The document discusses acute aortic emergencies, including aortic dissection and its associated conditions, with a focus on risk factors, pathophysiology, clinical features, diagnosis, and treatment options. It emphasizes the importance of rapid identification and intervention to reduce mortality rates, detailing various classifications and imaging techniques for assessments. Additionally, it covers aneurysmal disease, its risk factors, symptoms, diagnosis, and treatment strategies, highlighting the complex nature of managing vascular emergencies.

1. ACUTE AORTIC EMERGENCIES
Dr Andrew Crofton
ED Registrar

2. INTRODUCTION
• Acute aortic syndromes
• Aortic dissection, penetrating atherosclerotic ulcer, intramural haematoma and
aortic aneurysm leakage/rupture
• 3-6 cases per 100 000 per year
• Most common cardiovascular complication of Marfan’s syndrome is aortic root
disease and type A dissection
• Identification of gene mutations associated with Marfan’s (TGFBR2 and FBN1),
combined with regular follow-up can reduce fatal outcomes

3. PATHOPHYSIOLOGY
• Degeneration of the media of the aortic wall with
intimal stress leading to:
• Aortic dilation
• Aneurysm formation
• Development of penetrating ulcer
• Intramural haemorrhage
• Aortic dissection
• Aortic rupture

4. RISK FACTORS
• Risk factors
• Male (65% of cases)
• Chronic hypertension (70-90% of cases)
• Arteritis/syphilis
• Bicuspid aortic valve
• Marfan’s syndrome
• Ehlers-Danlos syndrome
• Family history of aortic dissection
• Chronic cocaine/amphetamine use
• Prior cardiac surgery

5. PATHOPHYSIOLOGY
• Aortic dissection
• Violation of intima allowing blood to enter media and dissect between the
intima and adventitia
• Dissecting column of blood forms a false lumen and can re-enter lumen
(spontaneous clinical recovery) or dissect through adventitia with
exsanguination
• First peak in younger patients with connective tissue disorders and second
peak in those >50yo with chronic hypertension
• Other atherosclerotic risk factors are relatively weak compared to chronic
HTN
• Atherosclerosis is NOT a major risk factor for aortic dissection and is rarely
present at site of dissection

6. PATHOPHYSIOLOGY
• Aortic dissection
• Classification
• Stanford A – Any involvement of the ascending aorta (proximal to ligamentum
arteriosum) – 60-70% of cases
• Stanford B – Descending aorta only
• DeBakey type I – Ascending, arch and descending aorta
• DeBakey type II – Ascending aorta only
• DeBakey III – Descending aorta only
• IIIa stops before diaphragm
• IIIb extends past diaphragm

7. AORTIC DISSECTION
• 5-10 patients per million per year
• 2-3x more common than ruptured AAA
• 90% fatal in 3 months; 28% fatal in 24 hours
• In-hospital mortality 25%
• Distribution
• 50% begin in ascending aorta
• 30% begin in the arch
• 20% begin distally
• Usually re-enter aorta just above bifurcation

8. COMPLICATIONS
• Dissection of other vessels
• Coronaries, brachiocephalic trunk, carotids, left
subclavian, spinal, mesenteric, renal, iliacs
• Free rupture – Haemothorax/sudden
death/retroperitoneal/peritoneal
• Acute aortic regurgitation
• Haemopericardium/tamponade
• Aneurysm formation

9. PATHOPHYSIOLOGY
• Aortic intramural haematoma
• Results from infarction of the aortic media due to injury to vasa vasorum
• May resolve spontaneously or dissect
• 5-20% of cases of acute aortic syndrome
• Treated as for dissection
• Penetrating atherosclerotic ulcer
• Can lead to intramural haematoma, aortic dissection or perforation of the aorta
• Poorer outcome than mural haematoma
• Treatment is with early surgical graft replacement of aorta

