severe burn. Fifty-three percent of the patients had central nervous system (CNS) complications-infections, cerebral infarcts and hemorrhages, metabolic encephalopathies, central pontine myelinolysis, and cerebral trauma. Children and adults were equally affected. Sixteen percent of the patients had a CNS infection. Candida species, Staphylococcus aureus and Pseudomonas aeruginosa caused almost 80% of them. S. aureus and candida caused cerebral microabscesses and septic infarcts. P. aeruginosa caused meningitis and infarcts due to meningitis. CNS infections arose as a result of spread from a systemic source. The major risk factors for CNS infection were an extensive burn, S. aureus endocarditis, and a burn wound infection due to candida or P. aeruginosa. Patients with burns of less than 30% of the surface area of their body, those without a systemic infection, and those in the first week after their burn were at low risk. Eighteen percent of the patients had cerebral infarcts. In almost half the patients, the infarcts were caused by septic arterial occlusions or other complications of the burn, viz, disseminated intravascular coagulation (DIC) and septic shock. In only one-third of the patients were infarcts due to atherosclerosis, atrial fibrillation, or other causes prevalent in the general population. Intracranial hemorrhages were only one-fifth as frequent as infarcts and were due to DIC and thrombocytopenia, caused by bacteremia. Diagnosis during life was difficult, because the neurologic picture of focal cerebral lesions and meningitis was indistinguishable from that of metabolic encephalopathies, and because many patients had more than 1 neurologic complication. However, our results suggest that a clinical approach that includes analysis of risk factors for CNS infection, cerebral imaging, examination of cerebrospinal fluid, and tests for DIC can lead to a neurologic and microbiologic diagnosis in most patients.
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PMID:Central nervous system complications of thermal burns. A postmortem study of 139 patients. 152 3

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

The influence of glucocorticosteroids (GKS) therapy on clinical status, T4 lymphocyte count in peripheral blood and T4/T8 lymphocyte ratio was investigated in five HIV infected patients: two were asymptomatic, while three had clinically overt disease. The reasons for GKS therapy were: thrombocytopenia in two patients, pancytopenia in two and sepsis with severe endocarditis in one. No influence of GKS on the clinical course of HIV infection was observed. The prospective determinations of T4 lymphocyte count and T4/T8 lymphocyte ratio were relatively constant in two cases, in one case increased and in two patients, one of whom had AIDS, a decrease in both parameters was observed. It seems that GKS therapy does not seriously influence the course of HIV infection in most patients and can be instituted without risk of severe worsening of the immune status.
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PMID:[Influence of therapy with glucocorticosteroids on clinical status, t4 lymphocyte count and t4/t8 lymphocyte ratio in people infected with AIDS]. 168 96


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