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PubMed1982

Primary mesenteric venous thrombosis.

To elucidate further the characteristics, optimal management and ultimate outcome of patients with primary mesenteric venous thrombosis, the records of nine such patients were analyzed. There were seven male and two female patients, with a mean age of 47 years. Abdominal pain, vomiting, fever and hematochezia were the characteristics presenting complaints. Tenderness, distention and diminished intestinal sounds were the prominent abdominal physical findings and were often associated with tachycardia and hypotension. No one of the laboratory findings were specifically diagnostic for mesenteric venous thrombosis, but leukocytosis and hemoconcentration were commonly found. Roentgenographic findings were consistent with intestinal obstruction in six patients. Thrombosis of the mesenteric veins could not be attributed to any specific cause in these nine patients, thereby warranting the classification of primary. At operation, all nine patients were found to have a segment of infarcted small intestine--132 +/- 105 centimeters--with obvious thrombosis of the mesenteric veins but with patent mesenteric arteries. Five patients had bloody ascites. Two deaths occurred in the immediate postoperative period, both being due to sudden and unexpected cardiopulmonary arrest. Neither of these two patients received anticoagulant therapy. Two patients had undergone segmental resection at other hospitals and were referred to our institution because of a recurrence of acute abdominal signs and symptoms. Neither of these patients received anticoagulant therapy. At reoperation, both had recurrent segmental mesenteric venous thrombosis. Familiarity with this condition is essential in making the correct diagnosis, so that resection may be undertaken promptly. Heparin should immediately be administered intravenously after establishing the diagnosis of mesenteric venous thrombosis to prevent recurrent thrombosis and other possible thrombotic complications. If these steps are taken expeditiously, the prognosis of mesenteric venous thrombosis is often favorable.

Adult↗
PubMedDate not supplied

[Echocardiographic diagnosis of atrial thrombosis].

Seventy patients with rheumatic mitral disease were studied by M-Mode and 2D echocardiography in order to detect left atrial thrombosis before surgery. Thrombosis were suspected by the observation of abnormal echoes in the left atrium. During surgery 17 (24%) patients had atrial thrombosis. It had been suspected by echocardiography in 12 (sensitivity 70%). In 53 patients thrombosis were not found during surgery; in 46 the echo had been also negative (specificity 86%). There was a false positive detection of thrombosis by echo in 7 patients (14%) and false negativity in 5 (30%). Patients with atrial thrombosis had atrial fibrilation in 91% of cases; and the most frequent valvular disease was mitral stenosis. There was not a direct relationship among existence of left atrial thrombosis and the anteroposterior diameter of the left atrium as measured by echo. We conclude that echocardiography has good specificity to rule out atrial thrombosis and moderate sensitivity to detect it in rheumatic mitral disease.

Adult↗
PubMed1995

Neonatal thrombosis: report of a prospective Canadian and international registry.

OBJECTIVE: We sought to obtain representative data on the risk factors, diagnosis, current management, and short-term outcome of neonatal thrombosis. RESEARCH DESIGN: A case registry was established at McMaster University. Standardized questionnaires were mailed to collaborators at participating centers every 4 to 6 months. SETTING: Eighty-five level III and modified level II neonatal units in North America, Europe, and Australia were invited to join the registry. PATIENTS: Eligible infants were born between January 1990 and June 1993. Large-vessel thrombosis was diagnosed during the first month of life or up to 44 weeks post-conception after premature birth. The clinical impression of thrombotic vessel obstruction was confirmed using at least one imaging technique. RESULTS: Physicians in 64 centers expressed their willingness to participate. A total of 97 cases (excluding stroke) were registered from 29 centers. Spontaneous renal venous thrombosis (n = 21) was diagnosed at a median age of 2 days. The other venous (n = 39), arterial (n = 33), and mixed (n = 4) thromboses presented later; 89% of them were associated with an intravascular catheter and 29% with systemic infection. Doppler ultrasonography was the definitive diagnostic test in 68% of cases; contrast angiography was performed infrequently (14%). A third of all patients (but 62% of infants with renal venous thrombosis) received supportive therapy only. Thrombolytic agents were prescribed for 28% of catheter-associated venous thromboses and 30% of all arterial thromboses. The remainder of the patients were given heparin. Most patients (82%) survived to hospital discharge. Mortality rates were highest among infants with aortic thrombosis or central venous line-associated thrombosis affecting the right atrium or the superior vena cava (33%). CONCLUSIONS: Neonatal thrombosis is diagnosed fairly rarely. With the exception of spontaneous renal venous thrombosis, almost all cases are associated with indwelling catheters. Doppler ultrasound techniques are the most popular means of confirming the diagnosis in virtually all centers. Treatment varies greatly among different centers, probably because of the lack of scientific evidence about the optimum management of affected infants.

