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 Table of Contents  
Year : 2019  |  Volume : 8  |  Issue : 3  |  Page : 182-190

Risk factors, pattern of presentation, methods of diagnosis, and results of treatment of acute portal vein thrombosis: A multicenter study

1 Department of Surgery, College of Medicine, Taif University, Taif, Saudi Arabia
2 Department of Surgery, College of Medicine, Taif University, Taif, Saudi Arabia; Department of Surgery, Damanhur Teaching Hospital, General Organization of Teaching Hospitals and Institutes, Damanhur, Egypt
3 Department of Surgery, College of Medicine, Taif University, Taif, Saudi Arabia; Department of Surgery, Benha Teaching Hospital, General Organization of Teaching Hospitals and Institutes, Benha, Egypt
4 Department of Surgery, College of Medicine, Taif University, Taif, Saudi Arabia; Department of Surgery, Faculty of Medicine, Ain Shams University, Cairo, Egypt
5 Ain Shams Organ Transplant Center, HBP and Liver Transplant Unit, Cairo, Egypt

Date of Web Publication9-Dec-2019

Correspondence Address:
Dr. Mohamed Salem Al Saeed
Department of Surgery, College of Medicine, Taif University, P.O. Box: 888, Taif 21947
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sjhs.sjhs_77_19

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Background and Aim of the Work: Portal vein thrombosis (PVT) is a serious condition; however, the outcome may be improved by early recognition and prompt management. The aim of this multicenter retrospective study is to evaluate the underlying risk factors, pattern of presentation, methods of diagnosis, and results of treatment of cases of acute/recent PVT in Taif tertiary hospitals.Methods: In this chart review and database study, 103 patients met the inclusion criteria. Data extracted from the medical records were analyzed for underlying risk factors, pattern of presentation, diagnostic tools, and results of treatment.Results: The underlying causes of PVT were cirrhosis (46.6%) and noncirrhotic causes (43.7%), and no obvious cause was recorded in 9.7% of cases. In 9.7% of the patients, PVT progressed to mesenteric venous occlusion. The diagnosis was established by initial duplex ultrasound scan or/and contrast-enhanced computed tomography scan in 97.1% of patients. Anticoagulation was started for all patients after established diagnosis except in patients with gastrointestinal bleeding. In all patients with mesenteric venous occlusion, infarcted segments were found and resected during abdominal exploration. The recorded overall mortality during follow-up was 51.5%, and it was significantly higher in cirrhotic than in noncirrhotic patients (P < 0.05).Conclusions: Cirrhosis is the main underlying cause of PVT in Taif, Saudi Arabia. Most of the findings in this study about epidemiological and risk factors were quite different from that of other global findings. More studies are required to assess the actual magnitude of PVT in Taif and other Saudi Arabia provinces.

Keywords: Cirrhosis, portal vein, thrombophilia, thrombosis

How to cite this article:
Al Saeed MS, Al-Jiffry BO, Younes A, Badr S, Abdel-Rahman T, Hatem M, El-Meteini M. Risk factors, pattern of presentation, methods of diagnosis, and results of treatment of acute portal vein thrombosis: A multicenter study. Saudi J Health Sci 2019;8:182-90

How to cite this URL:
Al Saeed MS, Al-Jiffry BO, Younes A, Badr S, Abdel-Rahman T, Hatem M, El-Meteini M. Risk factors, pattern of presentation, methods of diagnosis, and results of treatment of acute portal vein thrombosis: A multicenter study. Saudi J Health Sci [serial online] 2019 [cited 2020 Sep 30];8:182-90. Available from: http://www.saudijhealthsci.org/text.asp?2019/8/3/182/272445

  Introduction Top

Portal vein thrombosis (PVT) is a serious complication of liver cirrhosis and other thrombophilic disorders.[1],[2],[3] Thrombosis usually begins intrahepatically in liver cirrhosis and hepatic malignancies; however, in other etiologies, it starts at the site of origin of the portal vein or splenic vein.[3],[4] The incidence of PVT is underestimated as it may be asymptomatic or present with nonspecific symptoms, especially in cirrhotic patients.[5],[6],[7],[8],[9],[10],[11] The magnitude of this problem may be exaggerated by the effect of hypobaric hypoxia on the coagulation system in altitude and high altitude environment as in Taif and its related districts.[12],[13],[14],[15] Early identification of patients with PVT would prevent potentially fatal complications such as bowel infarction or development of portal hypertension.[7] Acute PVT is diagnosed when the patient presents with abdominal pain >24 h with radiological evidence of variable degrees of obstruction of portal veins or/and mesenteric veins.[8],[16] In chronic PVT serpiginous collaterals will replace the portal vein, and it takes 12–60 days to be radiologically evident.[8] In cirrhotic patients, PVT accelerates the liver impairment and worsens the prognosis; however, in noncirrhotic patients, hepatic derangement is minor.[4],[7] D-dimer testing may help in rolling out PVT sparing patients the unnecessary risks of anticoagulation, but its diagnostic accuracy is low.[17],[18],[19] Early diagnosis and prompt treatment would help recanalization that improves outcome.[12],[20],[21],[22],[23] The aim of this multicenter retrospective study is to evaluate the underlying risk factors, pattern of presentation, methods of diagnosis, and results of the treatment of cases of acute/recent PVT in Taif tertiary hospitals.

