Surgery for Obesity and Related Diseases ] (2014) 00–00
Case report
Sleeve gastrectomy and mesenteric venous thrombosis: report of 3 patients and review of the literature Amihai Rottenstreich*, Abed Khalaileh, Ram Elazary Department of General Surgery, Hadassah-Hebrew University Medical Center, Ein Kerem, Jerusalem, Israel Received July 3, 2014; accepted July 7, 2014
Keywords:
Bariatric; Laparoscopic; Thrombosis; Portal; Mesenteric
Mesenteric venous thrombosis (MVT) is a rare but potentially lethal pathology. Although first described by Balfour and Stewart in 1869 [1], it was first presented as a distinct cause of mesenteric ischemia by Warren and Eberhand only in 1935 [2]. MVT accounts for 5%–15% of all mesenteric ischemic events [2,3]. In the past, MVT has been described after procedures involving manipulation of the portal venous system, such as splenectomy or liver transplantation [4,5]. However, since the beginning of the minimal invasive era, MVT has occurred in several cases after various laparoscopic procedures [6]. During the last decade, a few cases of MVT have been published to occur after laparoscopic bariatric operations, including laparoscopic sleeve gastrectomy (LSG) [7]. Nevertheless, MVT has been shown to be a major morbidity during the perioperative period of LSG with an incidence of 1% [8]. The aim of this article is to present 3 cases of MVT that have occurred after 900 LSG procedures in our center, discuss the pathophysiology and management of this complication and suggest preventive strategy. Case 1 A 24-year-old man, height 168 cm, weight 110 kg, and body mass index (BMI) of 39 kg/m2, with a medical history of glucose 6 phosphokinase deficiency (G6 PD) deficiency and osteoarthritis of both knees. He underwent an uneventful LSG. The operative time was 1 hour. Prophylactic perioperative low molecular weight heparin (LMWH) was given. He * Correspondence: Amihai Rottenstreich, Department of Surgery, Hadassah-Hebrew University Medical Center, P.O. Box 12000 Jerusalem, Israel, 91120. E-mail: [email protected]
was discharged on postoperative day 4. On the 9th day postsurgery, he presented to the emergency department (ED) suffering from a 1-day history of epigastric pain. He also complained of nausea without vomiting, diarrhea, or other symptoms. His vital signs were normal. Physical examination revealed mild epigastric tenderness. Laboratory tests were within the normal limits, except for mild leukocytosis of 10,300/mm3 and elevated, twice normal, amylase level. Chest and plain abdominal radiographs were normal. Computed tomography (CT) demonstrated normal postoperative changes. The patient was discharged. Five days later, he came back to the ED with escalating abdominal pain accompanied by nausea and vomiting. On physical examination, mild epigastric tenderness was found. Amylase levels were increased up to 3 times normal. He was hospitalized for further evaluation. Additional interpretation of the CT taken at his initial ED visit revealed filling defects in the superior mesenteric vein (SMV) and right portal vein (RPV). An additional CT scan was performed and a thrombosis of both SMV and RPV were demonstrated with no change in comparison to the previous scan, alongside stranding fat around the pancreas and little edema noted in the right colon. Anticoagulation with LMWH was initiated and its effect monitored using antiXa levels. Duplex ultrasonography performed during admission demonstrated no evidence of flow in either SMV or RPV. The patient's symptoms improved, and he was discharged after 9 days of hospitalization. Postdischarge evaluation revealed positive lupusanticoagulant antibodies. Follow-up duplex ultrasonography scans done on 1, 2, and 5 months after discharge revealed lack of flow in the SMV and RPV. Only 9 months after discharge did recanalization of the veins and restoration of flow occur; however, their diameters were decreased.
http://dx.doi.org/10.1016/j.soard.2014.07.002 1550-7289/r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved.
