Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed1990

Very low doses of warfarin can prevent thrombosis in central venous catheters. A randomized prospective trial.

OBJECTIVE: To determine whether very low doses of warfarin are useful in thrombosis prophylaxis in patients with central venous catheters. DESIGN: Patients at risk for thrombosis associated with chronic indwelling central venous catheters were prospectively and randomly assigned to receive or not to receive 1 mg of warfarin, beginning 3 days before catheter insertion and continuing for 90 days. Subclavian, innominate, and superior vena cava venograms were done at onset of thrombosis symptoms or after 90 days in the study. RESULTS: One hundred twenty-one patients entered the study, and 82 patients completed the study. Of 42 patients completing the study while receiving warfarin, 4 had venogram-proven thrombosis. All 4 had symptoms from thrombosis. Of 40 patients completing the study while not receiving warfarin, 15 had venogram-proven thrombosis, and 10 had symptoms from thrombosis (P less than 0.001). There were no measurable changes in the coagulation values assayed due to this warfarin dose, except in occasional patients who had become anorectic because of their disease or chemotherapy. CONCLUSIONS: Very low doses of warfarin can protect against thrombosis without inducing a hemorrhagic state. This approach may be applicable to other groups of patients.

Adult↗
PubMed1999

Risk of thrombosis in patients with antiphospholipid antibodies and factor V Leiden mutation.

OBJECTIVE: Antiphospholipid antibodies (aPL) are thrombophilic risk markers in patients with systemic lupus erythematosus (SLE) or primary antiphospholipid syndrome (APS). The risk factors for recurrent venous or arterial thrombosis and indications for longterm anticoagulation therapy are debated. We hypothesized that carrying a second thrombophilic defect, factor V Leiden mutation, would increase the risk for thrombosis in patients with aPL. METHODS: Seventy-five patients with primary APS and 83 with SLE and aPL with or without thrombosis followed at 2 university hospitals were studied. Factor V mutation rate was analyzed in patients and in 200 healthy blood donors by polymerase chain reaction analysis. RESULTS: The prevalence of factor V Leiden mutation in patients with SLE and aPL or primary APS was similar to controls. Patients with deep vein thrombosis or arterial thrombosis did not have a significantly increased rate of factor V mutation compared to controls or to patients with aPL without thrombosis. CONCLUSION: Factor V Leiden mutation is not significantly associated with vein thrombosis in patients with aPL. However, due to the sample size we cannot rule out synergy between both factor V Leiden and aPL. A trend toward increased risk for thrombosis was detected in patients with the mutation and this should be analyzed in a larger study.

Adult↗
PubMed1999

Increased levels of factor VIII and fibrinogen in patients with venous thrombosis are not caused by acute phase reactions.

Factor VIII activity (factor VIII:C) levels > or =150 IU/dl are associated with a 5- to 6-fold increased risk of venous thrombosis compared to levels <100 IU/dl, and fibrinogen levels > or =5.0 g/l increase the thrombosis risk 4-fold. These high levels are present in 25% resp. 3% of the patients with a first episode of venous thrombosis. These findings were based on measurements after the thrombotic event, so the factor VIII and fibrinogen levels in thrombosis patients may have been influenced by acute phase reactions or ongoing inflammatory responses. In the present study we measured plasma C-reactive protein (CRP) as a sensitive marker of an acute phase reaction in 474 thrombosis patients and 474 age- and sex-matched healthy controls, that were part of the Leiden Thrombophilia Study (LETS). Mean and median CRP levels were higher in thrombosis patients than in the controls, suggesting inflammation in some patients. CRP affected both factor VIII and fibrinogen levels, in patients and controls alike. After adjustment for the effect of CRP, high factor VIII:C levels still increased the thrombosis risk 6-fold and high fibrinogen levels 4-fold, which is for both very similar to the risk before correction for CRP levels. These results show that although systemic inflammation may be present in some of the patients, elevated levels of factor VIII:C and fibrinogen were in general not caused by acute phase reactions. This further supports a causal relationship between both high factor VIII:C and fibrinogen levels and venous thrombosis.