  Methods Top

In this retrospective chart review and database study, the patients were identified in the computerized hospital administrative registration system of Taif tertiary hospitals, Saudi Arabia. One hundred and three patients met the inclusion criteria in the examined files from January 2012 to December 2017. The inclusion criteria included the patients who had PVT of duration <5 weeks with or without associated mesenteric venous thrombosis and their files are complete and include the underlying risk factors, presentation, diagnostic tools, treatment, and follow-up events. Exclusion criteria included: patients with chronic PVT, traumatic cases, incomplete, and unclear files. We reviewed demographic data, associated risk factors, pattern of presentation, laboratory, radiological, treatment, and intraoperative findings if the operation was done in addition to the recorded mortality during the follow-up. The mean period of follow-up was 67.2 ± 16.1 months. Survival was determined from the date of diagnosis to the date of documented death or loss of follow-up. SPSS version 22 was used for carrying out statistical analysis (IBM Corp. Released 2013. IBM SPSS Statistics for Windows, Version 22.0. IBM Corp., Armonk, NY, USA). Group differences were further analyzed by Chi-squre and Fisher's exact (FE) tests, and the difference between means of continuous variables was tested by Student's t-test. The level of statistical significance was determined at P < 0.05.

The study was conducted after approval of the hospitals' ethical boards.

  Results Top

[Table 1] shows that the number of males was significantly higher than females. It also shows a significantly higher mean age in males than in females and cirrhotic patients than noncirrhotics. [Table 2] shows the underlying risk factors of PVT where the most common cause was cirrhosis wherein the most common cause was nonalcoholic steatohepatitis (NASH) followed by intra-abdominal inflammatory and neoplastic condition (most common was pancreatitis), then myeloproliferative disorder (MPD), unidentified cause, then inherited and acquired thrombophilic disorders. The table shows also associated conditions with cirrhosis. [Table 3] shows the relation between PVT and pregnancy or/and delivery and associated other risk factors. [Table 4] shows postoperative PVT and associated other risk factors. [Table 5] shows a comparison of different presentations in cirrhotic and noncirrhotic patients. Pain and tachycardia were the outstanding features in all patients that progressed to microvascular obstruction (MVO), and only 30% of patients had marked peritoneal signs and shock at the time of presentation. [Table 6] shows a comparison of the laboratory findings in cirrhotic and noncirrhotic patients with PVT where it shows a significant derangement in liver function test (LFT) of cirrhotic patients than noncirrhotics and that the mean level of alpha-fetoprotein of cirrhotic patients is significantly higher than that in noncirrhotics. The diagnosis was established by duplex ultrasound scan or/and contrast-enhanced computed tomography (CECT) scan. The diagnosis of cirrhosis was established by ultrasound examination and confirmed by liver biopsy and serology for the underlying cause. In patients with liver masses biopsy were not done, and triphasic CT was used to determine the nature of the mass. In noncirrhotic patients, specific tests of the underlying causes were done. Upper gastrointestinal (GI) endoscopy was used to diagnose and stop upper GI bleeding by banding or sclerotherapy. In cirrhotic patients, esophageal varices were the main cause of bleeding (12/20 patients, 60%) and hypertensive portal gastropathy in 8/20 patients (40%), while in noncirrhotics hypertensive portal gastropathy was the cause in all cases. Anticoagulation was initiated immediately in 66/103 patients (64.1%). In the other 37 patients, 34 patients started anticoagulation after control of GI bleeding and in the other three patients with associated MVO with marked peritoneal signs; the diagnosis was established after exploratory laparotomy and followed by anticoagulation. In the patient of perforated appendicitis, abdominal exploration, peritoneal toilet, appendectomy, and drainage were done. Intravenous (IV) metronidazole was given for the amebic liver abscess patient, and ultrasound-guided drainage was done. Specific treatment of the underlying causes was performed. In patients presented with PVT associated with MVO preoperative resuscitation was done with IV antibiotics. During operation, all MVO patients were found to have a segment of infarction of the small intestine with obvious thrombosis of the mesenteric veins and portal vein but with patent mesenteric arteries and resections with primary anastomosis were done of the affected intestinal segments. Second-look operation was performed in 3/10 patients (30%) with MVO, and further resection was required in the three patients (100% of the second-look operations). The mean period of follow-up was 67 ± 16.1 months and the overall recorded mortality during this period was 53/103 patients (51.5%); 16/55 (29.1%) of noncirrhotic patients; and 37/48 (77.1%) of the cirrhotic patients. The mean survival was significantly lower in cirrhotic patients than noncirrhotic (35.4 ± 8.1 months vs. 65.6 ± 13.2 months; P <0.05). The mean survival in females was higher than male but did not reach a statistically significant value (P >0.05).
Table 1: Demographic data

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Table 2: Underlying causes

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Table 3: Portal vein thrombosis related to pregnancy and/or delivery

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Table 4: Postoperative portal vein thrombosis

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Table 5: Presentation of patients with portal vein thrombosis

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Table 6: Laboratory findings in portal vein thrombosis

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The perioperative mortality in the MVO group of patients was 2/10 patients (20%); one patient died intraoperatively from cardiac arrest, and the other patients died in the early postoperative period from the sequelae of sepsis. The dead patients presented with marked peritoneal signs and in shock status. [Table 7] summarizes the findings in patients progressed to MVO.
Table 7: Findings in the patients with portal vein thrombosis progressed to mesenteric vascular occlusion

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  Discussion Top

The incidence of PVT is variable, where it reaches 15% in advanced cirrhosis versus <0.5% in autopsy studies.[1] The actual incidence in Saudi Arabia is not known; however, it has been recorded that PVT is more commonly encountered as a cause of portal hypertension in developing than in developed societies (40% in the former vs. 10% in the latter).[1],[2],[3]

