Splenic vein thrombosis and chronic pancreatitis: therapeutic approach

10% of chronic pancreatitis (CP) cases are complicated by splenic vein thrombosis (SVT) which is responsible for upper digestive haemorrhages. To improve our approach to treatment we reviewed 30 cases of SVT associated with CP treated in our centre from 1985 to 1995. 14 patients were treated conservatively. Six of them were refused for surgery due to extension of splenic vein thrombosis into the portal vein. Two patients without extrinsic compression of the vein were treated with anticoagulants. 16 patients were treated by surgery with low morbidity and without mortality. The standard treatment in fourteen cases was splenopancreatectomy. The average follow-up of seven years shows that these patients have preserved their body mass index (BMI). The results suggest that early surgical intervention is beneficial in preventing progression of SVT to the portomesenteric vein.     

Splenic vein thrombosis with pancytopenia and fever: antiphospholipid antibody syndrome

Antiphospholipid antibody syndrome (APS) is now recognized as one of the most important causes of hypercoagulability. The most common site for venous thrombosis in APS is deep venous thrombosis of the lower extremities. Other sites of venous thrombosis include retinal veins, renal veins, and hepatic veins. The authors report a case of splenic vein thrombosis disclosing antiphospholipid syndrome in which also the cytolytic effect of aPL may play a role of "cofactor" in the genesis of thrombosis through the release of thromboplastin from the lysis of red cells, granulocytes and platelets, making them vulnerable to clearance by splenic macrophages. Important considerations are stressed about differential diagnosis, etiopathogenetic factors, therapy and follow-up of the patient.     

Cockett syndrome. Initial results with percutaneous treatment in 6 patients

Intimal hypertrophy with venous spur formation caused by compression of the left common iliac vein by the right common iliac artery is advanced as the etiology of the higher incidence of deep venous thrombosis involving the left leg. In most cases of left iliofemoral thrombosis no underlying compression syndrome is detected or treated because the left common iliac vein has to be cleared from thrombi before compression can be identified. A series of 6 consecutive retrospectively analyzed patients with acute left iliofemoral thrombosis is presented. In these patients a left iliac vein compression syndrome was detected after percutaneous intraluminal thrombolysis with Actilyse (rt-PA). This compression was successfully relieved by insertion of a wall stent. Percutaneous treatment of Cockett's syndrome seems an attractive alternative for conservative and/or surgical management.     

The middle colic vein: an alternative source of portal inflow in orthotopic liver transplantation complicated by portal vein thrombosis

BACKGROUND: Portal vein thrombosis (PVT) was previously considered a contraindication to orthotopic liver transplantation (OLT) since adequate portal blood supply is mandatory for graft function and patient survival. Improvements in surgical technique, however, have meant that this problem now can be circumvented in most instances. Nevertheless portal vein thrombosis remains an obstacle in OLT and is associated with increased incidence of primary non-function and long-term liver failure. METHODS: A 55-yr-old patient underwent OLT for secondary biliary cirrhosis associated with hepatitis C infection and complicated by long standing PVT. Involvement of the portal, mesenteric, and splenic veins prevented standard portal venous reconstruction. Portal inflow was accomplished by a side-to-end anastomosis between the middle colic vein and the donor portal vein. RESULTS: Hepatic reperfusion and subsequent liver function were excellent. Portal blood flow, as measured by color-enhanced Doppler ultrasound, was normal following surgery until discharge. The post-operative course was complicated by abdominal wound dehiscence and recurrent cytomegalovirus (CMV) infection. The patient was discharged in good clinical condition, with excellent liver function and patent portal vein 89 d after OLT. CONCLUSIONS: The middle colic vein is a novel, not previously described, source of portal venous inflow for OLT complicated by extensive splanchnic venous inflow thrombosis.     

