Chest pain? We also think of aortic dissection if we are not convinced that the patient has an acute coronary syndrome!
Anatomically we divide the thoracic aorta into 4 segments:
1 the aortic root which starts from the aortic valvular anulus and arrives at
the synotubular junction;
in it are included the sinuses of Valsalva with the coronary hosts;
2 the tubular segment of the ascending aorta that arrives at the emergence from
the synotubular junction
anonymous artery;
3 the aortic arch, between the emergence of the anonymous artery and the
emergence of the left subclavian artery;
4 the descending thoracic aorta, which from the emergence of the subclavian
artery reaches the diaphragm and then
continue as the abdominal aorta, subdivided in turn into the upper and the lower
back.
A dissection of the vessel wall is defined as a laceration of the intima thath propagates distally and
proximally. The blood penetrates into the myintimal flap and forms a hematoma
that propagates in the muscular tunic both distal and proximal.
The dissection may stop near a large collateral artery, but may also continue within or
beyond it. Or the hematoma may re-enter through a distal myo-intimal breach, thus
creating a double lumen of sliding a true and a false. By convention,
dissections are defined as "acute" when observed within the first 14 days and "chronic"
after this period. The real incidence is not known, because many dissections
lead to sudden death and are interpreted as cardiac infarcts. However, it is
estimated that in the Western world there are about 10 cases per year per
100,000 inhabitants, with a ratio between men and women 3: 1 and an average age
of around 60.
The ascending aortic aneurysms represent a pathological dilatation of the vessel, usually caused by weakening of the wall, secondary to atherosclerotic processes or to luetic arteritis (now rare); they have an incidence of about 6 cases every 100,000 per year. Morphologically we can distinguish fusiform and saccular aneurysms.
In patients with aneurysm of the ascending aorta and the arch, intervention is indicated when the diameter of the aneurysm is equal to or greater than 55 mm, or there is evidence of an increase in the caliber of 5 mm in a year. In patients with Marfan syndrome, surgery is indicated in patients with dilatation greater than or equal to 50 mm. But this threshold is lowered to 45 mm in patients with Marfan syndrome and risk factors such as familiarity with aortic dissection, increase in aortic diameter of 2 mm per year, desire for pregnancy
Never as in these cases the reanimation is of vital importance. Only after obtaining the hemodynamic stabilization can proceed to the diagnostic instrumental confirmation and the possible surgical correction. In the event of hypotension or shock, the systolic blood pressure should be reported to at least 70-80 mm Hg by vasoconstrictors and liquid infusion and, if the shock is cardiogenic, it's necessary to support the cardiac output pharmacologically. On the contrary, if hypertension is present, it is necessary to reduce it with nitroprusside to about 100 mm Hg, associating beta-blockers to counter the consequent raising of the range, of the frequency and of the contractile force of the heart.
Angio CT of a dissection of the ascending
aorta that continues along the descending aorta,
the true and false lumen are appreciated.
Rapid diagnosis is essential to modify the substantially poor prognosis of aortic dissections. ECG and chest radiography, almost always performed in the presence of acute chest pain, can hardly allow diagnosis by providing non-specific signs. The ECG can demonstrate signs of hypertensive heart disease, overload of the ventricle due to acute valvular insufficiency, atrioventricular block due to involvement of the sinus node, myocardial ischemia by coronary involvement. In chest X-rays are almost always evident mediastinal enlargement, dislocation of aortic parietal calcifications versus the inside of the lumen, double aortic profile on the left edge. Less specific is the enlargement of the cardiac shadow, the pleural opacification, the deviation to the right of the trachea. Transparietal echocardiography has good specificity for type A dissection, the ascending aorta being directly under the anterior thoracic pacet with poor interposition of pulmonary tissue; but it has considerable problems in evaluating the distal extension of the dissection and the type B dissections. The sign of a floating veil inside the lumen is patognomonic, whose rapidity of fluctuation can make it invisible to other imaging techniques, such as MRI and TC if not multislice. Transesophageal ultrasound, by eliminating the interaction of the costal wall and the pulmoral tissue, can provide reliable information on the whole thoracic aorta, and specify the location of the intimal flap. the double lumen or thrombosis of one of the two lumens, the valvular insufficiency, the involvement of the coronary hosts, the pericardial and pleural effusion.
