Aortic Dissection

Question 1

What are dissecting aneurysms

Answer 1

A dissecting aneurysm (or dissection) occurs when there is a tear in the vessel intima that allows blood to flow into the wall, creating an additional channel (the false lumen) between the intima and media through which blood can flow. This intimal tear can result from shear forces acting on the intima from within the vessel lumen or from internal rupture of a small haematoma within the vessel media.

Question 2

Summarise aortic dissection

Answer 2

Typically presents in men older than 50 years of age, with sudden onset of severe ripping or tearing substernal or interscapular pain.

May present with syncope, heart/renal failure, or mesenteric or limb ischaemia; oxygen/advanced life support protocol and haemodynamic support should be instituted without delay when the condition is suspected.

Diagnostic modalities include computed tomography scan, magnetic resonance imaging, or trans-thoracic/trans-oesophageal echocardiography.

Involvement of the ascending aorta and/or arch warrants urgent surgical repair. Dissections of the descending aorta are managed medically with beta blockade; surgery in this group is reserved for those with end-organ malperfusion, persistent pain, rapid aneurysmal degeneration, or rupture.

Lifelong surveillance is needed with regular imaging to detect delayed aneurysmal degeneration of the remaining aorta, which may later require surgery.

Question 3

Define aortic dissection

Answer 3

Aortic dissection describes the condition when a separation has occurred in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media. Dissection most commonly occurs with a discrete intimal tear, but can occur without one. An aortic dissection is considered acute if the process is less than 14 days old

Question 4

Describe the epidemiology of aortic dissection

Answer 4

The worldwide incidence of aortic dissection is 0.5 to 2.95 cases per 100,000 people annually. The incidence in the US is 0.2 to 0.8 cases per 100,000 people annually, resulting in about 2000 new cases each year. The highest rate is in Italy with 4.04 cases per 100,000 per year.[5] Men are predominantly affected, typically older than 50 years of age.

Question 5

What does aortic dissection result from

Answer 5

Aortic dissection results from an intimal tear that extends into the media of the aortic wall. Cystic medial degeneration predisposes to intimal disruption and is characterised by elastin, collagen, and smooth muscle breakdown in the lamina media. Bleeding from the vasa vasorum can also lead to this condition.

Question 6

Describe the inherited conditions and iatrogenic factors that can lead to aortic dissection

Answer 6

Inherited conditions that lead to medial degeneration provide a morphological substrate for developing aortic dissection. Marfan syndrome and Ehlers-Danlos syndrome lead to weakening of the media, thus predisposing to aortic dilation and dissection. Bicuspid aortic valve may be associated with a non-specific connective-tissue disease, predisposing to aortic aneurysm and/or dissection. Aortic atherosclerosis with dilation, and inflammatory or traumatic conditions or infections, may also predispose to aneurysmal degeneration and dissection. Although rare, iatrogenic causes of aortic dissection include aortic manipulation associated with cardiac surgery or interventional procedures.[6] It is unclear if these iatrogenic complications occur in patients already predisposed by the aetiologies described above.

Question 7

What is the initial event in the pathophysiology of aortic dissection

Answer 7

An intimal tear is the initial event, with subsequent degeneration of the medial layer of the aortic wall. Blood then passes through the media, propagating distally or proximally and creating a false lumen. As the dissection propagates, flow through the false lumen can occlude flow through branches of the aorta, including the coronary, brachiocephalic, intercostal, visceral and renal, or iliac vessels

Question 8

Where do the intimal tears of dissection most commonly occur

Answer 8

The intimal tears of dissection most commonly occur just above the sinotubular junction or just distal to the left subclavian artery.[7] Regardless of where tears occur in the aorta, there may be both a retrograde and antegrade extension of the dissection. Retrograde dissections starting in the ascending aorta can lead to aortic incompetence by separating the aortic valve from the aortic root.

Question 9

Describe the effects of aortic dissection on side-branches

Answer 9

Static narrowing of side-branches occurs when the line of dissection intersects the vessel origin and the aortic haematoma has propagated into the vessel wall, leading to stenosis or occlusion of the side-branch. Dynamic compression occurs when the dissection flap is on the opposite side of the side-branch origin. Obstruction of the side-branch occurs during diastole, when the true lumen collapses and the intimal flap closes over the ostium of the branch vessel. Flow is restored during systole. Both static and dynamic compression of a side-branch or a combination of both can lead to total flow occlusion and end-organ ischaemia. Subsequent clinical manifestations occur depending on the extent of propagation of the dissection with subsequent organ malperfusion

Question 10

What does Laplace’s law describe

Answer 10

Laplace’s law describes wall stress as directly proportional to pressure and radius, and inversely proportional to wall thickness. Thus, factors that weaken the aortic wall, particularly the lamina media, lead to increased risk of aneurysm formation and dissection, and a cycle of increasing wall stress.

