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[Thrombosis of the basilar artery--a rare differential sudden deafness diagnosis and vestibular failure].

BACKGROUND: Occlusion of basilar artery is a rare and life-threatening event. A quick and safe diagnosis and initiation of adequate therapy are decisive. For the ENT-specialist it is important to know that this thrombosis, which runs a lethal course in many cases, can develop with a disturbance of hearing and/or vestibular function as initial symptoms. PATIENTS: Reported are four cases of thrombosis of the basilar or vertebral artery. Two out of four patients contacted the ENT emergency unit because of symptoms of acute vestibular neuritis, one patient was previously diagnosed with sudden deafness by a local ENT-specialist, one patient was treated for hypertension induced epistaxis in one of our wards. Only one patient initially presented additional neurological symptoms, causing suspicion for a brainstem lesion as well. However these symptoms were only noticed on close examination. By immediate anticoagulation therapy (with Heparin) progress of thrombosis could be avoided. The patient showed a complete recovery and was free of any symptoms two years after thrombosis. Two of the other two patients developed a delayed onset of neurological symptoms next to the initial symptoms of vestibular and cochlear affection (within 24 hours), therefore diagnosis of thrombosis was late and despite of immediate anticoagulation therapy (with Heparin) both patients died. The one patient treated for hypertension induced epistaxis developed only discrete symptoms of basilar artery thrombosis, nevertheless he was diagnosed and treated immediately. He made a complete recovery and was dismissed two weeks later. CONCLUSIONS: It is therefore necessary to carefully control and sometimes correct diagnosis in cases of sudden deafness and acute vestibular neuritis. Especially additional neurological symptoms indicate the necessity of a MRI-angiogram or CT-(angiography)scan to exclude thrombosis of the basilar artery.

Adult↗

[Guidelines for the diagnostics of deep pelvic/lower limb vein thrombosis].

As a result of availability and failing invasiveness the technique of compression sonography led to a change in the indication of thrombosis examination - from the proof of thrombosis shown by phlebography to exclusion of thrombosis by ultrasound. Compression sonography showed the same sensitivity and specificity as phlebography for proximal limb thrombosis and reaches high safety due to actual treatment studies in the diagnosis of deep vein thrombosis. For the distal limb the compression sonography has provided > 90 % specificity, with an examinator dependent sensitivity of 50 to 95 %, and hence examination of the distal limb must be recommended. These guidelines for the diagnosis of deep vein thrombosis are recommendations by the Section of Vascular Ultrasound of DEGUM for examination technique and documentation. It also contains an algorithm of diagnosis for thrombosis as a result of the actual treatment studies.

Diagnosis, Differential↗

[Informed consent on heparin-induced thrombocytopenia during thrombosis prophylaxis. A pilot study including 460 patients].

BACKGROUND: The practicability and acceptance of written information about heparin thrombosis prophylaxis and the associated risk of heparin-induced thrombocytopenia (HIT) was evaluated in a pilot study. PATIENTS AND METHODS: All patients consecutively admitted to the department of trauma- and reconstructive surgery at the Ernst-Moritz-Arndt-University, Greifswald, Germany, with an indication for heparin thrombosis prophylaxis were give written information about thrombosis prophylaxis and the undesired drug effect HIT. After this, acceptance was evaluated using a standardized questionnaire. Primary endpoint was refusal of heparin for thrombosis prophylaxis, secondary endpoint acceptance and comprehensibility of the information. RESULTS: None of the 460 patients included in the study subsequently refused thrombosis prophylaxis with heparin. The majority welcomed the information and thought it should be given to all patients that are about to be treated with heparin. Only 0.9 % of patients judged comprehensibility of the information to be insufficient. Anticipation of imminent heparin therapy (good/very good in 90 %) and appreciation of the quality of care was not judged to be unacceptable by any patient. CONCLUSIONS: The present study demonstrates that giving information about heparin-induced thrombocytopenia during explanation of the risks and benefits of heparin thrombosis prophylaxis is feasible. This information--given in writing in our pilot study--was judged by patients to be comprehensible and necessary and did not lead to refusal of treatment. Lower incidence of HIT with use of low molecular weight heparins should be considered in the choice of drug for thrombosis prophylaxis.

Adult↗

Hyperhomocysteinemia and venous thrombosis.

