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PubMed1976

The prevention of postoperative deep vein thrombosis and pulmonary embolism with low dose subcutaneous heparin and dextran.

The standard low dose of heparin for the prevention of deep venous thrombosis in patients who are operated upon is 5,000 units administered subcutaneously two hours before operation and at eight or 12 hourly intervals for the next seven days. Heparin in low doses can at present be recommended as an effective agent in the prevention of deep venous thrombosis in patients over the age of 40 years who are undergoing a major abdominothoracic or gynecologic operation. There is reasonable evidence that heparin in low doses also offers a satisfactory protection against fatal pulmonary embolism for patients at high risk after general abdominothoracic operations. The evidence of the effectiveness of low doses of heparin in the prevention of deep venous thrombosis is less well established in other patients and particularly those at high risk, as after urologic and hip operations. This important distinction is to be made in terms of the population at risk and the efficacy of heparin in low doses. Considering the evidence so far available, it appears that the postoperative state in which dextran has been shown to reduce the incidence of phlebographically confirmed deep venous thrombosis most convincingly is after orthopedic operations. Major orthopedic operations are precisely the type in which the superiority of heparin in low doses is controversial. Unless proved otherwise, dextran 70 in an infusion of 500 to 1,000 milliliters of a 6 per cent solution started before operation and 500 milliliters the following and next three alternate days may be the agent of choice in preventing deep venous thrombosis in major orthopedic operations. Using this scheme, the prophylaxis of postoperative deep venous thrombosis appears equally effective with dextran 70 as with oral anticoagulants. Whether the protection offered by dextran 70 will also prevent fatal and nonfatal pulmonary embolism is still an open question. Low doses of heparin and dextran do not expose patients to serious risks of bleeding after operation, and with the recommended doses of the latter drug, other untoward effects are rare. At the doses recommended, neither of these two drugs requires laboratory monitoring.

Abdomen↗

PubMed2004

Cerebral venous thrombosis in a patient with Evans syndrome: a rare association.

In this report we describe a case of extensive cerebral venous thrombosis in a patient with Evans syndrome. A 19-year-old male patient with Evans syndrome was admitted to the hospital with the complaints of headache, convulsive seizure, and vomiting. The cerebral venous thrombosis including left lateral, left sigmoid, straight sinus, and vena jugularis interna was diagnosed by cerebral magnetic resonance angiography. When the thrombosis developed, he was in hematological remission and he was not receiving any medications except lamivudine for chronic hepatitis B infection. As a genetic prothrombotic risk factor, he had heterozygous prothrombin G20210A gene mutation. His clinical and radiologic findings improved after unfractionated heparin and subsequently with coumadin therapy. On follow-up, cerebral venous thrombosis reoccurred in different localizations, but complete recanalization could be obtained with antithrombotic therapy. We present the case since the association of cerebral venous thrombosis and Evans syndrome is very rare.

Adult↗

PubMed2000

Mouse models of focal arterial and venous thrombosis.

Mouse models of arterial and venous thrombosis have gained increasing interest over the last 15 years, due to direct availability of a growing number of genetically modified mice, improved technical feasibility, standardization of new models of local thrombosis, and low maintenance costs. In order to provide an overview of suitable models for the study of arterial and venous thrombosis in mice, we have systematically searched MEDLINE electronic databases for publications reporting on murine thrombo-embolic models from 1966-1999. We found that the variety of murine thromboembolic models through 1995 was rather limited, as most methods used intravenous injections of strong coagulation triggers such as thrombin, thromboplastin and collagen, causing lethal thromboembolism. Between 1996 and the end of 1999, a number of more sophisticated murine models of local acute or chronic thrombosis have been established. They seem to be more suitable for mimicking the natural scenario of thrombosis and, therefore, are preferable models for pathophysiological or drug evaluation studies. In this paper various models are described and their advantages and limitations discussed.

Animals↗

PubMed2006

Cerebral venous thrombosis as a first presentation of diabetes.

