An Emergency of the Aortic Kind

Air Transport Case of the Month

You are called to the emergency room of a community hospital to transport a 57-year-old male with a 12-hour history of chest pain. The patient is to be delivered directly to the cardiac catheterization lab of an academic medical center 50 miles away.

He has received a 12-lead EKG and portable chest x-ray. Initial laboratory studies have been drawn and sent. The bedside nurse reports that the patient has received chewable aspirin, three sublingual nitroglycerin tablets with minimal relief, a total of 5mg of morphine sulfate IV and the first of three 5mg IV metoprolol doses. Heparin and nitroglycerin infusions have been prepared but not yet started. A dose Retavase (Reteplase), 10 units IV have also been ordered but not yet administered.

Upon your arrival, the patient is in obvious distress. He has 7/10 chest pain and pale, cool skin. He is also complaining of tearing back pain radiating to the left side of his neck. Vital signs include a heart rate of 94 beats/minute, a respiratory rate of 20 breaths/minute (regular and non-labored), a blood pressure of 154/96, and an oxygen saturation of 97 percent on two liters/minute of oxygen by nasal cannula. The 12-lead EKG shows ST-segment elevation in leads I, aVL, V5 and V6. Chest x-ray shows a widened mediastinum and a blunted aortic knob.

What are your treatment priorities? Are there any differential diagnoses to consider at this time? Should the nitroglycerin and heparin drips be initiated? When would you start the ordered thrombolytic therapy?

The Underlying Clinical Issue

Further clinical and diagnostic examination, including a non-contrast chest and abdominal CT, showed that the gentleman in the above scenario was suffering from a thoracic aortic dissection. While he presented very similarly to a typical patient suffering from a lateral wall myocardial infarction (MI), treatment priorities are not quite parallel. In fact, some therapies (thrombolytic and anticoagulation therapy) could prove to be deleterious to the patient in this situation.

Pathophysiology

The aorta consists of three distinct but connected layers. The inner-most layer, or tunica-intima, is composed of an elastic membrane lining and smooth endothelial tissue. The middle layer, tunica-media, contains smooth muscle and elastic fibers. The outer layer, tunica-adventitia, is a tough outer covering.

Any number of physical defects or medical conditions can cause the inner layer of the aorta to tear:

• uncontrolled hypertension
• atherosclerosis
• cocaine abuse
• medical syndromes
• diseases such as Marfan’s
• inflammatory conditions, such as vasculitis or Ehlers-Danlo syndrome

Continuous hydrodynamic or shearing forces causing forceful ejection of blood in to the aorta can increase tearing². Eventually, degeneration of the medial layer occurs. As blood travels in between the layers of the aorta, it separates or “dissects” the layers of the aorta².

Prognosis and Classification

Undiagnosed aortic dissection can have a mortality rate as high as 33 pecent within the first 24 hours, 50 percent within 48 hours, and 75 percent within two weeks. There are two commonly used anatomic classifications1.

The Stanford classification divides dissections into two types: type A and type B. Type A involves the ascending aorta and type B does not¹. Type A dissections are surgical emergencies while type B dissections are generally treated medically — although certain conditions may warrant surgery.

The DeBakey classification system divides dissections into the following 3 types:

• Type I involves the ascending aorta, aortic arch, and descending aorta.
• Type II involves the ascending aorta.
• Type III involves the descending aorta distal to the left subclavian artery.

The formula “1=2+3” helps to delineate the Debakey classification system – the type I dissection involves both aspects of a type II and type III.

