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PubMed1997

Spontaneous erythroid colony formation as the clue to an underlying myeloproliferative disorder in patients with Budd-Chiari syndrome or portal vein thrombosis.

Budd-Chiari syndrome is a severe disease characterized by occlusion of large hepatic veins leading to death if untreated. Using the classical criteria for the diagnosis of polycythemia vera (PV), essential thrombocythemia (ET), and idiopathic myelofibrosis (IMF), overt PV was the underlying cause in about 10% of the cases and ET or IMF in only a very few. Using spontaneous endogenous erythroid colony (EEC) formation in vitro and/or bone marrow biopsies, a primary myeloproliferative disorder (PMD) was present in 78% of the patients with apparently idiopathic Budd-Chiari syndrome and in about half of the patients with portal, splenic, and/or mesenteric vein thrombosis. The diagnoses in 40 reported cases with hepatic vein thrombosis and spontaneous EEC were overt PV in 25 and latent unclassified PMD in 15 patients. The diagnoses of 40 reported cases with splanchnic vein thrombosis and spontaneous EEC were overt PV in 12, ET in 2, IMF in 2, and latent unclassified PMD with the presence of EEC in 24 patients. Thrombocytosis as a manifestation of myeloproliferative disease was recorded in 34 of 80 (42.5%) patients with spontaneous EEC and Budd-Chiari syndrome or portal vein thrombosis. Thrombocythemia was present in 15 of 41 patients with a proven and in 19 of 39 patients with a latent myeloproliferative disorder. Patients with hepatic vein or splanchnic vein thrombosis associated with a PMD are predominantly females younger than 45. It is concluded that both spontaneous EEC and histopathology from bone marrow biopsy provide specific information as sensitive clues to the diagnosis of all variants of overt and latent myeloproliferative disorders. The association of hepatic and splanchnic vein thrombosis and PMD is not fully understood. Therapeutic options of Budd-Chiari syndrome include anticoagulation with heparin, fibrinolysis followed by oral anticoagulation, and appropriate treatment of the underlying PMD. In case of failure, invasive options include local procedures such as angioplasty or stenting, venous decompression by portal-systemic shunts, or liver transplantation.

Biomarkers↗
PubMed1996

Coexistence of hereditary homocystinuria and factor V Leiden--effect on thrombosis.

BACKGROUND: Venous and arterial thromboembolism occurs in only about one third of patients homozygous for homocystinuria, which suggests that other, contributory factors are necessary for the development of thrombosis in these patients. Factor V Leiden, an R506Q mutation in the gene coding for factor V, is the most common cause of familial thrombosis and could be a potentiating factor. METHODS: We determined activated partial-thromboplastin times in the presence and absence of activated protein C and tested for the factor V Leiden mutation in 45 members of seven unrelated consanguineous kindreds in which at least 1 member was homozygous for homocystinuria. RESULT: Thrombosis (venous, arterial, or both) occurred in 6 of 11 patients with homocystinuria (age, 0.2 to 8 years). All six also had the factor V Leiden mutation. One patient with prenatally diagnosed homocystinuria who was also heterozygous for factor V Leiden has received warfarin therapy since birth and has not had thrombosis (age, 18 months). Of four patients with homocystinuria who did not have factor V Leiden, none had thrombosis (ages at this writing, 1 to 17 years). Three women who were heterozygous for both homocystinuria and factor V Leiden had recurrent fetal loss and placental infarctions. CONCLUSIONS: Patients with concurrent homocystinuria and factor V Leiden can have an increased risk of thrombosis. Screening for factor V Leiden may be indicated in patient with homocystinuria and their family members.

Adolescent↗
PubMed2003

A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.

BACKGROUND: Many patients with the antiphospholipid antibody syndrome and recurrent thrombosis receive doses of warfarin adjusted to achieve an international normalized ratio (INR) of more than 3.0. However, there are no prospective data to support this approach to thromboprophylaxis. METHODS: We performed a randomized, double-blind trial in which patients with antiphospholipid antibodies and previous thrombosis were assigned to receive enough warfarin to achieve an INR of 2.0 to 3.0 (moderate intensity) or 3.1 to 4.0 (high intensity). Our objective was to show that high-intensity warfarin was more effective in preventing thrombosis than moderate-intensity warfarin. RESULTS: A total of 114 patients were enrolled in the study and followed for a mean of 2.7 years. Recurrent thrombosis occurred in 6 of 56 patients (10.7 percent) assigned to receive high-intensity warfarin and in 2 of 58 patients (3.4 percent) assigned to receive moderate-intensity warfarin (hazard ratio for the high-intensity group, 3.1; 95 percent confidence interval, 0.6 to 15.0). Major bleeding occurred in three patients assigned to receive high-intensity warfarin and four patients assigned to receive moderate-intensity warfarin (hazard ratio, 1.0; 95 percent confidence interval, 0.2 to 4.8). CONCLUSIONS: High-intensity warfarin was not superior to moderate-intensity warfarin for thromboprophylaxis in patients with antiphospholipid antibodies and previous thrombosis. The low rate of recurrent thrombosis among patients in whom the target INR was 2.0 to 3.0 suggests that moderate-intensity warfarin is appropriate for patients with the antiphospholipid antibody syndrome.