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A. Rottenstreich et al. / Surgery for Obesity and Related Diseases ] (2014) 00–00
LMWH therapy was switched to warfarin and discontinued after 6 months without any further sequella. Case 2 A 50-year-old man, height 180 cm, weight 184 kg, and BMI of 56 kg/m2, with a medical history of H. pylori gastritis, epididymitis, essential hypertension, and G6 PD deficiency. He had undergone laparoscopic adjustable gastric banding 5 years before, and, because of insufficient weight loss and recurrent vomiting, he was referred to our department for conversion to LSG and band removal. The operation time was 2 hours. Prophylactic anticoagulation was given perioperatively. He was discharged on the 3rd postoperative day. Postoperative outpatient clinic follow-up was on the 6th and 23rd day postoperatively; he had no complaints and physical examination was unremarkable. On the 36th postoperative day, he presented to the ED suffering from epigastric pain lasting for 4 days, without nausea, vomiting, diarrhea, or other complaints. His vital signs were normal. Physical examination revealed moderate epigastric tenderness. The initial white blood cells count was 12,800/mm3, hemoglobin 12.5 g/dL, platelets 433,000/mm3, and bilirubin 1.5 mg/dL. Chest and plain abdominal radiographs were normal. CT demonstrated normal postoperative changes with fat stranding around the duodenum. The patient was treated with a proton pump inhibitor symptoms resolved and was discharged home. Two days later, he returned to the ED with severe abdominal pain associated with vomiting. His vital signs were normal. Periumbilical tenderness was noted without other peritoneal signs. Blood tests showed a leukocytosis of 17,000/mm3, gamma-glutamyl transferase (GGT) level was 113 U/L, and alkaline phosphatase level was 140 U/L. Total bilirubin remained 1.5 mg/dL, lactic acid 5.5 mmol/L, and C-reactive protein 14 mg/dL. He was admitted for further evaluation. A repeated CT scan was performed and thrombus in the SMV was demonstrated, alongside bowel wall thickening in the proximal ileum and a small to moderate amount of ascites. We initiated conservative treatment, which included nothing per oram and LMWH. Five days later, an additional CT scan demonstrated the same findings without improvement; however, a larger amount of ascites was noted. During hospitalization, his symptoms improved, and he was discharged after 24 days. CT scan performed 2 months after discharge showed chronic changes in the SMV. Doppler studies were not done. Workup after discharge for hypercoagulable states was normal. LMWH injections were converted to warfarin for completion of 6 months of anticoagulant therapy.
was given perioperatively. He was discharged on the third postoperative day. On the 13th postoperative day, he presented to the ED complaining of right upper quadrant and epigastric pain from the morning of admission, without nausea, vomiting, diarrhea, or other complaints. His vital signs were normal. Physical examination revealed mild epigastric tenderness. Laboratory findings showed an elevated alanine aminotransferase and aspartate aminotransferase 3.5, 2 times normal, respectively. GGT was 113 U/L. CT demonstrated MVT involving the splenic vein, SMV, and RPV (Fig. 1). He was admitted and anticoagulation with LMWH was started immediately after diagnosis, using antiXa levels for monitoring. During admission, we learned his family history of a brother who suffered from deep vein thrombosis and a mother who sustained multiple abortions. A family workup for thrombophilia had not been carried in the past. Duplex ultrasonography performed before discharge revealed complete occlusion of both RPV and SMV. The patient's symptoms improved, and he was discharged after 29 days of hospitalization. The patient refused to undergo workup for thrombophilia, and he was withdrawn from anticoagulants after 6 months and did well. Follow-up CT scan was not performed. Discussion Bariatric procedures have become quite common but are not entirely free of complications, which occur in up to 40% of patients [9]. MVT was first described to occur after LSG by Berthet et al. [7] in 2009. Recently, Salinas et al. [8] reported that among 1,713 patients undergoing LSG, 17 patients developed this complication.
Case 3 A 29-year-old man, height 174 cm, weight 133 kg, and BMI 43.8 kg/m2, with a medical history of hyperlipidemia and essential hypertension. He underwent uneventful LSG. The operative time was 1 hour. Prophylactic anticoagulation
Fig. 1. Computed tomography scan demonstrating a large filling defect in the superior mesenteric vein.
Sleeve Gastrectomy and Mesenteric Venous Thrombosis / Surgery for Obesity and Related Diseases ] (2014) 00–00
Mesenteric venous thrombosis is a rare but potentially lethal condition that requires a high index of suspicion. It could be classified as primary, where no obvious cause could be found, and secondary, where a specific cause or predisposing condition is identified. Primary cases represent 50%, although recent studies found that in 80% of cases an identifiable cause could be found [10,11]. Therefore a diagnostic workup for hypercoagulable states should be done after the diagnosis of MVT. Only assays for heparinplatelet factor 4 antibodies, hyperhomocysteinemia, anticardiolipin antibodies, and prothrombin 20210 and factor V leiden mutations are reliable during the initial event, and other tests should be performed remote from the initial presentation at least 2–3 weeks after cessation of anticoagulation [12]. Goitein et al. [13] reported that a third of the patients who suffered from MVT after laparoscopic bariatric surgery had a personal history of venous thromboembolism (VTE). A personal or familial history of VTEs should be elicited at the preoperative evaluation. The etiology of this complication after laparoscopic surgery and specifically bariatric surgery is probably multifactorial. Obesity itself is a known risk factor for VTE especially deep vein thrombosis of the lower limbs [14]. This could be attributed to several factors, such as a chronic inflammatory state associated with obesity, the metabolic syndrome found in a significant portion of these obese patients, increased abdominal pressure, venous stasis in the lower limbs and a sedentary lifestyle [13,15,16]. Regarding the laparoscopic surgical technique, several mechanisms might be involved. Hypercarbia, induced by CO2 insufflation, decreases splanchnic blood flow by mesenteric vasoconstriction [17]. Moreover, the increased intra-abdominal pressure (IAP) leads to decreased mesenteric and portal venous flow via direct pressure-induced compression [6]. Haglund et al. [18] demonstrated an inverse correlation between IAP and portal venous flow. Other factors that might contribute are visceral vasoconstriction induced by intraoperative vasopressin release, increased portal pressure due to retained CO2, the reverse Trendelenberg position, and prolonged operative times [19– 22]. One study suggested that the use of bipolar coagulation during the procedure, which denature collagen and elastin found in the blood vessels’ wall, may promote coagulation, which would extend into the SMV and RPV [23]. It was also postulated that laparoscopic bariatric surgery, could have specific mechanisms contributing to the development of MVT [8,13]. First, a change in the pattern of blood flow is created during LSG in which the short gastric vessels are divided. This could enhance MVT in a way similar to Nissen fundoplication, after which MVT has been described [6]. Second, it was proposed that direct contact with the splenic or SMV could occur during surgery and cause thrombosis. Third, some of the patients may be in negative fluid balance after discharge which predisposes them to VTE, including MVT.
