Author
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Editor
Jose Varghese, MD
Associate Professor of Radiology
Boston University School of Medicine
Boston, Massachusetts
Disclosure: Jose Varghese, MD, has disclosed no relevant financial relationships.
Thromboembolic disease of the abdominal vasculature has a wide variety of manifestations. Acute mesenteric artery ischemia and portal vein thrombosis (PVT) may be life threatening if not identified and treated emergently. Chronic mesenteric ischemia, renal vein thrombosis, mesenteric vein thrombosis, and Budd-Chiari syndrome (BCS) may develop insidiously but lead to significant morbidity and mortality if not appropriately managed. Clinicians have a wide variety of tools available to detect thromboemoblic disease of the abdominal vasculature but must maintain a high degree of suspicion. The image shown demonstrates portal venous gas (white arrow) and thickening of the small bowel (yellow arrow), classic findings of mesenteric ischemia on CT.
Acute mesenteric ischemia is a true medical emergency frequently requiring urgent surgical or intravascular intervention due to an all-cause mortality of 70%. Arterial emboli are the most common etiology, usually when thrombus from the heart dislodge and travel to the mesenteric arteries. As a result, common risk factors include atherosclerosis, arrhythmia, congestive heart failure, recent myocardial infarction, and valvular heart disease. The 2-chamber transthoracic echocardiogram shown demonstrates a large apical thrombus (arrow) in the left ventricle, which, if untreated, could migrate into the mesenteric vasculature.
The splanchnic blood flow claims 10%-40% of cardiac output. When the blood flow is cut off, ischemia and infarction of the bowel develop rapidly. Within 4 hours of ischemia, the mucosal villi (black arrow) become necrotic. Within 6 hours, full-thickness infarction begins to occur. Submucosal edema and hemorrhage (red arrow) produce changes that can be seen on a macroscopic level. Eventually perforation and rupture of intraluminal contents occur, which can lead to lethal sepsis.
The classic presentation for a patient with acute mesenteric ischemia is severe abdominal pain with a relatively benign abdominal examination. The pain is visceral and often very difficult to localize. Nausea, vomiting, and diarrhea are found in roughly one half of patients. Early in the process, stool occult blood testing may be negative. Initial imaging with plain radiographs is often normal, but pneumatosis intestinalis is a classic finding. Pneumatosis intestinalis refers to air within the intestinal wall (arrows) from necrosis. Late findings on plain radiographs include free gas within the abdomen.
Fluoroscopic studies may reveal intraluminal pathology. Thickening of the bowel wall due to edema will change the intraluminal contour producing an appearance termed "thumb printing" (arrowheads) as seen on this single-contrast enema study. Other potential findings include focal areas of narrowing from ischemic strictures and more diffuse areas of narrowing from ischemia induced bowel spasm.
CT with oral and intravenous contrast is the imaging modality of choice to evaluate for mesenteric ischemia. The specificity is greater than 95% to detect primary or secondary findings of mesenteric ischemia. Typical findings are irregular thickening of the bowel wall (arrows) in a distribution consistent with vascular territories. The celiac axis supplies the foregut, which includes the lower esophagus, stomach, duodenum, liver, pancreas, and spleen. The superior mesenteric artery (SMA) supplies the intestines from the jejunum to the mid-transverse colon. The inferior mesenteric artery then supplies the mid-transverse colon to the rectum.
Thrombosis within the vessel wall is a direct finding of mesenteric ischemia on CT. Other CT findings include mucosal necrosis with ulceration, pneumatosis intestinalis, free intraperitoneal gas, portal venous gas, absent intestinal gas, and lack of bowel wall enhancement. Portal venous gas develops secondary to bowel wall ischemia and in the setting of mesenteric ischemia is an ominous finding. It accumulates in the least dependent portion of the abdomen, typically the left hepatic lobe (arrows), which differentiates it from pneumobilia, which localizes centrally in the biliary system.
