# Aortic Emergencies: Dissection, Aneurysm, and Mimics

## Acute Aortic Dissection

### Pathophysiology

Acute aortic dissection begins with a tear in the aortic intima, allowing blood to enter the media and create a false lumen that propagates along the length of the aorta. Propagation can be anterograde (toward the iliac arteries) or retrograde (toward the aortic root). The false lumen can compress branch vessels, producing malperfusion syndromes that affect virtually any organ system. Hypertension and connective tissue disorders are the primary risk factors. Peak incidence is between 60 and 80 years, with a 3:1 male predominance.

### Stanford Classification

The Stanford classification divides dissections into two types based on whether the ascending aorta is involved. Type A involves the ascending aorta regardless of where the intimal tear originates and is a surgical emergency. Type B involves only the descending aorta distal to the left subclavian artery and is typically managed medically. Type A accounts for approximately 60 percent of acute dissections. The older DeBakey classification subdivides further: Type I involves both ascending and descending aorta, Type II is ascending only, and Type III is descending only.

| Classification | Stanford | DeBakey | Location | Management |
|---|---|---|---|---|
| Ascending ± descending | Type A | Type I | Ascending + descending | Emergent surgery |
| Ascending only | Type A | Type II | Ascending only | Emergent surgery |
| Descending only | Type B | Type III | Distal to left subclavian | Medical (BP/HR control); TEVAR if complicated |

### Clinical Presentation

The classic presentation is sudden-onset severe "tearing" or "ripping" chest or back pain. Anterior chest pain is more common in Type A, while interscapular back pain is more common in Type B. A critical distinguishing feature is that dissection pain is maximal at onset, unlike ACS pain, which often crescendos. Atypical presentations occur in up to 20 percent of cases and include syncope without pain, stroke, acute heart failure, abdominal pain, and limb ischemia. Physical examination may reveal a blood pressure differential greater than 20 mmHg between arms (though present in only 20-30 percent of cases), an aortic regurgitation murmur in Type A, pulse deficits (asymmetric radial, femoral, or carotid pulses), and neurologic deficits from carotid or spinal artery involvement.

### Malperfusion Syndromes

The false lumen can compromise virtually any branch vessel. Coronary malperfusion produces acute MI, most commonly inferior STEMI from RCA involvement. Cerebral malperfusion causes stroke, typically right-sided due to innominate artery involvement. Mesenteric malperfusion leads to bowel ischemia with abdominal pain and lactic acidosis. Renal malperfusion causes acute kidney injury, hematuria, and refractory hypertension. Limb malperfusion produces acute ischemia with a cool, pulseless extremity. Spinal cord malperfusion can cause paraplegia or paraparesis.

| Malperfusion Syndrome | Vessel Involved | Clinical Presentation |
|---|---|---|
| Coronary | RCA (most common) | Inferior STEMI, acute MI |
| Cerebral | Innominate / carotid | Stroke (typically right-sided) |
| Mesenteric | SMA / celiac | Bowel ischemia, abdominal pain, lactic acidosis |
| Renal | Renal arteries | AKI, hematuria, refractory hypertension |
| Limb | Iliac / subclavian | Cool, pulseless extremity |
| Spinal cord | Intercostal / lumbar arteries | Paraplegia or paraparesis |

### Diagnostic Approach

#### ADD-RS (Aortic Dissection Detection Risk Score)

The ADD-RS assigns one point each for high-risk conditions (Marfan syndrome, family history, aortic valve disease, recent aortic manipulation), high-risk pain features (abrupt onset, severe, tearing or ripping quality), and high-risk examination findings (pulse deficit, BP differential, new aortic regurgitation murmur, hypotension or shock). A score of 0-1 combined with a negative D-dimer (below 500 ng/mL) can effectively rule out dissection without advanced imaging.

#### Imaging

CT angiography is the gold standard with sensitivity and specificity exceeding 95 percent. It demonstrates the intimal flap, true and false lumens, extent of dissection, and branch vessel involvement. Transesophageal echocardiography is excellent for Type A and can be performed at the bedside in unstable patients. Transthoracic echocardiography has low sensitivity for dissection but can identify aortic root dilation, pericardial effusion, and aortic regurgitation. On point-of-care ultrasound, a dilated aortic root greater than 4 cm on the parasternal long-axis view should raise concern. MRA has excellent diagnostic accuracy but is impractical in the acute setting.

