A case report of spontaneous intercostal artery bleed in the emergency department in a patient with malignancy and anticoagulation: managed with transarterial embolization and discharged hemodynamically stable

Introduction

Background

Spontaneous rupture of an intercostal artery (ICA) is rare, and only a handful of case reports exist in the literature (1-5). ICA rupture most commonly occurs due to trauma, iatrogenic injury, or aneurysm rupture secondary to conditions such as neurofibromatosis type 1, Kawasaki disease, or coarctation of the aorta (6-10). Despite its rarity, the clinical significance of ICA rupture lies in its potential to progress to life-threatening hemorrhagic shock rapidly.

The intercostal arteries are paired branches of the thoracic aorta that supply blood to the chest wall, including the ribs, intercostal muscles, and overlying skin (6). When ruptured, they may present with sudden onset chest, back, or flank pain and can rapidly lead to hemothorax and hemodynamic compromise (1-5). Although spontaneous ICA rupture is rare, it carries a high risk for morbidity and mortality without prompt recognition and intervention. Transcatheter arterial embolization (TAE) is typically the preferred first-line treatment, with surgical evacuation sometimes required in cases of persistent bleeding or retained hemothorax (3,4,11).

Rationale and knowledge gap

Although case reports exist, limited literature describes the successful multidisciplinary management of spontaneous ICA rupture, particularly in patients with complex comorbidities. Our case expands the existing literature by presenting a rare instance of spontaneous ICA rupture in a patient with multiple overlapping risk factors, including malignancy, pathological rib fractures, and anticoagulation therapy. Existing case reports describe a wide range of presentations. Izumoto et al. reported idiopathic rupture in an otherwise healthy individual managed successfully with TAE alone (1); Dua et al. detailed a case without known comorbidities that required multiple surgeries after failed initial control (2); Jang et al. described rupture following severe cough in a healthy patient, treated effectively with embolization (5); Sundram-Novelend et al. presented a case during air travel in an anticoagulated patient that required both embolization and thoracotomy (4); and Ohtaka et al. reported multifocal bleeding in a patient on antithrombotic therapy and mechanical support, which required both TAE and open surgery due to persistent hemorrhage (3). In contrast, our case involved a single-vessel rupture likely due to rib erosion in malignancy and anticoagulation, successfully managed through a staged, multidisciplinary approach without recurrence or rebleeding, illustrating a favorable outcome in a complex clinical context.

Objective

This report aims to broaden the clinical understanding and guide treatment approaches for patients with complex risk factors related to ICA rupture. In this case report, we present a 50-year-old woman who presented to the emergency department complaining of right flank pain. Computed tomography (CT) imaging revealed a right hemothorax and active bleeding from a ruptured ICA, which was subsequently treated with TAE. This case emphasizes the value of rapid recognition and intervention to manage spontaneous ICA rupture effectively. We present this case in accordance with the CARE reporting checklist (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-9/rc).

Case presentation

The patient is a 50-year-old postmenopausal female with a past medical history significant for metastatic hormone receptor-positive, HER2-negative breast cancer diagnosed in 2010. She was treated with bilateral mastectomies, adjuvant chemotherapy, and long-term endocrine therapy. In 2016, she experienced a local skin recurrence that required re-excision, and in 2022, she developed biopsy-proven hepatic metastases treated with stereotactic body radiation therapy. She is currently maintained on abemaciclib and letrozole, with stable disease on recent imaging. Her cancer history is complicated by chronic posterolateral pathological fractures of the right eighth and ninth ribs, first noted one year prior, and hepatic vein thrombosis for which she is on long-term anticoagulation with apixaban. She presented to the emergency department with the acute onset of right flank pain.

Upon arrival, the patient reported being in her usual state of health, but while urinating at home two hours prior, she developed acute right flank pain. The pain radiated to her right shoulder, neck, and down into her right leg, was exacerbated by inspiration, and had no relieving factors. She stated that she had never experienced pain this severe before and felt unable to take a full breath. She denied any recent falls or trauma, dizziness, lightheadedness, nausea, vomiting, hematuria, or dysuria. After the onset of pain, she self-medicated with 400 mg of ibuprofen, which provided only minimal relief.

