scholarly journals Deep Vein Thrombosis Caused by Heparin-induced Thrombocytopenia Thrombosis

2013 ◽  
Vol 52 (8) ◽  
pp. 929-929 ◽  
Author(s):  
Yoji Neishi ◽  
Hiroyuki Okura ◽  
Kiyoshi Yoshida
Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3049-3051 ◽  
Author(s):  
Aaron P. Hong ◽  
Deborah J. Cook ◽  
Christopher S. Sigouin ◽  
Theodore E. Warkentin

Abstract Heparin-induced thrombocytopenia (HIT) is a transient antibody-mediated hypercoagulability state strongly associated with lower-limb deep-vein thrombosis (DVT). Whether HIT is additionally associated with upper-limb DVT—either with or without central venous catheter (CVC) use—is unknown. We therefore studied 260 patients with antibody-positive HIT to determine the influence of CVC use on frequency and localization of upper-extremity DVT in comparison with 2 non-HIT control populations (postoperative orthopedic surgery and intensive-care unit patients). Compared with the control populations, both upper- and lower-extremity DVTs were found to be associated with HIT. Upper-extremity DVTs occurred more frequently in HIT patients with a CVC (14 of 145 [9.7%]) versus none of 115 (0%) patients without a CVC (P = .000 35). All upper-extremity DVTs occurred at the CVC site (right, 12; left, 2; kappa = 1.0; P = .011). We conclude that a localizing vascular injury (CVC use) and a systemic hypercoagulability disorder (HIT) interact to explain upper-extremity DVT complicating HIT.


2016 ◽  
Vol 03 (03) ◽  
pp. 245-248
Author(s):  
Arun Thangavel ◽  
Shalvi Mahajan ◽  
Amarjyoti Hazarika

AbstractUnfractionated heparin is a widely used drug to prevent deep vein thrombosis and pulmonary emboli in patients at risk. With the advent of newer anticoagulants having lesser side effects, its use has diminished but not out of service. Here, we report a case of deep venous thrombosis, in a patient on prophylactic dose of heparin, which was later found to be a manifestation of heparin-induced thrombocytopenia (HIT). Thrombosis in the presence of heparin prophylaxis should be considered as HIT rather than a failure of anticoagulation.


1998 ◽  
Vol 79 (03) ◽  
pp. 517-519 ◽  
Author(s):  
Stephane Heymans ◽  
Raymond Verhaeghe ◽  
Luc Stockx ◽  
Désiré Collen

SummaryThe feasibility of catheter-directed thrombolysis with recombinant staphylokinase was evaluated in six selected patients with deep vein thrombosis. The patients underwent intrathrombus infusion of recombinant staphylokinase (2 mg bolus followed by a continuous infusion of 1 mg/h). Heparin was given via the catheter as a bolus (5000 U) and as a continuous infusion (1000 U/h). Complete lyis was obtained in five patients and partial lysis in one patient. Complications consisted of minor bleeding in four subjects. Symptomatic reocclusion occurred in one. Debulking of the thrombus mass by a high speed rotating impeller (n = 1) and stenting (n = 3) were used as additional interventions. An underlying anatomical abnormality was present in two patients. Long term follow up revealed normal patency in all patients and normal valve function in four patients. Symptomatic venous insufficiency with valve dysfunction was present in the two with a second thrombotic episode.Thus catheter-directed infusion of recombinant staphylokinase in patients with deep vein thrombosis appears feasible and may be associated with a high frequency of thrombolysis. Larger studies to define the clinical benefit of this treatment appear to be warranted.


1991 ◽  
Vol 66 (04) ◽  
pp. 426-429 ◽  
Author(s):  
Marcel Levi ◽  
Anthonie W A Lensing ◽  
Harry R Büller ◽  
Paolo Prandoni ◽  
Gerard Dooijewaard ◽  
...  

SummaryIn the present study 57 consecutive patients with a first episode of venographically proven deep vein thrombosis were investigated to evaluate the release of tissue-type plasminogen activator (t-PA) and of urokinase-type plasminogen activator (u-PA) in response to DDAVP stimulation as well as the resting plasminogen activator inhibitor (PAI) concentration, comparing this to the results obtained in 66 similar patients with a clinical suspicion of thrombosis but with a normal venogram. All assays were performed without knowledge of the patient's status.Four patients in the deep vein thrombosis-group (7%) had an absent u-PA antigen response upon DDAVP infusion, while a normal response was observed in all control subjects. Patients and controls showed similar increases in t-PA antigen level upon DDAVP. High resting PAI antigen levels were encountered in 5 patients in the deep vein thrombosis-group (9%) and in 6 subjects in the control group (9%).The results from this controlled study indicate that a defective release of u-PA may occur in patients with deep vein thrombosis and may have pathogenetic significance. Furthermore it is concluded that elevation of PAI levels cannot be considered as a specific risk factor for venous thrombosis.


1974 ◽  
Vol 32 (02/03) ◽  
pp. 468-482 ◽  
Author(s):  
O Storm ◽  
P Ollendorff ◽  
E Drewsen ◽  
P Tang

SummaryThe thrombolytic effect of pig plasmin was tested in a double blind trial on patients with deep venous thrombosis in the lower limb. Only patients with not more than three days old thrombi were selected for this study. The diagnosis of deep vein thrombosis was made clinically and confirmed by phlebography. Lysofibrin Novo (porcine plasmin) or placebo (porcine plasminogen) was administered intravenously to the patients. The enzyme and the placebo were delivered as lyophilized powder in labelled bottles - the contents of the bottles were unknown to the doctor in charge of the clinical administration of the trial. An initial dose of plasmin/plasminogen of 30 unit per kg body weight given slowly intravenously (1-1% hours infusion) was followed by a maintenance dosis of 15 per cent the initial dose per hour for the following 5-7 hours. In most cases a similar maintenance dosis was given the next day. In all patients heparin was administered after ending the plasmin/plasminogen infusion. The results of the treatment was evaluated clinically as well as by control phlebo- grams the following days.A statistically significant improvement was found in the plasmin treated group compared with the placebo (plasminogen) treated group. Thrombolysis was obtained clinically and phlebographically in 65 per cent of the plasmin treated group, but only in 15 per cent of the control patients were improvements found.This study has thus demonstrated that plasmin treatment according to a standard scheme was able to induce thrombolysis. There were only a few and insignificant side effects. Allergic reactions have not been seen and only very simple tests are required.


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