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| CASE REPORT |
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| Year : 2018 | Volume
: 3
| Issue : 1 | Page : 36-40 |
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Portal vein thrombosis occurring after laparoscopic sleeve gastrectomy: A short series and review of literature
Yasmine Shafik, Tariq Jaber
Department of General Surgery, King Abdulaziz Medical City, Ministry of the National Guard-Health Affairs, Jeddah, Saudi Arabia
| Date of Web Publication | 17-Aug-2018 |
Correspondence Address:
Tariq Jaber
Department of General Surgery, King Abdulaziz Medical City, Ministry of the National Guard-Health Affairs, P. O. Box. 6366, Jeddah 21423
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/SJL.SJL_4_18
The prevalence of obesity in Saudi Arabia was 28.7% in 2013, and similar to the west, laparoscopic sleeve gastrectomy (LSG) is nowadays one of the most commonly performed bariatric procedures in Saudi Arabia. Portal vein thrombosis (PVT) was at first thought to be a rare and potentially fatal occurrence postoperatively. Recent data suggest that it is much more prevalent following LSG of all other bariatric procedures, and prognosis is favorable given early diagnosis and treatment. The aim of this article was to describe three cases of PVT post-LSG encountered at our institution and provide a brief review of the literature. Keywords: Bariatric surgery, laparoscopic sleeve gastrectomy, mesenteric vein thrombosis, portal vein thrombosis, portomesenteric vein thrombosis
How to cite this article:
Shafik Y, Jaber T. Portal vein thrombosis occurring after laparoscopic sleeve gastrectomy: A short series and review of literature. Saudi J Laparosc 2018;3:36-40 |
How to cite this URL:
Shafik Y, Jaber T. Portal vein thrombosis occurring after laparoscopic sleeve gastrectomy: A short series and review of literature. Saudi J Laparosc [serial online] 2018 [cited 2023 Mar 23];3:36-40. Available from: https://www.saudijl.org/text.asp?2018/3/1/36/239214 |
| Introduction | |  |
Portal vein thrombosis (PVT) refers to the complete or partial obstruction of blood flow in the portal vein, due to the presence of a “thrombus” in the vessel lumen. It can be intra- or extrahepatic and may also extend upstream to the splenic and/or the mesenteric veins.[1] Laparoscopic sleeve gastrectomy (LSG) has recently become a very popular weight loss surgery because of good results and low morbidity.[2] PVT was once thought to be a rare complication following LSG;[3] however, there are reports suggesting that its incidence surpasses that of pulmonary embolism.[3],[4],[5] The first report of PVT occurring after LSG was by Berthet et al. in 2009.[6] To the best of our knowledge, at least 60 other cases have been reported ever since then. PVT occurs after various bariatric procedures but not as frequently as seen with LSG.[7] A retrospective review of 4386 patients who underwent bariatric surgery observed 10 cases of PVT, all occurring after LSG.[7] Another report even concluded that LSG appears to be an independent risk factor for PVT.[8] With an incidence of 0.55%–1%,[4],[5],[7],[9],[10],[11] PVT post-LSG is not without sequelae and can cause nonsalvageable bowel ischemia and death, especially in the setting of delayed treatment.[11] Signs and symptoms are often nonspecific,[12] and the diagnosis is readily made with computed tomography (CT).[3],[13],[14] The etiology is multifactorial with local and systemic factors working in concert.[3] Herein, we report three cases and present a review of current literature.
| Case Reports | | |
Case 1
A 33-year-old medically free gentleman presented to our bariatric service due to Class I obesity with a body mass index (BMI) of 35 kg/m 2 after several unsuccessful attempts at weight reduction following conventional diet regimens and exercise plans. He was a heavy hookah smoker and had dyslipidemia, back pain, and a family history of unprovoked deep venous thrombosis.
All preoperative laboratory investigations were unremarkable, and he was offered an LSG as management for his weight. The patient consented accordingly.
On call to the operating theater, the patient was given 5000 IU of intravenous (IV) unfractionated heparin. Intraoperatively, pneumatic sequential devices were applied to the lower limbs, insufflation pressure was set to 14 mmHg, a liver retractor was not used, and the entire procedure lasted for 2 h and 8 min.
Our patient tolerated the procedure well and was kept on IV unfractionated heparin 5000 IU BID till he was discharged on postoperative day (POD) 2 after a gastrografin study ruled out the presence of a leak. He was discharged on subcutaneous injections of low-molecular-weight heparin (LMWH) at 40 mg OD for a total of 21 days.
On POD 28, the patient presented with abdominal pain radiating to the back that progressively worsened and became associated with back pain, nausea, and vomiting. His symptoms had started on POD 14. On presentation, his abdomen was soft and lax with maximal tenderness at the epigastric area and no signs of peritonitis. All laboratory values were within normal. A CT scan of the abdomen and pelvis with oral and IV contrast was performed and revealed extensive filling defects involving the right, left, and main portal veins, as well as the proximal splenic and superior mesenteric veins. Bowel loops did not show any evidence of ischemia, and there were no intra-abdominal collections.