This report presents a case of cerebral venous thrombosis and venous infarction in a diabetic patient, the third in the world literature (the second in a child). An 8-year-old male was admitted to the hospital due to abdominal pain, vomiting, polydypsia, and polyuria, lasting for 4 days. Laboratory studies revealed marked hyperglycemia and ketoacidosis. Two hours after admission the child lost consciousness. Emergency computed tomography performed 3 hours after admission (4 days after the onset of symptoms) revealed hyperdensity in the vein of Galen and superior sagittal sinus, consistent with thrombosis, accompanied by bilateral venous infarction. Follow-up computed tomography performed 6 days after admission (10 days after the onset of symptoms) documented evolution of thrombosis. Magnetic resonance imaging and magnetic resonance venography performed 22 days after admission (26 days after the onset of symptoms) confirmed venous infarction and thrombosis. This report discusses possible mechanisms of cerebral venous thrombosis in diabetic hyperglycemia and stresses the importance of imaging studies despite the extreme rarity of such cases.

Cerebral Infarction↗

PubMed2000

Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease.

BACKGROUND: Although reduced intracellular levels of magnesium have been described in patients with acute myocardial infarction, its significance as a regulator of thrombosis remains unknown. METHODS AND RESULTS: To determine whether reduced intracellular levels of magnesium enhance platelet-dependent thrombosis, we evaluated 42 patients with coronary artery disease (CAD) by exposing porcine aortic media to their flowing unanticoagulated venous blood for 5 minutes by using an ex vivo perfusion (Badimon) chamber. Baseline analysis demonstrated significant associations between intracellular levels of magnesium, platelet-dependent thrombosis (P =.02), and platelet P-selectin (CD62P) expression (P <.05). Patients were divided into 2 groups: below (n = 22) and above (n = 20) the median intracellular levels of magnesium (1.12 microg/mg protein). There were no significant differences in age, body mass index, serum lipids, fibrinogen, platelet count, or serum magnesium levels between the two groups. Platelet-dependent thrombosis was significantly higher in patients with intracellular levels of magnesium below compared with above median (150 +/- 128 vs 45 +/- 28 microm(2)/mm, P <.004). Neither platelet aggregation nor CD62P expression was significantly different between the two groups. CONCLUSIONS: Platelet-dependent thrombosis was significantly increased in patients with stable CAD with low intracellular levels of magnesium, suggesting a potential role for magnesium supplementation in CAD.

Aged↗

PubMedDate not supplied

Atrial and venous thrombosis secondary to septic arthritis of the sacroiliac joint in a child with hereditary protein C deficiency.

Septic arthritis and osteomyelitis in children is seldom accompanied by calf vein thrombosis and rarely by atrial thrombosis. We report the case of an 11-year, 5-month-old boy with septic arthritis and osteomyelitis of the sacroiliac region who developed deep venous thrombosis, in addition to life-threatening right atrial thrombosis. After an intensive hematologic investigation, a hereditary protein C deficiency was revealed. The association of venous thrombosis with septic arthritis or osteomyelitis should raise the possibility of the presence of protein C deficiency.

Arthritis, Infectious↗

PubMed2006

Murine model of ferric chloride-induced vena cava thrombosis: evidence for effect of potato carboxypeptidase inhibitor.

BACKGROUND/OBJECTIVE: Thrombin-activatable fibrinolysis inhibitor (TAFI) is a plasma carboxypeptidase that renders a fibrin-containing thrombus less sensitive to lysis. In the present study, we describe the development of a murine model of vena cava thrombosis and its use to characterize the antithrombotic activity of potato carboxypeptidase inhibitor (PCI) of TAFIa (activated TAFI) in mice. METHODS/RESULTS: Vena cava thrombosis was induced by various concentrations of FeCl(3) in C57BL/6 mice. A relatively mild stimulus (3.5% FeCl(3)) induced thrombosis that was consistent and sensitive to reference antithrombotic agents such as clopidogrel and heparin. Dose-response studies identified a PCI dose (5 mg kg(-1) bolus plus 5 mg kg(-1) h(-1), i.v.) that produced a maximum 45% decrease in vena cava thrombus mass as assessed by protein content (n = 8, P < 0.01 compared to vehicle) in the 3.5% FeCl(3)-induced model without exogenous tissue plasminogen activator administration. In contrast, PCI had no effect on 3.5% FeCl(3)-induced carotid artery thrombosis in mice. In a tail transection bleeding model, the 5 mg kg(-1) bolus plus 5 mg kg(-1) h(-1) dose of PCI increased tail-bleeding time up to 3.5 times control (n = 8, P < 0.05). The ex vivo activity of antithrombotic doses of PCI was also demonstrated by the enhanced lysis of whole blood clots formed in a thrombelastograph with the addition of a sub-threshold concentration of tPA. CONCLUSION: These studies provide evidence for a role of TAFIa in venous thrombosis in mice, and describe an optimized vena cava injury model appropriate for the evaluation of antithrombotic drugs and the characterization of novel therapeutic targets.

