AORTIC DISSECTION

AND
AORTIC ANEURYSM

Dr. Sarthak Mishra

PG1 – Emergency Medicine
SMSR, Greater Noida

REFERENCE: 1. Tintinalli’s Textbook of Emergency Medicine

2. Bailey and Love Textbook of Surgery
 INTRODUCTION
• Acute aortic syndromes encompass a number of life-threatening aortic emergencies.
These include aortic dissection, penetrating atherosclerotic ulcer, intramural
hematoma, and aortic aneurysmal leakage and ruptured abdominal aortic aneurysm.
• The most common cardiovascular complication of Marfan’s syndrome is aortic root
disease and type A dissection (ascending aorta).
• Acute aortic syndromes predisposing factors include - chronic hypertension, Bicuspid
aortic valve, Marfan’s syndrome, Ehlers-Danlos syndrome, and familial history of
aortic dissection all predispose to aortic syndromes.
• Chronic cocaine or amphetamine use accelerates atherosclerosis and increases the
risk for dissection.
• Prior cardiac surgery is also a risk factor for aortic dissection. All mechanisms involve
weakening of the medial layer and increasing intimal wall stress.
• Response to stress may include aortic dilation, aneurysm formation, development of
a penetrating ulcer, intramural hemorrhage, aortic dissection, and aortic rupture.
• Aortic dissection occurs after a violation of the intima allows blood to enter
the media and dissect between the intimal and adventitial layers.
• The two most common intimal tear sites are the sinotubular junction at the
start of the acending aorta (50% to 65%) and just beyond the left subclavian
artery (20% to 30%) at the junction between the acending and descending
aorta.
• Bimodal age distribution: The first peak involves younger patients with specific
predisposing conditions such as connective tissue disorders. The second peak
includes those aged >50 years with chronic hypertension and/or ischemic
heart disease.
• An aortic intramural hematoma results from infarction of the aortic media,
usually from injury to the vasa vasorum.
• Penetrating atherosclerotic ulcer can lead to intramural hematoma, aortic
dissection, or perforation of the aorta.
PRESENTATION OF PATIENT
Chest pain is classically ripping or tearing in nature, that occurs suddenly and is maximal at onset –
however, chest pain is not always present!
• retrosternal chest pain – anterior dissection
• interscapular pain – descending aorta
• severe pain (‘worst ever-pain’) (90%)
• sudden onset (90%)
• sharp (64%) or tearing (50%)
• migrating pain (16%)
• down the back (46%)
• maximal at onset (not crescendo build up, as in an AMI)

Other features
• end-organ symptoms: neurological, syncope, seizure, limb paraesthesias, pain or weakness, flank pain,
SOB + haemoptysis
• aortic regurgitation
• hypertension
• most have ischaemic heart disease,
• A pulse deficit in radial arteries or femoral arteries may be found (15%).
• A blood pressure difference >20 mm Hg between arms is independently associated with aortic dissection.
• Hypertenstion is common (49%), but hypotension occurs in 18% to 25% of patients.
• Aneurysmal dilation of the aorta may compress regional structures such as the esophagus, the recurrent
laryngeal nerve, or the superior cervical sympathetic ganglion, causing dysphagia, hoarseness, or Horner’s
syndrome.

The clinical features listed in Table 59-1 form the basis of the Aortic Dissetion Detection Risk Score; 1 point
is given for each category with a feature present by history or physical exam, and scores range from 0 to 3.
Two studies published in 2018 support the strong association of the features listed in Table 59-1 with acute
aortic dissection in symptomatic patients.
DIAGNOSIS OF AORTIC DISSECTION:

• Abnormal ECG findings include new Q waves or ST-segment elevation in 3%

to 4%, ST-segment depression in 15% to 22%, and nonspecific ST- and T-wave
changes in 41% to 62%. The ECG is normal in only 19% to 31% of patients.
• BIOMARKERS: d-Dimer is the marker most thoroughly investigated;
sensitivity of 98%, using a d-dimer cut point of 500 nanograms/mL.
Guidelines do not endorse the use of d-dimer as the sole means of excluding
aortic dissection. Despite extensive study, there is no clinical decision rule that
can be reliably used to identify very-low-risk patients for whom no further
diagnostic workup is needed.
• The Diagnostic Accuracy of the Aortic Dissection Detection Risk Score Plus d-
Dimer for Acute Aortic Syndromes study needs to be externally validated.
• A plain chest radiograph may provide important clues for the diagnosis. The most
common radiographic abnormality is a widened mediastinum or abnormal aortic
contour. Other possible findings include pleural effusion, displacement of aortic
intimal calcification, and deviation of the trachea, mainstream bronchi, or
esophagus.
• CT is the imaging modality of choice for diagnosis of dissection.
• CT can reliably identify a false lumen and can provide additional
details such as the anatomy of the dissection, the location of the
dissection flap, extension of the flap into great vessels signs of aortic
rupture, and signs of end-organ damage.
• CT protocols should be both with and without IV contrast.
• In experienced hands, transesophageal echocardiography may be as
sensitive and specific as CT. The procedure generally must be
performed under moderate sedation or even general anesthesia.
Known esophageal disease is a relative contraindication.
• Coronary/pulmonary/aortic CT angiography, or the “triple rule-out,”
which is used to differentiate acute coronary artery disease,
pulmonary embolism, and acute aortic dissection,32,33 has not been
shown to improve diagnostic yield, reduce clinical events, or diminish
Treatment of Aortic Dissection:
• Negative inotropic Agents: While aortic dissections may cause
hypotension that requires fluid or blood product resuscitation, suspected
aortic dissection commonly requires antihypertensive treatment.
• Initial treatment should be a negative inotropic agent in order to lower
blood pressure without increasing the shear force on the intimal flap of
the aorta.
• β-Blockade is ideal, and short-acting β-blockers such as esmolol or
labetalol are preferred over long-acting β-blockers.
• A systolic pressure of 120 to 130 mm Hg is a reasonable starting point;
some guidelines suggest a goal of 100 to 120 mm Hg (in the absence of
aortic regurgitation).
• Esmolol may be given as an initial bolus of 0.1 to 0.5 milligram/kg IV over 1 minute
followed by an infusion of 0.025 to 0.2 milligram/kg/min.
• Labetalol (a β-blocker with limited α-blocking characteristics in a 7:1 ratio) also may
be used at an initial dose of 10 to 20 milligrams IV with repeat doses of 20 to 40
milligrams every 10 minutes to desired effect or a maximum dose of 300 milligrams.
• Vasodilators may be added for further antihypertensive treatment after successful
administration of esmolol or labetelol. IV nicardipine, clevidipine, nitroglycerin, or
nitroprusside.

• SURGICAL MANAGEMENT OF AD:

• Definitive treatment in case of Stanford A or DeBakey I & II is repair with Dacron
Graft.

• In case of Stanford B or DeBakey III – BP monitoring and Anti-HTN medications is the