In the current report, male predominance is much higher than that recorded in the literature in both cirrhotic and noncirrhotic patients.[1],[2],[3],[4]

This study also verified that the age distribution was significantly higher in cirrhotic than in noncirrhotic patients, which is concordant with the findings in previous studies.[1],[2]

Said et al.[4] and Khayyat[5] emphasized that cirrhosis was the most common cause and NASH was the most common entity, and these findings were in accordance with our study. Similar results were recorded by Stine et al.,[6] as they found that NASH was considered as a higher risk for the development of PVT than the other forms of cirrhosis. However, in our study, Said et al.,[4] and Khayyat[5] studies the reported incidence of cirrhosis as a cause of PVT was higher than that recorded in the English literature.

Investigators found that PVT was much more prevalent in patients with advanced cirrhosis than in patients with compensated cirrhosis.[3],[4],[7] In agreement with these findings, Child C patients represented over 60% of the PVT patients in the current report. In advanced cirrhosis, extensive fibrosis would impede venous flow causing venous stasis and congestion that increase vascular stress and endothelial injury.[24],[25] Although the synthesis of clotting factors are diminished in advanced liver impairment, recent evidence suggests that cirrhosis is considered to be a thrombophilic disorder as the synthesis of anticoagulant proteins is decreased especially protein C with increase in the levels of certain procoagulants as factor VIII.[1],[2],[20],[24],[25]

Intra-abdominal neoplasms as hepatocellular carcinoma, secondary liver tumors, and pancreatic carcinoma may cause compression and/or invasion of portal vein in addition to the associated hypercoagulable state, and these conditions are reported to be responsible for >20% of PVT.[1],[3],[4]

Pancreatitis and intra-abdominal sepsis, especially when peritonitis is established are involved in the development of PVT.[3] Hamidi et al.[26] isolated bacterial endotoxins from the portal blood in advanced cirrhosis emphasizing its role in the activation of thrombus formation mechanisms. Ni et al.[27] reported that  Bacteroides fragilis Scientific Name Search eremia is frequently encountered in cases of PVT, especially in developing counties. In our study, intra-abdominal neoplasms and inflammatory conditions represented the second-most common cause of PVT.

In the absence of cirrhosis, MPDs appear as a major cause of PVT reaching 20%–50% of those patients, yet, the incidence decreases to 10%–12% if cirrhosis is taken into consideration.[28],[29],[30],[31] Similar results were encountered in the current study. The studies that show the correlation between MPD and PVT in Saudi patients are still lacking.

D'Amico et al.[32] found that the prevalence of inherited or secondary thrombophilic disorders among PVT patients is encountered in about 15% of patients and more than one risk factor may be detected especially if the patient had a parenchymal liver disease which is the site of synthesis of anticoagulant factors. Qi et al.[33] found in their meta-analysis that protein C deficiency is seen in 5.6% of cases, antithrombin III deficiency in 3.9%, and protein S deficiency in 2.6%. The findings of the previous study were quite different from our results, and this may be related to actual ethnic difference or just due to the limited number of our patients. However, the results of Al-Jaouni[34] in her study about primary thrombophilia in Saudi Arabia in patients with venous thromboembolic disorders support our findings. Lisman and Porte[25] emphasized that more than one risk factor may be present in the same patients, so, it is reasonable to check for an inherited coagulation disorders even when a local factor for PVT is obvious and conversely, also checking for local factors even in the presence of inherited coagulation disorders. In the present retrospective study, only one risk factor was recorded, which may reflect that more meticulous workup might not be done.

Mohanty et al.,[35] Sharma et al.,[36] Koshy and Jeyakumari,[37] and Shah et al.[38] documented the role of other inherited hypercoagulable disorders carry a risk for PVT such as factor V Leiden mutation, factor II mutation (G20210A in 0%–22%), paroxysmal nocturnal hemoglobinuria, antiphospholipid syndrome, hyperhomocysteinemia, methylenetetrahydrofolate reductase gene mutation, mutation in thrombin activatable fibrinolysis inhibitor gene, and high levels of factor VIII.

Savoia et al.[39] and Dasari and Balusamy[40] recorded in their reports that the data about the exact prevalence, etiology, and outcome of PVT in pregnancy and after delivery are lacking, even though, the risk of PVT is reported to be increased. In our study, PVT as a complication of pregnancy and delivery was 2.9% and 8.7%, respectively, this figure is higher than that recorded in the previous reports and further studies are required to assess the actual magnitude of the problem in the KSA. During pregnancy and puerperium, the coagulation mechanisms are modified with increased coagulant and reduced fibrinolytic activity to prevent undue bleeding during these periods.[41],[42]

The incidence of PVT in adult living donor liver transplantation (LDLT) is not much higher than that in orthotopic liver transplantation (OLT) (4% in the former vs. <3% in the latter) this slightly higher incidence in LDLT may be related to the difficulties in portal vein reconstructions as the vascular pedicle is shorter in addition to the limitation of the vessel graft.[43],[44],[45],[46],[47],[48] Woo et al.[47] found that technical errors and anatomic variations such as venous redundancy, kinking, and/or stenosis of the anastomosis are the most common causes leading to PVT after OLT. Audet et al.[48] reported other additional factors as; the presence of portal thrombosis prior to OLT, development of acute rejection, and previous splenectomy. Ghabril et al.[9] found that PVT was detected in 50%–70% of explanted cirrhotic livers during liver transplantation, a finding which has been documented in other studies.[9],[43],[44],[45],[46],[47],[48],[49],[50],[51] In the present study, the sample was very small, yet, 2.9% of the patients were diagnosed as PVT following LDLT, two of three patients had PVT prior to the transplantation, and in the third patient, the condition was developed secondary to acute rejection.

