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FOAM
http://emcrit.org/podcasts/aortic-dissection/
http://lifeinthefastlane.com/education/ccc/acute-aortic-dissection/
http://lifeinthefastlane.com/2010/03/cardiovascular-curveball-008/
http://lifeinthefastlane.com/2010/09/die-like-a-king/
http://lifeinthefastlane.com/2008/11/aortic-dissection-lecture-notes/
http://flippedemclassroom.wordpress.com/2013/06/07/aortic-dissection/
http://academiclifeinem.com/paucis-verbis-international-registry-on-aortic-dissection-irad/
Pathophysiology
Aortic disection is caused by a disruption of the media layer of the aorta. For this to start, this needs a tear of intima with the formation of a false lumen between layers. An important variation of ATAD is an acute intramural haematoma - bleeding within the wall without an intimal defect. The treatment is the same.
There are three possibilities as to how the blood gets into the media:
- Atherosclerotic ulcer leading to intimal tear
- Disruption of vasa vasorum causing intramural haematoma
- De novo intimal tear
Most tears occur in the ascending aorta due to greater pressure on the aortic wall. Once the dissection process occurs blood tracks through the media to varying degrees and may dissect down from the aortic root to the bifurcation of the common iliac arteries in a matter of seconds.
Location of primary aortic tear Incidence
Ascending aorta 70%
Descending thoracic aorta 15-20%
Arch of the aorta 10%
Abdominal aorta <5%
Risk Factors
Thrombus - 2/3 of patients
Embolism - 1/3 of patients
White (79%)
Men (68%)
over 40
Inherited disease (especially younger patients < 40 yrs)
- Marfan’s syndrome (fibrillin gene mutations)
- Ehlers-Danlos syndrome type IV (collagen defects)
- Turner syndrome
- annulo- aortic ectasia
- familial aortic dissection.
Aortic wall stress
- Hypertension (72%)
- Previous cardiovascular surgery
- Bicuspid or unicommisural aortic valve
- Aortic coarctation
- Iatrogenic
- Infection (syphilis)
- Arteritis such as Takayasu’s or giant cell, aortic dilatation / aneurysm, wall thinning
- ‘crack’ cocaine (abrupt catecholamine-induced hypertension).
Reduced resistance aortic wall
- Increasing age
- pregnancy (debatable).
Clinical Symptoms
The clinical symptoms vary depending on which branch vessel is occluded:
Coronary vessel(s) ST elevation myocardial infarction
Common carotid(s) any type of stroke
Subclavian(s) an acutely ischaemic upper limb
Coeliac/mesenteric vessel(s) ischaemic bowel
Renal vessel(s) frank haematuria
Spinal artery(ies) sudden onset painless paraplegia
Ascending aorta: haemopericardium (syncope and /or sudden death)
right haemothorax (invariably sudden death)
Arch of aorta: mediastinal haematoma
interatrial septal haematoma (cardiac conduction defects)
compression of pulmonary trunk/ artery
Descending aorta: left haemothorax (sudden death)
rarely into oesophagus (profuse haematemesis)
Abdominal aorta: retroperitoneal haemorrhage (back pain with shock)
rarely intraperitoneal haemorrhage (shock and acute abdomen)
Aortic root: aortic regurgitation can occur when the dissection process extends into or around the aortic valvular support. The aortic root can dilate so much that the aortic leaflets cannot fully appose during diastole, allowing regurgitation of blood.
Pain
Pain is the most common symptom.
The pain is said to be severe or ‘worst ever’ (90%), abrupt (90%), sharp (64%) or tearing (50%) retrosternal or interscapular pain (50%), migrating (16%), down the back (46%), maximal at onset (not crescendo build up, as in an AMI).
The pain in aortic dissection occurs in the anterior chest 70-80% of the time in patients with a type A dissection and back pain occurs only in 50% of all patients. Abdominal pain was found to be the third commonest site of initial pain and other sites described were the throat, neck and extremities.
Patients may also describe the classic migration of pain from the chest, back or abdomen to one or more limbs or to the neck and this is thought to be due to peripheral extension of the dissection from the primary intimal tear.
In 5-15% of patients however, no pain occurs at all. This is typically the case in those patients presenting with syncope, stroke, congestive cardiac failure or the elderly.
Cardiac Signs
- Aortic incompetence (32%)
- cardiac tamponade,
- myocardial ischaemia (although only 2-5% of ECGs mimick AMI)
- BP differences >20 mmHg in arms
- missing pulse (15%).
Other Signs
- Pleural rub or effusion, haemothorax
- Altered consciousness
- syncope (13 %),
- hemiplegia (5%)
- paraplegia.
- abdominal pain (43% descending, 22% ascending)
- intestinal ischaemia
- oliguria
Diagnosis
Transthoracic Echocardiography - 78.3% sensitivity and 83.0% specificity for diagnosing proximal dissection. Cannot accurately visualise the descending aorta in most patients. Can diagnose aortic incompetence.
May identify a free intimal flap within the aortic lumen - sensitivity is approximately 80% for type A dissections but only 50% for type B.
CT - 83-100% sensitive
Will reveal pericardial fluid which will suggest dissection diagnosis in the right clinical context.
ECG - normal in 30% of cases
STEMI patterns in 3% (Changes consistently with AMI do not rule out dissection)
15% acute ischaemic changes
41% had non-specific ST segment and T wave changes
Chest X-ray - normal in 12% of cases
Mediastinal widening in 60% of cases
Abnormal aortic contour 50% of cases
Soft tissue shadow behind a calcified aortic annulus (15%)
Globular heart (haemopericardium)
Pleural effusion (haemothorax)
Bloods - D-dimer has a sensitivity of below 95%
Treatment
The most important step in treatment is diagnosis - 40% cases are initially misdiagnosed. Mortality increases every hour from onset of disease.
Even if there are signs of tamponade, do not perform pericardiocentesis.
There are two main types of disection:
Stanford A: De Bakey 1 and II: Proximal
Stanford B: Proximal
Stanford B: DeBakey IIIa and IIIb: Distal
Stanford A dissections normally have surgical treatment, and type B has medical management.
Medical Management
Analgesia
Blood Pressure Control:
- Control blood pressure with labetalol (a mixed alpha and beta blockers)
- Causes vasodilatation and reduces cardiac contractility
- Doesn't cause reflex tachycardia that is seen with other vasodilators.
Best to use a mixture of beta blockers and vasodilators - so metoprolol and GTN
Ten year survival rates of patients who are discharged from hospital range from 30% to 60%
