Clinical Images

Critical Ostial Celiac Trunk Stenosis Presenting as Abdominal Angina during Massive Pulmonary Embolism with Cardiogenic Shock

Jan Belohlavek, MD, Stanislav Beran, MD, Ales Linhart, MD, PhD
Jan Belohlavek, MD, Stanislav Beran, MD, Ales Linhart, MD, PhD
From the Department of Internal Medicine II, Cardiology and Angiology, General Teaching Hospital, Charles University Prague, Czech Republic. The authors report no financial relationships or conflicts of interest regarding the content herein. Manuscript submitted September 12, 2008 and accepted December 2, 2008. Address for correspondence: Jan Belohlavek, MD, Department of Internal Medicine II, Cardiology and Angiology, General Teaching Hospital, Vseobecna fakultni nemocnice U Nemocnice 2, Prague 2 128 00, Czech Republic. E-mail: jbelo@vfn.cz

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ABSTRACT: Massive pulmonary embolism complicated by cardiogenic shock and severe abdominal pain represents both a diagnostic and therapeutic challenge. We present the case of a critically ill patient in whom acute abdominal ischemia, which was caused by splanchnic hypoperfusion secondary to critical ostial celiac trunk stenosis, manifested during the course of massive pulmonary embolism complicated by a cardiogenic shock.

J INVASIVE CARDIOL 2009;21:139–140

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Pulmonary embolism accompanied by abdominal pain suggests possible paradoxical embolization with potentially deleterious end-organ damage if not diagnosed and treated promptly.1,2 We report the case of a patient with severe abdominal pain that occurred during the course of massive pulmonary embolism complicated by cardiogenic shock and was attributed to hypoperfusion due to critical celiac trunk stenosis. Hemodynamic stabilization following successful systemic thrombolysis was promptly followed by relief of the abdominal pain. Case Presentation. A 60-year-old hypertensive male with diabetes suffered from sudden shortness of breath, chest pain and two bouts of syncope while working. On ambulance arrival he also complained of abdominal pain. An anterior ST-elevation myocardial infarction (STEMI) (Figure 1A) was suspected and he was referred to our institution for primary percutaneous coronary intervention (PCI). On admission, he was in shock, with a blood pressure of 65/30 mmHg and a pulse rate of 88 pulses/minute. He was agitated, anxious, dyspneic and showed signs of peripheral hypoperfusion, cyanosis, distended jugular veins and an enlarged liver. He complained of severe abdominal pain and persistent shortness of breath. An urgent echocardiogram revealed a dilated right ventricle with signs of acute overload (Figure 1B). PCI was cancelled and the patient was transferred to the coronary care unit (CCU), where his blood pressure remained at 70/30 mmHg despite volume and catecholamines. Ultrasound examination excluded abdominal aortic aneurysm rupture or dissection. His condition was considered to represent a massive pulmonary embolism with abdominal pain of an unclear origin, and heparin and thrombolysis were administered 25 minutes after admission to the CCU. After only 40 mg of intravenous recombinant tissue plasminogen activator (rtPA), the patient quickly stabilized, hypoperfusion disappeared and his abdominal pain resolved. The entire dose of 100 mg of rtPA was then completed. Cardiac Troponin I subsequently rose to 4.86 µg/l (normal ≤ 0.03). A chest computed tomographic (CT) scan 5 hours later verified bilateral pulmonary embolism (Figure 1C), whereas an abdominal CT revealed celiac trunk ostial stenosis (Figure 1D), further confirmed the next day on angiography (Figure 1E) and treated by percutaneous stent implantation (Figure 1F). Signs of subacute left femoro-popliteo-crural thrombosis were confirmed by duplex ultrasound imaging. The course of his hospitalization remained unremarkable. Transthoracic echocardiography did not show a patent foramen ovale, and further work-up revealed no secondary cause of pulmonary embolism. The patient was initially treated with low-molecular-weight heparin (LMWH) and clopidogrel. During the following days, LMWH was switched to long-term coumadin and clopidogrel was discontinued after one month. He remained asymptomatic at a 1-year follow-up examination; an echocardiogram showed borderline right-sided pressures and a V/Q scan was normal. Discussion. While paradoxical embolization resulting in splanchnic ischemia during pulmonary embolism is a widely recognized complication associated with a preserved or temporarily opened right-to-left shunt (usually PFO),1–4 the hemodynamic instability underlying acute abdominal ischemia caused by critical ostial celiac trunk stenosis has not been described in recent literature to our knowledge. Moreover, symptomatic abdominal angina is considered to occur only when two or three major vessels are occluded or have critical stenosis.5,6 In our case, however, massive pulmonary embolism was complicated by profound hypotension and accompanied by severe abdominal pain. The initial differential diagnosis thus included acute necrotizing pancreatitis and dissecting/ruptured abdominal aneurysm. The patient’s rapidly deteriorating clinical condition precluded us from performing any further diagnostic workup, and thrombolysis as a rescue therapy had been administered. Both the hemodynamic status and abdominal pain resolved quickly following only a partial dose of thrombolytics. Later, critical ostial celiac trunk stenosis, diagnosed by a CT scan and confirmed by angiography, suggested that this lesion may have been responsible for the abdominal angina. The critical pattern of this stenosis on angiography and the substantial clinical manifestation during the “stress test” of systemic hypotension contributed to our decision to treat the lesion by percutaneous stent implantation.7–9

References

1. Fan Z, Roedersheimer R, Lohr J. Systemic thrombolysis using tissue plasminogen activator for a patient with paradoxic embolism: A case report. Vasc Endovascular Surg 2007;41:136–139. 2. Edoga JK, Widmann WD, McLean ER. Paradoxical embolism to the superior mesenteric artery. Clin Cardiol 1987;10:54–56. 3. Turedi S, Gunduz A, Eroglu O, et al. Paradoxical embolism involving 4 organ systems (pulmonary, renal, splenic, and hepatic artery). Am J Emerg Med 2007;25:737. 4. Duman D, Demirtunc R, Duman D, et al. Paradoxical mesentery embolism and silent myocardial infarction in primary antiphospholipid syndrome: A case report. Heart Surg Forum 2006;9:E592–E594. 5. Rosenblum JD, Boyle CM, Schwartz LB. The Mesenteric Circulation. Anatomy and Physiology. Surg Clin North Am 1997;77:289–306. 6. Agarwal AK, Youssef MK, Doyle GJ, Wood CP. Coeliomesenteric trunk stenosis — A rare variation causing mesenteric ischaemia. Eur J Vasc Endovasc Surg 2000;20:405–406. 7. Ikeda O, Tamura Y, Nakasone Y, Yamashita Y. Celiac artery stenosis/occlusion treated by interventional radiology. Eur J Radiol 2008 Jun 16. (Epub ahead of print) 8. Sharafuddin MJ, Olson CH, Sun S, et al. Endovascular treatment of celiac and mesenteric arteries stenoses: Applications and results. J Vasc Surg 2003;38:692–698. 9. AbuRahma AF, Stone PA, Bates MC, Welch CA. Angioplasty/stenting of the superior mesenteric artery and celiac trunk: Early and late outcomes. J Endovasc Ther 2003;10:1046–1053.