Acute-Phase Reaction↗
PubMed2000

[Diagnosis and therapy of leg and pelvic deep vein thrombosis in pregnancy].

OBJECTIVE: To establish differences in the management of acute thrombosis in the deep venous system associated with pregnancy in patients undergoing thrombectomy and in patients receiving heparin therapy. MATERIALS AND METHODS: From 1984 to 1995 the course of pregnancy was assessed retrospectively in 26 patients with acute deep vein thrombosis. Thirteen patients underwent thrombectomy with establishment of an arteriovenous fistula and 13 patients received conservative treatment with heparin therapy. In addition to the assessment of clinical symptoms, signs of thrombosis, diagnoses established with imaging techniques and of laboratory parameters, early complications and obstetric data obtained in surgically and conservatively treated patients were compared. RESULTS: The incidence of deep vein thrombosis in the 26 patients (median age 28 years) was 0.21%. In 53.8% of the cases the occurrence of thrombosis was observed in the second trimester (median: 27.5 weeks of gestation). The presence of risk factors was demonstrated in 58% of cases. The most frequently reported symptoms were swelling of the affected leg (88.5%) and pain (61.5%). A marked predilection for the left leg was recorded in 88% of cases. In contrast to phlebography, twice the number of sonographic studies were performed. The comparison of both therapeutic regimes showed a three-fold increase in the rate of early complications in patients after thrombectomy. The rate of recurrent thrombosis in these patients was 58.3% compared to a recurrence rate of 15.4% in patients undergoing heparin therapy. CONCLUSIONS: Recurrent thrombosis and pulmonary embolism represent the most frequent complications associated with thrombosis in the deep venous system during pregnancy. Although currently there is a lack of conclusive data on the development of postthrombotic syndrome, heparin therapy appears to be associated with fewer maternal risks. Interdisciplinary cooperation is urgently needed.

Adult↗
PubMed2000

Deep vein thrombosis after total knee replacement.

INTRODUCTION: The prevalence of deep vein thrombosis after total knee replacement has been quoted to be between 46% and 84% in the Western literature. The aims of this study were to determine its prevalence in the Singapore population and to assess the need for prophylaxis against deep vein thrombosis. MATERIALS AND METHODS: We examined data on 100 consecutive patients undergoing total knee replacement at the Adult Reconstructive Service, Department of Orthopaedic Surgery, Singapore General Hospital and assessed the possible risk factors: age, sex, weight, previous surgery, unilateral or bilateral surgery, postoperative rehabilitation, tourniquet and operating time. Functional and knee scores based on the Knee Society Clinical Rating System were also assessed. No prophylaxis was given to these patients. These patients underwent a duplex scan of both lower limbs on the seventh postoperative day. Treatment was instituted only if proximal deep vein thrombosis was detected. RESULTS: The overall incidence of deep vein thrombosis was 14% with 64.3% of it occurring distally. Deep vein thrombosis was more common in bilateral total knee replacement (22.2%) compared to unilateral total knee replacement (13.2%). Partial thrombosis was present in 71.4% and occurred predominantly in the ipsilateral leg. There was no evidence of propagation. Only 1 patient developed pulmonary embolism and was treated successfully but there was no evidence of deep vein thrombosis on duplex scan in this patient. CONCLUSION: There was no significant difference in the risk factors between patients who did and those who did not develop deep vein thrombosis.

Adult↗
PubMed2001

Deep vein thrombosis in patients admitted for exacerbation of chronic obstructive pulmonary disease.

INTRODUCTION: There is a lack of data on the prevalence of deep vein thrombosis and pulmonary embolism in patients admitted to hospital for exacerbation of chronic obstructive pulmonary disease. Studies have found that most pulmonary embolism originate from deep vein thrombosis in the lower limbs, thus the prevalence of deep vein thrombosis may give an accurate reflection of the prevalence of pulmonary embolism. The aim of our study was to determine the prevalence of deep vein thrombosis in these patients, using duplex ultrasound of the lower limbs as the screening tool. METHODS: Thirty-three male patients admitted to the general ward for exacerbation of chronic obstructive pulmonary disease were screened for presence of deep vein thrombosis of the lower limbs using duplex ultrasound scan. RESULT: No patient in this study was found to have deep vein thrombosis of the lower limbs. CONCLUSIONS: The prevalence of deep vein thrombosis in local patients admitted for exacerbation of chronic obstructive pulmonary disease is likely to be low. We do not recommend the use of duplex ultrasound to screen for deep vein thrombosis in this group of patients.