CT
and resonance demonstrate the presence of a double lumen in the aorta, but they
have difficulty in visualizing the entrance door, the internment of the aortic
valve and the coronary valve, so they are preferably used in the chronic phase
to follow the evolution the type B dissections. If the false lumen is channeled
because an exit door has been created, a contrast medium is present in both
lumens, separated by a thin intimal veil. Angiography remains the fundamental
examination because it provides precise data on the entrance door, and extension
of the dissection, the state of the bulb and the aortic valve, the involvement
of the coronary arteries and other branches of the aorta, but can only be
ratized on stable patients. However, it fails to demonstrate intramural
thrombosis or parietal thrombosis of an aneurysm and presents the risks of
invasion and the use of contrast agent in patients with pre-existing or acute
renal insufficiency. Urgent arteriography is currently indicated only when the
other investigations have not been proven to be due to the presence of a
dissection, or to clarify the site of the entrance breach, when there is a
history of coronary artery disease, or when visceral involvement is suspected .
Symptoms associated with acute aortic dissection can mimic those of acute
myocardial infarction. The electrocardiogram (ECG) can demonstrate myocardial
ischemia, and the level of cardiac enzymes such as serum creatine kinase can be
high. Because thrombolytic therapy is often given to patients with acute
myocardial infarction and ST-segment abnormalities, thrombolytic drugs may be
given to patients with acute aortic dissection, with potentially disastrous
effects. ST segment elevation rarely occurs in acute aortic dissection, while ST
segment depression is more common (in about 32% of patients). Therefore,
thrombolytic therapy can be safely administered to patients with ST segment
elevation, in the absence of physical signs or other symptoms related to aortic
dissection, without the need for further diagnostic tests.
After the initial resuscitation, the treatment of these patients differs fundamentally in relation to the type of lesion, the present complications and the evolution. No protracted drug treatment is able to stabilize a dissection for long when it reaches the aortic valve plane. Therefore, in the face of the very high risk of immediate death, it is imperative that all type A dissatations be carried out urgently, with the exception of very old age or presence of too serious complications (multi-organ failure, stroke with loss of consciousness, mesenteric infarction). massive). In contrast, the majority of patients with type B dissection, uncomplicated by rupture shock, periaortic hematoma or visceral involvement, respond favorably to protracted drug treatment, with maintenance of the result in 70-80% of patients at one year. Therefore, for these the emergency correction is indicated only in a minority of cases, ie when medical therapy is not able to control both pressure and pain and when complications are present or imminent. Surgical correction in urgency must achieve three purposes: close the entry breach, replace the compromised stretch and restore the flow into the true lumen. All operations on the ascending aorta require cardio-circulatory arrest with cardio-pulmonary bypass, as well as deep hypothermia with cerebral protection, when arch reconstruction is also planned. Interventions on the descending or thoracoabdominal aorta alone do not require cardiopulmonary bypass and can be performed with or without a partial atrio-femoral bypass using a pump without an oxygenator.
We can have types A and B, depending on the dissection site
According to Stanford: Type A involves the ascending aorta and possibly also
the aortic arch and the descending thoracic aorta. Type B involves only the
descending aorta.
Type A:
Via median sternotomy
Cardiocirculatory arrest and total CEC
Replacement ascending aorta + / - coronary + / - valve
If involved the bow (type I of De Bakey): as above + deep hypothermia + elephant
trunk
Type B
Via left thoracotomy
No partial + / - C EC circle stop
Replacement of thoracic aorta
Femoral or iliac pathway
Endoluminal exclusion
If thoraco-abdominal (chronic):
Via: thoraco-brake-laparotomy Replacement thoracic and abdominal aorta +
intercostal reimplantation + replanting visceral arteries
+/- bifurcated prosthesis for the iliac
The replacement surgery of the aortic arch consists in replacing with a vascular prosthesis the thoracic aorta segment that goes from the emergence of the anonymous trunk to the emergence of the left subclavian artery. There is an indication in the case of aneurysm> 5.5 cm or in the case of an aortic dissection with the presence of intimate breccias at this level. It is performed in extracorporeal circulation, with suspension of blood flow that physiologically arrives at the brain through the carotid and vertebral arteries. This aspect involves a considerable technical difficulty, to overcome which over the years various techniques have been developed for the protection of brain tissue during the circulation stop. The basis of the brain protection strategy is the choice of the arterial cannulation site for the connection to the >> extra-corporal circulation, CEC, which may be the femoral or axillary artery.
