Portal vein thrombosis is a well-described, infrequent complication of operations that involve the portal or mesenteric veins. It is a rare complication of laparoscopic general surgery that may be potentially life threatening due to mesenteric ischemia or infarction.3–7
In a literature search, spanning a 17-y time period, James et al.3
identified a total of 18 case reports of portomesenteric vein thrombosis after laparoscopic surgery, excluding operations involving splenectomy.
Case reports of PVT in the bariatric population have emerged as the prevalence of laparoscopic weight loss surgery has increased over the past decade. Portomesenteric thrombosis has been noted after laparoscopic Roux-en-Y gastric bypass and laparoscopic adjustable gastric banding.14–19
While commonly reported complications after laparoscopic sleeve gastrectomy include staple-line leak, respiratory insufficiency, pulmonary embolism, hemorrhage, stricture, and splenic injury,11
to our knowledge this is the second known report of a PVT after sleeve gastrectomy.
Clinical presentation may be subtle and requires a high index of suspicion. In retrospect, larger than expected drainage fluid in the postoperative period in this case may have represented early ascites and PVT in our patient. Most commonly, patients present approximately 2 wk postoperatively with nonfocal abdominal pain, nausea, vomiting, and low-grade fever.1,3
Laboratory values are typically within normal limits; however, leukocytosis and mild elevation of liver function tests can also be seen. Thus, physical examination findings can be normal, or alternatively, if associated with bowel ischemia, patients could present with peritonitis and septic shock. In this case, our patient returned to the hospital with a typical clinical presentation of PVT. However, this presentation is nonspecific, especially since vague abdominal pain, nausea, and vomiting can also be seen for a few weeks in the normal postoperative course of sleeve gastrectomy. In addition, our patient presented with ascites, which was identified on CT. Ascites is found in approximately 1/3 of patients who present with PVT, and may be associated with delayed initiation of anticoagulation treatment or thrombus resistant to recanalization.20
In noncirrhotic patients, the etiology of PVT is generally divided into local and systemic causes.1
Local surgical factors known to predispose to venous thrombosis include direct surgical manipulation of portomesenteric vessels, as in splenectomy. Portal vein thrombosis is known after splenectomy, where ligation of the splenic vein incites endothelial damage that in turn increases thrombogenicity of the vein. Whereas gastric bypass involves some transection of the gastric and mesenteric veins causing endothelial damage, the sleeve gastrectomy involves transection of the short gastric veins alone, and is thus less likely to cause PVT. In these cases, other causes of PVT are considered. Genetic coagulopathies that have been associated with PVT include factor V Leiden, the prothrombin G20210A mutation, protein C and S deficiency, antithrombin III deficiency, the homozygous MTHFR mutation, and hyperhomocysteinemia.21
Our patient had no known prothrombotic hematologic condition and no family history suggesting a genetic coagulopathy.
Portal venous flow is affected by increased intraabdominal pressure with carbon dioxide pneumoperitoneum. It is unclear at what pressure this effect becomes clinically significant; however, it is suspected that a decrease in portal blood flow may contribute to a prothrombotic state in the portomesenteric circulation.10,22
Controversy exists over how clinically relevant this is, as the changes in blood flow vary between patients, and pneumoperitoneum results in venous thrombosis so infrequently.23,24
In addition, the steep reverse-Trendelenburg position during laparoscopic bariatric surgery may augment the flow effects of pneumoperitoneum. While bariatric surgery patients are often treated with routine pharmacologic deep vein thrombosis (DVT) prophylaxis, it is yet unclear what role routine pharmacologic DVT prophylaxis has in prevention of PVT.
The definitive diagnosis of PVT is made with noninvasive imagining. More invasive portal venography is typically not necessary. The diagnosis can be established with contrast-enhanced CT or color Doppler ultrasonography.25,26
Our patient had both studies to confirm the diagnosis, prior to initiation of anticoagulation treatment.
Treatment of PVT is guided by the acuity of the disease and the underlying cause, if known. Therapeutic anticoagulation is recommended in stable, noncirrhotic patients with acute PVT. The suggested duration of treatment is 6 to 12 mo. For patients with known systemic prothrombotic states, treatment may be life long, with the goal of recanalization of the portal vein.27
In addition, any underlying predisposing condition should be treated as well. We initiated treatment with unfractionated heparin, which was later transitioned to warfarin, immediately after the diagnosis was made. In addition, treatment for C. difficile
colitis was started concurrently. Symptoms gradually resolved over the course of 1 wk. It is feasible that the inflammatory response to the C. difficile
infection contributed to the prothrombotic state. However, inflammatory bowel disease, rather than C. difficile
colitis, has been associated with PVT.28,29
We found a single report of mesenteric vein thrombosis (not PVT) in the setting of C. difficile
colitis, in a patient who also had a urinary tract infection.30
Clinical improvement in this patient was rapid following the initiation of systemic anticoagulation and specific antibiotic treatment. Follow-up may include imaging studies to confirm recanalization of the portal vein after 3 mo to 6 mo of treatment.
Although still a subject of debate, some studies suggest that the risk of thromboembolism following bariatric surgery extends long after discharge from the hospital, and prophylaxis should therefore be continued for several weeks into the postoperative period.31
This aggressive approach, however, which could also theoretically lower the risk of PVT, is not considered standard.32
In the setting of persistent thrombosis, or with concerns for bowel ischemia, more aggressive therapy may include endovascular thrombolysis or percutaneous thrombectomy.33,34
No large studies exist to support the routine use of thrombolytics; however, this treatment has been shown to be effective in cases resistant to standard anticoagulation therapy.35
In addition, this treatment has to be weighed against the potential for life-threatening hemorrhage. In this case, there was no indication to initiate thrombolytic therapy.
As mentioned, acquired thrombophilias may also contribute to PVT, particularly in the bariatric population. Obesity is associated with an increased risk of thromboembolism, and consequently all bariatric surgery patients carry an increased risk.36
Additionally, the postoperative bariatric patient on a stringent diet may be micronutrient deficient, and vitamin K deficiency in particular could lead to decreased protein C and S concentrations with an increased prothrombin time. Additional acquired thrombophilias including myeloproliferative disorders and antiphospholipid syndrome should be considered. In this case, the cause of PVT was unclear and likely multifactorial. The patient was morbidly obese, underwent laparoscopic surgery in a reverse-Trendelenburg position, and suffered from C. difficile
colitis, all potential factors contributing to development of PVT in the early postoperative period. As the prevalence of bariatric surgery continues to increase, PVT may become an increasingly identified diagnosis.