To the Editor:
Acute pancreatitis (AP) is an acute inflammatory process of the pancreas and the annual incidence ranges from 13 to 45 per 100,000 population.1 Complications of AP include pancreatic necrosis, fluid collection, organ failure, and so on.2 Portal hypertension, a complication of pancreatitis, gives rise to esophagogastric varices which may lead to fatal upper gastrointestinal hemorrhage. It is commonly reported in chronic pancreatitis cases where it is mainly caused by splenic vein thrombosis or occlusion.3,4 However, in AP cases, portal hypertension resulted from superior mesenteric vein (SMV) stenosis is rarely concerned and there has been no report about the systemic treatment. Here, we address a case of SMV stenosis in a patient of AP with total minimally invasive treatment, including laparoscopic surgery and stent implantation.
A 62-year-old male presented with sudden onset of upper abdominal pain after high-fat diet, associated with nausea and vomiting. Physical examination was significant for epigastric tenderness. Laboratory tests showed serum calcium of 1.06 mmol/L (reference range, 2.1–2.5 mmol/L) and an elevated amylase of 2612 U/L (reference range, <100 U/L). Abdominal enhanced computed tomography (CT) revealed swollen pancreas with extensive effusion around epigastrium (Fig. 1A). The patient was accompanied with persistent respiratory failure (PaO2/FiO2 was 185) and sequential organ failure assessment score was 4. The diagnosis was severe AP (SAP) with multiple organ failure.
Liquid resuscitation, tracheal intubation, mechanical ventilation, and other organ function supportive treatment were performed. The organ function was gradually stable, but infectious symptom, such as fever, was present. Pancreatic necrosis with infection was considered. After the percutaneous catheter drainage for abdominal abscess, surgery was still considered to control the infection. Meanwhile, CT indicated intrahepatic bile duct expanded mildly with lower part of common bile duct (CBD) stenosis and portal vein (PV) compression. Serum total bilirubin was 156.9 μmol/L (reference range, 0–20.5 μmol/L). Percutaneous biliary drainage was performed because of obstructive jaundice. We performed a laparoscopy-assisted debridement of peripancreatic necrosis and indwelled two irrigation tubes for drainage. Infection was quickly controlled, and the patient resumed oral diet. However, bile drainage and ascites volume were large. Postoperative vascular ultrasonography indicated the left PV sagittal diameter of 0.56 cm. Postoperative CT indicated ascites increased (Fig. 1B). The coronal reconstruction of CT showed SMV stenosis (Fig. 1C). Cholangiography showed the upper segment of CBD was dilated, and the middle and lower segments were not developed (Fig. 1D). Biliary plastic stent and PV stent implantation were then executed. Intraoperative PV angiography indicated a stenosis in the SMV with collateral circulation (Fig. 1E). The PV stent and biliary plastic stent were implanted separately. Postoperative PV angiography showed smooth blood flow and cholangiography showed biliary patency (Figs. 1F-G). The patient recovered smoothly and was discharged in good condition. Computed tomography after 3 months of discharge showed a little necrosis around the pancreas without obstruction of the section from SMV to PV stent and without expansion of CBD. Low molecular weight heparin was used for anticoagulation inhouse, and warfarin was continued for 6 months as outpatient.
There are devastating complications of AP, including pancreatic necrosis, portal hypertension, organ failure, leading to severe prognosis, even death. Extrahepatic portal venous system (PV, splenic vein, and SMV) stenosis, including thrombosis, embolism and occlusion, is more noticeable in chronic pancreatitis and rarely mentioned in AP. Only a retrospective study focusing on CT scans found the prevalence of SMV thrombosis was 14% in 100 AP patients and risk factors included formation of pseudocysts, alcoholic pancreatitis, necrotizing pancreatitis.2 Also, another study demonstrated that 13% of 832 patients with extrahepatic portal venous system thrombosis had pancreatitis (including acute and chronic pancreatitis).5 Moreover, there has been no standard program of prevention and treatment for AP with SMV stenosis.
In AP cases, causes of SMV stenosis include local inflammation, stasis, spasm, and mass effect from surrounding necrotic pancreas as well as direct damage of the venous wall by liberated enzymes.4,6,7 It is more prone to happen in SAP, especially SAP with systemic inflammatory response syndrome, because of more severe inflammation, damage to the vascular endothelium, and hypovolemia.
Mortality associated with acute SMV thrombosis is extremely high, at 20% to 50%.8 Incidence of SMV stenosis is positively correlated with the severity of pancreatitis.2,3 Therefore, it is necessary to pay attention to SMV stenosis in AP, especially regarding prevention and clinical treatment. On one hand, anticoagulation is considered to be the first choice. However, Gonzelez et al9 observed that almost one third of patients had recanalization, regardless of whether they received systemic anticoagulation. The patient's acquired or inherited prothrombotic states is not related to the occurrence of extrahepatic portal venous system thrombosis.2 Whether early anticoagulation can prevent SMV stenosis in AP remains to be studied. On the other hand, debridement and drainage to remove pancreatic necrotic tissue can prevent further inflammation progression and stent implantation can help recanalization of SMV. However, there is no study on the systemic treatment about SMV stenosis in AP. In our case, we used total minimally invasive therapy, including laparoscopic-assisted debridement of pancreatic necrotic tissue and implantation of endovascular stent in SMV stenosis. The prognosis of the patient is currently good. Limited by the number of cases, systemic treatment of AP-associated SMV stenosis remains to be further studied.
Zhe Wan, MD
Bo Shen, MD, PhD
Dong Cen, MD
Hong Yu, MD, PhD
Xiujun Cai, MD, PhD
Zhejiang Provincial Key Laboratory of Laparoscopic Technology
Department of General Surgery Sir Run Run Shaw Hospital School of Medicine Zhejiang University Hangzhou, China firstname.lastname@example.org
This study was supported by Natural Science Foundation of Zhejiang Province (grant number: LY18H030003).
Z.W., B.S., and D.C. contributed equally to this work.
The authors declare no conflict of interest.
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