Animals↗

PubMed2002

Intimatan prevents arterial and venous thrombosis in a canine model of deep vessel wall injury.

Resistance of fibrin-bound thrombin to inactivation by the heparin/antithrombin III complex is considered a limitation in the use of heparin as an antithrombotic agent. Intimatan (dermatan 4,6-di-O-sulfate) is a heparin cofactor II agonist that inhibits both free and bound forms of thrombin. The present study examines the hypothesis that Intimatan prevents thrombotic occlusion in response to vascular wall injury in a canine model of carotid artery/jugular vein thrombosis. The left carotid artery and right jugular vein served as vehicle-treated control vessels, whereas the right carotid artery and left jugular vein were subjected to electrolytic injury after administration of Intimatan (9 mg/kg bolus + 300 microg/kg/min infusion, i.v.) or dalteparin (Fragmin) (400 IU/kg, s.c.). Intimatan significantly increased time to carotid artery (226.0 +/- 14.0 min) and jugular vein (240.0 +/- 0.0 min) thrombosis, compared with control vessels (carotid artery, 87.1 +/- 7.9 min; jugular vein, 60.6 +/- 7.4 min). Vessel patency was maintained in eight of eight jugular veins and seven of eight carotid arteries during treatment with Intimatan. Dalteparin significantly increased time to carotid artery thrombosis (122.1 +/- 17.5 min) compared with control (64.3 +/- 8.2 min), but did not change the time to thrombosis in the jugular vein. Only one carotid artery remained patent at the end of the dalteparin protocol. The two drugs produced minimal increases in bleeding times, and Intimatan increased the activated partial thromboplastin time above that observed with dalteparin. The results demonstrate that Intimatan is effective in preventing occlusive arterial and venous thrombosis in an experimental model of deep vascular wall injury.

Animals↗

PubMedDate not supplied

Concurrent thrombosis of cerebral and femoral arteries in a patient with nephrotic syndrome.

Although venous thrombosis is a frequently encountered problem in nephrotic syndrome, the occurrence of arterial thrombosis is much less common, and is usually associated with a poor prognosis. To the best of our knowledge, there has been only one reported case of concurrent cerebral and femoral artery thrombosis, that of a 23-year-old male who finally died. Herein, we report a case of a 35-year-old woman with nephrotic syndrome. She developed cerebral and femoral arterial thrombosis simultaneously when the nephrotic syndrome relapsed. Immediate thrombectomy of the femoral artery, followed by anticoagulation and immunosuppressive therapy, were employed. The patient recovered completely and is now doing well. Our experience indicates that multiple artery thrombosis in nephrotic patients may not necessarily carry a poor outcome if early and aggressive treatment can be undertaken.

Adult↗

PubMed2001

Diffusion-weighted mr in cerebral venous thrombosis.

