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Mesenteric Venous Thrombosis - 2/15/2013

posted Feb 15, 2013, 7:12 AM by Rohit Das   [ updated Feb 15, 2013, 7:12 AM by Purnema Madahar ]

At Chief of Service this Wednesday, we discussed a case of a man in his mid-40s who presented with 4 weeks of post-prandial pain, occurring about 30-40 minutes after eating. The day prior to presenting, he had an episode of “tarry stools.” Ultimately, imaging showed diffuse thrombosis of his mesenteric venous system, including the superior mesenteric vein, splenic vein and portal vein, all in the context of being found to be heterozygote for the Prothrombin gene mutation (thus conferring a 3-4-fold increased risk for VTE disease)…quite fascinating.

Mesenteric ischemic disease comes in a host of flavors. Specifically, it can be arterial (more common) or venous, and can be acute or chronic. Acute arterial mesenteric ischemia is generally a disease of older, atherosclerotic ridden patients, and has a very high mortality (around 60%). It is due to either emboli lodging in the superior mesenteric artery (SMA) (50%), Nonocclusive ischemia (20-30% - usually in the context of hypotension…think of it as “demand” ischemia of the intestines), and SMA Thrombosis (15-20%). Chronic mesenteric ischemia, a.k.a “intestinal angina,” has a more indolent presentation with postprandial pain, classic “fear of eating,” and invariably leads to weight loss (80-90% of patients). Mesenteric venous thrombosis (MVT) is a bit of a different animal – it effects a different population of patients, etiologically and pathophysiologically unique, and has a better prognosis. So, shall we?

·         What’s the epidemiology of MVT? What causes it?

·         What’s the pathophysiology behind MVT leading to intestinal ischemia? How do the acute and chronic forms of MVT differ in this respect?

·         How does MVT present? How is it diagnosed?

·         What are the treatment options, and what’s the overall prognosis?

What’s the epidemiology of MVT? What causes it?

·         MVT is rare, with incidence estimates of around 2-3 cases per 100,000 patient-years. It was first recognized as an etiology for mesenteric ischemia in the 1890s, and recent reports attribute MVT as the cause of mesenteric ischemia/infarction in about 5-10% of cases. As compared to arterial mesenteric disease, MVT affects patients across a broad age range, mainly depending on the etiology. Overall, the mean age range is 45-60 years old based on previous case series.

·         MVT is idiopathic in 20-40% of patients, and most usually have an identifiable risk factor. Table 2 provides a nice overview…non-idiopathic etiologies include hereditary hypercoagulability (JAK2 mutation, hypercoagulability), acquired hypercoagulability (pregnancy, OCPs, nephrotic syndrome…etc.), or direct intra-abdominal causes (cirrhosis, pancreatitis, other intra-abdominal infections…). The distribution between these different categories is very difficult to tease out, mainly due to the rarity of MVT and the fairly limited literature surrounding it.

 

What’s the pathophysiology behind MVT leading to intestinal ischemia? How do the acute and chronic forms of MVT differ in this respect?

·         Just to refresh ourselves on the anatomy – the SMV drains basically the entire small intestinal tract as well as the colon up to the splenic flexure. The SMV runs superiorly, joining with the splenic vein (which itself combines with the inferior mesenteric vein) to form the portal vein. The majority of cases of MVT are associated with concurrent splenic and portal vein thrombosis. The IMV is rarely involved (only around 5%) for unclear reasons.

·         When venous thrombosis leads to significant blockage of venous return from the intestines into the portal system, the intestine becomes engorged with blood. Bowel wall edema occurs, leads to a state of high viscosity flow and consequent impairment of arterial blood delivery à ischemia. In addition, for unclear reasons, venous engorgement seems to also directly lead to arterial vasospasm in the intestines, further compounding the issue.

·          It’s thought that the worst outcomes with MVT are seen when the thrombus initiates in the smaller vessels in the SMV system – i.e., the arcuate veins and intramural veins. This is more commonly associated with cases of inherited hypercoagulability, which makes our case a little odd…On the other side of the coin, when the thrombus originates in the larger vessels (more often the case with local, intra-abdominal causes), infarction takes longer to happen due to formation of collaterals, and outcomes are better.

 

How does MVT present? How is it diagnosed?

·         Virtually all patients with acute MVT present with abdominal pain, which is classically “out of proportion” to their physical exam. Other associated symptoms, like nausea/vomiting, diarrhea, anorexia occur at variable rates and are nonspecific. Most patients present within 2 weeks of symptom onset, with more than 75% having at least 2 days of pain before seeking medical care. When thrombus begins in the larger vessels, MVT can have a “chronic” presentation, where abdominal pain may not be the predominant presenting symptom. Instead, patients may present with complications of portal hypertension, like bleeding or ascites.

·         MVT is a diagnosis dependent on imaging. CT with adequate venous phase is preferred, and when thrombus is extensive and involving the splenic and portal systems, the sensitivity approaches 97%. MRA is also very accurate. Doppler ultrasound is specific, but cannot properly evaluate the smaller mesenteric vessels, so is not particularly sensitive (70-80%).

·         Important in the evaluation of any patient with mesenteric ischemic disease, regardless of etiology, is evaluation for signs of infarction. Hemodynamic instability and/or peritoneal signs are obviously fairly concerning. Lactic acid is also helpful, which has a high sensitivity (80-90%) for intestinal ischemia/infarction. On CT imaging, a “layered” enhancement of the bowel wall is consistent with bowel wall edema/ischemia, whereas bowel with a homogeneous, non-enhancing appearance is concerning for infarction/necrosis – Figure 1 gives a nice a pictorial example of both.

 

What are the treatment options, and what’s the overall prognosis?

·         Anticoagulation is the standard of care. Similar to other VTE scenarios, when there’s an identified, transient risk factor, treatment duration should be for at least 3-6 months. For those who have idiopathic MVT or MVT in the context of a persistent hypercoagulability issue, lifelong treatment should be considered.

·         Thrombolysis, either mechanical or pharmacologic, is often done for MVT. The literature around this subject is limited to small case series, and there are no good recommendations as to when this may be beneficial as an adjunct to anticoagulation.

·         The prognosis for MVT is generally good. Around 90% of patients receiving anticoagulation will recanalize at 5 months (as compared to <10% of patients not on anticoagulation). Excluding patients with malignancy, the one and five-year survival rates approach 90%.

 

The attached review article on MVT is right from home, as Dr. Brandt is one of the experts in the intestinal ischemia world. Also attached is a general review on mesenteric ischemia from 2004. Overall, the presented case was a bit weird…he had symptoms and signs of both acute MVT (abdominal pain, 2 week presenting before seeking medical care) and chronic MVT (gastric variceal bleeding, collateral formation on imaging). Someone should have asked him to read the review article.

 

Have a good weekend!


Acute Mesenteric Ischemia
Oldenburg et. al., Arch Int Med 2004, Volume 164: 1054-62

Harnik et. al., Vasc Med 2010, Volume 15: 407-418
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