Canada↗
PubMed1995

[Thrombosis in patients with SLE and antiphospholipid syndrome].

Clinical and serological features in SLE patients with arterial or venous thrombosis were studied. The subjects consisted of 140 patients with SLE who met the revised criteria for the classification of SLE by the American Rheumatism Association. Forty patients (29%) had arterial or venous thrombosis. Arterial thrombosis such as stroke was found in 30 patients, and venous thrombosis such as deep vein thrombosis was seen in 24 patients. Average age at the disease onset was 34.5 +/- 12.5 years old. Renal disorder was found as a clinical feature, and IgG anticardiolipin antibodies (aCL), IgG phospholipid-dependent anti-beta 2-glycoprotein I (beta 2-GPI) antibodies and IgG anti-Annexin V antibodies were identified as serological features in SLE patients with thrombosis. These patients were diagnosed as having antiphospholipid syndrome. It was necessary to perform primary prevention therapy as well as secondary prevention therapy. Multiple thrombotic events in the past history and sustained positive reactions of IgG aCL were suggested as predictors of recurrent thrombosis. These data indicated the clinical and serological characteristics in SLE patients with arterial or venous thrombosis.

Adult↗
PubMed1995

Increased rate of thrombin generation in hepatitis C virus cirrhotic patients. Relationship to venous thrombosis.

BACKGROUND: Venous thrombosis may complicate the clinical course of liver cirrhosis (LC), but the pathogenesis is still uncertain. We have previously demonstrated that antiphospholipid (aPL) antibodies were a risk factor for thrombosis. In the same study it was also evident that there was a higher prevalence of hepatitis C virus (HCV) infection in patients with thrombosis, and an association between anti-HCV positivity and aPL. METHODS: In a case-control study, 18 consecutive patients with LC, who had suffered from splanchnic venous thrombosis (n = 12), or thrombophlebitis (n = 6), were matched for age, sex, and degree of liver failure with 36 LC patients without thrombosis. RESULTS: In comparison to patients without thrombosis, patients with thrombosis had higher prevalence of HCV infection (p = 0.0027), positivity for aPL antibodies (p = 0.0003), and higher values of fragment F1+2, a marker of thrombin generation (p = 0.0083). While F1+2 values were similar in aPL (+) and aPL (-) patients, HCV patients had significantly higher values of F1+2 than patients with hepatitis B virus (HBV) infection and/or alcoholism (2.6 +/- 0.94 vs 1.5 +/- 0.66, p = 0.0001). CONCLUSIONS: These data suggest that in LC, HCV infection may contribute to clotting system activation, thus predisposing patients to venous thrombosis.

Adult↗
PubMed1997

[Primary subclavian vein thrombosis after intensive physical exertion].

Subclavian vein thrombosis accounts for approximately 1-2% of recorded deep venous thromboses. It may be primary or secondary, and insertion of a central venous catheter is the most common cause of secondary subclavian vein thrombosis. Traumas, anatomic abnormalities and carcinoma are important additional risk factors for secondary thrombosis. Primary thrombosis of the subclavian veins is known as Paget-Schroetter syndrome. New criteria for its diagnosis include a history of increased upper extremity use prior to onset of symptoms, the presence of a venographically demonstrated thrombus and absence of any definable causes. We describe a 42-year-old woman with a history of intensive physical exertion admitted with swelling, pain and difficulty moving her arm. The diagnosis of primary subclavian vein thrombosis was established from the history of physical effort, results of Doppler ultrasound, and exclusion of other causes of subclavian vein thrombosis. This case suggests that primary subclavian vein thrombosis should be considered in young patients with subclavian vein thrombosis after exclusion of secondary disease.