Question 11

What is the Stanford classification of aortic dissections

Answer 11

Stanford[2]
Type A: Dissection involves the ascending aorta with or without involvement of the arch and descending aorta.
Type B: Dissection does not involve the ascending aorta. Predominantly involves only the descending thoracic (distal to the left subclavian artery) and/or abdominal aorta.

Question 12

Describe a typical case history of a patient with aortic dissection

Answer 12

A 59-year-old man presents to the emergency department with a sudden onset of excruciating chest pain, which he describes as tearing. There is a history of hypertension. On physical examination, his heart rate is 95 beats per minute. Blood pressure is 195/90 mmHg in the right arm and 160/80 mmHg in the left arm. Pulses are absent in the right leg and diminished in the left.

Question 13

Describe some other presentations of aortic dissection

Answer 13

The pain of aortic dissection usually manifests as acute, tearing chest and back pain (Stanford Type A) or tearing back pain (Stanford Type B). It may also migrate through the thorax or abdomen. Symptoms of stroke or visceral or acute limb ischaemia may be present. It may also migrate through the thorax or abdomen. Symptoms of stroke or visceral or acute limb ischemia may be present. Patients may be haemodynamically stable or in hypovolaemic shock. Occasionally, depressed mental status or neurological changes, limb pain, paraesthesias or weakness, paraplegia, or syncope are presenting symptoms. Infrequently (less than 10%), patients present atypically without pain.[4] There may be signs of heart failure, pericardial tamponade, or a left pleural effusion. Younger patients can present with a recent history of heavy lifting or cocaine use.

Patients with connective-tissue disorders such as Marfan syndrome often present in their 30s, most often due to aortic root enlargement. Patients with Marfan syndrome with a normal diameter aorta may also be at risk.

Question 14

When should aortic dissection be suspected

Answer 14

Aortic dissection should be suspected when an abrupt onset of tearing or ripping chest or back pain is reported. Missing the diagnosis may be catastrophic, hence the importance of acute history taking to prompt further investigation.[14]

The usual presentation is a patient in their 50s, but the condition may occur in younger patients who have Marfan syndrome, Ehlers-Danlos syndrome, or other connective-tissue disorders. Because of the severity of the condition, the diagnosis should be considered in young patients, even when predisposing factors are absent.

Question 15

What do most patients who suffer from aortic dissection have

Answer 15

Most patients have prior hypertension, often poorly controlled. Younger patients may have a connective-tissue disorder, or a recent history of heavy lifting or cocaine use. Family history may reveal aortic aneurysms, dissection, or a connective-tissue disorder.

Question 16

Where is the pain from aortic dissection often located

Answer 16

The pain associated with aortic dissection may be located retrosternally, interscapularly, or in the lower back. Anterior chest pain is typically associated with an ascending dissection; interscapular pain usually occurs with a descending dissection. Pain may migrate through the thorax or abdomen, and the location of pain may change with time as the dissection extends. A minority of patients present with syncope or without pain. It is important to recognise that no single symptom of aortic dissection is pathognomonic of the condition, as there is overlap with cardiac, pulmonary, abdominal, and musculoskeletal disorders.

Question 17

Describe some other signs and symptoms in patients with aortic dissection

Answer 17

Patients may be haemodynamically stable or in hypovolaemic shock. Blood pressure differences in the upper extremities or pulse deficits in the lower extremities should be sought. Neurological deficits may indicate involvement of cerebral or intercostal vessels. There may be depressed mental status, limb pain, paraesthesia, weakness, or paraplegia. Symptoms of visceral ischaemia may be present. Occasionally, a diastolic decrescendo murmur may be discovered, indicating aortic insufficiency. There may be symptoms or signs of heart failure, pericardial tamponade, or a left pleural effusion.

