Secondary Logo

Journal Logo

Acute Coronary Artery Thrombus After Tranexamic Acid During Total Shoulder Arthroplasty in a Patient With Coronary Stents: A Case Report

Bridges, Kathryn H. MD; Wilson, Sylvia H. MD

doi: 10.1213/XAA.0000000000000667
Case Reports

Tranexamic acid (TXA), an antifibrinolytic, is routinely used to decrease transfusion rates in total joint replacement surgery. While recent publications have indicated a low risk of TXA-associated thromboembolic events in this orthopedic population, few studies specifically address the safety of TXA administration in high-risk patients. We present a case of acute coronary thrombus requiring emergent intervention in a patient with indwelling coronary stents who underwent shoulder arthroplasty with TXA administration.

From the Department of Anesthesia and Perioperative Medicine, Medical University of South Carolina, Charleston, South Carolina

Accepted for publication September 20, 2017.

Funding: None.

The authors declare no conflicts of interest.

Presented at IARS Poster Session on Medically Challenging Cases, May 2017, Washington, DC.

Address correspondence to Kathryn H. Bridges, MD, Department of Anesthesia and Perioperative Medicine, Medical University of South Carolina, 25 Courtenay Dr, Suite 4200, MSC 240, Charleston, SC 29425. Address e-mail to

Following the CRASH-2 trial (Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage 2) publication, tranexamic acid (TXA) utilization surged for trauma and surgery-associated bleeding.1 TXA is now routinely administered during joint replacement to decrease blood loss and transfusion.2,3 Studies have reported low risk of thromboembolic events in this orthopedic population.4–7 However, few studies have specifically addressed the safety of TXA in high-risk patients with prior thromboembolic events. We present a patient with multiple coronary artery stents and prior in-stent rethrombosis who underwent shoulder arthroplasty with TXA administration and developed acute coronary artery thrombosis requiring emergent coronary intervention. Written consent was obtained from the patient for the publication of this report.

Back to Top | Article Outline


A 71-year-old man with a history of coronary artery disease and 4 indwelling coronary drug-eluting stents (DES) presented for shoulder arthroplasty. His complex cardiac history began with myocardial infarction in 2011 at which time angiography revealed stenosis of the left circumflex artery at the bifurcation of the first obtuse marginal branch. This was treated with DES placement at the bifurcation. Six months later, acute chest pain prompted cardiac catheterization. This revealed 90% restenosis of the first obtuse marginal, which was treated with balloon angioplasty. In 2012, after a positive cardiac stress test, coronary angiography revealed severe stenosis of the first diagonal and right coronary artery requiring DES placement. A patent stent was noted at the left circumflex bifurcation, but complete in-stent thrombosis of the first obtuse marginal was treated with placement of another DES. Surveillance catheterization in 2014 revealed widely patent stents in all vessels. On evaluation in 2017, 2 weeks before surgery, the patient reported excellent exercise tolerance and denied angina. The resting electrocardiogram (ECG) revealed sinus rhythm at 65 beats per minute without abnormalities. Transthoracic echocardiogram (TTE) 2 months prior showed normal systolic and diastolic function without wall motion abnormalities. The patient saw his outside cardiologist 1 week before surgery. Although dual antiplatelet therapy (DAPT) with prasugrel and aspirin had been uninterrupted since 2011, this was stopped 7 days before surgery by his cardiologist.

Figure 1.

Figure 1.

Figure 2.

Figure 2.