In recent years hyperhomocysteinemia has been established as a new risk factor for neural tube defects, arterial cardiovascular disease, and venous thrombosis. Concerning vascular problems, it first became clear that hyperhomocysteinemia might be (though not proven) a risk factor for arterial disease as observed in case-control studies, as well as in prospective analysis. More recently, the subject of hyperhomocysteinemia and venous thrombosis has received much attention. In this article, we discuss the issue of hyperhomocysteinemia, in general, the known causes of hyperhomocysteinemia and the association with venous thrombosis. Special attention is given to the value of the methionine loading test to diagnose hyperhomocysteinemia. An association of venous thrombosis and hyperhomocysteinemia has now been documented in several case control studies, but only in one prospective analysis. Thus far, there is limited evidence for a causal relationship for mild hyperhomocysteinemia in venous thrombosis. Briefly, the possible mechanisms of how hyperhomocysteinemia can lead to venous thrombosis are discussed. The article ends with therapeutic options to treat hyperhomocysteinemia (hyperhomocysteinemia can easily be treated with vitamins) and the description of a study that is presently being undertaken in an international multicenter design. This placebo-controlled study might resolve the question of whether lowering of homocysteine levels is of any clinical relevance in preventing recurrent venous thrombosis.

Case-Control Studies↗

The management of thrombosis in the antiphospholipid-antibody syndrome.

BACKGROUND: The antiphospholipid-antibody syndrome is a thrombophilic disorder in which venous or arterial thrombosis, or both, may occur in patients with antiphospholipid antibodies. The optimal treatment of these patients is unclear. We assessed the efficacy of warfarin, low-dose aspirin, or both in the secondary prevention of thrombosis in patients with the syndrome. METHODS: One hundred forty-seven patients (124 [84 percent] of whom were female) with the antiphospholipid-antibody syndrome and a history of thrombosis were studied retrospectively. The syndrome was primary in 62 patients and was associated with systemic lupus erythematosus in 66 patients and lupus-like disease in 19. Each patient's history was reviewed. RESULTS: One hundred one patients (69 percent) had a total of 186 recurrences of thrombosis. The median time between the initial thrombosis and the first recurrence was 12 months (range, 0.5 to 144 months). Treatment with high-intensity warfarin (producing an international normalized ratio of > or = 3) with or without low-dose aspirin (75 mg per day) was significantly more effective (P < 0.001 by the log-rank test) than treatment with low-intensity warfarin (producing an international normalized ratio of < 3) with or without low-dose aspirin or treatment with aspirin alone in preventing further thrombotic events (recurrence rates per patient-year, 0.013, 0.23, and 0.18, respectively). The rate of recurrence of thrombosis was highest (1.30 per patient-year) during the first six months after the cessation of warfarin therapy. Complications involving bleeding occurred in 29 patients during warfarin therapy and were severe in 7 (0.071 and 0.017 occurrence per patient-year, respectively). CONCLUSIONS: The risk of recurrent thrombosis in patients with the antiphospholipid-antibody syndrome is high. Long-term anticoagulation therapy in which the international normalized ratio is maintained at or above 3 is advisable in these patients.

Adolescent↗

Deep venous thrombosis and superficial venous reflux.

OBJECTIVE: Although superficial venous reflux is an important determinant of post-thrombotic skin changes, the origin of this reflux is unknown. The purpose of this study was to evaluate the frequency and etiologic mechanisms of superficial venous reflux after acute deep venous thrombosis (DVT). METHODS: Patients with a documented acute lower extremity DVT were asked to return for serial venous duplex ultrasound examinations at 1 day, 1 week, 1 month, every 3 months for the first year, and every year thereafter. Reflux in the greater saphenous vein (GSV) and lesser saphenous vein (LSV) was assessed by standing distal pneumatic cuff deflation. RESULTS: Sixty-six patients with a DVT in 69 lower extremities were followed up for a mean of 48 (SD +/- 32) months. Initial thrombosis of the GSV was noted in 15 limbs (21.7%). At 8 years, the cumulative incidence of GSV reflux was 77.1% (SE +/- 0.11) in DVT limbs with GSV involvement, 28.9% (+/- 0.09%) in DVT limbs without GSV thrombosis, and 14.8% (+/- 0.05) in uninvolved contralateral limbs (P <.0001). For LSV reflux, the cumulative incidence in DVT limbs was 23.1% (+/- 0.06%) in comparison with 10% (+/- 0.06%) in uninvolved limbs (P =.06). In comparison with uninvolved contralateral limbs, the relative risk of GSV reflux for DVT limbs with and without GSV thrombosis was 8.7 (P <.001) and 1.4 (P =.5), respectively. The relative risk of LSV reflux in thrombosed extremities compared with uninvolved extremities was 3.2 (P =.07). Despite these observations, the fraction of observed GSV reflux that could be attributable to superficial thrombosis was only 49%. CONCLUSIONS: Superficial venous thrombosis frequently accompanies DVT and is associated with development of superficial reflux in most limbs. However, a substantial proportion of observed reflux is not directly associated with thrombosis and develops at a rate equivalent to that in uninvolved limbs.

