A 70-year-old man was admitted to internal medicine department with complaints of heartburn and intolerable chest pain with irradiation to the left arm and shoulder, neck and back. Pain had appeared a day before during domestic physical activity. Based on positive troponine blood test, electrocardiography (ECG), echocardiography and standard clinical diagnostic measures the patient was diagnosed with: Coronary artery disease, non-ST segment elevation myocardial infarction of front-side and apex; Killip class II; heart failure class IV (NYHA classification); Grace scale 174 scores. The patient underwent primary coronarography, balloon angioplasty and left circumflex artery stenting. The time between admission and primary percutaneous coronary intervention (PCI) was 70 min. The patient tolerated the intervention well and was transferred from the IC unit to the internal medicine department ward on the second day after the PCI.
On the 3rd day after breakfast the patient complained of severe diffuse abdominal pain and diarrhea. Clinical examination showed abdominal distention, active peristalsis and no signs of peritoneal irritation. Antispasmodic and nonsteroidal anti-inflammatory drugs did not cease the pain. Blood tests revealed leukocytosis of 21.2 x 10*12/L, alanine transaminase 49 IU/L, aspartate transaminase 89 IU/L, alkaline phosphatase 207 IU/L, D-dimer level of 500 ng/ml (laboratory test dynamics see Table 1).
Abdominal ultrasound showed intense flatulence, no intraabdominal free fluid and no other pathology. Duplex scan was impossible due to poor visualization with bowel gas.
In a view of this sudden diffuse continuous abdominal pain with no findings on clinical examination, patient's anamnesis data (age, myocardial infarction followed by vascular manipulation, hypertension, dyslipidemia) AMI was suspected. Then computed tomography with intravenous contrast was performed (Fig. 1). It revealed CT-signs of generalized abdominal aorta atherosclerosis and circular thrombus with 30 mm length in superior mesenteric artery right below its takeoff from the aorta. Small intestine was dilatated with horizontal liquid levels.
The decision to perform superior mesenteric angiography with aspiration thrombectomy, percutaneous transluminal angioplasty and stenting was made. The time between abdominal pain onset and endovascular intervention was 8 h.
Under local anesthesia with 0.5% lidocaine solution (5 ml), JR-4 6 F guide catheter (Vista Bright Tip, Cordis) was installed to the SMA through right femoral approach. The angiogram was performed showing proximal SMA occlusion in 35 mm from its arising (Fig. 2 (2.1)). 10,000 IU of heparin were administered intra-arterial. The guidewire (Hi-Torque Whisper ES, Abbott) was inserted through the occlusion into the distal segment of SMA (Fig. 2 (2.2)). Thrombus was aspired with extraction catheter (QuickCat, Spectranetics), and blood clots were removed (Fig. 3). During a control angiography, SMA was permeable; there was a stenosis and dissection of the artery in the proximal third.
The coronary stent with a drug coating (3.5 x 23 mm, Abbott Xience) was positioned and expanded under the pressure of 14 atm to the dissection zone of the proximal part of the SMA. The control angiography showed a satisfactory result; residual stenosis and vessel dissection were not detected (Fig. 2 (2.3), (2.4)). The guidewire and catheter were removed; introducer was left until hemostasis was normalized. In total 200 ml of Ultravist contrast were introduced.
Then the patient was transferred to ICU. The next day (4th in-hospital day) abdominal pain still persisted. Clinical examination showed abdominal distention, no peristalsis, no signs of peritoneal irritation. A diagnostic laparoscopy to exclude possible progression of bowel ischemia and recurrent thrombosis, and also in order differentiate with other possible reasons of abdominal pain, was performed.
The operation revealed the dilated small bowel, but there seemed to be no necrotic bowel macroscopically. To confirm adequate bowel perfusion and viability a 0.25 mg of ICG was injected. We observed the bowel using the OPAL1 System (Karl Storz) (Fig. 4). The entire intestine wall showed satisfactory fluorescence emission, indicating no ischemia and necrotic changes. No other pathological changes in the abdominal cavity were detected.
The patient tolerated the surgery well and was transferred to the intensive care unit where, together with cardiologists, we carried out infusion, cardioprotective, detoxification and antibiotic therapy. On the day 6 after SMA stenting (9th in-hospital day), the patient was prescribed enteral nutrition. On the 15th day the patient was discharged in a good state of health with medical recommendations. We had a confirmation that he was alive at 4 months after the operative treatment of AMI.