Hemothorax as an infrequent complication of aortic dissection in a young patient: a case report

Introduction

Acute aortic dissection (AAD) is part of the acute aortic syndrome (AAS). It is an infrequent but highly lethal condition defined by the separation of the layers of the aortic wall caused by blood entering through an intimal tear. The estimated incidence is 3–6 cases per 100,000 inhabitants per year, increasing to 30 or more cases among individuals older than 65 years (1). Most epidemiological data on AAD are derived from high-income countries, and the burden in Latin American populations may be underreported (1). Approximately 49% of patients die before reaching a hospital (2), highlighting the critical nature of early recognition and management (3). Diagnosis in the emergency department can be particularly challenging due to the wide spectrum of clinical presentations. It is estimated that 1 out of every 3 patients is initially misdiagnosed, leading to a significant increase in mortality with each hour of diagnostic delay, and many patients die before a definitive diagnosis is established (4).

Recognized risk factors include male sex, systemic arterial hypertension (particularly poorly controlled), atherosclerosis, connective tissue disorders, smoking, use of sympathomimetic drugs, blunt thoracic trauma, pregnancy, large-vessel vasculitis, and iatrogenic causes (1-4). The mean age at presentation is 65 years; only 25% of cases occur before the age of 50 years, and cases occurring before 40 years of age are usually associated with connective tissue disorders (1,2).

The pathophysiology of AAD involves three main mechanisms: (I) an initial intimal tear allowing blood to penetrate the media; (II) formation of a false lumen that propagates longitudinally; and (III) pressure differences between the true and false lumens, leading to collapse of the true lumen, organ malperfusion, and contained or free rupture (5).

Massive hemothorax is a very rare form of presentation, reported in at least 9% of Stanford type B dissections (descending aorta). It results from rupture of the dissected aortic wall into the pleural cavity and is associated with increased in-hospital mortality (1,6,7). Clinical manifestations may range from sudden dyspnea, severe chest or back pain, decreased breath sounds on the left hemithorax, syncope, and neurological deficits (7). Differential diagnoses include pneumonia, acute coronary syndrome, pulmonary embolism, pleural effusion, and abdominal pathology, all of which may contribute to diagnostic delay (6).

Diagnosis is established by computed tomography angiography (CTA), with a sensitivity and specificity of 98–100%. Initial treatment of AAD focuses on strict blood pressure and heart rate control. Stanford type A dissections require urgent surgical intervention, while uncomplicated type B dissections are managed conservatively; complicated type B dissections require endovascular intervention (4). Regarding hemothorax management, although chest tube drainage is necessary to relieve respiratory compromise, it does not control the source of bleeding, which is aortic in origin (5). This article is presented in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0023/rc).

Case presentation

A 39-year-old male presented to the emergency department of Hospital General de Zona No. 1, Aguascalientes, Mexico, with acute chest pain of approximately 50 minutes duration prior to hospital arrival. The patient reported being asleep when he was awakened by sudden, intense chest pain described as constant and tearing, accompanied by diaphoresis, nausea, and dyspnea. Identifiable risk factors included obesity and systemic arterial hypertension under treatment. He denied other comorbidities, tobacco use, or illicit drug use. A structured timeline of the patient’s clinical course is presented below (Table 1) to facilitate understanding of the sequence of events. 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 Helsinki Declaration and its subsequent amendments. Written informed consent could not be obtained due to the patient’s death and inability to contact next of kin despite reasonable efforts. All efforts were made to ensure patient anonymity.

On arrival to the resuscitation area, vital signs were as follows: blood pressure 195/138 mmHg, heart rate 79 beats per minute, respiratory rate 20 breaths per minute, temperature 36.3 ℃, and oxygen saturation 94% on room air. The patient was awake, anxious, and diaphoretic. Pulmonary examination revealed preserved vesicular breath sounds, and cardiac auscultation showed a regular rhythm without tachycardia or additional sounds.

A 12-lead electrocardiogram was obtained due to suspicion of acute coronary syndrome, showing mild ST-segment elevation of 1 mV in V1, 2 mV in V2, and 1 mV in V3, without fully meeting electrocardiographic criteria for myocardial infarction, and a Sokolow-Lyon index of 35 mm. The absence of more definitive changes was attributed to the short duration of symptoms. Treatment was initiated with an angiotensin II receptor blocker, acetylsalicylic acid, low-molecular-weight heparin, high-intensity statin therapy, and opioid analgesia with tramadol. Due to persistent pain, analgesia was escalated to buprenorphine.

