Aortic Dissection

by Shanaz Sajeed


Aortic dissection carries high morbidity and mortality. Although patients generally present with acute symptoms and classic signs, a subset of patients may present with syncope, GI bleeding, and neurological deficits. The clinician needs to remain vigilant for such atypical presentations. There are two standard anatomical classifications – Stanford and De Bakey. Stanford type A dissections (De Bakey I and II) involve the ascending aorta. Stanford type B (De Bakey III) dissections arise distal to the left subclavian artery (Figure 1). Stanford A dissections are more common than Stanford B dissections (62% vs. 38%). Figure 1. De Bakey and Stanford classification of aortic dissection. Aortic Dissection The aortic wall consists of 3 layers – the intima, media and an outer layer known as the adventitia. Classic nontraumatic aortic dissection is usually due to a tear in the intimal layer of the aorta, leading to an intimal flap. The bridge between the media layer and the aortic lumen causes a subintimal hematoma. Then intima gets separated from the underlying media and adventitia. This false lumen of varying size may result in complete occlusion of major arteries that branch from the aorta leading to major ischemic complications such as limb ischemia, paralysis, stroke, renal failure as well as cardiac events.

Case Presentation

A 56-year-old male presented to the emergency department with sudden onset of severe tearing chest pain radiating to the back. He had a history of hypertension and hyperlipidemia. He was a smoker. Upon arrival, he appeared to be diaphoretic and in severe pain. He denied any prior history of chest pain. He had been without any infective symptoms lately. He was compliant with his medications, namely, amlodipine and simvastatin. At triage, his blood pressure was noted to be 80/60 mmHg with a pulse rate of 130 bpm. His oxygen saturation was 95% on room air, and his respiratory rate was 22 breaths per minute. On examination, he had muffled heart sounds, jugular venous distention, and radio-radial pulse delay.

Critical Bedside Actions and General Approach

The initial management of a patient with chest pain and hypotension warrants observation in a monitored area with continuous SpO2 and cardiac documentation. The physician needs to assess airway, breathing, and circulation. A compromise in any of these necessitates immediate action. In this case scenario, for example, the next priority would be to determine the etiology of this patient’s hypotension and to initiate resuscitative and stabilizing measures. The physician should

  • Administer supplemental oxygen and assess the patient’s airway, breathing, and circulation to determine the need for any immediate critical interventions.
  • Secure venous access by inserting two large bore IV cannulas into the antecubital fossa.
  • In the hypotensive patient, administer an initial IV fluid bolus of 20 ml/kg crystalloid.

Note: A small initial bolus of fluid would not be harmful. Even in cardiogenic shock, it is likely to improve cardiac output and blood pressure transiently. Thus, one should not be hesitant to give an initial bolus of fluid in the hypotensive patient even if the etiology of shock is not immediately apparent.

History Taking and Physical Examination Hints

History Taking Hints

As initial resuscitation is going on, a focused history should be obtained at the bedside. Inquire about the site, onset, nature, duration, radiation as well as aggravating and relieving factors of the chest pain. Patients with acute Type A dissection classically present with :

  • Sudden onset of ‘ripping’ or ‘tearing’ chest pain (85%) and/or interscapular back pain (46%)
  • Pain is usually maximal at onset, unlike MI where pain usually gradually increases in intensity.
  • Pain may migrate distally to the abdomen as dissection progresses
  • However, a minority of patients may present atypically with abdominal pain (22%), syncope (13%) and stroke (6%).
  • Patients often describe the pain as knife-like.

Other symptoms include dyspnea, dysphagia, focal weakness and altered mental status. Type B dissections present similarly. Occlusion of the main abdominal aortic branches may lead to mesenteric and solid organ ischemia. Patients may present with gastrointestinal bleeding, oliguria or anuria. Therefore, asking about gastrointestinal symptoms is an essential part of the history. Risk factors for aortic dissection should be assessed. These are;

  • An aortic aneurysm
  • Atherosclerosis
  • Chronic Hypertension
  • Coarctation of the aorta
  • Congenital aortic valvular defects (e.g., bicuspid aortic valve)
  • High-intensity weight lifting
  • Increasing Age
  • Infection leading to aortitis
  • Inflammatory processes due to vasculitis. e.g., Takayasu’s aortitis
  • Inherited connective tissue disease (e.g., Marfan’s, Ehlers Danlos Syndrome Type IV, familial forms of a thoracic aneurysm and dissection)
  • Male gender
  • Substance abuse such as cocaine, methamphetamine, MDMA

Past medical history findings that should prompt consideration of aortic dissection include:

  • A family history of aortic dissection, aneurysm, or sudden death
  • Chronic hypertension (most common predisposing factor)
  • Documented aortic pathology
  • History of tuberculosis or syphilis
  • Known connective tissue disorder
  • Previous cardiac surgery (especially valve repair) or vascular surgery
  • Vasculitis

The physician should also assess the patient’s anticoagulants use for increased bleeding risk, such as Warfarin/Novel Oral Anticoagulants or antiplatelet agents, which would increase their bleeding risk. It is also vital to elicit any specific allergies that may affect therapy or prohibit the use of IV contrast for imaging purposes. Elicit any relevant social history including questions about illicit drug use. Note: Cocaine use is associated with acute dissections.

Physical Examination Hints

As initial stabilization and initial resuscitation take place, a focused clinical examination should simultaneously be performed. The physician should assess for signs of shock (e.g., cold extremities, delayed capillary refill, weak, thready pulse.) and aim to determine the etiology of hypotension if present. The physician should always consider bedside ultrasonography (RUSH protocol) to facilitate diagnosis as soon as possible. Assess for pulse deficits. Pulse deficits are diminished or absent pulses caused by compression of the true lumen by the false lumen. Blood pressure difference between the left and right arm suggests aortic dissection. BP difference >20 mmHg between the two limbs is significant. Data analysis from the International Registry of Acute Aortic Dissection (IRAD) revealed that fewer than 20% of patients with proven acute aortic dissection had reported pulse deficits. The cardiopulmonary examination should focus on signs of cardiac ischemia, aortic insufficiency, cardiac tamponade and cardiogenic shock. When listening to the heart sounds, listen for:

  • Distant/muffled heart sounds suggest pericardial effusion.
  • Gallop rhythm, S3, S4 suggestive of heart failure.
  • Diastolic murmur indicating aortic insufficiency. It is seen up to 75% of Type A dissections.

In the setting of the hypotensive patient, pulsus paradoxus and distended neck veins suggest cardiac tamponade. Examine for pulmonary findings of:

  • Rales or Ronchi suggestive of heart failure
  • Tachypnea and retractions indicating respiratory distress

Examine for signs of stroke or paraplegias/paresthesias suggestive of spinal cord infarcts due to occlusion of the spinal arteries. Examine the abdomen for pulsatile expansile masses suggestive of aneurysmal dilation. Signs of peritonitis may suggest mesenteric ischemia, a known complication of an aortic dissection.

Differential Diagnosis

Aortic dissection should be considered in all patients with chest pain. The typical pain in acute thoracic aortic dissection is abrupt onset, severe and with radiation to the back. However, there is significant overlap between patients with myocardial infarction, and the two can be difficult to distinguish. A patient with aortic dissection may experience ischemic pain due to the involvement of the coronary arteries. There is a wide range of differential diagnosis in a patient with chest pain. Potentially life-threatening causes of chest pain include:

  • Acute coronary syndrome
  • Pericarditis/Myocarditis
  • Pulmonary embolism
  • Pneumonia/Pleural effusion
  • Pneumothorax
  • Rib fractures
  • Esophageal rupture
  • Mediastinitis

Emergency Diagnostic Tests and Interpretations

Bedside Tests

  • Electrocardiogram(ECG) – may be normal, show nonspecific ST changes, or changes suggestive acute coronary syndrome. The most common coronary artery involved is the right coronary artery, leading to an inferior STEMI.
  • Bedside transthoracic echocardiography may yield useful information such as the presence of pericardial fluid suggestive of tamponade. It can also give information on cardiac contractility. A dilated aortic root or dissection flap may be visualized on the parasternal long axis view.
  • Chest X-ray – Abnormalities suggestive of dissection are present between 60-90% of cases.

These are;

  • Depression of the left mainstem bronchus
  • Displaced intimal calcification
  • Indistinct or irregular aortic contour
  • Left apical pleural cap
  • Opacification of the “AP window” (i.e., clear space between the aorta and the pulmonary artery)
  • Pleural effusion (left > right)
  • Tracheal or esophageal deviation
  • Widened aortic knob or mediastinum (present in only 63% and 56% of patients with type A and type B dissections, respectively).

469 - wide mediastinum - chest X-ray

Laboratory Tests

Blood investigations should include a full blood count, urea and electrolytes, coagulation, cardiac enzymes and crossmatch.

Imaging Modalities

  • Contrast-enhanced CT aortogram (Figure 2 and Figure 3) is usually the investigation of choice. In cases where CT poses a significant risk (e.g., pregnancy), MR Angiography of the aorta can be done.
  • Transesophageal echocardiogram (TEE) can be done at the bedside where there is a risk of contrast-induced nephropathy (Patients with impaired renal function) or contrast allergy, or in unstable patients.