Question 18

What are the key features of Marfan’s syndrome

Answer 18

Patients may exhibit typical marfanoid features including tall stature, arachnodactyly, pectus excavatum, hypermobile joints, high-arched palate, and narrow face

Question 19

What are the features of Ehlers-Danlos syndrome

Answer 19

Type IV Ehlers-Danlos syndrome predisposes to both aneurysms and/or dissections.[1] Features include translucent skin, easy bruising, hypermobility of small joints, and premature ageing of the skin (acrogeria)

Question 20

What sign is a hallmark feature of aortic dissection

Answer 20

A blood pressure differential between the 2 arms is a hallmark of aortic dissection. Pulse differences in the lower limbs may also be evident.

Question 21

Describe the pulse deficit

Answer 21

A pulse deficit (reduction or absence of a pulse) is particularly common in a proximal dissection affecting the aortic arch. The deficit may be unilateral or bilateral depending on the level of the intimal flap. Pulse deficits may also feature in more distal aortic dissections (e.g., of the descending aorta) but these are less common.

Question 22

Describe the diastolic murmur in aortic dissection

Answer 22

Crescendo pattern, indicating aortic incompetence. Common in proximal dissections, but uncommon in distal dissections.

Question 23

Describe some uncommon presentations of aortic dissection

Answer 23

syncope
Up to 20% of patients may present with syncope and no pain

hypotension
Associated with cardiac tamponade and/or hypovolaemic shock.

Question 24

What is a common diagnostic factor of aortic dissection

Answer 24

hypertension

Due to pre-existing hypertensive condition or increased sympathetic drive.

Question 25

Describe some uncommon diagnosis factors of aortic dissection

Answer 25

paraplegia Due to compromise of intercostal vessels and subsequent spinal cord ischaemia. hemiparesis/paraesthesia Due to cerebral or peripheral ischaemia. abdominal pain Visceral ischaemia resulting from compromised organ perfusion. limb pain/pallor Due to compromised limb perfusion. left-sided decreased breath sounds/dullness Left pleural effusion. dyspnoea May indicate new-onset heart failure because of acute aortic insufficiency during proximal dissections, or cardiac tamponade. altered mental status Due to cerebral ischaemia.

Question 26

Describe the strong risk factors for aortic dissection

Answer 26

hypertension The International Registry of Acute Aortic Dissection found that 72% of patients with aortic dissection had a history of hypertension and 32% had a history of atherosclerosis.[8] atherosclerotic aneurysmal disease Approximately 1% of sudden deaths are attributable to aortic rupture. Of these, two-thirds are due to dissection and one third to degenerative aneurysms.[9] Marfan syndrome Predisposes to both aneurysms and/or dissections, presumably related to weakness of the aortic wall.[1] Ehlers-Danlos syndrome Ehlers-Danlos syndrome type IV predisposes to both aneurysms and/or dissections, presumably related to weakness of the aortic wall.[1] bicuspid aortic valve Predisposes to both aneurysms and/or dissections, presumably related to weakness of the aortic wall.[1] annulo-aortic ectasia Predisposes to both aneurysms and/or dissections, presumably related to weakness of the aortic wall. coarctation Untreated coarctation in adults is associated with dissection and is probably related to longstanding hypertension. smoking Tobacco use is closely associated with atherosclerotic and vascular disease and therefore dissections. Family history

Question 27

What is annuloaortic ectasia

Answer 27

Annuloaortic ectasia is a dilation of the proximal ascending aorta and aortic annulus. It may cause aortic regurgitation, thoracic aortic dissection, aneurysm and rupture. It is often associated with connective tissue diseases like Marfan syndrome and Ehlers Danlos Syndrome.

Question 28

What is the aortic annulus

Answer 28

The aortic annulus is a fibrous ring at the aortic orifice to the front and right of the atrioventricular aortic valve and is considered the transition point between the left ventricle and aortic root. The annulus is part of the fibrous skeleton of the heart.

