Case Report

Intra-Aortic Balloon Pump Related Thrombus in the Proximal Descending Thoracic Aorta with Peripheral Emboli

*Geoffrey T. L. Kloppenburg, MD, Uday Sonker, FRCS(I), FRCS(Ed), Marc A. A. Schepens, MD, PhD
*Geoffrey T. L. Kloppenburg, MD, Uday Sonker, FRCS(I), FRCS(Ed), Marc A. A. Schepens, MD, PhD
ABSTRACT: The intra-aortic balloon pump (IABP) is a mechanical circulatory assist device commonly used for patients with cardiogenic shock or perioperative cardiac failure. The use of IABPs is, however, associated with severe complications occurring in 6–15% of patients. We report a case and present images of a patient who died of sequelae after thrombus formation in the thoracic aorta as an exceedingly rare complication of IABP use.

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J INVASIVE CARDIOL 2009;21:e110–e112 Key words: Thrombosis, intra-aortic balloon pump, aorta The intra-aortic balloon pump (IABP) is a mechanical circulatory assist device commonly used for patients with cardiogenic shock or perioperative cardiac failure. IABPs decrease ventricular afterload and improve diastolic coronary perfusion. The use of IABPs is, however, associated with severe complications occurring in 6–15% of patients.1,2 Local vascular complications at the insertion site are most common and include dissection, thrombosis, false aneurysms or infection, although distal limb ischemia and compartment syndrome may also occur. Incidental serious complications include aortic dissection, perforation, hemorrhage, systemic sepsis, renal failure, paraplegia and visceral ischemia.1–3 We report a case and present images of a patient who died of sequelae from thrombus formation in the thoracic aorta as an exceedingly rare complication of IABP use. Case Report. A 70-year-old male was admitted to our hospital with sudden onset of acute chest pain radiating to the left arm, electrocardiographic changes showing ischemia and positive troponin-T levels. Coronary arteriography confirmed a severe left main stem stenosis and a total occlusion of the proximal obtuse marginal branch. This procedure was complicated by a short episode of ventricular fibrillation after which a 7 Fr IABP was placed percutaneously through the right femoral artery. Balloon counterpulsation was initiated at a 1:1 ratio with 100% augmentation. Emergency surgery for coronary artery bypass with the left internal thoracic artery anastomosed to the obtuse marginal coronary artery and a left main stem plasty with a vein patch was performed. The surgical procedure was uncomplicated, intra-operative transesophageal echocardiography (TEE) showed good left ventricular function and the patient was easily weaned from cardiopulmonary bypass. The IABP remained in situ as a safety measure. The patient’s initial intensive care unit stay was uneventful. He received anticoagulation with low-dose heparin and acenocoumarol until an international normalized ratio (INR) > 2 IU/l was achieved. The patient was extubated after 8 hours and the IABP was removed on the second postoperative day. Two days later, he developed fever due to a pulmonary infection with decreased oxygen saturation, requiring re-intubation. Pseudomonas was identified in the sputum and adequate antibiotic therapy was initiated. On the tenth postoperative day, a percutaneous tracheotomy was performed to facilitate the prolonged respiratory weaning process. On the twelfth postoperative day, ischemic changes were noted on clinical examination of the right leg. Angiography (Figure 1) showed multiple thrombi for which thrombosuction was performed; continuous intravenous heparin infusion was started and urokinase 4,400 IE/kg local intra-arterially was administered. Unfortunately, his clinical condition deteriorated, resulting in necrosis of the toes and a right below-knee amputation had to be performed on the fourteenth postoperative day. TEE was performed to exclude a cardiac origin of the thrombi, revealing a large bulbous mass in the proximal descending thoracic aorta (Figure 2). This location was confirmed to be related to the initial site of the IABP by reviewing previous chest X-rays. The presence of the thrombus and no other aortic pathology were later confirmed on computed tomographic scanning (Figure 2). The patient’s condition remained poor with signs of critical illness polyneuropathy, a poor hemodynamic state and a high ventilation requirement. Gradual onset of subcutaneous emphysema was observed, for which a video-assisted thoracoscopic surgery (VATS) with adequate sealing of the air leak was performed. A small apical pneumothorax persisted for several days. Four days later, the patient deteriorated and experienced severe respiratory failure due to acute respiratory distress syndrome, resulting in asystole and death. Post-mortem examination revealed diffuse alveolar damage combined with extensive broncho-pneumonia. The venous patch plasty of the left main stem and bypass with the left internal thoracic artery were patent. Surprisingly, the thrombus in the thoracic descending aorta was not seen on gross examination of the aorta. No intimal damage could be identified. Discussion. In this report we describe a rare case of thrombus formation in the aorta with peripheral thrombo-embolic sequelae related to the use of IABP. IABP therapy is commonly used as a mechanical circulatory support in high-risk cardiac