Aged↗
PubMed2001

Contribution of prothrombin 20210A allele and factor V Leiden mutation to thrombosis risk in thrombophilic families with other hemostatic deficiencies.

BACKGROUND AND OBJECTIVES: The aims of this study were to compare the lifetime probability of developing thrombosis in 722 relatives of 132 thrombophilic families of symptomatic probands with recognized thrombophilic defects and to determine the prevalence of the factor V Leiden (FVL) mutation and the 20210A allele of the prothrombin gene (PT20210A) in these families. DESIGN AND METHODS: The study included 722 members belonging to 132 unrelated families. The propositi were patients who had been referred to our Thrombosis Unit. The families were selected through a symptomatic proband. Once a patient with a deficiency or mutation was identified, family members were screened for the same defect. RESULTS: The prevalence of FVL and PT20210A in families with other thrombophilic defects was higher than expected. Compared with non-deficient individuals, the risk of venous thrombosis was increased in subjects with antithrombin (AT), protein S (PS) and protein C (PC) deficiencies, and in carriers of FVL and PT20210A mutations. The risk of thrombosis was significantly increased for individuals with combined genetic defects (PC-FVL, PS-FVL, PS-PT20210A and FVL-PT20210A). The ages at the time of 50% thrombosis-free survival were as follows: 34 years for AT deficiency, (19 years with FVL, 21 years with PT20210A), 62 years for PC deficiency (33 years with FVL, 44 years with PT20210A), 37 years for PS deficiency (24 years with FVL, 36 years with PT20210A), 50 years for the FVL mutation (52 years with PT20210A), and 65 years for the PT20210A mutation. As for clinical characteristics, no differences were observed except for the higher frequency of oral contraceptive-related thrombosis in women who were carriers of PT20210A or FVL. INTERPRETATION AND CONCLUSIONS: Based on these results, screening for FVL and PT20210A mutation is recommended in patients with other thrombophilic defects. To the best of our knowledge, this is the first family study, including the PT20210A mutation, that compares genetic risk factors for thrombosis and the lifelong probability of developing thrombosis.

Adolescent↗
PubMed2002

[Air travel and venous thrombosis].

BACKGROUND AND METHODS: The paper reviews air travel and venous thrombosis. The risk of venous thrombosis increases with distance flown. The mechanisms that cause thrombosis are unknown, but may be related to hypobaric hypoxia, i.e. reduced air pressure inside the aeroplane, stasis of the lower limbs, often referred to as economy class syndrome (ECS), and dehydration. RESULTS: Symptomless deep venous thrombosis may occur in 10% of healthy long-haul airline travellers over 50 years of age, and up to 4.5% of passengers under 50 at high risk of thrombosis. Wearing of elastic compression stockings during the flight is associated with reduced risk of deep venous thrombosis. INTERPRETATION: Passengers should be encouraged to use the muscle-vein pump regularly, ensure adequate hydration, and in some cases wear elastic compression stockings. A majority of passengers will not need any thromboprophylaxis. Aspirin may have a protective role, but its efficacy in preventing venous thrombosis is much smaller than that of low molecular weight heparins. A high prophylactic dose of a low molecular weight heparin should be considered in passengers at high risk of thrombosis.

Aerospace Medicine↗
PubMed1992

The incidence of portal vein thrombosis at liver transplantation.

