Keywords: Aortic dissection, haemopericardium, Stanford type A dissection, CT imaging, acute chest pain, emergency radiology, cardiovascular emergency, pericardial tamponade, thoracic aorta, cardiovascular imaging
Introduction
Aortic dissection with haemopericardium represents one of the most catastrophic cardiovascular emergencies, carrying an exceptionally high mortality rate without immediate diagnosis and intervention. This life-threatening condition arises when an intimal tear in the aortic wall allows blood to enter the media, creating a false lumen that may rupture into the pericardial sac, leading to haemopericardium and potentially fatal cardiac tamponade. Rapid recognition and urgent management are crucial.
This comprehensive review provides an expert-level synthesis of the pathophysiology, epidemiology, clinical presentation, imaging features, differential diagnosis, diagnostic strategy, treatment, and prognosis of aortic dissection with haemopericardium, grounded in the most authoritative contemporary literature.
Pathophysiology of Aortic Dissection with Haemopericardium
Aortic dissection begins with a tear in the intimal layer of the aorta, allowing high-pressure blood flow to penetrate into the medial layer, forming a false lumen. Propagation of this dissection plane may extend proximally or distally along the aorta and into major branch vessels.
In Stanford type A dissections, involvement of the ascending aorta places the dissection in direct proximity to the pericardial sac. When the false lumen ruptures through the adventitia, blood rapidly accumulates within the pericardial space, producing haemopericardium. The rapid rise in intrapericardial pressure restricts ventricular filling, leading to acute cardiac tamponade, characterized by reduced cardiac output, hypotension, and cardiogenic shock.
Structural factors contributing to aortic wall vulnerability include medial degeneration, fragmentation of elastic fibers, and smooth muscle cell apoptosis. These changes are accelerated by chronic hypertension, genetic connective tissue disorders, and aging. The sudden hemodynamic stress imposed by systolic blood pressure can precipitate rupture, particularly at sites of maximal wall tension, such as the ascending aorta.
Epidemiology
The incidence of acute aortic dissection is estimated at 2.6–3.5 cases per 100,000 person-years, with Stanford type A dissections accounting for approximately 60–65% of cases. Haemopericardium complicates up to 20–25% of type A dissections, significantly increasing mortality.
Risk factors include:
Advanced age (peak incidence: 60–80 years)
Male sex (male-to-female ratio ~2–3:1)
Chronic hypertension
Atherosclerosis
Genetic syndromes (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
Bicuspid aortic valve
Prior cardiac surgery
The presence of haemopericardium is a strong independent predictor of early death, with in-hospital mortality rates exceeding 50% in untreated cases.
Clinical Presentation
Typical Symptoms
Sudden onset of severe chest pain, often described as tearing or ripping
Radiation of pain to the back, neck, or jaw
Dyspnea
Syncope
Signs of Haemopericardium and Tamponade
Hypotension
Tachycardia
Elevated jugular venous pressure
Muffled heart sounds
Pulsus paradoxus
Neurological and Vascular Complications
Stroke or transient ischemic attack
Upper limb ischemia
Acute renal failure
Mesenteric ischemia
In elderly patients, symptoms may be atypical, presenting as confusion, syncope, or heart failure, underscoring the importance of high clinical suspicion.
Imaging Features
Role of CT Angiography (CTA)
Multidetector CT angiography is the gold standard for diagnosis, offering rapid, high-resolution visualization of the aorta and its branches.
Key CT features include:
Intimal flap separating true and false lumens
Dilated ascending aorta
Extension into the supra-aortic branches
Pericardial effusion with high attenuation (haemopericardium)
Figure Descriptions
Figure 2. Sagittal Image: Shows longitudinal propagation of the dissection flap along the thoracic aorta, highlighting the full craniocaudal extent of the Stanford type A dissection.
Figure 3. Coronal image: Reveals extension of the dissection into the left common carotid artery, increasing the risk of cerebrovascular complications. The dashed line outlines the affected vessel.
These imaging findings collectively confirm aortic dissection with haemopericardium, requiring immediate surgical intervention.
Differential Diagnosis
Acute coronary syndrome (myocardial infarction)
Pulmonary embolism
Pericarditis
Tension pneumothorax
Esophageal rupture (Boerhaave syndrome)
Imaging and laboratory correlation are essential for accurate differentiation.
Diagnosis
Diagnosis relies on the integration of:
Clinical suspicion
Electrocardiography and biomarkers (to exclude myocardial infarction)
Emergency CT angiography
Transesophageal echocardiography (TEE) may be used when CT is unavailable or contraindicated, especially in unstable patients.
Treatment
Emergency Surgical Management
All Stanford type A dissections with haemopericardium require immediate surgical repair, including:
Resection of the intimal tear
Replacement of the ascending aorta with a prosthetic graft
Management of pericardial tamponade
Medical Stabilization
Rapid blood pressure control (target systolic BP 100–120 mmHg)
Beta-blockers to reduce shear stress
Analgesia
Postoperative Care
Intensive hemodynamic monitoring
Long-term antihypertensive therapy
Serial imaging surveillance
Prognosis
Without surgery, mortality increases by 1–2% per hour after symptom onset. With prompt intervention, survival rates improve significantly, though overall in-hospital mortality remains 15–30%.
Long-term survival depends on:
Adequacy of surgical repair
Blood pressure control
Absence of major complications
Quiz
Question 1. A 78-year-old man presents with sudden chest pain and hypotension. CT reveals a Stanford type A aortic dissection with pericardial effusion. What is the most likely immediate cause of shock?
A. Myocardial infarction
B. Pulmonary embolism
C. Cardiac tamponade
D. Aortic valve stenosis
Answer: C. Explanation: Haemopericardium leads to cardiac tamponade, restricting ventricular filling and causing shock.
Question 2. Which CT feature most reliably distinguishes true from false lumen in aortic dissection?
A. Wall calcification
B. Intimal flap
C. Aortic diameter
D. Pleural effusion
Answer: B. Explanation: The intimal flap directly separates true and false lumens.
Question 3. Which risk factor is most strongly associated with Stanford type A aortic dissection?
A. Diabetes mellitus
B. Chronic hypertension
C. Hyperlipidemia
D. Smoking
Answer: B. Explanation: Chronic hypertension is the most significant modifiable risk factor.
References
[1] E. M. Isselbacher et al., “Contemporary management of acute aortic dissection,” Circulation, vol. 134, no. 3, pp. 184–196, 2023.
[2] H. Suzuki et al., “Clinical profiles and outcomes of acute type A aortic dissection,” J Am Coll Cardiol, vol. 80, no. 12, pp. 1105–1117, 2022.
[3] M. McMahon et al., “Multidetector CT of aortic dissection: A pictorial review,” Radiographics, vol. 30, no. 2, pp. 445–460, 2010.
[4] R. Erbel et al., “2014 ESC Guidelines on the diagnosis and treatment of aortic diseases,” Eur Heart J, vol. 35, no. 41, pp. 2873–2926.
[5] J. A. Elefteriades, “Natural history of thoracic aortic aneurysms and dissections,” Ann Thorac Surg, vol. 74, pp. S1877–S1880, 2021.
[6] S. Nienaber and C. Clough, “Management of acute aortic dissection,” Lancet, vol. 385, pp. 800–811, 2020.
[7] H. J. Patel et al., “Surgical strategies for acute type A aortic dissection,” J Thorac Cardiovasc Surg, vol. 164, no. 2, pp. 334–346, 2022.
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