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Clinical suspicion has utmost importance because of the wide spectrum of the initial presentation. Patients may present with nonspecific abdominal pain (90% of patients), nausea (54%), vomiting (77%), and diarrhea (36%) [24]. Others may experience anorexia, colicky pain, and gastrointestinal bleeding. A minority of patients present with peritonitis or shock. Most patients have had symptoms for 42 days before seeking medical care [25]. Symptoms usually appear within 45 days after surgery [8]. Physical examination may be unrevealing or may include low grade fever, mild abdominal tenderness, peritoneal signs, splenomegaly, and hypotension because of bowel ischemia [13]. Laboratory studies are often within the normal limits. Leukocytosis and mild elevations of liver enzymes may be detected, whereas, lactic acidosis is a late finding [6]. Abdominal radiograph may show an ileus, pneumatosis intestinalis, bowel wall edema with thumb-printing, and intraperitoneal or portal vein air [26]. CT performed with intravenous contrast media is the test of choice for diagnosing MVT, having a sensitivity of 90%. It can also examine signs of bowel ischemia, where an unnecessary laparotomy could be avoided without its evidence [27]. Findings include an intraluminal filling defect with central lucency, mesenteric venous congestion, mesenteric fat stranding, and venous collateral circulation [28]. Other diagnostic modalities include magnetic resonance imaging, which has an excellent sensitivity and specificity but is not widely available and requires time for its completion. Mesenteric angiography, although useful in diagnosing mesenteric arterial thrombosis, cannot be used for diagnosing MVT because it requires delayed images [12]. Despite its wide availability, Doppler ultrasonography has the lowest sensitivity among all imaging modalities for detecting MVT; however, it is very useful for follow-up of restoration of flow in the thrombotic veins [6]. Late diagnosis and treatment could lead to mesenteric ischemia or to the formation of thrombus with a secondary portal cavernomatosis, including the sequel of portal hypertension and variceal bleeding [29]. Therefore, once the diagnosis is made, treatment should be started promptly. In patients presenting with peritonitis or shock, an exploratory laparotomy is required with possible resection of necrotic bowel. In most cases without suspicion of bowel ischemia, systemic anticoagulation alone is the mainstay of treatment. An intravenous unfractionated heparin drip should be started with the goal to achieve activated partial thromboplastin times above twice normal or alternatively, LMWH can be used in a dose of 1.5 mg/kg divided into 2 daily dosages [30,31]. A retrospective study showed that the use of anticoagulation reduced the rate of recurrence and extension of MVT by 66% without increasing the risk of gastrointestinal bleeding [32].The use of either heparin or LMWH was shown to result in complete or partial recanalization of MVT in 92% of patients [33]. Anticoagulation is continued for 6–12
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months after the event, in the absence of ongoing thrombotic disorder [34]. Thrombectomy and transhepatic venous thrombolysis have been described in small series and case reports [35,36]. Hollingshead et al. [37] showed that partial or complete recanalization of portal vein thrombosis was achieved in 15 out of 20 patients who did not respond to anticoagulation therapy, but was associated with 60% rate of major complications. Therefore, thrombolysis should be considered in patients with persistent symptoms or deteriorating condition despite anticoagulation. VTE prophylaxis is used by most bariatric centers, with different regimens regarding time of initiation, type of anticoagulation used, dose, duration, and adjuncts measures, such as compression devices or inferior vena caval filters. Early ambulation is recommended for all bariatric surgery patients [38]. All 3 patients described above developed MVT despite perioperative prophylactic anticoagulation. Some studies showed that the risk of development of VTE after bariatric surgery extends well beyond the hospital discharge and suggest that prophylactic anticoagulation should be continued for several weeks [39]. MVT is a common complication after laparoscopic splenectomy, where it was suggested that more aggressive perioperative anticoagulation may prevent its occurrence [21]. This approach, which may also potentially reduce the rate of MVT, should be considered in high-risk patients according to current guidelines, although the specific duration, dose, and agent used are not mentioned [38].We believe that this complication is much more common than cited. Therefore, we recommend that in this high-risk obese population of patients undergoing laparoscopic bariatric surgery, anticoagulation should be given for 1–2 weeks after surgery. Conclusion The 3 cases reported here are based on our single-center experience of over 900 cases. All 3 patients were treated conservatively with anticoagulation alone and were discharged home. There is a need for high clinical suspicion among clinical practitioners to diagnose this rare complication and avoid its potentially catastrophic consequences. We also concluded that in this high-risk obese patients undergoing LSG, anticoagulation must be given for at least 2 weeks postoperatively to prevent development of VTEs. Disclosures The authors have no commercial associations that might be a conflict of interest in relation to this article. References [1] Balfour GW, Stewart TG. Case of enlarged spleen complicated with ascites, both depending upon varicose dilatation and thrombosis of the portal vein. Edinburgh Med J 1869;14:589–98.