The incidence of portal vein thrombosis was examined in 885 patients who received orthotopic liver transplantations for various end-stage liver diseases between 1989 and 1990. The thrombosis was classified into four grades. Grade 1 was thrombosis of intrahepatic portal vein branches, grade 2 was thrombosis of the right or left portal branch or at the bifurcation, grade 3 was partial obstruction of the portal vein trunk, and grade 4 was complete obstruction of the portal vein trunk. Among the 849 patients without previous portosystemic shunt, 14 patients (1.6%) had grade 1, 27 patients (3.2%) had grade 2, 27 patients (3.2%) had grade 3 and 49 patients (5.8%) had grade 4 portal vein thrombosis. The incidence of portal vein thrombosis was highest (34.8%) in the patients with hepatic malignancy in the cirrhotic liver, followed by those with Budd-Chiari syndrome (22.2%) and postnecrotic cirrhosis of various causes (15.7%). The patients with encephalopathy, ascites, variceal bleeding, previous splenectomy and small liver had significantly higher incidences of portal vein thrombosis than the others. The total incidence of portal vein thrombosis among the 36 patients with previous portosystemic shunt was 38.9%, which was significantly higher than that (13.8%) of those without shunt.

Adolescent↗
PubMedDate not supplied

Thrombolytic treatment of portal thrombosis.

BACKGROUND/AIMS: The authors present their experience with thrombolytic treatment of "acute" portal thrombosis. METHODOLOGY: Since 1980, portal thrombosis has been diagnosed in 305 patients treated in our Department. Portal thrombosis, mostly chronic, was associated with liver cirrhosis, Budd-Chiari syndrome, inflammatory and malignant liver tumors, as well as hypercoagulation conditions. In half of the patients the etiology of portal thrombosis remained obscure. Herewith, the authors present a retrospective review of 33 cases of rapidly developing portal thrombosis. Abdominal pain, ascites and jaundice were the most frequent initial symptoms. Time interval from the first symptoms appearance to hospitalization ranged from 8 to 60 days. The acute form of portal thrombosis was confirmed by Doppler sonography, spiral computed tomography and angiography. Sixteen female patients were regularly using oral contraceptives, in 8--portal thrombosis coexisted with the Budd-Chiari syndrome, in another 8--with polycythemia or myeloproliferative disorders and in 1 was observed during acute liver failure following paracetamol ingestion. RESULTS: Conservative treatment was unsuccessful in the first 5 cases: all of them died from esophageal variceal bleeding and liver failure. The next 28 patients received fibrinolytic treatment with streptokinase (3 cases) or recombinated tissue plasminogen activator. The results of therapy were evaluated on the basis of clinical picture and Doppler sonography monitoring. Rapid improvement of general condition, with Doppler sonography signs of the portal vein recanalization was noted in 10 patients, in all of whom the history of the disease did not exceed 14 days. In 13 patients with the longer history, partial portal vein occlusion persisted, but restored hepatopetal flow was sufficient to assure normal liver function. In the remaining 5 patients, with the history of the disease lasting longer than 30-40 days, the treatment failed and no clinical or Doppler sonography evidence of restoring of the portal flow were demonstrated. Four patients died: 2 from portal rethrombosis, 1 from liver failure and 1 from cerebral stroke (12, 16 months, 3 months and 4 years after therapy, respectively). Twenty-four patients are alive, the time of follow-up ranging from 9 months to 6 years. In 8 cases, five years after portal system recanalization the first symptoms of portal hypertension occurred. CONCLUSIONS: Thrombolytic treatment of acute portal thrombosis, if administered promptly, appears to be the only way to improve, or even restore, the portal system patency.

Acute Disease↗
PubMed2005

Inflammation in patients with lupus anticoagulant and implications for thrombosis.

