scholarly journals Rapid anticoagulation using ancrod for heparin-induced thrombocytopenia [see comments]

Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Bleeding Episode ◽  
Heparin Therapy ◽  
Heparin Induced Thrombocytopenia ◽  
Normal Platelet ◽  
Reasonable Approach ◽  
History Of ◽  
Recurrent Venous Thrombosis ◽  
Phlegmasia Cerulea Dolens

In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.

scholarly journals Rapid anticoagulation using ancrod for heparin-induced thrombocytopenia [see comments]

Blood ◽  
1991 ◽  
Vol 78 (9) ◽  
pp. 2194-2197 ◽  
Author(s):  
C Demers ◽  
JS Ginsberg ◽  
P Brill-Edwards ◽  
A Panju ◽  
TE Warkentin ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Bleeding Episode ◽  
Heparin Therapy ◽  
Heparin Induced Thrombocytopenia ◽  
Normal Platelet ◽  
Reasonable Approach ◽  
History Of ◽  
Recurrent Venous Thrombosis ◽  
Phlegmasia Cerulea Dolens

Abstract In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin- induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.

The Prevalence of Hereditary Antithrombin-III Deficiency in Patients with a History of Venous Thromboembolism

1985 ◽  
Vol 54 (04) ◽  
pp. 744-745 ◽  
Author(s):  
R Vikydal ◽  
C Korninger ◽  
P A Kyrle ◽  
H Niessner ◽  
I Pabinger ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Antithrombin Iii ◽  
Positive Family History ◽  
Normal Range ◽  
The Family ◽  
History Of ◽  
Antithrombin Iii Deficiency ◽  
Recurrent Venous Thrombosis ◽  
Antithrombin Iii Activity ◽  
Slight Deficiency

SummaryAntithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.

scholarly journals Fibrinopeptide A (FPA) Levels in Venous Thrombosis and Pulmonary Embolism Before and During Anticoagulant Therapy

1977 ◽  
Author(s):  
I. Yudelman ◽  
H. L. Nossel ◽  
K. L. Kaplan ◽  
J. Hirsh
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Heparin Therapy ◽  
Fibrinopeptide A ◽  
Normal Range ◽  
Monitoring Therapy ◽  
Asymptomatic Patients ◽  
Initial Symptoms ◽  
Lung Scan ◽  
Marked Drop

FPA levels were measured in 60 patients subjected to venography and to lung scan for symptoms suggestive of venous thromboembolism. In all 23 patients with negative venography and/or lung scan, FPA levels were in the normal range (<1.3 pmol/ml, mean 0.6 pmol/ml). The FPA levels were elevated in 34 of the 37 patients with a positive lung scan and/or venogram. The range was 0.4–112 pmol/ml, median 6.2 pmol/ml. The FPA levels were measured serially in patients with confirmed thromboembolism who were treated with heparin. In 14 of the 15 patients there was a marked drop in FPA levels in the first 15 minutes after the initial dose of heparin. In 1 patient the FPA levels only reached the normal range after 48 hours of heparin therapy. FPA levels were measured daily in 10 patients while on anticoagulant therapy. In 4 patients FPA levels became normal and remained so and no symptoms recurred. In the other 6 patients there were 13 episodes of FPA elevations.10 of these were preceded by a recurrence of the initial symptoms. In one patient FPA elevations occurred in the absence of symptoms while the repeat lung scan showed new lesions. Suboptimal anticoagulation and/or the transition from heparin to Coumadin preceded the recurrence of symptoms in 6 out of 10 episodes. FPA levels were frequently normal in asymptomatic patients with evidence of venous thrombosis as shown byfibrinogen uptake scan. These results suggest that FPA measurements may be useful in the diagnosis and in monitoring therapy of symptomatic thromboembolism.

scholarly journals Recurrent Venous Thrombosis following Free Flap Surgery: The Role of Heparin-Induced Thrombocytopenia

