Keywords

Physical Examination and History

A 57-year-old female was admitted via emergency room to the hospital on November 24, 2019, with abdominal pain, nausea, and vomiting of 48 hours duration. She was experiencing worsening postprandial pain for the past 2 days. She had poor oral intake and experienced weight loss for the past 6 weeks. Medical comorbidities included Type II diabetes mellitus, hypertension, hyperthyroidism, and hyperlipidemia. Patient was a nonsmoker. She had absent right axillary pulse, right brachial pulse, and right radial pulse. Pulses were not palpable in both lower extremities (femoral, popliteal posterior tibial, and dorsalis pedis). Examination of the abdomen of the showed diffuse tenderness but without any guarding or rigidity. Lab data showed hemoglobin 10.4 g, hematocrit 30.4, platelet count 527,000, sodium 112, potassium 5.5, creatinine 0.9, and lactate 4.9. With medical management (fluid restriction and resuscitation), the lactate level decreased to 2 mg/dL and WBC count to 8600 from 13,000/ml. Sodium level increased to 124 mg/L over the next 24 hours. Contrast-enhanced CT scan of the abdomen, and pelvis showed occlusion of the infrarenal abdominal aorta and bilateral common iliac arteries with reconstitution of external iliac arteries and severe narrowing of both internal iliac arteries. There was 60–70% stenosis of the celiac artery, 80% superior mesenteric artery (SMA), and occlusion of the inferior mesenteric artery (IMA, Fig. 97.1).

Fig. 97.1
figure 1

CTA showing severe SMA stenosis and marked calcification of the infrarenal aorta

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Procedure

Patient underwent abdominal and visceral arteriography on November 26, 2019, in the interventional radiology suite using left brachial puncture. Using ultrasound guidance, a 5 F sheath was inserted. A 260-cm-long 035 GLIDEWIRE® (Terumo, Tokyo, Japan) was advanced into the supraceliac aortogram in AP, and extreme RAO projection showed occlusion of the infrarenal abdominal aorta, moderate stenosis of the celiac artery, severe stenosis of the SMA at its origin, and occlusion of the IMA with large gastroduodenal collaterals (Fig. 97.2). The 5 F sheath was exchanged for a 65-cm-long Arrow® sheath (Teleflex, Wayne, PA). Celiac artery angioplasty was performed with a 6 mm × 2 cm Armada® (Abbott, Abbott Park, IL) balloon (Fig. 97.3). Using Kumpe catheter (Cook Medical, Bloomington, IN), SMA origin was engaged using a 035 mm Glidewire (Fig. 97.4). Glidewire was positioned distally near the terminal branches of the SMA, and a pre-angioplasty was performed with a 6 mm × 2-cm-long Armada balloon followed by deployment of an 8 × 19 mm Omnilink (Abbott, Abbott Park, IL) balloon expandable stent with flaring of the stent for 2 mm into the aorta. Completion arteriogram showed less than 20% stenosis (Fig. 97.5) Gastrointestinal symptoms showed marked improvement, and she was discharged on December 2, 2019.

Fig. 97.2
figure 2

Abdominal aortogram via left brachial approach shows infrarenal aortic occlusion with large gastroduodenal arteries as collaterals

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Fig. 97.3
figure 3

Celiac artery balloon angioplasty with guidewire extending into hepatic artery

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Fig. 97.4
figure 4

Wire access into SMA with associated high-grade stenosis of SMA at its origin

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Fig. 97.5
figure 5

Post-stenting SMA with <20% residual stenosis. There is diminished filling of the gastroduodenal collaterals following stenting

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Discussion

Patients with celiac and mesenteric artery occlusive disease with symptoms of intestinal angina may experience acute exacerbation secondary to low cardiac output (dehydration, hypercoagulability, cardiac arrhythmia). In such patients, careful monitoring in the intensive care unit should be performed as progression of ischemia may result in full-thickness necrosis of the small or large intestine. Patient may need laparotomy for bowel resection, in addition to the endovascular treatment of the mesenteric artery occlusion. Correction of fluid and electrolyte imbalance in addition to endovascular treatment as described in this report may result in reversal of the mucosal ischemia and thus halt the progression to bowel infarction.

Acute mesenteric ischemia is a rare clinical problem that accounts for 0.09–0.2% of all emergency department admissions representing an uncommon cause of abdominal pain. The underlying causes can be nonocclusive or occlusive with the embolic etiology in 50%, thrombotic in 15–25%, and mesenteric venous thrombosis in 5–15%. Mortality rates for 16–80% have been reported [1]. Prognosis of patients of thrombotic occlusion of the SMA with bowel infarction continues to remain poor in spite of modern intensive care unit management, availability of endovascular treatment, and better control of cardiac arrhythmia [1]. In patients with chronic mesenteric ischemia (intestinal angina) and elective mesenteric revascularization, two vessel revascularization is preferred. In emergency settings, bypass to the superior mesenteric artery usually suffices. Scali et al. reported 82 patients who underwent aortomesenteric bypass (aortoceliac/SMA n = 44, aortomesenteric n = 38) for acute mesenteric ischemia with 76% undergoing antegrade bypass. Concurrent bowel resection was evenly distributed (antegrade 45% and retrograde 45%). Incidence of complication was 78% with mortality 37%. The 1-year and 3-year primary patency rate for both was 82% [1]. There was higher rate of reintervention in patients undergoing retrograde bypass. In some patients there is anatomic variation as celiac and SMA may arise as a common trunk. More commonly, the hepatic artery may arise from SMA. Bulut et al. reported excellent long-term secondary patency of celiac and SMA with percutaneous mesenteric stenting. They reported primary patency of 77% at 12 months and 45% at 16 months with primary assisted patency of 90.3% and 69.8% with overall secondary patency of 98.3% and 93.6% [2].

Superior mesenteric artery stenting with use of embolic protection devices (EPD) have been reported by Mendes et al. among 65 patients. The indication for use of EPD was severe calcification in 22 patients (34%) and total occlusion in 16 (25%) and acute thrombosis in 18 (28%). They retrieved large microscopic debris in one third of the patients [3].