Question 29

Describe coarctation of the aorta

Answer 29

Coarctation of the aorta is a narrowing, or constriction, in a portion of the aorta. The condition forces the heart to pump harder to get blood through the aorta and on to the rest of the body. The aorta is the largest artery in your body

Question 30

Describe some weak risk factors for aortic dissection

Answer 30

The usual presentation is a man in his 50s. However, aortic dissection can occur in younger patients, even in the absence of connective-tissue disorders, and should be considered given the severity of the process.[1] giant cell arteritis Can weaken the media of the aorta and lead to expansion or dissection. overlap connective-tissue disorders Clinical or laboratory features of several connective tissue diseases such as rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, polymyositis, dermatomyositis, and Sjogren syndrome, without meeting the criteria for a specific diagnosis. surgical/catheter manipulation Manipulation of at-risk aortas: examples of procedures include cardiac catheterisation, aortic valve replacement, or thoracic stent-grafting.[6][10] cocaine/amfetamine use Acute hypertension, vasoconstriction, increased stroke volume, and vasospasm as a result of the misuse of these agents may lead to aortic dissection. Case reports involving young patients have been described, and the increased risk associated with misuse of these substances has also been demonstrated using the Nationwide Inpatient Sample.[11][12] heavy lifting Typically confined to young patients and theoretically attributed to the elevated aortic pressure during straining. pregnancy Case reports; for example, in conjunction with Marfan syndrome

Question 31

Describe the initial work up

Answer 31

Initial work-up includes chest x-ray, ECG, and cardiac enzymes to exclude pneumonia or myocardial infarction. Blood tests including a complete metabolic panel and full blood count, including blood type and cross match, should also be requested. Despite a high sensitivity, D-dimer is not recommended as the sole screening tool for acute aortic dissection; while negative D-dimer may be helpful to rule out aortic dissection in low-risk patients, a positive D-dimer lacks specificity, thereby limiting its clinical role.[15][14] However, D-dimer will be of value when considering the differential diagnosis (e.g., pulmonary embolus).[14] Other biomarkers with the potential to assist in the diagnosis of aortic dissection include C-reactive protein, elastin degradation products, calponin, and smooth muscle myosin heavy chain, but none of these have been validated

Question 32

What should be done if aortic dissection is suspected

Answer 32

If aortic dissection is suspected because of the patient's history or widened mediastinum on chest x-ray, computed tomography angiography (CTA) is the primary modality used for diagnosis. CTA has a sensitivity greater than 90% and specificity greater than 85% The diagnosis is made by imaging an intimal flap separating 2 lumens. If the false lumen is completely thrombosed, central displacement of the intimal flap, calcification, or separation of intimal layers are definitive signs of aortic dissection. CTA also allows visualisation of the extent of dissection and involvement of side-branches. Trans-thoracic echocardiography (TTE) may be done in the emergency department, intensive care unit (ICU), or operating theatre for acute proximal dissections if the patient is clinically unstable and there is any question about the diagnosis, or if CTA is unavailable or contraindicated.

Question 33

Describe the difference in the investigation of type A and type B aortic dissections

Answer 33

For type A dissections (ascending), trans-oesophageal echocardiography may be done in the ICU or operating theatre to confirm the diagnosis and better evaluate the aortic valve. Sensitivity and specificity are higher than for TTE. Magnetic resonance angiogram is the most accurate, sensitive, and specific test for aortic dissection, but is rarely used in the acute setting because it is more difficult to obtain than CTA.[17] In the setting of type B dissections (descending), if medical therapy fails and surgery is required, intra-operative intravascular ultrasound helps define the morphology of the dissection and assists in the treatment plan.

Question 34

Describe the importance of the ECG

Answer 34

Important first-line test to look for evidence of myocardial ischaemia. ST segment depression may occur with acute dissection; ST elevation occurs rarely

Question 35

Describe the purpose of the CXR

Answer 35

Excludes other pulmonary causes of pain. may show widened mediastinum

Question 36

Describe the purpose of cardiac enzymes

Answer 36

Important to exclude myocardial infarction; however, myocardial ischaemia and infarction can occur if the dissection extends to the coronary ostium. cardiac enzymes usually negative

Question 37

Describe the importance of the CT angiography

Answer 37

Should be ordered as soon as diagnosis suspected. Should include chest, abdomen, and pelvis to visualise extent of the aneurysm. Intimal flap

Question 38

Describe the purpose of renal function tests

Answer 38

If renal perfusion is compromised. elevated creatinine and urea

Question 39

Describe the purpose of liver function tests

Answer 39

If hepatic perfusion is compromised. elevated aspartate transaminase and alanine transaminase

Question 40

Describe the purpose of lactate

Answer 40

Indicative of malperfusion. elevated or normal

Question 41

Describe the purpose of the FBC

Answer 41

Anaemia may be present in the case of haemorrhage. reduced or normal

Question 42

Describe the purpose of the type and cross

Answer 42

Surgical intervention/transfusion may be necessary in some cases. preparation for surgery