On initial presentation, the patient appeared visibly uncomfortable and in considerable pain, but was non-toxic appearing. She was slightly tachycardic with a heart rate of 107 beats per minute but remained warm and well-perfused centrally and peripherally. Breath sounds were clear to auscultation bilaterally on initial presentation, with a regular respiratory rate and unlabored effort. The abdominal exam revealed mild tenderness in the right upper quadrant, overlying the liver, and in the right flank, without tenderness to percussion over the flank. She was hemodynamically stable with a blood pressure of 126/73 mmHg.

The initial diagnosis closely aligned with a clinical picture of ureterolithiasis versus nephrolithiasis. However, given her history of metastatic breast cancer and a known pathological rib fracture, the differential diagnosis was broadened to include pulmonary embolism, pulmonary infarct, pneumonia, complications of pathological rib fractures, intra-abdominal or gastrointestinal processes, and retroperitoneal etiologies. The initial workup included a complete blood count, comprehensive chemistry panel, coagulation studies, liver function tests, point-of-care glucose, urinalysis, and a CT scan of the chest, abdomen, and pelvis with contrast. Given her anticoagulated status, the patient’s pain was initially managed with acetaminophen.

The urinalysis demonstrated trace protein and small leukocyte esterase but no significant micro- or macroscopic hematuria. White blood cells (WBCs) were 4–10 per high-power field (HPF) (reference range, 0–5 WBCs/HPF), and red blood cells (RBCs) were 1–2 per HPF (reference range, 0–3 RBCs/HPF), with few bacteria and many squamous epithelial cells, lowering suspicion for ureterolithiasis. The CBC revealed mild macrocytic anemia with a hemoglobin of 10.5 g/dL (reference range, 12.0–15.5 g/dL) and hematocrit of 31.3% (reference range, 35.5%–44.9%). Platelet and WBC counts were within normal limits. Liver function tests showed a mildly elevated alkaline phosphatase of 129 U/L (reference range, 44–147 U/L). The coagulation panel was unremarkable, with a prothrombin time of 12.9 seconds (reference range, 11.0–13.5 seconds) and an international normalized ratio (INR) of 1.1 (reference range, 0.8–1.2).

The patient’s CT scan revealed a linear blush of contrast at the right costophrenic angle (shown in Figure 1), raising suspicion of active bleeding from an ICA adjacent to a pathological fracture of the right ninth rib. The patient’s CT scan, combined with the absence of trauma or procedural intervention, supported a diagnosis of spontaneous ICA rupture.

Figure 1 Computed tomography of the chest with contrast in the arterial-phase of the right chest with a linear hyperdensity of arterial extravasation in the posterior thorax adjacent to pathological eighth and ninth rib fractures in the sagittal view (A) and axial view (B). Arrows indicate hyperdensities on contrast-enhanced arterial-phase CT of the right chest, consistent with active arterial extravasation. CT, computed tomography.

Additionally, a new moderate right-sided pleural effusion with scattered hyperdensities and heterogeneous material at the right lung base, consistent with a hemothorax, was identified, as shown in Figure 2A. The pathological fractures of the eighth and ninth ribs were also visualized on imaging and remained unchanged compared to a CT chest performed three weeks earlier, as shown in Figure 2B.

Figure 2 Computed tomography of the chest with contrast in the arterial phase demonstrating (A) a heterogenous hyperdense pleural fluid collection suggestive of hemothorax in the coronal view (arrow highlights a heterogeneous, hyperdense pleural collection suggestive of hemothorax) and (B) a sagittal view of the healing pathological eighth and ninth rib fractures (arrows indicate fractures of the eighth and ninth ribs).

Interventional radiology (IR) and thoracic surgery were consulted, and the patient was administered a 4-factor prothrombin complex concentrate (PCC) for anticoagulation reversal of apixaban. She was scheduled for embolization in the IR suite. Before the procedure, the patient became progressively more hypotensive, with blood pressure dropping as low as 72/46 mmHg, consistent with hemorrhagic shock. One unit of packed RBCs was transfused. To manage her escalating pain, she received 4 mg of morphine, followed by 0.5 mg of intravenous (IV) hydromorphone.

