Recommendations
Key Recommendations
Give initial resuscitation measures, which may include oxygen, fluids, and inotropes, and ensure adequate pain relief using opioids.[2]
Monitor the patient’s vital signs closely.
Once aortic dissection is confirmed, give medical therapy to achieve:[2][14][18]
Heart rate <60 beats per minute
Systolic blood pressure (SBP) 100-120 mmHg.
If aortic regurgitation is excluded, use an intravenous beta-blocker.[2][14][18] A non-dihydropyridine calcium-channel blocker (i.e., verapamil or diltiazem) is an alternative.[14][18]
Add a vasodilator if SBP and heart rate are not adequately controlled.[18]
Further definitive management of acute dissection depends on the type of dissection and the presence of complications.[2] If the patient has a:
Type A (ascending) dissection, refer for emergency surgery[2]
Complicated type B (descending) dissection, refer for urgent thoracic endovascular aortic repair (TEVAR) or open surgery if TEVAR is contraindicated or not feasible[2][14][18]
Uncomplicated type B (descending) dissection, continue medical therapy. TEVAR may be considered in the subacute phase (14 days to 6 weeks after the onset of symptoms) in some patients, including those with features that indicate they are at high risk of developing complications.[2][18]
Treatment of chronic dissection involves careful management of blood pressure and heart rate, modification of risk factors for atherosclerotic disease, and close surveillance for complications.[2]
Give supplemental oxygen and haemodynamic support if needed.
Monitor controlled oxygen therapy. An upper SpO2 limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.
Evidence suggests that liberal use of supplemental oxygen (target SpO2 >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[41]
A lower target SpO2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[42]
Evidence: Target oxygen saturation in acutely ill adults
Too much supplemental oxygen increases mortality.
Evidence from a large systematic review and meta-analysis supports conservative/controlled oxygen therapy versus liberal oxygen therapy in non-hypercapnic acutely ill adults.
Guidelines differ in their recommendations on target oxygen saturation in acutely unwell adults who are receiving supplemental oxygen.
The 2017 British Thoracic Society (BTS) guideline recommends a target SpO2 range of 94% to 98% for patients not at risk of hypercapnia, whereas the 2022 Thoracic Society of Australia and New Zealand (TSANZ) guideline recommends 92% to 96%.[42][43]
The Global Initiative for Asthma (GINA) guidelines recommend a target SpO2 range of 93% to 96% in the context of a severe exacerbation of asthma.[44]
A systematic review including a meta-analysis of data from 25 randomised controlled trials, published in 2018, found that, in adults with acute illness, liberal oxygen therapy (broadly equivalent to a target saturation >96%) is associated with higher mortality than conservative oxygen therapy (broadly equivalent to a target saturation ≤96%).[41]
In-hospital mortality was 11 per 1000 higher for the liberal oxygen therapy versus conservative therapy group (95% CI, 2 to 22 per 1000 more).
Mortality at 30 days was also higher in the group who had received liberal oxygen (RR 1.14, 95% CI 1.01 to 1.29).
The trials included adults with sepsis, critical illness, stroke, trauma, myocardial infarction, or cardiac arrest, and patients who had emergency surgery. The review excluded studies that were limited to people with chronic respiratory illness or psychiatric illness, patients on extracorporeal life support, those receiving hyperbaric oxygen therapy, or those having elective surgery.
An upper SpO2 limit of 96% is therefore reasonable when administering supplemental oxygen to patients with acute illness who are not at risk of hypercapnia. However, a higher target may be appropriate for some specific conditions (e.g., pneumothorax, carbon monoxide poisoning, cluster headache, and sickle cell crisis).[45]
In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis and decided an interim update was not required.[42]
The committee noted that the systematic review supported the use of controlled oxygen therapy to a target.
While the systematic review showed an association between higher oxygen saturations and higher mortality, the BTS committee felt the review was not definitive on what the optimal target range should be. The suggested range of 94% to 96% in the review was based on the lower 95% confidence interval and the median baseline SpO2 from the liberal oxygen groups, along with the TSANZ guideline recommendation.
Subsequently, experience during the COVID-19 pandemic has also made clinicians more aware of the feasibility of permissive hypoxaemia.[46]
Management of oxygen therapy in patients in intensive care is specialised and informed by further evidence (not covered in this summary) that is more specific to this setting.[47][48][49]
Give intravenous fluid resuscitation and consider inotropes if the patient is haemodynamically unstable, particularly if they have incipient renal failure and hypovolaemic shock. See Acute kidney injury and Shock.