OBJECTIVE: The underlying mechanism of the prothrombotic state associated with the lupus anticoagulant (LAC) has not been fully elucidated. Evidence suggests involvement of inflammation in arterial and venous thrombosis, and it may be hypothesized that subclinical inflammation aggravates the tendency to thrombosis in patients with LAC. METHODS: Levels of high sensitivity C-reactive protein (hs-CRP), fibrinogen, and factor VIII (VIII) were measured in 38 patients with LAC and a history of thrombosis, 27 with LAC and no history of thrombosis, and 33 healthy controls. RESULTS: Hs-CRP, fibrinogen, and factor VIII levels were significantly higher in patients with LAC with thrombosis (hs-CRP median = 0.3 mg/dl, interquartile range, IQR, 0.11-0.62, p < 0.001 vs controls; fibrinogen mean = 395 +/- 90 SD mg/dl, p < 0.001; factor VIII mean = 181 +/- 50%, p = 0.005) as well as in those without thrombosis (median = 0.21, IQR 0.10-0.12, p < 0.001; mean = 378 +/- 91, p = 0.003; mean = 179 +/- 39, p = 0.015) compared to controls (median = 0.07, IQR 0.03-0.12; mean = 308 +/- 48; mean = 137 +/- 39). After adjustment for age, body mass index, smoking status, and blood group (only for factor VIII) the differences between LAC groups and controls remained significant, except for the comparison of fibrinogen between patients without thrombosis and controls. The association between LAC and markers of inflammation was confirmed using linear regression analysis. Markers of systemic inflammation did not differentiate between LAC patients with and without thrombosis (p = 0.829 for hs-CRP, p = 0.649 for fibrinogen, p = 0.996 for factor VIII). CONCLUSION: Our results show that LAC is associated with an inflammatory state. However, there was no evidence for an association between inflammatory markers and thromboembolism in patients with LAC.

Adult↗
PubMed2006

Dural sinus thrombosis in melioidosis: the first case report.

Melioidosis which is infection with Burkholderia pseudomallei, is an important cause of sepsis in India, southeast Asia and northern Australia. Mortality is high and treatment is problematic. Neurological melioidosis is unusual but meningoencephalitis, encephalomyelitis and brain microabscess can occur Dural sinus thrombosis is not an uncommon cerebrovascular disorder with various etiologies. Hypercoagulable state, pregnancy, dehydration, certain blood dyscrasia and contraceptive pills are common causes however meningitis and local head & neck infections may lead to this condition. Dural sinus thrombosis complicating septicemic melioidosis has never been reported. The authors report a 42-year-old Thai man suffering from septicemic melioidosis with dural sinus thrombosis. He had high fever, headache, left hemiparesis, focal seizure and increased intracranial pressure. Diabetes and mild alcoholic cirrhosis were diagnosed in this admission. CT scan, MRI brain and MRV revealed superior saggital sinus thrombosis with complicating venous infarction over right posterior parietal lobe. Hemoculture demonstrated Burkholderia pseudomallei and CSF was acellular Investigations for causes of dural sinus thrombosis were all negative. This patient gradually improved after treatment with ceftazidime, antiepileptic drug and heparin without clinical recurrence. Neuromelioidosis is a rare syndrome that may present as brain abscess, encephalitis or meningoencephalitis. The authors report dural sinus thrombosis associated with septicemic melioidosis. The authors' hypothesis of venous thrombosis in the presented case is sepsis induced hypercoagulable state. Physicians should be aware of cerebral venous thrombosis in case of suspicious melioidosis with neurological involvement. Prompt treatment with intravenous heparin and antibiotic is potentially effective.

Adult↗
PubMed2006

[Correlation of thrombosis with increased platelet turnover in essential thrombocythemia].

This study was aimed to investigate the correlation of thrombosis with increased platelet turnover in essential thrombocythemia. According to presence or absence of thrombosis, 26 patients with ET were divided into two groups. Reticulated platelets (RP) were measured by flow cytometry and 26 healthy volunteers were selected as healthy controls. The ET patients with thrombosis were treated with hydroxyurea and interferon-alpha. The results demonstrated that the ET patients with thrombotic events had a significantly higher RP percentage (14.8% +/- 7.2%) than that in both asymptomatic ET patients (4.5% +/- 2.3%) and normal control (3.3% +/- 1.5%), (P < 0.05); the RP percentage in asymptomatic ET patients did not differ significantly from controls. ET patients with thrombosis also had a significantly higher absolute RP (ARP) count than those in ET patients without thrombosis [(176 +/- 37) x 10(9)/L vs (46 +/- 12) x 10(9)/L]. The ET patients with thrombosis were successfully treated with hydroxyurea plus INF-alpha, the RP percentage and ARP counts obviously reduced. In conclusion, when the ET patients had thrombotic events, those patients had a significantly higher RP percentage and ARP compared with patients without thrombosis and healthy controls. The ET patients with thrombosis were successfully treated with hydroxyurea plus INF-alpha.