Adult↗
PubMed2000

Genetic factors associated with thrombosis in pregnancy in a United States population.

OBJECTIVE: Polymorphisms in the genes for factor V (factor V Leiden), prothrombin, methylenetetrahydrofolate reductase, and angiotensin-converting enzyme have been associated with the occurrence of venous thrombosis. The objective of this study was to determine the relationships of these polymorphisms to thrombosis during pregnancy. STUDY DESIGN: This case-control study included 41 case patients with venous thrombosis during pregnancy and 76 control subjects matched for hospital and for race (white vs black) who had a normal pregnancy. RESULTS: Among white subjects, mutations in the genes for factor V and prothrombin were associated with increased risks of venous thrombosis during pregnancy (factor V: odds ratio, 18.3; 95% confidence interval, 2.7-432; P =.001; prothrombin: odds ratio infinity; 95% lower confidence limit, 1.7; P =.01). No black subject had either of these two mutations. For both black and white subjects the D/D genotype of the gene for angiotensin-converting enzyme entailed increased risk compared with the other genotypes (odds ratio, 2.7; 95% confidence interval, 1.2-6.3; P =.02). The polymorphism in the gene for methylenetetrahydrofolate reductase was unrelated to thrombosis during pregnancy among both blacks and whites. CONCLUSION: Women who had thrombotic complications during pregnancy demonstrated an increased prevalence of genetic mutations related to coagulation. The additional risk of thrombosis during pregnancy associated with such genetic mutations can be substantial.

Black People↗
PubMed1987

Prevention of occlusive coronary artery thrombosis by a murine monoclonal antibody to porcine von Willebrand factor.

A murine monoclonal antibody (mAb) against porcine von Willebrand factor (vWF) induced an antithrombotic state in normal pigs. Thrombosis was induced by a standard procedure of stenosis and mechanical injury of the artery. The mAb was an IgG1 kappa that inhibited vWF-induced platelet aggregation at a titer of 1:6250 and bound to immobilized vWF at a maximal dilution of 1:512,000. The antibody did not affect two other vWF functions, platelet adhesion and binding of coagulant factor VIII (factor VIII:C). The antithrombotic state was characterized by a prolonged bleeding time and lack of plasma vWF activity, but with near-normal levels of factor VIII:C and von Willebrand antigen. The circulating Ag.mAb complex demonstrated a multimeric distribution comparable to that of native plasma vWF. Three groups of pigs were studied: group A consisted of nine untreated animals, eight of which developed occlusive coronary thrombosis; group B, four treated animals with a long bleeding time, none of which developed occlusive thrombosis; and group C, two animals with preexisting thrombosis treated with mAb, in which stable blood flow was reestablished. Morphologically, the group B animals showed adherent platelets covering the injured intima but no thrombosis. This mAb is an antithrombotic agent that prevents platelet thrombosis without affecting intrinsic platelet function.

Animals↗
PubMed2004

Prevention of catheter thrombosis increases survival, but does not modify lung injury in rats receiving long-term parenteral nutrition.

