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PubMed2005

Deep venous thrombosis in medical-surgical critically ill patients: prevalence, incidence, and risk factors.

OBJECTIVE: Critically ill patients may be at high risk of venous thromboembolism. The objective was to determine the prevalence, incidence, and risk factors for proximal lower extremity deep venous thrombosis among critically ill medical-surgical patients. DESIGN: Prospective cohort. SETTING: Closed university-affiliated intensive care unit. PATIENTS: We enrolled consecutive patients > or =18 yrs of age expected to be in intensive care unit for > or =72 hrs. Exclusion criteria were an admitting diagnosis of trauma, orthopedic surgery, pregnancy, and life support withdrawal. INTERVENTIONS: Interventions included bilateral lower extremity compression ultrasound within 48 hrs of intensive care unit admission, twice weekly, and if venous thromboembolism was clinically suspected. Thromboprophylaxis was protocol directed and universal. We recorded deep venous thrombosis risk factors at baseline and daily, using multivariate regression analysis to determine independent predictors. Patients were followed to hospital discharge. RESULTS: Among 261 patients with a mean Acute Physiology and Chronic Health Evaluation II score of 25.5 (+/-8.4), the prevalence of deep venous thrombosis was 2.7% (95% confidence interval 1.1-5.5) on intensive care unit admission, and the incidence was 9.6% (95% confidence interval 6.3-13.8) over the intensive care unit stay. We identified four independent risk factors for intensive care unit-acquired deep venous thrombosis: personal or family history of venous thromboembolism (hazard ratio 4.0, 95% confidence interval 1.5-10.3), end-stage renal failure (hazard ratio 3.7, 95% confidence interval 1.2-11.1), platelet transfusion (hazard ratio 3.2, 95% confidence interval 1.2-8.4), and vasopressor use (hazard ratio 2.8, 95% confidence interval 1.1-7.2). Patients with deep venous thrombosis had a longer duration of mechanical ventilation (p = .03), intensive care unit stay (p = .005), and hospitalization (p < .001) than patients without deep venous thrombosis. CONCLUSIONS: Despite universal thromboprophylaxis, medical-surgical critically ill patients remain at risk for lower extremity deep venous thrombosis. Further research is needed to evaluate the risks and benefits of more intense venous thromboembolism prophylaxis.

APACHE↗
PubMed2006

Thrombosis in children with malignancy.

PURPOSE OF REVIEW: The association between thrombosis and malignancy in adults is well known. Children are now surviving malignancies that previously resulted in mortality. Complications, however, occur including thrombosis that result in mortality and morbidity. This review will explore the association in children and discuss the epidemiology and evidence-based diagnosis and treatment of thrombosis in this cohort. RECENT FINDINGS: Thrombin is an important link between malignancy, metastases, and inflammation. The accurate diagnosis of thrombosis in the upper venous system is directly related to the diagnostic technique used. Antithrombotic treatment is challenging owing to higher risks of bleeding, for example, decreased platelet counts, tiffelitis, large vascular tumor, etc. SUMMARY: Thrombosis and malignancy are associated in children. Properly designed studies are urgently required to further define the epidemiology of thrombosis in different malignancies and to find the best way to diagnose and treat thrombosis in children.

Blood Coagulation↗
PubMed2005

Sonography for deep venous thrombosis: current and future applications.

Deep venous thrombosis (DVT) is a one of the most common problems facing the clinician in medicine today. It is often asymptomatic and goes undiagnosed with potentially fatal consequences. Ultrasound has become the "gold standard" in the diagnosis of deep venous thrombosis and with proper attention to technique sensitivity of this test is approximately 97%. An understanding of anatomy, pathophysiology, and risk factors is important. Thrombus formation usually begins beneath a valve leaflet below the knee. Approximately 40% will resolve spontaneously, 40% will become organized, and 20% will propagate. Whether or not a calf vein thrombus is identified, a repeat examination in 7 to 10 days is recommended in patients with risk factors or when deep venous thrombosis is suspected. The three main risk factors for thrombus formation are age greater than 75 years, previous history of deep venous thrombosis, and underlying malignancy. Other diagnostic studies include the contrast venogram, CT or MRI venogram, Tc99m Apcitide study, and the laboratory test D-Dimer. The D-Dimer study is being used more frequently as a screening test with 99% sensitivity in detecting thrombus, whether deep venous thrombosis or pulmonary embolism. However, specificity is only approximately 50% with many conditions leading to false-positive exams. Therefore, a negative examination is useful in avoiding other diagnostic studies, but a positive one may be misleading. Conditions that can lead to a false-positive examination include, but are not limited to diabetes, pregnancy, liver disease, heart conditions, recent surgery, and some gastrointestinal diseases. Like the sonogram, two negative D-Dimer studies a week apart exclude the diagnosis of deep venous thrombosis. Compression sonography with color Doppler remains the best overall test for deep venous thrombosis. It is easy to perform, less expensive than most "high tech" studies, can be performed as a portable examination, and is highly reliable when done properly.