Adult↗
PubMed2006

Arteriovenous fistula thrombosis in patients on regular hemodialysis: a report of 171 patients.

BACKGROUND: Fistula thrombosis in patients on maintenance hemodialysis is an important morbidity factor. Arterial or venous thrombotic events have been described as complications in patients on regular hemodialysis. This study was designed to evaluate the risk factors for arteriovenous fistula thrombosis. METHODS: One hundred and seventy-one patients with arteriovenous fistula on maintenance hemodialysis were studied prospectively during a period of 14 months for any episode of arteriovenous fistula thrombosis, after anticardiolipin antibodies were assayed by ELISA. Other risk factors for thrombosis such as the presence of diabetes or hypertension, the use of erythropoietin (rhEPO), fistula site, gender, age, ultrafiltration, hypotension during dialysis, and the number of dialysis visits in a week were assessed. RESULTS: Fifty-six percent of patients had IgG-anticardiolipin antibodies > or = 10GPL, which was significantly correlated with dialysis duration (23.18 +/- 24.56 months in patients with anticardiolipin antibodies < or = 10GPL vs. 37.73 +/- 36.35 months in patients with 20 < or = IgG-anticardiolipin antibodies < 40GPL). Within the 14 months of follow-up, 36 episodes of arteriovenous fistula thrombosis occurred in 31 patients (18.1%). Considering anticardiolipin antibodies and other risk factors in a Cox proportional hazard model, only fistula site (P = 0.021, RR = 2.48, Cl = 1.14 - 5.37) and erythropoietin (Eprex) use (P = 0.021, RR = 10.92, Cl = 1.43 - 83.02) seemed to have an influence on fistula patency. According to fistula site, the survival of brachiocephalic fistulas were significantly (P = 0.007) better than radiocephalic ones (1- and 3-year survival were 95% and 87% for upper, and 88% and 72% for lower ones, respectively). CONCLUSION: Although the incidence of the anticardiolipin antibody was high in our patients, in the presence of other risk factors for thrombosis, we found no correlation between IgG-anticardiolipin antibodies and arteriovenous fistula thrombosis. Instead, erythropoietin (Eprex) use and fistula site seem to have an important role in the correlation between IgG-anticardiolipin antibodies and arteriovenous fistula thrombosis.

Antibodies, Anticardiolipin↗
PubMed1991

Compression ultrasonography in hospitalized patients with suspected deep venous thrombosis.

Compression ultrasonography was compared with contrast venography in 215 hospitalized patients (218 limbs) with suspected deep venous thrombosis. All scans were performed using a 5-MHz linear-array scanner. The calf veins were not assessed owing to their small caliber. Distribution of deep venous thrombosis was proximal in 113 of 215 patients (number of limbs with deep venous thrombosis being the same as the number of patients) and limited to the calf veins (distal) in 29 patients. Deep venous thrombosis was detected by compression ultrasonography in 101 of 113 patients (sensitivity, 89%) and falsely diagnosed in two of 76 limbs (73 patients) with negative venographic results (specificity, 97%). The method was less sensitive below the knee, where deep venous thrombosis of the distal popliteal vein was not detected in five of 10 patients as compared with seven of 103 patients with thrombus extension above the knee. Pelvic vein deep venous thrombosis (n = 34) was detected by compression ultrasonography in 71% of the patients. The results of this study indicate that venography may be omitted in patients where compression ultrasonography demonstrates proximal deep venous thrombosis. In patients with negative compression ultrasonographic results, however, venographic verification is needed since venography has a considerably higher sensitivity than compression ultrasonography in detecting isolated iliac and calf vein deep venous thrombosis.

Aged↗
PubMed1990

Angiographic arterio-venous shunt and venous thrombosis in the prognosis of hepatoma.

