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CASE REPORT
Year : 2015  |  Volume : 3  |  Issue : 1  |  Page : 29-31

Liver and bowel infarction secondary to portomesenteric vein thrombosis following laparoscopic sleeve gastrectomy


Department of General and Minimally Invasive Surgery, Asian Institute of Medical Sciences, Faridabad, Haryana, India

Date of Web Publication12-Jun-2015

Correspondence Address:
Anushtup De
Flat No. 603, Onyxe Towers, Sector 21c, Faridabad - 121 001, Haryana
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2347-2618.158700

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  Abstract 

Portal vein thrombosis is a rare and life-threatening complication following surgery. Extension of thrombosis with involvement of the mesenteric vein is rarer. There have been some case reports documenting successful management of portomesenteric venous thrombosis (PMVT) following laparoscopic surgery. This case report describes a patient developing extensive hepatic and bowel infarction due to PMVT following laparoscopic sleeve gastrectomy.

Keywords: Bowel infarction, laparoscopic, sleeve gastrectomy, portomesenteric vein thrombosis


How to cite this article:
Roy P, De A. Liver and bowel infarction secondary to portomesenteric vein thrombosis following laparoscopic sleeve gastrectomy. Saudi J Obesity 2015;3:29-31

How to cite this URL:
Roy P, De A. Liver and bowel infarction secondary to portomesenteric vein thrombosis following laparoscopic sleeve gastrectomy. Saudi J Obesity [serial online] 2015 [cited 2019 Aug 26];3:29-31. Available from: http://www.saudijobesity.com/text.asp?2015/3/1/29/158700


  Introduction Top


Portal vein thrombosis (PVT) is recognized as a serious and life threatening condition requiring early recognition and effective management for a favorable outcome. [1]

Postoperative PVT has been recognized since some time and was found to be associated with both, procedures involving handling of portomesenteric system and also those that had no such issue. Reports of PVT have been published following laparoscopic surgery also. Two authors have reported PVT following laparoscopic sleeve gastrectomy (LSG) that was managed with systemic anticoagulation. [2],[3] This case report describes hepatic and bowel ischemia subsequent to portomesenteric venous thrombosis (PMVT) following LSG.


  Case report Top


A 26-year-old lady (body mass index 52.7 Kg/m 2 ) presented for LSG. Patient had no associated comorbidity and did not use contraceptive pills. After a preoperative workup and consent, LSG was carried out over a 36 Fr gastric calibration tube. Intraoperative leak test was negative. The patient had an uneventful postoperative recovery and discharged on the second postoperative day on a clear liquid diet. As per protocol DVT prophylaxis (enoxaparin 40 mg) was administered 12 h preoperatively and once daily for 2 weeks after surgery. Compression stocking for 2 weeks and a sequential compression device for the duration of surgery and postoperatively were used. The patient defaulted on subcutaneous enoxaparin after 1-week. However, the patient was adequately hydrated as she was consuming desired quantity of liquid diet and passing urine.

On 18 th day of post operation, she presented with severe upper abdominal pain, nausea, and vomiting for 4 days. Physical examination revealed tachycardia (pulse 144/min) and tachypnea (respiratory rate 26/min) with adequate hydration. Blood work showed leukocytosis (total count 24,900 cells/mm 3 ). Blood gases showed respiratory alkalosis (pH 7.52, pCO 2 30.4 mm Hg, HCO 3 − 24.0 mmol/L). Kidney and liver functions were within normal limit. Contrast-enhanced computed tomography (CECT) of the abdomen did not show any evidence of a leak. However, there was suspicion of PVT with mild ascites [Figure 1]b.
Figure 1: (a) Liver infarct. (b) Portal vein thrombus

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The rarity of PVT and likely possibility of staple line dehiscence led the surgical team to decide on undertaking a diagnostic laparoscopy. On laparoscopy, hemorrhagic fluid was found in the peritoneal cavity. The staple line was intact and intra-operative leak test was negative. The entire small bowel was mildly congested and liver did not show any abnormality. Peritoneal fluid was sent for culture but the result did not show any bacterial growth. Blood samples were sent for coagulation abnormalities. Results showed functional protein S deficiency (<10%), while Antithrombin, protein C, and cardiolipin antibody levels were within normal. Lupus anticoagulant factor was not detected and serum homocysteine level were elevated (level - 19.58 umol/L).(normal value −4.44-13.56 umol/L).

Patient was put on 60 mg enoxaparin twice daily and she was discharged after 18 days on the same medication. At the time of discharge she was pain-free and tolerating orally. She was advised to follow-up after 8 weeks. Over the next month, she had a steady weight loss of about 20 kg by 2 months.

The patient presented 10 weeks after initial surgery with diffuse abdominal pain for 1-day with 4-5 episodes of vomiting. She had tachycardia (rate −170/min). Abdomen was distended and had a tender central abdominal lump. Lab investigations showed mild leukocytosis (WBC = 13,000 cells/mm3), metabolic acidosis (pH 7.08, pCO2 = 36.8 mm Hg, HCO3 = 10.6 mmol/L). A CECT abdomen showed infarcted liver and diffuse edema of entire small intestines and mild ascites [Figure 1]a. Patient was continued on injection enoxaparin 60 mg s/c twice daily. Considering a possibility of mesenteric or intestinal infarction, an exploratory laparotomy was carried out. There was presence of a moderate quantity of hemorrhagic fluid in the abdomen. The entire small bowel and colon up to sigmoid colon along with its mesentery was infarcted and unviable. The liver was small and pale. No further procedure after exploratory laparotomy was carried out. The outcome of the patient was discussed with the patient's family. Patient succumbed to irreversible metabolic acidosis (pH 7.058, pCO 2 − 33.4, HCO 3 − 9 mmol/L) with multiorgan dysfunction syndrome (Anuria with ventilatory and high inotropic support).