Aged↗
PubMed2005

Relationship between ABO and Secretor genotype with plasma levels of factor VIII and von Willebrand factor in thrombosis patients and control individuals.

In contrast to earlier reports, this study examined the relationship between plasma levels of factor VIII (FVIII) and von Willebrand factor (VWF) and ABO blood group and secretor status at the genetic level in 355 patients with venous thrombosis as well as in 236 controls. ABO glycosyl transferase alleles A(1) and B were more frequent in the thrombosis collective and alleles O(1), O(2) and A(2) were more frequent in the controls. A low-risk group for venous thrombosis of individuals with genotypes O(1)O(1), O(1)O(2) and O(1)A(2) (H-antigen rich) could be distinguished from a high-risk group with genotypes A(1)A(1), A(1)B, O(1)A(1) and O(1)B (H-antigen poor). In both the thrombosis and control groups, the H-antigen rich group showed significantly lower levels of FVIII coagulant activity (FVIII:C) and VWF antigen (VWF:Ag) than the H-antigen poor group. The frequency of the different secretor genotypes in the thrombosis group was not different from that in the control group. No significant differences of FVIII:C and VWF:Ag levels were seen between SeSe, Sese and sese individuals in the thrombosis and in the control group. Thus the risk of venous thrombosis is associated with the ABO blood group genotype but not with secretor status.

ABO Blood-Group System↗
PubMed2006

Rabbit antithymocyte globulin related decrease in platelet count reduced risk of pediatric renal transplant graft thrombosis.

Graft thrombosis is a serious complication in pediatric renal transplantation. We assess a potential protective effect for the decrease in platelet count associated with RATG therapy against pediatric renal transplant graft vascular thrombosis. Between January 1986 and December 1998, 120 kidney transplants were performed in 95 pediatric recipients. Patients were divided into two groups. Group 1 (n = 61), non-RATG group received cyclosporine, azathioprine and steroids, while group 2 (n = 59), RATG group, received in addition, RATG at day 1 and continued for 4-10 days postoperatively. Platelet count prior to transplant, median change in absolute platelet count at 1 and 3 days post-transplant was recorded. Graft thrombosis incidence was examined. Six grafts (5%) developed thrombosis. All were in group 1 (p = 0.028). Median pretransplant platelet count (x10(9)/L) in group 1 was 283 vs. 280 in group 2 (p = 0.921). Median decrease in absolute platelet count (x10(9)/L) from pretransplant levels at one and three days post-transplant for group 1 and 2 was 18 vs. 83 (p </= 0.001) and 39 vs. 105 (p </= 0.001), respectively. Graft thrombosis risk factors were similar in both groups. RATG use was statistically significant (p = 0.044) for reduced risk of graft thrombosis in multivariate analysis. Patients receiving RATG showed significant decrease in both platelet count and graft thrombosis incidence. A role for RATG related effect on platelet count is assumed.

Adolescent↗
PubMed2004

Thrombosis and ELISA optical density values in hospitalized patients with heparin-induced thrombocytopenia.

