EASILY MISSED?
Acute aortic dissection
Aaron M Ranasinghe Walport clinical lecturer 1lecturer2, Daniel Strong clinical fellow3, Barry Boland
consultant in emergency medicine4, Robert S Bonser consultant cardiac surgeon1honorary professor2
1Department of Cardiac Surgery, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham B15 2TH, UK;
2School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT; 3New Cross Hospital, Royal Wolverhampton
Hospitals NHS Trust, Wolverhampton WV10 0QP, UK; 4Emergency Department, Queen Elizabeth Hospital, University Hospitals Birmingham NHS
Foundation Trust, Birmingham B15 2TH
This is one of a series of occasional articles highlighting conditions that
may be more common than many doctors realise or may be missed at
first presentation. The series advisers are Anthony Harnden, university
lecturer in general practice, Department of Primary Health Care,
University of Oxford, and Richard Lehman, general practitioner, Banbury.
To suggest a topic for this series, please email us at
Acute aortic dissection is caused by an aortic intimal tear with
propagation of a false channel in the media. Depending on the
site and extent of the tear, it may cause chest, back, or abdominal
pain, or collapse caused by rupture or malperfusion (transient
or persistent ischaemia of any organ as a result of arterial branch
obstruction). It is anatomically categorised according to
involvement of the ascending aorta (type A, DeBakey type I/II)
(fig 1); the categorisation dictates management.
Why is aortic dissection missed?
Although most patients present within two hours of onset of
symptoms (usually to non-cardiac surgical centres), definitive
diagnosis may be delayed by over 12 hours6and half of patients
do not have surgery until more than 24 hours have elapsed.7
Patients with dissection are commonly hypertensive men in
their 60s, but all ages are affected (27% are aged 17-59 years,
40% aged 60-74 years, 33% aged >75 years),5including young
adults, some with connective tissue disorders, such as
undiagnosed Marfan syndrome. In older patients, other
conditions are more prevalent, and in the young, the diagnosis
may not be considered.
The clinical features at presentation (table ) may be sensitive
but highly non-specific indicators and in some instances may
include features of ischaemia from malperfusion (such as
neurological deficits), which may confuse the clinical
diagnosis.8 9 Electrocardiographic and troponin abnormalities
resulting from coronary malperfusion are common and
diagnostically misleading. Although changes in chest
radiographs are common (89%), a normal chest radiograph does
not exclude the diagnosis, and anterioposterior projections are
unreliable. Guidelines for evaluating chest pain from the
National Institute for Health and Clinical Excellence (NICE)
concentrate on acute coronary syndrome (which is more
common and less lethal). The need for chest radiographs, and
their timing, is discretional and inquiry for transient neurological
deficits is not mandatory.10
Why does this matter?
For type A acute aortic dissection, untreated mortality is 1-2%
per hour in the first day, with a 90% mortality at 30 days. With
surgery, this can be converted to 75-90% survival, and no more
than two patients need treatment to gain survival advantage.8
Rapid recognition and treatment (within hours) may prevent
the survival attrition and maximise recovery of reversible
malperfusion phenomena (including neurological deficit).11
Misdiagnosis as acute coronary syndrome may lead to
inappropriate administration of anti-platelets and thrombolysis,
complicating surgery. For all cases of acute aortic dissection,
delayed diagnosis may delay antihypertensive treatment,
allowing propagation and worsening of prognosis.
How is acute aortic dissection diagnosed?
Clinical
A triad of symptoms—characteristic chest pain (usually abrupt
and/or severe), a pulse deficit or blood pressure differential, and
an abnormal chest radiograph—increases the likelihood of
dissection but is present in only a third of patients. A pulse
deficit is the unilateral absence or diminution of a pulse
compared with contralateral palpation.4To detect this, a full
peripheral pulse examination is mandatory (radial, brachial,
carotid, and femoral pulses). The blood pressure differential is
defined as a difference in systolic blood pressure between both
arms of >20 mm Hg.9
Correspondence to: R S Bonser rober[email protected].uk
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Practice
PRACTICE
Case scenario
A 64 year old hypertensive man presented to an emergency department with sudden onset, severe, sharp chest pain.
Right arm blood pressure was 100/70 mm Hg and an electrocardiogram showed inferior ST segment depression. Troponin
T was raised (0.2 ng/mL). Acute coronary syndrome was provisionally diagnosed, anti-platelet therapy administered, and
coronary angiography planned. On later questioning, he described a left arm weakness that had resolved. Further examination
noted left arm hypertension (155/90 mm Hg), a right carotid bruit, and diastolic murmur. Computed tomography showed a
type A acute aortic dissection (see fig 2) for an example from another case) involving the right coronary ostium and
brachiocephalic artery. He was transferred for emergency surgery.