An evaluation of splenopancreatic disconnection as a modification of the distal splenorenal shunt, studied in nonalcoholic patients by sequential angiography

To evaluate the validity and complications of modifying the distal splenorenal shunt (DSRS) by performing splenopancreatic disconnection (SPD), hemodynamic changes in the portal system were assessed by visceral angiography in 93 patients with nonalcoholic portal hypertension during early postoperative follow-up after DSRS. There were 40 patients who underwent DSRS alone and 53 who underwent DSRS plus SPD. Early follow-up angiography showed that portal vein perfusion was well maintained, and that the diameter of the portal vein had decreased significantly by the same degree in both groups. Hepatofugal collaterals for the shunt had developed to a greater extent in the DSRS group, while they were almost completely absent in the DSRS with SPD group. Nevertheless, partial portal vein thrombosis was not detected in the DSRS group, although it was seen in seven (13.2%) of the patients who underwent DSRS plus SPD, in whom the left proximal splenic vein was not visible. The proximal splenic vein was seen in significantly less of the DSRS with SPD patients (47.2%) than the DSRS group patients (85%). In conclusion, SPD more effectively prevented the early postoperative development of collateral pathways for the shunt compared with standard DSRS; however, the possible stagnation of blood flow in the left proximal splenic vein may predispose to a risk of partial portal vein thrombosis developing during the early postoperative period after DSRS with SPD.     

Complications of superficial thrombophlebitis

Phlebitis and varicophlebitis are regarded as harmless diseases easily treated by compression and local measures such as incisions and applications. However, recent experience has revealed that they are often complicated by growth of the superficial thrombus into the deep veins, by noncontiguous calf thrombosis, and by usually asymptomatic pulmonary embolism. We prospectively examined 25 consecutive patients using duplex scanning (21x) and/or ascending venography (15x). The phlebitic process involved a varicose greater saphenous vein or a branch thereof (19x), the lesser saphenous vein (3x) or a nonvaricose superficial vein (3x). In 11 cases (44%) we found direct extension to involve the deep vein system and/or noncontiguous isolated calf or popliteal vein thrombosis. The presence of risk factors for deep vein thrombosis and a painful calf muscle were good clinical indicators of such complications. Patients with complications were anticoagulated on an outpatient basis. The course was uneventful in most cases. Our study confirms the notion that superficial thrombophlebitis is often part of a more extended thromboembolic process. This implies diagnostic and therapeutic consequences, although the prognostic significance of such complications is not clear at the moment.     

Levels of tumor necrosis factor alpha, gamma interferon, and interleukins 4,6, and 10 as determined in mice infected with virulent or attenuated strains of Trypanosoma cruzi

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.     

Prospective study of thromboses of the subclavian vein after setting implantable venous access systems in cervico-facial cancerology

Seventy-eight consecutive patients treated by chemotherapy for ENT cancers and having a subclavian catheter for venous access were studied prospectively to assess the prevalence of venous thrombosis. Thrombosis of the subclavian vein was demonstrated clinically in 4 patients and by ultrasonography in 7 patients. The prevalence of thrombosis was 14.1%. No clinical or biological predisposition factor could be identified. Subclavian thrombosis mostly occurred during the second month after implantation (91% of cases). Ultrasonography seems the most useful non-invasive technique for the diagnosis of subclavian thrombosis.     

Pattern of circulating eosinophils in allergic children suffering from infectious disease

We report a patient presenting with melena. Endoscopic examination showed gastric fundal varices as well as colonic varices. The latter is rarely encountered and is usually associated with portal hypertension. On angiography there appeared to be a splenic vein thrombosis which is only reported once earlier as a cause of colonic varices. A short review of the literature concerning colonic varices is added.     

Portal decompression using the inferior mesenteric vein

We report five patients with variceal hemorrhage, in three cases secondary to diffuse thrombosis of the portal, superior mesenteric and splenic veins. Mesenteric angiography demonstrated patency of the inferior mesenteric vein (IMV) in each, and successful portal decompression by anastomosis of the IMV to the left renal vein (n = 4) or the inferior vena cava (n = 1) was accomplished. Bleeding was permanently controlled: four patients have survived from one to eight years post-operatively. Because shunt procedures utilizing the IMV are technically straightforward, subtotally decompress the portal system and avoid the right upper quadrant, they may be advantageous in certain clinical settings.     

Treatment of venous thromboembolism

This review provides meta-analytic data of studies aiming at improved treatment of deep vein thrombosis and pulmonary embolism. The introduction of low molecular weight heparin has considerably ameliorated the initial treatment of deep vein thrombosis, and should now be regarded as the treatment of choice for most patients with deep vein thrombosis. Oral anticoagulant treatment is presently considered safe and effective for the long-term treatment of venous thromboembolism, provided that the INR is maintained at 2.0-3.0. However, the optimal duration as well as the optimal intensity of anticoagulation have still to be determined. Patients with submassive pulmonary embolism should presently be treated with adjusted dose unfractionated heparin and coumarins. Studies determining the efficacy and safety of low molecular weight heparin in this condition deserve priority. Thrombolytic therapy should be restricted to patients with massive pulmonary embolism, unless safer methods of thrombolysis have been developed. Surgical embolectomy and catheter fragmentation of emboli seem alternative options but deserve further investigations.     