2003 ◽  
Vol 11 (1) ◽  
pp. 37-40 ◽  
Author(s):  
Andreas Nikolis ◽  
Apostolos Christopoulos ◽  
Michel Saint-Cyr ◽  
Carlos Cordoba ◽  
Louis Guertin ◽  
...  
Keyword(s):  
Free Flap ◽  
Free Tissue Transfer ◽  
Tobacco Consumption ◽  
Heparin Induced Thrombocytopenia ◽  
Flap Failure ◽  
Free Flap Surgery ◽  
History Of ◽  
Recurrent Venous Thrombosis ◽  
High Index Of Suspicion

Complications following free tissue transfer have been well established in the literature. Common and rare causes of free flap failure must be addressed by the treating surgeon when microvascular patency is threatened. With the evolution and prevalence of microsurgery, ‘rare’ causes of free flap failure will become increasingly frequent. A high index of suspicion must be established in patients with multiple failed operative interventions. A case of recurrent free flap failure secondary to heparin-induced thrombocytopenia is presented in a patient with a history of squamous cell carcinoma of the floor of the mouth, and a long-standing history of alcohol and tobacco consumption.

scholarly journals Phlegmasia Cerulea Dolens: A Life- and Limb-threatening Disease

2021 ◽  
Vol 5 (0-2) ◽  
pp. 16
Author(s):  
Wan Nuraisyah Azzahrah Wan Zuki
Keyword(s):  
Venous Thrombosis ◽  
Lower Limb ◽  
Early Recognition ◽  
Vena Cava ◽  
Common Iliac Vein ◽  
Venous Thrombectomy ◽  
Catheter Directed Thrombolysis ◽  
Left Lower Limb ◽  
History Of ◽  
Phlegmasia Cerulea Dolens

Phlegmasia cerulea dolens (PCD) is a rare syndrome caused by venous thrombosis and characterised by a triad of limb oedema, cyanosis and pain. It requires early recognition as delay of treatment can cause gangrene, limb amputation and in extreme cases, death. A 67- year-old Chinese lady, with underlying hypertension, diabetes mellitus and dyslipidaemia presented to the emergency department with a 2 days history of pain, oedema and bluish discoloration over the entire left leg. She had a history of fall 6 months prior and since then she used a walking stick for mobilization. This patient underwent ultrasound doppler left lower limb , which showed features suggestive of long-segment left lower limb deep vein thrombosis. A diagnosis of PCD was made. Subsequently, she went for a CT angiogram and venography of the left lower limb which confirmed thrombosis of the left calf vein extending to the long segment of the left common iliac vein. She was commenced on intravenous heparin infusion and then underwent inferior vena cava filter insertion and catheter directed thrombolysis. Repeat venogram showed successful catheter directed thrombolysis of the left lower limb deep venous thrombosis (DVT). Treatment should be initiated as soon as the diagnosis of PCD is suspected. Currently, guidelines for treatment are lacking however 3 therapeutic options are advocated alone or in combination: anticoagulants, thrombolytic therapy, and venous thrombectomy. An early recognition of PCD and appropriate decision regarding the treatment is essential to preserve the limb.International Journal of Human and Health Sciences Supplementary Issue-2: 2021 Page: S16

scholarly journals Recidivne tromboze arterij spodnjega uda pri bolniku s trombocitopenijo, povzročeno s heparinom – Prikaz primera

2017 ◽  
Vol 86 ◽  
Author(s):  
Blanka Mahne ◽  
Mladen Gasparini ◽  
Matija Kozak
Keyword(s):  
Platelet Count ◽  
Venous Thrombosis ◽  
Lower Limb ◽  
Early Recognition ◽  
Coronary Bypass ◽  
Posterior Tibial Artery ◽  
Heparin Therapy ◽  
Limb Amputation ◽  
Heparin Induced Thrombocytopenia ◽  
Acute Thrombosis

