Massive Portal Vein Thrombosis Three Weeks Following Laparoscopic Sleeve Gastrectomy

| June 1, 2017

by Bryce m. Bludevich, MS-IV; Sean M. Wrenn, MD; and Wasef Abu-Jaish, MD, FACS, FASMBS

AUTHOR AFFILIATION: Bryce M. Bludevich, MSIV, and Sean M. Wrenn, MD, are from the Department of Surgery, University of Vermont Medical Center, Burlington Vermont. Wasef Abu-Jaish MD, FACS, FASMBS, is Associate Professor of Surgery, The Robert Larner, M.D. College of Medicine at The University of Vermont, Burlington, Vermont, and Director, The Bariatric & Metabolic Surgery Program, Department of Surgery, The Univesity of Vermont Medical Center, Burlington, Vermont.

FUNDING: No funding was provided.

DISCLOSURES: The authors report no conflicts of interest relevant to the content of this manuscript.


The authors present a case of portal vein thrombosis three weeks postoperatively following a laparoscopic sleeve gastrectomy, which was also complicated by a concurrent episode of diverticulitis. They discuss the case and provide a review of the literature pertaining to postoperative portal vein thrombosis, a rare and potentially fatal complication that can follow bariatric surgery. They retrospectively review the case as compared to others reported in the literature and conclude that alarmingly vague presenting symptoms of abdominal pain, diarrhea, or constipation, nausea, and vomiting are similar throughout. The authors conclude that both physicians and patients should be made aware of the possible complication of portal venous thrombosis, and the potential symptoms. They conclude that further study is needed to determine if the standard of care anticoagulation given to bariatric patients is sufficient to prevent possible venous thromboembolisms or if the surgical technique used to complete a sleeve gastrectomy needs to be standardized. Additionally, further study should focus on increasing the length of anticoagulation therapy post-operation, along with identifying the most effective anticoagulant agent.

KEYWORDS: Laparoscopic sleeve gastrectomy, portal vein thrombosis, diverticulitis, morbid obesity

Bariatric Times. 2017;14(6):18–22


Obesity is epidemic in the United States and worldwide. The adverse effects of obesity on health and longevity were formally recognized and established by the National Institutes of Health in 1985.[1] Metabolic and bariatric surgery have been shown to be safe, and remain the most effective and durable treatments for clinically severe obesity with a documented reduction in all-cause mortality and long-term survival benefit.[2] Laparoscopic Roux-en-Y gastric bypass (RYGB) was the most common bariatric procedure performed in the United States from 2004 to 2012, after which sleeve gastrectomy (SG) became the most common procedure.[3] Laparoscopic sleeve gastrectomy was originally designed as the first step procedure in a duodenal switch or a Roux-en-Y gastric bypass procedure, but has gained popularity as a stand-alone procedure given its similar results in weight loss and resolution in comorbid conditions.[4] As worldwide obesity rates and, in turn bariatric procedures increase, complications of these surgeries are being reported in the literature. Venous thromboembolism (VTE) is one of the most common postoperative complications following bariatric surgery, with deep venous thrombosis (DVT) being the most common etiology, followed by pulmonary embolism.[5] In 2013 the American Society of Metabolic and Bariatric Surgeons (ASMBS) issued an update on prophylactic measures to reduce the risk of VTE in bariatric patients.

Case Report

A 36-year-old Caucasian woman with a history of a recent laparoscopic sleeve gastrectomy (weight: 162.478kg, body mass index [BMI]: 58.96kg/m2) and hiatal hernia repair with anterior cruroplasty in late 2015 presented to the emergency department three weeks following surgery with increasing abdominal pain. She also complained of mustard brown diarrhea, dark urine, weakness, and fatigue; her remaining review of systems was negative.

Her past medical history was significant for asthma, obstructive sleep apnea (treated with continuous positive airway pressure therapy [CPAP]), gastroesophageal reflux disease (GERD), alpha thalassemia (a blood disorder that reduces the production of hemoglobin), depression, and morbid obesity. Her medications at the time of presentatin were as follows: aspirin 81mg daily, omeprazole 40mg PO (by mouth) daily, bupropion 300mg PO daily, fluticasone/salmetrol inhaler, levalbuterol, montelukast, ondansetron, loratidine, and an oral contraceptive pill (OCP [ethinyl estradiol and levonorgestrel]). Patient reported that she had been on the OCP for 10 to 15 years except during pregnancy; she had two full-term pregnancies. She stopped taking the medication prior to several days prior to surgery as per pre-operative instructions.