Expanding eligibility for outpatient treatment of deep venous thrombosis and pulmonary embolism with low-molecular-weight heparin: a comparison of patient self-injection with homecare injection

BACKGROUND: The outpatient treatment of patients with deep vein thrombosis and pulmonary embolism using low-molecular-weight heparin has the potential to reduce health care costs, but it is unclear if most patients with deep vein thrombosis and pulmonary embolism can be treated as outpatients. In the published studies, more than 50% of patients were excluded from outpatient treatment for reasons such as comorbid conditions, short life expectancy, concomitant pulmonary embolism, and previous deep vein thrombosis, and many patients were not treated entirely at home. We sought to determine if expanding patient eligibility for the outpatient treatment of deep vein thrombosis and pulmonary embolism affects the safety and effectiveness of the treatment, and to determine if patient self-injection compared with injections administered by a homecare nurse affected these outcomes. PATIENTS AND METHODS: We treated as outpatients all patients with deep vein thrombosis and pulmonary embolism, except for those with massive pulmonary embolism, high risk for major bleeding or an active bleed, phlegmasia, and patients hospitalized for reasons that prevented discharge. We compared 2 models of outpatient care to determine feasibility, safety, and efficacy. Both models involved nurse managers who provided daily patient contact and ongoing treatment; however, in one model the patients were taught to inject themselves and in the other model homecare nurses administered the injections. We expanded the population of patients eligible for outpatient treatment by including many patients not treated at home in previous studies. Most patients in our study were treated with dalteparin sodium, 200 U/kg every 24 hours, for a minimum of 5 days. Therapy with warfarin sodium was started on the day of diagnosis or the following day. Patients were followed up for 3 months to determine rates of recurrent venous thromboembolism, bleeding, and death. RESULTS: In this study, 194 (83%) of 233 consecutive patients were deemed eligible and treated as outpatients. Of the 39 patients who did not receive home therapy, 20 had concomitant medical problems responsible for their admission or were already inpatients, 6 had massive pulmonary embolism, 6 refused to pay for the dalteparin therapy, 4 had active bleeding, and 3 had phlegmasia cerulea dolens, which required treatment with intravenous narcotics for pain control. More than 184 (95%) of the 194 patients were treated entirely at home. There was no significant difference (P>.99) in the rate of recurrent venous thromboembolic events between the patients who were injected by homecare nurses (3/95 [3.2%]) and those who injected themselves (4/99 [4.0%]). Combining the 2 models, the overall recurrent event rate was 3.6% (95% confidence interval, 1.5%-7.4%). Similarly, there were no significant differences in rates of major hemorrhage (2/95 vs 2/99; P>.99), minor hemorrhage (8/95 vs 2/99; P = .06), and death (6/95 vs 8/99; P = .63). The overall rate of major hemorrhage was 2.0% (95% confidence interval, 0.6%-5.2%). CONCLUSIONS: We demonstrate that more than 80% of patients at our tertiary care hospital could be treated at home using 1 of the 2 models of care we describe. Our results demonstrate that patients can safely and effectively perform home self-injection under the supervision of a hospital-based nurse. Injections at home by a homecare nurse are similarly effective. Our overall rates of recurrent venous thromboembolism, bleeding, and death are at least as favorable as those previously reported despite using 1 dose per day of dalteparin for most patients.     

The CT nephrogram: implications for evaluation of urinary tract disease

The urographic nephrogram is an important indicator of underlying functional and structural renal disease. With expansions in use of cross-sectional imaging, the computed tomographic (CT) nephrogram (ie, contrast material enhancement within the renal parenchyma) has assumed a greater role in the evaluation of urinary tract disorders. Both quantitative and qualitative nephrographic abnormalities are well demonstrated by CT, including global or segmental absence or persistence of the nephrogram, slowed temporal progression, striated pattern, and rim pattern. Global absence is nearly always unilateral and is most often seen with blunt abdominal trauma with renal pedicle injury. Segmental absence is attributable to focal renal infarction, most likely due to arterial emboli. Global persistence, which is much more common than segmental persistence, may be unilateral (caused by renal artery stenosis, renal vein thrombosis, or urinary tract obstruction) or bilateral (due to systemic hypotension, intratubular obstruction, or abnormalities in tubular function). Striated nephrograms may be unilateral or bilateral and are caused by ureteric obstruction, acute pyelonephritis, contusion, renal vein thrombosis, tubular obstruction, hypotension, and autosomal recessive polycystic kidney disease. The rim pattern is most often associated with renal infarction and occasionally with acute tubular necrosis and renal vein thrombosis. Careful evaluation of the CT nephrogram is an integral part of the abdominal CT examination.     