Adult↗
PubMed1998

Antagonism of vWF inhibits both injury induced arterial and venous thrombosis in the hamster.

von Willebrand factor (vWF) is instrumental in arterial but has also been implicated in venous thrombogenesis. To address its role in venous thrombosis, experimental thrombosis was induced in the carotid artery and the femoral vein of hamsters, following which thrombus prevention by two different antagonists of vWF was studied. The first antagonist was the anti-human vWF monoclonal antibody AJvW-2, which inhibits the botrocetin and ristocetin induced aggregation of human blood platelets. AJvW-2 reacts with an epitope present in the A1 domain of vWF in very different species (human, pig, rabbit, dog, Guinea pig and rat). This epitope was found to be conformational and overlapping with vWF binding sites for aurin tricarboxylic acid (ATA), but not for botrocetin and heparin. AJvW-2 has affinities for vWF in the absence (Kd = 0.5 +/- 0.03 nmol/l in solution) and in the presence of shear stress (Kd = 3.3 +/- 0.6 nmol/l during perfusion at 1,300 s over subendothelial matrix associated vWF) sufficiently elevated to neutralize vWF. During perfusion of subendothelial matrix with anticoagulated human blood, the surface covered by adhering platelets was reduced by AJvW-2, with IC50s equal to 6.6 +/- 0.34 microg/ml at 1,300 s(-1) and to 1 +/- 0.01 microg/ml at 2,700 s(-1). As a second antagonist, molecular size gel filtered ATA was selected. Fractionated ATA inhibited platelet adhesion to matrix with IC50s equal to 0.27 +/- 0.09 mmol/l at 1,300 s(-1) and 0.16 +/- 0.008 mmol/l at 2,700 s(-1). When administered to hamsters, AJvW-2 prevented thrombosis in the injured carotid artery dose-dependently (ED50 = 0.15 +/- 0.01 mg/kg). Thrombosis in the similarly injured femoral vein was however also inhibited (ED50 = 0.37 +/- 0.06 mg/kg). Likewise, fractionated ATA completely inhibited carotid artery thrombosis (ED50 = 0.42 +/- 0.13 mg/kg), but also interfered with femoral vein thrombosis (apparent ED50 between 2 and 3 mg/kg). We conclude that antagonizing the vWF A1 domain by AJvW-2 and to a lesser extent also by fractionated ATA, inhibits thrombosis not only in the arterial but also in the venous circulation. Since venous thrombi were prevented at only 3-5-fold higher doses of antagonist, vWF participates in injury induced venous thrombosis.

Animals↗
PubMed1999

Puerperal ovarian vein thrombosis with extension into the inferior vena cava.

The incidence of puerperal ovarian vein thrombosis is estimated to range between 1 in 600 and 1 in 2000 deliveries. The cardinal signs of puerperal ovarian vein thrombosis include fever, leukocytosis, and right lower quadrant abdominal pain, most often in a recently delivered female patient. These patients are classically described as failing to improve with intravenous antibiotic therapy alone; resolution of symptoms and presumptive diagnosis is made on defervescence with the addition of intravenous heparin therapy. Objective diagnostic modalities include venography, ultrasound, laparoscopy, and MRI, although CT remains the gold standard for the identification of this under-diagnosed entity. We present a case report of a 20-year-old female treated at our facility for puerperal ovarian vein thrombosis. She was transferred to our vascular surgery service after developing the classic signs of puerperal ovarian vein thrombosis and undergoing CT demonstrating ovarian vein thrombosis with extension of free-floating thrombus into her inferior vena cava (IVC). This degree of thrombosis was particularly concerning when one considers the 3 to 33 per cent rate of pulmonary embolism reported in patients with puerperal ovarian vein thrombosis. Treatment modalities for such extensive degrees of thrombosis are described in the literature and range from hysterectomy and thrombectomy to ligation of the IVC. In our case, we prophylactically placed a suprarenal IVC Greenfield filter to protect against pulmonary embolism and proceeded with the standard regimen of anticoagulation and antibiotics. This treatment approach has been reported only twice previously in the literature, to our knowledge.