Her past surgical history was significant for a recent laparoscopic sleeve gastrectomy and hiatal hernia repair with anterior cruroplasty (2015) laparoscopic cholecystectomy (2004), and two caesarian sections (2002, 2008).

She was a former smoker (1pack per day for 15 years), having quit one year prior to presentation (quit date of 8/2014). She denied alcohol or recreational drug use. Her family medical history was unknown given that she was adopted.

Upon arrival to the emergency room, the patient was hemodynamically stable. Her physical exam was only remarkable for tenderness to palpation in the epigastric region, right upper quadrant and left lower quadrant without peritoneal signs. Her recent surgical incisions were all healing well without erythema or drainage. Laboratory findings were significant for leukocytosis (15.45 k/mm), thrombocytosis (526 k/mm), and elevated ALT (983 U/L), AST (647 U/L), and alkaline phosphatase (147 U/L). Her lipase, electrolytes, urinalysis, and hepatitis viral panel were all within normal limits.

An initial computerized tomography (CT)scan of her abdomen with PO contrast showed clear lung bases, and no abnormality of the spleen, pancreas, or adrenal glands. The portal venous system demonstrated hypoattenuation and mild dilation with adjacent stranding beginning at the confluence of the superior mesenteric and splenic veins consistent with an extensive acute portal venous thrombosis (PVT). There was no intrahepatic biliary ductal dilation (Figure 1). The gastric sleeve was without evidence of obstruction or contrast extravasation. There was no adjacent stranding or fluid (Figure 2). There were several diverticula noted throughout the colon. Within the sigmoid colon there was an area of complex fluid collection with a small tract extending toward the collection. The complex collection of fluid and gas anterior to the uterus and superior to the urinary bladder measuring 5 x 5.2 x 4 cm with significant fat stranding noted around the collection (Figure 3). There was no evidence of a high-grade obstruction or mural thickening. There was no free air in the peritoneal cavity.

She was started on therapeutic low-molecular weight heparin (LMWH)and was treated for her pelvic abscess. The collection was drained by interventional radiology (IR). Subsequent tube studies showed a communicating fistula between the abscess cavity and the colon. She displayed improvement following the drainage of the abscess and was discharged home on therapeutic anticoagulation (Figure 3).

Two weeks following drain removal she presented again with the same symptoms. A repeat CT scan showed another fluid collection in the left lower quadrant and showed that the PVT remained stable and was beginning to decrease in caliber. The thrombosis of the peripheral branches of the portal vein were unchanged. There was an increase in the caliber of multiple collateral vessels in the porta hepatis, which was compatible with cavernous transformation (Figure 4). The new fluid collection was again drained by IR. Following these imaging studies, the care team decided to leave the drain in place until the patient’s colon resection was completed.


Portal vein thrombosis (PVT) can be a potentially devastating complication of laparoscopic surgeries, especially bariatric laparoscopic surgeries. Portomesenteric thrombosis can lead to mesenteric ischemia or infarction which can be life threatening.[6] Common risk factors that may lead to acute PVT are myeloproliferative disease, Janus kinase 2 (JAK 2) positive gene mutation, antiphospholipid syndrome (an autoimmune disease which can cause frequent clotting in arteries and veins), hormonal contraception or replacement therapy use, along with a personal history or family history of DVT.[7] Local factors, like acute pancreatitis, cholecystitis, or cholangitis, liver abscesses, or gastritis have also been found to be more common risk factors of PVT.[7]

PVT have been identified as possible complications of laparoscopic adjustable gastric banding and laparoscopic Roux-en-Y gastric bypass surgeries.[6],[8–13] There have been an increasing number of case reports about PVT following laparoscopic sleeve gastrectomies (LSG), which may be due to the increasing popularity of LSG.[6],[14],[15] Recently , Salinas et al completed a retrospective analysis of 1,713 LSGs and reported a one-percent incidence of portomesenteric vein thrombosis (PMVT).[16] LSG procedures have been found to be associated with a lower 30-day risk adjusted serious morbidity compared to laparoscopic gastric bypass and an equivalent 30-day mortality; which may in part explain its increasing popularity.[15] More commonly, possible complications of LSG include: staple line leaks, pulmonary embolism, DVTs, respiratory insufficiency, hemorrhage, stricture, and splenic injury.[6],[15] The vast majority of cases of PMVT that have been reported occur following LSG, and not laparoscopic gastric bypass surgery, potentially indicating that this particular complication may be procedurally related.[17]