The diagnosis of cerebral venous thrombosis is often difficult both clinically and radiologically and until now there is no method available to predict if brain lesions, detected clinically and using conventional brain imaging methods, may lead to full recovery, as expected in vasogenic edema or ischemic infarcts and even a hematoma. New fast neuroimaging techniques such as diffusion-weighted imaging (DWI) are sensitive to different reasons of changes in local tissular water concentration thus giving further insight into the pathophysiological mechanism as well as prognosis of cerebral venous thrombosis. We report the cases of 18 consecutive patients with a diagnosis of cerebral venous thrombosis based on clinical and imaging criteria. All patients underwent magnetic resonance imaging (MRI) of the brain, which comprised isotropic diffusion-weighted MR. Diffusion-weighted MRI showed positive findings in 17/18 cases. In 7 cases the clot could be directly visualized as an area of hyperintensity in the affected vein on DWI. In 7 cases DWI showed areas of signal loss corresponding to hematomas. In 6 cases DWI showed changes in signal intensity that were more subtle. In 4 cases of superficial venous thrombosis, there were areas of decreased ADC values (0.65-0.79 x 10(-3) mm(2)/s) whereas in 2 cases of deep venous thrombosis, increased DWI intensities could be found that corresponded to both an increase and a decrease in ADC, corresponding to a coexistence of cytotoxic and vasogenic edemas. Diffusion-weighted MRI can demonstrate directly the presence of an intravenous clot in a select number of patients. It can also demonstrate early ischemic changes, and can differentiate conventional T2-weighted MR areas of cytotoxic from vasogenic edema.

Adult↗

PubMed1995

Thrombolysis and reocclusion in experimental jugular vein and coronary artery thrombosis. Effects of a plasminogen activator inhibitor type 1-neutralizing monoclonal antibody.

BACKGROUND: Thrombolytic therapy for acute myocardial infarction is often complicated by reocclusion of the initially reperfused artery. Platelets have been shown to play an important role in this process. We determined the contribution of plasminogen activator inhibitor type 1 (PAI-1), stored in the alpha-granules of platelets, to thrombolysis resistance and to reocclusion. METHODS AND RESULTS: In a rabbit jugular vein thrombosis model, the effect of a PAI-1-neutralizing monoclonal antibody (CLB-2C8) on thrombolysis and thrombus growth was assessed. The effect on reperfusion, reocclusion, and duration of vessel patency was studied in a canine model of coronary artery thrombosis superimposed on a high-grade stenosis and endothelial damage. In the rabbit jugular vein model, the intravenous administration of 1 mg/kg anti-PAI-1 antibody significantly enhanced the endogenous thrombolysis from 5.5 +/- 1.3% in the animals treated with a nonspecific monoclonal antibody (control) to 13.7 +/- 2.6% in the animals treated with the anti-PAI-1 antibody. Thrombus growth was reduced significantly, from 41.3 +/- 2.6% in the control animals to 22.8 +/- 2.8% in the animals treated with the anti-PAI-1 antibody. In combination with a single bolus injection of recombinant tissue-type plasminogen activator (rTPA; 0.25 mg/kg), the anti-PAI-1 antibody reduced thrombus growth significantly, from 21.5 +/- 2.7% in the animals treated with rTPA alone to 12.2 +/- 2.6% in the animals treated with rTPA and the antibody. No additional effect of the anti-PAI-1 antibody was observed on rTPA-induced thrombolysis. In the canine coronary artery thrombosis model, the administration of a suboptimal dose of rTPA (0.45 mg/kg) induced reperfusion in 7 of the 8 dogs after 19.5 +/- 8.2 minutes. Reperfusion was followed by reocclusion in all animals after 3.3 +/- 2.6 minutes. Administration of the anti-PAI-1 antibody in combination with rTPA significantly reduced time to reperfusion (8.1 +/- 5.2 minutes) and delayed the occurrence of reocclusion to 11.6 +/- 12.5 minutes. CONCLUSIONS: Administration of the anti-PAI-1 antibody (CLB-2C8) results in increased endogenous thrombolysis and inhibition of thrombus growth in a venous thrombosis model in rabbits and facilitated reperfusion and reduction of reocclusion in a canine model of coronary artery thrombosis.

Animals↗

PubMed2001

Dacarbazine-induced carotid artery and deep venous thrombosis in a patient with leiomyosarcoma: case report.

Thromboembolic events are a common and important cause of morbidity and mortality in cancer patients that require early diagnosis and treatment. Reports have suggested that chemotherapeutic agents may contribute to this risk. In this case report, a 60-year-old male patient on chemotherapy (dacarbazine and doxorubicin) for leiomyosarcoma with no previous history of thromboembolism developed left carotid artery thrombosis 3 days after the first cycle of chemotherapy. A low molecular weight heparin was started for a possible cerebrovascular accident-related thrombosis. In the second cycle, he developed right femoral vein thrombosis only 2 days after initiating the chemotherapy. The chemotherapy protocol was changed and the patient did not develop any thrombosis during the 1-year follow-up. In the literature, no thrombotic complications have previously been reported due to either dacarbazine or doxorubicin. In conclusion, elderly patients on chemotherapy should be carefully monitored for thromboembolic complications and, in case of thrombosis, the chemotherapy protocol should be changed.