Figure 2. Type A dissection involving the ascending aorta demonstrating dissection flap as well as the true and false lumen. (Case courtesy of Dr. Frank Gaillard,, rID: 8886)

Stanford A - aortic dissection
Stanford A – aortic dissection

Figure 3. Type B aortic dissection with dissection flap in descending aorta. (Case courtesy of Dr. Avni K P Skandhan,, rID: 25409)

Stanford B - aortic dissection
Stanford B – aortic dissection

Emergency Treatment Options

Investigations and diagnostic workup should be done in parallel with the resuscitation of the patient. After initial assessment and stabilization and the definitive diagnosis made, reassess the patient and determine further management. Patients with aortic dissection may be hypotensive, normotensive or hypertensive.

Hypotensive Patient

The priority is to maintain organ perfusion until definitive management:

  • Administer IV crystalloid bolus of 20 ml/kg
  • Consider vasopressors (if needed) to maintain a MAP: 70-80 mmHg
  • If pericardial tamponade is present, emergent pericardiocentesis is indicated
  • Blood transfusion is indicated if the hypotension is due to internal bleeding

Hypertensive Patient

Aggressive blood pressure control is essential to reduce shear stress:

  • Target a systolic pressure between 100-120 mmHg or MAP 70-80 mmHg. Heart rate should be between 60-80.
  • IV ß-blockers are the first-line therapy.
    • Labetalol: 20 mg IV slow injection, then 40-80 mg IV q10 min PRN, up to 300 mg IV total. An infusion of 0.5 to 2.0 mg/min can also be run.
  • Calcium channel blockers such as diltiazem or verapamil may be used in patients with contraindication to ß-blockers
  • Sodium Nitroprusside may be added as adjunctive therapy for elevated blood pressure refractory to ß-blockers or Calcium Channel Blocker therapy. Avoid using as sole therapy as it can cause reflex tachycardia.

Practical Point: Hypotensive and drowsy patients need secured airway or intubation before any advanced imaging. Induction agents with cardiovascular stability are advised. Push dose vasopressors should be available in case of a precipitous drop in blood pressure. Investigations and diagnostic workup should be done in parallel with the resuscitation of the patient. Emergent surgical/interventional consult should be sought for definitive management.

  • Type A dissections are usually managed surgically. The principal objectives are 1) relieve the symptoms, 2) reduce the complications, and 3) prevent aortic rupture and death. The affected layers of the aorta are sutured together, and the aorta is reinforced with a graft. Endovascular therapy is now becoming increasingly popular.
  • Type B dissections are usually managed medically with aggressive blood pressure and pain control as well as continual monitoring for signs and symptoms of complications. Surgical management indications include:
    • Signs of bowel ischemia, limb ischemia or solid organ ischemia
    • Persistent pain
    • Expanding hematoma or impending rupture
    • Associated aneurysmal dilatation of the aorta


Patients with acute aortic dissection should be managed in a high dependency or intensive care unit. The overall in-hospital mortality of aortic dissection is 27%. 30-day mortality of type A dissection with and without surgery is 26% and 58%, respectively. Type B dissection treated medically has 11% and surgically has 31% 30-day mortality.

References and Further Reading

  • Aziz S, Ramsdale DR. Acute dissection of the thoracic aorta. Hosp Med 2004;65(3):136-142. (Review)
  • Kevin C Reed, Liesl A Curtis. Aortic Emergencies: Part I- Throacic dissections and aneurysms. Emergency Medicine Practice. Feb 2006. Vol 8, num 2.
  • Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: Part I: from etiology to diagnostic strategies. Circulation 2003;108(5):628-635. (Review)
  • Gomez-Jorge J. Aorta, dissection. Updated July 28, 2005. Available at: Accessed January 31, 2006. (Online article)
  • Rashid J, Eisenberg MJ, Topol EJ. Cocaine-induced aortic dissection. Am Heart J 1996;132(6):1301-1304. (Case report)
  • Mochizuki Y, Zhang M, Golestaneh L, et al. Acute aortic thrombosis and renal infarction in acute cocaine intoxication: a case report and review of literature. Clin Nephrol 2003;60(2):130-133. (Case report)
  • Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283(7):897- 903. (Retrospective, 464 patients)
  • Nienaber CA1, Eagle KA.Aortic dissection: new frontiers in diagnosis and management: Part II: therapeutic management and follow-up. Circulation 2003 Aug 12;108(6):772-8

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