Thrombosis of the splenoportal axis after splenectomy

Romano, Fabrizio; Caprotti, Roberto; Conti, Matteo; Piacentini, Maria Gaia; Uggeri, Fabio; Motta, Vittorio; Pogliani, Enrico Maria; Uggeri, Franco

doi:10.1007/s00423-006-0075-z

Cited by 48 publications

(57 citation statements)

References 39 publications

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“…The incidence of only symptomatic SPVT was evaluated in eight retrospective cohort studies, three after OS [19][20][21] and two after LS, 22,23 in three other studies OS and LS were performed in the same study, but OS and LS evaluated separately. 5,24,25 The incidence of symptomatic SPVT in these studies was 2.6% with a range of 0.35% to 13% (Table 2). Overall, the incidence of symptomatic SVPT in prospective and retrospective studies with open and laparascopic splenectomy was 3.3% (85/2590).…”

Section: Resultsmentioning

confidence: 85%

“…The median time from splenectomy to asymptomatic SPVT was six days (range 3-11 days) in a study with contrast-enhanced CT. 17 The median interval between splenectomy and symptomatic SPVT in three retrospective studies was 10.7 (range 4-27) days, 24 11.6 days (range 2-22) 5 and 12 days (range 6-99), 21 while it was eight days (range 2->28) in published reports on single or small series of cases in which data on the interval between splenectomy and SPVT were provided ( Figure 1). Considering all data, we infer that the latency period from the onset of thrombosis to clinical symptoms is on average one week or more.…”

Section: Time From Surgery To Asymptomatic or Symptomatic Splenic/pormentioning

confidence: 97%

“…9,12,21,24 The duration of heparin prophylaxis ranged from three to more than seven days after surgery. In only a few studies 9,11,24,25,30 was heparin treatment extended beyond seven days in some of the patients.…”

Section: Antithrombotic Prophylaxismentioning

confidence: 99%

“…In the majority of cases in whom a follow-up investigation was performed (n=90) 5,9,11,12,[15][16][17][20][21][23][24][25]28,33 there was a documented complete (57/90, 63.3%) or at least partial resolution (13.3 %) of the thrombus. However, in 7.7% the thrombus persisted and in 15.5% cavernoma or portal hypertension were documented.…”

Section: Response To Treatment and Late Complicationsmentioning

confidence: 99%

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The postoperative splenic/portal vein thrombosis after splenectomy and its prevention - an unresolved issue

Krauth¹,

Lechner²,

Neugebauer³

et al. 2008

Haematologica

122

103

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Patients undergoing splenectomy have an increased risk of splenic/portal vein thrombosis. We used several databases to identify publications dealing with this risk and analyzed incidence, risk factors and outcome. The risk of splenic portal vein thrombosis has been addressed in prospective and retrospective randomized or non-randomized studies. All studies combined, the overall risk is 3.3%. Risk factors are big spleens (i.e. myeloproliferative disorders) and hereditary hemolytic anemias, whereas the risk is low in autoimmune thrombocytopenia and trauma. The incidence is approximately the same in laparascopic and open splenectomy. The median time from splenectomy to symptomatic splenic vein thrombosis is 8-12 days. Postoperative antithrombotic prophylaxis ranged from no prophylaxis to heparin for seven days or longer. Treatment of symptomatic splenic vein thrombosis with heparin and warfarin leads to complete resolution of thrombosis in 67%, to partial resolution in 13%, but persistent occlusion, portal hypertension or cavernoma occurred in 20%. The long-term outcome of treatment failures is unknown. Well-designed randomized studies on the prophylaxis of venous thromboembolism after splenectomy are urgently needed.Key words: portal vein thrombosis, risk factors, splenectomy, thromboembolism, treatment. Citation: Krauth M-T, Lechner K, Neugebauer EAM and Pabinger I. The postoperative splenic/portal vein thrombosis after splenectomy and its prevention -an unresolved issue.

