Aortic Emergencies

Diseases of the aorta are occurring more frequently with the aging of the population. Imaging with CT and ultrasound has led to increased recognition of aortic pathology. These diseases present in both dramatic and subtle ways, but left untreated they are almost universally fatal. Therefore, the Emergency Physician must be aware of the various presentations of aortic emergencies and have a complete understanding of their management.

Aortic Dissection

Epidemiology/Pathophysiology

• The most important cause of aortic dissection is long-standing systemic hypertension.
  The forceful ejection of the cardiac output results in repeated sheer stress on the intimal wall, ultimately leading to the wall disruption that causes dissection.
• Patients with Marfan’s syndrome or Ehlers-Danlos syndrome have a congenitally weakened aortic wall, thus predisposing these patients to aortic dissection.
• Dissection of the thoracic aorta is caused by a disruption of the intimal wall of the aorta. Blood is transmitted through the tear creating a false lumen in the aortic wall.
  Once the medial wall is weakened by the false lumen, the dissection can rupture through the remainder of the outer wall, rupture through the side branches of the aorta, or rarely rupture back into the true lumen of the aorta.
• Occasionally, dissections of the ascending aorta may also damage the coronary arteries or the aortic valve.

Diagnosis and Evaluation
History and Physical Exam

• The presentation of aortic dissection usually involves the acute onset of severe chest pain. Classically, the pain is described as "tearing" and is most severe at its onset.
• Occasionally, dissections will present with pain in other locations due to the migration of the dissection and damage to side branch vessels.
• Neurologic symptoms may also be present if the carotid or spinal arteries are involved.
• Syncope may be a presenting symptom and is usually associated with ascending aorta dissections.
• On clinical exam, hypertension is usually present, unless there are pulse deficits in the arms being measured.
• Hypotension in the face of an aortic dissection is indicative of a dissection into the pericardium causing tamponade or severe hypovolemia secondary to hemorrhage.
• Pulse deficits may be present on exam and should be sought initially and on reexamination to check for propagation of the dissection.
• If the dissection spreads proximally, dissection through the aortic valve may occur, resulting in the findings of acute aortic insufficiency and congestive heart failure.
• As mentioned above, neurologic deficits may be present.

  Laboratory and Studies

• Laboratory results are variable in aortic dissections; the only lab test of true importance is the type and cross.
• The electrocardiogram usually indicates evidence of long-standing hypertension. Proximal dissections may disrupt coronary blood flow, thus causing myocardial infarctions with related EKG changes. Most commonly, the right coronary artery is involved, leading to inferior myocardial infarctions.
• The chest X-ray is almost always abnormal. Most commonly, mediastinal widening is present. Other X-ray signs include obliteration of the aortic knob, right-sided deviation of a nasogastric tube, depression of the left mainstem bronchus, or a small left-sided pleural effusion, or a left apical cap.
• Definitive diagnosis of an aortic dissection involves direct imaging of the aorta. The gold standard remains aortography, which allows complete aortic visualization but is being rapidly replaced by other modalities.
• Contrast CT scanning allows visualization of the extent of the dissection, as well as pericardial and pleural effusions. CT scanning does not precisely localize intimal tears, unreliably demonstrates side branch involvement, and is not able to define aortic regurgitation. Furthermore, the contrast load needed for the CT scan issubstantial and can have adverse consequences, especially for patients with renal insufficiency.
• Transesophageal echocardiography (TEE) is highly accurate for proximal aortic dissections. Benefits of TEE include speed and safety. TEE is also able to quickly evaluate for aortic insufficiency and pericardial effusions and evaluate myocardial function. Drawbacks to TEE include the need for an experienced operator and the inability to evaluate the descending aorta in its entirety or the side branch arteries.

  ED Management

• The anatomic location of a dissection is the major determinant for therapy. Two classification schemes are widely used to describe dissections, the Stanford and DeBakey classifications.
• The Stanford classification labels dissection as type A if the ascending aorta is involved and type B if there is no ascending aorta involvement.
• The DeBakey classification describes dissections as Type I involving both the ascending and descending aorta, Type II if the dissection involving the ascending aorta only, and Type III involving the descending aorta only.
• The treatment of an aortic dissection begins with control of hypertension. These patients can be very sensitive to blood pressure manipulation. Short acting, titratable medications are therefore appropriate in this setting. ß blockade (esmolol, labetolol, or propranolol are appropriate) is used to decrease the sheer stress placed on the aorta by the systolic pulse. Nitroprusside is used in conjunction with ß blockade to control hypertension. The goal of blood pressure control is to lower the blood pressure to the lowest level which still allows organ perfusion.
• Definitive treatment is based on anatomy.
• Dissections involving the ascending aorta are treated surgically with replacement of the involved segment. Concurrent aortic insufficiency or coronary insufficiency can be corrected surgically during the procedure.
• The treatment of isolated dissections of the descending aorta is intensive blood pressure control alone. Indications for surgical management include uncontrollable hypertension, rupture, or involvement of a major aortic branch with subsequent end-organ ischemia.