Initial laboratory tests showed hemoglobin 15.8 g/dL, leukocyte count 9,050/µL, and platelet count 170,000/µL. Coagulation parameters were within normal limits [prothrombin time (PT) 11.1 s, international normalized ratio (INR) 1.01, activated partial thromboplastin time (aPTT) 27.4 s]. Initial troponin was 0.012 ng/mL, with subsequent values of 0.290 ng/mL and 0.250 ng/mL. Serial troponin measurements were obtained to assess for dynamic changes suggestive of evolving myocardial infarction in the context of the initial clinical suspicion of acute coronary syndrome.

After ruling out myocardial infarction based on three cardiac biomarker measurements and a non-diagnostic electrocardiogram, a non-contrast chest computed tomography (CT) scan was requested as part of the diagnostic protocol for acute chest pain to evaluate potential alternative diagnoses. At that time, aortic dissection was not the primary clinical suspicion (Table 1). The time interval between symptom onset and the first non-contrast CT scan was approximately 2 hours and 43 minutes (Figure 1). Point-of-care ultrasound was not performed prior to imaging. This study revealed a left hemothorax occupying approximately 70% of the left hemithorax, based on visual estimation from imaging. Chest tube placement was considered; however, it was not performed due to clinical decision-making priorities and limitations in available resources at the institution.

Figure 1 Non-contrast chest computed tomography findings. (A) Non-contrast chest computed tomography showing left hemothorax. (B) Same study with lung window settings. Images obtained from original clinical imaging records; resolution reflects source material.

A contrast-enhanced CT scan was subsequently performed as part of the hemothorax evaluation protocol, revealing a dissection of the descending aorta without evidence of visceral branch involvement or organ malperfusion (Figure 2).

Figure 2 Contrast-enhanced computed tomography angiography findings. (A) Massive left hemothorax. (B,C) Intimal flap (arrows) in the descending aorta (Stanford type B), defining a true and a false lumen. Images obtained from original clinical imaging records; resolution reflects source material.

Transfer for evaluation by cardiothoracic and vascular surgery at a higher-level center was considered. However, a few hours later, the patient developed acute neurological deterioration followed by hypotension and cardiac arrest. Advanced cardiopulmonary resuscitation was performed without return of spontaneous circulation.

Discussion

AAS is a term used to describe a group of life-threatening aortic pathologies whose main symptom is chest pain and which require prompt recognition and appropriate management due to their high mortality.

This case involved a 39-year-old patient with obesity and treated hypertension presenting with acute chest pain and no other cardiovascular risk factors (no smoking, no known dyslipidemia, and no metabolic, endocrine, or genetic diseases). Although genetic testing and detailed family history assessment were not performed in this case due to the patient’s rapid clinical deterioration and the emergent context, his relatively young age raises the possibility of an underlying heritable aortic disorder. Genetic testing is not routinely available in the emergency setting at our institution. No prior clinical features suggestive of connective tissue disease were documented at presentation. This represents a limitation of the present report and highlights the importance of considering genetic evaluation and family screening in similar cases. Initial management was directed toward suspected acute coronary syndrome. After this diagnosis was excluded, other possibilities such as pneumonia, pulmonary embolism, and pancreatitis were considered. Chest CT revealed a large left hemothorax, which progressed within 24 hours to shock and subsequent cardiac arrest, without timely diagnosis allowing urgent surgical management.

From a clinical perspective, this case highlights the potential impact of diagnostic anchoring in the emergency setting. The initial presentation with acute chest pain and nonspecific electrocardiographic findings led to a working diagnosis of acute coronary syndrome, which may have delayed consideration of alternative life-threatening conditions such as aortic dissection. Importantly, the identification of a large non-traumatic hemothorax should prompt consideration of underlying vascular causes, including aortic pathology. The clinical course in this case underscores the importance of maintaining a broad differential diagnosis and reassessing initial assumptions when patient evolution is not fully explained by the working diagnosis.

