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R.C. Hyzy (ed.), Evidence-Based Critical Care, DOI 10.1007/978-3-319-43341-7_18
Management of Acute Aortic
cardiothoracic surgeons with emergent repair. All other dissections are usually managed with strict blood pressure control and urgent Cardiothoracic and Vascular Surgery consultations, unless there is evidence of end-organ hypoperfusion [1–3].
As pain can contribute to elevated blood pres- sures, the patient was given 4 mg Morphine IV with a modest improvement in his pain. However, he continued to have significant anxiety, shortness of breath and diaphoresis. After a discussion with the patient and his family, he was orotracheally intubated. An arterial line was placed into his right radial artery and his pressures were noted to be 170/100 s mmHg. Bilateral upper extremity cuff pressures correlated with pressures obtained from his arterial line. He was started on an esmolol drip at 10 mcg/kg/minute. This agent was quickly titrated up to 150 mcg/kg/minute (maximum infu- sion rate of 300 mcg/kg/minute) in order to obtain a goal heart rate <60 beats per minute (bpm) and a systolic blood pressure <120 mmHg. Despite high doses of esmolol with a heart rate <60 bpm, the patient’s blood pressure remained uncon- trolled so a nitroprusside infusion was started at 0.25 mcg/kg/minute and increased up to 0.35 mcg/kg/minute (maximum dose 2 mcg/kg/min- ute). Blood pressures remained poorly controlled with the two agents and so a third agent, labetalol was added at 1 mg/minute and increased up to 6 mg/minute. The initiation of labetalol improved his BP and the esmolol drip was weaned off.
Concurrent to the patient’s blood pressure control, a STAT CTA chest was obtained upon the patient’s arrival, and was read as a dissection of the aortic arch starting at the innominate artery (brachiocephalic trunk) and extending to the descending aorta. Cardiothoracic Surgery and Vascular Surgery evaluated the patient and opted to medically manage him as the ascending aorta was not involved. Twelve hours later, a transtho- racic echocardiogram (TTE) was performed and was concerning for aortic valve involvement. A transesophageal echocardiogram (TEE) was immediately performed which confirmed ascend- ing aortic dissection with aortic insufficiency without pericardial tamponade (Figs. 18.3, 18.4, and 18.5, Video 18.1 and 18.2).
Principles of Management Definition
Acute aortic syndromes comprise a spectrum of disease involving the aorta, including penetrating aortic ulcers (PAU), intramural hematomas (IMH), and aortic dissection [2, 4]. Intramural hematomas develop as a result of a micro-tear within the vasa vasorum resulting in an intrame- dial hematoma that is characterized by the absence of an aortic entry or exit tear. The prevalence of IMH in patients found to have aortic dissections ranges from 4 to 22 %. The IMH may evolve to overt dissection or even rupture, with progression that may occur suddenly or be heralded by ongo- ing acute aortic syndrome. Fifty to 80 % may resolve completely but patients may also progress to dissection or develop an aneurysm later in their disease course. Resolution occurs more often in younger patients, and those with aortic diame- ter < 4–4.5 cm, hematoma thickness <1 cm, and therapy with beta-blockers [1, 2, 5, 6].
Penetrating aortic ulcers represent atheroscle- rotic plaques that have ulcerated into the medial layer of the aortic wall. The high pressure pulsa- tile flow of blood through the aorta can cause fur- ther erosion of this ulcerated plaque which, in turn, can result in instability of the aortic wall and can lead to IMH, dissection, and even aortic
Fig. 18.2 CTA chest showing the dissection flap (black arrow) at the level of the descending aorta
rupture. These lesions are uncommon in the ascending aorta because high flow is protective against atherosclerosis. However, if present, they usually rupture and are commonly fatal. Lesions in the ascending aorta can initially be treated medically with close observation. PAUs more commonly arise in the descending thoracic aorta [2, 4–6].
Anatomically, the ascending aorta is the sec- tion proximal to the brachiocephalic trunk and the
descending aorta is distal to the left subclavian artery. The DeBakey and the Stanford classifica- tions are the two most frequently utilized classifi- cation systems. The DeBakey classification system divides the dissection into 3 types. Type I involves both the ascending and descending aorta;
Type II affects the ascending aorta only; and Type III is a dissection distal to the left subclavian artery. The Stanford classification simplifies this further. The dissection either affects the ascending
Fig. 18.3 Apical 5 cham- ber view demonstrating marked dilatation of the proximal ascending aorta and dissection flap (arrow). AoV aortic valve, LV left ventricle, LA left atrium (Image courtesy of Priscilla Peters, BA, RDCS, FASE)
Fig. 18.4 Apical 5 cham- ber view revealing aortic regurgitation. White arrow points to the dissection flap. Red asterisk (*) at area of aortic regurgitation (Image courtesy of Priscilla Peters, BA, RDCS, FASE)
aorta (Type A) or it remains distal to the left subclavian (Type B) [7]. Isolated aortic arch dis- sections do not fit neatly into any of these classifi- cation types, and there is debate as to whether they should be grouped with Type A or Type B dissections. Some have argued that the natural history approximates more closely that of Type B dissections and as such, isolated arch dissections do not require emergent surgical intervention.