The natural history of heparin-induced thrombocytopenia (HIT) in the absence of thrombosis was previously established using functional assays for confirmation of diagnosis (e.g. 14C serotonin release assay). An enzyme-linked immunosorbent assay (ELISA) that detects the presence of antibodies directed against the heparin-platelet factor-4 (PF4) complex has largely replaced functional assays in many medical centers. Although the ELISA is highly sensitive for detecting HIT antibodies, its usefulness for predicting thrombotic outcomes has not been clearly established. We performed a retrospective chart review of all hospitalized patients at a university hospital who tested seropositive for HIT by a commercial ELISA during 2001 and 2002. A total of 63 inpatients were identified as HIT positive by ELISA. Forty-eight patients had no apparent HIT-associated thrombosis at the time of HIT seropositivity (i.e. isolated HIT) and only one was treated prophylactically with a direct thrombin inhibitor. The 30-day thrombosis rate for patients with isolated HIT was 17% (eight of 48). Higher ELISA optical density (OD) measurements correlated significantly with thrombosis (1.41 +/- 0.87 vs. 0.79 +/- 0.46, P <0.001). Patients with isolated HIT and an OD measurement of > or = 1.0 demonstrated nearly a 6-fold increased risk of thrombosis compared with those with OD values between 0.4 and 0.99 (odds ratio 5.74, 95% confidence interval 1.73, 19.0; absolute rate of thrombosis, 36% vs. 9%, respectively, P=0.07). We conclude that in hospitalized patients with isolated HIT, the presence of heparin-PF4 antibodies detected by ELISA was associated with a significant risk of subsequent thrombosis and higher ELISA values were observed among patients suffering thrombotic events.

Aged↗
PubMed2005

Old and new risk factors for upper extremity deep venous thrombosis.

BACKGROUND: Well known risk factors for upper extremity deep venous thrombosis are the presence of a central venous catheter (CVC) and malignancy, but other potential risk factors, such as surgery, injury and hormone replacement therapy (HRT), have not yet been explored. METHODS: We performed a population-based case-control study including 179 consecutive patients, aged 18-70 years with upper extremity deep venous thrombosis and 2399 control subjects. Participants reported on acquired risk factors in a questionnaire and factor V Leiden and prothrombin 20210A mutation were ascertained. Information on CVC was obtained from discharge letters. RESULTS: Forty-two patients (23%) and one control subject (0.04%) had a CVC (ORadj: 1136, 95% CI: 153-8448, adjusted for age and sex). Cancer patients without a CVC had an eightfold increased risk of venous thrombosis of the arm (ORcrude: 7.7, 95% CI: 4.6-13.0). Other evident risk factors were prothrombotic mutations, surgery, immobilization of the arm (plaster cast), oral contraceptive use and family history, with odds ratios varying from 2.0 up to 13.1. The risk in the presence of injury and during puerperium was twofold or more increased, although not significantly. In contrast HRT, unusual exercise, travel and obesity did not increase the risk. Hormone users had an increased risk in the presence of prothrombotic mutations or surgery. Obese persons (BMI > 30 kg m(-2)) undergoing surgery had a 23-fold increased risk of arm thrombosis compared with non-obese persons not undergoing surgery. CONCLUSION: A CVC is a very strong risk factor for arm thrombosis. Most risk factors for thrombosis in the leg are also risk factors for arm thrombosis.

Adolescent↗
PubMed1992

Superior sagittal sinus thrombosis and pulmonary embolism: a syndrome rediscovered.

Pulmonary emboli as a fatal complication of superior sagittal sinus thrombosis was once well recognized in the literature but appears to have been forgotten. The sagittal sinus appeared to be the source of pulmonary emboli in previously reported cases. Even in patients with no evidence of systemic thrombosis, but who have sagittal sinus thrombosis, the possibility of dislodging pulmonary emboli should be strongly considered. We report a case of nontraumatic sagittal sinus thrombosis complicated by multiple pulmonary emboli and a fatal saddle embolism, likely originating from the thrombosed sinus. Our review of the literature between 1942 and 1990 yielded 203 cases of intracranial venous thrombosis. The overall mortality rate was 49.3%. In 23 cases (11.3%), the venous sinus thrombosis was associated with pulmonary emboli and in these the overall mortality rate was 95.6%. In the 203 cases in our review, those patients who received anticoagulation therapy also had a statistically significant better outcome. Therefore, the presence of pulmonary emboli in association with sagittal sinus thrombosis mandates a sober assessment of the need of anticoagulation therapy in the absence of obvious contraindication.

Adult↗
PubMed1999

Antiphospholipid-thrombosis syndromes.