Case reports of PVT in the bariatric population continue to note the importance of clinical suspicion when faced with a potential PVT in a recent operative patient given their non-specific presentations.[14],[18] Most patients tend to present with vague abdominal pain, diarrhea, or constipation, nausea, and vomiting, which are similar to the symptoms that generally follow major bariatric surgery.[4],[6],[18] Some surgeons have begun listing PVT as a formal complication of bariatric surgery and have begun to include it in the differential diagnosis for abdominal pain following bariatric surgery.[14]

The etiology of PVT can be divided into local and systemic causes, some of which can be controlled.[6],[19] Surgical manipulation of the portomesenteric vessels has been known to predispose patients to PVT, and can be avoided with good surgical technique.[6] Portal venous flow during the procedure is affected inversely by increased intraabdominal pressure with carbon dioxide pneumoperitoneum.[4] It is suspected that this inverse relationship may contribute to the prothrombotic state in the portomesenteric circulation, but it is unclear what intra-abdominal pressure level needs to be reached before this change in flow becomes clinically significant.[4],[6] Other factors that may contribute to increased prothrombotic state during LSG are the pro-inflammatory state associated with baseline obesity, visceral vasoconstriction secondary to intraoperative release of vasopressin, steep reverse Trendelenburg position, and retained CO2 causing increased portal pressure.[4],[6] In particular, this patient’s continued use of oral contraceptive pills after her surgery may have also contributed to her pro-coagulable state.[4]

Our Surgical Technique

For VTE (venous thromboembolic complications) prophylaxis, 5,000 units of unfractionated heparin is injected subcutaneously on the morning of the surgery. Following surgery, LMWH is continued during the patient’s hospitalization. Sequential compression devices are also used throughout surgery and following surgery. A second generation cephalosporin is also given prophylactically before surgery, and continued for 24 hours following surgery.

After the patient is prepped, draped, and trocars are placed; the patient is placed in slight reverse Trendelenburg position. Creation of pneumoperitoneum of 15mmHg then occurs and the liver is retracted with a liver retractor. The gastroesophageal (GE) junction is inspected for possible hiatal hernia, and the pylorus is identified. Dissection of the stomach from the greater omentum up to the GE junction then occurs. The left crus of the diaphragm at the GE junction is identified to ensure complete mobilization of the gastric fundus.

In this case the peritoneum covering over the left crus, as well as the right crus was taken down and the hernia sac was dissected. The esophagus was freed from nearby connective tissue and mobilized with confirmation of about 3cm intraabdominally. The hernia sac was excised together with a Murphy’s esophageal fat pad. The 40-French ViSiGi 3D™ (Boehringer Laboratories Inc., Phoenixville, Pennsylvania) bougie was then advanced under direct vision until the proximal pyloric channel, secured against the lesser curvature of the stomach and placed to suction. Hiatal hernia repair was completed by approximating the 2 crus anteriorly, anterior cruroplasty, using interrupted #1 figure-of-eight Ethibond (Ethicon, Inc., Cincinnati) one sutures while the bougie in place. The integrity of the repair was tested and confirmed to be tight enough, but without compressing the esophagus.

Insertion of the transoral bougie occurs, followed by vertical transaction of the stomach to create the gastric sleeve. Imbrication of the stable line is followed by the removal of the bougie. After testing the staple, a drain is placed and closure of the skin follows.

The definitive diagnosis of PVT can be made with non-invasive imaging, such as PO contrast enhanced CT abdomen imaging and/or color Doppler ultrasonography. Our patient received both of these imaging modalities, along with magnetic resonance angiogram (MRA) to monitor the stability of her clot.

