Portal de Periódicos da CAPES

Nonocclusive Mesenteric Ischemia: Findings at Multidetector CT Angiography

2007; Elsevier BV; Volume: 18; Issue: 10 Linguagem: Inglês

10.1016/j.jvir.2007.06.024

1535-7732

Uğur Bozlar, Ulku C. Turba, Klaus D. Hagspiel,

Abdominal Surgery and Complications

Nonocclusive mesenteric ischemia is thought to be responsible for approximately 25% of cases of acute mesenteric ischemia, with a high mortality rate (1Bassiouny H.S. Nonocclusive mesenteric ischemia.Surg Clin North Am. 1997; 77: 319-326Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar, 2Shih M.C. Hagspiel K.D. CTA and MRA in mesenteric ischemia I. Role in diagnosis and differential diagnosis.AJR Am J Roentgenol. 2007; 188: 452-461Crossref PubMed Scopus (98) Google Scholar). Nonocclusive mesenteric ischemia usually develops during an episode of cardiogenic shock or a state of hypoperfusion in which excessive sympathetic activity results in secondary vasoconstriction of the mesenteric arteries (2Shih M.C. Hagspiel K.D. CTA and MRA in mesenteric ischemia I. Role in diagnosis and differential diagnosis.AJR Am J Roentgenol. 2007; 188: 452-461Crossref PubMed Scopus (98) Google Scholar). The only generally accepted diagnostic imaging modality for this entity is catheter angiography with papaverine infusion. Due to the subtlety of the arterial findings related to vasoconstriction, the noninvasive diagnosis of this entity is difficult. Herein, we describe the computed tomographic (CT) angiography findings of this entity in a case with angiographic and clinical confirmation.A 93-year-old man with a history of coronary atherosclerosis, severe left ventricular dysfunction (ejection fraction, approximately 15%), and hypertension presented with anterior chest pain associated with nonspecific changes at electrocardiography and an elevated troponin level of 1.5 μg/L (a normal level is less than 0.02 μg/L). This episode was also associated with transient hypotension and severe abdominal pain. At this time, the lactic acid level was normal at 1.6 mmol/L (reference range, 0.5–2.2 mmol/L), aspartate aminotransferase level was slightly elevated at 77 U/L (reference range, <35 U/L), and the alanine aminotransferase level was 32 U/L (reference range, <55 U/L), which is within the normal range. Twenty-four hours later, the patient's serum lactic acid level significantly increased to a maximum of 9.2 mmol/L, with an interval increase in aspartate aminotransferase and alanine aminotransferase levels to 372 and 182 U/L, respectively. Compromised mesenteric arterial flow was suspected, and biphasic multidetector CT angiography of the abdomen and pelvis was performed with a 16-channel multidetector CT unit (LightSpeed 16; GE Medical Systems, Milwaukee, Wis). The collimation and pitch were 1.25 mm and 1.375:1, respectively, in the arterial phase and 5 mm and 1.375:1 in the portal venous phase. One hundred milliliters of an iodinated contrast medium (Omnipaque 350; Nycomed Amersham, Princeton, NJ) was given via the antecubital vein at a flow rate of 4 mL/sec. Automated bolus tracking (Smart Prep; GE Medical Systems) was used for imaging in the arterial phase. Portal venous scans were obtained with a 70-second scan delay after the initial injection. CT angiograms demonstrated an approximately 40% ostial stenosis of the celiac axis and a 90% ostial stenosis of the inferior mesenteric artery secondary to atherosclerotic plaque. The superior mesenteric artery (SMA) was widely patent at its origin and the main trunk, but all of its branches were diffusely small and could only be visualized to within 3 cm of the mesenteric border of the small bowel, despite very good arterial enhancement in the range of 400 Hounsfield units (Figure, part a). The wall of the small bowel did not enhance on the arterial phase scan, and no bowel wall thickening was seen. The portal venous phase scan was also highly abnormal, again reflecting diminished circulation. There was only a minimal increase in the enhancement of the superior mesenteric vein, up to 80 HU from 15 HU in the arterial phase (Figure, part b). The normal