management of choice.
ANEURYSMAL DISEASE:
• An aneurysm is dilation of the arterial wall to >1.5 times its normal diameter.
• Aneurysms have been classically distinguished as true aneurysms,
pseudoaneurysms, and mycotic aneurysms.
• The wall of a true aneurysm involves of all layers of the vessel.
• Risk factors for these include smoking, increasing age, white race, hypertension,
hyperlipidemia, connective tissue disorders, and familial history of aneurysm.
• The wall of a pseudoaneurysm consists partly of the vessel wall and partly of
fibrous or other surrounding tissue.
• Mycotic aneurysms and infected aneurysms occur due to an infection in the
vessel wall, often in an immunocompromised patient - IV drug abuse is a
significant risk factor for both types of these aneurysms.
• Peripheral and visceral aneurysms are less frequent but an important subset of
arterial aneurysmal disease. Visceral artery aneurysms may occur anywhere but
are most common in the renal, splenic, and hepatic arteries.
• Screening for abdominal aortic aneurysm with USG should be done in
all patients of age >= 65 years – look for aortic wall calcification,
dilatation, psoas hematoma, draping sign over vertebra.
• Chance of rupture is more in males than females.
• Blue Toe syndrome: the aneurysm can act as a source of embolus and
leading to the cyanosis of the lower limb.
•
• Pseudoaneurysms show to and fro movement on Doppler USG known
as Yin-Yang sign.
SYMPTOMATIC ABDOMINAL AORTIC ANEURYSMS:
• An abdominal aortic aneurysm is defined as an aorta ≥3.0 cm in diameter;
repair is considered for an aneurysm ≥5.0 cm in diameter.
• RISK FACTORS: Age > 60 years; males > females; aneurysms involving other major
arteries and PVOD; Smoking (smoking is a major risk factor for accelerated
aneurysmal growth and rupture).
CLINICAL ASSESSMENT
• asymptomatic AAA may be an incidental finding on clinical examination or
imaging
• palpation of an expansile mass
 pass two fingers on either side of the pulsating mass and observe for separation of the
fingers with each pulsation
 may be detectable at 4-5cm diameter depending on body habitus
• isolated pain in abdomen, epigastrium or back (contained leaks typically present
with back pain)
• ‘classic’ triad of AAA rupture (often not present e.g. guarding, obese,
hypotensive or large retroperitoneal haemorrhage)
 Pain, typically severe and predominantly located in the back
 Signs if circulatory compromise, often the patient is frankly shocked
 The presence of a pulsatile mass in the abdomen

• atypical presentations in the elderly

 back pain (may mimic renal colic)
 +/- radiation to the legs (mimicking sciatica)
 chronic severe back pain (contained rupture)

• tender AAA on palpation is an aortic emergency unless proven

otherwise
COMPLICATIONS:
1. AAA Rupture:
• Most common site of rupture of abdominal aortic aneurysm is
posterior which bleeds into the left retroperitoneum.
• Anterior aneurysmal ruptures are about 20% and mostly fatal.

2. Aorto-Caval Fistula leading to increased cardiac output failure.

3. Aorto-Enteric Fistula especially into the 3rd or 4th part of duodenum

leading to severe lower GI bleeds.
DIAGNOSIS:
• Bedside US is the imaging modality of choice for unstable patients. A
technically adequate US study has >90% sensitivity for demonstrating the
presence of an aneurysm and measuring its diameter. An aortic diameter
<3.0 cm excludes acute aneurysmal disease.
• Occasionally, an aneurysm may be picked up on plain abdominal radiography.
• Plain abdominal films may show a calcified and bulging aortic contour,
implying the presence of an aneurysm.
• CT scanning with IV contrast best detects the anatomic details of the
aneurysm and associated hemorrhage. Scan all stable patients with suspected
abdominal aneurysmal disease or rupture. For those who cannot have IV
contrast, unenhanced CT can reveal aneurysm size and retroperitoneal
hemorrhage.
Management protocol:
• Dacron graft repair is indicated in all symptomatic patients.
• In c/o asymptomatic patients, criteria are following:
1. Diameter > 5.5cm; or
2. Rate of growth > 0.5cm/ 6m or >1cm/ 1 year; OR
3. Distal Emboli;
4. Compression symptoms

• Dacron Graft Repair can be of 2 types:

1. Open Surgery involving the following techniques i.e. Mattox Maneuvre,
Cattle Brasch Maneuvre or Kocherization.
2. Endovascular Aneurysm Repair with stent made of nitinol/ polyester
consisting of 3 parts – head, body and hooks.
Endoleaks: a complication of EVAR
Some key points on aneurysms:
• M/C vessels involved – Circle of Willis
• M/C extra-cranial vessel – Infra-renal Abdominal Aorta
• M/C peripheral vessel – Popliteal artery
• M/C blood vessel a/w mycotic aneurysm – Aorta
• M/c BV associated with pseudoaneurysm – Femoral Artery
• Most important risk factor associated with aneurysm formation is
Atherosclerosis.
• Critical diameter for Popliteal aneurysm – 2 cm
THANK
YOU