How common is acute aortic dissection?
•The estimated annual incidence is 30-43 per million of the population2and may be increasing3
•However, it is relatively uncommon, accounting for 1 in 300-350 emergency admissions for chest pain4
•For every emergency admission for dissection, there are 100 patients with acute myocardial infarction and 25 with
pulmonary embolism5
Ask about any new neurological symptoms (transient or
permanent) or symptoms of limb ischaemia, as these may
highlight malperfusion phenomena and because focal
neurological deficits occur in 17% of patients with type A
dissection.12 In addition, for patients who are admitted with
neurology or limb ischaemia, questioning about chest pain
should be done to identify potential triggering causes of the
presenting symptoms. The table outlines the key clinical features
of both type A and B dissection.
Investigations
Patients with a suspected clinical diagnosis of acute aortic
dissection should have basic investigations. These include
electrocardiography, chest radiography, and blood tests for
markers of myocardial ischaemia. Normality or abnormality of
any of these does not exclude dissection; however, if further
imaging rules out dissection, then they may be of use in future
patient management. Once clinically suspected, a definitive
diagnosis is made with cross sectional imaging (computed
tomography of the aorta or magnetic resonance angiography)
or transoesophageal echocardiography; each of these imaging
techniques has high diagnostic accuracy. If computed
tomography is done, images of the thoracic aorta should be
obtained before injection of contrast to allow the detection of
intramural haematoma (a condition that may progress to
dissection). In the absence of trauma, computed tomography is
not routine. Transthoracic echocardiography may be specific
but is insensitive and operator dependent and does not exclude
the diagnosis. Biomarkers may have a role: raised concentration
of D-dimer is sensitive but non-specific, raising the suspicion
for both dissection and the differential diagnosis of pulmonary
embolus.13 14
How is acute aortic dissection managed?
Administer analgesia for pain relief and control hypertension
with intravenous β blockade, and refer all patients to cardiac
surgical centres: (a) in patients with type A dissection, for
emergency surgery to prevent intrapericardial rupture, restore
true luminal flow and aortic valve competence, and to correct
malperfusion; (b) in patients with type B dissection, for medical
management and assessment for complications, which may
require surgical or endovascular intervention.15
Contributors: AMR and RSB conceived the manuscript, interpreted the
data from the literature, and drafted and revised the manuscript. DS
and BB interpreted data from the literature and helped to revise the
manuscript. All authors have approved the final version. RSB is the
guarantor.
Competing interests: All authors have completed the ICMJE uniform
disclosure form at www.icmje.org/coi_disclosure.pdf (available on
request from the corresponding author) and declare: no support from
any organisation for the submitted work; no financial relationships with
any organisations that might have an interest in the submitted work in
the previous three years; no other relationships or activities that could
appear to have influenced the submitted work.
Provenance and peer review: Not commissioned; externally peer
reviewed.
Patient consent not required (patient anonymised, dead, or hypothetical).
1 Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management.
Part I: From etiology to diagnostic strategies. Circulation 2003;108:628-35.
2 Meszaros I, Morocz J, Szlavi J, Schmidt J, Tornoci L, Nagy L, et al. Epidemiology and
clinicopathology of aortic dissection. Chest 2000;117:1271-8.
3 Olsson C, Thelin S, Stahle E, Ekbom A, Granath F. Thoracic aortic aneurysm and
dissection: increasing prevalence and improved outcomes reported in a nationwide
population-based study of more than 14 000 cases from 1987 to 2002. Circulation
2006;114:2611-8.
4Von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection.
Arch Intern Med 2000;160:2977-82.
5 Information Centre for Health Education and Social Care. Hospital epsiode statistics
online. www.hesonline.nhs.uk.
6Raghupathy A, Nienaber CA, Harris KM, Myrmel T, Fattori R, Sechtem U, et al. Geographic
differences in clinical presentation, treatment, and outcomes in type A acute aortic
dissection (from the International Registry of Acute Aortic Dissection). Am J Cardiol
2008;102:1562-6.
7 Sabik JF, Lytle BW, Blackstone EH, McCarthy PM, Loop FD, Cosgrove DM. Long-term
effectiveness of operations for ascending aortic dissections. J Thorac Cardiovasc Surg
2000;119:946-62.
8 Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al.
The International Registry of Acute Aortic Dissection (IRAD): new insights into an old
disease. JAMA 2000;283:897-903.
9Bossone E, Rampoldi V, Nienaber CA, Trimarchi S, Ballotta A, Cooper JV, et al. Usefulness
of pulse deficit to predict in-hospital complications and mortality in patients with acute
type A aortic dissection. Am J Cardiol 2002;89:851-5.