Angiograms and clinical data for 249 patients with hepatoma were evaluated, with particular attention paid to the arteriovenous (A-V) shunt and venous thrombosis (including occlusion). There were 43 cases (17.3%) with A-V shunt and 140 cases (56.2%) with venous thrombosis. A statistically significant difference in survival was noted among the unresectable patients with and without these vascular changes. Furthermore, in the resectable patients, presence of venous thrombosis also showed a poor prognosis. A-V shunt did not influence the survival in the unresectable patients with venous thrombosis, and 93.0% of A-V shunt was associated with venous thrombosis. This seemed to imply that these two vascular changes might be the same entity. In the presence of either A-V shunt or venous thrombosis, the survival rate in the surgical group was still better than that of medical groups treated by either transarterial embolization (TAE) or conservative methods. Most of the A-V shunt (81.4%) and venous thrombosis (56.4%) occurred in the diffuse type of hepatoma, and the prognosis for unresectable patients was the worst in this type, with a mean survival time of 3 months. Since A-V shunt and venous thrombosis are factors in poor prognosis and occur frequently, careful preoperative evaluation of these vascular changes is mandatory. However, in patients with localized tumor, coexisting with such vascular involvement, surgical resection is still recommended.

Arteriovenous Fistula↗
PubMed1989

Reexploration for thrombosis in carotid endarterectomy.

We reviewed the records of patients undergoing carotid endarterectomy and manifesting either postoperative stroke or thrombosis by oculopneumoplethysmography (OPG-Gee) to analyze the etiology of stroke and to determine the indications for reexploration. Of 900 consecutive elective endarterectomies performed during an 8-year period, 41 patients experienced a perioperative stroke, carotid thrombosis, or both. These patients were subdivided into three groups: group 1, 22 patients with perioperative stroke and carotid thrombosis; group 2, six patients with carotid thrombosis but without symptoms; and group 3, 13 patients with postoperative stroke but no thrombosis. In group 1, 17 patients were reexplored (group 1a), and five were observed without reexploration (group 1b). In group 2, three of the patients were reexplored (group 2a), and the remaining three were observed (group 2b). None of the group 3 patients were reexplored. In group 1a, four (23%) patients awoke from anesthesia with neurological deficits, whereas in group 3, nine (69%) patients awoke with such deficits. Follow-up at 30 days revealed that 76% of group 1a patients demonstrated improvement in symptoms, whereas similar results were seen in only 20% of group 1b patients and 23% of group 3 patients. These trends were maintained throughout the follow-up period of 1-5 years. Those patients who were asymptomatic, group 2, with thrombosis were more likely to have been operated on for asymptomatic carotid stenosis. with thrombosis were more likely to have been operated on for asymptomatic carotid stenosis. Thrombosis was the most common cause of postoperative stroke (63%) in patients after carotid endarterectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Mesenteric venous thrombosis.

Sixteen patients with mesenteric venous thrombosis were reviewed retrospectively during a period from 1983 to 1987. Twelve patients had progressive abdominal pain, three had gastrointestinal bleeding, and one had general malaise. Seven of these 16 patients had previous deep-vein thrombosis. After negative routine gastrointestinal and hepatobiliary evaluation, 11 patients underwent an infusion computerized tomographic scan. Of these, 10 had superior mesenteric vein thrombosis; three of these 10 patients had portal vein thrombosis. Selective arteriography was done in two patients because of gastrointestinal bleeding, and a diagnosis of mesenteric vein thrombosis was made on the venous phase of the examination. The remaining four patients developed acute abdominal symptoms requiring surgical exploration, at which time mesenteric venous thrombosis was discovered. An identifiable coagulopathy was detected in nine patients (protein C deficiency in six, protein S deficiency in two, and factor IX deficiency treated with factor IX concentrate in one). No case of congenital antithrombin-III deficiency was identified. Six of these nine patients had a past history of deep venous thrombosis. Of five patients who underwent surgical exploration, all required bowel resection. In follow-up, two patients died of intestinal necrosis and a third died of associated pancreatic cancer. Thirteen patients were discharged from the hospital. Treatment of coagulopathy was by heparin in three patients and sodium warfarin (Coumadin) in four patients. Long-term anticoagulation was not instituted because of gastrointestinal bleeding in three and cirrhosis in three patients. Mesenteric venous thrombosis can occur without gangrenous bowel. Diagnosis should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes and a coagulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