Currently, no randomized control trials have been completed in the bariatric surgery population to determine the ideal chemoprophylaxis anticoagulation protocol for this patient population.[4] The routine chemoprophylaxis protocol used by many institutions continues to follow the protocol created by Carmody et al,[20] which was instituted in 1998 and includes a preoperative injections of 5,000 units of subcutaneous heparin and a daily injection of 40 units of LMWH following completion of the procedure.[4] Following the diagnosis of an acute PVT, previously recommended treatment algorithms have included systemic therapeutic anticoagulation in stable, non-cirrhotic patients along with treatment of any possible predisposing conditions. The suggested duration of anticoagulation was 6 to 12 months depending on the extent of the thrombus.6 However, these treatment algorithms remain in debate regarding optimum medical management of postoperative patients with acute PVT.

While treatment of PVT is essential, modifying risk factors prior to bariatric surgery may also be helpful. Factors associated with a high risk of VTE include: older age, elevated BMI, prior history of VTE, male gender, long procedure time (>3 hours), and procedure type (Duodenal switch > open gastric bypass > laparoscopic sleeve gastrectomy).[6],[4] Prolonging post-procedure anticoagulation in patients with many risk factors may be beneficial.


PVT is a rare and potentially fatal complication that can follow bariatric surgery. Recently, more reports of PVT following sleeve gastrectomy have been published, all with alarmingly vague presenting symptoms of abdominal pain, diarrhea, or constipation, nausea, and vomiting.[14],[18] Given this case presentation was complicated by a concurrent episode of diverticulitis, it is hard to know which issue occurred first—the portal venous thrombosis or the diverticular abscess. Physicians and patients should be made aware of the possible complication of PVT and the potential symptoms. Further study is needed to determine if the standard of care anticoagulation given to bariatric patients is sufficient to prevent possible venous thromboembolisms or if the surgical technique used to complete a sleeve gastrectomy needs to be standardized.


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3. Nguyen NT, Nguyen B, Gebhart A, et al. Changes in the makeup of bariatric surgery: a national increase in use of laparoscopic sleeve gastrectomy. J Am Coll Surg. 2013;216(2):252–257.

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12. De Roover A, Detry O, Coimbra C, et al. Pylephlebitis of the portal vein complicating intragastric migration of an adjustable gastric band. Obes Surg. 2006;16(3):369–371.

13. Pigeyre M, Seguy D, Arnalsteen L, et al. Laparoscopic gastric bypass complicated by portal venous thrombosis and severe neurologicalcomplications. Obes Surg. 2008; 18(9):1203–1207.

14. Bhatia P, John S, Kalhan S, et al. Portomesenteric venous thrombosis after laparoscopic sleeve gastrectomy: a case report and a call for prevention. J Minim Access Surg. 2015; 11(4):276–278.

15. Young M, Gebhart A, Phelan M, et al. Use and outcomes of laparoscopic sleeve gastrectomy vs laparoscopic gastric bypass: analysis of the American College of Surgeons NSQIP. J Am Coll Surg. 2015; 220(5):880–885.

16. Salinas J, Barros D, Salgado N, et al. Portomesenteric vein thrombosis after laparoscopic sleeve gastrectomy. Surg Endosc. 2014;28:1083–1089.

17. Lakis M, Pozzi A, Chamieh J, et al. Portomesenteric vein thrombosis after laparoscopic sleeve gastrectomy and laparoscopic Roux-en-Y gastric bypass: a 36-case series. Surg Endosc. 2017; 31:1005–1011.

18. Bellanger D, Hargroder A, Greenway F. Mesenteric venous thrombosis after laparoscopic sleeve gastrectomy. Surg Obes Relat Dis. 2010; 6(1):109–111.

19. Parikh S, Shah R, Kapoor P. Portal vein thrombosis. Am J Med. 2010; 123(2):111-119.

20. Carmody B, Sugerman H, Kellum J, et al. Pulmonary embolism complicating bariatric surgery: detailed analysis of a single institution’s 24 year experience. J Am Coll Surg. 2006; 203(6):831–837.

21. Jamal M, Corcelles R, Shimizu H, et al. Thromboembolic events in bariatric surgery: a large multi-institutional referral center experience. Surg Endosc. 2015; 29(2):376–380.

22. Rocha A, de Vasconcellos A, Luz Neto E, et al. Risk of venous thromboembolism and efficacy of thromboprophylaxis in hospitalized obese medical patients and in obese patients undergoing bariatric surgery. Obes Surg. 2006;16(12):1645–1655.

23. Goitein D, Matter I, Raziel A, et al. Portomesenteric thrombosis following laparoscopic bariatric surgery. JAMA Surg. 2013; 148(4):340–334.

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