Adolescent↗

Combined liver vein and spleen pulp pressure measurements in patients with portal or splenic vein thrombosis.

BACKGROUND: Patients with thrombosis of the portal or splenic vein may develop portal hypertension with bleeding from oesophageal or gastric varices. The relevant portal pressure cannot be measured by liver vein catheterization or transhepatic puncture of the portal vein because the obstruction is peripheral to the accessible part of the portal system. METHODS: Liver vein catheterization was combined with percutaneous splenic pressure measurement in 10 patients with portal or splenic vein thrombosis and no cirrhosis, and 10 cirrhotic patients without thrombosis. The splenic pressure was measured by percutaneous puncture below the curvature of the ribs with an angle of the needle to skin of 30 degrees in order to minimize the risk of cutting the spleen if the patient took a deep breath. RESULTS: None of the patients in whom the described procedure was followed had complications. Pressure measurements in the spleen pulp and splenic vein were concordant. The pressure gradient across the portal venous system (splenic-to-wedged hepatic vein pressure) was -1.3 to 8.5 mmHg (median, 2.8 mmHg) in cirrhosis patients and 0-44 mmHg (median, 18 mmHg) in thrombosis patients, the variation reflecting various degrees of obstruction to flow in the portal venous system. Peripheral portal pressure (splenic-to-free liver vein pressure gradient) was 1.1-28 mmHg (median, 17 mmHg) in cirrhotic patients and 11-52 mmHg (median, 23 mmHg) in thrombosis patients. CONCLUSIONS: Liver vein catheterization combined with percutaneous splenic pressure measurement is feasible in quantifying pressure gradient across a thrombosis of the portal/splenic vein and in quantifying portal pressure peripheral to this kind of thrombosis.

Adult↗

Central venous line thrombosis in children and young adults with thalassemia major.

High doses of intravenous deferoxamine via central venous line (CVL) has recently been shown to improve survival in patients with noncompliant thalassemia major (TM). The aim of this retrospective study was to evaluate the extent of CVL-related thrombosis and to determine the presence of prothrombotic factors in children and young patients with TM on such a regimen. Twenty-three patients (median age 13, range 5-25 years) with TM in whom a tunneled CVL was inserted for intensification of iron chelation were evaluated for signs and symptoms of thrombosis and for inherited and acquired risk factors of thrombosis. Mean duration of CVL placement was 37 +/- 31 months (range 6-98 months). Eight patients (35%) had CVL-related thrombosis diagnosed clinically or by echocardiography. Nine patients (39%) had prothrombotic factors, but the thrombosis subgroup did not differ from the other group in age, platelet counts, duration of CVL placement, or the presence of predisposing prothrombotic factors. Based on the high rate of CVL-related thrombosis, routine monitoring is suggested for CVL thrombosis in this population.

Adolescent↗

Detection of perivenous inflammation in a rat model of venous thrombosis using MRV.