It has previously been shown that rats receiving total parenteral nutrition (TPN) or each component of TPN die within 40 days of treatment. Central catheter thrombosis and lung injury were constant findings. The aim of the present study was to examine the impact of central thrombosis on lung injury and survival in rats receiving long-term parenteral nutrition. In the first part of the study TPN was infused via the jugular vein and incidence of central venous thrombosis and rate of survival were recorded. Addition of low molecular weight heparin (LMWH) reduced central thrombosis from 6 out of 7 animals to 2 out of 7 animals (p=0.027) and increased survival from 17.1+/-4.5 days to 32.4+/-4.9 days (p=0.04). In the second part of the study four infusion groups were established. Group 1 (controls) received saline 100 mL/kg/day via the jugular vein (n=6). Group 2 received Intralipid 40 mL/kg/day via the jugular vein (n = 7). Group 3 received Intralipid 40 mL/kg/day via the portal vein (n = 7). Group 4 received Intralipid 40 mL/kg/day with added LMWH 70 U/kg/day (n = 7). Lung injury and occurrence of central thrombosis were investigated. Lung injury was assessed by measuring pulmonary arterial pressure (Ppa), clearance of serotonin by the vascular endothelium and the capillary filtration coefficient (CFC). Either infusion via the portal vein or the addition of LMWH to the infusion via the jugular vein prevented central thrombus formation, but the lung injury was not modified by this method compared with infusing Intralipid via the jugular vein without LMWH. In conclusion, central thrombus formation contributes to death in rats receiving parenteral nutrition. The mechanism of the injurious effect of central thrombosis remains unknown, but central thrombus formation seems not to increase lung injury caused by Intralipid.

Animals↗
PubMed2006

In vivo veritas: thrombosis mechanisms in animal models.

Experimental models have enhanced our understanding of atherothrombosis pathophysiology and have played a major role in the search for adequate therapeutic interventions. Various animal models have been developed to simulate thrombosis and to study in vivo parameters related to hemodynamics and rheology that lead to thrombogenesis. Although no model completely mimics the human condition, much can be learned from existing models about specific biologic processes in disease causation and therapeutic intervention. In general, large animals such as pigs and monkeys have been better suited to study atherosclerosis and arterial and venous thrombosis than smaller species such as rats, rabbits, and dogs. On the other hand, mouse models of arterial and venous thrombosis have attracted increasing interest over the past two decades, owing 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. To simulate rupture of an atherosclerotic plaque, models of arterial thrombosis often involve vascular injury, which can be achieved by several means. There is no animal model that is sufficiently tall, that can mimic the ability of humans to walk upright, and that possesses the calf muscle pump that plays an important role in human venous hemodynamics. A number of spontaneous or genetically engineered animals with overexpression or deletion of various elements in the coagulation, platelet, and fibrinolysis pathways are now available. These animal models can replicate important aspects of thrombosis in humans, and provide a valuable resource in the development of novel concepts of disease mechanisms in human patients.

Animals↗
PubMed2006

Septic thrombosis of the cavernous sinus: two different mechanisms.

PURPOSE: Septic thrombosis of the cavernous sinus is a rare condition that may lead to significant morbidity and mortality if not diagnosed and treated urgently. We present two recent cases of bilateral septic cavernous sinus thrombosis with differing etiologies, the first of dental origin and the second a complication of sphenoid sinusitis. METHODS: Case report. RESULTS: A diagnosis of cavernous sinus thrombosis was made based on clinical findings and confirmed by imaging in both patients. The etiology in the first patient was related to poor dental hygiene, with resultant spread of infection to the cavernous sinuses. The second had bilateral sphenoid sinusitis, with intravascular gas noted in both orbits and cavernous sinuses. This is the first reported occurrence of such an event associated with septic cavernous sinus thrombosis. Bilateral sphenoidotomies with evacuation of the sinuses were performed, and Haemophilus influenzae was cultured from the sphenoidotomy fluid and blood. Broad spectrum intravenous antibiotics were given in both patients, and complete recovery achieved within weeks. CONCLUSION: In septic thrombosis of the cavernous sinus, early recognition and prompt management with broad spectrum intravenous antibiotics is crucial for full recovery. The primary source of sepsis may be a distant focus with septicemia preceding thrombosis of the cavernous sinus. Alternatively, infection may spread from facial regions via the facial venous plexus or from the sphenoid sinus directly to the adjacent cavernous sinus.

Adult↗
PubMed2005

Prothrombin G20210A mutation in Turkish children with thrombosis and the frequency of prothrombin C20209T.

