THE KURSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF SURGICAL DISEASES № 1
AORTA ANEURYSMS. ACUTE AORTA DISSECTION.
Information for self-training of English-speaking students
The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)
By PROFESSOR O.I. OCHOTNICKOV
ass. professor A.V. BELCHENKOV
KURSK-2010
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AORTA ANEURYSMS
I. INTRODUCTION
An aortic aneurysm is a general term for any swelling (dilatation or aneurysm) of
the aorta, usually representing an underlying weakness in the wall of the aorta at that
location. While the stretched vessel may occasionally cause discomfort, a greater
concern is the risk of rupture, which causes severe pain; massive internal
hemorrhage; and, without prompt treatment, results in a quick death.Abdominal
aortic aneurysm, also written as AAA and often pronounced 'triple-A', is a localized
dilatation of the abdominal aorta, that exceeds the normal diameter by more than
50%. The normal diameter of the infrarenal aorta is 2 cm. It is caused by a
degenerative process of the aortic wall, but the exact etiology remains unknown. It is
most commonly located below the kidneys (infrarenally; 90%), other possible
locations are above or at the level of the kidneys (suprarenal and pararenal). The
aneurysm can extend to include one or both of the iliac arteries. An aortic aneurysm
may also occur in the thorax.
An abdominal aortic aneurysm occurs most commonly in older individuals
(between 65 and 75), and more in men and smokers. There is moderate evidence to
support screening in individuals with these risk factors. The majority of abdominal
aortic aneurysms do not cause symptoms. Symptomatic and large aneurysms (>5.5
cm in diameter) are considered for repair.
The most important complication of an abdominal aortic aneurysm is rupture,
which is most often a fatal event. An abdominal aortic aneurysm weakens the walls
of the blood vessel, leaving it vulnerable to bursting open, or rupturing, and spilling
large amounts of blood into the abdominal cavity, leading to only minutes of life
remaining.
II. GENERAL AIM OF THE SESSION
General aim of the session includes acquisition the following by students:
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1. Knowledges on clinical signs, diagnose, medicine treatment and surgical
management of aortic aneurysms.
2. Practical skills of disease anamnesis accumulation and objective examination of
the patients.
3. Opportunity to create plan of laboratory and instrumental investigation, ability to
create and to prove clinical diagnosis, to make indications and contra-indication for
surgical treatment and to choose the mode of it or conservative therapy in patient
with aortic aneurysms.
III. TRAINING-AIM TASKS FOR SELF-TRAINING
After individual studying of the material every student have to:
A/ to know:
• Classification of this diseases
• Pathogenesis of more spread forms of the diseases
• Clinical picture of this diseases
• Diagnostic value of different instrumental methods.
• Indications and contra-indication for surgical treatment
•Complex conservative treatment
•Principles of surgical treatment and technics of operation.
B/ be able
• To find main complains, symptoms and signs of the deep veins thrombosis,
accumulate anamnesis in cases and staging this disease.
• To realize objective examination of patients with this diseases.
• Be able to assess received datas of US-scanning, X-Ray
examination, angiography, CT-examination, laboratory datas
• To create indications and contra-indication for surgical treatment.
III. INITIAL LEVEL OF KNOWLEDGES
4
Anatomo-physiological datas about the aorta have been studied on 3-4-th courses.
Different modes of surgical procedures have been studied on course of operative
surgery. You should restore this study material.
IV. MATERIAL, IS OBL1GATIVE FOR TOPIC MASTERING
History
The first historical records about AAA are from Ancient Rome in the 2nd
century AD, when Greek surgeon Antyllus tried to treat the AAA with proximal
and distal ligature, central incision and removal of thrombotic material from the
aneurysm. However, attempts to treat the AAA surgically were unsuccessful until
1923. In that year, Rudolph Matas (who also proposed the concept of
endoaneurysmorrhaphy), performed the first successful aortic ligation on a human.
Other methods that were successful in treating the AAA included wrapping the
aorta with polyethene cellophane, which induced fibrosis and restricted the growth
of the aneurysm. Albert Einstein was operated on by Rudolf Nissen with use of
this technique in 1949, and survived five years after the operation.
Epidemiology
AAA is uncommon in individuals of African, Asian, and Hispanic heritage.
The frequency varies strongly between males and females. The peak incidence is
among males around 70 years of age, the prevalence among males over 60 years
totals 2-6%. The frequency is much higher in smokers than in non-smokers (8:1),
and the risk decreases slowly after smoking cessation. Other risk factors include
hypertension and male sex. In the U.S., the incidence of AAA is 2-4% in the adult
population. AAA is 4-6 times more common in male siblings of known patients,
with a risk of 20-30%. Rupture of the AAA occurs in 1-3% of men aged 65 or
more, the mortality is 70-95%.