Al Saeed[52] found in his study on postsplenectomy PVT that the pesence of malignancy was the most important preoperative risk factor. Jiang et al.[53] emphasized on the surgical intervention itself including duration, open or laparoscopic splenectomy. Mesa et al.[54] and Mohren et al.[55] found that the type of the underlying disease and the size of the spleen are considered the most important factors as seen in the patients with big spleens as MPD, lymphoma, and patients with hereditary hemolytic anemia. In the present study, the most common underlying risk factors for PVT following splenectomy was MPD, followed by congestive splenomegaly in cirrhotic patients and chronic hemolytic anemia; unfortunately, the incidence of this complication in relation to the mean size of spleens were missing. Al Saeed[52] reported in his study of PVT after splenectomy in Taif tertiary hospitals a significantly higher incidence (16%) than reported in literature (8%–12%) and attributed that to the effect of hypobaric hypoxia on coagulation system and emphasized that 62.5% of the patients developed PVT in spite of receiving prophylactic low molecular weight heparin. He reported also that the mean size of the removed spleens was above 1500 g.

Amitrano et al.[56] found in their study that 43% of their cirrhotic patients with PVT were asymptomatic and that gastro-intestinal bleeding was the commonest presentation in symptomatic patients (39.2%). Sogaard et al.[57] reported in their study on acute PVT in cirrhotic patients with malignancy that abdominalia (abdominal pain, anorexia, nausea, vomiting, and diarrhea) was seen in 63%, bleeding in 58%, splenomegaly in 63%, fever in 37%, ascites in 32%, and weight loss in 16% of patients. In the present study, the findings were in accordance with the findings in the previous studies including a single Saudi Arabian study about the survival of patients with PVT in the Western Saudi Arabia.[5],[56],[57]

Amitrano et al.[56] attested in their study that PVT with mesenteric venous involvement is never asymptomatic and lead to intestinal ischemia or infarction. Al Saeed et al.,[12] Al Saeed et al.,[13] Brandt and Feuerstadt,[58] and Abu-Daff et al.[59] authenticated in their studies that the involvement of superior mesenteric vein and the mesenteric venous arches would lead to intestinal ischemia ending in bowel infarction and the patients may then present with abdominal pain, bloody diarrhea, fever, and peritoneal signs which will be marked if bowel infarction occurs. The results of the current report are similar to that in the previous studies.

Mild derangement of LFT is only seen in PVT unless there is cirrhosis or advanced hepatic malignancy.[1] These findings are in agreement with our results.

Dai et al.,[17] Zhang et al.,[18] and Altinyollar et al.,[19] notarized that D-Dimer assay would have a high negative predictive value, and this test may be useful for the exclusion of patients with suspected mesenteric/PVT. In the current study, D-Dimer level was high in all patients.

Ultrasound is nonexpensive efficient modality for the diagnosis of PVT, and it is the investigation of choice in spite of being operator dependent; however, its results may be limited in obese patients particularly in the presence of bowel gas.[59],[60],[61],[62],[63] The ultrasound sensitivity and specificity for detection of PVT ranges from 80% to 100% with a diagnostic accuracy of 88%–98%.[59]

CECT scanning is superior to ultrasound in detecting variceal disease, extension of thrombus to mesenteric veins, and parenchymal hepatic lesions, yet, if both modalities are combined their diagnostic accuracy would be increased.[63],[64],[65],[66],[67] The findings, in this study, were in agreement with the recommendations of the previous studies where ultrasound was the initial step in the diagnosis of all patients, and CECT scanning was done to establish diagnosis except in conditions requiring urgent therapeutic interference.

Other diagnostic modalities include magnetic resonance imaging/magnetic resonance angiography which can detect hepatic parenchymal details, and if angiography is added, quantitative portal and hepatic vessel flow can be determined before shunt surgery or liver transplantation.[67],[68],[69],[70]

Endoscopic ultrasound has high sensitivity and specificity, but its specificity is low in severe portal hypertension as portosystemic collaterals lead to shunting of blood away from a patent portal vein.[59],[63],[67],[68],[69],[70]

In cases present with acute bleeding management must include restoration of the blood volume followed by stopping bleeding, and investigators found that endoscopic variceal banding or sclerotherapy has a success rate of 95%.[71],[72] Octreotide infusion has over 80%–90% success rate in control of acute variceal bleeding, especially if concomitant portal gastropathy is found; in addition, it can be used with propranolol to minimize rebleeding.[72] The guidelines for anticoagulation, TIPSS, shunt surgery, or liver transplantation are lacking, and the choice of treatment depends on the local expertise and the patient conditions; however, the aim of the treatment is to stop advancement of thrombosis, to prevent or minimize complications, and to allow recanalization of the portal vein.[73],[74] Loffredo et al.[75] advocated the use of anticoagulation in noncirrhotic acute PVT, compensated cirrhotic patients, especially if there is associated MVO with intestinal ischemia heralding an infarction and they affirmed starting anticoagulation after control of GI bleeding. The results of this study were in accordance with the findings of previous studies.