#### Laboratory

D-dimer is elevated in more than 95 percent of acute dissections within the first 24 hours. A negative D-dimer combined with a low ADD-RS (0-1) has a negative predictive value approaching 99 percent, though D-dimer cannot be used alone to rule out dissection. Troponin may be elevated from coronary malperfusion or demand ischemia. Lactate is elevated in mesenteric or limb malperfusion. Type and screen should be sent to prepare for potential massive transfusion.

### Management

#### Type A — Surgical Emergency

Emergent cardiothoracic surgery consultation is the priority. Blood pressure should be controlled to a target SBP of 100 to 120 mmHg and heart rate below 60 bpm. Beta-blockers must be given first to reduce aortic shear stress by decreasing the rate of pressure change (dP/dt). Esmolol (500 mcg/kg bolus, then 50-200 mcg/kg/min infusion) is easily titratable, and labetalol (20 mg IV bolus, then infusion) is an alternative. Vasodilators are added only after heart rate is controlled: nicardipine at 5 to 15 mg/hr IV, or nitroprusside (which must never be given without concurrent beta-blockade because reflex tachycardia worsens shear stress). IV morphine or fentanyl controls pain and reduces sympathetic drive. Anticoagulation and antiplatelet agents must be withheld until dissection is excluded.

#### Type B — Medical Management (Uncomplicated)

Uncomplicated Type B dissection is managed with aggressive blood pressure and heart rate control using the same targets as Type A, ICU admission for monitoring, and serial imaging to assess for progression. Complicated Type B (with malperfusion, rupture, or refractory pain and hypertension) requires thoracic endovascular aortic repair (TEVAR).

## Abdominal Aortic Aneurysm (AAA)

### Epidemiology and Risk Factors

AAA prevalence is 4 to 8 percent in men over 65. Risk factors include male sex, age over 65, smoking (the strongest modifiable risk factor), hypertension, and family history. Screening recommendations call for a one-time ultrasound for men aged 65 to 75 who have ever smoked.

### Ruptured AAA

The classic triad of ruptured AAA is abdominal, flank, or back pain, hypotension, and a pulsatile abdominal mass — but this complete triad is present in only 25 to 50 percent of cases. Most ruptures are contained initially in the retroperitoneal space, allowing temporary hemodynamic stability. Free intraperitoneal rupture is rapidly fatal without intervention. Fifty percent of patients die before reaching the hospital, with an overall mortality of 80 to 90 percent.

### Clinical Presentation

Sudden-onset severe abdominal, flank, or back pain is the most common presentation. Syncope and near-syncope occur frequently. The condition is frequently misdiagnosed as renal colic, diverticulitis, musculoskeletal back pain, or MI. A high index of suspicion is essential in any older male with abdominal or back pain and risk factors. A critical rule: never assume renal colic in a patient over 60 without a prior history of kidney stones.

### Diagnosis

Bedside ultrasound rapidly identifies AAA with greater than 95 percent sensitivity — any aortic diameter above 3 cm is an aneurysm, and diameters above 5.5 cm carry high rupture risk. Ultrasound cannot reliably identify active rupture, but any AAA with hemodynamic instability should be treated as ruptured until proven otherwise. CT angiography confirms rupture by showing retroperitoneal hematoma and active contrast extravasation, and defines anatomy for surgical planning, but should only be performed if the patient is hemodynamically stable enough for transport. Surgical consultation should never be delayed for imaging in an unstable patient with a known AAA.

### Management of Ruptured AAA

The massive transfusion protocol should be activated immediately. Permissive hypotension targeting SBP 80 to 100 mmHg is critical — aggressive fluid resuscitation can dislodge the tamponading clot. Emergent vascular surgery consultation is required. Definitive repair involves open surgical repair or endovascular aneurysm repair (EVAR) depending on anatomy and institutional capability.