Etiology
The exact causes of the degenerative process remain unclear. There are, however,
some theories and risk factors defined.
Genetic influences: The influence of genetic factors is highly probable. The high
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familial prevalence rate is most notable in male individuals. There are many
theories about the exact genetic disorder that could cause higher incidence of
AAA among male members of the affected families. Some presumed that the
influence of alpha 1-antitrypsin deficiency could be crucial, some experimental
works favored the theory of X-linked mutation, which would explain the lower
incidence in heterozygous females. Other theories of genetic etiology were also
formulated.
Hemodynamic influences: Abdominal aortic aneurysm is a focal degenerative
process with predilection for the infrarenal aorta. The histological structure and
mechanical characteristics of infrarenal aorta differ from those of the thoracic
aorta. The diameter decreases from the root to the bifurcation, and the wall of the
abdominal aorta also contains a lesser proportion of elastin. The mechanical
tension in abdominal aortic wall is therefore higher than in the thoracic aortic
wall. The elasticity and distensibility also decline with age, which can result in
gradual dilatation of the segment. Higher intraluminal pressure in patients with
arterial hypertension markedly contributes to the progression of the pathological
process.
Atherosclerosis: The AAA was long considered to be caused by atherosclerosis,
because the walls of the AAA are frequently affected heavily. However, this
theory cannot be used to explain the initial defect and the development of
occlusion, which is observed in the process.
Other causes: Other causes of the development of AAA include: infection,
trauma, arteritis, cystic medial necrosis (m. Erdheim) and connective tissue
disorders (e.g. Marfan syndrome, Ehlers-Danlos syndrome).
Pathophysiology
The most striking histopathological changes of aneurysmatic aorta are seen in
tunica media and intima. These include accumulation of lipids in foam cells,
extracellular free cholesterol crystals, calcifications, thrombosis, and ulcerations
and ruptures of the layers. There is an adventitial inflammatory infiltrate.
However, the degradation of tunica media by means of proteolytic process seems
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to be the basic pathophysiologic mechanism of the AAA development. Some
researchers report increased expression and activity of matrix metalloproteinases
in individuals with AAA. This leads to elimination of elastin from the media,
rendering the aortic wall more susceptible to the influence of the blood pressure.
Classification
Aortic aneurysms are classified by where on the aorta they occur; aneurysms
can appear anywhere. An aortic root aneurysm, or aneurysm of sinus of Valsalva,
appears on the sinuses of Valsalva or aortic root. Thoracic aortic aneurysms are
found on the thoracic aorta; these are further classified as ascending, aortic arch,
or descending aneurysms depending on the location on the thoracic aorta
involved. Abdominal aortic aneurysms, the most common form of aortic
aneurysm, are found on the abdominal aorta, and thoracoabdominal aortic
aneuryms involve both the thoracic and abdominal aorta. There are other
classifications that might help treatment.
Manifestations and Diagnosis
AAAs are commonly divided according to their size and symptomatology. An
aneurysm is usually considered to be present if the measured outer aortic diameter
is over 3 cm (normal diameter of aorta is around 2 cm). The natural history is of
increasing diameter over time, followed eventually by the development of
symptoms (usually rupture). If the outer diameter exceeds 5.5 cm, the aneurysm is
considered to be large. For aneurysms under 5.5 cm, the risk of rupture is low, so
that the risks of surgery usually outweigh the risk of rupture. Aneurysms less than
5.5 cm are therefore usually kept under surveillance until such time as they
become large enough to warrant repair, or develop symptoms. The vast majority
of aneurysms are asymptomatic. The risk of rupture is high in a symptomatic
aneurysm, which is therefore considered an indication for surgery. Possible
symptoms include low back pain, flank pain, abdominal pain, groin pain or
pulsating abdominal mass. The complications include rupture, peripheral
embolisation, acute aortic occlusion, and aortocaval (beteween the aorta and
inferior vena cava) or aortoduodenal (between the aorta and the duodenum)
7
fistulae. On physical examination, a palpable abdominal mass can be noted. Bruits
can be present in case of renal or visceral arterial stenosis.
CT image showing an abdominal aortic aneurysm.
As most of the AAAs are asymptomatic, their presence is usually revealed
during an abdominal examination for another reason - the most common being
abdominal ultrasonography. A physician may also detect the presence of an AAA
by abdominal palpation. Ultrasonography provides the initial assessment of the
size and extent of the aneurysm, and is the usual modality for surveillance.
Preoperative examinations include CT, MRI and special modes thereof, like
CT/MR angiography. Angiography may be useful also, as an additional method of
measurement for the planning of endoluminal repair. Note that an aneurysmal
aorta may appear normal on angiogram, due to thrombus within the sac.