Thrombolysis may be used in acute PVT through the transhepatic route followed by anticoagulation for 3–6 months; another alternative is to perform shunt surgery in compensated cirrhotic patients followed by anticoagulation.[73]

Further management of the underlying local or systemic risk factors must be followed and transfer to a liver transplantation center is recommended for cirrhotic patients with hepatic dysfunction in the setting of PVT.[76] Until recently, the presence of PVT was considered a relative contraindication of OLT; yet, Woo et al.,[47] Audet et al.,[48] and Schmitz et al.[49] advocated the use of recent surgical techniques as the use of portal vein tributaries, venous jump graft, and thrombectomy. However, if the thrombus extends to the splenic and mesenteric veins in otherwise healthy young patient with end-stage liver disease, multivisceral transplantation would be considered.[50]

Angiography and infusion of vasodilator, thrombolytic agent before the appearance of peritoneal signs, hemodynamic derangements, and other nonsurgical modalities are still investigatory and may replace surgical intervention in a large number of patients with extension of thrombosis to mesenteric veins.[76]

Once intestinal infarction is suspected, the abdomen must be explored with resection of the nonviable segments of intestine.[12],[13],[77],[78],[79],[80] Lindblad and Håkansson[80] and Kaminsky et al.[81] advocated second-look operation during the first 12–48 postoperative h to assess the viability of doubtful intestinal segments to limit the extent of the initial resection. In the present study, resections with primary anastomosis were done of the affected intestinal segments. The second-look operation was performed in three patients with MVO, and further resection was required in all of them.

The mortality rate of cirrhotic patients with PVT ranges from 30% to 70%, and this variation depends on the child grade of the patient, the presence of associated malignancy, and the management including liver transplantation.[1],[2],[3],[4],[9],[10],[11] In noncirrhotic patients, the overall prognosis is good, and the 10-year survival reaches 75% with overall mortality rate of about 10%–30%, and this difference is primarily related to the normal hepatic function of those patients.[1],[2] The previous findings are concordant with that reported in the current study.

  Conclusions Top

Cirrhosis is the main underlying cause of PVT in Taif, Saudi Arabia. Most of the findings in this study about epidemiological and risk factors were quite different from that of other global findings. More studies are required to assess the actual magnitude of PVT in Taif and other Saudi Arabia provinces.