The prothrombin G20210A mutation has been described as the second most common genetic risk factor in thrombotic patients. Recently a new prothrombin gene variant namely prothrombin C20209T has also been found to be associated with thrombosis. In the present study the frequency of these two thrombin variants have been searched in two different groups. Group 1: A total of 377 children with thrombosis were analyzed during 7 years between January 1997 and 2004 and screened for prothrombin G20210A mutation. Twenty-four of 387 children (6.3%) with thrombosis were diagnosed as having PT G20210A mutation. The mean age of the patients was 6.1 years (median: 6 years, range: 4 months to 17 years, 15 male, 9 female). Six of 24 children were below 2 years of age (25%). Fifteen of 24 children (62.5%) had arterial thrombosis, most of whom (93.3%) had cerebral infarct. Group 2: The prothrombin C20209T variant has been analyzed in 200 thrombotic patients and in 200 healthy subjects. None of the thrombotic patients and healthy individuals carried the prothrombin C20209T variant. In conclusion, arterial thrombosis as the cerebral infarct is the most prominent type of thrombosis in children with prothrombin G20210A mutation. It seems that the prothrombin C20209T variant is not an important risk factor for the population studied.

Adolescent↗
PubMed1991

Oral contraceptives, sex steroid-induced antibodies and vascular thrombosis: results from 1318 cases.

The role of antiethinyl estradiol antibodies (anti EE Ab) and associated risk factors was evaluated in 1318 cases of venous or arterial thrombosis in oral contraceptives (OC) users, and compared to 61 non-users and 124 healthy current users. Anti EE Ab were absent in non-users and present in 33% of healthy users and 72% of those with thrombosis, either arterial or venous. Age, duration of use, hyperlipidaemia and smoking were factors associated with thrombosis only in women with an arterial disease. While the two predominant factors, anti EE Ab and smoking may be risk factors in their own right, the combination of both was found in 47.7% of women with thrombosis. It is proposed that thrombosis associated with OC use may be explained by an immunological disease in which anti EE Ab and their complexes with the circulating synthetic hormones may be harmful to the vessels, as also suggested by the type of lesions already described in OC users. The determination of anti EE Ab in healthy users may identify a group at risk of thrombosis.

Adult↗
PubMed1993

Diagnosis of prosthetic heart valve thrombosis. The respective values of transthoracic and transoesophageal Doppler echocardiography.

Early diagnosis of acute prosthetic thrombosis remains a challenge. In 20 patients with 23 thrombosed cardiac valves, we evaluated the respective value of transthoracic (TTE) and transoesophageal (TEE) Doppler echocardiography. According to the presence or absence of prosthetic obstruction by continuous-wave Doppler, prostheses were separated into two groups. Group 1 included nine thrombosed prostheses (8 mitral, 1 aortic) with severe obstruction. All patients presented with severe symptoms of heart failure. Transthoracic Doppler echocardiography allowed immediate diagnosis of prosthetic thrombosis, even in critically ill patients, showing (1) eccentric transprosthetic colour flow jets in all eight mitral prostheses, (2) severe obstruction on Doppler examination (mean gradient = 18 to 36 mmHg in eight mitral prostheses, and 69 mmHg in one aortic valve), and (3) direct echocardiographic evidence of thrombosis (i.e. thrombus or abnormal disc or leaflet motion) in four patients. All nine patients were immediately treated by surgery (n = 8) or fibrinolysis (n = 1) on the basis of TTE results only. TEE allowed better visualization of thrombus and restricted leaflet or disc motion, but had little influence on patient management. Group 2 included 14 thrombosed prostheses (10 mitral, 4 aortic) with mild or absent obstruction. In three patients with massive mitral prosthetic thrombosis, an associated minimal thrombosis of a prosthetic aortic valve was found at surgery, but was detected neither by TTE, nor by TEE. The 11 remaining patients with isolated partial mitral (n = 10) or aortic (n = 1) thrombosis. Clinical presentation was fever, cerebral embolism, or mild dyspnoea, but no heart failure. TTE was normal in all.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗
PubMed2005

The elusive clot: the controversy over coronary thrombosis in myocardial infarction.

UNLABELLED: After Heberden's description of patients with "angina pectoris" in 1768, for over 125 years most physicians believed that the disease was immediately fatal. The growing realization early in the twentieth century that in fact patients could survive an acute myocardial infarction led to a search for mechanisms and treatment. Coronary thrombosis was the primary candidate for the inciting event, but this supposition was based on rather piecemeal and uncritical reports. It became apparent that coronary thrombosis and acute myocardial infarction (AMI), terms that had often been used interchangeably, actually represented separate pathological entities. A few physicians even proposed that AMI caused coronary thrombosis rather than the other way around. The reasons for some investigators rejecting the coronary thrombosis hypothesis were ultimately shown to be the result of faulty pathological techniques and interpretations. This debate ended only when in vivo studies (i.e., coronary arteriography in living patients during AMI episodes) finally settled the matter. These events indicate that older theories, even when derived from faulty reasoning or poorly substantiated documentation, might ultimately prove valid. Newer investigative techniques can suddenly clarify issues that have previously seemed irresolvable. The identification of coronary thrombosis in AMI has led to major advances in the treatment of this serious and ubiquitous disease. KEYWORDS: coronary artery disease, coronary thrombosis, angina pectoris, acute myocardial infarction, coronary arteriography, anticoagulation.