surgery patients during the perioperative period. The IABP was designed and experimentally tested by Moulopoulos et al in the early 1960s and introduced into clinical use in the setting of cardiogenic shock by Kantrowizt and colleagues in 1968.4,5 Balloon counterpulsation favorably influences cardiac function by augmenting diastolic pressure, resulting in a redistribution of coronary blood flow toward ischemic areas of the myocardium. Afterload is reduced and diastolic pressure augmented, resulting in increased stroke volume and cardiac output. Initially, the use of IABP was restricted to cases of cardiogenic shock during acute myocardial infarction and post-operative cardiac failure. Later indications were extended to include unstable angina pectoris and ventricular arrhythmia. The efficacy of preoperative IABP has been demonstrated, especially in high-risk patients including those with poor left ventricular function, re-do surgery, left main stenosis and patients with unstable angina.6 Complications related to IABP use are frequent and are usually categorized as peripheral ischemia, infection and hematological complications. The presence of low cardiac output with diminished blood flow, thrombotic catheter occlusion and local arterial trauma predisposes patients to peripheral ischemia despite the adequate use of heparin. The incidence of vascular complications is high (6–15%), with the most commonly reported being lower-limb ischemia requiring thrombo-embolectomy.7 The mortality rates associated with IABP use are relatively low, ranging from 0–2.6%, and can be largely attributed to aortic perforation and dissection despite the high incidence of vascular complications.1,2 A benchmark registry including over 16,000 patients reported an overall IABP-related morbidity rate of 2.6% and a mortality rate of 0.05%.8 The known risk factors for development of vascular complications during IABP usage are age, female sex, presence of peripheral arterial disease, obesity, hypertension, smoking, triple-vessel disease, indication for IABP therapy (unstable angina, cardiac arrhythmia and hemodynamic instability), left ventricular aneurysm surgery and the use of a balloon with a sheath.1,2,7,8 Since its introduction, there have been significant technical improvements in IABP catheters including a reduction in size and percutaneous and sheathless insertion. The use of a smaller-diameter catheter was expected to decrease the incidence of vascular complications since the ratio of femoral artery size-to-catheter size has been implicated as an important causative factor in arterial occlusion. Indeed, a significant decrease in vascular complications with risks as low as 1% has been observed during the last decade.9 The observed complications tend to be less severe with the use of smaller-diameter catheters.10 In a large prospective study, Cohen et al were unable to confirm this finding.1 Thrombus formation in the thoracic aorta following IABP therapy, as presented here, is exceedingly rare, and to our knowledge, only one previous case has been reported.11 Several mechanisms for thrombus formation in the aorta have been proposed. First, the use of IABP may cause increased vascular resistance due to local narrowing of the aortic lumen, however, this would lead to thrombus formation during counterpulsation. Second, IABP can cause local trauma to the thoracic aorta, not only during placement and removal, but during balloon counterpulsation as well, especially in the presence of an atherosclerotic aorta. Finally, reduced cardiac output after weaning from IABP support can result in a low-flow state, which predisposes the patient to thrombotic events, though this was not the case in our patient. The thrombus could not be identified on post-mortem examination in our patient, which could be due to full resorption by adequate therapy or to inappropriate post-mortem handling. Diagnosis of lower-limb ischemia in a sedated, ventilated and cardiovascularly compromised patient can be difficult, but diligent clinical observation of the limb, use of serial Doppler ultrasonography, oxygen saturation monitoring, ankle or brachial indices and prophylactic administration of low-molecular-weight heparin may help reduce and more quickly diagnose complications associated with IABP therapy. Conclusion. IABP therapy is an effective means of supporting the failing circulation in high-risk patients. However, serious morbidity and mortality rates should be taken into account. Adverse vascular events, as presented here, are common, and even a thrombus in the proximal descending thoracic aorta may be seen. During IABP use, the patient’s lower limbs should be monitored closely with Doppler ultrasound to detect signs of an early-phase thrombo-embolic phenomenon. When possible, ischemia can often be relieved simply by removing the balloon. _________________________ From the Department of Cardiothoracic Surgery, Nieuwegein, St. Antonius Hospital, The Netherlands. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 31, 2008, provisional acceptance given March 2, 2009, and final version accepted March 4, 2009. Address for correspondence: Geoffrey Kloppenburg, MD, Department of Cardiothoracic Surgery, St. Antonius Hospital, Koekoekslaan 1, 3435 CM Nieuwegein, The Netherlands. E-mail: g.kloppenburg@antonius.net

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