Antiphospholipid antibodies are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Based upon our experience, approximately 25% of patients with unexplained venous thrombosis, approximately 60% of patients with cerebrovascular thrombosis, approximately 37% of patients with transient ischemic attacks, approximately 18% with premature coronary artery thrombosis and approximately 60% of patients with recurrent fetal loss (recurrent miscarriage syndrome) harbor antiphospholipid antibodies. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. Since the aPTT is unreliable in patients with lupus anticoagulant and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests, ELISA for IgG, IgA and IgM anticardiolipin antibodies and the dilute Russel's viper venom time (followed by cephalin correction for confirmation) for lupus anticoagulant should be immediately ordered when suspecting the antiphospholipid syndrome in individuals with otherwise unexplained thrombotic or thromboembolic events or recurrent fetal loss. However, if one strongly suspects antiphospholipid thrombosis syndrome clinically and assays for lupus anticoagulants and anticardiolipin antibodies are negative, specific assays for all three idiotypes of phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine, phosphatidylinositol and phosphatidylglycerol are available and should be considered. These may clearly be indicated for difficult diagnostic cases of fetal wastage syndrome, and cerebrovascular events, but their significance in other types of thrombosis, particularly venous, remains unclear at present. Since about 65% of patients with antiphospholipid antibodies will fail warfarin therapy (rethrombose), it is important to define this common defect and institute appropriate antithrombotic therapy for appropriate time periods.

Antiphospholipid Syndrome↗
PubMedDate not supplied

Venous thrombosis: the history of knowledge.

Venous thrombosis is a frequent disease. It is surprising, therefore, that no case truly compatible with a diagnosis of venous thrombosis was apparently reported in the antiquity. There is no case that could be reasonably attributed to a venous thrombus in the writings of Hippocrates, Galenus, Celius Aurelianus, Ibn an-Nafiz, Avicenna and others. Venous thrombosis is not among the many diseases mentioned in the Bible. The term "leucophlegmasia", first used by Hippocrates and then by Celius Aurelianus, refers to cases of bilateral leg edema, most likely due to conditions such as heart failure, liver cirrhosis and renal insufficiency. Nothing compatible with a diagnosis of venous thrombosis can be found in pieces of art from ancient Egypt, Greece, Rome, Persia and South America. While in these sources there are sometimes representations of varicose veins and ulcers, unilateral leg edema or other pictures compatible with venous thrombosis are not featured. The first well documented case of venous thrombosis is depicted in a beautifully illustrated manuscript written in the 13th century and currently preserved in Paris at the Bibliothèque Nationale (MS Fr 2829, Folio 87). The manuscript describes the case of a young man from Normandy named Raoul who at the age of twenty developed unilateral edema in the right ankle that subsequently extended up to the thigh, with no obvious symptoms in the contralateral leg. Raoul was advised to visit the tomb of Saint Louis who was buried in the church of Saint Denis, where the patient spent several days confessing his sins and praying the saint. Afterwards he chose to collect the dust accumulating below the stone that covered the tomb and to apply it on the fistulae and ulcers of his foot. The openings stopped running and were filled with flesh. He was first obliged to use crutches but subsequently he could walk with a cane, to be eventually able to dispose of all devices, even though his foot throbbed a little. Raoul was cured as described above in the year 1271 and was still alive and well in 1282. Not only this is the first case of venous thrombosis, the young age of the patients leads us to suspect that Raoul had a thrombophilic condition.

History, 15th Century↗
PubMedDate not supplied

Unusual forms of venous thrombosis and thrombophilia.

Venous thromboembolism (VTE) results from multiple interactions between inherited and environmental risk factors. The lower limbs are the most common site of VTE, but more rarely other venous sites can be involved. The role of risk factors for VTE can be different in the various thrombotic manifestations, and there are specific risk factors for specific sites. Coagulation abnormalities causing inherited thrombophilia are frequently found in patients with cerebral vein thrombosis, but are more rare in those with "isolated" pulmonary embolism, upper limb or retinal vein thrombosis. Transient situations, such as surgery, trauma, prolonged immobilization, the use of oral contraceptives or hormone replacement therapy, and pregnancy or puerperium, are often recognized in patients with lower limb deep vein thrombosis, "isolated" pulmonary embolism, abdominal and cerebral vein thrombosis, but not in patients with upper limb deep vein thrombosis. Major risk factors for deep vein thrombosis of the upper limbs are strong efforts with the arms, whereas for abdominal vein thrombosis are myeloproliferative disorders and liver cirrhosis. In conclusion, there is increasing evidence that inherited and environmental risk factors may interact differently in determining VTE in different sites.