  Discussion Top


Portomesenteric venous thrombosis is a rare but recognized phenomenon. Possible etiologies are varied from systemic (inherited hypercoagulable or acquired prothrombotic states) or local (inflammatory or neoplastic states or portal hypertension or direct surgical manipulation of portosystemic vessels). [1] PVT as a postsurgical complication was described by Delatour (1895) following splenectomy. Gastric bypass involves transection of the gastric and mesenteric veins causing endothelial damage, but in sleeve gastrectomy the transection of short gastric veins alone is less likely to cause PVT. [4]

Genetic coagulopathies that have been associated with PVT include factor V leiden, protein C and protein S deficiency, Antithrombin III deficiency, and hyperhomocysteinemia. Our patient had protein S deficiency and hyperhomocysteinemia. Berthet et al. [2] reported factor 2 leiden deficiency and 7 out of 17 patients in the series by Sailnas et al. [3] had a positive thrombophilic study [Table 1]. However, importantly most of the cases reported had negative hematologic work up.
Table 1: Studies comparing postoperative presentation and work up of patients with postoperative PMVT

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It is unclear as to the mechanism by which laparoscopic surgery increases the risk of development of PMVT. [5],[6],[7] However, studies have reported significantly higher incidence of PVT following Laparoscopic surgery from 8% to 52% [8] compared to around 10% after open surgery. [9]

A noticeable feature regarding the presentation of PMVT in this patient is the delayed presentation of the disease. Most of the cases reported usually present within 1-2 weeks postoperatively [Table 1]. In the series of 17 patients, the median postoperative day of presentation was 14 th . This feature gives a possibility that there may be other factors than intraoperative splanchnic perfusion that is responsible.

The diagnosis of PMVT in postoperative patients is often difficult since symptoms are frequently nonspecific. Physical findings range from low-grade fever, mild to severe abdominal pain radiating to the back and ileus. Features of severe disease include hematochezia, ascites, metabolic acidosis, and renal or respiratory failure. Salinas et al. reported [3] epigastric pain as an initial symptom in their series.

The diagnosis of PMVT is usually done by CECT abdomen. It may also allow detection of signs of bowel ischemia which is the most severe complication of PMVT. The treatment is guided by the acuity of disease and any known underlying cause. Therapeutic anticoagulation is recommended for a duration of 6-12 months. However, this may be continued lifelong in patients with known prothrombotic states with the goal of recanalization of the portal vein. [10] Follow-up may include imaging studies to confirm recanalization of the portal vein after 3-6 months of treatment.

Bariatric surgery has rapidly gained acceptance due to the huge metabolic benefits a patient gets. Leaks and DVT have predominated the discussion and literature among the complications.


  Conclusion Top


Portomesenteric venous thrombosis is an uncommon but known and potentially life-threatening complication following LSG. With the gaining popularity of LSG considering it to be simpler and safer than Roux-en-Y gastric bypass, the possibility of this complication must be kept in mind in patients presenting with nonspecific and unexplained abdominal pain.

 
  References Top

1.
Goitein D, Matter I, Raziel A, Keidar A, Hazzan D, Rimon U, 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.  Back to cited text no. 1
    
2.
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.  Back to cited text no. 2
    
3.
Salinas J, Barros D, Salgado N, Viscido G, Funke R, Pérez G, et al. Portomesenteric vein thrombosis after laparoscopic sleeve gastrectomy. Surg Endosc 2014;28:1083-9.  Back to cited text no. 3
    
4.
Rosenberg JM, Tedesco M, Yao DC, Eisenberg D. Portal vein thrombosis following laparoscopic sleeve gastrectomy for morbid obesity. JSLS 2012;16:639-43.  Back to cited text no. 4
    
5.
Sternberg A, Alfici R, Bronek S, Kimmel B. Laparoscopic surgery and splanchnic vessel thrombosis. J Laparoendosc Adv Surg Tech A 1998;8:65-8.  Back to cited text no. 5
    
6.
Abdelrazeq AS, Dwaik MA, Aldoori MI, Lund JN, Leveson SH. Laparoscopy-associated portal vein thrombosis: Description of an evolving clinical syndrome. J Laparoendosc Adv Surg Tech A 2006;16:9-14.  Back to cited text no. 6
    
7.
Poultsides GA, Lewis WC, Feld R, Walters DL, Cherry DA, Ruby ST. Portal vein thrombosis after laparoscopic colectomy: Thrombolytic therapy via the superior mesenteric vein. Am Surg 2005;71:856-60.  Back to cited text no. 7
    
8.
Ikeda M, Sekimoto M, Takiguchi S, Kubota M, Ikenaga M, Yamamoto H, et al. High incidence of thrombosis of the portal venous system after laparoscopic splenectomy: A prospective study with contrast-enhanced CT scan. Ann Surg 2005;241:208-16.  Back to cited text no. 8
    
9.
van′t Riet M, Burger JW, van Muiswinkel JM, Kazemier G, Schipperus MR, Bonjer HJ. Diagnosis and treatment of portal vein thrombosis following splenectomy. Br J Surg 2000;87:1229-33.  Back to cited text no. 9
    
10.
Condat B, Pessione F, Hillaire S, Denninger MH, Guillin MC, Poliquin M, et al. Current outcome of portal vein thrombosis in adults: Risk and benefit of anticoagulant therapy. Gastroenterology 2001;120:490-7.  Back to cited text no. 10
    


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