Accordingly, the patient was admitted to the surgical ward, given nil by mouth nil per oral, and started on therapeutic anticoagulation with 90 mg of subcutaneous LMWH followed by warfarin titrated to keep the international normalized ratio (INR) between 2 and 3. Antithrombin III, functional protein C, and protein S levels were within normal levels along with no mutations in the JAK2 gene. Throughout the hospital course, the patient's abdominal pain and food intolerance gradually improved and he was eventually discharged home.
The patient received warfarin for a total of 6 months, and a follow-up ultrasound at the end of his treatment period revealed patency of the splenic, superior mesenteric, and portal veins with evidence of cavernous transformation in the porta hepatis.
Case 2
A medically free 52-year-old woman who suffered from Class III morbid obesity (BMI 43.9) presented to our bariatric service seeking LSG for weight management. She reported being a heavy hookah smoker. Again, preoperative workup was unremarkable.
On call to the operating theater, the patient was given 5000 IU of IV unfractionated heparin. Intraoperatively, pneumatic sequential devices were applied to the lower limbs, insufflation pressure was set to 14 mmHg, a liver retractor was not used, and the entire procedure lasted for 2 h and 20 min.
The patient tolerated the procedure well and her hospital course was unremarkable. No leak was evident on the postoperative gastrografin study, and the patient was discharged on POD 2 with LMWH for 14 days.
On POD 21, the patient returned complaining of epigastric abdominal pain that was radiating to the back and flanks with associated nausea. She was uncompliant with the postoperative prophylactic anticoagulation regimen. Vitally, she was stable, and physical examination revealed a soft and lax abdomen with maximal tenderness at the epigastric region. Blood works were unremarkable, and CT with IV and oral contrast revealed main portal vein, right portal vein, and superior mesenteric vein thromboses associated with fat stranding. Focal wall thickening of the proximal jejunum was present as well without any evidence of pneumatosis intestinalis, leak, bowel obstruction, or intra-abdominal collections.
The patient was treated conservatively and was started on full anticoagulation followed by warfarin titrated to antifactor X levels between 0.6 and 1 and INR levels between 2 and 3, respectively. The patient's pain and ability to tolerate an enteral diet responded well to treatment, and there were no complications throughout her admission. She was discharged after 5 days on warfarin.
During the patient's 3-month follow-up visit and upon completion of her course of anticoagulation, a review of a repeat CT of the abdomen revealed complete resolution of the thromboses with normal appearance of the previously affected bowel loops.
Case 3
A 43-year-old gentleman who is known to have hypertension, dyslipidemia, ischemic heart disease, and Class III obesity (BMI 41.3) presented to our service for weight reduction. Besides being a heavy smoker, the patient had no other evident risk factors for thrombosis. His pre-LSG workup was unremarkable after which he underwent a standard uneventful LSG. The procedure lasted 2 h and 33 min and venous thromboembolic precautions taken were like those followed in the abovementioned cases. He was discharged on POD 2 after ensuring that there was no anastomotic site leak on 40 mg of subcutaneous enoxaparin for 3 weeks.
The patient returned to the emergency department on the 18th day postoperatively complaining of colicky abdominal pain that was radiating to the back and was associated with vomiting and decreased oral intake for a week. His epigastrium was tender; however, the abdomen was soft and lax without any signs of peritonitis. Laboratory parameters including the white blood cell count were within normal ranges. An enhanced CT scan of the abdomen and pelvis revealed thrombosis of the main and right portal veins and the entirety of the splenic and superior mesenteric veins as well. Furthermore, there was segmental bowel wall thickening in the mid-jejunum but no other signs of vascular compromise.
Accordingly, the patient was started immediately on therapeutic enoxaparin (100 mg subcutaneously Q12 h) followed by warfarin. Gradually, the patient's symptoms improved and he regained the ability to tolerate orally, responding to anticoagulation and conservative management alone.
| Discussion | | |
Since 2005, at least 64 cases of PVT post-LSG have been reported in the literature, with 50% of reports being in 2015 and 2016 alone. LSG was first described in 1988 by Hess as part of biliopancreatic diversion with duodenal switch (BPD/DS). Today, LSG is recognized as a stand-alone procedure and has gained increased support and popularity.[15] According to the American Society for Metabolic and Bariatric Surgery, numbers of LSG have steadily risen from 17.8% in 2011 to 53.8% in 2015. Rates of Roux-en-Y gastric bypass and BPD/DS, on the contrary, are much lower with 23.1% and 0.6%, respectively.[16] The current documented incidence of PVT post-LSG reaches up to 1% which is much higher than that observed after other/abdominal/bariatric procedures.[4],[5] In our practice, 3 out of our first 500 patients undergoing LSG developed PVT with an incidence of 0.6%. There are higher rates of PVT post-LSG even compared with those occurring post-BPD/DS.[12] Rottenstreich et al. recently published a retrospective review of 4386 patients who underwent bariatric surgery between 2006 and 2016. Ten patients developed PVT, all occurring after LSG.[7] Similarly, Goitein et al.'s multicenter retrospective review of 5706 patients who underwent bariatric surgery between 2007 and 2012 showed that all but one cases of PVT occurred after LSG.[15] Carlin et al. also concluded that LSG appears to be an independent risk factor for the development of PVT.[8] It remains unclear if this increased incidence is merely due to the increasing frequency of the procedure or is because LSG might be an actual independent risk factor for the occurrence of PVT.