attenuation value of superior mesenteric vein at the portal venous phase is approximately 180 HU (3Tozaki M. Naruo K. Fukuda K. Dynamic contrast-enhanced MDCT of the liver: analysis of the effect of different iodine concentrations with the same total iodine dose in the same chronic liver disease patients.Radiat Med. 2005; 23: 533-538PubMed Google Scholar). There was no imaging evidence of hypovolemia. These CT angiographic findings, coupled with poor cardiac output, abdominal pain, and an acutely elevated lactic acid level, were suggestive of nonocclusive mesenteric ischemia. Therefore, it was decided to perform angiography with the intention of diagnostic and therapeutic administration of papaverine.Digital subtraction angiography of selective SMA injection demonstrated diffusely small mesenteric arterial branches, reflux of contrast medium into the aorta, slow flow in the mesenteric arteries with a decreased rate of filling of peripheral vessels, and delayed filling of the mesenteric veins (Figure, part c). After arterial administration of 60 mg papaverine, there was increased filling of the distal branch vessels of the SMA, no more reflux into the aorta despite the use of the same injection parameters, and earlier and more robust bowel wall and mesenteric venous enhancement (Figure, part d). Continuous papaverine infusion was begun with an infusion rate of 1 mg/min. The patient reported improvement of the abdominal pain, and there was normalization of the serum lactic acid level (2.1 mmol/L) 24 hours after treatment. The patient was weaned off papaverine 48 hours later and, to improve his cardiac output, was started on milrinone at 0.25 mcg/kg/min. He continued to do well with milrinone, and was then weaned off it. The patient was discharged 4 days after the onset of symptoms to a skilled nursing facility.The described angiographic findings of mesenteric arterial vasoconstriction are as follows: diffusely small mesenteric arterial branches; a greater degree of contrast medium reflux into the aorta during selective superior mesenteric arteriography than usual; slow flow in the mesenteric arteries with a decreased rate of filling of peripheral vessels; narrowing at the origins of major branches of the SMA; luminal irregularities in branch vessels with segments of narrowing, zones of beading, and abnormal tapering and spasm of the intestinal arcades; and delayed filling of the mesenteric veins (4Trompeter M. Brazda T. Remy C.T. Vestring T. Reimer P. Non-occlusive mesenteric ischemia: etiology, diagnosis, and interventional therapy.Eur Radiol. 2002; 12: 1179-1187Crossref PubMed Scopus (239) Google Scholar). The definitive diagnostic sign is the reversibility of these angiographic findings after the intraarterial administration of papaverine.Although catheter angiography is the only definitive method with which to diagnose this condition, it is rarely performed initially in patients presenting with abdominal pain even if a vascular cause is suspected. CT angiography is the most frequently performed diagnostic procedure in this setting. The ability to diagnose this condition with CT angiography has not been established with certainty because the only previously published report did not have angiographic correlation (2Shih M.C. Hagspiel K.D. CTA and MRA in mesenteric ischemia I. Role in diagnosis and differential diagnosis.AJR Am J Roentgenol. 2007; 188: 452-461Crossref PubMed Scopus (98) Google Scholar, 5Wildermuth S. Leschka S. Alkadhi H. Marincek B. Multislice CT in the pre- and postinterventional evaluation of mesenteric perfusion.Eur Radiol. 