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Section: Resultsmentioning

confidence: 85%

Section: Time From Surgery To Asymptomatic or Symptomatic Splenic/pormentioning

confidence: 97%

Section: Antithrombotic Prophylaxismentioning

confidence: 99%

Section: Response To Treatment and Late Complicationsmentioning

confidence: 99%

See 2 more Smart Citations

The postoperative splenic/portal vein thrombosis after splenectomy and its prevention - an unresolved issue

Krauth¹,

Lechner²,

Neugebauer³

et al. 2008

Haematologica

122

103

View full text Add to dashboard Cite

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“…LS might increase the risk of P/SVT because it reduces the blood flow in the portal system due to the pneumoperitoneum; however, on the other hand, it seems to be associated with fewer postoperative modifications of coagulation parameters and of fibrinolytic postoperative pathways than OS, thus preventing P/SVT itself (6,17,19,(21)(22)(23)64). Because P/SVT constitutes a potentially lethal complication following LS, literature shows that patients with myeloproliferative disorders, hemolytic diseases and marked splenomegaly are at higher risk for its development, thus ultrasonographic screening as routine on the seventh postoperative day is now justified (65).…”

Section: Critical Evaluationmentioning

confidence: 99%

Laparoscopic Splenectomy for Benign Hematological Disorders in Adults: A Systematic Review

Moris

Dimitriou

Grınıatsos

2017

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Postsplenectomy vascular complications: Feasibility of studying patients with splenectomy following trauma

et al. 2009

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To the editor: The interesting article by van Beers et al. states that functional studies does not offer clues as to the presence of mild pulmonary hypertension (PH) in patients with sickle cell disease (SCD) [1]. However, they did show that although not statistically significant, lung function findings do vary in hemoglobin-SS patients.Studies examining lung function in adults with SCD conclude that pulmonary function is abnormal in 90% of patients and gradually declines over time [2,3]. The most common patterns observed were restrictive lung disease and low diffusing capacity (D LCO ). Few publications include data on both the D LCO and the transfer coefficient (K CO ). However, measuring K CO provides information on pathophysiology, which cannot be obtained just from the D LCO . These measurements help us understand when lung disease is due to a loss of lung units (e.g., pneumonectomy), a process interfering with the alveolar surface (e.g., fibrosis) or the capillaries (e.g., PH).Studies on patients with pulmonary arterial hypertension show that a low D LCO can be used as an early marker of PH, before echocardiographic signs develop [4]. When patients with SCD are screened with echocardiogram up to 36% have evidence of PH depending on the hemoglobin genotype [5,6]. However, in autopsy studies there is histological evidence of PH in up to 75% of patients [7]. D LCO may therefore be a more reliable tool than echocardiogram in predicting PH. Van Beers study shows both the D LCO and K CO were reduced in patients with mild PH [1].We examined lung function results from 32 adults with SCD, average age was 34 years and 30 patients had hemoglobin-SS. The mean forced expiratory volume in 1 sec (FEV 1 ) was 81.8% predicted and the mean forced vital capacity (FVC) was 80.9% predicted. Two patients had an obstructive defect (FEV 1 /FVC < 70%) and 18 patients had a FEV 1 /FVC >80%. The mean D LCO (82.6% AE 3.2%) was lower than predicted but the mean K CO (110.4% AE 3.2%) was higher than predicted. There was no statistical difference between patients with or without a history of acute chest syndrome. The results suggest that in these patients the pathophysiological process may be the loss of lung units.To our knowledge, only two other studies on adults with SCD included data on K CO [8,9]. These studies had similar patient numbers, characteristics and spirometry results. Unlike our study both these studies found the K CO lower than predicted. This implies in these patients a different pathophysiological mechanism was operating. The difference with our patient group may be one of disease severity. The high K CO we found is consistent with an increased blood flow to normal lung. A lower than predicted K CO could imply the patients had developed PH, as suggested by the findings in van Beers study, or diffuse alveolar damage. Only two studies performed in children examined D LCO and K CO and found results similar to our study, perhaps reflecting their lower exposure to pulmonary complications [10,11].We feel both our study and ...

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Thrombosis of the splenoportal axis after splenectomy

Cited by 48 publications

References 39 publications

The postoperative splenic/portal vein thrombosis after splenectomy and its prevention - an unresolved issue

The postoperative splenic/portal vein thrombosis after splenectomy and its prevention - an unresolved issue

Laparoscopic Splenectomy for Benign Hematological Disorders in Adults: A Systematic Review

Postsplenectomy vascular complications: Feasibility of studying patients with splenectomy following trauma

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