On the day of surgery, baseline blood pressure (BP) was 119/77 mm Hg, heart rate (HR) 67 bpm, respiratory rate 16 per minute, and peripheral oxygen saturation 97% on room air. An interscalene perineural catheter was placed preoperatively for postoperative analgesia (preoperative bolus 20 mL, 0.5% ropivacaine; postoperative infusion 0.2% ropivacaine, 6 mL/h). General endotracheal anesthesia was induced with propofol, fentanyl, and rocuronium and maintained with sevoflurane. TXA (20 mg/kg) was intravenously (IV) administered over 30 minutes after anesthetic induction and positioning. BP was noninvasively monitored by a BP cuff. An arterial line was not placed given the patient’s excellent exercise tolerance, lack of angina symptoms, and recent normal TTE. A low-dose phenylephrine infusion served to maintain BP at baseline values. Because the patient was in the sitting position, cerebral oximetry was used to monitor cerebral perfusion. Normocapnia was maintained during pressure-controlled ventilation. The surgery was uneventful with stable hemodynamics and no ECG abnormalities throughout. Preoperative hemoglobin was 12.5 g/dL, and estimated blood loss was 150 mL. The patient emerged from anesthesia without complication and was monitored in the postanesthesia care unit for approximately 1.5 hours with vital sign assessment every 15 minutes. He did not require any pain medications. On discharge by the anesthesiologist, he was alert and comfortable with excellent pain control from the perineural catheter. Approximately 3 hours later, during routine postoperative evaluation, the orthopedic resident noted an awake, comfortable, and conversant patient. Shortly after, the patient called to the nurse’s station complaining of “feeling sweaty.” A nurse quickly responded and found him diaphoretic but arousable. He complained of dyspnea (respiratory rate, 16 per minute; peripheral oxygen saturation 92% on room air) and was hypotensive (BP, 60/40 mm Hg) and bradycardic (HR, 33 bpm). The emergency medical response team was activated. Atropine (0.5 mg IV) was given for bradycardia with little improvement (HR, 42 bpm). Electrocardiography showed complete heart block and acute inferior wall ST elevation consistent with myocardial infarction. High-flow oxygen therapy was initiated by nonrebreather mask and epinephrine infusion administered for hemodynamic support (0.025 µg/kg/min). Aspirin (325 mg) was given orally. The patient was immediately taken to the cardiac catheterization laboratory. He was alert and hemodynamically stable (114/79 mm Hg) on arrival. He complained of 8/10 chest pain and remained bradycardic with heart block. Epinephrine infusion was continued throughout the 2-hour catheterization procedure without sedation. Coronary angiography showed an acute thrombus at the bifurcation of the circumflex coronary artery and first obtuse marginal artery with total occlusion and restenosis of the bifurcation stent (Figure 1). Successful aspiration thrombectomy of the circumflex and kissing balloon angioplasty of the bifurcation lesion were performed and followed by placement of a DES in the left circumflex artery at the level of the atrioventricular groove. Unfortunately, the occlusion of the first obtuse marginal, suspected to be caused by an acute thrombus, could not be repaired (Figure 2). The patient experienced intermittent hemodynamic instability and increased oxygen requirements over the next 24 hours requiring intensive care unit admission with concern for cardiogenic shock. TTE revealed an ejection fraction of 0.42 with inferior wall hypokinesis. Inotropic support with dobutamine and aggressive diuresis improved the patient’s condition. Aspirin (325 mg) and clopidogrel (75 mg) were administered daily for 2 days and then aspirin reduced to 81 mg daily. He was transitioned to the floor on postoperative day 3 and discharged home on postoperative day 8 on daily clopidogrel (75 mg) and aspirin (81 mg) with instructions to continue DAPT for a minimum of 1 year.

Back to Top | Article Outline


TXA administration combined with DAPT cessation in a cardiac high-risk patient likely contributed to stent rethrombosis. Because TXA inhibits fibrinolysis, its administration may increase the risk of thromboembolic events, such as deep venous thrombosis, pulmonary embolism, or myocardial infarction. While few prior reports have described temporal associations between acute myocardial ischemia and oral TXA administered for menorrhagia or hemoptysis, only 2 prior cases of thromboembolic events after IV TXA administration for orthopedic surgery have been published. In 2016, Gerstein et al8 described left ventricular thrombus formation in a patient with human immunodeficiency virus who received intraoperative TXA (1 g bolus followed by 1 mg/kg/h infusion) for spine surgery. Similar to our case, Garg et al9 described a patient in 2014 who experienced a ST elevation myocardial infarction after hip arthroplasty with intraoperative TXA administration (10 mg/kg IV). Notably, in all these published case reports, the patients did not have any cardiac history. While meta-analyses of TXA administration for arthroplasty have not noted an increased risk for thromboembolic events, patients with elevated risk for thromboembolic events were excluded from many of these trials.4–7 One retrospective review of over 1000 arthroplasty surgeries, which included 240 patients with a risk factor for thromboembolic events who received TXA, did not find an increased rate of thromboembolic events.10 However, large prospective trials are needed to confirm those findings.6,7,10 Our case suggests that the prothrombotic nature of TXA may contribute to life-threatening complications in high-risk patient populations.

Our case differs from prior reports because our patient had several risk factors for coronary artery thrombosis. Coronary DES cause impairment in arterial healing characterized by incomplete reendothelialization which contributes to late stent thrombosis.10 Additional risk factors for late stent thrombosis include overlapping stent placement, excessive stent length, and bifurcation stents.11 Additionally, DAPT was held 7 days before surgery by the patient’s cardiologist without discussion with an anesthesiologist. This management is not consistent with the 2016 American College of Cardiology/American Heart Association guidelines, which recommend continuation of aspirin throughout the perioperative period when possible for patients on DAPT who must discontinue P2Y12 inhibitor therapy.12 These guidelines further state that the patient, surgeon, anesthesiologist, and cardiologist should all be included in the decision-making process. Given that prasugrel was discontinued because of concern for intraoperative bleeding, perioperative continuation of aspirin in this high-risk cardiac patient should have been discussed among care providers. Administration of aspirin on the morning of surgery should have been considered when aspirin cessation was noted. A randomized, double-blind, placebo-controlled trial found that perioperative aspirin reduced the risk of major adverse cardiac events in high-risk patients undergoing noncardiac surgery.13 Although this study was not powered to evaluate bleeding complications, a recent meta-analysis of over 30,000 patients undergoing noncardiac surgery found antiplatelet therapy (aspirin, clopidogrel, or DAPT) to convey minimal bleeding risk.14 The authors concluded that antiplatelet agents were safe to continue when indicated. Although our patient’s most recent stents were placed 5 years prior, DAPT cessation combined with TXA administration likely increased his risk for rethrombosis.