The patient was then taken to the IR suite, where digital subtraction angiography (DSA) of the right T10–T11 ICA demonstrated a small focus of distal extravasation, as shown in Figure 3A. Embolization successfully achieved hemostasis of an arterial bleed involving the distal segment of the right T10–T11 ICA via TAE through the right common femoral artery. Post-embolization DSA demonstrated adequate hemostasis with no active extravasation, as shown in Figure 3B. Intraprocedural DSA of the right T8–T9, T9–T10, and T11–12 intercostal arteries was negative for extravasation. Following the IR procedure, the initial plan was to place a pigtail chest tube for drainage; however, given the patient’s anticoagulated state and after further evaluation by thoracic surgery, the plan was revised to proceed with video-assisted thoracoscopic surgery (VATS) for decortication and relief of the residual hemothorax burden.

Figure 3 Digital subtraction angiography of the intercostal arteries demonstrates (A) a small area of active arterial extravasation at the distal T10–T11 intercostal artery (arrow identifies a small focus of active arterial extravasation from the distal T10–T11 intercostal artery) and (B) no remaining contrast extravasation post-embolization (arrow shows the same site post-embolization with no residual contrast extravasation on digital subtraction angiography).

Following IR management and admission to the intensive care unit, the patient’s hemoglobin was 8.6 g/dL. Overnight, hemoglobin declined to 7.5 g/dL, and repeat imaging revealed a slight increase in the patient’s right hemothorax burden. After a detailed risk-benefit discussion regarding chest tube placement versus surgical intervention, the decision was made to perform a right thoracoscopic hematoma evacuation. During the procedure, 1.8 L of dark, bloody fluid and hematoma were removed, the hemithorax was thoroughly irrigated, and hemostasis was confirmed. A chest tube was placed at the conclusion of the surgery, and the patient was stable post-operatively. The chest tube was removed on postoperative day one, and the patient was subsequently discharged home in a hemodynamically stable condition. There were no adverse or unanticipated events during the patient’s hospitalization, embolization procedure, or surgical intervention.

At her two-week post-hospital follow-up with the cardiovascular surgery team, the patient reported doing well overall, continually improving appetite, energy, and sleep. She noted mild residual pain while sleeping on her right side, which was attributed to the recent VATS procedure and not out of proportion to expected postoperative discomfort. Notably, her initial flank pain had resolved, and she had no complaints related to hemothorax recurrence or respiratory symptoms. A repeat anteroposterior chest X-ray at that visit showed resolution of the trace right apical pneumothorax, no new focal consolidation, and improved bibasilar atelectasis. Although her residual pain was deemed malignant in origin, she was referred to her palliative care team for continued pain management and support.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

key findings

This case describes a 50-year-old woman with metastatic breast cancer, pathological rib fractures, and anticoagulation who presented with spontaneous ICA rupture. Unlike previously reported cases, this presentation involved multiple overlapping risk factors and was successfully managed with TAE and VATS. The differential diagnosis for acute flank pain can be broad, and spontaneous ICA rupture is extremely rare. ICA rupture is most commonly due to trauma or vessel fragility and aneurysm formation secondary to conditions such as neurofibromatosis type 1 (6,8,11). However, the literature on spontaneous ICA rupture is limited and isolated to case reports. Thus, clear guidelines for diagnosis and management have yet to be established.

Presentations of ICA rupture may include flank, chest, or back pain and can range from mild symptoms to signs of hemorrhagic shock, depending on the extent of bleeding (1-5). Diagnosis is typically made by contrast-enhanced CT, which may show active extravasation or hemothorax and can be confirmed with DSA (2,3,11). In existing literature, TAE is generally considered the first-line treatment for hemodynamically significant bleeding due to its minimally invasive nature and high technical success rate (1,3,11). Surgical intervention, including thoracotomy or VATS, may be necessary for ongoing hemorrhage or evacuation of retained hemothorax. Conservative management has been reported in stable patients without active extravasation but is uncommon (2). Complications of TAE, although rare, can include non-target embolization, vessel injury, or recurrent bleeding (11).