## Aortic Mimics and Differential Diagnosis

### Conditions That Mimic Aortic Dissection

ACS produces chest pain and ECG changes, but the pain typically crescendos rather than being maximal at onset. Pulmonary embolism presents with acute dyspnea, chest pain, and tachycardia. Pericarditis and tamponade cause chest pain with a friction rub and electrical alternans. Musculoskeletal chest pain is sharp, positional, and reproducible. Esophageal rupture (Boerhaave syndrome) produces severe chest or epigastric pain with subcutaneous emphysema. Acute pancreatitis causes epigastric pain radiating to the back.

### Aortic Intramural Hematoma

Aortic intramural hematoma involves hemorrhage within the aortic media without an intimal tear. On CT, it appears as a crescent-shaped thickening of the aortic wall without flow in the thickened segment. It is managed similarly to dissection (Type A requires surgery; Type B is managed medically) and can progress to classic dissection.

### Penetrating Aortic Ulcer

A penetrating aortic ulcer occurs when an atherosclerotic plaque ulcerates through the intima into the media. It is more common in the descending aorta in elderly patients with severe atherosclerosis and can lead to intramural hematoma, dissection, or rupture. It is usually managed medically unless complications develop.

<image>A CT angiography image series showing the three major acute aortic syndromes in axial view. Panel A shows a Stanford Type A aortic dissection with a clearly visible intimal flap in the ascending aorta, with true and false lumens labeled. Panel B shows an aortic intramural hematoma as a crescent-shaped hyperdense thickening of the descending aortic wall without a visible intimal flap. Panel C shows a penetrating aortic ulcer with a focal outpouching of contrast beyond the intimal surface of the descending aorta into the media. Each panel includes anatomical labels and arrows pointing to key diagnostic features.</image>

<image>An anatomical diagram of the aortic arch and its branches illustrating the malperfusion syndromes of aortic dissection. The aorta is shown from the root to the bifurcation, with a dissection flap extending from the ascending aorta distally. Branch vessels are labeled (coronary arteries, brachiocephalic, left common carotid, left subclavian, celiac trunk, superior mesenteric artery, renal arteries, common iliacs). Each branch has an icon and text box describing the malperfusion syndrome that results from its compromise: coronary (MI), cerebral (stroke), mesenteric (bowel ischemia), renal (AKI), and limb (acute ischemia).</image>

<image>A bedside ultrasound image showing measurement of the abdominal aorta in the transverse plane. The aorta is measured outer-wall to outer-wall at 6.2 cm, indicating a large abdominal aortic aneurysm. Adjacent to it, the IVC is visible for anatomic reference. An inset panel shows the normal aortic diameter (less than 3 cm) for comparison. Anatomical labels include the vertebral body posteriorly and the liver anteriorly. A callout box lists the ultrasound screening criteria: normal (less than 3 cm), aneurysm (3 cm or more), high rupture risk (5.5 cm or more).</image>

## Clinical Pearls

Aortic dissection pain is classically maximal at onset and migrates — this temporal pattern is what distinguishes it from ACS, where pain typically builds gradually. Always give beta-blockers before vasodilators in dissection, because vasodilators alone cause reflex tachycardia that increases aortic shear stress and promotes propagation. Type A dissection can present as inferior STEMI from RCA involvement — if dissection is discovered on CTA, anticoagulation and thrombolytics must not be given. An ADD-RS of 0-1 combined with a negative D-dimer can effectively rule out dissection without CTA. Bedside ultrasound rapidly identifies AAA but cannot reliably detect rupture — an unstable patient with a known AAA needs the operating room, not the CT scanner. Never assume renal colic in an elderly male presenting with first-time flank or back pain without excluding AAA. In ruptured AAA, permissive hypotension is essential because aggressive fluid resuscitation before surgical control worsens outcomes by dislodging the tamponading clot. The classic triad of ruptured AAA is present in fewer than half of cases, so clinical suspicion must remain high.

## References

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- Nazerian P, et al. ADD-RS plus D-dimer for the diagnosis of acute aortic syndromes. *Circulation*. 2018;137:250-258.
- Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. *Circulation*. 2022;146:e334-e482.
- Hiratzka LF, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease. *Circulation*. 2010;121:e266-e369.
- Stable M, et al. Bedside ultrasound for detection of abdominal aortic aneurysm: a systematic review. *Emerg Med J*. 2012;29:881-882.