Question 43

Describe the potential role of the D-dimer

Answer 43

Despite a high sensitivity, D-dimer is not recommended as the sole screening tool for acute aortic dissection; while negative D-dimer may be helpful to rule out aortic dissection in low-risk patients, a positive D-dimer lacks specificity, thereby limiting its clinical role.[15][14] However, D-dimer will be of value when considering the differential diagnosis (e.g., pulmonary embolus).[14]

Question 44

Describe the potential role of the transthoracic echo

Answer 44

Can be ordered as supplementary test, or in unstable patients when acute proximal dissection is suspected. intimal flap

Question 45

Describe the potential role for the trans-oesophageal echo

Answer 45

Can be done to confirm the diagnosis and better evaluate the aortic valve, or if computed tomography angiography is unavailable. Sensitivity and specificity are higher than for trans-thoracic echocardiography. Intimal flap

Question 46

Describe the potential for MRI angiography

Answer 46

Very accurate, but rarely used in the acute setting because difficult to obtain. intimal flap

Question 47

Describe the potential role for intravascular ultrasound

Answer 47

In the setting of type B dissections, if medical therapy fails and surgery required, helps define morphology of the dissection and assists in treatment plan. intimal flap

Question 48

Describe the potential role for smooth muscle myosin heavy chain protein

Answer 48

A protein released from damaged aortic medial smooth muscle.[16][20] elevated

Question 49

Describe the different sub-classes of type B aortic dissections

Answer 49

``` Uncomplicated type B (descending) Type B (descending) with end-organ ischaemia. ```

Question 50

Summarise the initial management of aortic dissection

Answer 50

Local resuscitation protocols should be followed. Supplemental oxygen and haemodynamic support with intravenous fluid resuscitation and judicious use of inotropes is recommended in cases of incipient renal failure and hypovolaemic shock. Initial management of both type A and B dissections involves intensive monitoring and anti-impulse therapy. Intravenous beta blockade is used to achieve a heart rate less than 60 beats per minute and systolic blood pressure less than 120 mmHg.[1][21] If beta blockade alone fails, vasodilator therapy (such as sodium nitroprusside or a calcium channel blocker) should be added. To decrease sympathetic tone and facilitate hemodynamic stability, pain should also be controlled with intravenous opioids. It should be noted that morphine causes vasodilation and reduces the heart rate by increasing vagal tone.

Question 51

What does a type A dissection require

Answer 51

Type A dissections require urgent surgical replacement of the diseased aorta. Depending on the extent of retrograde extension, the aortic valve may or may not need to be repaired or replaced in order to prevent cardiac tamponade or fatal exsanguination from aortic rupture.

Question 52

Describe management of a complicated type B aortic dissection

Answer 52

Urgent surgical or endovascular intervention is required if the patient's course is complicated by rupture, visceral or extremity ischaemia, aneurysmal expansion, or persistent pain. Although both open and endovascular therapies are acceptable options, the endovascular approach is gaining preference over the open technique for patients presenting with complications

Question 53

What is the evidence regarding the treatment of a complicated type B aortic dissection showing

Answer 53

here is a growing body of experience with endovascular interventions for the treatment of complicated type B dissections, including fenestration and stenting.[23][24][25] 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. Long-term outcomes will need to be evaluated. In the US, there is currently no approved endovascular stent specifically approved for placement in patients with type B aortic dissection. However, this approach is rapidly becoming the treatment of choice for complicated type B dissection, because of good outcomes compared with historical open surgical controls and reduced invasiveness compared with conventional surgery.

Question 54

When should TEVAR be considered

Answer 54

Based on the 2017 European Society for Vascular Surgery guidelines, thoracic endovascular aortic repair (TEVAR) should be considered in patients with descending thoracic aneurysms more than 60 mm, and may be considered for aneurysms 56 mm to 59 mm. In women and patients with connective tissue disorders, the recommended threshold is lower at 50 mm to 55 mm

Question 55

Describe the treatment of uncomplicated type B aortic dissections

Answer 55