Check your local protocols for specific recommendations on fluid choice and inotrope dose and choice. There is debate, based on conflicting evidence, on whether there is a benefit in using normal saline or balanced crystalloid in critically ill patients.
Practical tip
Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloraemic acidosis.
Also note that use of lactate-containing fluid in a patient with impaired liver metabolism may lead to a spuriously elevated lactate level, so results need to be interpreted with other markers of volume status.
Evidence: Choice of fluids
Evidence from two large randomised controlled trials (RCTs) suggest there is no difference between normal saline and a balanced crystalloid for critically ill patients in mortality at 90 days, although results from two meta-analyses including these RCTs point to a possible small benefit of balanced solutions compared with normal saline.
There has been extensive debate over the choice between normal saline (an unbalanced crystalloid) versus a balanced crystalloid (such as Hartmann’s solution [also known as Ringer’s lactate] or Plasma-Lyte®). Clinical practice varies widely, so you should check local protocols.
In 2021-2022, two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte) versus normal saline: the Plasma-Lyte® 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; N=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; N=11,052).[50][51]
In the PLUS study, 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis, and 79.0% were receiving mechanical ventilation at the time of randomisation.
In BaSICS, almost half the patients (48.4%) were admitted to ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
Both found no difference in 90-day mortality overall or in pre-specified subgroups for patients with acute kidney injury (AKI), sepsis, or post-surgery. They also found no difference in the risk of AKI.
In BaSICS, for patients with traumatic brain injury, there was a small decrease in 90-day mortality with normal saline - however, the overall number of patients was small (<5% of total included in the study) so there is some uncertainty about this result. Patients with traumatic brain injury were excluded from PLUS as the authors felt these patients should be receiving saline or a solution of similar tonicity.
A meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[52]
A subsequent individual patient data meta-analysis included six RCTs of which only PLUS and BaSICS were assessed as being at low risk of bias. There was no statistically significant difference in in-hospital mortality (OR 0.96, 95% CI 0.91 to 1.02). However, the authors argued that using a Bayesian analysis there was a high probability that balanced solutions reduced in-hospital mortality, although they acknowledged that the absolute risk reduction was small.[53]
A pre-specified subgroup analysis of patients with traumatic brain injury (N=1961) found that balanced solutions increased the risk of in-hospital mortality compared with normal saline (OR 1.42, 95% CI 1.10 to 1.82).
Previous evidence has been mixed.
A 2015 double-blind, cluster randomised, double-crossover trial conducted in 4 ICUs in New Zealand (N=2278), the 0.9% Saline vs Plasma-Lyte for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, AKI, or use of renal-replacement therapy.[54]
However, a 2018 US multi-centre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs 11.1%; odds ratio [OR] 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4% respectively (OR 0.91, 95% CI 0.84 to 0.99).[55]
A 2019 Cochrane review included 21 RCTs (N=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[56]
The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (N=19,054).
There was no difference in in‐hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), acute renal injury (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).
Initial management of acute aortic dissection involves intensive monitoring and medical therapy, regardless of definitive treatment.[2][14][18]
The aim of medical therapy is to control the patient’s pain, heart rate, and blood pressure to decrease wall stress in order to limit the extension of the dissection and reduce the risk of developing end-organ damage and rupture.[18]
Once aortic dissection is confirmed, give medical therapy while monitoring the patient’s vital signs closely.[2][14]
If aortic regurgitation is excluded, give an intravenous beta-blocker to achieve:[2][14][18]
Heart rate <60 beats per minute
Systolic blood pressure (SBP) 100-120 mmHg.
If a beta-blocker is not suitable for the patient, a non-dihydropyridine calcium-channel blocker (i.e., verapamil or diltiazem) is an alternative.[18]
Ensure adequate pain relief using intravenous opioids to decrease sympathetic tone and facilitate haemodynamic stability.[2][18] Be aware that morphine causes vasodilation and reduces the heart rate by increasing vagal tone.
If heart rate and SBP are not adequately controlled with a beta-blocker (or a calcium-channel blocker) and analgesia, add a vasodilator (e.g., sodium nitroprusside).[18]
Further definitive treatment is determined by accurate diagnosis of the type of aortic dissection according to the following criteria:[2][18]
Type A: involves the ascending aorta with or without involvement of the arch and descending aorta.
Complicated type B: involves only the descending thoracic aorta (distal to the left subclavian artery) and/or abdominal aorta, with any of the following complications:[2][14][18]
Signs of rupture (haemothorax, increasing periaortic or mediastinal haematoma) and/or hypotension or shock
Malperfusion (visceral, renal, limb, or spinal)
Early or rapid aortic aneurysm expansion
Periaortic haematoma
Hypertension not controlled despite full medication
Persistent or recurrent pain.