Rupture
The clinical manifestation of ruptured AAA can include low back, flank,
abdominal or groin pain, but the bleeding usually leads to a hypovolemic shock
with hypotension, tachycardia, cyanosis, and altered mental status. The mortality
of AAA rupture is up to 90%. 65–75% of patients die before they arrive at
hospital and up to 90% die before they reach the operating room. The bleeding can
be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval or
aortointestinal (between the aorta and intestine) fistula.. Flank ecchymosis
(appearance of a bruise) is a sign of retroperitoneal hemorrhage, and is also called
the Grey-Turner sign. Ruptured AAA is a clinical diagnosis: the presence of the
triad of abdominal pain, shock and pulsatile abdominal mass makes the diagnosis;
no further investigations are required for diagnostic purposes, and imaging should
not delay surgery. The operative mortality has slowly decreased over several
decades but remains higher than 40%.
Treatment
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The treatment options for asymptomatic AAA are immediate repair,
surveillance with a view to eventual repair, and conservative management. There
are currently two modes of repair available for an AAA: open aneurysm repair
(OR), and endovascular aneurysm repair (EVAR).
Conservative treatment is indicated in patients where repair carries a high risk
of mortality and also in patients where repair is unlikely to improve life
expectancy. The two mainstays of the conservative treatment are smoking
cessation and blood pressure control. Recent studies have suggested possible
protective effects of therapy with angiotensin converting enzyme inhibitors or
statins.
Surveillance is indicated in small aneurysms, where the risk of repair exceeds
the risk of rupture. As an AAA grows in diameter the risk of rupture increases.
Surveillance until the aneurysm has reached a diameter of 5.5cm has not been
shown to have a higher risk as compared to early intervention.[26][27] The
threshold for repair varies slightly from individual to individual, depending on the
balance of risks and benefits when considering repair versus ongoing surveillance.
The size of an individual's native aorta may influence this, along with the presence
of comorbitities that increase operative risk or decrease life expectancy.
Open repair (operation) is indicated in young patients as an elective procedure,
or in growing or large, symptomatic or ruptured aneurysms. Open repair has been
the mainstay of intervention from the 1950s until recently.
Endovascular repair first became practical in the 1990s and although it is now
an established alternative to open repair, its role is yet to be clearly defined. It is
generally indicated in older, high-risk patients or patients unfit for open repair.
However, endovascular repair is feasible for only a proportion of AAA's,
depending on the morphology of the aneurysm. The main advantage over open
repair is that there is less peri-operative mortality, less time in intensive care, less
time in hospital overall and earlier return to normal activity. Disadvantages of
endovascular repair include a requirement for more frequent ongoing hospital
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reviews, and a higher chance of further procedures being required. According to
the latest studies, the EVAR procedure doesn't offer any benefit for overall
survival or health-related quality of life compared to open surgery, although
aneurysm-related mortality is lower. In patients unfit for open repair, EVAR plus
conservative management was associated with no benefit and more complications
and subsequent procedures and higher costs compared to conservative
management alone. Endovascular treatment for paraanastomotic aneurysms after
aortobiiliac reconstruction is also a possibility.
New endovascular devices are being developed that are able to treat more
complex and tortuous anatomies.
Endovascular treatment of other aortic aneurysms. The endoluminal exclusion
of aortic aneurysms has seen a real revolution in the very recent years. It is now
possible to treat thoracic aortic aneurysms, abdominal aortic aneurysms and other
aneurysms in most of the body's major arteries (such as the iliac and the femoral
arteries) using endovascular stents and avoiding big incisions. Still, in most cases
the technique is applied in patients at high risk for surgery as more trials are
required in order to fully accept this method as the gold standard for the treatment
of aneurysms.
Prevention
Attention to patient's general blood pressure, smoking and cholesterol risks
helps reduce the risk on an individual basis. There have been proposals to
introduce ultrasound scans as a screening tool for those most at risk: men over the
age of 65. The tetracycline antibiotic Doxycycline is currently being investigated
for use as a potential drug in the prevention of aortic aneurysm due to its
metalloproteinase inhibitor and collagen stabilising properties.
V. LITERATURE
1. Lections
2. Vascular Surgery/ European Manual of Medicine/ Chief editor C.D. Liapis –
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Springer – 2007.
3. Short Practice of Surgery by Charles v. Mann and al.
VI. APPROXIMATE ACTIONS BASE
1. Introduction /5 min/
Teacher short characterizes topic actuality, meets students with main aims of
the study and its plan.