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  References Top

von Köckritz L, De Gottardi A, Trebicka J, Praktiknjo M. Portal vein thrombosis in patients with cirrhosis. Gastroenterol Rep (Oxf) 2017;5:148-56.  Back to cited text no. 1
Nery F, Chevret S, Condat B, de Raucourt E, Boudaoud L, Rautou PE, et al. Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: Results of a longitudinal study. Hepatology 2015;61:660-7.  Back to cited text no. 2
Ogren M, Bergqvist D, Björck M, Acosta S, Eriksson H, Sternby NH, et al. Portal vein thrombosis: Prevalence, patient characteristics and lifetime risk: A population study based on 23,796 consecutive autopsies. World J Gastroenterol 2006;12:2115-9.  Back to cited text no. 3
Said H, Mamdouh K, Hilal AF. Portal vein thrombosis with cirrhosis: Is it an indication for early liver transplantation? Egypt J Surg 2018;37:191-5.  Back to cited text no. 4
  [Full text]  
Khayyat YM. Survival of patients with portal vein thrombosis: Analysis based on disease onset. Hepatogastroenterology 2013;60:65-9.  Back to cited text no. 5
Stine JG, Shah NL, Argo CK, Pelletier SJ, Caldwell SH, Northup PG. Increased risk of portal vein thrombosis in patients with cirrhosis due to nonalcoholic steatohepatitis. Liver Transpl 2015;21:1016-21.  Back to cited text no. 6
Harding DJ, Perera MT, Chen F, Olliff S, Tripathi D. Portal vein thrombosis in cirrhosis: Controversies and latest developments. World J Gastroenterol 2015;21:6769-84.  Back to cited text no. 7
Sarin SK, Philips CA, Kamath PS, Choudhury A, Maruyama H, Nery FG, et al. Toward a comprehensive new classification of portal vein thrombosis in patients with cirrhosis. Gastroenterology 2016;151:574-7.e3.  Back to cited text no. 8
Ghabril M, Agarwal S, Lacerda M, Chalasani N, Kwo P, Tector AJ, et al. Portal vein thrombosis is a risk factor for poor early outcomes after liver transplantation: Analysis of risk factors and outcomes for portal vein thrombosis in waitlisted patients. Transplantation 2016;100:126-33.  Back to cited text no. 9
Englesbe MJ, Schaubel DE, Cai S, Guidinger MK, Merion RM. Portal vein thrombosis and liver transplant survival benefit. Liver Transpl 2010;16:999-1005.  Back to cited text no. 10
Yerdel MA, Gunson B, Mirza D, Karayalçin K, Olliff S, Buckels J, et al. Portal vein thrombosis in adults undergoing liver transplantation: Risk factors, screening, management, and outcome. Transplantation 2000;69:1873-81.  Back to cited text no. 11
Al Saeed M, Hatem M, Abu Duruk A, Mohamed HA, Al-Nashar N, Ahmed M, et al. Prevalence, pattern of presentation, risk factors and outcome of acute mesenteric venous thrombosis in Taif Province, Saudi Arabia, a single center study. Egypt J Hosp Med 2013;52:642-9.  Back to cited text no. 12
Al Saeed M, Abu Shady M, Hatem M, Alzahrani K, Al Nashar M, Al Nashar H. Acute occlusive mesenteric ischemia in Taif Province, Saudi Arabia. Egypt J Hosp Med 2012;47:158-65.  Back to cited text no. 13
Al-Shraim MM, Zafer MH, Rahman GA. Acute occlusive mesenteric ischemia in high altitude of southwestern region of Saudi Arabia. Ann Afr Med 2012;11:5-10.  Back to cited text no. 14
[PUBMED]  [Full text]  
Bendz B, Rostrup M, Sevre K, Andersen TO, Sandset PM. Association between acute hypobaric hypoxia and activation of coagulation in human beings. Lancet 2000;356:1657-8.  Back to cited text no. 15
Ma J, Yan Z, Luo J, Liu Q, Wang J, Qiu S. Rational classification of portal vein thrombosis and its clinical significance. PLoS One 2014;9:e112501.  Back to cited text no. 16
Dai J, Qi X, Li H, Guo X. Role of D-dimer in the development of portal vein thrombosis in liver cirrhosis: A meta-analysis. Saudi J Gastroenterol 2015;21:165-74.  Back to cited text no. 17
[PUBMED]  [Full text]  
Zhang DL, Hao JY, Yang N. Value of D-dimer and protein S for diagnosis of portal vein thrombosis in patients with liver cirrhosis. J Int Med Res 2013;41:664-72.  Back to cited text no. 18
Altinyollar H, Boyabatli M, Berberoǧlu U. D-dimer as a marker for early diagnosis of acute mesenteric ischemia. Thromb Res 2006;117:463-7.  Back to cited text no. 19
Valla DC, Condat B. Portal vein thrombosis in adults: Pathophysiology, pathogenesis and management. J Hepatol 2000;32:865-71.  Back to cited text no. 20
Primignani M, Tosetti G, La Mura V. Therapeutic and clinical aspects of portal vein thrombosis in patients with cirrhosis. World J Hepatol 2015;7:2906-12.  Back to cited text no. 21
Schultheib M, Bettinger D, Thimme R. Nonsurgical therapeutic options in portal vein thrombosis. Viszeralmedizin 2014;30:388-92.  Back to cited text no. 22
Cerini F, Gonzalez JM, Torres F, Puente Á, Casas M, Vinaixa C, et al. Impact of anticoagulation on upper-gastrointestinal bleeding in cirrhosis. A retrospective multicenter study. Hepatology 2015;62:575-83.  Back to cited text no. 23
Tripodi A, Primignani M, Mannucci PM, Caldwell SH. Changing concepts of cirrhotic coagulopathy. Am J Gastroenterol 2017;112:274-81.  Back to cited text no. 24
Lisman T, Porte RJ. Rebalanced hemostasis in patients with liver disease: Evidence and clinical consequences. Blood 2010;116:878-85.  Back to cited text no. 25
Hamidi K, Pauwels A, Bingen M, Simo AC, Medini A, Jarjous N, et al. Recent portal and mesenteric venous thrombosis associated with Fusobacterium bacteremia. Gastroenterol Clin Biol 2008;32:734-9.  Back to cited text no. 26
Ni YH, Wang NC, Peng MY, Chou YY, Chang FY. Bacteroides fragilis bacteremia associated with portal vein and superior mesentery vein thrombosis secondary to antithrombin III and protein C deficiency: A case report. J Microbiol Immunol Infect 2002;35:255-8.  Back to cited text no. 27