Adult↗
PubMedDate not supplied

Hepatic vein thrombosis (Budd-Chiari syndrome).

Hepatic vein thrombosis (Budd-Chiari Syndrome) is a rare disorder resulting from obstruction to the outflow of blood from the liver. The characteristic pathologic findings are intense congestion most pronounced around the terminal hepatic venules, cell necrosis, and a scant inflammatory reaction. Major clinical manifestations include hepatomegaly, right upper quadrant abdominal pain, and ascites. Disorders associated with hepatic vein thrombosis include those associated with a thrombotic tendency, such as polycythemia vera and paroxysmal nocturnal hemoglobinuria. Use of oral contraceptive agents probably increases tendency to develop hepatic vein thrombosis. Biochemical tests of the liver are of little value. The hepatic scan may be useful in suggesting the diagnosis with a marked decrease in uptake of isotope over affected areas of the liver. The diagnosis is confirmed by inferior vena caval and attempted hepatic venous catheterization. An associated thrombosis of the inferior vena cava is frequently found. Therapy in hepatic vein thrombosis is directed towards correction, in so far as possible, the underlying disorder, prevention of further extention of thrombosis, and management of ascites. Side-to-side portacaval or mesocaval shunt operation may convert the portal vein into an effective hepatic outflow vessel and reduce intrahepatic pressure and decrease injury. Mesoatrial shunts have proven useful in a few patients with hepatic vein thrombosis and either an inferior vena caval thrombosis or a marked pressure gradient from the abdomen to the thorax from ascites and an hypertrophied caudate lobe of the liver. For patients with extensive hepatocellular disease and portal hypertension, hepatic transplantation would seem to offer the best chance for survival.

Budd-Chiari Syndrome↗
PubMed1990

Hepatic vein thrombosis in Behçet's disease.

We describe four patients with hepatic vein thrombosis caused by Behçet's disease and review the 17 previously published cases. In addition, we compared these 21 cases of hepatic vein thrombosis to our 24 cases of hepatic vein thrombosis caused by primary myeloproliferative disorders. In patients with Behçet's disease, a male predominance (male/female ratio, 19:1) contrasted with the female predominance found in patients with hepatic vein thrombosis complicating primary myeloproliferative disorders (sex ratio = 1:3). The mean age at clinical onset was younger in patients with Behçet's disease than in those with primary myeloproliferative disorders (29 vs. 35 yr). Obstruction of the inferior vena cava was found in 90% of patients with hepatic vein thrombosis caused by Behçet's disease. Inferior vena caval thrombosis appears to be the main pathophysiological mechanism of hepatic vein thrombosis in patients with Behçet's disease. Unlike patients with primary myeloproliferative disorders who often had a progressive course, one third of patients with Behçet's disease had acute liver failure and died within 2 wk of clinical onset. These findings suggest that, in patients with Behçet's disease, hepatic vein thrombosis is a sudden event usually related to the extension of a caval thrombus to the ostium of the hepatic veins.

Adolescent↗
PubMed2005

Stent underexpansion and residual reference segment stenosis are related to stent thrombosis after sirolimus-eluting stent implantation: an intravascular ultrasound study.

