Mesenteric Vein Thrombosis following Sleeve Gastrectomy: A Case Report and Review of the Literature

Abstract

Introduction

Acute mesenteric ischemia (AMI) is a rare but lethal disease. Mesenteric vein thrombosis (VAMI) is a subtype of AMI. Morbid obesity is usually accompanied by hypertension, hyperlipidemia, or diabetes mellitus, which are risk factors associated with AMI.

Case Presentation

We present a 28-year-old man with VAMI post-laparoscopic sleeve gastrectomy. He was first misdiagnosed with intestinal obstruction. Superior VAMI was confirmed after computed tomography angiography. Laparotomy, resection of the necrotic small bowel, and ostomy were performed immediately.

Conclusion

Patients with morbid obesity accompanied by hypertension, hyperlipidemia, or diabetes mellitus have a high risk of AMI. Abdominal pain with sudden onset should be considered AMI. Anticoagulation therapy post-sleeve gastrectomy might help reduce the incidence of AMI.

Introduction

The incidence of morbid obesity has increased recently [1–3]. Bariatric surgery has shown effectiveness in the management of morbid obesity. Laparoscopic sleeve gastrectomy (LSG) has become the most popular bariatric procedure due to its simple management, effective treatment outcome, and low morbidity [4]. However, some severe postoperative complications have not yet been noticed. Acute mesenteric ischemia (AMI) is a rare disease. A British study [5] suggested that the incidence was 0.63/100,000/year. A study in Sweden [6] based on autopsy reports showed that the incidence was 12.90/100,000/year. Despite its low incidence, the mortality rate of this disease is as high as 50–69% [7]. AMI is categorized into four subtypes according to its cause: mesenteric artery embolism, mesenteric artery thrombosis, nonocclusive mesenteric ischemia, and mesenteric vein thrombosis (VAMI). Mesenteric artery embolism accounts for 25% of cases, mesenteric artery thrombosis accounts for approximately 40%, VAMI accounts for approximately 15%, and nonocclusive mesenteric ischemia accounts for approximately 20% [8]. The guidelines conclude that hypertension, diabetes mellitus, and hyperlipidemia are the risk factors associated with AMI [9]. Morbid obesity is usually accompanied by hypertension, hyperlipidemia, or diabetes mellitus. Therefore, abdominal pain with sudden onset in patients who are morbidly obese should be considered AMI, and computed tomography angiography (CTA) should be performed as soon as possible.

We present a case of a patient with morbid obesity with VAMI post-LSG. Laparotomy, resection of necrotic small bowel, and ostomy were performed 24 days after LSG.

Case Presentation

Chief Complaints

A 28-year-old man with morbid obesity was admitted to Beijing Tsinghua Changgung Hospital in 2021. His body mass index was 44.2 kg/m². He had a past medical history of hypertension and hyperlipidemia. LSG was performed after laboratory tests and preoperative examination. Patient was placed in supine position. After general anesthesia and sterilization, a 12 mm Hg pneumoperitoneum was formed by inflation with carbon dioxide. Laparoscopic instruments were placed through the trocars. The gastrocolic ligament was cut off by Ligasure from 3–4 cm left to the pylorus. The His angle was completely separated, and the posterior wall of the gastric fundus, the esophagus, and the foot of the diaphragm were exposed. Sleeve gastrectomy was performed with staplers under the guidance of the gastric tube. The greater curvature of the stomach was removed completely. The stump of the stomach was closed by continuous suture. Neither the superior mesenteric vein nor the portal vein was retracted during the surgery. The operation time was 116 min. The patient began to drink on postoperative day (POD) 1 and consumed liquid food on POD 2. Because of good food tolerance, pain control, and no signs of infection, he was discharged on POD 3. We prescribed aspirin 100 mg (oral intake OD) for him. He returned to the emergency room (ER) on POD 16. He experienced intermittent abdominal pain for 2 days. It was a colic pain without radiation. The pain was accompanied by nausea and abdominal distension. He had stopped passing stool or gas for 2 days. There was no fever, vomiting, melena, hematochezia, or hematemesis.

