DEEP VENOUS THROMBOSIS PROPHYLAXIS BY LOW MOLECULAR WEIGHT HEPARININ NEUROSURGICAL PATIENTS

1991 ◽  
Vol 75 (3) ◽  
pp. A214-A214 ◽  
Author(s):  
E. Melon ◽  
Y. Keravel ◽  
A. Gaston ◽  
Y. Huet ◽  
S. Combes
2004 ◽  
Vol 17 (4) ◽  
pp. 1-6 ◽  
Author(s):  
Samuel R. Browd ◽  
Brian T. Ragel ◽  
Gary E. Davis ◽  
Amy M. Scott ◽  
Elaine J. Skalabrin ◽  
...  

The incidence of deep venous thrombosis (DVT) and subsequent pulmonary embolism (PE) in patients undergoing neurosurgery has been reported to be as high as 25%, with a mortality rate from PE between 9 and 50%. Even with the use of pneumatic compression devices, the incidence of DVT has been reported to be 32% in these patients, making prophylactic heparin therapy desirable. Both unfractionated and low-molecular-weight heparin have been shown to reduce the incidence of DVT consistently by 40 to 50% in neurosurgical patients. The baseline rate for major intracranial hemorrhage (ICH) following craniotomy has been reported to be between 1 and 3.9%, but after initiation of heparin therapy this rate has been found to be as high as 10.9%. Therefore, neurosurgeons must balance the risk of PE against the increased risk of postoperative ICH from prophylactic heparin for DVT. The authors review the literature on the incidence of DVT and PE in neurosurgical patients, focusing on the incidence of ICH related to the use of unfractionated and low-molecular-weight heparin in this patient population


1993 ◽  
Vol 70 (06) ◽  
pp. 0909-0914 ◽  
Author(s):  

SummaryFibrin D-Dimer (D-Di), prothrombin activation fragment (F 1+2) and thrombin-antithrombin III complexes (TAT) were measured using ELISA procedures in the plasma of patients with an acute deep venous thrombosis (DVT), at presentation and on days 2, 6 and 10 after initiation of heparin treatment. Patients were randomly allocated into two treatment groups: 44 patients received adapted doses of continuous intravenous unfractionated heparin (UH) whereas 47 received 1 mg/kg every twelve hours of a low molecular weight heparin (enoxaparin) subcutaneously. A phlebography and a perfusion lung scan were performed before inclusion and on day 10. Failure of therapy (n = 9) was defined by venogram worsening or confirmed pulmonary embolism. Improvement (n = 44) or stationary state (n = 38) were defined by venogram evolution in the absence of new leg scan defects.At presentation, D-Di, F 1 + 2 and TAT were above cut-off values in 97, 66 and 89% of patients respectively. D-Di levels correlated with the extent of venous thrombosis whereas TAT and F 1 + 2 did not. Mean levels of D-Di decreased sharply during the first days of treatment but were still abnormal on day 10. A secondary increase of D-Di on days 6 or 10 by more than 3 μg/ml occurred in 4 of the 9 patients who developed a thromboembolic recurrence but in none of the 72 patients who had a more favorable outcome. F 1 + 2 and TAT time-courses were not related to clinical evolution. In the Enoxaparin group, there was no relationship between antifactor Xa activities and any biological markers. TAT and F 1 + 2 levels fell on day 2 and remained stable until day 10. In contrast, in the UH group, TAT and F 1 + 2 did not significantly decrease on day 2, probably due to a delay in dose adaptation, but they declined slowly until day 10.In conclusion, D-Di displays a higher sensitivity than F 1 + 2 or TAT for the diagnosis of D\T. D-Di, but not TAT or F 1 + 2, follow-up seems to be of potential value for early detection of recurrency. Hemostatic activation is controlled earlier by fixed doses of a low molecular weight heparin, irrespective of the plasma anti-factor Xa activities, than by unfractionated heparin at adapted doses.


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