[2] Warren S, Eberhard TP. Mesenteric venous thrombosis. Surg Gynecol Obstet 1935;61:102–21. [3] Ottinger LW, Austen WG. A study of 136 patients with mesenteric infarction. Surg Gyencol Obstet 1967;124:251–61. [4] Fujita F, Lyass S, Otsuka K, et al. Portal vein thrombosis following splenectomy: identification of risk factors. Am Surg 2003;69:951–6. [5] Stieber AC, Zetti G, Todo S, et al. The spectrum of portal vein thrombosis in liver transplantation. Ann Surg 1991;213:199–206. [6] James AW, Rabl C, Westphalen AC, Fogarty PF, Posselt AM, Campos GM. Portomesenteric venous thrombosis after laparoscopic surgery: a systematic literature review. Arch Surg 2009;144:520–6. [7] Berthet B, Bollon E, Valero R, Ouaissi M, Sielezneff I, Sastre B. Portal vein thrombosis due to factor 2 leiden in the post-operative course of a laparoscopic sleeve gastrectomy for morbid obesity. Obes Surg 2009;19:1464–7. [8] Salinas J, Barros D, Salgado N, et al. Portomesenteric vein thrombosis after laparoscopic sleeve gastrectomy. Surg Endosc 2014;28: 1083–9. [9] Encinosa WE, Bernard DM, Du D, Steiner CA. Recent improvements in bariatric surgery outcomes. Med Care 2009;47:531–5. [10] Kumar S, Kamath PS. Acute superior mesenteric venous thrombosis: one disease or two? Am J Gastroenterol 2003;98:1299–304. [11] Bayraktar Y, Harmanci O. Etiology and consequences of thrombosis in abdominal vessels. World J Gastroenterol 2006;12:1165–74. [12] Johnson CM, de la Torre RA, Scott JS, Johansen T. Mesenteric venous thrombosis after laparoscopic Roux-en-Y gastric bypass. Surg Obes Relat Dis 2005;1:580–2; discussion 582–3. [13] Goitein D, Matter I, Raziel A, et al. Portomesenteric thrombosis following laparoscopic bariatric surgery: incidence, patterns of clinical presentation, and etiology in a bariatric patient population. JAMA Surg 2013;148:340–6. [14] Abdollahi M, Cushman M, Rosendaal FR. Obesity: risk of venous thrombosis and the interaction with coagulation factor levels and oral contraceptive use. Thromb Haemost 2003;89:493–8. [15] Herron DM. C-reactive protein and adiposity: obesity as a systemic inflammatory state. Surg Obes Relat Dis 2005;1:385–6. [16] Ay C, Tengler T, Vormittag R, et al. Venous thromboembolism–a manifestation of the metabolic syndrome. Haematologica 2007;92: 374–80. [17] Epstein RM, Wheeler HO, Frumin MJ, Habig DV, Papper EM, Bradley SE. The effect of hypercapnia on estimated hepatic blood flow, circulating splanchnic blood volume, and hepatic sulfobromophthalein clearance during general anesthesia in man. J Clin Invest 1961;40:592–8. [18] Haglund U, Norlen K, Rasmussen I, Flowers JL. Complications related to pneumoperitoneum. In: Bailey RW, Flowers JL, eds. Complications of laparoscopic surgery. St. Louis, MO: Quality Medical Publ; 1995. p. 26–57. [19] Viinamki O, Punnonen R. Vasopressin release during laparoscopy: role of increased intra-abdominal pressure. Lancet 1982;1:175–6. [20] Ivankovich AD, Miletich DJ, Albrecht RF, Heyman HJ, Bonnet RF. Cardiovascular effects of intraperitoneal insufflation with carbon dioxide and nitrous oxide in the dog. Anesthesiology 1975;42: 281–7. [21] Pietrabissa A, Moretto C, Antonelli G, Morelli L, Marciano E, Mosca F. Thrombosis in the portal venous system after elective laparoscopic splenectomy. Surg Endosc 2004;18:1140–3. [22] Chan MM, Hamza N, Ammori BJ. Duration of surgery independently influences risk of venous thromboembolism after laparoscopic bariatric surgery. Surg Obes Relat Dis 2013;9:88–93. [23] Pineda L, Sarhan M, Ahmed L. Superior mesenteric vein thrombosis after laparoscopic sleeve gastrectomy. Surg Laparosc Endosc Percutan Tech 2013;23:e162–3. [24] Boley SJ, Kaleya RN, Brandt LJ. Mesenteric venous thrombosis. Surg Clin North Am 1992;72:183–201.