Physical Examination

The heart rate was 127/min and the blood pressure was 126/101 mm Hg. The other vital signs were normal. The abdomen was soft. There was mild tenderness in the upper abdomen. There were no signs of peritonitis. The bowel movement sound could not be heard.

Laboratory Test and Imaging Test

Laboratory tests suggested that the white blood cell (WBC) count and C-reactive protein (CRP) levels were elevated. The CT scan without contrast demonstrated the dilated bowel.

Pre-Second Operation Management

The ER doctor diagnosed the patient with intestinal obstruction. Fasting, IV antibiotics, fluid resuscitation, and enema were prescribed. The symptoms did not disappear, and the patient was admitted to the gastrointestinal department on POD 19. After admission, IV antibiotics, fluid resuscitation, enema, and enoxaparin (6,000 IU ih QD) were prescribed. On POD 24, the abdominal pain became severe and peritonitis appeared suddenly. Laboratory test results showed that WBC levels and D-dimer levels were elevated, as shown in Table 1. We performed CTA immediately. The results suggested thrombosis in the superior mesenteric vein and the portal vein, ascites in the abdomen, and small intestine wall thickening, as shown in Figure 1. We confirmed the diagnosis of VAMI and suspected intestinal necrosis.

Table 1.

Laboratory test results

	POD 18	POD 24
WBC, 109/L	11.03	11.72
CRP, mg/L	64.13	70.30
Neutrophil percentage	64.3	78.7
D-dimer, mg/L	–	9.18
PH	–	7.45
Lactate, mmol/L	–	1.3

Fig. 1.

CTA on POD 24. Thrombosis in the portal vein.

Second Operation

The patient underwent laparotomy on POD 24. During the operation, we found 70-cm necrotic bowel in the jejunum, as shown in Figure 2. Resection of the necrotic bowel and ostomy of the proximal and distal jejunum were performed. The operation time was 283 min. The amount of intraoperative blood loss was 50 mL.

Fig. 2.

Necrotic bowel on POD 24.

Post-Second Operation Management

IV antibiotics, fluid resuscitation, parenteral nutrition, and anticoagulation therapy (10,000 IU ih Q12 h) were prescribed. We inserted a tube into the distal stoma. The enteral nutrition and the fluid collected from the proximal stoma were infused through the tube. He was discharged after 30 days of hospitalization. The CTA on POD 39 showed nearly no thrombosis in the portal vein but still in the superior mesenteric vein, as shown in Figure 3. Home enteral nutrition and rivaroxaban (20 mg once a day) were prescribed. The continuity of the jejunum was restored 3 months after the second operation.

Fig. 3.

CTA on POD 39. The portal vein without thrombosis.

Discussion

With the increased number of morbid obesity cases, bariatric surgery has become the most important procedure. The complication rate of bariatric surgery ranges from 7.3–15% [1, 10]. LSG is a popular surgical method. In a survey in 2018, 55.4% of patients with morbid obesity underwent LSG [2]. Compared with Roux-en-Y gastric bypass surgery, LSG has shown lower morbidity [11]. The morbidity rate associated with LSG ranges from 0–16.7% [4, 12]. In a meta-analysis of 1,112 cases post-LSG, 1.35% included gastric bleeding, 0.84% included abdominal abscess, 0.17% included internal abdominal hernia, 0.17% included gastric leakage, 4.9% included reflux, and 0.34% included gastric ulcers [11]. Few studies have reported mesenteric ischemia post-LSG. Park reviewed LSG cases from 2019–2021 and reported that the morbidity of portal vein thrombosis was 0.3–0.4% and the mortality was 4.8%.

AMI is a rare but lethal disease. The overall incidence is 0.09–0.2% of all acute admissions to emergency departments, according to the guidelines [8]. The high mortality was mainly due to the difficulty of early diagnosis and treatment. Dupree et al. [13] reported that irreversible intestinal necrosis occurred after 10 h of AMI in an animal experiment. The complaints of AMI include abdominal pain, fever, nausea, vomiting, diarrhea, and gastrointestinal bleeding [14]. All of the above symptoms are common in other acute abdominal conditions. Therefore, the patients were usually misdiagnosed at the beginning. This patient was first misdiagnosed due to unspecific symptoms. The risk factors for AMI include hypertension, diabetes mellitus, hyperlipidemia, and hypercoagulable disorders. This always occurred in cases with morbid obesity and postoperative cases, similar to our case. According to the obesity surgery guidelines, routine anticoagulation therapy before surgery is not required. Therefore, no preoperative prophylaxis prevention of deep vein thrombosis was performed in this case. Doctors should consider AMI when patients with morbid obesity are accompanied with sudden onset of abdominal pain. As the accuracy of CTA in diagnosing AMI is above 90% [15], CTA should be performed for such patients as soon as possible.