Humans↗
PubMed2004

Serum lipid levels and the risk of venous thrombosis.

OBJECTIVE: Lipids, through effects on the coagulation and fibrinolytic systems, may contribute to the development of venous thrombosis. This association has been investigated in a few studies, with conflicting results. METHODS AND RESULTS: We conducted a population-based, case-control study at a health maintenance organization in Washington State, to assess the association of serum lipid levels with the risk of venous thrombosis. Cases were 477 postmenopausal women with a first venous thrombosis during January 1995 through December 2001. Control subjects (1986) were a random sample of postmenopausal women. Medical records, computerized pharmacy databases, and a cancer registry served to collect data on lipid levels and risk factors for thrombosis. Total cholesterol levels were not associated with venous thrombosis. Only high HDL cholesterol levels were associated with a decreased risk of venous thrombosis after adjustment for hospitalization, malignancy, height and weight, postmenopausal hormone therapy, and vascular disease (for high-density lipoprotein [HDL] cholesterol levels >1.79 mmol/L versus those <1.79 mmol/L; odds ratio [OR], 0.71; 95% confidence interval [CI], 0.52 to 0.97). In contrast, elevated triglyceride levels were associated with an increased risk (OR, 2.13; 95% CI, 1.34 to 3.37) for women with triglyceride levels >1.05 mmol/L compared with women with lower levels. CONCLUSIONS: Elevated triglyceride levels were associated with a doubling of risk of venous thrombosis in postmenopausal women, whereas elevated HDL cholesterol levels were associated with a decreased risk.

Adult↗
PubMed2004

In vivo induction of endothelial apoptosis leads to vessel thrombosis and endothelial denudation: a clue to the understanding of the mechanisms of thrombotic plaque erosion.

BACKGROUND: The mechanisms of thrombosis on plaque erosion are poorly understood. We examined the potential role of endothelial apoptosis in endothelial erosion and vessel thrombosis. METHODS AND RESULTS: Segments of New Zealand White rabbit femoral arteries were temporarily isolated in vivo. One artery was incubated with staurosporin for 30 minutes, whereas the contralateral artery was incubated with saline and served as control. Three days later, thrombosis was evaluated angiographically and histologically. TUNEL score in the endothelial layer was significantly increased in staurosporin-treated arteries compared with controls (2.43+/-0.30 versus 0.93+/-0.44, respectively; P=0.001). Large areas of endothelial denudation were detectable in staurosporin-treated vessels, whereas endothelium integrity was almost preserved in the saline group. Vessel thrombosis occurred in 58% of staurosporin-treated arteries (7 of 12) but in only 8% of saline-treated segments (P<0.01). Immunoreactivities for tissue factor, platelets, and fibrin were detectable within the thrombus. Addition of ZVAD-fmk (0.1 mmol/L) significantly reduced the occurrence of thrombosis (1 of 7 arteries or 14%, P=0.04). These results were confirmed in balloon-injured atheromatous arteries. CONCLUSIONS: In vivo induction of endothelial apoptosis leads to both vessel thrombosis and endothelial denudation. Endothelial apoptosis may be a critical step in the transition from a stable endothelialized plaque to plaque erosion and thrombosis.

Amino Acid Chloromethyl Ketones↗
PubMed1998

Arm edema, subclavian thrombosis, and pacemakers--a case report.

This reports an arm edema that was initially treated as cellulitis and later diagnosed to be subclavian thrombosis due to pacemaker wire irritation. We present an 87-year-old Caucasian man with 5 weeks duration of left arm swelling and pain that was treated with two courses of antibiotics. An axillary venous Doppler study was interpreted as normal with no evidence of venous thrombosis. However, a venogram showed evidence of thrombosis involving the left innominate, subclavian, and axillary veins with multiple collateral veins diverting the blood to the contralateral side and into the superior vena cava. Intravenous anticoagulation was initiated and subsequently the patient was maintained on warfarin (Coumadin). The thrombosis subsequently improved and the original pacemaker was maintained. Arm edema are commonly mistaken for cellulitis, causing a delay in a more definite diagnosis of subclavian thrombosis. In a setting of a patient with pacemaker, subclavian thrombosis should be considered even with a normal screening venous ultrasound test. The incidence, manifestation, venous Doppler, and venogram findings are reviewed and discussed. Upper arm edema and superior vena cava syndrome are the most common presentation of this subclavian thrombosis associated with pacemakers. Venous ultrasound tests may be normal and a venogram is usually required to establish a diagnosis.

