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Thrombosis Prophylaxis (thrombosis + prophylaxis)
Selected AbstractsEffect of time of admission on compliance with deep vein thrombosis prophylaxis in a tertiary medical intensive care unitJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2009O. DABBAGH Summary.,Objective:,We sought to evaluate deep vein thrombosis (DVT) prophylaxis compliance according to time of admission in a medical intensive care unit (MICU). Methods:,This was a retrospective cohort study at a closed tertiary MICU. We classified patients into three groups (week days, weekends, and week nights), according to time of admission. An unweighted risk factor score (RFS) was calculated from 20 known risk factors. We defined DVT prophylaxis compliance as any type of prophylaxis (mechanical or pharmacologic) for RFS , 3 or both types of prophylaxis for RFS > 3. Non-compliance was defined as no prophylaxis or single-type prophylaxis for RFS > 3. Results:,We analyzed 105 admissions. Eighty (76.19%) patients received compliant DVT prophylaxis, and 25 (23.81%) patients received non-compliant regimens of whom 11 (10.48%) were not on any prophylaxis. DVT prophylaxis compliance was not different across the three admission groups. The non-compliant DVT prophylaxis group had a higher RFS (3.48 ± 2.1 vs. 2.25 ± 1.5; P = 0.011), a trend towards fewer female patients (40% vs. 60%; P = 0.079), and a higher percentage of admissions by interns at the first postgraduate year (PGY) level (28% vs. 5.4%; P = 0.01). Logistic regression revealed that only RFS and PGY level were independent predictors for compliance (P = 0.015 and 0.005 respectively). Time of admission was not a significant factor. Conclusions:,Time of admission did not influence DVT prophylaxis compliance. Compliance improved with higher PGY level and lower RFS. A higher level of knowledge probably explains the association with PGY level; however, we cannot explain the inverse relationship between RFS and compliance. [source] Hemostatic complications of angiogenesis inhibitors in cancer patients,AMERICAN JOURNAL OF HEMATOLOGY, Issue 11 2008Francesca Elice Tumor vasculature and tumor-associated neo-angiogenesis have recently become major targets for rational drug design of antineoplastic agents. Five such agents with angiogenesis inhibiting activity (thalidomide, lenalidomide, bevacizumab, sunitinib, sorafenib) have already obtained US Food and Drug Administration approval for clinical use and many others have entered clinical trials. Vascular complications, including venous or arterial thromboembolism and hemorrhage, have emerged as relevant toxicities in several clinical trials with angiogenesis inhibitors. Given the well-known interplay between the blood clotting system, angiogenesis, and tumor growth, a better understanding of the impact of these new drugs on overall hemostatic balance is required. In this brief overview, we discuss the incidence of hemostatic complications, the likely pathogenetic mechanisms involved, and the critical need to establish in randomized clinical trials the usefulness of thrombosis prophylaxis to prevent these complications. Careful documentation of hemostatic complications during treatment with each of the new antiangiogenic drugs is warranted. Further studies are urgently required to better define the causal association of these new agents with hemostatic complications and to establish the best prophylactic strategy. Am. J. Hematol., 2008. © 2008 Wiley-Liss, Inc. [source] Low-molecular-weight heparins and angiogenesis,APMIS, Issue 2 2006KLAS NORRBY The involvement of the vascular system in malignancy encompasses not only angiogenesis, but also systemic hypercoagulability and a pro-thrombotic state, and there is increasing evidence that pathways of blood coagulation and angiogenesis are reciprocally linked. In fact, cancer atients often display hypercoagulability resulting in markedly increased thromboembolism, which requires anti-coagulant treatment using heparins, for example. Clinical trials reveal that treatment with various low-molecular-weight heparins (LMWHs) improves the survival time in cancer patients receiving chemotherapy compared with those receiving unfractionated standard heparin (UFH) or no heparin treatment, as well as in cancer patients receiving LMWH as thrombosis prophylaxis during primary surgery. This anti-tumor effect of the heparins appears to be unrelated to their anti-coagulant activity, but the mechanisms involved are not fully understood. Tumor growth and spread are dependent on angiogenesis and it is noteworthy that the most potent endogenous pro- and anti-angiogenic factors are heparin-binding proteins that may be affected by systemic treatment with heparins. Heparin and other glycosaminoglycans play a role in vascular endothelial cell function, as they are able to modulate the activities of angiogenic growth factors by facilitating the interaction with their receptor and promoting receptor activation. To date, preclinical studies have demonstrated that only LMWH fragments produced by the heparinase digestion of UFH, i.e. tinzaparin, exert anti-angiogenic effects in any type of tissue in vivo. These effects are fragment-mass-specific and angiogenesis-type-specific. Data on the effect of various LMWHs and UFH on endothelial cell capillary tube formation and proliferation in vitro are also presented. We hope that this paper will stimulate and facilitate future research designed to elucidate whether the anti-angiogenic or anti-tumor effects of commercial LMWHs in their own right are agent specific and whether anti-angiogenic properties increase the anti-tumor properties of the LMWHs in the clinic. [source] Kidney retransplants after initial graft loss to vascular thrombosisCLINICAL TRANSPLANTATION, Issue 1 2001Abhinav Humar Background: Vascular thrombosis early after a kidney transplant is an infrequent but devastating complication. Often, no cause is found. These recipients are generally felt to be good candidates for a retransplant. However, their ideal care at the time of the retransplant and their outcomes have not been well documented. We studied outcomes in 16 retransplant recipients who had lost their first graft early posttransplant (<1 month) to vascular thrombosis. Methods: Of 2 003 kidney transplants between 1 January 1984 and 30 September 1998, we identified 32 recipients who had lost their first graft early posttransplant to vascular thrombosis. Of these 32 recipients, 16 were subsequently retransplanted and detailed chart reviews were done. Results: Of the 16 retransplant recipients, 12 lost their first graft to renal vein thrombosis and 4 to renal artery thrombosis. Thrombosis generally occurred early (mean, 3.6 d). Five recipients underwent a complete hematologic workup to rule out a thrombophilic disorder before their retransplant: 4 had a positive result (presence of antiphospholipid antibodies, n=3; increased homocysteine levels, n=1). These 4 recipients, along with 1 other recipient who had a strong family history of thrombosis, underwent thrombosis prophylaxis at the time of their retransplant. Prophylaxis consisted of low-dose heparin for the first 3,5 d posttransplant, followed by acetylsalicylic acid or Coumadin. Of the 16 retransplant recipients, none developed thrombosis. Of the 5 who underwent thrombosis prophylaxis, none had significant bleeding complications. At a mean follow-up of 5.4 yr, 10 (63%) recipients have functioning grafts. Causes of graft loss in the remaining 6 recipients were death with function (n=5, 31%) and acute rejection (n=1, 6%). Graft and patient survival rates after these 16 retransplants were equivalent to results after primary transplants. The incidence of acute and chronic rejection was also no different (p=ns). Conclusion: Vascular thrombosis in the absence of obvious technical factors should prompt a workup for a thrombophilic disorder before a retransplant. Recipients with an identified disorder should undergo prophylaxis at the time of the retransplant. Results in these retransplant recipients are equivalent to those seen in primary transplant recipients. [source] | ||||||||||