  Aortic Aneurysm
  Epidemiology/Pathophysiology

• Aneurysms are defined as dilatation of an aortic segment >3 cm.
• They are true aneurysms, indicating a dilatation of all three layers of the aortic wall.
• Men older than 70, smoking, hypertension, and a family history of aneurysms are predisposing factors. Most aortic aneurysms are diagnosed in the seventh decade of life.
• Abdominal aortic aneurysms (AAA) are most commonly located in an infrarenal location, but may occur at any level of the aorta.
• Aneurysms enlarge at a rate of 0.5 cm per year on average, with larger aneurysms enlarging at a faster rate.
• The risk of aneurysm rupture is largely based on size. While small aneurysms may rupture, the risk of rupture increases dramatically as aneurysms enlarge to >5cm.
• The mortality rate of ruptured aortic aneurysms is approximately 90% with over half of patients dying before reaching the hospital.

  Diagnosis and Evaluation
  History and Physical Examination

• The most important factor in diagnosing AAA is entertaining the diagnosis.
• Middle-aged patients presenting with abdominal or flank pain should always have the diagnosis entertained. Unruptured aneurysms are usually asymptomatic.
• Chronic abdominal pain, back pain, and ureteral colic-like symptoms are common presentations of aneurysms.
• Physical exam findings may include palpation of a pulsatile abdominal mass, but this finding is neither sensitive nor specific enough to rule in or out aneurysmal disease.
• A ruptured aneurysm classically presents with pain, hypotension and a pulsatile mass.
• However, many patients present without these findings. The location and quality of pain is variable, most commonly presenting as acute, severe abdominal, back, or flank pain. Hypotension is a late and grave finding. Other presentations include syncope and altered mental status.

  Laboratory and Studies

• Lab work is not helpful except for a type and cross which is imperative in cases of ruptured AAA.
• Imaging studies are indicated and the choice of study is largely dependent on the clinical stability of the patient.
• Plain films of the abdomen can be helpful if positive but are not sensitive enough to rule out aneurysms. Calcification of the aortic wall can be seen with obvious enlargement of the aorta. These studies are almost universally available and can be done rapidly in the case of an unstable patient.
• Ultrasound is the test of choice to detect aneurysmal disease. It is very sensitive and can evaluate the size of an aneurysm as well as identify intraperitoneal free fluid indicative of rupture. Bedside ultrasound can be done rapidly, making it especially useful for unstable patients. Drawbacks of ultrasound include operator-dependent accuracy and difficulty in visualization of the aorta in patients with excess bowel gas or obesity.
• CT scanning is almost 100% sensitive for the detection of AAA. It has better sensitivity than ultrasound for the detection and location of rupture and is better in defining the surrounding anatomy. IV contrast is helpful, but not imperative for the examination. The main disadvantage of CT scanning is the inability to monitor critically ill patients during the exam.

  ED Management

• Treatment of AAA depends on the stability of the patient. Asymptomatic aneurysms discovered during physical exam or during evaluation for other problems may be referred for further evaluation and treatment. Generally, aneurysms less than 5 cm. are observed with repeat ultrasound evaluation and elective surgical management based on patients concurrent illnesses and the size of the aneurysm.
• Newer intravascular stent techniques are beginning to be used and are appropriate for a select group of patients.
• Treatment of ruptured AAA includes rapid medical resuscitation with blood products as needed. Definitive treatment is surgical and arrangements for surgery should be made as quickly as possible.
• Complications of AAA repair include infection, thrombosis, erosion, and dilation of the graft. These are often life-threatening.
• Infections may occur immediately postoperatively or from hematogenous spread of other infections later in life. Staph species are generally responsible. Treatment includes IV antibiotics and removal and repair of the infected graft.
• Thrombotic complications present in multiple ways with embolic phenomena or ischemic symptoms. Evaluation includes visualization of the aorta and anticoagulation and repair as necessary.
• Erosion of the graft may lead to rupture and/or fistula formation. Aorto-enteric fistulae are caused by erosion into the GI tract. The duodenum is the most common site of fistulae. Fistulae present with GI bleeding and can range from a slow, chronic process, to an acute life-threatening hemorrhage. Many patients with aorto-enteric fistulae also have septic complications necessitating antibiotics. Treatment for fistulae is surgical.