Page 487 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 42: Aortic Dissection 357

is manifested by the loss of smooth muscle cells and accumulation of can lead to late death. Endostenting has been proposed as an interven-
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basophilic amorphous material with or without associated “cysts” in tion to improve survival in these patients. 11-13
the aortic media. This is believed to be due to inborn errors of metabo-
lism (Marfan or Ehlers-Danlos syndrome). There is a reduction in the AORTIC INTRAMURAL HEMATOMA
cohesiveness of the layers of the aortic wall as a result. Other causes of
reduced wall strength causing aortic dissection include annuloaortic Aortic intramural hematoma (IMH) results from hemorrhage within the
ectasia, coarctation, and pregnancy (especially in the third trimester). A aortic wall without disruption of the intima. It is likely due to rupture of
bicuspid aortic valve is present in up to 22% of type A dissections and the vasa vasorum and may progress to rupture through the intima to form
dissections occur 5 to 10 times more commonly than in trileaflet aortic a classic dissection in up to 33% to 47% of cases while only 10% regress. 14
valves. The aortic wall has been found to be abnormal in these patients It is an entity that is frequently confused with aortic dissection. The
5
with increased expression of genes associated with cell death (eg, the diagnosis, management, and prognosis of IMH remain debatable. 15-17
gene for interleukin-1B) causing reduced collagen content similar to Most authors believe the clinical course is similar enough to warrant
that seen in Marfan syndrome. Iatrogenic injuries occur during open treatment of IMH the same as a classical dissection (Fig. 42-5). 18-21
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heart surgical procedures at any point where the aorta is invaded, such The diameter of the aorta is important in that if the aortic diameter
as the aortotomy for an aortic valve replacement or the proximal anas- is <45 mm at 1 month follow-up, then most will resolve. Complications
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tomosis of an aortocoronary bypass graft. Stresses applied to the aortic appear to occur mainly in patients with an aortic diameter over 45 mm.
wall increase wall tension and lead to dissections. Most important are The same consideration is given to atherosclerotic penetrating ulcers. It
intraluminal shear stresses, which are related both to the level of the is suggested that these ulcers, IMH, and dissection might all be related
systolic blood pressure and to the steepness of the aortic pulse wave. and should be treated in similar fashion. 22,23
2
This is referred to as dP/dT max and represents the speed with which the
maximal systolic pressure is attained in the aortic root. As this increases, CLINICAL PICTURE
so too does the shear stress on the ascending aorta. 7
Human genetic and biomarkers studies and findings from ani- Men, particularly African-Americans, are at two to three times the risk
mal models suggest the possibility of identifying some genetic and of developing an aortic dissection as women. More than 90% will have a
biomarker risk factors for dissection. This could potentially lead to history of hypertension requiring treatment. The presentation of an acute
improved targets for drug development to stabilize the aortic wall in dissection can be subtle, demanding great attention to detail to make the
high-risk patients and prevent dissections. 8 diagnosis, or classic and obvious. A new murmur of aortic insufficiency
is present in 50% to 66% of type A dissections due to the loss of support
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of the valve at the commissures as the inner layer of the aorta collapses
CLASSIFICATION inward. A continuous murmur suggests rupture of the dissection into the
right ventricle or atrium. The signs and symptoms are related to the loca-
Dissections are classified by timing and location to identify the morbid-
ity and mortality for the specific lesions. tion of the tear and the extent of the hematoma dissection. These are man-
ifested mainly by pain, poor peripheral perfusion despite an increased
■ TIMING blood pressure, and signs and symptoms of aortic branch occlusion.

• Acute: <2 weeks ■ PAIN
• Chronic: >2 weeks Typically, the pain is either retrosternal or central interscapular back
pain, but it may be epigastric. Classically, it begins in the chest, moves
Acute dissections are very high-risk lesions with an estimated mortal- to the back, and then moves down to the abdomen or lower extremi-
ity for type A of 50% for the first 48 hours (~1% per hour). ties as the dissection progresses, but this pattern is rarely seen. Patients
■ LOCATION describe the pain as “sharp,” “tearing,” or “knife-like,” and it is most
often excruciating in intensity. To differentiate it from angina, the pain
• Type A (Fig. 42-2A-E): The ascending aorta is involved independent is maximal immediately upon onset, and it is often difficult to obtain
of the site of the intimal tear (since 15% of transverse arch and 5% of relief with opiates. Clinical diagnostic accuracy may approach 90% if
descending aortic tears will involve the ascending aorta by retrograde three basic questions are asked regarding the pain’s quality (tearing or
dissection), and may include the aortic arch and part or all of ripping), radiation (beginning between the scapulae and radiating down
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the descending thoracic and abdominal aorta. In autopsy series, type the back), and the intensity at onset (abrupt onset of 10/10 pain).
A dissections outnumber type B dissections almost 2:1. 9 ■ POOR PERFUSION
• Type B (Fig. 42-3A and B): Descending aorta (beyond the left sub-
clavian artery). Patients frequently present with evidence of shock, with a cool, clammy
periphery, ashen coloring, and depressed level of consciousness, and
This classification system, proposed by Daily and colleagues and pop- yet markedly elevated systolic blood pressure frequently exceeding
ularized by the Stanford group, replaces the original system proposed by 200 mm Hg. Most often this is due to reflex sympathetic discharge from
DeBakey (Fig. 42-4). The classification system is based on the risk of the intense pain. It can occur, however, with myocardial infarction due
sudden death from the dissection, which is highest in type A. Here the to coronary artery occlusion (especially the right coronary artery) by
dissection may cause tamponade or severe aortic insufficiency with con- the dissection, or from severe aortic insufficiency with congestive heart
gestive heart failure as well as coronary thrombosis, especially involving failure, which is present in 30% to 60% of patients with type A dissec-
the right coronary artery, with acute myocardial infarction. Type B tions. If the blood pressure is depressed, the dissection may have rup-
dissections do not have these risks and generally can be approached tured into the pericardium with tamponade (as occurs in up to 30% of
and managed conservatively. As a result, therapeutic interventions are type A dissections) or into the pleural space (left more often than right)
dependent on location with almost all type A dissections requiring with resulting hypovolemia. Hypotension occurred in >25% of patients
urgent operative intervention, whereas type B dissections are managed with acute aortic dissection among patients enrolled in the International
primarily pharmacologically or with endostenting and, less commonly, Registry of Acute Aortic Dissection (IRAD) and was associated with
surgery for specific complications. Long-term surveillance is imperative much higher rate of in-hospital adverse events. Cardiac tamponade is a
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to follow potential dilatation of the descending aorta (especially if the life-threatening complication and the leading cause of death. Emergency
false lumen is patent), as in up to 40% of patients the type B dissections echo-directed percutaneous drainage of pericardial effusions causing

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