|Year : 2019 | Volume
| 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
Mohamed Salem Al Saeed1, Bilal O Al-Jiffry1, Alaa Younes1, Samir Badr2, Tamer Abdel-Rahman3, Mohamed Hatem4, Mahmoud El-Meteini5
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 Publication||9-Dec-2019|
Dr. Mohamed Salem Al Saeed
Department of Surgery, College of Medicine, Taif University, P.O. Box: 888, Taif 21947
Source of Support: None, Conflict of Interest: None
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 Jan 25];8:182-90. Available from: http://www.saudijhealthsci.org/text.asp?2019/8/3/182/272445
| Introduction|| |
Portal vein thrombosis (PVT) is a serious complication of liver cirrhosis and other thrombophilic disorders.,, 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., The incidence of PVT is underestimated as it may be asymptomatic or present with nonspecific symptoms, especially in cirrhotic patients.,,,,,, 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.,,, Early identification of patients with PVT would prevent potentially fatal complications such as bowel infarction or development of portal hypertension. 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., In chronic PVT serpiginous collaterals will replace the portal vein, and it takes 12–60 days to be radiologically evident. In cirrhotic patients, PVT accelerates the liver impairment and worsens the prognosis; however, in noncirrhotic patients, hepatic derangement is minor., D-dimer testing may help in rolling out PVT sparing patients the unnecessary risks of anticoagulation, but its diagnostic accuracy is low.,, Early diagnosis and prompt treatment would help recanalization that improves outcome.,,,, 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|| |
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|| |
[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).
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|| |
The incidence of PVT is variable, where it reaches 15% in advanced cirrhosis versus <0.5% in autopsy studies. 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).,,
In the current report, male predominance is much higher than that recorded in the literature in both cirrhotic and noncirrhotic patients.,,,
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.,
Said et al. and Khayyat 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., 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., and Khayyat 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.,, 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., 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.,,,,
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.,,
Pancreatitis and intra-abdominal sepsis, especially when peritonitis is established are involved in the development of PVT. Hamidi et al. isolated bacterial endotoxins from the portal blood in advanced cirrhosis emphasizing its role in the activation of thrombus formation mechanisms. Ni et al. reported that Bacteroides fragilis 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.,,, 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. 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. 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 in her study about primary thrombophilia in Saudi Arabia in patients with venous thromboembolic disorders support our findings. Lisman and Porte 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., Sharma et al., Koshy and Jeyakumari, and Shah et al. 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. and Dasari and Balusamy 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.,
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.,,,,, Woo et al. 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. reported other additional factors as; the presence of portal thrombosis prior to OLT, development of acute rejection, and previous splenectomy. Ghabril et al. found that PVT was detected in 50%–70% of explanted cirrhotic livers during liver transplantation, a finding which has been documented in other studies.,,,,,,,,, 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 found in his study on postsplenectomy PVT that the pesence of malignancy was the most important preoperative risk factor. Jiang et al. emphasized on the surgical intervention itself including duration, open or laparoscopic splenectomy. Mesa et al. and Mohren et al. 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 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. 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. 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.,,
Amitrano et al. attested in their study that PVT with mesenteric venous involvement is never asymptomatic and lead to intestinal ischemia or infarction. Al Saeed et al., Al Saeed et al., Brandt and Feuerstadt, and Abu-Daff et al. 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. These findings are in agreement with our results.
Dai et al., Zhang et al., and Altinyollar et al., 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.,,,, The ultrasound sensitivity and specificity for detection of PVT ranges from 80% to 100% with a diagnostic accuracy of 88%–98%.
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.,,,, 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.,,,
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.,,,,,
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%., 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. 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., Loffredo et al. 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.
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. Until recently, the presence of PVT was considered a relative contraindication of OLT; yet, Woo et al., Audet et al., and Schmitz et al. 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.
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.
Once intestinal infarction is suspected, the abdomen must be explored with resection of the nonviable segments of intestine.,,,,, Lindblad and Håkansson and Kaminsky et al. 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.,,,,,, 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., The previous findings are concordant with that reported in the current study.
| 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.
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]