2. Initial knowledges control /15 min/
3. Individual students work with patients. /30 min/ The teacher explains some
more difficult and important parts of problem. The choice is realized by asking of
students and their answers correction.
4. Clinical analisys of topical patients. /100 min/
Students observe topical patients under teacher control. After it finishing, the
students report about receiving results.
Work in dressing-room and operational theater.
Teacher and students change the dressings of patients after different
surgical procedures on the pancreas
Study of X-Ray pictures, US- and CT-scanns, laboratory datas
5. Final knowledge control. Solution of test-questions /25 min/
6. Conclusion /5min/
The teacher concludes the session and gives new task for the next once.
VII. QUESTION.
1. Aortic aneurysm: definition of the idea.
2. Epidemiology of the aortic aneurysms.
3. Etiology of the aortic aneurysms.
4. Pathophysiology of the aortic aneurysms.
5. Classification.
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6. Manifestations and Diagnosis.
7. Clinical manifestation of ruptured aneurysm.
8. Conservative treatment: indication, drug management.
9. Open repair: indication, types of the operations.
10. Endovascular repair: indication, types of the procedures.
11. Endovascular treatment of other aortic aneurysms.
12. Prevention to complications.
Acute aortic dissection.
I. INTRODUCTION
Aortic dissection is a tear in the wall of the aorta that causes blood to flow
between the layers of the wall of the aorta and force the layers apart. Aortic
dissection is a medical emergency and can quickly lead to death, even with optimal
treatment. If the dissection tears the aorta completely open (through all three layers),
massive and rapid blood loss occurs. Aortic dissections resulting in rupture have an
80% mortality rate, and 50% of patients die before they even reach the hospital. If the
dissection reaches 6 cm, the patient must be taken for emergency surgery. The
surgery to repair a dissection takes about 20 hours. The patient would be in a drug
induced coma for three days.
II. GENERAL AIM OF THE SESSION
General aim of the session includes acquisition the following by students:
1. Knowledges on clinical signs, diagnose, medicine treatment and surgical
management of acute aortic dissections.
2. Practical skills of disease anamnesis accumulation and objective examination of
the patients.
3. Opportunity to create plan of laboratory and instrumental investigation, ability to
12
create and to prove clinical diagnosis, to make indications and contra-indication for
surgical treatment and to choose the mode of it or conservative therapy in patient
with acute aortic dissections..
III. TRAINING-AIM TASKS FOR SELF-TRAINING
After individual studying of the material every student have to:
A/ to know:
• Classification of this diseases
• Pathogenesis of more spread forms of the diseases
• Clinical picture of this diseases
• Diagnostic value of different instrumental methods.
• Indications and contra-indication for surgical treatment
•Complex conservative treatment
•Principles of surgical treatment and technics of operation.
B/ be able
• To find main complains, symptoms and signs of the deep veins thrombosis,
accumulate anamnesis in cases and staging this disease.
• To realize objective examination of patients with this diseases.
• Be able to assess received datas of US-scanning, X-Ray
examination, angiography, CT-examination, laboratory datas
• To create indications and contra-indication for surgical treatment.
III. INITIAL LEVEL OF KNOWLEDGES
Anatomo-physiological datas about the aorta have been studied on 3-4-th courses.
Different modes of surgical procedures have been studied on course of operative
surgery. You should restore this study material.
IV. MATERIAL, IS OBL1GATIVE FOR TOPIC MASTERING
ETIOLOGY
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As with all other arteries, the aorta is made up of three layers. The layer that is
in direct contact with the flow of blood is the tunica intima, commonly called the
intima. This layer is made up of mainly endothelial cells. The next layer is the tunica
media, known as the media. This "middle layer" is made up of smooth muscle cells
and elastic tissue. The outermost layer (furthest from the flow of blood) is known as
the tunica adventitia or the adventitia. This layer is composed of connective tissue.
In an aortic dissection, blood penetrates the intima and enters the media layer.
The high pressure rips the tissue of the media apart, allowing more blood to enter.
This can propagate along the length of the aorta for a variable distance, dissecting
towards or away from the heart or both. The initial tear is usually within 100 mm of
the aortic valve.
The risk in aortic dissection is that the aorta may rupture, leading to massive
blood loss resulting in death. Several different classification systems have been used
to describe aortic dissections. The systems commonly in use are either based on the
anatomy of the dissection or the duration of onset of symptoms prior to presentation.
DeBakey classification system
The DeBakey system, named after surgeon and aortic dissection sufferer
Michael E. DeBakey, is an anatomical description of the aortic dissection. It
categorizes the dissection based on where the original intimal tear is located and the
extent of the dissection (localized to either the ascending aorta or descending aorta,
or involves both the ascending and descending aorta.
