Intramural Esophageal Hematoma as a Complication of Percutaneous Coronary Intervention: A Case Report

Introduction

Intramural esophageal hematoma (IEH) is characterized by blood accumulation between the mucosal and muscular layers of the esophagus, usually confined within the esophageal wall without transmural extension. It is a form of esophageal mucosal tear syndrome or mural injury. It was first reported by Williams in 1957 [1]. A systematic search of PubMed using the term “Intramural Esophageal Hematoma” retrieved fewer than 50 publications, underscoring the rarity of this condition in clinical practice. IEH is an uncommon condition affecting the esophagus, which can emerge independently or as a complication after certain medical procedures. These procedures include esophageal dilation, variceal band ligation, and endotracheal intubation [2]. Patients with a history of taking antithrombotic medications, particularly anticoagulants like heparin, warfarin, and novel oral anticoagulants (NOACs), face an elevated risk of spontaneous hemorrhaging [3]. Percutaneous coronary intervention (PCI) is one of the primary methods for revascularization, with numerous patients undergoing this procedure each year to alleviate symptoms of coronary artery disease [4]. However, complications after PCI are not uncommon. Complications include acute in-stent thrombosis, gastrointestinal bleeding, and cardiac tamponade [5]. We report a case of a patient who experienced complications with IEH after PCI.

Case Report

A 67-year-old man visited the Cardiology outpatient clinic, experiencing episodes of chest pain for the past 24 hours. His medical history included 2 stents implanted in the left circumflex artery (LCX) and the right coronary artery (RCA) 5 years ago, as well as another stent placed in the right coronary artery 2 years ago. He had hypertension for the past 10 years. He was on aspirin, ticagrelor, metoprolol, and statins.

Upon initial assessment, his blood pressure was 119/67 mmHg, body temperature was 36.6°C, and heart rate was 68 beats per minute. The electrocardiography results indicated a normal sinus rhythm, as well as an unremarkable electrocardiogram (Figure 1). Echocardiography revealed the dimensions and shapes of the heart chambers were normal. The concentrations of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I were 0.004 ng/mL and below 20 pg/mL, respectively. Computed tomography (CT) of the lungs indicated bronchitis and coronary stent artifacts (Figure 2).

Two days after admission, the patient received a standard ticagrelor 180 mg and aspirin 300mg loading dose before PCI. Coronary angiography revealed significant stenoses in the left anterior descending artery (LAD) and diagonal branches. PCI was successfully performed on the LAD and D1 using a drug-eluting stent and drug-coated balloon, respectively. Intraprocedural anticoagulation with unfractionated heparin was administered. After surgery he was maintained on DAPT and prophylactic low-molecular-weight heparin (Figure 3). Intraprocedural unfractionated heparin (UFH) was dosed at 7500 IU, with ACT achieved in 300 seconds.

After 18 hours after the operation, he had chest pain accompanied by sweating, followed by nausea, vomiting, and hiccups. Repeated electrocardiograms showed no abnormalities (Figure 1), and myocardial enzymes and troponin tests were negative. The symptoms continued to persist, and a subsequent CT scan of the lungs revealed a hyperdense area within the esophageal wall, suggesting possible bleeding (Figure 3). After obtaining consent from the family, an esophagogastroscopy was performed, which confirmed the presence of IEH (Figure 4). Given the patient’s history of stent implantation and ongoing anticoagulation therapy, the risk of surgical intervention was deemed high, leading to the final decision of conservative treatment with medications. After weighing bleeding versus ischemia risks, we switched to ticagrelor monotherapy to prevent stent thrombosis, with close monitoring for bleeding.

After 8 days of conservative treatment, chest CT indicated a reduction in the size of the esophageal hematoma (Figure 3). An upper-gastrointestinal He was ultimately discharged successfully, and subsequent follow-up indicated his condition remained stable. An upper gastrointestinal tract contrast study revealed no significant strictures in the esophagus (Figure 5). The patient was ultimately discharged successfully, and subsequent follow-up indicated that the patient’s condition remained stable.