Intrarenal arterial Doppler sonography in the detection of renal vein thrombosis of the native kidney

OBJECTIVE: Previous studies of transplant kidneys and recent reports on native kidneys have suggested intrarenal arterial Doppler findings can be helpful in the noninvasive workup of renal vein thrombosis. We used arterial Doppler sonography to evaluate cases of possible acute renal vein thrombosis in native kidneys that had equivocal results on standard Doppler analysis of the renal vein. MATERIALS AND METHODS: Twenty native kidneys in 12 patients with clinical findings suggestive of acute renal vein thrombosis had Doppler studies of the main renal vein that failed to show normal flow. In all 20 kidneys, duplex Doppler study of arcuate/interlobar intrarenal arteries was done and the resistive index was determined. The Doppler findings were compared with subsequent findings on either renal venograms (n = 11) or MR images (n = 9), which served as the reference "gold" standards. RESULTS: The prevalence of renal vein thrombosis was 25% (5/20). Ten kidneys had very abnormal findings on arterial Doppler studies (absent or reversed end-diastolic flow), but only two of these were proved to have renal vein thrombosis. In six other kidneys, end-diastolic flow was identified but the resistive index was still elevated (> or = 0.70), and only one of these kidneys was proved to have renal vein thrombosis. Four kidneys had normal arterial Doppler studies, and 50% (two) of these were proved to have renal vein thrombosis. When absent or reversed end-diastolic flow was used as a sign of renal vein thrombosis, intrarenal arterial Doppler analysis had a sensitivity of 40% (2/5) and a specificity of 47% (7/15). CONCLUSION: Unlike the reported experience in transplanted kidneys, intrarenal arterial Doppler analysis is neither sensitive nor specific for renal vein thrombosis in native kidneys. An intrarenal arterial Doppler study with normal findings should not prevent further workup if Doppler findings in the renal vein are equivocal, nor should absent or reversed end-diastolic arterial signals be considered highly suggestive of renal vein thrombosis.     

Different risks of thrombosis in four coagulation defects associated with inherited thrombophilia: a study of 150 families

Deficiency of the naturally occurring anticoagulant proteins, such as antithrombin, protein C and protein S, and activated protein C resistance due to the factor V Leiden gene mutation is associated with inherited thrombophilia. So far, no direct comparison of the thrombotic risk associated with these genetic defects is available. In this study, we wish to compare the lifetime probability of developing thrombosis, the type of thrombotic symptoms, and the role of circumstantial triggering factors in 723 first- and second-degree relatives of 150 index patients with different thrombophilic defects. We found higher risks for thrombosis for subjects with antithrombin (risk ratio 8.1, 95% confidence interval [CI], 3.4 to 19.6), protein C (7.3, 95% CI, 2.9 to 18.4) or protein S deficiency (8.5, 95% CI, 3. 5 to 20.8), and factor V Leiden (2.2, 95% CI, 1.1 to 4.7) than for individuals with normal coagulation. The risk of thrombosis for subjects with factor V Leiden was lower than that for those with all three other coagulation defects (0.3, 95% CI, 0.1 to 1.6), even when arterial and superficial vein thromboses were excluded and the analysis was restricted to deep vein thrombosis (0.3, 95% CI, 0.2 to 0.5). No association between coagulation defects and arterial thrombosis was found. The most frequent venous thrombotic manifestation was deep vein thrombosis with or without pulmonary embolism (90% in antithrombin, 88% in protein C, 100% in protein S deficiency, and 57% in factor V Leiden), but a relatively mild manifestation such as superficial vein thrombosis was common in factor V Leiden (43%). There was a predisposing factor at the time of venous thromboembolism in approximately 50% of cases for each of the four defects. In conclusion, factor V Leiden is associated with a relatively small risk of thrombosis, lower than that for antithrombin, protein C, or protein S deficiency. In addition, individuals with factor V Leiden develop less severe thrombotic manifestations, such as superficial vein thrombosis.     