10. CLINICAL FEATURES
• History
• Always think if chest pain PLUS
• Back pain
• Abdominal pain
• Neurological deficits
• Limb ischaemia
• Classically tearing chest pain radiating to interscapular region with impending doom
• 60% of patients had anterior chest pain (most common in Stanford A); 50% have back pain
• Abdominal pain (30%) and back pain are more common in Stanford B
• 25% have no chest pain
• 5% have no pain at all
• Most patients describe pain as worst pain they’ve ever had and abrupt onset (85%) - if not rapid onset LR -0.3 to -0.07
• 64% describe sharp pain and 50% as tearing

11. CLINICAL FEATURES
• History
• Syncope seen in 10% (mostly Stanford A)
• 22% occur in patients with prior cardiac surgery
• May present with stroke symptoms with carotid involvement
• 20% of type A dissections display neurological findings (poor prognosis)
• Focal neuro deficit + chest pain = LR + 6.6 to 33
• Paraplegia if blood supply to spinal cord interrupted
• Further distal dissection may lead to flank/back or abdominal pain
• Cardiac tamponade if more proximal dissection ensues +- ECG showing ACS-type
findings if coronary arteries involved

12. CLINICAL FEATURES
• Examination
• 1/3 have aortic insufficiency murmur – LR + 9.0
• 15% have pulse deficit in radial or femoral arteries
• 20% sensitive but 95% specific – LR + 29-33
• BP discrepancy of >20mmHg between arms – significant
• 30% sensitive and 85% specific for dissection
• 50% have hypertension (>150mmHg)
• Seen in 35% of Type A and 70% of type B
• Hypotension in 18-25% (worse prognosis)
• Pericardial tamponade occurs in 25% of type A dissections
• Aneurysmal aortic dilatation can compress surrounding structures
• Oesophagus (dysphagia)
• Recurrent laryngeal nerve (hoarsenss)
• Superior cervical sympathetic ganglion (Horner’s)

13. CLINICAL FEATURES
• DDx
• MI/ACS
• Pericardial disease
• Stroke
• Spinal cord injury/disorders
• Intra-abdominal disorders
• PE, pneumonia, pleurisy, pneumothorax

14. DIAGNOSIS
• ECG – Normal in 19-31%. Majority have non-specific
ST/T wave changes or ST depression
• 25% have features suggestive of ACS (usually type I
dissection)
• D-dimer
• False negative rate as high as 18%. Especially useless in
younger patients with short dissection length and
thrombosed false lumen
• Not to be used as sole rule-out criterion and not routinely
used in workup at all

15. DIAGNOSIS
• Imaging
• 12-37% of patients have normal CXR; conversely 90% of cases have
some abnormality
• 60% widened mediastinum; 50% abnormal aortic contour
• Normal CXR more common if younger (connective tissue) or
pregnancy-related
• CT (MDCT) is the modality of choice
• Highly sensitive/specific and can diagnose atherosclerotic ulcers and intramural haematomas
• Provides information on extent of dissection, other organs involved and signs of aortic rupture
• More accurate for proximal than distal aortic dissections; Sensitivity 95%, specificity 95-
100%

16. DIAGNOSIS
• Imaging continued…
• TTE
• Limited sensitivity but highly specific if intimal flap seen. Sensitive for ascending dissections within 2-3cm of
aortic valve
• TOE may be as sensitive and specific as CT
• Requires moderate sedation and highly operator dependent
• Sensitivity 80-100%; specificity 70-95%
• Less accurate for aortic ulcers and intramural haematomas
• Coronary CT angiography (triple rule-out)
• Can diagnosed and differentiate coronary artery disease, PE and acute aortic dissection
• Requires special infusion protocol and has not been shown to improve diagnostic yield, reduce clinical events
or diminish downstream resource use