Anticoagulants↗

PubMed2003

Hyperhomocysteinemia in cerebral vein thrombosis.

High plasma levels of total homocysteine (tHcy) are a risk factor for deep vein thrombosis. Because no information on the relationship between cerebral vein thrombosis and hyperhomocysteinemia is available, a case-control study of 121 patients with a first episode of cerebral vein thrombosis and 242 healthy control subjects was carried out. Fasting plasma levels of tHcy and their postmethionine load (PML) increments, together with other laboratory markers of thrombophilia, were measured in plasma or DNA. Hyperhomocysteinemia (high fasting tHcy and/or PML increments) was diagnosed in 33 patients (27%) and 20 control subjects (8%) (odds ratio, 4.2; 95% confidence interval [CI], 2.3-7.6). Low levels of serum folate and the 677TT methylene tetrahydrofolate reductase were associated with hyperhomocysteinemia, but in a multivariate model hyperhomocysteinemia only was associated with an increased risk of cerebral vein thrombosis. Oral contraceptive intake was associated with the disease with an odds ratio of 6.1 (95% CI, 3.3-11.0). The combined presence of the latter and hyperhomocysteinemia increased the risk of the disease with an odds ratio of 19.5 (95% CI, 5.7-67.3). In conclusion, hyperhomocysteinemia is associated with a 4-fold increased risk of cerebral vein thrombosis; whether or not its correction with vitamins reduces the risk of the disease remains to be demonstrated.

Adolescent↗

PubMed1998

Stroke and intracranial venous thrombosis during pregnancy and puerperium.

OBJECTIVES: To determine nationally representative estimates of the incidence of stroke and intracranial venous thrombosis during pregnancy and the puerperium, and to identify potential risk factors for these conditions. METHODS: National Hospital Discharge Survey data were analyzed for the period 1979 to 1991. Nationally representative estimates of risk were calculated by age, race, presence of pregnancy-related hypertension, census region, hospital ownership, and number of hospital beds. Multivariate models were developed using logistic regression. RESULTS: There were an estimated 8,918 cases of stroke and 5,723 cases of intracranial venous thrombosis during pregnancy and the puerperium in the United States among 50,264,631 deliveries, giving risks of 17.7 cases of stroke and 11.4 cases of intracranial venous thrombosis per 100,000 deliveries. In the multivariate models, stroke was associated strongly with pregnancy-related hypertension, larger hospital size, and proprietary hospital ownership, and inversely associated with living in the South. Intracranial venous thrombosis was associated with maternal age. CONCLUSIONS: Stroke and intracranial venous thrombosis are relatively common complications of pregnancy and the puerperium. Collectively, rates for these conditions are about 50% greater for the entire period of pregnancy and the puerperium than for the immediate peripartum period.

Adolescent↗

PubMedDate not supplied

[Pulmonary thromboembolism and acute renal insufficiency caused by renal artery thrombosis].

INTRODUCTION: Pulmonary thromboembolism is a clinical and pathophysiological condition caused by occlusion of pulmonary arteries by thrombotic embolus. Deep venous thrombosis needn't necessarily be evident. Acute renal insufficiency is a syndrome manifested by rapid decrease or even complete urinary retention, which may be due to obturation of renal arteries by a thrombus. The condition is clinically manifested by hematuria, oliguria, anuria and death due to uremia. CASE REPORT: The patient had a history of disease and a chest X-ray finding both irrelevant for establishing the working diagnosis. Blood gas analysis presented prominent hypoxemia with hyperventilation and ECG finding exhibited right heart overload, pointing to pulmonary thromboembolism. On the third day of treatment with heparin, the patient developed hematuria, oliguria and excessive elevation of nitrogen in blood as a sign of acute renal insufficiency, leading to fatal outcome. Autopsy revealed deep venous thrombosis of the left femoral vein, with massive pulmonary thromboembolism and thrombosis of both femoral arteries, inducing acute renal failure. DISCUSSION: Although the patient had a typical radiologic presentation of pulmonary thromboembolism, treatment with heparin was initiated on the basis of his blood gas analysis and ECG findings. Deep venous thrombosis was not clinically evident and acute renal failure could not be explained during patient's lifetime. CONCLUSION: This is a rare case of acute renal failure due to a rare occurrence of bilateral acute thrombosis of renal arteries.