OBJECTIVES: We sought to determine the predictors of stent thrombosis after sirolimus-eluting stent (SES) implantation. BACKGROUND: A number of cases of stent thrombosis have been reported after commercial release of the SES in the "real world," such that the U.S. Food and Drug Administration issued a warning. METHODS: Fifteen patients who developed stent thrombosis after successful SES implantation were analyzed and compared with 45 matched control patients who had no evidence of stent thrombosis. RESULTS: Minimum stent cross-sectional area (MSA) (4.3 +/- 1.6 mm(2) vs. 6.2 +/- 1.9 mm(2), p < 0.001) and stent expansion (0.65 +/- 0.18 vs. 0.85 +/- 0.14, p < 0.001) were significantly smaller in the stent thrombosis group than in the matched control patients. There was no significant difference in the rate of SES malapposition between the groups. However, the presence of a significant residual reference segment stenosis was more common in the stent thrombosis group compared with the matched control group (67% vs. 9%, p < 0.001). Independent predictors of stent thrombosis were stent underexpansion (p = 0.03) and a significant residual reference segment stenosis (p = 0.02). CONCLUSIONS: Stent underexpansion and residual reference segment stenosis are associated with stent thrombosis after successful SES implantation.

Aged↗
PubMed1995

Catheter-related thrombosis in critically ill children: comparison of catheters with and without heparin bonding.

OBJECTIVE: To compare the incidence of and factors associated with vascular thrombosis after placement of heparin-bonded and standard femoral venous catheters. DESIGN: Prospective, masked, clinical study. SETTING: Multidisciplinary, tertiary, pediatric intensive care unit. PATIENTS: Consecutive cases (n = 50) of critically ill children admitted to a pediatric intensive care unit in whom either a heparin-bonded (n = 25) or a standard (n = 25) femoral venous catheter was placed. MEASUREMENTS AND MAIN RESULTS: Patients were examined by ultrasonography within 3 days of catheter insertion, weekly while the catheter was in place, and after catheter removal for evidence of vascular thrombosis. Data were collected prospectively regarding clinical evidence of catheter thrombosis, infusate composition, and positive blood culture results. Of 50 patients, 13 (26%) had thrombotic complications, 11 (44%) of the 25 patients in the standard-catheter group, in comparison with 2 (8%) of the 25 patients in the heparin-bonded catheter group (p = 0.004). In addition, there was a significantly higher incidence of positive blood culture results among patients in the standard-catheter group (24% vs 0%; p = 0.009). Positive catheter blood culture results were obtained in 38% of patients with thrombosis versus 3% without thrombosis (p = 0.001). Clinical evidence of thrombosis was found in 69% of patients with, versus 27% of patients without, ultrasound-proved thrombosis (p = 0.007). CONCLUSION: Heparin bonding of catheters is associated with significantly fewer thrombotic complications. A reduced incidence of positive catheter-related blood culture results may be associated with the absence of thrombosis.

Catheterization, Central Venous↗
PubMed1994

Increased risk of venous thrombosis in oral-contraceptive users who are carriers of factor V Leiden mutation.

We investigated whether the occurrence of venous thrombosis in young women who use oral contraceptives might be explained by the factor V Leiden mutation, which leads to resistance to activated protein C and enhances susceptibility to thrombosis. We compared 155 consecutive premenopausal women, aged 15 to 49, who had developed deep venous thrombosis in the absence of other underlying diseases, with 169 population controls. The risk of thrombosis among users of oral contraceptives was increased 4-fold (relative risk 3.8 [95% CI 2.4-6.0]). The risk of thrombosis among carriers of the mutation compared with non-carriers was increased 8-fold (7.9 [3.2-19.4]). Compared with women who did not use oral contraceptives and were not carriers of the mutation, the risk of thrombosis among those with both risk factors was increased more than 30-fold (34.7 [7.8-154]). Recalculation of population incidences from these relative risks shows that the absolute risk of venous thrombosis in young women who use oral contraceptives is much larger when they carry the factor V Leiden mutation. When a young woman develops thrombosis, her factor V Leiden status should be considered in counselling about her future method of contraception.

Adolescent↗
PubMed1990

Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis.