Sleeve Gastrectomy and Mesenteric Venous Thrombosis / Surgery for Obesity and Related Diseases ] (2014) 00–00 [25] Rhee RY, Gloviczki P, Mendonca CT, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s J Vasc Surg 1994;20:688–697. [26] Swartz DE, Felix EL. Acute mesenteric venous thrombosis following laparoscopic Roux-en-Y gastric bypass. JSLS 2004;8:165–9. [27] Bradbury MS, Kavanagh PV, Bechtold RE, et al. Mesenteric venous thrombosis: diagnosis and noninvasive imaging. Radiographics 2002;22:527–41. [28] Cakmak O, Elmas N, Tamsel S, et al. Role of contrast-enhanced 3 D magnetic resonance portography in evaluating portal venous system compared with color Doppler ultrasonography. Abdom Imaging 2008;33:65–71. [29] Sorrentino D, Labombarda A, Debiase F, Trevisi A, Giagu P. Cavernous transformation of the portal vein associated to multiorgan developmental abnormalities. Liver Int 2004;24:80–3. [30] Abdu RA, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosis– 1911 to 1984. Surgery 1987;101:383–8. [31] Joh JH, Kim DI. Mesenteric and portal vein thrombosis: treated with early initiation of anticoagulation. Eur J Vasc Endovasc Surg 2005;29:204–8. [32] Condat B, Pessione F, Hillaire S, et al. Current outcome of portal vein thrombosis in adults: risk and benefit of anticoagulant therapy. Gastroenterology 2001;120:490–7.
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[33] Condat B, Pessione F, Helene Denninger M, Hillaire S, Valla D. Recent portal or mesenteric venous thrombosis: increased recognition and frequent recanalization on anticoagulant therapy. Hepatology 2000;32:466–70. [34] Kumar S, Sarr MG, Kamath PS. Mesenteric venous thrombosis. N Engl J Med 2001;345:1683–8. [35] Kaplan JL, Weintraub SL, Hunt JP, Gonzalez A, Lopera J, Brazzini A. Treatment of superior mesenteric and portal vein thrombosis with direct thrombolytic infusion via an operatively placed mesenteric catheter. Am Surg 2004;70:600–4. [36] Demertzis S, Ringe B, Gulba D, Rosenthal H, Pichlmayr R. Treatment of portal vein thrombosis by thrombectomy and regional thrombolysis. Surgery 1994;115:389–93. [37] Hollingshead M, Burke CT, Mauro MA, Weeks SM, Dixon RG, Jaques PF. Transcatheter thrombolytic therapy for acute mesenteric and portal vein thrombosis. J Vasc Interv Radiol 2005;16:651–61. [38] American Society for Metabolic and Bariatric Surgery Clinical Issues Committee. ASMBS updated position statement on prophylactic measures to reduce the risk of venous thromboembolism in bariatric surgery patients. Surg Obes Relat Dis 2013;9:493–7. [39] Steele KE, Schweitzer MA, Prokopowicz G, et al. The long-term risk of venous thromboembolism following bariatric surgery. Obes Surg 2011;21:1371–6.