Acute Kidney Injury↗

PubMedDate not supplied

[Cerebral venous thrombosis and familial prothrombin gene G20210a mutation].

INTRODUCTION: The prothrombin gene variant G20210A was first described as a risk factor for deep vein thrombosis, and recently for cerebral venous thrombosis, although reported cases had other concomitant risk factors. CLINICAL CASES: A 33 years old woman, with no previous vascular nor thrombotic risk factors, was admitted with thrombosis of superior longitudinal, lateral and sigmoid right sinus. The father had deep venous thrombosis 3 years before. One year later, the 29 year old sister of the proband, developed massive deep venous thrombosis, when she was 8 months pregnant. Laboratory investigations showed elevated anticardiolipin antibodies titer in the proband. Prothrombin activity was in the normal range in the 3 patients. Prothrombin gene mutation G 20210A was detected in the 3 patients. CONCLUSION: As the presence of more than one thrombophilic factor (in the reported case, prothrombin G20210A mutation and anticardiolipin antibodies) increases the likehood of a thrombotic event, it is useful to screen for thrombotic genetic conditions, even when other vascular risks are present, and vice versa.

Adult↗

PubMedDate not supplied

[Intracranial venous thrombosis: a study of 16 cases and a review of the literature].

INTRODUCTION: The clinical picture and aetiology of intracranial venous thrombosis are highly variable. Early descriptions reported it as a rare disease with a poor prognosis but the advent of neuroimaging techniques, and a deeper knowledge of the clinical picture, have shown it to have a higher frequency and a better prognosis. OBJECTIVE: To report the clinical and neuroimaging findings in patients diagnosed as having intracranial venous thrombosis in our department and review the state of the literature. PATIENTS AND METHODS: We reviewed all discharge reports from patients admitted to the neurology department of the Juan Canalejo Hospital between 1975 and 2000. Of these, we reviewed the medical records of those patients diagnosed as having intracranial venous thrombosis in order to obtain data relating to the clinical manifestations, complementary tests, etiological and topographical diagnosis, treatment and outcome. RESULTS: Diagnosis of intracranial venous thrombosis was made in 16 patients. The most common symptom was headache. The superior sagittal was the most frequently affected sinus. In almost all patients CT results led to the suspicion, and in some cases the confirmation, of the diagnosis. The most frequently found aetiology was oral contraceptive consumption. Outcome was generally good both with anticoagulation and symptomatic treatments. CONCLUSIONS: The most important difference between the present study and earlier reports is in the frequency of the different aetiologies. Our findings provide further evidence that intracranial venous thrombosis is not an infrequent disease and that the prognosis is generally good.

Adult↗

PubMedDate not supplied

"Effort" thrombosis of the axillary and subclavian vein associated with cervical rib and oral contraceptives in a young woman athlete.

"Effort" thrombosis, also called the Paget-Schroetter syndrome or primary thrombosis of the upper extremity, has been well documented in the literature. However, in our review of the United States, Canadian, and British literature, we found only 52 cases in which it was related to sports participation. We report a case of axillary and subclavian vein "effort" thrombosis in a young woman athlete, who was predisposed to thrombosis by all three postulates of the Virchow triad: namely, (1) stasis caused by constriction from a cervical rib, (2) increased coagulability as a result of oral contraceptive use, and (3) vessel wall injury because of competitive softball participation. Of the available therapeutic plans, we believe that athletes with "effort" thrombosis should have aggressive treatment that is initiated as early as possible to prevent swelling, tingling numbness, easy fatigue of the arm, and pain on prolonged use of the affected extremity.

Adolescent↗