17. CXR FINDINGS
• Double density of aorta
• Tracheal deviation to the right and
anteriorly
• Depression of left main bronchus
• NGT deviation to the right
• Cardiomegaly
• Left sided pleural effusion
• Apical capping
Left mediastinal width at level of aortic
knob >5cm – 90% sensitive and specific
Blurred aortic knob – 70% sensitive
Loss of aortopulmonary window
Mediastinum > 7.5cm at level of aortic
knob – 90% sensitive and specific
Mediastinum >25% chest width
Subjective widening – Sensitivity of
65%; LR + 2.0
Disparity between ascending and
descending aorta diameter

18. TREATMENT
• Target HR<60 and then SBP 100-120mmHg
• Esmolol 0.1-0.5mg/kg IV bolus then 0.025-0.2mg/kg/min
• Labetalol 10-20mg IV bous, then repeat 20-40mg q10min up to 300mg
• Metoprolol 1-5mg IV boluses q3-5min
• Improved survival with beta-blocker use
• If significant aortic regurgitation, more vasodilator vs. rate control may improve haemodynamics
(tachycardia shortens time of regurgitation)
• Vasodilators
• Nitroprusside can be added once HR <60
• GTN preferred if coronary ischaemia evident
• Hydralazine 5-10mg IV over 5-10 min repeated q15-20min

19. TREATMENT
• Definitive repair
• Type A require prompt surgical repair
• Endovascular stent repairs with fenetrations can be used
for some type A and complicated type B dissections
(malperfusion, resistent hypertension, persistent severe
pain, persistent false lumens or expanding aortic
diameter), penetrating ulcers and intramural
haematomas
• All other Type B get medical management and
ongoing management from Cardiology/Vascular
Surgery

20. ANEURYSMAL DISEASE
• Aneurysm = Dilatation >1.5x normal diameter
• True aneurysm - involves all three layers of wall
• Risk factors:
• Connective tissue disorders
• Family Hx of aneurysm
• Atherosclerosis risk factors
• Thinning of media and reduced tensile strength
• Increased wall force and dilatation are intertwined as per LaPlace law: wall tension = pressure x
radius
• Larger aneurysms expand more quickly due to this (0.25-0.5cm per year)
• Abrupt expansion and rupture can occur and is not predictable

21. ANEURYSMAL DISEASE
• Pseudoaneurysm – Partly vessel wall and partly fibrous tissues
• Usually at site of previous cannulation, anastamoses of prior reconstructions, trauma or
infection
• Small ones may thrombose spontaneously
• Mycotic aneurysm – Infection in blood vessel wall, often in
immunocompromised
• Can be direct extension or embolisation from IE
• Peripheral and visceral aneurysms
• Popliteal artery most common (often co-exist with AAA)
• Renal, splenic and hepatic arteries most common visceral aneurysms
• Usually silent until rupture or thrombosis/embolic phenomena

22. SYMPTOMATIC AAA
• Defined as aorta >=3cm in diameter
• Repair considered for aneurysm >5cm
• 20% have first-degree relative with AAA
• Most patients >60 and more commonly male
• Clinical features
• Syncope, back, flank, abdominal pain, GI bleeding, extremity ischaemia from embolisation from intramural thrombus, shock or sudden death
• Sudden death usually occurs from intraperitoneal rupture
• Syncope without warning symptoms and subsequent severe pain suggests rupture with some temporary containment
• Patients may regain consciousness but irreversible haemorrhagic shock ensues if not promptly diagnosed
• Typically back or abdominal pain, 50% describe as ripping/tearing and 10% have syncope
• Non-classic sites of pain are still common (flank, groin, isolated quadrants, hip)
• Uncommon presentations are Grey-Turner, Cullen, scrotal haematoma, inguinal mass and femoral neuropathy from compression

23. AAA
• Prevalence
• 1% at age 50
• 4% at age 60
• 5-10% at age 70
• 10% at age 80
• Rupture <1% per year if <5cm and 17% per year if >6cm
• Risk of rupture higher in women (growth rate is faster) and in current
smokers/hypertension
• 0.3cm/year expansion if <5cm and 0.5cm/year if >5cm