Patients with uncomplicated type B aortic dissection are usually managed medically with blood pressure and pain control during the acute phase (less than 14 days). However, updated analysis of data from the International Registry of Aortic Dissection suggests that there may be some benefit to endovascular intervention in patients with refractory pain and hypertension.[28] Additionally, long-term results of the randomised INSTEAD-XL trial demonstrated that endovascular stent-grafting in uncomplicated subacute patients improved aorta-specific survival and aortic remodelling compared with optimal medical therapy at 5 years.

Question 56

Describe the potential role of TEVAR in uncomplicated type B aortic dissections

Answer 56

With the advent of endovascular stent-graft technology, there has been an interest in performing TEVAR in patients with uncomplicated dissections to promote false lumen thrombosis and prevent aneurysmal degeneration. Results from one study (ADSORB trial) demonstrated that uncomplicated dissection can be treated safely with TEVAR and promote aortic remodelling at one-year postoperatively.[30] Subsequent analysis of the ADSORB trial database showed that the number of vessels originating from the false lumen is an independent predictor of false lumen growth, suggesting that patients with more complex dissection flaps may benefit from TEVAR, even if they do not suffer from malperfusion.[31] There is some evidence that TEVAR in the subacute phase of type B dissection (i.e., between 2 and 6 weeks of presentation) has a lower risk of complications, particularly retrograde type A dissection.[32] Therefore, in patients who are stable it is generally recommended to wait until the subacute time period before stenting.

Question 57

Describe the management of type B aortic dissection

Answer 57

A chronic type B dissection primarily requires treatment due to aneurysmal dilation of the dissected segment of the aorta. The use of TEVAR for chronic type B dissection is becoming more common. The goals of TEVAR therapy 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. ```

Question 58

What have studies shown regarding the use of TEVAR in chronic type B aortic dissections

Answer 58

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%. Five-year overall survival was 70%.[33] 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.[34] There currently are no longer-term data on the efficacy of TEVAR for chronic type B aortic dissection.

Question 59

Describe ongoing management of aortic dissections

Answer 59

Blood pressure control is continued after discharge from hospital.[35] Beta-blockers and ACE inhibitors are usually required, with additional antihypertensives such as diuretics or calcium-channel blockers used if necessary. A systolic blood pressure less than 120 mmHg and heart rate less than 80 beats per minute should be targeted. At least 40% of patients will require combination treatment to control blood pressure. In patients with connective tissue disorders, particularly Marfan syndrome, Iosartan plus beta blockade has been shown to slow the progression of aortic dilation compared with beta blockade alone.

Question 60

What should be done if the patient is initially haemodynamically unstable

Answer 60

– advanced life support with haemodynamic support Primary options noradrenaline (norepinephrine): 0.5 to 1 microgram/min intravenously initially, adjust according to response, usual dose range 2-12 micrograms/min, maximum 30 micrograms/min -- AND / OR -- dobutamine: 0.5 to 1 microgram/kg/min intravenously initially, adjust according to response, usual dose range 2-20 micrograms/kg/min, maximum 40 micrograms/kg/min Local resuscitation protocols should be followed. Supplemental oxygen and haemodynamic support with intravenous fluid resuscitation and judicious use of inotropes is recommended in cases of incipient renal failure and hypovolaemic shock.

Question 61

Describe the 1st line for confirmed aortic dissections

Answer 61

labetalol: 1-5 mg/min intravenous infusion More OR esmolol: 500 micrograms/kg intravenously initially, followed by 50 micrograms/kg/min for 4 min, may repeat loading dose and increase infusion up to 200 micrograms/kg/min if necessary More OR metoprolol: 5 mg intravenously every 5-10 minutes, maximum 15 mg/total dose Intravenous beta blockade is essential to reduce the continued pulsatile force (dP/dt) on the already-thinned walls of the false channel. Beta blockade may prevent further propagation of the dissection and reduces the risk of acute rupture. The risk of therapy is low. Intravenous beta blockade is used to achieve a heart rate less than 60 beats per minute and systolic blood pressure less than 120 mmHg PLUS opioid analgesia Treatment recommended for ALL patients in selected patient group Primary options morphine sulfate: 2-5 mg intravenously every 5-30 minutes as needed Pain control is an important first-line therapy to reduce sympathetic tone and facilitate haemodynamic stability. It should be noted that morphine causes vasodilation and reduces the heart rate by increasing vagal tone.

Question 62

What should be prescribed if the beta blockade is insufficient

Answer 62