Case report
Sleeve gastrectomy and mesenteric venous thrombosis: report of 3 patients and review of the literature Amihai Rottenstreich*, Abed Khalaileh, Ram Elazary Department of General Surgery, Hadassah-Hebrew University Medical Center, Ein Kerem, Jerusalem, Israel Received July 3, 2014; accepted July 7, 2014
Keywords:
Bariatric; Laparoscopic; Thrombosis; Portal; Mesenteric
Mesenteric venous thrombosis (MVT) is a rare but potentially lethal pathology. Although first described by Balfour and Stewart in 1869 [1], it was first presented as a distinct cause of mesenteric ischemia by Warren and Eberhand only in 1935 [2]. MVT accounts for 5%–15% of all mesenteric ischemic events [2,3]. In the past, MVT has been described after procedures involving manipulation of the portal venous system, such as splenectomy or liver transplantation [4,5]. However, since the beginning of the minimal invasive era, MVT has occurred in several cases after various laparoscopic procedures [6]. During the last decade, a few cases of MVT have been published to occur after laparoscopic bariatric operations, including laparoscopic sleeve gastrectomy (LSG) [7]. Nevertheless, MVT has been shown to be a major morbidity during the perioperative period of LSG with an incidence of 1% [8]. The aim of this article is to present 3 cases of MVT that have occurred after 900 LSG procedures in our center, discuss the pathophysiology and management of this complication and suggest preventive strategy. Case 1 A 24-year-old man, height 168 cm, weight 110 kg, and body mass index (BMI) of 39 kg/m2, with a medical history of glucose 6 phosphokinase deficiency (G6 PD) deficiency and osteoarthritis of both knees. He underwent an uneventful LSG. The operative time was 1 hour. Prophylactic perioperative low molecular weight heparin (LMWH) was given. He * Correspondence: Amihai Rottenstreich, Department of Surgery, Hadassah-Hebrew University Medical Center, P.O. Box 12000 Jerusalem, Israel, 91120. E-mail: [email protected]
was discharged on postoperative day 4. On the 9th day postsurgery, he presented to the emergency department (ED) suffering from a 1-day history of epigastric pain. He also complained of nausea without vomiting, diarrhea, or other symptoms. His vital signs were normal. Physical examination revealed mild epigastric tenderness. Laboratory tests were within the normal limits, except for mild leukocytosis of 10,300/mm3 and elevated, twice normal, amylase level. Chest and plain abdominal radiographs were normal. Computed tomography (CT) demonstrated normal postoperative changes. The patient was discharged. Five days later, he came back to the ED with escalating abdominal pain accompanied by nausea and vomiting. On physical examination, mild epigastric tenderness was found. Amylase levels were increased up to 3 times normal. He was hospitalized for further evaluation. Additional interpretation of the CT taken at his initial ED visit revealed filling defects in the superior mesenteric vein (SMV) and right portal vein (RPV). An additional CT scan was performed and a thrombosis of both SMV and RPV were demonstrated with no change in comparison to the previous scan, alongside stranding fat around the pancreas and little edema noted in the right colon. Anticoagulation with LMWH was initiated and its effect monitored using antiXa levels. Duplex ultrasonography performed during admission demonstrated no evidence of flow in either SMV or RPV. The patient's symptoms improved, and he was discharged after 9 days of hospitalization. Postdischarge evaluation revealed positive lupusanticoagulant antibodies. Follow-up duplex ultrasonography scans done on 1, 2, and 5 months after discharge revealed lack of flow in the SMV and RPV. Only 9 months after discharge did recanalization of the veins and restoration of flow occur; however, their diameters were decreased.
http://dx.doi.org/10.1016/j.soard.2014.07.002 1550-7289/r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved.
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A. Rottenstreich et al. / Surgery for Obesity and Related Diseases ] (2014) 00–00
LMWH therapy was switched to warfarin and discontinued after 6 months without any further sequella. Case 2 A 50-year-old man, height 180 cm, weight 184 kg, and BMI of 56 kg/m2, with a medical history of H. pylori gastritis, epididymitis, essential hypertension, and G6 PD deficiency. He had undergone laparoscopic adjustable gastric banding 5 years before, and, because of insufficient weight loss and recurrent vomiting, he was referred to our department for conversion to LSG and band removal. The operation time was 2 hours. Prophylactic anticoagulation was given perioperatively. He was discharged on the 3rd postoperative day. Postoperative outpatient clinic follow-up was on the 6th and 23rd day postoperatively; he had no complaints and physical examination was unremarkable. On the 36th postoperative day, he presented to the ED suffering from epigastric pain lasting for 4 days, without nausea, vomiting, diarrhea, or other complaints. His vital signs were normal. Physical examination revealed moderate epigastric tenderness. The initial white blood cells count was 12,800/mm3, hemoglobin 12.5 g/dL, platelets 433,000/mm3, and bilirubin 1.5 mg/dL. Chest and plain abdominal radiographs were normal. CT demonstrated normal postoperative changes with fat stranding around the duodenum. The patient was treated with a proton pump inhibitor symptoms resolved and was discharged home. Two days later, he returned to the ED with severe abdominal pain associated with vomiting. His vital signs were normal. Periumbilical tenderness was noted without other peritoneal signs. Blood tests showed a leukocytosis of 17,000/mm3, gamma-glutamyl transferase (GGT) level was 113 U/L, and alkaline phosphatase level was 140 U/L. Total bilirubin remained 1.5 mg/dL, lactic acid 5.5 mmol/L, and C-reactive protein 14 mg/dL. He was admitted for further evaluation. A repeated CT scan was performed and thrombus in the SMV was demonstrated, alongside bowel wall thickening in the proximal ileum and a small to moderate amount of ascites. We initiated conservative treatment, which included nothing per oram and LMWH. Five days later, an additional CT scan demonstrated the same findings without improvement; however, a larger amount of ascites was noted. During hospitalization, his symptoms improved, and he was discharged after 24 days. CT scan performed 2 months after discharge showed chronic changes in the SMV. Doppler studies were not done. Workup after discharge for hypercoagulable states was normal. LMWH injections were converted to warfarin for completion of 6 months of anticoagulant therapy.