The etiology of PVT post-LSG is probably multifactorial where local and systemic factors concur.[3] Metabolic syndrome and the thromboembolic risk of obesity, smoking, use of oral contraception, dehydration secondary to subsequent poor oral intake, and undiagnosed inherited thrombophilias are systemic contributors.[10] Vascular wall injury to the left gastroepiploic arcade or short gastric vessels and probable splenic vein contact during LSG are also plausible local predisposing factors.[3],[5],[17] Laparoscopy particularly renders splanchnic vascular physiology vulnerable to thrombosis.[5] Flow in the splanchnic and portal vessels has been found to be inversely proportional to pneumoperitoneum, and intra-abdominal pressure >14 mmHg results in >50% reduction in portal blood flow. In addition, hypercapnia induced by CO2 insufflation causes vasoconstriction of the splanchnic system, which further reduces blood flow.[10],[12] A systemic procoagulant etiology is identified in approximately 60% of patients [14] and an additional local predisposing factor in 30%.[18] Nevertheless, 20% of cases have been reported to be idiopathic.[7] All three of our patients suffered from morbid obesity and were avid smokers. One patient was worked up for thrombophilia and results came back negative.
As per clinical practice guidelines set forward by the American College of Chest Physicians, all bariatric patients have a moderate-to-high risk of developing thromboembolic events. Accordingly, chemical prophylaxis, with or without mechanical prophylaxis, is normally offered to all bariatric patients. These guidelines, although standard of treatment today, are based on randomized controlled trials in patients undergoing abdominal and pelvic surgery. To top that, there is a lack of consensus with regard to the dose, frequency, and duration of thromboprophylaxis in the bariatric population.[7] Evidence suggests that over 74% of venous thromboembolic events occur after discharge and well beyond 30 days after surgery.[19] Extended thromboprophylaxis has been advocated by several authors for the prevention of PVT post-LSG.[20] The exact duration, however, is yet to be determined.[7] We have recently changed our practice where patients are discharged on prophylactic low-molecular-weight heparin BID for a period of 28 days. Operative times have been cut in half, and in the last 500 cases, no symptomatic PVT has been encountered. Patients in our case series responded to conservative management and anticoagulation alone.
The clinical presentation of PVT is vague, and a high index of suspicion is essential to making the diagnosis.[7] Patients most commonly complain of colicky abdominal pain that radiates to the back.[17] The presence of nausea, vomiting, and fever is less consistent; abdominal examination often reveals tenderness but is otherwise unremarkable unless the patient has associated bowel ischemia. No laboratory investigation is pathognomonic, but it is not uncommon to find leukocytosis, an increase in inflammatory markers, and elevated liver enzymes. The diagnosis is often made when patients undergo a CT scan to rule out more common complications post-LSG such as leak.[7] Enhanced CT scans are 90% sensitive and considered the diagnostic modality of choice. Doppler ultrasonography has low sensitivity; however, it provides an accessible and cost-effective means for follow-up of patency of the splanchnic veins.[10]
Prompt anticoagulation should always be instituted once the diagnosis is confirmed.[10] Besides limiting the propagation of thrombosis and leaving the bowel more liable to ischemia, early anticoagulation was found to correlate with a survival benefit, decreased recurrence rates, and decreased secondary portal cavernomatosis.[12] Portal cavernomatosis, also called cavernous transformation of the portal vein, is a sequela of PVT and is the replacement of the normal single channel portal vein with numerous tortuous venous channels. As these collateral channels are usually insufficient to bypass the entire splenomesenteric inflow, the signs of portal hypertension frequently coexist.[3],[6] Anticoagulation is continued for 3–6 months and until there is complete resolution of the thrombus.[12] Lifelong anticoagulation is necessary for patients with thrombophilia.[21] Surgery is reserved for patients presenting with severe ischemia and peritonitis.[10],[11],[12],[13],[22] Thrombolysis and thrombectomy have also been described for the management of high-grade nonocclusive and occlusive PVT, respectively.[23]
| Conclusion | | |
PVT post-LSG is a unique entity and is not an uncommon complication. Most patients have favorable outcomes and management is as simple as anticoagulation. A multitude of risk factors contribute to the development of thrombosis and a high index of suspicion is essential for ensuring a head start with management. Further research is required to identify the true incidence of PVT post-LSG, evaluate independent risk factors for the development of such complication, and determine the dose and duration of optimal postoperative prophylactic anticoagulation.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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