In this case, we presented a patient with multiple comorbidities that increased her risk for spontaneous ICA rupture, such as metastatic breast cancer, pathological rib fractures, and anticoagulation. Prompt identification of these risk factors facilitated early diagnosis and timely multidisciplinary management, leading to a successful outcome. While the term spontaneous is often used to describe vessel rupture in the absence of trauma or procedural intervention, it is important to distinguish this from idiopathic, which implies no identifiable cause. Although there was no direct inciting trauma, the likely etiology was rib erosion of the vessel in the setting of anticoagulation, rendering the event spontaneous but not idiopathic.

Strenths and limitations

A key strength of this case is the successful multidisciplinary management of an ICA bleed using TAE and VATS in a patient with risk factors underrepresented in the literature, including metastatic cancer, pathological rib fractures, and ongoing anticoagulation therapy. The case also contributes detailed documentation of the clinical presentation, imaging findings, treatment decision-making, and follow-up. However, as with all case reports, generalizability is limited. Additionally, while the rupture was presumed to be spontaneous, the precise mechanism remains uncertain, and causality cannot be definitively established in a single patient.

Comparison with similar research

Several previously published cases of ICA rupture differ significantly in etiology and management from our patient’s presentation. For example, Izumoto et al. reported idiopathic rupture in a healthy patient successfully treated with TAE alone (1), while Dua et al. described a case without comorbidities that ultimately required multiple surgeries after initial management failure (2). Jang et al. noted a rupture after a severe cough in a patient without underlying disease (5), and Sundram-Novelend et al. reported a rupture during air travel in a patient on anticoagulation requiring both embolization and thoracotomy (4). Ohtaka et al. presented one of the most severe cases involving multifocal ICA bleeding in a patient on antithrombotic therapy and mechanical circulatory support, necessitating both embolization and open thoracic surgery (3).

Compared to these reports, our case is distinct in its association with malignancy-related pathological rib fractures and concurrent anticoagulation, representing a more complex risk profile. Additionally, our patient underwent a successful staged multidisciplinary approach, with embolization followed by VATS for hemothorax evacuation, resulting in a favorable recovery without recurrence.

The most likely etiology for the patient’s ICA rupture in this case is the adjacent pathological rib fractures. Pathological or atraumatic fractures occur secondary to conditions that weaken bone structure, such as osteoporosis, inherited bone disorders, or malignancy, particularly breast cancer (12,13). Pathological fractures are present in 8–13% of patients with advanced-stage cancer; metastatic disease accounts for approximately 30% of spontaneous rib fractures in these patients (12,13). Osteoporosis may also increase the risk of rib fracture and can be exacerbated by cancer treatment, including chemotherapy-induced menopause and radiation therapy fibrosis (13).

Explanation of findings

In patients with cancer, the development of a hypercoagulable state is common and often exacerbated by anti-cancer therapies (14). Tumor cells and many anti-cancer therapies induce a hypercoagulable state. The complications of hypercoagulability, such as thrombus formation, account for a significant portion of morbidity and mortality in cancer patients (14). Hence, as seen in our patient, many patients are placed on anticoagulant medications to prevent or treat thrombus formation. However, anticoagulant medications have been shown to increase the risk of spontaneous vessel rupture and life-threatening hemorrhage and increase the difficulty of management (11). In our case, the patient’s use of apixaban in the setting of metastatic disease and pathological rib fractures likely contributed to vessel fragility and rupture. Patients with a history of malignancy or undergoing cancer treatment are often on anticoagulant medications and at higher risk of hemorrhagic complications, particularly when structural compromise is also present.

Implications and actions needed

This case reinforces the importance of maintaining a high index of suspicion for ICA rupture in patients presenting with acute chest, back, or flank pain, particularly those with malignancy, pathological rib fractures, or anticoagulation therapy. Providers should consider early imaging with contrast-enhanced CT when ICA rupture is suspected, as delayed recognition may lead to rapid progression to hemorrhagic shock. Prompt involvement of the IR and surgical teams is critical for stabilizing these patients. As case reports accumulate, there is a growing need to develop standardized diagnostic and treatment protocols for the timely identification and multidisciplinary management of ICA rupture.