Treatment recommended for ALL patients in selected patient group Primary options nitroprusside: 0.3 to 0.5 micrograms/kg/min intravenously initially increase by 0.5 micrograms/kg/min increments; maximum 10 micrograms/kg/min Secondary options diltiazem: 0.25 mg/kg intravenous bolus initially, followed by 5-10 mg/hour infusion; maximum 15 mg/hour If beta blockade (and analgesia) fails to achieve a heart rate less than 60 beats per minute and systolic blood pressure less than 120 mmHg, then intravenous anti-hypertensive vasodilator therapy (such as sodium nitroprusside or a calcium-channel blocker) should be added. The risk of therapy is minimal.

Question 63

What should then be done if its type A or complicated type B

Answer 63

OPEN SURGERY OR ENDOVASCULAR STENT-GRAFT REPAIR

Question 64

What should then be done if its uncomplicated type B or chronic type B

Answer 64

end-vascular stent-graft repair will be an adjunct

Question 65

What should be done after hospital discharge

Answer 65

metoprolol: 100-450 mg/day orally (immediate-release) given in 2-3 divided doses; 25-100 mg orally (modified-release) once daily and/or enalapril: 5-40 mg orally once daily or given in 2 divided doses Secondary options metoprolol: 100-450 mg/day orally (immediate-release) given in 2-3 divided doses; 25-100 mg orally (modified-release) once daily and enalapril: 5-40 mg orally once daily or given in 2 divided doses - - AND -- hydrochlorothiazide: 12.5 to 50 mg orally once daily and/or nifedipine: 30-60 mg orally (extended-release) once daily No patient is considered cured. Blood pressure control is continued after discharge from hospital. Beta-blockers and ACE inhibitors are usually required, with additional antihypertensives such as diuretics or calcium-channel blockers used if necessary. At least 40% of patients will require combination treatment to control blood pressure.

Question 66

Describe some emerging treatments for aortic dissection

Answer 66

Hybrid surgical repair/frozen elephant trunk operation For type A dissection, there is a late risk of aortic dilation and other complications of up to 50%. New surgical approaches combining open repair of the proximal aorta under deep hypothermic circulatory arrest combined with open placement of thoracic stent grafts into the distal aortic arch and upper descending aorta have been shown to increase late thrombosis and remodelling of the aortic false lumen. A 2015 meta-analysis of outcomes of the frozen elephant trunk technique for acute type A aortic dissection found acceptable morbidity and mortality with the approach.[36] Longer term follow-up is necessary, but these techniques have the promise to redefine treatment of acute aortic dissection.[37][38] Endovascular stent-grafting of the ascending aorta Although several case series have demonstrated feasibility of stent-grafting the ascending aorta, there have been no larger series to confirm the safety of these techniques and it remains investigational

Question 67

Describe the primary prevention for aortic dissection

Answer 67

Hypertension should be assessed for and treated appropriately in all patients. Other cardiovascular risk factors (e.g., dyslipidaemia and diabetes mellitus) should also be intensively managed. Smokers should be encouraged to cease smoking.

Question 68

Describe the secondary prevention for aortic dissection

Answer 68

Patients with known Marfan or Ehlers-Danlos syndrome should be regularly monitored with echocardiography for aortic root aneurysm (predisposing to dissection). Blood pressure control to less than 150 mmHg (preferably less than 120 mmHg) systolic and less than 90 mmHg is recommended. No data support exact goals, but shear forces are excessive when systolic blood pressure exceeds 150 mmHg. Heart rate should be maintained less than 80 beats per minute. Beta blockade is first-line treatment.

Question 69

Describe some important patient discussions in patients with aortic dissection

Answer 69

Heavy lifting of more than 30 lb to 50 lb should be avoided. Aerobic exercise is acceptable after discussion with the physician, ideally keeping the heart rate less than 100 beats per minute. Patients should follow up for surveillance imaging and blood pressure control. Smoking cessation and control of hyperlipidaemia is important for overall vascular health. It is recommended that patients maintain a heart-healthy diet.

Question 70

Describe the monitoring of patients with aortic dissection

Answer 70

Imaging of the aorta should be performed before discharge. Patients with uncomplicated aortic dissection should be followed up with serial surveillance imaging with computed tomography angiography (CTA) or magnetic resonance angiography (MRA) at 1, 3, 6, and 12 months after discharge, and then annually thereafter to monitor for aneurysmal degeneration of the descending thoracic aorta. Patients undergoing thoracic endovascular aortic repair should undergo CTA at 1 and 12 months postoperatively, followed by CTA or MRA annually for 3 years. If there is no evidence of endoleak or other complications by 3 years, postoperative surveillance can be performed every 2 to 3 years.