Aged↗
PubMedDate not supplied

Subclavian venous thrombosis due to indwelling catheters: a prospective study on 52 patients.

Clinical occurrence of subclavian venous thrombosis due to indwelling catheters is rare, but there is some evidence that subclinical thrombosis frequently occurs. It is purpose of this study to report the results of a prospective investigation in patients with subclavian vein catheters. Fifty-two patients admitted to the Istituto Nazionale Tumori of Milan and candidate to infraclavicular percutaneous catheterization of the subclavian vein were evaluated. There were 26 polyvinyl chloride and 26 rubber silicone catheters, which were correctly positioned in the superior vena cava-atrium. Average duration of the intravenous stay was 12.8 days. Asymptomatic thrombosis was venographically demonstrated in 46.1% of the polyvinyl chloride catheters and in 11.5% of the silicone ones (p = 0.005). The average age of catheters with or without thrombosis was 10.8 and 13.8 days, respectively. Addition of heparin to the infusate (1 U/ml) did not reduce the thrombosis rate in polyvinyl chloride or in silicone catheters, but risk of thrombosis was significantly higher (p = 0.03) in polyvinyl chloride catheters without heparin in comparison to the silicone ones. Osmolarity of the infusional fluid, manipulation during the cannulation, colonization of the catheter tip, and duration of the intravenous stay of the catheter apparently did not influence the rate of thrombosis. Since the natural history of the thrombotic subclavian veins is not known, some caution must be paid to repeat the percutaneous cannulation of the same vein and the change the catheter over a guidewire.

Adult↗
PubMed1995

Thrombosis and the pharmacology of antithrombotic agents.

OBJECTIVE: To provide an overview of the current state of knowledge regarding the physiology of hemostasis, the pathophysiology of thrombosis, and the pharmacology of antithrombotic agents. DATA SOURCES: A MEDLINE search was conducted to identify pertinent literature published since 1984. Recently published textbooks devoted to the subjects of hematology, hemostasis, and thrombosis also were reviewed, particularly their bibliographies. The bibliographies of selected review articles also were reviewed. STUDY SELECTION: As the amount of literature was vast, only the most significant and noteworthy published studies were reviewed. Review articles and book chapters authored by researchers of international reputation also were reviewed. DATA EXTRACTION: Identified studies from the primary literature and selected reviews were analyzed carefully. Information regarding hemostasis, thrombosis, and antithrombotic drugs was extracted. Particular attention was given to data regarding drugs currently available or soon to be available on the US market. DATA SYNTHESIS: Knowledge regarding the regulation of blood coagulation has expanded substantially in recent years. Hemostasis involves the dynamic interplay of numerous intravascular constituents, including the vessel wall, circulating procoagulants and anticoagulants, platelets, and fibrinolytic proteins. Thrombosis is the abnormal formation of a clot within the vascular system. When sufficiently large, thrombi can prevent the flow of blood and nutrients to vital tissues. Thrombosis is associated with many common diseases and is among the leading causes of death in developed countries. Many drugs are now available to prevent the formation and propagation of thrombi. These agents work by different pharmacologic mechanisms and are useful in different clinical situations. CONCLUSIONS: Thrombosis research has increased our understanding of the pharmacology of antithrombotic drugs and promoted the discovery of new agents targeted more specifically toward the critical steps in pathologic clot formation. New agents have the potential for greater efficacy and fewer adverse effects. An increased understanding of hemostasis, thrombosis, and the pharmacology of antithrombotic drugs should enable the clinician to use these agents appropriately.

Animals↗
PubMed2004

Erythropoietin-induced thrombosis as a result of increased inflammation and thrombin activatable fibrinolytic inhibitor.