Uncomplicated type B: involves only the descending thoracic aorta (distal to the left subclavian artery) and/or abdominal aorta with none of the complications above.
Type A dissection involves the ascending aorta with or without involvement of the arch and descending aorta.
Immediately refer the patient for emergency surgery if they have a type A dissection.[2]
The mortality rate of patients receiving medical management alone for acute type A aortic dissection is two to three times that of those treated with surgical intervention.[30]
Depending on the extent of retrograde extension, the aortic valve may or may not need to be repaired or replaced.[2] This is in order to prevent cardiac tamponade or fatal exsanguination from aortic rupture.
Therapeutic options include:[14]
Open aortic arch replacement
Transposition of supra-aortic branches with subsequent endovascular repair
Total endovascular repair
The frozen elephant trunk repair technique, which combines open repair of the proximal aorta under deep hypothermic circulatory arrest, together with placement of thoracic stent grafts into the distal aortic arch and upper descending thoracic aorta. Of note, stent grafts designed for total endovascular aortic arch repair are currently only available as part of a clinical trial, and thus the use of this approach using off-the-shelf stent graphs is off-label.
More info: Techniques for repair
One meta-analysis of comparator observational studies reported that the frozen elephant trunk technique was associated with lower stroke and mortality rates, but higher spinal cord ischaemia events, compared with conventional aortic arch surgery.[57] Longer term follow-up is necessary, and ideally evidence from randomised controlled trials; however, the technologies designed to treat aortic arch pathology continue to evolve.[58]
Type B dissection involves only the descending thoracic aorta (distal to the left subclavian artery) and/or abdominal aorta.
Urgently refer the patient for thoracic endovascular aortic repair (TEVAR) or open surgery if they have a type B dissection that is complicated by:[2][14][18]
Signs of rupture (haemothorax, increasing periaortic or mediastinal haematoma) and/or hypotension or shock
Malperfusion (visceral, renal, limb, or spinal)
Early or rapid aortic expansion
Periaortic haematoma
Hypertension not controlled despite full medication
Persistent or recurrent pain.
TEVAR is the treatment of choice for most patients with complicated type B aortic dissection.[2][14][18] However, open surgery may be indicated if the patient has:[2]
Arterial disease of the lower extremities
Severe tortuosity of the iliac arteries
A sharp angulation of the aortic arch
Absence of a proximal landing zone for the stent graft.
More info: TEVAR
One Cochrane review noted a lack of randomised controlled trials (RCTs) and controlled clinical trials investigating the effectiveness and safety of TEVAR compared to open surgical repair for patients with complicated chronic type B aortic dissection. The investigators were therefore unable to provide any evidence to inform decision-making on the optimal intervention for these patients.[59] Several studies have demonstrated high technical success rates for endovascular stenting to seal proximal entry tears. This promotes false lumen thrombosis and aortic remodelling. Static or dynamic side-branch obstruction can be relieved with additional endovascular stents. Compromised branches can be treated with ostial bare stents or stent grafts that enlarge the compressed true lumen. Survival rates and neurological complications with endovascular treatment of type B dissections are favourable compared with those of open surgery.[60][61][62]
Type B dissection involves only the descending thoracic aorta (distal to the left subclavian artery) and/or abdominal aorta.
Medical management
Continue medical management used in the initial phase with intensive monitoring (see Initial management section above) if the patient has an acute type B aortic dissection without any of the following complications:[2][14][18]
Signs of rupture (haemothorax, increasing periaortic or mediastinal haematoma) and/or hypotension or shock
Malperfusion (visceral, renal, limb, or spinal)
Early or rapid aortic aneurysm expansion
Periaortic haematoma
Hypertension not controlled despite full medication
Persistent or recurrent pain.
Thoracic endovascular aortic repair
Thoracic endovascular aortic repair (TEVAR) may be considered in some patients with uncomplicated type B dissection, including those who have features that indicate they are at high risk of developing complications, such as bloody pleural effusion, aortic diameter >40 mm, and malperfusion that is only detectable on imaging.[14][18] If TEVAR is indicated, it is performed in the subacute phase (14 days to 6 weeks after the onset of symptoms) to promote false lumen thrombosis and prevent aneurysmal degeneration.
More info: TEVAR for uncomplicated acute type B dissection
Although TEVAR is increasingly performed in patients with acute uncomplicated type B aortic dissection (TBAD), there is considerable heterogeneity of published data; results from meta-analyses evaluating TEVAR in patients with type B aortic dissection should be interpreted with caution.