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During the brain cycle arrest in hypothermia the recommended time limit, to
avoid deficit of postoperative cognitive function, is less than 30 minutes. To
prolong this period and to obtain greater safety against possible complications,
anterograde and retrograde cerebral perfusion techniques have been developed.
Their use made it possible to lengthen the time of circulatory arrest in
hypothermia at about one hour, as described by various authors, with
significantly reduced mortality and complications compared to the arrest only in
deep hypothermia. Selective anterograde cerebral perfusion consists in the
selective cannulation of the anonymous trunk and the left common carotid artery
or, in case of cannulation of the anonymous subclavian / trunk for the CEC, only
of the left common carotid artery, through which cerebroplegia is administered
during the arrest of circle in hypothermia. Its use has allowed to increase the
time of circulatory arrest in hypothermia with an average duration of cerebral
perfusion greater than 60 minutes, with a significant improvement in outcomes
for what concerns mortality and neurological complications
The positioning of an endoprosthesis is performed through a vascular access,
usually from the femoral artery, followed by success involves the exclusion of
the aneurysmal sac from any blood supply, with consequent deterrence and loss of
pulsatility, re-adjustment of the endoluminal thrombus, previously formed inside
the bag, and subsequent reduction of the diameters. The non-reduction of the
same, the persistence of a pulsation, and / or the presence of "endotension" are
an expression of a supply of the sac by pulsating blood, a phenomenon that goes
by the name of "endofeak (endoleak)".
In type A dissections, by means of sternotomy the ascending aorta is
substituted with a straight prosthesis and the distal false lumen is sutured
circumferentially. The coronary vessels and the aortic valve are repaired or
replaced because of the damage suffered (there are already pre-packaged
prostheses with a mechanical valve). If the dissection includes the arch, this
should also be replaced by replanting or bypassing the supra-aortic trunks. If
it extends beyond the arch, the so-called technique of the elephant trunk is
adopted, which consists in replacing the ascending aorta and the arch, suturing
the prosthesis beyond the subclavian sin and leaving a stretch of about 7-10 cm
free in the downstream light. This will serve at a distance of time for 9
prolongation necessary to correct the aneurysmal evolution of the false lumen in
the descending aorta (2/3 of cases) as if it were a type B aneurysm.
In type B dissections, by sin or thoraco-brake-laparotomic thoracotomies, at
least the proximal half of the descending aorta is substituted, comprising the
initial laceration and reaching to where the aorta reacquires a diameter of less
than 4 cm. To prevent the risk of paraplegia, one or more pairs of intercostal
arteries are re-implanted, generally T9-T11, in order to preserve the artery of
Adamkievicz born at this level. If the diaphragmatic and / or abdominal aorta is
also replaced, the visceral arteries (tripod, superior mesenteric and renal)
must be re-inserted. The distal anastomosis can occur at any level, possibly
also iliac or femoral through further grafting of a bifurcated prosthesis. In
recent years, in highly specialized centers, the type B dissections have begun
to be treated endovascularly, with a view to reducing the surgical trauma: in
selected cases the endopotesis release technically succeeds in 95%, with
apparent reduction in mortality.
Aortic arch reconstruction remains a challenge, particularly in elderly patients, in patients treated urgently or in those with significant co-morbidities. In 20 years, the endovascular treatment of descending thoracic aortic aneurysms has positioned itself as a valid alternative to open surgery. However, for lesions of the aortic arch, the emergence of supra-aortic trunks does not allow endovascular treatment. To obtain a proximal collar, a hybrid approach has been recently proposed that combines a transposition of one or more supraortic trunks followed by endovascular exclusion of the lesion. The transposition is made to create a proximal anchorage zone (proximal collar) suitable for implantation of the endoprosthesis, while at the same time maintaining cerebral perfusion and upper limbs. The results of the aortic arch hybrid treatment are similar in terms of mortality and neurological morbidity to those of conventional surgery.