After 8 days of treatment for the misdiagnosis of intestinal obstruction, our patient was finally diagnosed with VAMI. Unfortunately, small bowel necrosis occurred. Can we confirm intestinal necrosis at the early stage of AMI? Since bacterial translocation occurs after intestinal necrosis, can we use laboratory tests of infection to predict intestinal necrosis? The results remain debated. Chou et al. reported that WBC ≥24 × 10⁹/L was a risk factor associated with intestinal necrosis [16]. Emile et al. reported that the odds ratio was 1.22 in predicting intestinal necrosis when the neutrophil count was >18.1 × 10⁹/L after a meta-analysis among AMI cases [17]. They also reported that the odds ratios were 7.57 and 5.04 in predicting intestinal necrosis when the neutrophil-lymphocyte ratio was >11.05 and the platelet-lymphocyte ratio was >156.26. However, other studies did not find that WBC or CRP were risk factors associated with intestinal necrosis [18–20]. In AMI cases, intestinal hypoxia leads to increased anaerobic glycolysis and lactate metabolites, which eventually leads to metabolic acidosis. Therefore, many studies have reported that pH and lactate are risk factors associated with intestinal necrosis [16, 17, 19, 21]. The guidelines suggest that laparotomy should be performed in patients with peritonitis due to the high possibility of bowel necrosis [8]. Our patient had elevated WBC and CRP levels on the day he returned to the ER on POD 18, but there was no significant change on POD 24. It revealed that the laboratory test of infection could not reveal the intestinal necrosis. Peritonitis in this case also revealed bowel necrosis, as the guidelines suggested.

On CTA on POD 24, we found thrombosis in the superior mesenteric vein and portal vein, ascites in the abdomen, and small intestine wall thickening. Mothes et al. [22] reported that the specificities of intestinal wall pneumatosis, portal vein pneumatosis, decreased intestinal wall enhancement, and dilated bowel >5 cm in judging intestinal necrosis were 98.6, 95.7, 88.6, and 83.3%, respectively. Although the specificity was high, the sensitivity ranged from 15–23%. Our case had the same result.

We performed resection of the necrotic bowel and ostomy of the proximal and distal jejunum instead of one-stage intestinal anastomosis. This operation could avoid postoperative anastomotic leakage, which was reported to have an incidence of 23.4–27% after one-stage intestinal anastomosis [23, 24]. The enteral nutrition path can be easily established through the stoma, and total nutrition can be started sooner after the operation. This is a key point for patient recovery.

Conclusion

For post-LSG morbid obesity cases, doctors should consider the diagnosis of AMI when sudden abdominal pain occurs. CTA can help confirm the diagnosis. Laparotomy should be performed when peritonitis occurs even if the levels from the laboratory tests are not significantly elevated. Ostomy should be the first choice after necrotic bowel resection to prevent anastomotic leakage. This is a case report, so the conclusion should be tested by a large number of studies.

Statement of Ethics

This study protocol was reviewed and approved by the Beijing Tsinghua Changgung Hospital Ethics Committee, approval number (No.: 23405-6-01). Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images.

Conflict of Interest Statement

The authors declare that they have no conflict of interest.

Funding Sources

There was no special funding for the writing of this paper and no grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author Contributions

Tianyi Ma: conceptualization and writing – original draft. Peng Zhang: conceptualization and supervision. Hongwei Zhao and Qian Zhang: data curation.

Funding Statement

There was no special funding for the writing of this paper and no grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data Availability Statement

Data are not available due to ethical reasons. Further inquiries can be directed to the corresponding author.