Venous thrombosis is associated with a significant inflammatory response in the vein wall, which can be imaged noninvasively with gadolinium (Gd)-enhanced magnetic resonance venography (MRV). Interleukin-10 (IL-10), a naturally occurring anti-inflammatory cytokine, has been found to decrease the inflammatory response at the proper dosage and timing of administration. The present study determines if MRV with Gd is useful in a rat model of stasis-induced venous thrombosis to document the anti-inflammatory effects of rIL-10. Rats underwent laparotomy and ligation of the inferior vena cava (IVC). Animals were infused with rIL-10 at 2.5 microg (n = 6), rIL-10 at 10 microg (n = 6), or rIL-10 at 40 microg (n = 6). Six animals without IVC ligation or drug infusion served as controls. Two days after thrombosis induction, the rats underwent MRV with both time-of-flight imaging and pre/post-Gd T1-weighted imaging. Inflammation was analyzed by measuring the area of Gd enhancement at the point of IVC thrombosis. Enhancement area was also measured in the distal IVC where flow persisted. All animals with IVC ligation developed thrombosis, and all control rats were free of thrombus. In areas where flow remained, the area of enhancement was 1.8 +/- 0.4 mm2, while controls demonstrated 3.8 +/- 1.0 mm2 enhancement. Enhancement was significantly greater in all groups at the level of thrombus compared to the area of distal IVC flow and control IVCs (p < .001). Animals receiving rIL-10 at 40 microg revealed the most enhancement, 32.7 +/- 6.2 mm2, while the least enhancement was noted with 2.5 microg, 14.7 +/- 1.5 mm2 (p < .05). In conclusion, Gd-enhanced MRV was found useful in this rat model of stasis-induced venous thrombosis to document inflammation noninvasively and to evaluate the effects of anti-inflammatory interventions during stasis-induced IVC venous thrombosis.

Animals↗

Thrombosis in Behçet's disease: a retrospective survey from a single UK centre.

OBJECTIVE: To contribute to knowledge of vascular occlusion in Behçet's disease (BD), prevalence and relative risk for thrombosis were ascertained retrospectively in a cohort of Caucasian patients with the disease. PATIENTS: The study included 73 BD patients (36 males, 37 females, mean age 45+/-11 yr) attending the Immunology/Rheumatology Department of Northwick Park Hospital. A group of 146 patients without BD, attending the same department, served as a control group. RESULTS: Thrombosis was more frequent in BD patients than in controls (23/73, 32% vs 7/146, 5%, P<0.001). This was accounted for by a higher prevalence of venous thrombosis in BD patients (18/73, 25% vs 4/146, 3%, P<0.001). Gender-adjusted data revealed an 11-fold risk of developing any thrombosis and a 14-fold risk of developing venous thrombosis in BD. After adjusting for differences in age at first symptoms, male BD patients showed a 6-fold higher risk of vein thrombosis. Males reported more often thrombophlebitis (13/36, 36% vs 0/0, P<0.001), folliculitis (8/36, 22% vs 1/37, 3%, P<0.01) and retinal vasculitis (13/36, 36%, vs 4/37, 11%, P=0.01) than females, in whom arthralgia prevailed (23/37, 62%, vs 12/36, 33%, P=0.01). CONCLUSION: In our population, BD confers a 14-fold risk of developing venous thrombosis. The risk is sixfold higher in male BD patients, who fare worse than females with regard to thrombophlebitis, folliculitis and retinal vasculitis.

Behcet Syndrome↗

Warfarin is safe as secondary prophylaxis in patients with cancer and a previous episode of venous thrombosis.

The purpose of this study was to establish the safety and efficacy of sodium warfarin in the secondary prophylaxis of venous thrombosis in patients with cancer. This was an inception cohort study of patients enrolled in an anticoagulation clinic between July 1991 and October 1996. The rates of bleeding and recurrent thrombosis were evaluated in all the patients, and the results in patients with cancer (n = 104) were compared with those without cancer (n = 208). The rate of major hemorrhage was 0.4% and 0.3% per treatment month in the patients with cancer and those without cancer, respectively. The rates of recurrent thrombosis were 1.2% and 0.2% per treatment month in the patients with cancer compared with those without cancer, respectively. We conclude that warfarin is safe when used for the secondary prophylaxis of patients with cancer who have had a venous or arterial thrombosis, and the risk of major hemorrhage is not significantly different when compared with the risk in patients without cancer. The rate of recurrent thrombosis is approximately sixfold higher in patients with cancer being treated with warfarin for secondary prophylaxis of thrombosis compared with patients without cancer. Nonetheless, the rate of recurrent thrombosis is not overly excessive, and warfarin can be viewed as a relatively effective form of therapy for these patients.

Anticoagulants↗

Clinical and laboratory evaluation of Turkish children with thrombosis for homozygous factor V G1691A mutation.