BACKGROUND: Isolated deficiencies of antithrombin III, protein C, protein S, and plasminogen have been implicated as a cause of deep-vein thrombosis. It is assumed that patients with recurrent, familial, or juvenile thrombosis are very likely to have such a deficiency. METHODS: We studied the prevalence of isolated deficiencies of these proteins in 277 consecutive outpatients with venographically proved acute deep-vein thrombosis, as compared with 138 age-matched and sex-matched controls without deep-vein thrombosis, and calculated the positive predictive value of a history of recurrent, familial, or juvenile venous thromboembolism for the presence of such a deficiency. RESULTS: The overall prevalence of deficiencies of any of these proteins in the patients with venous thrombosis was 8.3 percent (23 of 277 patients) (95 percent confidence interval, 5.4 to 12.4), as compared with 2.2 percent in the controls (3 of 138 subjects) (95 percent confidence interval, 0.5 to 6.1; P less than 0.05 for the comparison between groups). The positive predictive values for the presence of an isolated protein deficiency in patients with recurrent, familial, or juvenile deep-vein thrombosis, defined as the proportion of patients with the clinical finding who had a deficiency of one or more of the proteins, were 9, 16, and 12 percent, respectively. CONCLUSIONS: The cause of acute venous thrombosis in most outpatients (91.7 percent) cannot be explained by abnormalities of coagulation-inhibiting and fibrinolytic proteins. The information obtained from the medical history concerning recurrent or familial venous thrombosis or the onset of the disease at a young age is not useful for the identification of patients with protein deficiencies.

Acute Disease↗
PubMed1994

Resistance to activated protein C as a basis for venous thrombosis.

BACKGROUND: In three families with various forms of venous thrombosis, we observed an apparently inherited poor response to the anticoagulant activated protein C (APC). The condition was due to a deficiency in a previously unrecognized anticoagulant factor that functioned as a cofactor to activated protein C. METHODS: We conducted the present study to determine the prevalence of resistance to APC in patients with venous thrombosis. We compared 104 consecutive patients with venous thrombosis confirmed by objective tests with 130 controls. In addition, 211 members of 34 families of persons with resistance to APC were studied. The anticoagulant response to APC was measured with a modified version of the activated partial-thromboplastin time test; the results were expressed as APC ratios. RESULTS: Forty-five percent of patients had a family history of thrombosis. A significant (P < 0.001) difference in APC ratios was observed between the controls and the patients with thrombosis. For 33 percent of patients, the APC ratio was below the 5th percentile of the control values, although the results of the family studies suggested that the prevalence of APC resistance may be even higher (approximately 40 percent) in the patients with thrombosis. The inherited nature of the defect was confirmed in a majority of cases, and the family studies suggested the mode of inheritance to be autosomal dominant. The thrombosis-free survival of APC-resistant family members was significantly less than that of non-APC-resistant family members. CONCLUSIONS: There was a high prevalence of APC resistance among young persons with a history of venous thrombosis, and this resistance appeared to be inherited as an autosomal dominant trait.

Adolescent↗
PubMed1998

Relation of three genetic traits to venous thrombosis in an African-American population.

A mutation in the Factor V gene (Factor V Leiden), a variant in the 5,10-methylenetetrahydrofolate reductase gene (MTHFR), and an insertion/deletion polymorphism of the angiotensin I-converting enzyme gene (ACE) may be related to abnormal blood clotting. The authors examined the associations between these genetic traits and venous thrombosis among African Americans. This study comprised 93 patients with venous thrombosis and 185 control subjects attending clinics at an urban, public hospital in Atlanta, Georgia, in 1995-1996. Subjects' DNA was extracted from blood and assayed for these genetic traits. Odds ratios were obtained from logistic regression and used as a measure of association between each genetic trait and venous thrombosis. Factor V Leiden was unrelated to venous thrombosis, but the mutation ws too rare among our African-American subjects to evaluate adequately its relation to venous thrombosis. The homozygous and heterozygous genotypes for the V allele of the MTHFR gene were unrelated to venous thrombosis (odds ratio = 0.9, 95% confidence interval 0.5-1.8). Subjects with the deletion/deletion ACE polymorphism experienced a moderate increase in venous thrombosis risk compared with persons with the other genotypes (odds ratio = 1.5, 95% confidence interval 0.9-2.6). However, women with this ACE genotype experienced no increased risk (odds ratio = 0.9, 95% confidence interval 0.5-1.9), whereas men with this genotype had nearly three times the risk (odds ratio = 2.8, 95% confidence interval 1.2-6.2; p value for interaction = 0.06). These data indicate that the prevalence of Factor V Leiden and the V allele of the MTHFR gene is low among African Americans. The D allele of the ACE gene is equally prevalent among African Americans and whites and may be related to venous thrombosis among African-American men.