Clinical Signs and Symptoms and Differentials²

Clinical signs and symptoms may include, but are not limited to:

• A sharp, often described as “tearing,” pain in the chest, neck and back
• Hyper- or hypo-tension and shock
• Pulse deficits
• Diastolic murmurs
• Evidence of acute myocardial ischemia or infarction if the coronary arteries are involved
• Cardiac rhythm disturbances
• Variation of blood pressures between arms
• Cardiac tamponade
• Neurologic deficits
  o Syncope
  o Evidence of stroke with carotid artery involvement
  o Spinal cord ischemia and peripheral neuropathy, paralysis and paresis
• Evidence of mesenteric ischemia and renal failure with descending aorta involvement

Potential differential diagnoses include, but are not limited to:

• Myocardial infarction
• Stroke
• Traumatic injury
• Orthopedic back pain
• Pulmonary embolus
• Pericardidts
• Isolated GI complaints such as indigestion, acute pancreatitis or cholecystitis

Management Options

Treatment options for the medical transport professional are based upon the patient’s clinical condition at the time of initial contact and transport. After determination of airway and circulatory status, a management plan can be formulated in order to treat either hypotension and shock or a potential hypertensive crisis.

Hypotension in the presence of an aortic dissection may be the result of pericardial tamponade, aortic leak or rupture, or pseudo hypotension caused by an intimal flap, which impedes blood flow to an extremity where blood pressure is measured. Placement of two large bore intravenous lines and volume resuscitation with isotonic crystalloid and packed red blood cells are the primary therapies for shock and hypotension. Patients who develop profound hypotension or Pulseless Electrical Activity (PEA) should be considered for emergent pericardiocentesis³.

Hypertension and tachycardia are dangerous conditions in the aortic dissection setting Extension of the dissection due to increased hydrostatic and hydrodynamic (shearing) forces is likely if blood pressure cannot be controlled. While target blood pressure is debatable, individual transport team protocols and referral center policies will more than likely dictate this situation.

Reducing blood pressure and minimizing shearing forces are best accomplished with a combination of antihypertensive agents that have different mechanisms of action. Beta blockers such as Esmolol or Labetalol will reduce heart rate and blood pressure, thus minimizing shear stress on the intima. Sodium nitroprusside is a powerful vasodilator. While it will quickly reduce blood pressure, sodium nitroprusside should not be used without beta blockade in patients with aortic dissections. Vasodilatation alone may cause a reflex activation of the sympathetic nervous system. This will cause increased ventricular contraction and increased aortic shear stress (as do any antihypertensive agents whose sole mechanism of action is vasodilatation)².

Fenoldopam (Corlopam®) is another agent with promise in treating the adverse effects of aortic dissection. Fenoldopam is a potent and effective vasodilator that acts upon dopamanergic (D1) receptors as well as alpha2 adrenoreceptors, thereby reducing bloodpressure while increasing renal blood flow^4,5. For additional information, such as uses, indications, mechanisms and prescribing information, visit www.fenoldopam.com.

Pain control is also a primary concern for patients with aortic dissection. Narcotic analgesics such as morphine or fentanyl will reduce the effects of chest pain, reduce anxiety, and reduce oxygen consumption. Clinical judgment should be used when administering narcotic analgesia in conjunction with antihypertensive therapy.

Conclusion

Transport of patients suffering from aortic dissections, while vital, is typically routine in nature. This type of transport can also be one of the most challenging that an air medical professional will encounter. Knowledge of clinical presentation, the ability to distinguish this diagnosis from a long list of differentials, and the ability to appropriately manage these patients are vital to a positive outcome in the uncontrolled setting of the transport environment.

References

• ¹ Wiesenfarth J. Dissection, Aortic. http://www.emedicine.com/emerg/topic28.htm.
  Updated November 8, 2007. Accessed February 17, 2008.
• ² Marx JA, Hockberger RS, Walls RM (Eds.). Rosen’s Emergency Medicine: Concepts and Clinical Practice (6th edition). 2006. Mosby-Elsevier, Philadelphia. pp. 1324-1330
• ³ University of Michigan Health System. Survival Flight Medical Protocols. Revised May 2006.
• ⁴ Micromedix on-line formulary. Licensed to the University of Michigan. 2008
• ⁵ http://www.fenoldopam.com. Accessed February 22, 2008.