Teaching Case

A 65-year-old man complains of a 4-day abdominal pain, constipation, and a 5 kg weight gain. Physical examination shows a distended abdomen with tympanic percussion without peripheral oedema or peristaltic sounds. He recently had a liver transplant and confessed to discontinuing anticoagulation.

Acute abdominal series (Figure 1) shows dilated small bowel loops on supine film and multiple air/fluid levels on erect film.

A thoracoabdominal contrast-enhanced CT on venous phase was performed (Figure 2).

The axial view shows a proximal superior mesenteric vein patency defect, reactive engorged ileal veins and free fluid. The affected intestinal segments show an oedematous thickened wall with mucosal layer enhancement (so-called target sign).

Coronal multiplanar reconstructions of the abdomen show dilated small bowel segments and a thrombus along the ileal veins extending to the portomesenteric axis, with dilated and tortuous vasa recta (so-called comb sign).

Background

Almost all of the venous drainage of the abdominal cavity is carried to the liver through the portal vein (PV), in which the superior mesenteric vein, the inferior mesenteric vein, and the splenic vein converge. Mesenteric vein thrombosis accounts for 5 to 15% of all cases of acute mesenteric ischemia [1]. Most frequent risk factors are trauma, surgery, portal hypertension, hypercoagulation, abdominal inflammatory diseases, and cancer [1].

Clinical perspective and imaging

Due to the insidious onset, clinical manifestations are variable and non-specific [1,4]. Acute abdominal series, although usually non-specific, may show signs of obstructive ileus (small bowel segments > 3 cm in diameter and air/fluid levels) and pneumoperitoneum. Although ultrasonography may demonstrate loss vascular patency, increased bowel wall thickness, and loss of the gut signature, contrast-enhanced CT shows higher sensitivity and specificity in confirming or ruling out suspicion of mesenteric ischaemia (MI) [2-4].

Unenhanced CT findings on venous MI include bowel dilatation and wall thickening (normal range ≤ 3 mm [5]) with low (oedema) or high attenuation values (if haemorrhagic) [2,3] as opposed to an arterial MI. Venous MI is characterised by hazy mesenteric fat, vasa recta engorgement (so-called comb sign), and ascites as opposed to arterial bowel ischemia [3].

Contrast-enhanced CT findings on MI include abnormal wall enhancement (diminished, absent, or increased) of the affected bowel loop (depending on time-to-onset) and filling defects. In early stages of venous MI, the wall stratification of the affected segment shows an inner (mucosa) and outer (muscularis propria) ring enhancement separated by a hypoattenuating oedematous submucosa, displaying the so-called "target sign" (highly suggestive of MI) [3]. Unlike arterial occlusion, the transition from an ischaemic to a normal bowel segment in venous occlusion is usually gradual, and bowel dilatation goes from moderate to prominent [3]. The advanced stage of ischaemia shows signs of established infarction and necrosis as peritonitis, pneumoperitoneum, pneumatosis intestinallis and portal venous gas [3].

CT protocol (from liver to perineum): non-contrast phase + arterial phase (2,5-4 mL/sec) + venous phase. Use of positive oral contrast is not advised as it masks bowel wall enhancement assessment.

Outcome

Anticoagulation is the mainstay of therapy, along with antibiotics, supplementary oxygen, and crystalloids [4]. Surgery is required if CT shows signs of established infarction. Mortality is highly variable and depends on numerous factors such as age, coexisting diseases, and the need for surgical intervention [2,4].

Our patient was treated with heparin and antibiotics, displaying an excellent clinical course.