In conclusion, the risk of perioperative hemorrhage must be weighed against the risk of a perioperative ischemic cardiac event. Our patient had a normal preoperative hemoglobin concentration and underwent a surgery with a low likelihood of transfusion. Considering the patient’s history of repeated coronary artery thromboses and a surgical procedure with low bleeding risk, aspirin–and possibly DAPT–should have been continued perioperatively. While it is impossible to define the exact cause of this patient’s coronary stent rethrombosis, the indication for TXA must be based on individual risk assessment. Fortunately, TXA-associated thromboembolic events are uncommon. However, further studies are needed to evaluate the safety profile of TXA in cardiac high-risk patients.

Back to Top | Article Outline


Name: Kathryn H. Bridges, MD.

Contribution: This author helped draft the original case report and perform the literature review.

Name: Sylvia H. Wilson, MD.

Contribution: This author helped edit the case report and search the literature.

This manuscript was handled by: Hans-Joachim Priebe, MD, FRCA, FCAI.

Back to Top | Article Outline


1. Shakur H, Roberts I, Bautista R, et al.; CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376:2332.
2. Friedman RJ, Gordon E, Butler RB, Mock L, Dumas B. Tranexamic acid decreases blood loss after total shoulder arthroplasty. J Shoulder Elbow Surg. 2016;25:614618.
3. Zhang H, Chen J, Chen F, Que W. The effect of tranexamic acid on blood loss and use of blood products in total knee arthroplasty: a meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2012;20:17421752.
4. Wu Q, Zhang HA, Liu SL, Meng T, Zhou X, Wang P. Is tranexamic acid clinically effective and safe to prevent blood loss in total knee arthroplasty? A meta-analysis of 34 randomized controlled trials. Eur J Orthop Surg Traumatol. 2015;25:525541.
5. Huang F, Wu D, Ma G, Yin Z, Wang Q. The use of tranexamic acid to reduce blood loss and transfusion in major orthopedic surgery: a meta-analysis. J Surg Res. 2014;186:318327.
6. Madsen RV, Nielsen CS, Kallemose T, Husted H, Troelsen A. Low risk of thromboembolic events after routine administration of tranexamic acid in hip and knee arthroplasty. J Arthroplasty. 2017;32:12981303.
7. Zhou XD, Tao LJ, Li J, Wu LD. Do we really need tranexamic acid in total hip arthroplasty? A meta-analysis of nineteen randomized controlled trials. Arch Orthop Trauma Surg. 2013;133:10171027.
8. Gerstein NS, Brierley JK, Culling MD. Left ventricle thrombus after tranexamic acid for spine surgery in an HIV-positive patient. Spine J. 2016;16:e77e82.
9. Garg J, Pinnamaneni S, Aronow WS, Ahmad H. ST elevation myocardial infarction after tranexamic acid: first reported case in the United States. Am J Ther. 2014;21:e221e224.
10. Whiting DR, Gillette BP, Duncan C, Smith H, Pagnano MW, Sierra RJ. Preliminary results suggest tranexamic acid is safe and effective in arthroplasty patients with severe comorbidities. Clin Orthop Relat Res. 2014;472:6672.
11. Finn AV, Nakazawa G, Joner M, et al. Vascular responses to drug eluting stents: importance of delayed healing. Arterioscler Thromb Vasc Biol. 2007;27:15001510.
12. Levine GN, Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines: an update of the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention, 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery, 2012 ACC/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease, 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction, 2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes, and 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery. Circulation. 2016;134:e123e155.
13. Oscarsson A, Gupta A, Fredrikson M, et al. To continue or discontinue aspirin in the perioperative period: a randomized, controlled clinical trial. Br J Anaesth. 2010;104:305312.
14. Columbo JA, Lambour AJ, Sundling RA, et al. A meta-analysis of the impact of aspirin, clopidogrel, and dual antiplatelet therapy on bleeding complications in noncardiac surgery. Ann Surg. 2017;[epub ahead of print].
Copyright © 2017 International Anesthesia Research Society