Type I - Originates in ascending aorta, propagates at least to the aortic arch and
often beyond it distally.
Type II – Originates in and is confined to the ascending aorta.
Type III – Originates in descending aorta, rarely extends proximally.
Stanford classification system
Divided into 2 groups; A and B depending on whether the ascending aorta is
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involved.
A = Type I and II DeBakey
B = Type III DeBakey
Pathophysiology
The initiating event in an aortic dissection is a tear in the intimal lining of the
aorta. Due to the high pressures in the aorta, blood enters the media at the point of the
tear. The force of the blood entering the media causes the tear to extend. It may
extend proximally (closer to the heart) or distally (away from the heart) or both. The
blood will travel through the media, creating a false lumen (the true lumen is the
normal conduit of blood in the aorta). Separating the false lumen from the true lumen
is a layer of intimal tissue. This tissue is known as the intimal flap.
The vast majority of aortic dissections originate with an intimal tear in either the
ascending aorta (65%), the aortic arch (10%), or just distal to the ligamentum
arteriosum in the descending thoracic aorta (20%).
As blood flows down the false lumen, it may cause secondary tears in the intima.
Through these secondary tears, the blood can re-enter the true lumen.
15
While it is not always clear why an intimal tear may occur, quite often it involves
degeneration of the collagen and elastin that make up the media. This is known as
cystic medial necrosis and is most commonly associated with Marfan syndrome and
is also associated with Ehlers-Danlos syndrome.
In about 13% of aortic dissections, there is no evidence of an intimal tear. It is
believed that in these cases the inciting event is an intramural hematoma (caused by
hemorrhage within the media). Since there is no direct connection between the true
lumen and the false lumen in these cases, it is difficult to diagnose an aortic
dissection by aortography if the etiology is an intramural hematoma. An aortic
dissection secondary to an intramural hematoma should be treated the same as one
caused by an intimal tear.
Causes
Aortic dissection is associated with hypertension (high blood pressure) and
many connective tissue disorders. Vasculitis (inflammation of an artery) is rarely
associated with aortic dissection. It can also be the result of chest trauma. 72 to 80%
of individuals who present with an aortic dissection have a previous history of
hypertension.
The highest incidence of aortic dissection is in individuals who are 50 to 70 years
old. The incidence is twice as high in males as in females (male-to-female ratio is
2:1). Half of dissections in females before age 40 occur during pregnancy (typically
in the 3rd trimester or early postpartum period).
A bicuspid aortic valve (a type of congenital heart disease involving the aortic
valve) is found in 7-14% of individuals who have an aortic dissection. These
individuals are prone to dissection in the ascending aorta. The risk of dissection in
individuals with bicuspid aortic valve is not associated with the degree of stenosis of
the valve.
Marfan syndrome is noted in 5-9% of individuals who suffer from aortic
dissection. In this subset, there is an increased incidence in young individuals.
Individuals with Marfan syndrome tend to have aneurysms of the aorta and are more
prone to proximal dissections of the aorta.
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Turner syndrome also increases the risk of aortic dissection, by aortic root
dilatation.
Chest trauma leading to aortic dissection can be divided into two groups based
on etiology: blunt chest trauma (commonly seen in car accidents) and iatrogenic.
Iatrogenic causes include trauma during cardiac catheterization or due to an intraaortic balloon pump.
Aortic dissection may be a late sequela of cardiac surgery. 18% of individuals
who present with an acute aortic dissection have a history of open heart surgery.
Individuals who have undergone aortic valve replacement for aortic insufficiency are
at particularly high risk. This is because aortic insufficiency causes increased blood
flow in the ascending aorta. This can cause dilatation and weakening of the walls of
the ascending aorta.
Of note, although this is extremely rare in this day and age, Syphilis can cause
aortic dissection. In the tertiary stage of this disease, the aorta gets Luetic lesions
which lead to dissection.
Signs and symptoms
About 96% of individuals with aortic dissection present with severe pain that
had a sudden onset. It may be described as tearing in nature, or stabbing or sharp in
character. 17% of individuals will feel the pain migrate as the dissection extends
down the aorta. The location of pain is associated with the location of the dissection.
Anterior chest pain is associated with dissections involving the ascending aorta,
while intrascapular (back) pain is associated with descending aortic dissections. If the
pain is pleuritic in nature, it may suggest acute pericarditis due to hemorrhage into
the pericardial sac.
While the pain may be confused with the pain of a myocardial infarction (heart
attack), aortic dissection is usually not associated with the other signs that suggest
myocardial infarction, including heart failure, and ECG changes. Also, individuals
suffering from an aortic dissection usually do not present with diaphoresis (profuse
sweating).
17
Individuals with aortic dissection who do not present with pain have chronic
dissection.
