Aortic dissection is a catastrophic cardiovascular emergency defined by a disruption of the medial layer of the aortic wall, precipitated by an intimal tear or primary medial hemorrhage^{1, 5}. This pathologic event leads to the propagation of a dissecting hematoma that splits the aortic wall longitudinally, creating a true lumen and a false lumen separated by an intimal flap^{5, 6}. With an incidence estimated between 30 and 35 cases per 100,000 individuals annually in older populations, it disproportionately affects elderly males with chronic systemic hypertension^{5, 7}. Swift diagnostic confirmation using cross-sectional imaging and immediate multidisciplinary management are essential to prevent fatal complications such as aortic rupture, cardiac tamponade, and end-organ ischemia^{2, 5}.

1. Etiology & Risk Factors

• Systemic Arterial Hypertension: The single most prevalent risk factor, present in over 70% of patients, generating chronic wall shear stress (dp/dt) that degrades medial elastic fibers^{5, 6}.
• Genetic Connective Tissue Disorders: Marfan syndrome (FBN1 mutations), Loeys-Dietz syndrome, and Ehlers-Danlos syndrome (vascular type IV) cause intrinsic weakness of the aortic media via cystic medial necrosis^{5, 6}.
• Congenital Aortic Valve Anomalies: Bicuspid aortic valve (BAV) is strongly associated with ascending aortopathy and premature dissection^{4, 5}.
• Aortic Structural Alterations: Pre-existing thoracic aortic aneurysm, coarctation of the aorta, and previous cardiac surgery or instrumentation^{4, 6}.
• Inflammatory & Vasculitic Conditions: Giant cell arteritis, Takayasu arteritis, and tertiary syphilis causing aortitis and vasa vasorum destruction^{1, 6}.
• Environmental & Acute Triggers: Severe physical exertion, heavy weightlifting, intense emotional stress, blunt chest trauma, cocaine or amphetamine abuse, and pregnancy (third trimester)^{1, 4}.

2. Pathophysiology

The pathogenesis of aortic dissection initiates with structural degradation of the aortic media, characterized by smooth muscle cell apoptosis, loss of elastic lamellar units, and accumulation of basophilic mucoid material (cystic medial necrosis)^{1, 5}. An initial tear in the intimal layer—most frequently located in the right lateral wall of the ascending aorta within 10 cm of the aortic valve, or just distal to the left subclavian artery in the descending aorta—allows high-pressure pulsatile blood to enter the medial layer^{2, 3}. The blood cleaves the media longitudinally, establishing a false lumen that propagates anterogradely or retrogradely^{6, 7}. The false lumen typically exhibits higher pressure or slower flow, leading to compression of the true lumen and subsequent branch vessel malperfusion syndromes involving the coronary, carotid, renal, visceral, or iliac arteries^{1, 6}. Progression of the hematoma can cause rupture into the pericardial sac (causing hemopericardium and cardiac tamponade), pleural space, or mediastinum, resulting in rapid circulatory collapse and death^{1, 5}.

3. Clinical Presentation & Classic Clinical Signs

• History & Cardinal Symptoms: Patients classically present with the abrupt onset of excruciating, severe chest or back pain described as "tearing," "ripping," or "sharp" in character. The pain frequently migrates as the dissection propagates down the aorta. Ascending aortic dissections (Type A) typically manifest with anterior chest pain radiating to the neck or jaw, whereas descending dissections (Type B) more commonly present with interscapular or back pain^{1, 5}.
• Physical Examination & Named Clinical Signs:
  • Pulse Deficits: Asymmetry or complete absence of carotid, brachial, radial, or femoral pulses due to false lumen compression or intimal flap occlusion of branch vessels^{1, 2}.
  • Blood Pressure Differential: An inter-arm systolic blood pressure discrepancy greater than 20 mmHg^{1, 3}.
  • Aortic Regurgitation (Early diastolic decrescendo murmur): Results from annular dilation or retrograde detachment of the aortic valve commissures (often termed "De Backer" or "Austin Flint" murmurs)^{1, 5}.
  • Neurological Deficits: Transient ischemic attacks, stroke, or spinal cord ischemia (paraplegia) secondary to carotid or intercostal artery involvement^{1, 6}.

4. Diagnostic Workup & Interpretation (Laboratory, Imaging & ECG/Pathology)

5. Staging, Classification & Clinical Scoring Systems

6. Differential Diagnosis

7. Management & Treatment Protocol

• Initial Stabilization & Resuscitation: Immediate admission to an intensive care unit (ICU), continuous invasive arterial blood pressure monitoring, large-bore intravenous access, and urgent cardiothoracic and vascular surgery consultation^{1, 2}.
• First-Line Medical / Pharmacological Therapy (with exact adult dosing):
  • Goal: Target heart rate <60 beats per minute and systolic blood pressure between 100 and 120 mmHg to minimize wall shear stress ($dp/dt$)^{1, 3}.
  • Beta-Blockers (Administered FIRST): Intravenous Labetalol (bolus 20–80 mg IV every 10 minutes, followed by continuous infusion 2–8 mg/min) or Esmolol (loading dose 500 mcg/kg/min over 1 minute, then maintenance infusion 50–200 mcg/kg/min)^{1, 2}.
  • Vasodilators (Added ONLY AFTER beta-blockade is established): Sodium Nitroprusside (infusion 0.5–10 mcg/kg/min) or Nicardipine (infusion 5–15 mg/h) if blood pressure remains elevated despite optimal beta-blockade^{1, 6}.
• Surgical / Interventional Indications:
  • Stanford Type A: Emergency open surgical repair involving replacement of the ascending aorta and/or aortic arch with a synthetic graft, restoration of aortic valve competence, and resection of the primary intimal tear^{1, 5}.
  • Stanford Type B (Uncomplicated): Continued aggressive medical anti-impulse therapy and strict blood pressure control in an ICU setting^{1, 7}.
  • Stanford Type B (Complicated - rupture, malperfusion, rapid expansion, intractable pain): Thoracic Endovascular Aortic Repair (TEVAR) to cover the primary entry tear and promote false lumen thrombosis^{3, 7}.

8. Complications & Prognosis

• Acute Complications: Aortic rupture leading to fatal hemothorax or cardiac tamponade, acute aortic regurgitation resulting in acute decompensated heart failure, visceral or renal ischemia/infarction, stroke, paraplegia due to spinal cord ischemia, and limb ischemia^{1, 5}.
• Chronic Complications: Formation of aneurysmal dilation of the false lumen, chronic aortic regurgitation, recurrent dissection, and persistent hypertension^{3, 6}.
• Mortality & Prognosis: Acute aortic dissection carries an untreated mortality rate of approximately 1–2% per hour in the first 24–48 hours. Long-term survival depends heavily on early surgical intervention for Type A dissections and rigorous blood pressure control during lifelong outpatient follow-up^{2, 5}.