10 National Institute for Health and Clinical Excellence. Chest pain of recent onset:
Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac
origin. (Clinical guideline 95.) 2010. www.nice.org.uk/guidance/CG95.
11 Estrera AL, Garami Z, Miller CC, Porat EE, Achouh PE, Dhareshwar J, et al. Acute type
A aortic dissection complicated by stroke: can immediate repair be performed safely? J
Thorac Cardiovasc Surg 2006;132:1404-8.
12 Collins JS, Evangelista A, Nienaber CA, Bossone E, Fang J, Cooper JV, et al. Differences
in clinical presentation, management, and outcomes of acute type A aortic dissection in
patients with and without previous cardiac surgery. Circulation 2004;110(11 suppl
1):II237-42.
13 Suzuki T, Distante A, Zizza A, Trimarchi S, Villani M, Salerno Uriarte JA, et al. Diagnosis
of acute aortic dissection by D-dimer: the International Registry of Acute Aortic Dissection
Substudy on Biomarkers (IRAD-Bio) experience. Circulation 2009;119:2702-7.
14 Sodeck G, Domanovits H, Schillinger M, Ehrlich MP, Endler G, Herkner H, et al. D-dimer
in ruling out acute aortic dissection: a systematic review and prospective cohort study.
Eur Heart J 2007;28:3067-75.
15 Fattori R, Tsai TT, Myrmel T, Evangelista A, Cooper JV, Trimarchi S, et al. Complicated
acute type B dissection: is surgery still the best option? A report from the International
Registry of Acute Aortic Dissection. J Am Coll Cardiol Intv 2008;1:395-402.
Accepted: 20 June 2011
Cite this as: BMJ 2011;343:d4487
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PRACTICE
Key points
•Consider acute aortic dissection in any patient with severe, sudden onset chest, back, or abdominal pain; although
uncommon, dissection is commonly lethal, and rapid diagnosis and intervention may save life and treat morbidity
from malperfusion
•If clinical suspicion is raised by detailed history taking of the pain and high risk features on examination (pulse deficit
or blood pressure differential; focal neurological deficits; murmur), confirm the diagnosis with imaging studies (such
as computed tomography of the aorta, magnetic resonance angiography, transoesophageal echocardiography)
•As malperfusion based symptoms may predominate, inquire about chest pain in patients presenting with neurological
or peripheral ischaemic symptoms
•A normal chest radiograph or abnormal electrocardiogram neither refutes nor confirms the diagnosis
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PRACTICE
Table
Table 1| Comparison of variables in patients presenting with acute type A and B aortic dissection. Values are percentages of patients
except where stated otherwise. Data adapted from publications from the International Registry of Aortic Dissection’s database8 9
Patients with type B dissectionPatients with type A dissection
Patient characteristics
6963Male
64 (13)61 (14)Age (mean (SD)) (years)
7769Hypertension
4224Known occlusive vascular disease
Pain
8485Acute onset
9090Severe or worst ever
4471Anterior chest
4133Posterior chest
4322Abdomen
6447Back
6862Sharp
5249Tearing or ripping
3027Radiating
26Painless
Physical examination
1244Aortic incompetence
930Pulse deficit
Electrocardiography
3231Normal
4343Non-specific ST-T wave changes
1317Ischaemia
3225Left ventricular hypertrophy
Chest radiography
1611Normal
5663Wide mediastinum
53 (24)47 (27)Abnormal aortic (or cardiac) contour
2217Pleural effusion
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PRACTICE
Figures
Fig 1 The two most common classifications of aortic dissection. The Stanford classification divides dissections into type A
(involving the ascending aorta) and type B (no ascending involvement). The DeBakey classification subdivides Stanford
type A into ascending and descending (type I) and ascending alone (type II). DeBakey type III is equivalent to Stanford
type B. Stanford type A (DeBakey types I and II) dissection requires surgery, whereas most Stanford type B dissection is
treated medically. DeBakey type I dissection has the greatest propensity for malperfusion. Neither classification reports the
site of the intimal tear, and some dissections may propagate in a retrograde way. Adapted and reproduced with permission
from Nienaber and Eagle1
Fig 2 Section of contrast enhanced computed tomogram at the level of the pulmonary artery bifurcation (labelled PA)
showing an acute dissection. An intimal flap is seen within the ascending (AA) and descending aorta (DA). Black arrows
indicate the intimal flap, and the true lumen is the smaller lumen. This therefore represents a Stanford type A (DeBakey
type I) dissection, which requires surgical intervention
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PRACTICE
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