OVERVIEW
Mesenteric vein thrombosis accounts for 5% to 15% of all ischemic disorders of the mesenteric vasculature and usually involves the superior mesenteric vein, while the inferior mesenteric vein is rarely involved. The disease is clinically insidious and the diagnosis is often delayed, with the majority of cases being diagnosed during laparotomy.
Etiology
Superior mesenteric vein thrombosis can be categorized as primary or secondary. Those with a clear etiology are called secondary, while those with an unknown etiology are called primary or idiopathic. As the diagnosis of hereditary coagulation disorders and the ability to recognize hypercoagulable states have increased, the proportion of idiopathic cases in the disease has been shrinking, and an etiologic diagnosis can now be obtained in approximately 75% of mesenteric vein thromboses. The most common causes are hypercoagulable states due to inherited or acquired conditions such as tumors, abdominal inflammation, postoperative, cirrhosis, and portal hypertension. The use of oral contraceptives accounts for 9% to 18% of patients with superior mesenteric vein embolism in young women.
Symptoms
Clinical manifestations of acute superior mesenteric vein thrombosis are mostly preceded by abdominal pain, abdominal discomfort, and changes in bowel patterns (diarrhea or constipation). At this stage, the patient’s symptoms are atypical, and there are no clear signs on physical examination, which only show uncertain deep pressure pain in the abdomen, and there are no specific changes in the laboratory tests and auxiliary examinations, which makes the diagnosis of superior mesenteric vein thrombosis very difficult. As the disease enters the progressive stage, the speed of development of the disease is accelerated significantly, the patient’s symptoms are more suddenly aggravated, abdominal pain is severe, persistent, but the localization is not precise, the general pain medication is ineffective, often need strong analgesic such as strong painkillers or dulcolax can be temporarily relieved, which can be accompanied by abdominal distension, nausea, vomiting. In the early stage of progression, the patient’s symptoms are obviously aggravated but the signs are few, and there are no obvious signs of peritoneal irritation such as muscle tension, pressure pain and rebound pain. Subsequently, the ischemia of the intestinal tube gradually aggravates, the intestinal wall becomes edematous and exudates, and secondary peritonitis occurs, then the corresponding signs will appear. In this period, due to the ischemia of abdominal organs and secondary infection, blood routine and blood and urine amylase will be abnormal.
Tests
Blood tests are usually not helpful in the diagnosis of superior mesenteric vein thrombosis. Metabolic acidosis and elevated serum lactate levels can be used to determine the presence of intestinal necrosis, but it is often a sign of advanced disease.
1. Abdominal radiography
Only 5% of patients show specific signs of intestinal ischemia: a finger-pressure sign in the intestinal lumen suggests ischemia of the intestinal mucosa, and an emphysema of the intestinal wall or free gas in the portal vein is characteristic of intestinal infarction due to mesenteric vein thrombosis.
2. Abdominal color Doppler ultrasonography
It can detect mesenteric vein thrombosis, but CT examination should be used in cases where mesenteric vein thrombosis is suspected.
3. CT examination can make the diagnosis in 90% of patients.
However, the diagnostic accuracy of small thrombi in the early portal vein is reduced.
4. Selective mesenteric angiography
It can show thrombi located in large veins or delayed visualization of superior mesenteric veins.
5. MRI
It has high sensitivity and specificity in diagnosing thrombosis of superior mesenteric vein, but its examination process is more complicated and its popularity is poor.
6.Other
Patients with mesenteric vein thrombosis can have plasma-blood peritoneal effusion, in which case diagnostic laparotomy may be helpful in the diagnosis. Pneumoperitoneum manipulation during laparoscopy may increase intra-abdominal pressure and decrease mesenteric blood flow and should be avoided. Colonoscopy and gastroduodenoscopy are of limited value because the colon and duodenum are rarely involved. Endoscopic ultrasonography can detect mesenteric vein thrombosis, but is best used in patients without acute symptoms because of the intestinal dilatation caused during the examination.
In cases of superior mesenteric vein thrombosis, CTA is a better test, not only to visualize the mesenteric vasculature and to determine the extent of the involved bowel, but also to rule out other diseases that cause abdominal pain. Mesenteric angiography, on the other hand, should be used in patients with a suspected tendency to thrombosis, in which case the thrombus tends to be located in the smaller vessels of the mesenteric venous system.
Diagnosis
The diagnosis of this disease relies primarily on imaging studies in addition to symptoms and signs.
Treatment
1. Surgical treatment
The treatment of mesenteric vein thrombosis includes anticoagulation and anticoagulation combined with surgery. For patients with acute or subacute mesenteric ischemia, heparin treatment should be started once diagnosed. Not all patients with superior mesenteric vein thrombosis require surgical exploration, but those with clear signs of peritonitis must be operated on urgently. If the diagnosis of mesenteric vein thrombosis is established intraoperatively, anticoagulation should be initiated. Due to the lack of a clear demarcation between ischemic and normal bowel, an emphasis on obtaining normal bowel breaks for bowel resection may result in the resection of too much viable bowel. Therefore, bowel resection in this disease should be performed more cautiously, with the principle of preserving as much viable bowel as possible.
To avoid removing too much potentially viable bowel, a second exploration after 24 hours is preferred. Secondary exploration is particularly useful in patients with extensive involvement of the bowel and the presence of some mesenteric blood flow. In some cases, the option of performing a conservative bowel resection without a one-stage anastomosis of the bowel and dragging the severed end out of the abdominal wall stoma, which serves as a window into the viability of the bowel, is also available, and may spare some less well off patients from a secondary exploration. In rare cases, thrombectomy can be performed if the thrombus is short-lived and confined to the superior mesenteric vein. Thrombectomy should not be performed for more extensive thrombi. Arterial spasm is a common scenario, and removal of potentially revitalized ischemic bowel can be avoided by a combination of intra-arterial opioid infusion, anticoagulation, and secondary exploration.
2. Medication
In the absence of intestinal necrosis, mesenteric vein thrombosis can be treated medically without surgery. However, there are no indicators that can accurately indicate the risk of intestinal necrosis in a patient. In patients without peritonitis or perforation, intravenous antibiotic therapy is not required. However, heparin anticoagulation given immediately in the early stages of the disease can significantly improve patient survival and reduce recurrence rates, even if applied during surgery. Systemic heparin therapy can be initiated by giving heparin 5000 U intravenously, followed by a continuous infusion to keep the activated partial thromboplastin time at more than twice the normal. Even in the presence of GI bleeding, anticoagulation may be given if the risk of intestinal necrosis is greater than the risk of GI bleeding.
3. Other treatments
Other supportive therapies include gastrointestinal decompression, fluid resuscitation, and fasting. After it is clear that there is no further ischemia in the bowel, oral anticoagulants may be given. Despite the possibility of esophageal varices and bleeding, the benefits of long-term anticoagulation still outweigh the risk of bleeding. In patients without new thrombosis, anticoagulation should be maintained for 6 months to 1 year.
Catheter placement into the portal vein for injection of urokinase or tissue fibrinolytic activator for direct thrombolysis has only been reported in a few attempts. The high risk of bleeding and the low success rate of thrombolytic therapy due to late patient presentation make this method successful in only a few cases. If the thrombus is located in a larger vessel, the prognosis is poor, and the expected benefits of performing direct thrombolysis outweigh the risk of bleeding, direct thrombolysis by cannulation may be considered.