was given perioperatively. He was discharged on the third postoperative day. On the 13th postoperative day, he presented to the ED complaining of right upper quadrant and epigastric pain from the morning of admission, without nausea, vomiting, diarrhea, or other complaints. His vital signs were normal. Physical examination revealed mild epigastric tenderness. Laboratory findings showed an elevated alanine aminotransferase and aspartate aminotransferase 3.5, 2 times normal, respectively. GGT was 113 U/L. CT demonstrated MVT involving the splenic vein, SMV, and RPV (Fig. 1). He was admitted and anticoagulation with LMWH was started immediately after diagnosis, using antiXa levels for monitoring. During admission, we learned his family history of a brother who suffered from deep vein thrombosis and a mother who sustained multiple abortions. A family workup for thrombophilia had not been carried in the past. Duplex ultrasonography performed before discharge revealed complete occlusion of both RPV and SMV. The patient's symptoms improved, and he was discharged after 29 days of hospitalization. The patient refused to undergo workup for thrombophilia, and he was withdrawn from anticoagulants after 6 months and did well. Follow-up CT scan was not performed. Discussion Bariatric procedures have become quite common but are not entirely free of complications, which occur in up to 40% of patients [9]. MVT was first described to occur after LSG by Berthet et al. [7] in 2009. Recently, Salinas et al. [8] reported that among 1,713 patients undergoing LSG, 17 patients developed this complication.
Case 3 A 29-year-old man, height 174 cm, weight 133 kg, and BMI 43.8 kg/m2, with a medical history of hyperlipidemia and essential hypertension. He underwent uneventful LSG. The operative time was 1 hour. Prophylactic anticoagulation
Fig. 1. Computed tomography scan demonstrating a large filling defect in the superior mesenteric vein.
Sleeve Gastrectomy and Mesenteric Venous Thrombosis / Surgery for Obesity and Related Diseases ] (2014) 00–00
Mesenteric venous thrombosis is a rare but potentially lethal condition that requires a high index of suspicion. It could be classified as primary, where no obvious cause could be found, and secondary, where a specific cause or predisposing condition is identified. Primary cases represent 50%, although recent studies found that in 80% of cases an identifiable cause could be found [10,11]. Therefore a diagnostic workup for hypercoagulable states should be done after the diagnosis of MVT. Only assays for heparinplatelet factor 4 antibodies, hyperhomocysteinemia, anticardiolipin antibodies, and prothrombin 20210 and factor V leiden mutations are reliable during the initial event, and other tests should be performed remote from the initial presentation at least 2–3 weeks after cessation of anticoagulation [12]. Goitein et al. [13] reported that a third of the patients who suffered from MVT after laparoscopic bariatric surgery had a personal history of venous thromboembolism (VTE). A personal or familial history of VTEs should be elicited at the preoperative evaluation. The etiology of this complication after laparoscopic surgery and specifically bariatric surgery is probably multifactorial. Obesity itself is a known risk factor for VTE especially deep vein thrombosis of the lower limbs [14]. This could be attributed to several factors, such as a chronic inflammatory state associated with obesity, the metabolic syndrome found in a significant portion of these obese patients, increased abdominal pressure, venous stasis in the lower limbs and a sedentary lifestyle [13,15,16]. Regarding the laparoscopic surgical technique, several mechanisms might be involved. Hypercarbia, induced by CO2 insufflation, decreases splanchnic blood flow by mesenteric vasoconstriction [17]. Moreover, the increased intra-abdominal pressure (IAP) leads to decreased mesenteric and portal venous flow via direct pressure-induced compression [6]. Haglund et al. [18] demonstrated an inverse correlation between IAP and portal venous flow. Other factors that might contribute are visceral vasoconstriction induced by intraoperative vasopressin release, increased portal pressure due to retained CO2, the reverse Trendelenberg position, and prolonged operative times [19– 22]. One study suggested that the use of bipolar coagulation during the procedure, which denature collagen and elastin found in the blood vessels’ wall, may promote coagulation, which would extend into the SMV and RPV [23]. It was also postulated that laparoscopic bariatric surgery, could have specific mechanisms contributing to the development of MVT [8,13]. First, a change in the pattern of blood flow is created during LSG in which the short gastric vessels are divided. This could enhance MVT in a way similar to Nissen fundoplication, after which MVT has been described [6]. Second, it was proposed that direct contact with the splenic or SMV could occur during surgery and cause thrombosis. Third, some of the patients may be in negative fluid balance after discharge which predisposes them to VTE, including MVT.