Question 71

What are the short-term high risks of aortic dissection

Answer 71

 pericardial tamponade short term high Occurs when an ascending aortic dissection extends proximally with rupture into the pericardial space. Emergency surgical repair of the aortic dissection is required. The team may wish to prepare the patient's chest for incision while the patient is awake in the event that the patient sustains cardiac arrest during the induction of anaesthesia. aortic incompetence short term high Occurs when dissection propagates proximally, leading to loss of commissural support for the valve leaflets. Urgent surgical repair of the dissected aorta with aortic valve repair or replacement is required.

Question 72

Describe a low risk short-term complication of aortic dissection

Answer 72

myocardial infarction short term low Occurs when the dissection propagates proximally and coronary ostial occlusion occurs. Urgent surgical repair of the aortic dissection with coronary reconstruction and/or coronary bypass grafting is required.

Question 73

Describe some variable term medium-low risk complications of aortic dissection

Answer 73

aneurysmal degeneration/rupture variable medium Complications from distal aortic dissection occur in 20% to 50% of patients. This occurs due to continued pulsatile force (dP/dt) on already-thinned walls of the false channel or new dissection. A multi-drug antihypertensive regimen including beta blockade to maintain systolic pressure less than 120 mmHg may alter the natural history of chronic dissection by diminishing the rate of aneurysmal dilation  regional ischaemia variable low Cerebral, renal, visceral, spinal cord, or lower-extremity ischaemia occur when the dissection propagates distally and true lumen occlusion occurs. Emergency surgical or endovascular repair of the dissected aorta with or without additional revascularisation of compromised branch vessels is required.  left arm ischaemia/subclavian steal syndrome variable low Occurs when the left subclavian artery is covered after endovascular aortic repair in approximately 15% of patients. The Society for Vascular Surgeons Practice Guidelines recommends routine preoperative revascularisation of the left subclavian artery for patients who need elective stent-graft repair where achievement of a proximal seal necessitates coverage of the left subclavian artery, and selective revascularisation in urgent indications.[44][45] This can result in subclavian steal syndrome.  endoleak variable low The risk of endoleak following thoracic endovascular aortic repair is low (estimated at 4.7%).[46] Depending on the location and type of endoleak, it may require re-intervention.[47][48] Endoleak is not a complication following open repair.

Question 74

Describe the prognosis of aortic dissection

Answer 74

Syncope at presentation is usually associated with worse outcomes. A deadly triad of hypotension/shock (not syncope), lack of chest or back pain (presumably related to delay in diagnosis), and branch vessel involvement is also described.[40] Left untreated, the natural history of proximal acute aortic dissection is of false channel rupture with fatal exsanguination in 50% to 60% of patients within 24 hours.[41] Late degeneration of the dissected aorta into a false lumen aneurysm occurs in 30% to 50% of patients.[8] Following treatment, patients remain at risk for further aneurysmal degeneration of remaining diseased aorta. The 10-year survival after surgery of ascending aortic dissection is 52%. Freedom from re-operation at both 5 and 10 years ranges from 59% to 95% The 5-year survival after thoracic endovascular aortic repair (TEVAR) for acute type B aortic dissection is 81%.[42] Longer term outcomes after TEVAR for the treatment of either acute or chronic type B aortic dissection are currently unknown.

Question 75

What is another important risk factor for aortic dissection

Answer 75

Pregnancy

Question 76

Describe the sequelae of dissection

Answer 76

Sequelae of dissection include: • Rupture, which is rapidly fatal. • Occlusion of aortic branches, especially coronary, cerebral, and renal arteries. • Proximal extension of the dissection can cause aortic regurgitation or cardiac tamponade.

Question 77

Describe the mortality rate of aortic dissections

Answer 77

Acute type A dissection has a mortality rate of 1–2% per hour during the first 48 h and a 90% mortality at 30 days if left untreated. Classically, type A dissections (high risk of rupture) are treated surgically by replacing the affected segment of the aorta with a synthetic graft, while type B dissections (which are not as immediately life-threatening) are treated medically with tight blood pressure control to reduce wall stress or with endovascular stenting.