Angiography provides the best radiographic means to identify intraluminal pathology including thrombosis, stenosis, vasoconstriction, and spasm. Thrombosis typically occurs at the artery origin, while emboli are usually found more distally. The classic appearance of mesenteric occlusion is an abrupt cutoff of an attenuated vessel (arrow) as seen on this selective angiogram of the SMA. The presence of collateral vessels can be used to help differentiate between acute and chronic processes. Depending on the cause of ischemia, endovascular therapy including stenting, thrombolysis, angioplasty, or a combination of these may be attempted to help restore blood flow.
Treatment for mesenteric ischemia depends on the duration and presence of necrotic bowel. In patients with nonocclusive disease, chronic symptoms, or hypovolemia, medical management is most appropriate. Patients with acute ischemia undergo emergent surgery to resect nonviable bowel. Patients with SMA occlusion may have the majority of their small bowel resected making it important to retain every centimeter of viable bowel during the operation. Frequently a repeat operation 24-48 hours after initial surgery is needed, because it may be difficult to differentiate at-risk bowel during the initial operation. A gross specimen demonstrating hemorrhagic dead bowel is shown.
Mesenteric venous thrombosis accounts for only 10% of cases of mesenteric ischemia and has the best prognosis. Risk factors include hypercoagulable states, sepsis, portal hypertension, pancreatitis, previous abdominal surgery, and perforated viscus. The presentation is typically insidious with 7-10 days of vague abdominal discomfort, which is thought to delay diagnosis and increase mortality. Intravenous contrast-enhanced CT is the diagnostic modality of choice, which may reveal an enlarged vein containing low-density intraluminal thrombus (arrow).
The goal of therapy for mesenteric venous thrombosis is reversal of the underlying etiology, typically a hypercoagulable state. Lytic therapy is initiated on a case by case basis. After initial anticoagulation, patients are commonly prescribed long-term anticoagulation with warfarin. The recurrence rate without anticoagulant therapy is 25%. Surgery is reserved for patients with bowel infarction. An intravenous contrast-enhanced CT of the upper abdomen is shown demonstrating thrombus within the portal vein (arrow).
Chronic mesenteric ischemia is a similar but distinct entity from acute mesenteric ischemia. The vast majority of cases are due to diffuse atherosclerotic disease with all 3 major mesenteric arteries involved. The classic presentation is postprandial pain, which leads to fear of eating and weight loss. Patients frequently have a history of vascular disease including myocardial infarction, cerebral vascular disease, or peripheral vascular disease. The disease course is usually progressive paralleling the degree of atherosclerosis. An angiogram is shown demonstrating diffuse collateral blood vessels consistent with chronic mesenteric ischemia.
Due to the rich collateral redundancy in the abdomen typically multiple vessels are involved before patients begin to develop symptoms. The gold standard for the diagnosis of chronic mesenteric ischemia is angiography. Classic findings are vessel narrowing, tortuous vessel pathways, and extensive collateralization. The angiogram shown demonstrates narrowing of the superior mesenteric artery (lower arrow). Duplex ultrasonography is a noninvasive method of analyzing blood flow and may be used to follow patients over time. CT and MR angiography are increasingly being utilized as noninvasive alternatives to traditional angiography.
Treatment for chronic mesenteric ischemia depends on the operative risk. In patients who are at high surgical risk, medical management with anticoagulation is most appropriate. Interventional options include endovascular therapy, with stenting or angioplasty, and surgical bypass. Although stenting decreases hospital stay and mortality, there is a high incidence of restenosis. Preoperative angiography may be helpful in surgical planning to determine appropriate bypass sites. An intraoperative image with exposure of the SMA in preparation for bypass graft surgery is shown.
BCS is obstruction of the hepatic venous outflow tract, most commonly at the level of the inferior vena cava (IVC). BCS leads to an increase in the sinusoidal pressure resulting in delay or reversal of portal venous flow, ascites, and morphologic changes to the liver including severe centrilobular congestion, hepatocellular necrosis, and atrophy. BCS may be caused by congenital webs, thrombosis, injury, inflammation, malignancy, liver disease, or it may be idiopathic. In most patients, accessory veins allow some limited forward flow of blood. The inferior vena cavogram shown demonstrates stenosis of the IVC (black arrow) with reflux of contrast into the hepatic venous circulation (yellow arrow).