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Clinical suspicion has utmost importance because of the wide spectrum of the initial presentation. Patients may present with nonspecific abdominal pain (90% of patients), nausea (54%), vomiting (77%), and diarrhea (36%) [24]. Others may experience anorexia, colicky pain, and gastrointestinal bleeding. A minority of patients present with peritonitis or shock. Most patients have had symptoms for 42 days before seeking medical care [25]. Symptoms usually appear within 45 days after surgery [8]. Physical examination may be unrevealing or may include low grade fever, mild abdominal tenderness, peritoneal signs, splenomegaly, and hypotension because of bowel ischemia [13]. Laboratory studies are often within the normal limits. Leukocytosis and mild elevations of liver enzymes may be detected, whereas, lactic acidosis is a late finding [6]. Abdominal radiograph may show an ileus, pneumatosis intestinalis, bowel wall edema with thumb-printing, and intraperitoneal or portal vein air [26]. CT performed with intravenous contrast media is the test of choice for diagnosing MVT, having a sensitivity of 90%. It can also examine signs of bowel ischemia, where an unnecessary laparotomy could be avoided without its evidence [27]. Findings include an intraluminal filling defect with central lucency, mesenteric venous congestion, mesenteric fat stranding, and venous collateral circulation [28]. Other diagnostic modalities include magnetic resonance imaging, which has an excellent sensitivity and specificity but is not widely available and requires time for its completion. Mesenteric angiography, although useful in diagnosing mesenteric arterial thrombosis, cannot be used for diagnosing MVT because it requires delayed images [12]. Despite its wide availability, Doppler ultrasonography has the lowest sensitivity among all imaging modalities for detecting MVT; however, it is very useful for follow-up of restoration of flow in the thrombotic veins [6]. Late diagnosis and treatment could lead to mesenteric ischemia or to the formation of thrombus with a secondary portal cavernomatosis, including the sequel of portal hypertension and variceal bleeding [29]. Therefore, once the diagnosis is made, treatment should be started promptly. In patients presenting with peritonitis or shock, an exploratory laparotomy is required with possible resection of necrotic bowel. In most cases without suspicion of bowel ischemia, systemic anticoagulation alone is the mainstay of treatment. An intravenous unfractionated heparin drip should be started with the goal to achieve activated partial thromboplastin times above twice normal or alternatively, LMWH can be used in a dose of 1.5 mg/kg divided into 2 daily dosages [30,31]. A retrospective study showed that the use of anticoagulation reduced the rate of recurrence and extension of MVT by 66% without increasing the risk of gastrointestinal bleeding [32].The use of either heparin or LMWH was shown to result in complete or partial recanalization of MVT in 92% of patients [33]. Anticoagulation is continued for 6–12
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A. Rottenstreich et al. / Surgery for Obesity and Related Diseases ] (2014) 00–00
months after the event, in the absence of ongoing thrombotic disorder [34]. Thrombectomy and transhepatic venous thrombolysis have been described in small series and case reports [35,36]. Hollingshead et al. [37] showed that partial or complete recanalization of portal vein thrombosis was achieved in 15 out of 20 patients who did not respond to anticoagulation therapy, but was associated with 60% rate of major complications. Therefore, thrombolysis should be considered in patients with persistent symptoms or deteriorating condition despite anticoagulation. VTE prophylaxis is used by most bariatric centers, with different regimens regarding time of initiation, type of anticoagulation used, dose, duration, and adjuncts measures, such as compression devices or inferior vena caval filters. Early ambulation is recommended for all bariatric surgery patients [38]. All 3 patients described above developed MVT despite perioperative prophylactic anticoagulation. Some studies showed that the risk of development of VTE after bariatric surgery extends well beyond the hospital discharge and suggest that prophylactic anticoagulation should be continued for several weeks [39]. MVT is a common complication after laparoscopic splenectomy, where it was suggested that more aggressive perioperative anticoagulation may prevent its occurrence [21]. This approach, which may also potentially reduce the rate of MVT, should be considered in high-risk patients according to current guidelines, although the specific duration, dose, and agent used are not mentioned [38].We believe that this complication is much more common than cited. Therefore, we recommend that in this high-risk obese population of patients undergoing laparoscopic bariatric surgery, anticoagulation should be given for 1–2 weeks after surgery. Conclusion The 3 cases reported here are based on our single-center experience of over 900 cases. All 3 patients were treated conservatively with anticoagulation alone and were discharged home. There is a need for high clinical suspicion among clinical practitioners to diagnose this rare complication and avoid its potentially catastrophic consequences. We also concluded that in this high-risk obese patients undergoing LSG, anticoagulation must be given for at least 2 weeks postoperatively to prevent development of VTEs. Disclosures The authors have no commercial associations that might be a conflict of interest in relation to this article. References [1] Balfour GW, Stewart TG. Case of enlarged spleen complicated with ascites, both depending upon varicose dilatation and thrombosis of the portal vein. Edinburgh Med J 1869;14:589–98.
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