Adolescent↗
PubMed1989

Allograft renal vascular thrombosis--lack of increase with cyclosporine immunosuppression.

Several recent reports have demonstrated an increased incidence of allograft renal vascular thrombosis in patients receiving cyclosporine alone or as part of multiple drug regimens when compared with patients receiving azathioprine (AZA) and prednisone (P). To determine whether CsA therapy is indeed a risk factor for renal artery or vein thrombosis, we examined the incidence of these complications in 224 adult renal allograft recipients who were prospectively randomized and stratified by risk to treatment with either CsA-P (n = 117) or AZA-P-antilymphocyte globulin (n = 107) between September 1980 and October 1983, and in 452 adult and 87 pediatric patients on triple (AZA-P-CsA) or quadruple (AZA-P-CsA-ALG) therapy protocols between July 1984 and November 1987. In the randomized trial, one of 107 AZA-P-ALG patients (0.9%) and two of 117 CsA-P patients (1.7%) developed renal vein thrombosis (P = 0.94), and there were no cases of arterial thrombosis. Though CsA levels were elevated in one of the two CsA-treated patients at the time of their events, and both these patients demonstrated other predisposing factors for thrombosis. In the triple/quadruple therapy era, there were no cases of renal vein thrombosis, and the only case of renal artery thrombosis occurred in a pediatric recipient who was not receiving CsA at the time. These data, when taken together with a critical review of the conflicting literature, strongly suggest that factors other than immunosuppression with CsA, including surgical technique, allograft rejection, use of multiple artery and/or pediatric donor kidneys, and postoperative hypotension, are important in the pathogenesis of allograft renal vascular thrombosis. It seems possible, however, that high initial dosing of CsA might trigger this complication in the early posttransplant period when other predisposing factors are present.

Antilymphocyte Serum↗
PubMed1996

Effect of preoperative donation of autologous blood on deep-vein thrombosis following total joint arthroplasty of the hip or knee.

The effect of preoperative donation of autologous blood on postoperative deep-vein thrombosis was retrospectively studied in men who had been managed consecutively with elective total joint replacement of the hip or knee because of osteoarthrosis. The patients had, on the average, two of nine considered risk factors for deep-vein thrombosis. Two hundred and thirty-seven patients were evaluated postoperatively with ascending venography, and they form the basis of this study. Fifty-four patients had venographic evidence of deep-vein thrombosis of the lower extremity, with most having asymptomatic clots distal to the knee. The prevalence of deep-vein thrombosis was nineteen (16 per cent) of 116 after total hip arthroplasty, compared with thirty-five (29 per cent) of 121 after total knee arthroplasty (chi square=4.6, p=0.03). Deep-vein thrombosis developed in twenty-eight (17 per cent) of the 161 patients who had donated blood preoperatively, compared with twenty-six (34 per cent) of the seventy-six patients who had not donated blood preoperatively (chi square=7.7, p=0.006). Through logistic regression analysis, the donation of autologous blood was shown to reduce significantly the development of postoperative deep-vein thrombosis for patients managed with total knee arthroplasty (p<0.01) but not for patients managed with total hip arthroplasty. Additional neural network analysis showed the donation of autologous blood to be the most important prognostic factor in predicting the absence of postoperative deep-vein thrombosis. In addition to diminishing the need for transfusion of homologous blood after total joint arthroplasty, preoperative donation of autologous blood appears to protect against postoperative deep-vein thrombosis after total knee arthroplasty.

Adult↗