2005; 15: 1203-1210Crossref PubMed Scopus (33) Google Scholar). We demonstrated several CT angiographic findings that were suggestive of the presence of nonocclusive mesenteric ischemia. These include a patent main trunk of the SMA, diffusely small side branches that cannot be visualized to within more than 3 cm of the mesenteric border of the small bowel, lack of visualization of the intestinal arcades, and absence of bowel wall thickening. The findings in the portal venous phase were as follows: a minimal increase in the enhancement of the superior mesenteric vein and a diminished increase in systemic venous circulation, reflecting systemic hypocirculation. Nonocclusive mesenteric ischemia is thought to be responsible for approximately 25% of cases of acute mesenteric ischemia, with a high mortality rate (1Bassiouny H.S. Nonocclusive mesenteric ischemia.Surg Clin North Am. 1997; 77: 319-326Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar, 2Shih M.C. Hagspiel K.D. CTA and MRA in mesenteric ischemia I. Role in diagnosis and differential diagnosis.AJR Am J Roentgenol. 2007; 188: 452-461Crossref PubMed Scopus (98) Google Scholar). Nonocclusive mesenteric ischemia usually develops during an episode of cardiogenic shock or a state of hypoperfusion in which excessive sympathetic activity results in secondary vasoconstriction of the mesenteric arteries (2Shih M.C. Hagspiel K.D. CTA and MRA in mesenteric ischemia I. Role in diagnosis and differential diagnosis.AJR Am J Roentgenol. 2007; 188: 452-461Crossref PubMed Scopus (98) Google Scholar). The only generally accepted diagnostic imaging modality for this entity is catheter angiography with papaverine infusion. Due to the subtlety of the arterial findings related to vasoconstriction, the noninvasive diagnosis of this entity is difficult. Herein, we describe the computed tomographic (CT) angiography findings of this entity in a case with angiographic and clinical confirmation. A 93-year-old man with a history of coronary atherosclerosis, severe left ventricular dysfunction (ejection fraction, approximately 15%), and hypertension presented with anterior chest pain associated with nonspecific changes at electrocardiography and an elevated troponin level of 1.5 μg/L (a normal level is less than 0.02 μg/L). This episode was also associated with transient hypotension and severe abdominal pain. At this time, the lactic acid level was normal at 1.6 mmol/L (reference range, 0.5–2.2 mmol/L), aspartate aminotransferase level was slightly elevated at 77 U/L (reference range, <35 U/L), and the alanine aminotransferase level was 32 U/L (reference range, <55 U/L), which is within the normal range. Twenty-four hours later, the patient's serum lactic acid level significantly increased to a maximum of 9.2 mmol/L, with an interval increase in aspartate aminotransferase and alanine aminotransferase levels to 372 and 182 U/L, respectively. Compromised mesenteric arterial flow was suspected, and biphasic multidetector CT angiography of the abdomen and pelvis was performed with a 16-channel multidetector CT unit (LightSpeed 16; GE Medical Systems, Milwaukee, Wis). The collimation and pitch were 1.25 mm and 1.375:1, respectively, in the arterial phase and 5 mm and 1.375:1 in the portal venous phase. One hundred milliliters of an iodinated contrast medium (Omnipaque 350; Nycomed Amersham, Princeton, NJ) was given via the antecubital vein at a flow rate of 4 mL/sec. Automated bolus tracking (Smart Prep; GE Medical Systems) was used for imaging in the arterial phase. Portal venous scans were obtained with a 70-second scan delay after the initial injection. CT angiograms demonstrated an approximately 40% ostial stenosis of the celiac axis and a 90% ostial stenosis of the inferior mesenteric artery secondary to atherosclerotic plaque. The superior mesenteric artery (SMA) was widely patent at its origin and the main trunk, but all of its branches were diffusely small and could only be visualized to within 3 cm of the mesenteric border of the small bowel, despite very good arterial enhancement in the range of 400 Hounsfield units (Figure, part a). The wall of the small bowel did not enhance on the arterial phase scan, and no bowel wall thickening was seen. The portal venous phase scan was also highly abnormal, again reflecting diminished circulation. There was only a minimal increase in the enhancement of the superior mesenteric vein, up to 80 HU from 15 HU in the arterial phase (Figure, part b). The normal attenuation value of superior mesenteric vein at the portal venous phase is approximately 180 HU (3Tozaki M. Naruo K. Fukuda K. Dynamic contrast-enhanced