Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The poor prognosis of acute mesenteric artery occlusion can be improved by reaching a rapid angiographic diagnosis and by instituting treatment at an early stage. In addition to operative embolectomy, success may be expected from the use of urokinase infused super-selectively into the superior mesenteric artery. This treatment is only likely to be successful if it is carried out within ten hours of the onset of clinical signs and symptoms. In patients with heart disease, angiography is recommended as soon as there is any suspicion of mesenteric occlusion, in order to confirm the diagnosis, localise the embolus and decide on the form of treatment. Urokinase treatment can be successful for embolic occlusion of the main branches or peripheral branches of the superior mesenteric artery. However, complete occlusion of the main superior mesenteric artery should be treated operatively. A contra-indication to urokinase therapy is occlusion due to infected emboli from an endocarditis.
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PMID:[Indications for the intra-arterial infusion of urokinase in the treatment of acute intestinal ischemia in patients with heart disease]. 300 57

In a proposed study of fibrinolytic therapy in experimental streptococcal endocarditis, this disease was induced in pigs by preinoculation damage to the aortic valve; the technique of this is described. If untreated, the disease runs a protracted course, similar to that in man. Fibrinolytic activity, normally low in the pig, can be increased by stress, by urokinase, by plasmin and briefly by streptokinase if supplemented by human plasminogen. The proposed experiments were abandoned in pigs, chiefly because of technical difficulties in obtaining frequent samples of blood and maintaining infusions. In experiments on the response of ADP-induced aggregation of pig platelets to prostacyclin, they were found to be about 10 times more resistant than human platelets. It is suggested that this resistance to prostacyclin, together with their usually low state of systemic fibrinolytic activity, may explain the susceptibility of pigs to bacterial endocarditis.
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PMID:A study of experimental endocarditis in pigs. 331 15

The authors report 2 cases of thrombolytic therapy by Urokinase at the dose of 4 500 U/kg/hour, for 24 hours, in patients with thrombosis of a Bjork aortic and Lillehei mitral valve prostheses, and assess the efficacy with a review of the world literature. The first case was a 65 year old woman who received a Bjork No 25 aortic valve prosthesis for aortic regurgitation. Two years later oral anti-vitamin K anticoagulants were replaced by an association of Aspirin-Persantine. She developed acute pulmonary oedema secondary to thrombosis of her valve during the fifth postoperative year. Treatment with Urokinase was successful (4 500 U/kg/hour for 24 hours). The second cases was a 33 year old woman who received a Lillehei No 27 mitral valve prosthesis for mitral regurgitation due to infective endocarditis. Six years later, during a period of apparently ineffective oral anticoagulation, she developed subacute pulmonary oedema due to thrombosis of her prosthesis. Urokinase therapy was successful after 4 hours, but the valve surface area on cardiac catheterisation was decreased and elective reoperation to change the prosthesis was decided upon. Prosthetic valve thrombosis is a serious complication with an operative mortality of 68.6% (35 deaths out of 51 reoperations in the worl literature) whilst the efficacy of thrombolytic therapy would appear to be about 80%. When thrombosis is progressive, the valve has to be changed surgically, but when it is secondary, thrombolytic therapy at least helps the patient survive the acute phase.
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PMID:[Role of thrombolytic treatment in thrombosis of valvular prostheses. Apropos of 2 cases and review of the world literature]. 643 46

Otherwise unexplained clinical signs of infection in patients with tunneled or totally implanted central venous access devices (CVAD) are highly suspicious of an underlying CVAD-associated infection. Diagnostic methods include catheter swabs, blood cultures and cultures of the catheter tip or port reservoir. In case of a suspected CVAD-related blood stream infection in pediatric cancer patients in situ treatment without prompt removal of the device can be tried. The removal of the CVAD should be considered, if bacteremia persists or relapses 72 hours or longer after the initiation of an (in vitro effective) antibacterial therapy administered through the line. The CVAD should be removed even earlier, if the patient suffers from hypotension or other signs of severe organ dysfunction related to the infection. If S. aureus, Pseudomonas aeruginosa, multiresistant Acinetobacter baumannii or Candida spp.are isolated from blood cultures taken through a CVAD, patients are at a high risk for severe complications and immediate device removal is also recommended. Duration of therapy depends on the immunological recovery of the patient (neutrophils counts), the pathogen isolated and on the presence of related complications like thrombosis, pneumonia, endocarditis, osteomyelitis. Antibiotic-lock techniques in addition to systemic treatment are beneficial in Gram-positive infections. Although prospectively controlled studies are missing, the concomitant use of urokinase- or taurolidine seems to favour catheter salvage.
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PMID:[Diagnostics and management of central venous line infections in pediatric cancer patients]. 1628 55

Otherwise unexplained clinical signs of infection in patients with long-term tunnelled or totally implanted central venous access devices (CVADs) are suspected to be CVAD-associated. Diagnostic methods include catheter swabs, blood cultures and cultures of the catheter tip or port reservoir. In the case of a suspected CVAD-related bloodstream infection in paediatric oncology patients, in-situ treatment without prompt removal of the device can be attempted. Removal of the CVAD should be considered if bacteraemia persists or relapses > or = 72 h after the initiation of (in-vitro effective) antibacterial therapy administered through the line. Timely removal of the device is also recommended if the patient suffers from a complicated infection, or if Staphylococcus aureus, Pseudomonas aeruginosa, multiresistant Acinetobacter baumannii or Candida spp. are isolated from blood cultures. Duration of therapy depends on the immunological recovery of the patient, the pathogen isolated and the presence of related complications, such as thrombosis, pneumonia, endocarditis and osteomyelitis. Antibiotic lock techniques in addition to systemic treatment are beneficial for Gram-positive infections. Although prospectively controlled studies are lacking, the concomitant use of urokinase locks and taurolidine secondary prophylaxis seem to favour catheter salvage.
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PMID:Diagnosis and treatment of catheter-related infections in paediatric oncology: an update. 1677 56

In immunocompromised patients, endovascular infection due to Candida albicans is associated with significant morbidity and mortality. Recommended management includes removal of any existing central venous catheter. Rarely, complications of endocarditis or infected mural thrombi may arise, with poorer clinical outcomes. For large endoluminal lesions, particularly of the great vessels or those that are intra-atrial, thrombolysis has been used in paediatric populations or before surgery for dissolution of infected thrombus. We describe the case of an adult patient with lung carcinoma who developed persisting candidaemia with a large endovascular fungal lesion adherent to the tip of a peripherally inserted central venous catheter. Local urokinase infusion enabled safe removal of the catheter without embolization. As an adjunct to antifungal therapy, local thrombolysis may play a contributory role in the management of central venous catheter-related candidal septic thrombosis.
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PMID:Thrombolytic therapy for management of complicated catheter-related Candida albicans thrombophlebitis. 1929 Sep 85