Discussion

Post-PCI chest pain should alert physicians, as common etiologies are often procedure-related. Conditions such as acute in-stent thrombosis or cardiac tamponade typically require urgent intervention [6]. However, it is crucial to differentiate these from other causes of chest pain. IEH is a rare disorder that must be considered in patients presenting with chest pain, hematemesis, and dysphagia or odynophagia in the appropriate clinical context [7]. Symptoms such as dysphagia, odynophagia, and hematemesis strongly suggest an esophageal pathology. In such scenarios, imaging plays a vital diagnostic role. Chest radiographs can reveal esophageal dilation, whereas CT provides detailed visualization of esophageal wall thickening, surface irregularities, and luminal narrowing. Esophageal endoscopy is essential for accurate and immediate evaluation of an intramural hematoma, confirming its presence, assessing extent, and predicting complications. In severe cases, endoscopic aspiration can obviate the need for surgery [8]. While endoscopy risks iatrogenic injury, CT is considered safer for monitoring esophageal healing [9]. Recurrent bleeding or new-onset odynophagia can indicate leakage or rupture, warranting prompt evaluation. Surgery for hematoma evacuation and repair is rarely required and is reserved for cases with serious injury. Nonetheless, mortality rates are approximately 7% to 9% regardless of surgical or medical management, which is a topic of ongoing academic discussion [10].

IEH, primarily characterized by hemorrhagic submucosal dissection, especially in the distal esophagus, is classically categorized into 5 etiologies: spontaneous, vomiting-induced, traumatic, coagulopathic, and aortic-related [11,12]. The development of IEH in this patient can be attributed to a confluence of factors: advanced age, long-standing hypertension potentially leading to microvascular fragility, and intensive antithrombotic therapy including aspirin, ticagrelor, and heparin. Ticagrelor, a potent P2Y12 inhibitor, and aspirin synergistically inhibit platelet aggregation, while heparin exerts its anticoagulant effect by enhancing antithrombin activity. These agents collectively impair hemostasis, making the esophageal submucosal vasculature vulnerable to even minor trauma, such as that induced by retching or vomiting.

Moreover, the therapeutic challenges in this case arose from the presence of IHE due to antithrombotic therapy during the perioperative period of PCI. Postoperative nausea and dry cough may have caused esophageal submucosal microvascular rupture, while anticoagulant/antiplatelet therapy contributed to IEH. After placement of a new stent, it was not feasible to discontinue antithrombotic therapy, as stopping the medication would significantly increase the risk of acute in-stent thrombosis. Furthermore, hemostatic agents could not be administered, nor was surgical intervention possible. Ultimately, since endoscopic evaluation indicated a substantial hematoma without any signs of active bleeding, we opted for conservative medical management. Our patient’s stable vitals and lack of active bleeding placed him in a lower-risk subgroup. Conservative treatment can result in spontaneous resolution of IEH with clinical improvement by 1 week and complete CT resolution by 2 months, although antiplatelet therapy complicates management [13].

IEH can be antithrombotic-related. Initially, we adjusted the antithrombotic therapy by discontinuing aspirin and low-molecular-weight heparin, and switching to ticagrelor for antiplatelet therapy. We also implemented a fasting strategy, administered intravenous esomeprazole to protect the esophageal mucosa, and initiated transfusion therapy. Additionally, we used sedation and interventions aimed at reducing hiccups and providing psychological support. As a result, the hematoma gradually resolved.

To mitigate the risk of IEH in patients undergoing PCI, a proactive approach is warranted. This includes assessing bleeding risk prior to initiating antithrombotic therapy, using proton pump inhibitors prophylactically in high-risk patients, and educating patients to avoid straining, retching, or vomiting post-PCI. In cases of unexplained chest pain after PCI, early imaging (eg, CT) should be considered to rule out non-cardiac causes. Multidisciplinary collaboration among cardiologists, gastroenterologists, and radiologists is crucial for timely diagnosis and management, ensuring that ischemic and bleeding risks are optimally balanced.

Conclusions

We described a patient with IHE after PCI. Although IHE is a self-limiting condition with a generally good prognosis following conservative management, it can have serious consequences. Our experience underscores the importance of regarding IHE as a potential adverse outcome of PCI, and our case report shows that although IEH is rare, it can still occur after PCI.