Less common symptoms that may be seen in the setting of aortic dissection
include congestive heart failure (7%), syncope (9%), cerebrovascular accident (36%), ischemic peripheral neuropathy, paraplegia, cardiac arrest, and sudden death. If
the individual had a syncopal episode, about half the time it is due to hemorrhage into
the pericardium leading to pericardial tamponade.
Neurologic complications of aortic dissection (i.e., cerebrovascular accident
(CVA) and paralysis) are due to involvement of one or more arteries supplying
portions of the central nervous system.
If the aortic dissection involves the abdominal aorta, compromise of the
branches of the abdominal aorta are possible. In abdominal aortic dissections,
compromise of one or both renal arteries occurs in 5-8% of cases, while mesenteric
ischemia (ischemia of the large intestines) occurs 3-5% of the time.
Blood pressure changes
While many patients with an aortic dissection have a history of hypertension,
the blood pressure is quite variable at presentation with acute aortic dissection, and
tends to be higher in individuals with a distal dissection. In individuals with a
proximal aortic dissection, 36% present with hypertension, while 25% present with
hypotension. In those that present with distal aortic dissections, 70% present with
hypertension while 4% present with hypotension.
Severe hypotension at presentation is a grave prognostic indicator. It is usually
associated with pericardial tamponade, severe aortic insufficiency, or rupture of the
aorta. Accurate measurement of the blood pressure is important. Pseudohypotension
(falsely low blood pressure measurement) may occur due to involvement of the
brachiocephalic artery (supplying the right arm) or the left subclavian artery
(supplying the left arm).
Aortic insufficiency
Aortic insufficiency (AI) occurs in 1/2 to 2/3 of ascending aortic dissections,
and the murmur of aortic insufficiency is audible in about 32% of proximal
18
dissections. The intensity (loudness) of the murmur is dependent on the blood
pressure and may be inaudible in the event of hypotension.
There are multiple etiologies for AI in the setting of ascending aortic dissection.
The dissection may dilate the annulus of the aortic valve, so that the leaflets of the
valve cannot coapt. Another mechanism is that the dissection may extend into the
aortic root and detach the aortic valve leaflets. The third mechanism is that if there
was an extensive intimal tear, the intimal flap may prolapse into the LV outflow tract,
causing intimal intussusception into the aortic valve preventing proper valve closure.
Myocardial infarction
Myocardial infarction (heart attack) occurs in 1-2% of aortic dissections. The
etiology of the infarction is involvement of the coronary arteries (the arteries that
supply the heart) in the dissection. The right coronary artery is involved more
commonly than the left coronary artery. If the myocardial infarction is treated with
thrombolytic therapy, the mortality increases to over 70%, mostly due to hemorrhage
into the pericardial sac causing pericardial tamponade.
Because aortic dissection may present to the emergency room physician similar
to a myocardial infarction, the physician must be careful to make the proper
diagnosis prior to initiating treatment for myocardial infarction, since the treatment
regimen for myocardial infarction can be lethal to an individual presenting with
aortic dissection.
Pleural effusion
A pleural effusion (fluid collection in the space between the lungs and the
chest wall or diaphragm) can be due to either blood from a transient rupture of the
aorta or fluid due to an inflammatory reaction around the aorta. If a pleural effusion
were to develop due to an aortic dissection, it is more commonly in the left
hemithorax rather than the right hemithorax.
Diagnosis
Because of the varying symptoms and signs of aortic dissection depending on
the initial intimal tear and the extent of the dissection, the proper diagnosis is
sometimes difficult to make.
19
In an individual with chest pain radiating to the back, the differentials to consider
include:
- Aortic dissection
- Myocardial infarction
- Acute aortic insufficiency
- Non-dissecting aortic aneurysm
- Pericarditis
- Musculoskeletal pain
- Mediastinal tumors
While taking a good history from the individual may be strongly suggestive of
an aortic dissection, the diagnosis cannot always be made by history and physical
signs alone. Often the diagnosis is made by visualization of the intimal flap on a
diagnositic imaging test. Common tests used to diagnose an aortic dissection include
a CT scan of the chest with iodinated contrast material and a trans-esophageal
echocardiogram. Other tests that may be used include an aortogram or magnetic
resonance angiogram (MRA) of the aorta. Each of these test have varying pros and
cons and they do not have equal sensitivities and specificities in the diagnosis of
aortic dissection.
In general, the imaging technique chosen is based on the pre-test likelihood of
the diagnosis, availability of the testing modality, patient stability, and the sensitivity
and specificity of the test.