Acute Disease↗
PubMed1994

Case report: acute renal vein thrombosis in patients with spinal cord injury and secondary amyloidosis.

Chronic spinal cord injury, when complicated by chronic suppurative infections, has replaced chronic tuberculosis as a leading cause of secondary amyloidosis. Renal involvement with secondary amyloidosis is characterized by the presence of nephrotic range proteinuria and an increased incidence of renal vein thrombosis. Two cases of acute renal vein thrombosis associated with secondary amyloidosis in patients with spinal cord injury are presented. In both cases, a past history of extensive decubitus ulcerations and urinary tract infections preceded the development of nephrotic range proteinuria. In case 1, nonoliguric acute renal failure occurred after the development of acute bilateral renal vein thrombosis. The patient declined dialytic therapy and expired with uremia. In case 2, worsening renal function and increased proteinuria resulted after the development of acute unilateral renal vein thrombosis. These cases include the clinical and anatomic findings of acute renal vein thrombosis that occur as a complication of secondary amyloidosis. Acute renal vein thrombosis should be considered whenever an acute change in renal function or increase in proteinuria is noted in this setting.

Aged↗
PubMed2003

Association of anti-heparin platelet factor 4 antibody levels and thrombosis in pediatric intensive care patients without thrombocytopenia.

Anti-heparin platelet factor 4 (anti-HPF4) antibodies have been demonstrated to play a pathogenetic role in the development of heparin-induced thrombocytopenia. In adults, the presence of anti-HPF4 antibodies without thrombocytopenia has been reported not to confer a thrombotic risk. To investigate whether this also holds true for children, we performed a case-control study in heparin-exposed patients from a pediatric intensive care unit. During the 30-month study period, 612 patients received heparin for at least 5 days. Of these, 10 patients developed thrombosis without thrombocytopenia and constituted the study group. These patients were compared with 19 matched control patients with neither thrombosis nor thrombocytopenia. Anti-HPF4 antibody levels were measured using an enzyme-linked immunosorbent assay (Asserachrom HPF4). All thrombosis patients and controls had lower anti-HPF4 antibody levels than the cut-off level recommended by the manufacturer for adults. However, median anti-HPF4 antibody levels were significantly higher in the thrombosis patients [51% of the manufacturer's cut-off; interquartile range (IQR), 47-53%] than in the control group (23%; IQR, 9-36%) (P = 0.004). At an anti-HPF4 cut-off level of 45%, the odds ratio for a thrombotic event amounted to 34 (95% confidence interval, 4.4-261.8), indicating an association between anti-HPF4 antibody levels and thrombosis despite the absence of thrombocytopenia. A role of anti-HPF4 antibodies in the development of catheter-related thrombosis is suggested.

Autoantibodies↗
PubMed2004

Intravenous apyrase administration reduces arterial thrombosis in a rabbit model of endothelial denudation in vivo.

The role of adenine nucleotides on vascular and platelet functions has long been established. Apyrase (CD39) takes part of a family of ecto-enzymes that hydrolyze adenosine diphosphate and adenosine triphosphate. The participation of apyrase in the thromboregulatory system is under study. An in vivo experimental model of acute arterial thrombosis was used to test the hypothesis that administering a soluble form of potato apyrase could prevent thrombus formation. Twenty-five white New Zealand male rabbits suffered balloon aortic endothelium denudation and, after 15 days, they were submitted to a thrombosis-triggering protocol with a procoagulant (Russel's viper venom) and epinephrine. After the thrombosis-triggering protocol, 12 animals received two soluble apyrase administrations intravenously (with 90 min intervals), while 13 control animals received no apyrase. Three hours after the triggering protocol, the animals were killed and the rate and area of arterial thrombosis were analyzed. The rate of thrombosis in the apyrase group was significantly lower than that of the control group (16.7 versus 69%, respectively; P = 0.015), as was the area of thrombosis (1.7 +/- 4.3 versus 21.7 +/- 37.4 mm2, respectively; P = 0.008). Our results confirm that apyrase participates in homeostasis through a potent anti-thrombotic effect.