Conclusions

We report a case of a spontaneous ICA rupture in a 50-year-old female patient with a history of metastatic breast cancer complicated by pathological rib fractures and right hepatic vein thrombosis on long-term anticoagulation. Although rare, spontaneous ICA ruptures are a life-threatening condition and may progress to hemorrhagic shock and death if not promptly recognized and treated. Clinicians should maintain a high index of suspicion for a ruptured ICA in patients with risk factors including malignancy, pathological rib fractures, or anticoagulation therapy who present with acute back, flank, or shoulder pain, especially if accompanied by hemodynamic instability. Early diagnosis with a contrast-enhanced CT and rapid treatment with TAE is crucial for preventing morbidity and mortality.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-9/rc

Peer Review File: Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-9/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2025-9/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Izumoto S, Abe T, Koroki T, et al. A 48-Year-Old Man Presenting as an Emergency with Severe Back Pain, a Large Anterior Paravertebral Hematoma, and Spontaneous Rupture of the Right 9th Intercostal Artery Successfully Managed by Transcatheter Arterial Embolization: A Case Report. Am J Case Rep 2022;23:e934173. [Crossref] [PubMed]
2. Dua A, Dua A, Jechow S, et al. Idiopathic spontaneous rupture of an intercostal artery. WMJ 2014;113:116-8. [PubMed]
3. Ohtaka K, Ohtake S, Ishii Y, et al. Spontaneous intercostal artery bleeding occurring simultaneously in numerous vessels during antithrombotic therapy with mechanical circulatory support: a case report. J Med Case Rep 2024;18:280. [Crossref] [PubMed]
4. Sundram-Novelend SY, Appleton DS, Screaton NJ, et al. Spontaneous rupture of an intercostal artery aneurysm during air flight. Thorax 2008;63:294. [Crossref] [PubMed]
5. Jang JY, Lim YS, Woo JH, et al. Spontaneous rupture of intercostal artery after severe cough. Am J Emerg Med 2015;33:131.e1-3. [Crossref] [PubMed]
6. Misao T, Yoshikawa T, Aoe M, et al. Recurrent rupture of intercostal artery aneurysms in neurofibromatosis type 1. Gen Thorac Cardiovasc Surg 2012;60:179-82. [Crossref] [PubMed]
7. Zhu R, Liu X, Li X, et al. Massive retroperitoneal hematoma caused by intercostal artery bleeding after blunt trauma: a case report. J Cardiothorac Surg 2024;19:248. [Crossref] [PubMed]
8. Arai K, Sanada J, Kurozumi A, et al. Spontaneous hemothorax in neurofibromatosis treated with percutaneous embolization. Cardiovasc Intervent Radiol 2007;30:477-9. [Crossref] [PubMed]
9. Neuwirth CA, Singh H. Intercostal artery aneurysm in a child with Kawasaki disease and known coronary artery aneurysms. J Vasc Interv Radiol 2010;21:952-3. [Crossref] [PubMed]
10. Luo ZQ, Lai YQ, Zhu JM, et al. Intercostal artery aneurysm associated with coarctation of aorta in an adult. J Card Surg 2010;25:719-20. [Crossref] [PubMed]
11. Patrini D, Panagiotopoulos N, Pararajasingham J, et al. Etiology and management of spontaneous haemothorax. J Thorac Dis 2015;7:520-6. [PubMed]
12. Higinbotham NL, Marcove RC. The management of pathological fractures. J Trauma 1965;5:792-8. [Crossref] [PubMed]
13. Harris SR. Differentiating the Causes of Spontaneous Rib Fracture After Breast Cancer. Clin Breast Cancer 2016;16:431-6. [Crossref] [PubMed]
14. Caine GJ, Stonelake PS, Lip GY, et al. The hypercoagulable state of malignancy: pathogenesis and current debate. Neoplasia 2002;4:465-73. [Crossref] [PubMed]