Chest X-ray
Widening of the mediastinum on an x-ray of the chest has moderate sensitivity
(67%) in the setting of an ascending aortic dissection[6]. However, it has low
specificity, as many other conditions can cause a widening of the mediastinum on
chest x-ray.
The calcium sign is a finding on chest x-ray that suggests aortic dissection. It is
the separation of the intimal calcification from the outer aortic soft tissue border by
10 mm.
20
Pleural effusions may be seen on chest x-ray. They are more commonly seen in
descending aortic dissections. If seen, they are typically in the left hemithorax.
Other findings include obliteration of the aortic knob, depression of the left
mainstem bronchus, loss of the paratracheal stripe, and tracheal deviation.
About 12%-20% of individuals presenting with an aortic dissection have a
"normal" chest x-ray.
ECG
There are no specific electrocardiographic findings associated with aortic
dissection. About 1/3 of the time, the ECG will show signs of left ventricular
hypertrophy, which is due to the long-standing hypertension seen in these
individuals. Another 1/3 of the time the ECG would be considered "normal". If the
ECG suggests cardiac ischemia in the setting of aortic dissection, involvement of the
coronary arteries should be suspected.
Biochemical markers
While there are currently no blood tests that can accurately diagnose aortic
dissection, research has been performed into the serial measurement of monoclonal
antibodies to smooth muscle myosin heavy chains that appears to be both sensitive
and specific for aortic dissection. The sensitivity of this test is about 90% and the
specificity is 97% within the first 12 hours of the beginning of the dissection, and this
assay can accurately differentiate myocardial infarction from aortic dissection. This
test is not currently available for the diagnosis of aortic dissection in the clinical
setting.
Transesophageal echocardiography
The transesophageal echocardiogram (TEE) is a relatively good test in the
diagnosis of aortic dissection, with a sensitivity of up to 98% and a specificity of up
to 97%. It is a relatively non-invasive test, requiring the individual to swallow the
echocardiography probe. It is especially good in the evaluation of AI in the setting of
ascending aortic dissection, and to determine whether the ostia (origins) of the
coronary arteries are involved. While many institutions give sedation during
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transesophageal echocardiography for added patient-comfort, it can be performed in
cooperative individuals without the use of sedation. Disadvantages of the TEE
include the inability to visualize the distal ascending aorta (the beginning of the aortic
arch), and the descending abdominal aorta that lies below the stomach. A TEE may
be technically difficult to perform in individuals with esophageal strictures or varices.
Aortogram
An aortogram involves placement of a catheter in the aorta and injection of
contrast material while taking x-rays of the aorta. The procedure is known as
aortography. The diagnosis of aortic dissection can be made by visualization of the
intimal flap and flow of contrast material in both the true lumen and the false lumen.
The aortogram was previously considered the gold standard test for the diagnosis
of aortic dissection, with a sensitivity of up to 88% and a specificity of about 94%. It
is especially poor in the diagnosis of cases where the dissection is due to hemorrhage
within the media without any initiating intimal tear.
The advantage of the aortogram in the diagnosis of aortic dissection is that it can
delineate the extent of involvement of the aorta and branch vessels and can diagnose
aortic insufficiency.
The disadvantages of the aortogram are that it is an invasive procedure and it
requires the use of iodinated contrast material.
Computed tomography angiography
Computed tomography angiography is a fast non-invasive test that will give an
accurate three-dimensional view of the aorta. These images are produced by taking
rapid thin cut slices of the chest and abdomen, and combining them in the computer
to create cross-sectional slices. In order to delineate the aorta to the accuracy
necessary to make the proper diagnosis, an iodinated contrast material is injected into
a peripheral vein. Contrast is injected and the scan performed using a Bolus Tracking
method. This is a type of scan timed to an injection, in order to capture the contrast as
it enters the aorta. The scan will then follow the contrast as it flows though the vessel.
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It has a sensitivity of 96 - 100% and a specificity of 96 to 100%. Disadvantages
include the need for iodinated contrast material and the inability to diagnose the site
of the intimal tear.
MRI
Magnetic resonance imaging (MRI) is currently the gold standard test for the
detection and assessment of aortic dissection, with a sensitivity of 98% and a
specificity of 98%. An MRI examination of the aorta will produce a threedimensional reconstruction of the aorta, allowing the physician to determine the
location of the intimal tear, the involvement of branch vessels, and locate any
secondary tears. It is a non-invasive test, does not require the use of iodinated
contrast material, and can detect and quantitate the degree of aortic insufficiency.
The disadvantage of the MRI scan in the face of aortic dissection is that it has
limited availability and is often located only in the larger hospitals, and the scan is
relatively time consuming. Due to the high intensity magnetic fields used during
MRI, an MRI scan is contraindicated in individuals with metallic implants. In
addition, many individuals experience claustrophobia while in the MRI scanning
tube.