One meta-analysis found no evidence for survival benefit at 1 year for patients with acute uncomplicated TBAD treated with TEVAR compared with those receiving best medical therapy.[63] Another meta-analysis found that TEVAR did not prevent aneurysmal degeneration in patients treated for acute or chronic (including complicated) TBAD, noting that long-term data are lacking.[64] Results from one meta-analysis of a mixed patient population (complicated/uncomplicated, acute/subacute TBAD) and one randomised study of patients with stable TBAD suggest that aneurysm-specific outcomes may be favourable over the longer term following TEVAR.[65][66]
Aortic dissection is a lifelong condition and is defined as chronic at >90 days since the first onset of symptoms.[2][5][18] This includes patients with type A dissection with persisting dissection of the descending aorta following surgical repair of the aortic arch.[2]
The patient may also be diagnosed with chronic dissection if the first diagnosis of aortic dissection is picked up as an incidental finding at the chronic stage (e.g., an incidental finding of mediastinal widening or prominent aortic knob on chest x-ray).[2]
The largest group of patients with chronic aortic dissection (approximately 60%) are those with surgically corrected ascending (Stanford type A) dissection with a persistent false lumen distal to the surgical repair.[5] Patients with non-operated type A dissection rarely live past the acute event; hence, chronic dissections of the ascending aorta are exceedingly rare.[5]
Manage patients with chronic aortic dissection in line with the same medical principles employed in the acute phase.
Manage the patient’s blood pressure and heart rate very carefully.
Aim for a target blood pressure of <120/80 mmHg and a heart rate <60 beats per minute.[18]
Use a long-acting beta-blocker (e.g., bisoprolol) as a first-line treatment.[2][18]
Most patients will require at least two antihypertensives. Additional drugs include an angiotensin-II receptor antagonist or an ACE inhibitor (as second line), and a calcium-channel blocker (as third line).[18] A thiazide-like diuretic may also be used.[67]
Advise the patient to avoid contact sports and strenuous physical activities (such as isometric heavy weight lifting, pushing, or straining that would require a Valsalva manoeuvre) to reduce aortic wall shear stress due to sudden rises in arterial blood pressure during exercise.[2][18] However, activities with low static and dynamic stress (mild aerobic exercise and daily activities) can be continued.[2][18] The patient should also avoid cocaine or other stimulating drugs such as methamphetamine.[18]
More info: Blood pressure control
At least 40% of patients will require combination treatment to control blood pressure. In patients with connective tissue disorders, particularly Marfan syndrome, losartan plus a beta-blocker did not improve clinical outcomes compared with those who did not receive losartan.[68]
Other interventions include management of risk factors for atherosclerotic disease; in particular:[18]
Smoking cessation
Lipid-lowering therapy: target of LDL-cholesterol <70 mg/dL (see Hypercholesterolaemia for more information).
Ensure the patient has close surveillance and follow-up to monitor for complications.[2] See Monitoring.
Organise thoracic endovascular aortic repair (TEVAR) or surgery if the patient has a chronic type B dissection and develops any of the following complications:[2]
Rupture
Chronic visceral or limb malperfusion
Progressive aneurysmal enlargement (growth of >10 mm/year)
False lumen aneurysms (with total aortic diameter >60 mm)
Persistent or recurrent pain.
Bear in mind that patients with connective tissue diseases and those with a family history of aortic dissection warrant more careful consideration and may be suitable for earlier intervention (diameter of 50-55 mm).[5][69][70]
More info: TEVAR for chronic type B dissection
A chronic type B dissection primarily requires TEVAR or surgery due to aneurysmal enlargement of the dissected segment of the aorta. The goals of treatment are to:
Cover the entry tear
Treat or prevent impending rupture
Re-establish organ perfusion
Restore flow in the true lumen
Induce the false lumen thrombosis.
In a retrospective analysis of 80 patients who underwent TEVAR for chronic type B aortic dissections, complete false lumen thrombosis was achieved in 52% and aneurysm diameter was stabilised or reduced in 65%. The 5-year overall survival was 70%.[71] In a prospective multi-centre trial from China, TEVAR for chronic type B aortic dissection decreased the risk of aortic-related mortality compared with optimal medical therapy alone at 4 years, but failed to improve overall survival. The thoracic aorta diameter decreased significantly in the TEVAR group, but increased in the medical therapy group.[72] There currently are no longer-term data on the efficacy of TEVAR for chronic type B aortic dissection.
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