24. AAA
• Diagnosis
• Abdominal palpation
• Sensitivity 29% for 3-4cm; 50% for 4-5cm; 76% for >5cm
• Lack of tenderness does not indicate intact aorta
• Periumbilical ecchymosis (Cullen sign) and flank ecchymosis (Grey-Turner sign) are rare
• Scrotal or vulvar haematomas or inguinal masses can be seen if retroperitoneal blood
dissects down
• Aortoenteric fistulas may present with small sentinel bleed
followed by catastrophic haemorrhage
• Aortovenous fistulas can cause high-output cardiac failure

25. AAA
• Imaging
• Plain film – May show calcified aneurysm but cannot determine rupture
• Bedside USS - >90% sensitivity for demonstrating aneurysm and measuring diameter if
technically adequate
• Obesity, bowel gas and abdominal tenderness make study difficult
• Need to measure transverse and longitudinally
• Identifying SMA distinguishes aorta from IVC
• If <3cm, this excludes aneurysmal disease
• CT with contrast
• Unenhanced CT still identifies aneurysm size and retroperitoneal haemorrhage

26. AAA
• Treatment
• Consultation
• Permissive hypotension to 90mmHg or LOC with blood products
• Pain control
• Use imaging only in those fully compensated or unlikely to have ruptured their aneurysm
• If asymptomatic
• >5cm needs follow-up within days
• >3cm needs follow-up at some point
• Repairing AAA <5.5cm does not improve survival in men but may do so in women
• Perioperative mortality for elective repair is 5% for open and 1.5% for endovascular repair (although 2 year survival rates are
the same for either method = 90%)
• Endovascular repair does NOT improve survival if deemed medically unfit for open repair
• Operative mortality is 15% if urgently repaired (non-ruptured) and 50% if ruptured

27. THORACIC AORTIC ANEURYSM
• Presenting symptoms often from compression of oesophagus, trachea,
bronchi, sympathetic ganglia or recurrent laryngeal
• If erodes into another structure, almost invariably fatal
• Refer any patient with asymptomatic TAA to surgeon and primary care
provider for operative repair and blood pressure control respectively

28. THORACIC AORTIC ANEURYSM
• Indications for repair
• Symptomatic
• Ruptured
• Dissection
• Asymptomatic
• Ascending
• End-diastolic aortic diameter >5.5cm
• Descending
• >5.5cm
• >7cm if high surgical risk
• Rapid expansion >1cm per year for aneurysms <5cm in diameter

29. SPONTANEOUS RETROPERITONEAL
HAEMORRHAGE
• Usually associated with vascular or malignant disease of the kidney or
adrenal gland, spontaneous rupture of retroperitoneal veins or with
anticoagulant therapy
• Presents as acute abdominal pain, shock and palpable abdominal or
groin mass
• Confirmed by CT
• IR is often the treatment of choice

30. VISCERAL ARTERIAL ANEURYSMS
• Defined as those affecting celiac, SMA, IMA and their branches
• Splenic artery (70%) and hepatic artery (20%) most commonly
• Often present with life-threatening haemorrhage due to delayed
diagnosis and high incidence of rupture
• Usual treatment is therefore early elective intervention rather than
watchful waiting
• Aneurysmal = 1.5x normal diameter

31. VAA
• Risk factors
• Atherosclerosis
• Pregnancy
• Portal HTN (splenic)
• Liver transplant (splenic)
• Marfan/Ehlers-Danlos
• Kawasaki
• Presenting complaints
• Usually vague abdominal pain, nausea/vomiting until rupture

32. VAA - SPLENIC
• Third most common true aneurysm after aortic and iliac artery
• 80% in those over 50

33. VAA - HEPATIC
• 80% extrahepatic
• Atherosclerosis is the most common underlying cause
• Symptomatic – Nausea and RUQ pain but most diagnosed incidentally
• Erosion into biliary tree leads to haemobilia
• Quincke’s triad = Jaundice, biliary colic and GI bleeding
• Occurs in 1/3

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