How J, Zhou A, Oh ST. Splanchnic vein thrombosis in myeloproliferative neoplasms: Pathophysiology and molecular mechanisms of disease. Ther Adv Hematol 2017;8:107-18.  Back to cited text no. 28
Barbui T, Carobbio A, Cervantes F, Vannucchi AM, Guglielmelli P, Antonioli E, et al. Thrombosis in primary myelofibrosis: Incidence and risk factors. Blood 2010;115:778-82.  Back to cited text no. 29
Barbui T, Finazzi G, Falanga A. Myeloproliferative neoplasms and thrombosis. Blood 2013;122:2176-84.  Back to cited text no. 30
Condat B, Valla D. Nonmalignant portal vein thrombosis in adults. Nat Clin Pract Gastroenterol Hepatol 2006;3:505-15.  Back to cited text no. 31
D'Amico M, Sammarco P, Pasta L. Thrombophilic genetic factors PAI-1, MTHFRC677T, V Leiden 506Q, and prothrombin 20210A in noncirrhotic portal vein thrombosis and Budd-Chiari syndrome in a Caucasian population. Int J Vasc Med 2013;2013:717480.  Back to cited text no. 32
Qi X, De Stefano V, Wang J, Bai M, Yang Z, Han G, et al. Prevalence of inherited antithrombin, protein C, and protein S deficiencies in portal vein system thrombosis and Budd-Chiari syndrome: A systematic review and meta-analysis of observational studies. J Gastroenterol Hepatol 2013;28:432-42.  Back to cited text no. 33
Al-Jaouni SK. Primary thrombophilia in Saudi Arabia. Saudi Med J 2003;24:614-6.  Back to cited text no. 34
Mohanty D, Shetty S, Ghosh K, Pawar A, Abraham P. Hereditary thrombophilia as a cause of Budd-Chiari syndrome: A study from Western India. Hepatology 2001;34:666-70.  Back to cited text no. 35
Sharma S, Kumar SI, Poddar U, Yachha SK, Aggarwal R. Factor V Leiden and prothrombin gene G20210A mutations are uncommon in portal vein thrombosis in India. Indian J Gastroenterol 2006;25:236-9.  Back to cited text no. 36
[PUBMED]  [Full text]  
Koshy A, Jeyakumari M. Factor V Leiden is not commonly associated with idiopathic portal vein thrombosis in Southern India. Indian J Gastroenterol 2006;25:140-2.  Back to cited text no. 37
[PUBMED]  [Full text]  
Shah SR, DasGupta A, Sharma A, Joshi A, Desai D, Abraham P. Thrombophilic conditions in non-cirrhotic portal vein thrombosis. Indian J Gastroenterol 2005;24:205-10.  Back to cited text no. 38
[PUBMED]  [Full text]  
Savoia F, Ferrara C, Sansone A, Bifulco G, Nappi C, Di Carlo C. Portal cavernoma during pregnancy. Case Rep Obstet Gynecol 2013;2013:396083.  Back to cited text no. 39
Dasari P, Balusamy S. Portal vein thrombosis during pregnancy. BMJ Case Rep 2013;2013. pii: bcr2012008325.  Back to cited text no. 40
Skupski DW, Brady D, Lowenwirt IP, Sample J, Lin SN, Lohana R, et al. Improvement in outcomes of major obstetric hemorrhage through systematic change. Obstet Gynecol 2017;130:770-7.  Back to cited text no. 41
Hall TC, Garcea G, Metcalfe M, Bilku D, Dennison AR. Management of acute non-cirrhotic and non-malignant portal vein thrombosis: A systematic review. World J Surg 2011;35:2510-20.  Back to cited text no. 42
Miura K, Sugawara Y, Uchida K, Kawabata S, Yoshii D, Isono K, et al. Adult living donor liver transplantation for patients with portal vein thrombosis: A single-center experience. Transplant Direct 2018;4:e341.  Back to cited text no. 43
Fukazawa K, Pretto EA Jr., Nishida S, Reyes JD, Gologorsky E. Factors associated with mortality within 24h of liver transplantation: An updated analysis of 65,308 adult liver transplant recipients between 2002 and 2013. J Clin Anesth 2018;44:35-40.  Back to cited text no. 44
Piardi T, Lhuaire M, Bruno O, Memeo R, Pessaux P, Kianmanesh R, et al. Vascular complications following liver transplantation: A literature review of advances in 2015. World J Hepatol 2016;8:36-57.  Back to cited text no. 45
Martinelli I, Ponziani FR, Maino A, Bhoori S, Abbattista M, Maggi U, et al. Thrombosis after liver transplantation for hepatocellular carcinoma. PLoS One 2017;12:e0186699.  Back to cited text no. 46
Woo DH, Laberge JM, Gordon RL, Wilson MW, Kerlan RK Jr. Management of portal venous complications after liver transplantation. Tech Vasc Interv Radiol 2007;10:233-9.  Back to cited text no. 47
Audet M, Piardi T, Panaro F, Cag M, Habibeh H, Gheza F, et al. Four hundred and twenty-three consecutive adults piggy-back liver transplantations with the three suprahepatic veins: Was the portal systemic shunt required? J Gastroenterol Hepatol 2010;25:591-6.  Back to cited text no. 48
Schmitz V, Schoening W, Jelkmann I, Globke B, Pascher A, Bahra M, et al. Different cava reconstruction techniques in liver transplantation: Piggyback versus cava resection. Hepatobiliary Pancreat Dis Int 2014;13:242-9.  Back to cited text no. 49
Charco R, Fuster J, Fondevila C, Ferrer J, Mans E, García-Valdecasas JC. Portal vein thrombosis in liver transplantation. Transplant Proc 2005;37:3904-5.  Back to cited text no. 50
Fayek SA, Quintini C, Chavin KD, Marsh CL. The current state of liver transplantation in the United States: Perspective from American Society of Transplant Surgeons (ASTS) scientific studies committee and endorsed by ASTS council. Am J Transplant 2016;16:3093-104.  Back to cited text no. 51
Al Saeed M. Portal Vein Thrombosis after Splenectomy. Egypt J Hosp Med 2012;48:496-503.  Back to cited text no. 52
Jiang GQ, Bai DS, Chen P, Xia BL, Qian JJ, Jin SJ. Predictors of portal vein system thrombosis after laparoscopic splenectomy and azygoportal disconnection: A retrospective cohort study of 75 consecutive patients with 3-months follow-up. Int J Surg 2016;30:143-9.  Back to cited text no. 53