Background: Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder following heparin therapy presenting with thrombocytopenia and associated arterial or/and venous thrombosis (heparin induced thrombocytopenia with thrombosis–HITT). Unrecognised HIT can lead to severe complications like limb amputation and death.Case report: We report a case of a patient who presented with HIT-associated recurrent lower limb arterial thrombotic occlusions and popliteal venous thrombosis 29 days after coronary bypass graf surgery. The patient underwent urgent thrombectomy of superfcial femoral, popliteal and posterior tibial artery. Because of recurrent thrombotic occlusions of lower limb arteries three surgical revisions were performed. Te platelet count decreased from 124 × 109/l to 53 × 109/l on the fifth day after the first intervention. After clinical suspicion of HIT, heparin was discontinued and fondaparinux was started. Arterial thrombosis did not recur and the patient recovered without consequences.Conclusions: HIT occurs in 1–3 % of patients after cardiac surgery. Strict following of international guidelines regarding the frequency of platelet count monitoring, assessing probability for HIT and laboratory testing is mandatory in order not to miss the diagnosis of HIT. HIT can manifest clinically several days after the first exposure to heparin. If a patient presents with acute thrombosis and thrombocytopenia, HITT should be suspected. Postoperative HIT is associated with higher morbidity and mortality. Early recognition is crucial to prevent severe complications and death.

scholarly journals Management of suspected and confirmed recurrent venous thrombosis while on anticoagulant therapy. What next?

2019 ◽  
Vol 180 ◽  
pp. 105-109
Author(s):  
Marc A. Rodger ◽  
Sebastien Miranda ◽  
Aurelien Delluc ◽  
Marc Carrier
Keyword(s):  
Venous Thrombosis ◽  
Anticoagulant Therapy ◽  
Recurrent Venous Thrombosis

Recurrent Venous Thrombosis Related To A Hereditary Dysfibrinogen With Abnormal Crossed Immunoelectrophoretic Pattern

1981 ◽  
Author(s):  
A C Papp ◽  
R M Snopko ◽  
E R Cole ◽  
R J Sassetti ◽  
K K Wu
Keyword(s):  
Venous Thrombosis ◽  
Relative Viscosity ◽  
Gravimetric Method ◽  
Fibrinogen Concentration ◽  
Thrombin Time ◽  
A Value ◽  
History Of ◽  
Abnormal Pattern ◽  
Recurrent Venous Thrombosis ◽  
Fibrinogen Molecule

A 24 year old man with a history of multiple recurrent venous thrombosis was found to have a qualitatively abnormal fibrinogen. Plasma fibrinogen concentration by a kinetic thrombin time method was 135mg% as compared to 150mg% by the gravimetric method of Ratnoff and Menzie. The thrombin, reptilase and Russell viper venom times were all approximately 50% longer than the normal values. Neither the thrombin time nor reptilase time was corrected upon addition of CaCl2. Antigenic quantitation by Laurell immunoelectrophoresis gave a value of 320mg%. On Ouchterlony immunodiffusion plate, the patient’s plasma and normal plasma showed a line of identity. The patient’s fibrinogen had a normal rate of migration by one-dimensional immunoelectrophoresis but it exhibited an abnormal pattern upon crossed immunoelectrophoresis. The abnormality is characterized by the presence of a shoulder on the anodal side of the fibrinogen peak. Family studies revealed that the fibrinogen defect was inherited as an autosomal dominant trait. To determine whether recurrent venous thrombosis is related to increased viscosity due to the abnormal fibrinogen, fibrinogen was purified by the method of BlombSck and the relative viscosity of fibrinogen solution was determined. Preliminary data were suggestive of an increased viscosity of the patient’s fibrinogen. These findings indicate that the immunologically abnormal dysfibrinogen may be responsible for recurrent venous thrombosis because of alteration of the physicochemical properties of the fibrinogen molecule.

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