Chronic inflammation is a major cause of morbidity and mortality in end-stage renal disease. The associated anemia in these patients due to renal cortical atrophy and erythropoietin deficiency is treated with recombinant erythropoietin. Recent reports suggest a growing incidence of symptomatic venous thrombosis in cancer patients treated with recombinant erythropoietin. Several investigators have reported on different mechanisms of thrombosis in these patients. We hypothesize that thrombosis in patients with end-stage renal disease due to increased expression of C-reactive protein (CRP) as a result of chronic inflammation promotes the release of thrombin activatable fibrinolytic inhibitor causing fibrinolytic deficit and eventually thrombosis. Furthermore, because endothelial nitric oxide is responsible for the maintenance of the normal vascular function, the decreased levels of nitric oxide in chronic inflammation cause endothelial damage and result in thrombosis. To test this hypothesis, blood samples were collected from 106 patients (49 male and 57 female, aged 59.8+/-15.7 years) with end-stage renal disease undergoing hemodialysis and treated with recombinant erythropoietin at a mean dose of 201.8 U/kg/week. Blood samples were drawn in 5-mL tubes containing 3.2% sodium citrate just before the hemodialysis procedure. These blood samples were immediately centrifuged to obtain platelet-poor plasma, which was aliquoted and frozen at -70 degrees C until further analysis. Erytropoietin antibodies were measured using an anti-EPO enzyme-linked immunosorbent assay (ELISA) method developed in our laboratory. Nitric oxide was measured using a NO analyzer (Sievers 280I, Ionics, Boulder, CO). Plasma CRP levels were measured with a highly sensitive ELISA method IMUNOCLONE CRP ELISA (American Diagnostica, Greenwich, CT). TAFI antigen levels in plasma were analyzed with an IMUCLONE TAFI ELISA kit (American Diagnostica, Greenwich, CT). TAFI functional activity was assayed with an ACTICHROME TAFI activity kit. The measured levels of nitric oxide, CRP, TAFI antigen, and TAFI functional were 37.36+/-36.8 (normal value, 37.49+/-18.96; range, 19.3-102 microM), 12.27+/-10.6 (normal value, < 1 microg/mL), 146.9+/-28.4% NHP (normal, 100% NHP), and 102.55+/-37% NHP (normal range, 22.3-165.7; mean, 89.5% NHP), respectively. The erythropoietin antibody was detected in 9.4% of the patient group. While 20% of the erythropoietin antibody-positive and 27.1% of the erythropoietin antibody-negative patients experienced chest pain, thrombotic events developed in 9.4% of the erythropoietin antibody-negative patients. These data provide the rationale for a novel mechanism of thrombosis through increased activity of CRP, nitric oxide, and TAFI, leading to fibrinolytic deficit and thrombosis in patients treated with erythropoietin.

Adult↗
PubMed2002

Successful treatment of aortic endograft thrombosis with rheolytic thrombectomy.

PURPOSE: To report the benefits of rheolytic thrombectomy for treating aortic endograft thrombosis. METHODS: Of 40 patients who received the Ancure bifurcated endograft to treat abdominal aortic aneurysm (AAA) during a 9-month period, 6 (15%) patients (6 men; mean age 62.6 years, range 53-77) developed thrombosis of the endograft at an average of 9 weeks (range 1-20 months). Five patients were taking aspirin, and 3 were on warfarin therapy for atrial fibrillation. Immediately after angiography, rheolytic thrombectomy was used to remove the thrombus, followed by adjunctive procedures to treat the underlying pathology. RESULTS: Causes were kinking or extrinsic compression of the graft limb in 5 cases and thrombosis of the surgical closure site in a common femoral artery. Mechanical thrombectomy was successful in restoring circulation in all cases; thrombolysis was used in 1. All 6 patients had additional stents placed in the graft limbs, re-establishing patency. There was no mortality or recurrent thrombosis in a follow-up that has extended to 26 months, but 1 patient required additional stenting for subsequent focal kinking of a graft limb above the previously implanted stent. CONCLUSIONS: Rheolytic thrombectomy can safely and effectively treat endograft thrombosis after endovascular AAA repair. Additional thrombolytic agents, angioplasty, and stenting may be needed to correct the underlying causes of the thrombosis. Prophylactic stenting of iliac limbs at the time of implantation in patients with complex anatomy may prevent thrombosis of unsupported bifurcated endografts.

Aged↗