Adenine Nucleotides↗
PubMed2001

Management of thrombosis in women with antiphospholipid syndrome.

1) Antiphospholipid antibody syndrome may be associated with unusual sites of thrombosis. 2) Laboratory evaluation involves testing for antiphospholipid antibodies: lupus anticoagulant and anticardiolipin antibodies. 3) Acute management of thrombosis involves immediate anticoagulation. Low-molecular-weight heparins are as safe and effective as unfractionated heparin in this setting. Arterial events may require emergent thrombolytic therapy. Monitoring of the APTT with unfractionated heparin in the presence of a lupus anticoagulant is ineffective; these patients require monitoring of antifactor Xa levels or the use of LMWH, which does not require monitoring. 4) The pharmacokinetics of LMWH change in pregnancy, resulting in a shorter plasma half-life and larger volume of distribution. Monitoring of antifactor Xa levels is necessary. 5) Chronic anticoagulation is best achieved with warfarin, with significantly decreased rates of recurrent events when the INR is > or = 3.0. Long-term, if not life-long, anticoagulation is often necessary. Warfarin is teratogenic, and individuals desiring pregnancy will need to convert to therapeutic, not prophylactic, doses of either unfractionated heparin or LMWH. 6) As part of optimal management of thrombosis in APS, additional risk factors for thrombosis should be eliminated or reduced. These include comorbid illnesses such as hypertension and hyperlipidemia, as well as smoking. 7) Tamoxifen, raloxifene, oral contraceptives, and hormone replacement therapy are all associated with an increased risk of DVT in the general population. In APS patients receiving therapeutic anticoagulation, the addition of these drugs should not increase thrombosis risk. In APS patients not receiving anticoagulant therapy, these hormonal therapies may increase the thrombosis risk.

Acute Disease↗
PubMed1999

Late deep venous thrombosis and delayed weightbearing after total hip arthroplasty.

One hundred ninety-nine patients who underwent primary total hip arthroplasty and used in hospital pneumatic compression stockings and aspirin as thromboembolic prophylaxis were screened for deep venous thrombosis using duplex ultrasonography on the fourth postoperative day. Of the initial 98 patients, 21 underwent noncemented arthroplasty, maintained touchdown weightbearing for 6 weeks after surgery, and then began progressive partial weightbearing. Of the subsequent 101 patients, 28 underwent noncemented arthroplasty and began progressive weightbearing immediately after surgery. All other patients underwent hybrid arthroplasty and began weightbearing to tolerance immediately after surgery. After duplex screening examination, patients with proximal deep venous thrombosis were given anticoagulation therapy, and patients with negative study results were observed clinically. The relative risk of proximal deep venous thrombosis after noncemented arthroplasty using delayed weightbearing was compared with that after noncemented arthroplasty using immediate progressive weightbearing. Of patients with noncemented arthroplasty, the prevalence of proximal deep venous thrombosis was significantly lower in those using progressive weightbearing immediately after surgery (none) than in those using delayed weightbearing rehabilitation (19%). This study showed that patients undergoing noncemented total hip arthroplasty with delayed weightbearing rehabilitation risk greater potential for deep venous thrombosis after hospital discharge. This study suggests consideration for continued thromboembolic prophylaxis or routine deep venous thrombosis surveillance, or both measures, after hospital discharge, unless more rapid progression of weightbearing is allowed.

Anticoagulants↗
PubMed1988

Thrombosis caused by polyurethane double-lumen subclavian superior vena cava catheter and hemodialysis.

During an 18-month period, 82 consecutive patients (37 women and 45 men), with a mean age of 50 yr (range 15 to 74), underwent hemodialysis with 91 polyurethane double-lumen subclavian superior vena cava catheters inserted via the right subclavian vein. Upon catheter removal, venograms were performed in 53 which revealed thrombosis in 13. Autopsy performed in 13 other patients revealed thrombosis in three. Mean catheter duration was 27 days (range 1 to 138). Catheter duration was significantly (p less than .01) longer in the 16 cases complicated by thrombosis. There was no significant difference in the frequency of thrombosis between men and women. Two patients developed symptoms of subclavian vein occlusion after the creation of an arteriovenous fistula on the same side as a previous hemodialysis catheter. Overall, thrombosis was found in 23% and increased with longer catheter duration. We recommend phlebography to exclude thrombosis before creating an arteriovenous fistula on the same side as the previous hemodialysis catheter. There was no case of clinical discernible pulmonary embolism.

Adolescent↗