Esophageal anastomotic stenosis is a common complication following esophageal cancer surgery, potentially leading to dysphagia and significantly impacting patients' quality of life. Endoscopic balloon dilation is widely regarded as an effective and safe treatment for esophageal stricture (1); however, common complications may include esophageal perforation, bleeding, and chest pain (2). Hoarseness can be caused by acute or chronic laryngitis, functional voice disorders, tumors, or neurogenic disorders; however, hoarseness resulting from endoscopic treatment is rare (3). A penetrating aortic ulcer, characterized by ulcerative lesions resulting from the rupture of atherosclerotic plaques in the aortic intima (4), represents a rare but serious complication after endoscopic therapy. Vigilance for potential complications following endoscopic procedures is crucial, as early detection and timely intervention are essential for improving patient outcomes. This study presents the case of a penetrating aortic ulcer following endoscopic balloon dilation, highlighting the importance of prompt recognition of such postoperative complications.

A 64-year-old male patient was admitted to Kunshan First People's Hospital in March 2023, reporting a six-month history of intermittent dysphagia.

The recurrent laryngeal nerve constitutes the primary motor nerve for the larynx and is vulnerable to compression or injury due to a variety of cervicothoracic disorders, including aortic aneurysms, mediastinal tumors, surgical interventions, trauma, exposure to neurotoxins, and viral infections (5). Such damage may produce vocal-cord paralysis and hoarseness, a symptom often attributed to benign factors. When hoarseness persists or occurs suddenly without an obvious cause, it may indicate serious underlying pathology and warrants further evaluation. Ortner syndrome, also known as cardiac-vocal cord syndrome, represents a rare etiology of hoarseness characterized by vocal cord paralysis stemming from cardiovascular conditions (6). Specifically, aortic aneurysms, pulmonary hypertension, and other primary cardiovascular diseases that induce dilation of the aorta or pulmonary artery, along with left atrial enlargement, can induce hoarseness by exerting pressure on the recurrent laryngeal nerve, located between the aortic arch and the pulmonary artery (7). Direct laryngoscopy frequently reveals reduced activity or paralysis of the left vocal cord in affected patients. In this case, the patient's postoperative discomfort is attributed to compression of the left recurrent laryngeal nerve by penetrating aortic ulcers and an intramural aortic hematoma.

A penetrating aortic ulcer is defined as the ulceration of an atherosclerotic plaque within the aorta that breaches the internal elastic lamina and extends into the media, typically associated with varying degrees of intramural hematoma formation (8). PAU represents a complex and potentially life-threatening condition characterized by rapid progression (9), which can culminate in catastrophic aortic rupture or other severe complications. The true prevalence of PAU remains elusive; however, risk factors such as smoking, advanced age, hypertension, hypercholesterolemia, and other associated comorbidities may increase the likelihood of developing this condition (10). On computed tomography (CT) imaging, PAUs characteristically present as contrast-filled, pouch-like protrusions within the thickened aortic wall, often accompanied by adjacent intramural hematoma formation (11). Given that PAUs are frequently identified as localized segmental wall lesions, endovascular stent grafting is considered the primary therapeutic modality, particularly for elderly patients with multiple underlying comorbidities and a prohibitively elevated risk associated with open surgery (12). Our management strategy with thoracic endovascular aortic repair (TEVAR) is strongly supported by contemporary clinical practice guidelines, which recommend endovascular repair as the first-line therapy for contained ruptures and traumatic injuries of the descending thoracic aorta (13–15).

The development of a PAU following endoscopic dilation likely results from a combination of patient-specific vulnerability and procedural factors. In our patient, the pre-existing aortic calcification seen on CT signifies a stiff, atherosclerotic aortic wall with limited elasticity. We postulate that the mechanical force exerted by the balloon dilation directly traumatized this compromised aortic segment. This trauma likely caused focal disruption of the atherosclerotic plaque and underlying intima, initiating PAU and intramural hematoma formation. While underlying atherosclerosis creates a predisposed environment, the clear temporal relationship between the procedure and the onset of symptoms strongly supports an iatrogenic etiology rather than a spontaneous event. While our case of a penetrating aortic ulcer following balloon dilation is exceptionally rare, it exists within a spectrum of documented, though scarce, iatrogenic aortic injuries resulting from esophageal interventions. The literature contains instructive parallels that underscore the potential for catastrophic vascular complications. Tezcan et al. reported a direct iatrogenic aortic injury in a child during esophagoscopy for foreign body removal, where a balloon dilator was subsequently used in an attempt to control the bleeding, necessitating emergent open surgical repair (16). This case highlights that mechanical instrumentation near the esophagus, even in the absence of pre-existing aortic disease, can directly traumatize the aortic wall. Furthermore, the risk extends beyond dilation to other procedures. Liao et al. described a fatal aortoesophageal fistula (AEF) that developed secondary to a pseudoaneurysm caused by an esophageal stent placed for malignancy (17). This illustrates that sustained pressure from an intraluminal device against the aorta, especially in the context of a compromised tissue plane, can lead to erosion and fistulization. Our case contributes a critical nuance to this clinical spectrum: unlike the immediate, massive bleeding seen in direct aortic injury or the classic “herald bleed” of an AEF, our patient presented with a contained aortic injury (PAU) whose primary manifestation was a neurologic symptom (Ortner's syndrome). This distinctive presentation underscores the need to consider vascular etiologies even in the absence of overt hemorrhagic signs, particularly when hoarseness arises post-procedure. The collective evidence from these cases solidifies the existence of this catastrophic complication pathway and mandates a high index of suspicion during any esophageal intervention close to the aorta.

In conclusion, the case delineated in this study, which involves aortic penetrating ulcers and hematomas following endoscopic balloon dilation, resulting in left vocal cord paralysis, represents a clinically rare but life-threatening phenomenon. This report serves as a critical reminder of the potential for serious vascular injury during seemingly routine endoscopic procedures. It underscores the importance of vigilant patient selection, consideration of pre-procedural imaging in high-risk cases, and the need for heightened awareness among endoscopists to promptly identify and manage such catastrophic complications.