This case is clinically relevant because it illustrates a very infrequent complication of aortic dissection—hemothorax—combined with an atypical patient age, as the patient was younger than the mean age of presentation and had no known genetic connective tissue disorders such as Marfan or Ehlers-Danlos syndrome. The only identified risk factor was systemic arterial hypertension, which is the most important risk factor for AAD (8). This case provides important clinical insights beyond the coexistence of aortic dissection and hemothorax. It highlights the occurrence of this life-threatening condition in a relatively young patient without known connective tissue disease, as well as the potential for initial misdiagnosis due to overlapping features with acute coronary syndrome. Furthermore, it underscores a critical diagnostic pitfall, as the presence of a large non-traumatic hemothorax should prompt consideration of underlying aortic pathology. Early recognition of these features may improve diagnostic accuracy and clinical outcomes.

Available reports are limited and often lack complete clinical data; however, they suggest that hemothorax associated with aortic dissection is uncommon and frequently associated with high morbidity and diagnostic challenges (Table 2) (9,10). Most reported cases involve older patients, and presentations in younger individuals without known connective tissue disorders remain rare. Management strategies vary depending on clinical stability and available resources, but delayed diagnosis is a recurrent factor associated with poor outcomes.

Diagnostic delay due to the complexity of the disease, as well as limited availability of resources and specialized medical services, led to a catastrophic outcome. Additionally, delay in performing the gold standard diagnostic method (aortic CTA) likely contributed to the poor prognosis; earlier diagnosis might have altered the clinical course (3,8). The initial management as acute coronary syndrome reflects the common clinical challenge in differentiating between these entities in the emergency setting, particularly when early electrocardiographic findings are inconclusive.

From an imaging perspective, this case highlights several important considerations. Although CTA is the gold standard for diagnosing aortic dissection, initial evaluation with non-contrast CT may occur in certain clinical settings due to logistical constraints or when alternative diagnoses are initially suspected. In this case, the non-contrast CT provided a critical clue by identifying a large hemothorax; however, it was insufficient to establish the underlying vascular etiology. This represents a potential diagnostic pitfall, as reliance on non-contrast imaging alone may delay definitive diagnosis. Early use of contrast-enhanced imaging should be strongly considered in patients with unexplained hemothorax or persistent chest pain to facilitate prompt identification of aortic pathology. A limitation of this report is the lack of detailed technical information regarding the CT acquisition protocol, including scanner specifications and contrast administration parameters, which were not available in the clinical records.

Management of Stanford type B aortic dissection depends on the presence of complications. While uncomplicated cases are typically managed with optimal medical therapy focused on strict blood pressure and heart rate control, complicated cases—defined by rupture, malperfusion, persistent pain, or hemodynamic instability—require urgent intervention. Thoracic endovascular aortic repair (TEVAR) has become the preferred treatment in many cases due to its lower morbidity and mortality compared to open surgery (4,5). In this context, the presence of a massive hemothorax suggests a complicated dissection with possible rupture, which may benefit from early endovascular or surgical management. Delayed diagnosis and lack of timely transfer to a higher-level center with cardiothoracic capabilities may significantly impact patient outcomes, as early intervention is a key determinant of survival.

The exact cause of cardiac arrest could not be definitively established due to the absence of post-mortem examination. However, the clinical presentation and imaging findings suggest hypovolemic shock secondary to aortic rupture into the pleural cavity as the most likely mechanism. No post-mortem examination was performed, which limits definitive confirmation of the extent of dissection and the exact site of rupture.

It is imperative to search for causes other than myocardial infarction in patients presenting with acute chest pain and to consider aortic dissection in all cases of non-traumatic hemothorax (6). In this case, delayed recognition of aortic dissection limited the opportunity for early referral to a higher-level center, highlighting the diagnostic complexity and potential consequences of atypical presentations.

Conclusions

AAS, particularly in its form as AAD, presents with a wide range of well-described symptoms; however, it may rarely present with atypical manifestations such as hemothorax, which has been reported in selected series as an uncommon but severe complication of aortic dissection and typically affects older male patients. A high index of suspicion is required to prompt appropriate diagnostic studies for early diagnosis and timely management. Prognosis is poor in most cases and even more lethal in the presence of atypical clinical features, which often represent a source of diagnostic confusion for clinicians.

Acknowledgments

Acknowledgments to Emergency Service Department for providing access to the patient’s medical record.

Footnote

Reporting Checklist: The author has completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0023/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0023/prf

Funding: None.

Conflicts of Interest: The author has completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0023/coif). The author has no conflicts of interest to declare.

Ethical Statement: The author is 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 Helsinki Declaration and its subsequent amendments. Written informed consent could not be obtained due to the patient’s death and inability to contact next of kin despite reasonable efforts. All efforts were made to ensure patient anonymity.

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/.

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