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Treatment
The risk of death due to aortic dissection is highest in the first few hours after
the dissection begins, and decreases afterwards. Because of this, the therapeutic
strategies differ for treatment of an acute dissection compared to a chronic
dissection. An acute dissection is one in which the individual presents within the
first two weeks. If the individual has managed to survive this window period, his
prognosis is improved. About 66% of all dissections present in the acute phase.
In all individuals with aortic dissections, medication should be used to control
high blood pressure, if present.
In the case of an acute dissection, once diagnosis has been confirmed, the
choice of treatment depends on the location of the dissection. For ascending aortic
dissection, surgical management is superior to medical management. On the other
hand, in the case of an uncomplicated distal aortic dissections (including
abdominal aortic dissections), medical management is preferred over surgical
treatment.
Individuals who present two weeks after the onset of the dissection are said to
have chronic aortic dissections. These individuals have been self-selected as
survivors of the acute episode, and can be treated with medical therapy as long as
they are stable.
Medical management is appropriate in individuals with an uncomplicated
distal dissection, a stable dissection isolated to the aortic arch, and stable chronic
dissections. Patient selection for medical management is very important. Stable
individuals who present with an acute distal dissection (typically treated with
medical management) still have an 8 percent 30 day mortality.
Medical management
The prime consideration in the medical management of aortic dissection is
strict blood pressure control. The target blood pressure should be a mean arterial
pressure (MAP) of 60 to 75 mmHg. Another factor is to reduce the shear-force
dP/dt (force of ejection of blood from the left ventricle).
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To reduce the shear stress, a vasodilator such as sodium nitroprusside should be
used with a beta blocker, such as esmolol, propranolol, or labetalol. The alphablocking properties of labetalol make it especially attractive in this situation.
Calcium channel blockers can be used in the treatment of aortic dissection,
particularly if there is a contraindication to the use of beta blockers. The calcium
channel blockers typically used are verapamil and diltiazem, because of their
combined vasodilator and negative inotropic effects.
If the individual has refractory hypertension (persistent hypertension on the
maximum doses of three different classes of antihypertensive agents),
involvement of the renal arteries in the aortic dissection plane should be
considered.
Surgical management
Indications for the surgical treatment of aortic dissection include an acute
proximal aortic dissection and an acute distal aortic dissection with one or more
complications. Complications include compromise of a vital organ, rupture or
impending rupture of the aorta, retrograde dissection into the ascending aorta, and
a history of Marfan's syndrome or Ehlers-Danlos Syndrome.
The objective in the surgical management of aortic dissection is to resect (remove)
the most severely damaged segments of the aorta, and to obliterate the entry of
blood into the false lumen (both at the initial intimal tear and any secondary tears
along the vessel). While excision of the intimal tear may be performed, it does not
significantly change mortality.
Some methods of repair are:
- Replacement of the damaged section with a tube graft (often made of dacron)
when there is no damage to the aortic valve.
- Bentall procedure - Replacement of the damaged section of aorta and
replacement of the aortic valve.
- David procedure - Replacement of the damaged section of aorta and
reimplantation of the aortic valve.
- Insertion of a stent, combined with on-going medical management
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V. LITERATURE
1. Lections
2. Vascular Surgery/ European Manual of Medicine/ Chief editor C.D. Liapis –
Springer – 2007.
3. Short Practice of Surgery by Charles v. Mann and al.
VI. APPROXIMATE ACTIONS BASE
1. Introduction /5 min/
Teacher short characterizes topic actuality, meets students with main aims of
the study and its plan.
2. Initial knowledges control /15 min/
3. Individual students work with patients. /30 min/ The teacher explains some
more difficult and important parts of problem. The choice is realized by asking of
students and their answers correction.
4. Clinical analisys of topical patients. /100 min/
Students observe topical patients under teacher control. After it finishing, the
students report about receiving results.
Work in dressing-room and operational theater.
Teacher and students change the dressings of patients after different
surgical procedures on the pancreas
Study of X-Ray pictures, US- and CT-scanns, laboratory datas
5. Final knowledge control. Solution of test-questions /25 min/
6. Conclusion /5min/
The teacher concludes the session and gives new task for the next once.
VII. QUESTION.
1. Aortic dissection: definition of the idea.
2. Etiology of the acute aortic dissection.
3. Classifications.
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4. Signs and symptoms of the acute aortic dissection.
5. Instrumental investigation with acute aortic dissection.
6. Differential diagnosis.
7. Medical management of the acute aortic dissection.
8. Indications for the surgical treatment of aortic dissection.
9. Some methods of repair are.
10. Non-invasive surgical treatment of aortic dissection.