Factor V (FV) G1691A mutation, in a heterozygous state, is one of the most common inherited risk factors for development of thrombosis. However, the clinical manifestations of homozygosity for the FV G1691A mutation in children is largely unknown because of the limited number of studies reported. The purpose of this study was to evaluate the clinical manifestations and laboratory findings of children with thrombosis who were homozygous for this mutation. Ten patients (four male/six female; mean age, 4.5 years; age range, 1-13 years) who were found to be homozygous for the FV G1691A mutation among 360 consecutive children with thrombosis (2.8%) were the subjects of this study. Six of the 10 patients had venous thrombosis, two had purpura fulminans, one had diffuse skin ecchymosis and one had arterial thrombosis. No history of thrombosis was present in their family members. Seven of the 10 children were under the age of 5 years. One or more additional risk factors (infection, protein S and protein C deficiencies, elevated factor VIII, etc.) were also present in nine of these patients. None of these patients had prothrombin G20210A mutation but one patient had risk-associated plasminogen activator inhibitor-1 gene 4G/4G genotype. These findings suggest that, in the presence of other underlying risk factors, homozygosity for FV G1691A mutation may lead to development of thrombosis at a very young age.

Adolescent↗

Analysis of some clinical and laboratory aspects of adolescent patients with thrombosis.

A total of 360 pediatric patients aged 1 month to 18 years were diagnosed as having thrombosis between January 1998 and April 2003. Of these patients, those aged 11-18 years (n=131) were regarded as adolescents and the rest as children. The proportion of adolescents in the whole group excluding the neonates was 36%. The peak age of diagnosis in adolescents was 11-14 years, comprising 58% of all thrombotic events in adolescents. In 73% of the adolescents, there was at least one risk factor. The four most common underlying disorders were infection, malignancy, connective tissue and cardiac disorders, in decreasing order of frequency. In children, on the other hand, infection was followed by congenital heart disease, malignancy and liver disease. Three common types of thrombosis in adolescents were deep venous thrombosis, cerebro-vascular events and portal venous thrombosis, while cerebro-vascular events were the most common in children. The frequency of factor V G1691A mutation in the adolescents (22.1%) was significantly higher than that found in a group of healthy controls (7.4%) and this mutation was associated with a 3.6-fold increase in the risk of developing thrombosis (95% confidence interval, 1.4-9.0). The carrier frequency of prothrombin G20210A mutation (3.1%) in adolescents did not differ significantly from that of the healthy population (2.3%) and no association was observed between this mutation and a risk of developing thrombosis in this group (odds ratio, 1.3; 95% confidence interval, 0.2-7.5). The rate of recurrent thrombosis was 6%.

Adolescent↗

Intervention based on monthly monitoring decreases hemodialysis access thrombosis.

We randomized 103 patients (68 arteriovenous [AV] fistulas, 35 polytetrafluoroethylene [PTFE] grafts; mean follow-up 197 days) to monthly measurement of access flow (QAT), monthly measurement of static venous pressure (VPS), or no monthly monitoring (control patients) to determine whether access thrombosis would decrease. Patients with access flow <750 cc/min or with static venous pressure > or =0.5 were referred for angiography and angioplasty of stenotic lesions > or =50%. Six of sixty-two (9.7%) of monthly monitored patients (MM) developed access thrombosis vs. 9 of 41 (22%) of control patients (p<0.05). Fewer MM patients developed thrombosis in AV fistulas (2.4% [2 of 42] vs. 15.4% [4 of 26] control patients; p<0.05). Monthly monitored patients had fewer thrombotic episodes than control patients (19 vs. 125 per 100 patient-years; p<0.01). Thrombosis rates were lowest in patients receiving monthly access flow measurement (5.9 [QAT] vs. 30.3 per 100 patient-years [VPS]; p<0.05). In conclusion, intervention based on monthly access flow measurement or static venous pressure decreased hemodialysis access thrombosis. Measurement of access flow tended to result in lower thrombosis rates than after static venous pressure. We believe that monthly access flow measurement will ensure the lowest incidence of thrombosis and decrease the cost of access maintenance.

Arteriovenous Anastomosis↗

Intrasplenic venous thrombosis: CT findings.

OBJECTIVE: To describe the CT findings of intrasplenic venous thrombosis in three cases. MATERIALS AND METHODS: Three adult patients had abdominal CT indicative of short-segment thrombosis of an intrasplenic blood vessel. Two patients underwent splenectomy; thrombosis of a segmental splenic vein was confirmed histologically in both cases. RESULTS: Segmental splenic vein thrombosis appeared on CT as a short, 1-2 cm, linear lucency surrounded by normal splenic parenchyma. The probable etiology of intrasplenic venous thrombosis was main splenic vein occlusion related to pancreatitis in two cases and splenic compression and inflammation by perisplenic abscess in the third case. CONCLUSION: Thrombosis of segmental intrasplenic veins is detectable with CT and can be a secondary CT finding of main splenic vein thrombosis.

