Endocarditis heparin

For premedication aspirin 300 mg twice a day 48 hours prior to the procedure and a loading dose of clopidogrel 300 mg (or ticlopidine 250 mg) is recommended. Endocarditis prophylaxis with a first generation cephalosporin (e.g., cefuroxime, 1, 5 g, i.v.) should be administered before and after intervention. After transseptal puncture, 10,000 units of heparin are administered. An activated clotting time of 200-300 seconds is desirable. 

Intravenous antibiotics are given before and after the procedure. Five thousand to ten thousand units of heparin should be administered after transseptal puncture. Aspirin (100-300 mg/day, p.o.) and clopidogrel (75 mg/day, p.o.) is prescribed for the following six months as well as endocarditis prophylaxis. A TEE is performed at six months. If the LAA is completely occluded, no further anticoagulation is required. 

With annuloplasty procedures heparin and endocarditis prophylaxis should be administered before the procedures. When the edge-to-edge technique is performed, heparin should not be administered until the transseptal puncture has been performed. Regular follow-up examination, anticoagulation, and endocarditis prophylaxis are recommended after mitral repair procedures. 

Before intervention heparin is administered (100 U/kg) in addition to endocarditis prophylaxis (e.g., cefuroxime, l,5g, i.v.). Endocarditis prophylaxis is repeated afterthe procedure. Aspirin (100mg, p.d.) and clopidogrel (75mg/day, p.o.) are prescribed for six months after implantation. The incidence of thrombus formation varies between devices (50). If thrombus is seen during follow-up, coumadin therapy should be commenced. 

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. 

Because of hemorrhage risk, check hematocrit and test for blood in stool. Administer with caution to menstruating women, or patients with subacute bacterial endocarditis, severe hypotension, liver disease, or blood dyscrasias. Protamine sulfate inactivates heparin and can be used as an antagonist if severe bleeding occurs. 

The prothrombin time of a 29-year-old patient stabilised on warfarin fell from a range of 20 to 25 seconds down to 16 seconds live days after intravenous nafcillin 2 g every 4 hours was started for endocarditis. Over the next 2 weeks the prothrombin time ranged between 14 and 17 seconds despite an eventual doubling of the warfarin dose, and heparin was substituted. In this patient the half-life of a single 30-mg dose of warfarin was 11 hours when nafcillin was taken, 17 hours 4 days after stopping nafcillin, and 44 hours eight months after the nafcillin was discontinued. At least 10 other cases of this warfarin resistance have been reported with high-dose nafcillin. " ... 

In 1950 (but not reported until 1975) a woman with subacute bacterial endocarditis was given probenecid orally and penicillin by intravenous drip, which was kept open with minimal doses of heparin. After a total of about 20 000 units of heparin had been given over a 3-week period, increasing epistaxes developed and the clotting time was found to be 24 minutes (normal 5 to 6 minutes). This was controlled with protamine. However, no reports of this interaction appear to have been made subsequently. This interaction seems unlikely to be of general significance. 

Heparin resistance is defined as the requirement of more than 35,000 units in a 24-h period to maintain a therapeutic activated partial thromboplastin time. In some cases, elevated factor VIII levels can factitiously lower the aPPT without influencing heparin activity measured by anti-Xa assays, leading to a misdiagnosis of heparin resistance. A case of apparent heparin resistance due to increased factor VIII levels in an elderly male with infective endocarditis was reported [18 ]. 

Thota R, Ganti AK, Subbiah S. Apparent heparin resistance in a patient with infective endocarditis secondary to elevated factor VIII levels. J Thromb Thrombolysis 2012 34(l) 132-4. 

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