Mesa RA, Nagorney DS, Schwager S, Allred J, Tefferi A. Palliative goals, patient selection, and perioperative platelet management: Outcomes and lessons from 3 decades of splenectomy for myelofibrosis with myeloid metaplasia at the Mayo Clinic. Cancer 2006;107:361-70.  Back to cited text no. 54
Mohren M, Markmann I, Dworschak U, Franke A, Maas C, Mewes S, et al. Thromboembolic complications after splenectomy for hematologic diseases. Am J Hematol 2004;76:143-7.  Back to cited text no. 55
Amitrano L, Guardascione MA, Brancaccio V, Margaglione M, Manguso F, Iannaccone L, et al. Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis. J Hepatol 2004;40:736-41.  Back to cited text no. 56
Sogaard KK, Astrup LB, Vilstrup H, Gronbaek H. Portal vein thrombosis; risk factors, clinical presentation and treatment. BMC Gastroenterol 2007;7:34.  Back to cited text no. 57
Brandt LJ, Feuerstadt P. Intestinal ischemia. In: Feldman M, Friedman LS, Brandt LJ, editors. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 9th ed. Philadelphia: WB Saunders; 2010.  Back to cited text no. 58
Abu-Daff S, Abu-Daff N, Al-Shahed M. Mesenteric venous thrombosis and factors associated with mortality: A statistical analysis with five-year follow-up. J Gastrointest Surg 2009;13:1245-50.  Back to cited text no. 59
Besa C, Cruz JP, Huete A, Cruz F. Portal biliopathy: A multitechnique imaging approach. Abdom Imaging 2012;37:83-90.  Back to cited text no. 60
Van Gansbeke D, Avni EF, Delcour C, Engelholm L, Struyven J. Sonographic features of portal vein thrombosis. AJR Am J Roentgenol 1985;144:749-52.  Back to cited text no. 61
Parvey HR, Eisenberg RL, Giyanani V, Krebs CA. Duplex sonography of the portal venous system: Pitfalls and limitations. AJR Am J Roentgenol 1989;152:765-70.  Back to cited text no. 62
Tessler FN, Gehring BJ, Gomes AS, Perrella RR, Ragavendra N, Busuttil RW, et al. Diagnosis of portal vein thrombosis: Value of color Doppler imaging. AJR Am J Roentgenol 1991;157:293-6.  Back to cited text no. 63
Parvey HR, Raval B, Sandler CM. Portal vein thrombosis: Imaging findings. AJR Am J Roentgenol 1994;162:77-81.  Back to cited text no. 64
Aguirre DA, Farhadi FA, Rattansingh A, Jhaveri KS. Portal biliopathy: Imaging manifestations on multidetector computed tomography and magnetic resonance imaging. Clin Imaging 2012;36:126-34.  Back to cited text no. 65
Lee HK, Park SJ, Yi BH, Yeon EK, Kim JH, Hong HS. Portal vein thrombosis: CT features. Abdom Imaging 2008;33:72-9.  Back to cited text no. 66
Attali J, Heurgue A, Loock M, Thiefin G, Marcus C, Long A. Computed tomography follow-up of acute portal vein thrombosis. Diagn Interv Imaging 2014;95:579-85.  Back to cited text no. 67
Berzigotti A, García-Criado A, Darnell A, García-Pagán JC. Imaging in clinical decision-making for portal vein thrombosis. Nat Rev Gastroenterol Hepatol 2014;11:308-16.  Back to cited text no. 68
Lai L, Brugge WR. Endoscopic ultrasound is a sensitive and specific test to diagnose portal venous system thrombosis (PVST). Am J Gastroenterol 2004;99:40-4.  Back to cited text no. 69
Palazzo L, Hochain P, Helmer C, Cuillerier E, Landi B, Roseau G, et al. Biliary varices on endoscopic ultrasonography: Clinical presentation and outcome. Endoscopy 2000;32:520-4.  Back to cited text no. 70
Shah TU, Semelka RC, Voultsinos V, Elias J Jr., N Altun E, Pamuklar E, et al. Accuracy of magnetic resonance imaging for preoperative detection of portal vein thrombosis in liver transplant candidates. Liver Transpl 2006;12:1682-8.  Back to cited text no. 71
Orloff MJ, Hye RJ, Wheeler HO, Isenberg JI, Haynes KS, Vaida F. Randomized trials of endoscopic therapy and transjugular intrahepatic portosystemic shunt versus portacaval shunt for emergency and elective treatment of bleeding gastric varices in cirrhosis. Surgery 2015;157:1028-45.  Back to cited text no. 72
D'Amico G, De Franchis R; Cooperative Study Group. Upper digestive bleeding in cirrhosis. Post-therapeutic outcome and prognostic indicators. Hepatology 2003;38:599-612.  Back to cited text no. 73
Boyer TD. Management of portal vein thrombosis. Gastroenterol Hepatol (N Y) 2008;4:699-700.  Back to cited text no. 74
Loffredo L, Pastori D, Farcomeni A, Violi F. Effects of anticoagulants in patients with cirrhosis and portal vein thrombosis: A systematic review and meta-analysis. Gastroenterology 2017;153:480-70.  Back to cited text no. 75
Francoz C, Valla D, Durand F. Portal vein thrombosis, cirrhosis, and liver transplantation. J Hepatol 2012;57:203-12.  Back to cited text no. 76
Ozdogan M, Gurer A, Gokakin AK, Kulacoglu H, Aydin R. Thrombolysis via an operatively placed mesenteric catheter for portal and superior mesenteric vein thrombosis: Report of a case. Surg Today 2006;36:846-8.  Back to cited text no. 77
Harnik IG, Brandt LJ. Mesenteric venous thrombosis. Vasc Med 2010;15:407-18.  Back to cited text no. 78
Grisham A, Lohr J, Guenther JM, Engel AM. Deciphering mesenteric venous thrombosis: Imaging and treatment. Vasc Endovascular Surg 2005;39:473-9.  Back to cited text no. 79
Lindblad B, Håkansson HO. The rationale for “second-look operation” in mesenteric vessel occlusion with uncertain intestinal viability at primary surgery. Acta Chir Scand 1987;153:531-3.  Back to cited text no. 80
Kaminsky O, Yampolski I, Aranovich D, Gnessin E, Greif F. Does a second-look operation improve survival in patients with peritonitis due to acute mesenteric ischemia? A five-year retrospective experience. World J Surg 2005;29:645-8.  Back to cited text no. 81


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]


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