Humans↗

Calf-thigh sequential pneumatic compression compared with plantar venous pneumatic compression to prevent deep-vein thrombosis after non-lower extremity trauma.

OBJECTIVE: To compare the effectiveness of calf-thigh sequential pneumatic compression devices with the effectiveness of plantar venous intermittent pneumatic compression devices in prevention of venous thrombosis after major trauma. SUBJECTS AND METHODS: We evaluated 181 consecutive patients after major trauma without lower extremity injuries that precluded the use of pneumatic compression devices. We randomly assigned 149 patients to either calf-thigh sequential pneumatic compression or plantar venous pneumatic compression. After blinding the observers to the method of prophylaxis against deep-vein thrombosis, we performed bilateral compression ultrasonography on or before day 8 after randomization. RESULTS: Among 149 randomized patients, 62 who received calf-thigh sequential pneumatic compression and 62 who received plantar venous intermittent pneumatic compression devices completed the trial. Thirteen patients randomized to plantar venous intermittent pneumatic compression (21.0%) and 4 patients randomized to calf-thigh sequential pneumatic compression (6.5%) had deep-vein thrombosis (p = 0.009). Seven of 13 patients with deep-vein thrombosis after prophylaxis with plantar venous intermittent pneumatic compression had bilateral deep-vein thromboses, whereas all 4 patients with deep-vein thrombosis after prophylaxis with calf-thigh sequential pneumatic compression had unilateral deep-vein thrombosis. CONCLUSION: Calf-thigh sequential pneumatic compression prevents deep-vein thrombosis more effectively than plantar venous intermittent pneumatic compression after major trauma without lower extremity injuries.

Adult↗

Asymptomatic patients at high risk for deep venous thrombosis who receive inadequate prophylaxis should be screened.

BACKGROUND: Patients after stroke and major orthopedic surgery have increased factors for developing deep vein thrombosis. We sought to determine the implications of screening high-risk patients to detect proximal deep vein thrombosis. METHODS: We used decision analysis to determine the implications of screening vs not screening asymptomatic high risk patients with duplex ultrasonography to detect proximal deep venous thrombosis. The outcomes were bleeding, pulmonary embolism, death, and number of patients with true-positive, false-positive, and false-negative tests. RESULTS: Screening with ultrasonography, all asymptomatic patients who receive appropriate prophylaxis, prevalence 5%, would result in the treatment of 3.1% patients with proximal deep vein thrombosis (true positives); 2.9% without proximal deep vein thrombosis (false positives) and in the lack of diagnosis in 1.9% patients (false negatives). At a prevalence of 20%, no prophylaxis, screening would result in the treatment of 12.4% patients with proximal deep vein thrombosis (true positives), 2.4% without proximal deep vein thrombosis (false positives), and in the lack of diagnosis in 7.6% of patients (false negatives). CONCLUSIONS: Screening high-risk patients who receive prophylaxis is not warranted. Patients who receive no prophylaxis should be screened with ultrasonography.

Anticoagulants↗

Outcome after splenic vein thrombosis in the pancreas allograft.

The outcome and management of isolated splenic vein thrombosis in the pancreas transplant is unknown. We retrospectively reviewed the records of 76 simultaneous pancreas-kidney transplantations (SPK) and 56 solitary pancreas transplantations (SPT) performed at the University of Maryland from January 1995 to December 1996. A total of 24 patients were identified (9 SPK and 15 SPT recipients). All were systemically anticoagulated for a period of 6-8 weeks after diagnosis. In the SPK thrombosis group, anticoagulation resulted in 1-year graft survival that was equivalent to that of SPK controls (86.1% vs. 95.3%). In contrast, in SPT, thrombosis and subsequent anticoagulation were associated with decreased graft survival compared with SPT controls (26.8% vs. 78.3%; P<0.01). Although the outcome of splenic vein thrombosis in the absence of anticoagulation is unknown, these data suggest that (1) in SPK, anticoagulation for splenic vein thrombosis maintains graft survival, and (2) in SPT, anticoagulation does not alter the ultimate progression of splenic vein thrombosis to complete graft thrombosis.

Adult↗