No evidence for thrombus embolization and a cranial CT scan discovered

No evidence for thrombus embolization and a cranial CT scan discovered no evidence of intracranial hemorrhage. A chest CT scan confirmed the diagnosis of cardiomegaly and hypodense structures in the apex of the left ventricle correlated with thrombus formation. After 7 days the CII was switched to a subcutaneous administration with similar anti-Xa levels and after 2 weeks the antithrombotic therapy was switched to acetylsalicylic acid because ofFigures 1 Cerebral arteriogram showing a right-sided middle cerebral artery infarction (a). Following thrombolytic therapy with enoxaparin, the MRI revealed normal perfusion of the cerebral arteries (b).Wiegand et Boc-D-Lys-OH al. Thrombosis Journal 2014, 12:19 http://www.thrombosisjournal.com/content/12/1/Page 3 ofFigures 2 Echocardiography of the left ventricle shows thrombus formation in the apex (a). Following thrombolytic therapy with enoxaparin, echocardiography revealed complete disappearance of the thrombus (b).expected poor compliance in a difficult family situation. During enoxaparin treatment, d-dimer levels increased to a maximum of 5.1 g/ml after 2 days of therapy. Cardiac catheterization including myocardial biopsy was performed and showed that the etiology of the severe heart failure was dilative cardiomyopathy of unknown origin. The CII of enoxaparin was paused 4 hours prior to the invasive procedure. To obtain a more efficient thrombolysis, anti-Xa levels were raised to the upper limits of the recommended therapeutic levels (between 0.7 and 1.0 IU/ml [7]). Platelet counts were monitored daily. None of the patients had renal dysfunction or manifested signs of heparin induced thrombycytopenia (HIT). Routine thrombophilia screening, including APC resistance, factor II mutation, protein C and S, antithrombin, homocysteine, lipoprotein (a), antiphospholipid antibodies and factor VIII, was negative in both patients prior to the enoxaparin therapy.Discussion LMWHs are prescribed for the treatment and prevention of several conditions including deep venous thrombosis, pulmonary embolism, acute coronary syndromes and atrial fibrillation [10,14,15]. The standardized method of administration for LMWH, including enoxaparin, is by subcutaneous injection, but Kane-Gill et al. found that the safety of enoxaparin administered by CII was comparable to that of subcutaneous administration [10]. Intravenous application Fmoc-Oic-OH has also been described in patients during percutaneous coronary interventions [16]. Few reports exist on the use of LMWHs by CII in the setting of deep vein thrombosis, hemodialysis and pulmonary embolism [11,17], and there is even less information regarding the use PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17591728 of LMWH administered as a CII in children [18]. In both of our patients, we started with an initial dosage of 2?.5 mg/kg as a CII. Despite being aware of the fact that the peak drug level is reached 4 hours following subcutaneous administration, we undertook a first sampling of the anti-Xa levels 6?hours after the start of the infusion. We chose to wait that long in order to obtain a steady-state, especially in view of the fact that PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/14445666 despite administering the same dosage over several days in the setting of CII the antiXa levels seemed to increase further. Therefore, daily blood sampling was performed because anti-Xa levels as we expected - continued to rise, especially during the first two to three days. In both patients, a therapeutic level of 0.6?.0 IU/ml was obtained with a dosage of 1.8?.5 mg/kg/d (Figure 3a and b). Administration o.