MDCT of the liver: analysis of the effect of different iodine concentrations with the same total iodine dose in the same chronic liver disease patients.Radiat Med. 2005; 23: 533-538PubMed Google Scholar). There was no imaging evidence of hypovolemia. These CT angiographic findings, coupled with poor cardiac output, abdominal pain, and an acutely elevated lactic acid level, were suggestive of nonocclusive mesenteric ischemia. Therefore, it was decided to perform angiography with the intention of diagnostic and therapeutic administration of papaverine. Digital subtraction angiography of selective SMA injection demonstrated diffusely small mesenteric arterial branches, reflux of contrast medium into the aorta, slow flow in the mesenteric arteries with a decreased rate of filling of peripheral vessels, and delayed filling of the mesenteric veins (Figure, part c). After arterial administration of 60 mg papaverine, there was increased filling of the distal branch vessels of the SMA, no more reflux into the aorta despite the use of the same injection parameters, and earlier and more robust bowel wall and mesenteric venous enhancement (Figure, part d). Continuous papaverine infusion was begun with an infusion rate of 1 mg/min. The patient reported improvement of the abdominal pain, and there was normalization of the serum lactic acid level (2.1 mmol/L) 24 hours after treatment. The patient was weaned off papaverine 48 hours later and, to improve his cardiac output, was started on milrinone at 0.25 mcg/kg/min. He continued to do well with milrinone, and was then weaned off it. The patient was discharged 4 days after the onset of symptoms to a skilled nursing facility. The described angiographic findings of mesenteric arterial vasoconstriction are as follows: diffusely small mesenteric arterial branches; a greater degree of contrast medium reflux into the aorta during selective superior mesenteric arteriography than usual; slow flow in the mesenteric arteries with a decreased rate of filling of peripheral vessels; narrowing at the origins of major branches of the SMA; luminal irregularities in branch vessels with segments of narrowing, zones of beading, and abnormal tapering and spasm of the intestinal arcades; and delayed filling of the mesenteric veins (4Trompeter M. Brazda T. Remy C.T. Vestring T. Reimer P. Non-occlusive mesenteric ischemia: etiology, diagnosis, and interventional therapy.Eur Radiol. 2002; 12: 1179-1187Crossref PubMed Scopus (239) Google Scholar). The definitive diagnostic sign is the reversibility of these angiographic findings after the intraarterial administration of papaverine. Although catheter angiography is the only definitive method with which to diagnose this condition, it is rarely performed initially in patients presenting with abdominal pain even if a vascular cause is suspected. CT angiography is the most frequently performed diagnostic procedure in this setting. The ability to diagnose this condition with CT angiography has not been established with certainty because the only previously published report did not have angiographic correlation (2Shih M.C. Hagspiel K.D. CTA and MRA in mesenteric ischemia I. Role in diagnosis and differential diagnosis.AJR Am J Roentgenol. 2007; 188: 452-461Crossref PubMed Scopus (98) Google Scholar, 5Wildermuth S. Leschka S. Alkadhi H. Marincek B. Multislice CT in the pre- and postinterventional evaluation of mesenteric perfusion.Eur Radiol. 2005; 15: 1203-1210Crossref PubMed Scopus (33) Google Scholar). We demonstrated several CT angiographic findings that were suggestive of the presence of nonocclusive mesenteric ischemia. These include a patent main trunk of the SMA, diffusely small side branches that cannot be visualized to within more than 3 cm of the mesenteric border of the small bowel, lack of visualization of the intestinal arcades, and absence of bowel wall thickening. The findings in the portal venous phase were as follows: a minimal increase in the enhancement of the superior mesenteric vein and a diminished increase in systemic venous circulation, reflecting systemic hypocirculation.