The classic presentation of BCS is ascites, hepatomegaly, and abdominal pain. Only one quarter of patients will present acutely and the diagnosis may be significantly delayed. Laboratory evaluation may reveal elevated transaminases and alkaline phosphatase. Ultrasonography is the most useful noninvasive study available in the detection of BCS. Color-flow Doppler allows for the evaluation of absent, slow, or reversed flow in the hepatic veins; it can detect collaterals. and can be used to follow patients over time after therapeutic intervention. The color-flow Doppler ultrasound shown demonstrates absent flow within the right hepatic vein (yellow arrow) with retained flow in the IVC (white arrow).
Although CT is most commonly ordered for patients with abdominal pain, in the evaluation of BCS it usually only reveals nonspecific changes. Detection of thrombus within the hepatic veins occurs in only half of patients. The intravenous contrast-enhanced CT of the upper abdomen shown demonstrates patchy liver enhancement, ascites, and thrombus within the IVC (arrow). MRI techniques, specifically angiography, are promising in the detection of BCS, but have not gained widespread use or validation. Angiography is the classically described gold standard for the evaluation of BCS as it provides direct visualization of the intraluminal vasculature and allows for pressure gradient measurements. A major advantage is the ability to provide simultaneous therapy in certain cases.
Treatment for BCS is etiology specific. Congenital defects are treated with membranectomy or stent placement. Systemic anticoagulation is used for patient with chronic BCS to help prevent disease progression while thrombolytic therapy may lyse acute or subacute thrombus. Interventional therapy includes angioplasty, stenting, or shunting. A transjugular intrahepatic portosystemic shunt (TIPS) may be placed to create an alternative conduit of flow between the portal veins and the IVC. The angiogram image shown demonstrates flow through a patent TIPS (arrow). Liver transplantation is reserved for patients with severe cirrhosis who have failed other treatment options.
PVT is most commonly caused by hepatic parenchymal disease and abdominal sepsis. The portal vein provides 75% of the blood flow to the liver. Longstanding occlusion can lead to cavernous transformation as well as bile duct varices, termed the pseudocholangiocarcinoma sign. PVT typically develops very slowly and usually is not discovered until there is gastrointestinal hemorrhage. Ultrasonography is the imaging modality of choice for the detection of PVT. The ultrasound image shown demonstrates thrombus within the portal vein (solid arrow) and an incidental mass (open arrow). The use of color-flow Doppler can evaluate the degree of occlusion and the presence of collaterals.
CT imaging can be useful to detect PVT as well as concomitant hepatic disease. The intravenous contrast-enhanced CT scan shown through the liver demonstrates multiple low-attenuation masses within the liver as well as absent flow within the portal vein (arrow). MR angiography is currently an active area of investigation. Angiography is the gold standard for the evaluation of PVT and is indicated for presurgical planning, the evaluation of resectable hepatic or pancreatic tumors, and transcatheter embolization. The development of PVT may precipitate emergency intervention with TIPS, thrombectomy, or thrombolysis; however, many subclinical self-resolving cases are suspected based on incidental detection during imaging for other causes.
Renal vein thrombosis (RVT) most commonly occurs in patients with nephrotic syndrome, secondary to the increased hypercoagulable state. The most consistent presentation is findings due to nephrotic syndrome, although flank or abdominal pain may also herald RVT. Thrombus within the renal vein may be directly visualized on CT (arrow) or ultrasound. Indirect findings on ultrasound are an enlarged, edematous kidney and on CT are decreased attenuation during the nephrographic phase, a loss of corticomedullary differentiation, and renal enlargement. Treatment is aimed at controlling the underlying nephrotic syndrome with steroids, diuretics, and angiotensin-converting enzymes inhibitors, while reducing the clot burden with systemic anticoagulation. Interventional therapy is rarely indicated.
Author
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Editor
Jose Varghese, MD
Associate Professor of Radiology
Boston University School of Medicine
Boston, Massachusetts
Disclosure: Jose Varghese, MD, has disclosed no relevant financial relationships.
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