IL-10 regulates thrombus-induced vein wall inflammation and thrombosis

Vein wall inflammation associated with venous thrombosis is mediated by an imbalance in proinflammatory as compared with antiinflammatory molecules. We hypothesize that IL-10 is an important antiinflammatory cytokine that influences vein wall inflammation and thrombus propagation during venous thrombosis. To test this hypothesis a model of inferior vena caval thrombosis was used. Studies were performed at sacrifice 2 days after thrombus induction and included leukocyte morphometrics, myeloperoxidase activity, vein wall permeability, thrombus weight, and IL-10 ELISA analysis from the vein wall. IL-10 was elevated in the vein wall during venous thrombosis. Neutralization of IL-10 increased inflammation, while supplementation with rIL-10 demonstrated a dose- and time-dependent decrease in inflammation. Interestingly, a low 2.5-microg rIL-10 dose given at time of initiation of thrombosis most significantly decreased inflammation. Thrombus weight was importantly diminished by reconstitution of IL-10. These studies support an important role for IL-10 in the regulation of thrombus-associated inflammation and thrombosis and suggest that IL-10 could be used as a therapeutic agent in the treatment of venous thrombosis.     

Management of chylothorax

BACKGROUND: Chylothorax is a rare primary or secondary condition the optimum management of which remains uncertain. METHODS: Twenty cases of chylothorax, including ten of primary chylothorax and ten secondary to either malignancy, subclavian vein thrombosis or lymphangioma treated between 1956 and 1986 have been reviewed. RESULTS: Open pleurectomy was the most successful treatment in preventing reaccumulation of the effusion. Three patients had thoracic duct-azygous vein anastomoses, but all anastomoses were probably occluded within a year of surgery. Three patients have been lost to follow-up and five died within 2 years of their treatment, but 12 patients were alive and free from an effusion 3-22 years after treatment. CONCLUSION: Patients with chylothorax should undergo lymphangiography to identify the cause and site of the lymphatic abnormality. Conservative treatment is successful in some patients but should be abandoned if the fluid loss exceeds 1.5 l/day for more than 5-7 days in an adult or more than 100 ml/day in a child. Parietal pleurectomy is the most successful treatment when no distinct chylous leak can be identified. Less commonly, an isolated chylous leak either in the chest or in the abdomen may be identified and this should be treated by direct ligation.     

Mesenteric vein thrombosis: a rare cause of abdominal pain in cirrhotic patients--two case reports

Mesenteric vein thrombosis is a rare disorder which can develop rapidly with intestinal infarction or subacutely with abdominal pain due to intestinal ischemia. Despite the availability of modern diagnostic tools, which allow an early diagnosis in most cases, the mortality from this disease has not significantly diminished over the years. The problem is that the syndrome is rare and unusual and the clinical presentation is usually vague or confusing. Particularly in cirrhotic patients, this diagnosis requires the exclusion of several other complications of liver disease, like spontaneous bacterial peritonitis, tense ascites or portal thrombosis. Here, we report the occurrence of acute mesenteric vein thrombosis in two patients with liver cirrhosis. Severe subcontinuous abdominal pain out of proportion to the physical findings and abdominal distension were the major symptoms in both patients. Magnetic resonance imaging in one case and ultrasound scan with color Doppler followed by computed tomography in the other patient confirmed the diagnosis and enabled an appropriate early therapy to be undertaken.     

Prevention of venous thrombosis with small, subcutaneous doses of heparin

The effect of low-dose heparin prophylaxis on venous thrombosis and bleeding after major elective surgery was studied in a prospective controlled study of 820 patients. The total incidence of venous thrombosis detected with leg-scanning using fibrinogen labeled with radioactive iodine (125I) was reduced from 16.0% in the control group to 4.2% in treated patients. More important, the incidence of popliteal or femoral vein thrombosis was reduced from 2.9% to 1.0%. Prophylaxis resulted in a slight increase in bleeding-minor wound hematoma, mean volume of blood transfused, and a post-operative hematocrit fall in treated patients. However, increased bleeding was clinically minor, and prophylaxis was well tolerated.     

Acute pre-hepatic portal thrombosis: diagnosis and therapy

Portal vein thrombosis is a rare pathology. The etiopathogenetic causes that most frequently lead to this pathology are myeloproliferative syndromes. The authors present a case of acute pre-hepatic portal vein thrombosis and discuss its etiopathogenesis, diagnosis and therapy.