Other experts disagree [7, 8] (Fig. 18.6).
Risk factors for acute aortic dissection are var- ied. Hypertension is a predominant risk factor [9]
but other factors include bicuspid aortic valve, cocaine use, Marfan syndrome (and other con- nective tissue disorders), blunt trauma, preg- nancy, weight lifting (Valsalva maneuvers), previous aortic surgery, and large-vessel vasculi- tis, among others [1].
Diagnosis
Chest pain is a ubiquitous presenting complaint.
In a patient with hypertension and chest pain radiating to the back, acute aortic syndrome must be considered and ruled out. While angiography had previously been the gold standard, CTA of the chest is now the standard of care to diagnose aortic dissection given its widespread availability and ease of use. MRI may also be used to aug- ment findings although it is not the diagnostic study of choice for emergently imaging the aorta
due to lesser availability and longer duration of image acquisition. TTE and TEE are other modalities that may be used to evaluate the aorta, particularly in a hemodynamically unstable patient for whom transport out of the department would be unsafe [2, 10, 11]. Although the quality of echocardiograms is operator dependent, TTE generally has a sensitivity of 59–83 % and a spec- ificity of 63–93 % for diagnosing an ascending aortic dissection [5]. TEE has a sensitivity of close to 100 % with a specificity of 89 % for iden- tifying an ascending aortic dissection, although it can be as low as 31–55 % for descending aortic aneurysms [6].
Medical Management
All Type B dissections, and rarely Type A dissec- tions, are initially medically-managed with strict blood pressure control. Although no randomized trials have been conducted, beta-blockers have been the mainstay of treatment. An esmolol, labetalol, or propranolol continuous infusion is initiated in order to reduce shear force (dP/dt) exerted on the aortic wall. Unless hypotension is present, the goal systolic blood pressure is 100–120 mmHg and the target heart rate is 50–60 beats per minute [1, 3]. Esmolol is often favored as the initial agent as it is short-acting and can be rapidly weaned off if the patient experiences severe hypotension or bronchospasm (patients
Fig. 18.5 Off-axis transesophageal echocardiogram revealing an ascending aortic dissection with a dissection flap (arrow)
with severe COPD or asthma). If blood pressure is still poorly controlled with intravenous beta- antagonist agents, nitroprusside may be added.
Nitroprusside should never be started as the ini- tial agent as it may promote reflex tachycardia and increase dP/dt, thus propagating the dissec- tion flap. If blood pressures are still poorly con- trolled or if beta-blocker use is contraindicated, an infusion of a non-dihydropyridine calcium- channel blocker may be used [1].
Patients with PAU and IMH are treated with blood pressure control similar to that used in
aortic dissection. Surgery may be necessary if there is refractory chest pain or extension. Both conditions should be recognized as part of the spectrum of acute aortic diseases that require close monitoring and treatment. They require lifelong anti-hypertensive therapy and repeat aor- tic imaging at 3, 6, 9 and 12 months based on the size of the aorta [2, 5].
Upon discharge, beta-blocking agents, calcium- channel blockers, or angiotensin- converting enzyme inhibitors should be pre- scribed to maintain blood pressure control. The
a b c
Fig. 18.6 Different types of aortic dissection. DeBakey classification: (a) DeBakey Type 1. (b) DeBakey Type 2.
(c) DeBakey Type 3. Stanford classification: (a, b)
Stanford Type A. (c) Stanford type B (Image courtesy of J. Heuser/Creative Commons)
International Registry of Acute Aortic Dissection (IRAD) researchers found that, in general, beta- blockers were associated with mortality benefit in Type A dissections and in patients that were treated surgically, while patients with medically- managed Type B dissections had improved sur- vival if discharged home with calcium channel blockers [3].
Surgical Intervention
Dissections involving the ascending aorta confer a high early mortality risk [12]. Previous studies reported a 1 % per hour mortality risk in patients with an untreated acute Type A aortic dissection [13]. Mortality is reduced from 90 % without sur- gical intervention to less than 20 % with surgery [13, 14]. Type B dissections are initially managed conservatively with strict blood pressure control unless there is evidence of malperfusion, persis- tent pain, or refractory hypertension; in such cases, emergent vascular surgery consultation and intervention is warranted. Delayed surgical intervention via endovascular repair is preferred to the open approach [9, 15, 16].
Complications
Aortic rupture and complications such as hypo- tension, neurologic deficits, shock, cardiac tam- ponade, pulse deficits, and kidney failure confer an even higher mortality rate [12]. Also, visceral malperfusion and extremity ischemia may occur.
Evidence Contour
A guideline-based approach to the management of patients with aortic dissection is provided in Fig. 18.7. However, the optimal approaches to diagnose and manage aortic dissection are still under investigation. Although no randomized control trials have been conducted to evaluate the best anti-hypertensive medication(s) to treat acute aortic syndromes, the mainstay of treat- ment is to start with an agent that will reduce
shear stress and decrease heart rate. Other aspects of diagnosing and treating dissections, however, are still under significant debate.
Diagnosis of Aortic Dissection
Various biomarkers have been evaluated to deter- mine their usefulness in ruling out aortic dissec- tion. Of the possible biomarkers, D-dimer seems to have the most clinical utility. D-dimer assays may be significantly elevated (greater than 1600 ng/mL) in the first 6 h [3, 4] and may be used to assist in the assessment of patients with suspected dissection. A low D-dimer level (<500 ng/mL) may offer a sufficiently high nega- tive predictive value to rule out aortic dissection [17]. However, professional guidelines do not endorse routine use of d-dimer for this purpose.
Other novel biomarkers are currently under investigation.
Medical Management of Type A Dissection
While surgical intervention has been established as the standard of care for an ascending aortic dissection, some proponents recommend that in patients with advanced age, coma, acute renal failure, shock, or need for re-do operation, medi- cal management alone may be warranted as the risk of surgery is prohibitive [18, 19]. Other con- siderations for medical management are given to patients with completed stroke, co-morbid condi- tions that preclude a good quality of life, prior aortic valve replacement, and presentation to the hospital more than 48–72 h after onset of aortic dissection [19].
Surgical Intervention for Aortic Arch Dissections
Treatment of aortic arch dissections is a matter of some controversy. In the DeBakey classification system, the aortic arch is a separate entity that is not clearly accounted for. As such, several studies
Acute aortic dissection
1. Initiate immediate medical management.
2. In house management or transfer to another facility
Check BP in both arms and treat highest reading
Hypotension or shock
Type B - Fluid boluses to obtain - MAP >70 mmHg - Review imaging for cause - Consider TEE
- Surgical consultation
Anatomy based management
Type A - Emergent surgical consult
- Fluid boluses to obtain MAP >70 mmHg - If still hypotensive use vasopressors
BP Control (lV) - Beta blocker - Diltiazem - Verapamil Pain control
-IV Opiates
Goal SBP < 120 mmHg?
Ascending aorta involvement?
Surgical or interventional management Etiology of hypotension
amenable to surgery
Ongoing medical management -Close hemodynamic monitoring -Keep SBP < 120 mmHg
Complications requiring surgical or interventional management - Malperfusion syndrome - Extension of dissection - Aneurysm expansion - Uncontrolled hypertension
Transition to outpatient - Transition to oral medications - Surveillance imaging
Yes No
Yes
No
Yes
No
No Yes
Yes No
Add IV vasodilator to titrate to < 120 mmHg
Fig. 18.7 Management of patients with aortic dissection
have evaluated whether aortic arch dissections require surgical intervention or if medical man- agement alone is sufficient in uncomplicated cases. The initial IRAD studies showed that there was no difference in in-hospital mortality when comparing Type B dissections with or without aortic arch involvement. Additionally, it was found that aortic arch involvement was not an independent risk factor for mortality [8].
Recently, the German Registry for Acute Aortic Dissection Type A (GERAADA) study evaluated early mortality and new neurologic and malper- fusion deficits among different surgical approaches for aortic arch replacement. They found that while there were more complications in the immediate post-operative period for the population treated with total arch replacement, there was no significant difference in 30-day mortality between the hemiarch and total arch groups [20]. They did not, however, compare arch replacement to medical management strate- gies. Nevertheless, other natural history studies suggest the risk of progression of isolated arch dissection is high and some experts argue for rou- tine surgical management. Because of this uncer- tainty, we favor a team-based approach to evaluation and individualized decision-making.
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R.C. Hyzy (ed.), Evidence-Based Critical Care, DOI 10.1007/978-3-319-43341-7_19