TY - JOUR
AU - Weigang, E
AB - Abstract Background Acute aortic dissection type A (AADA) is a life-threatening vascular emergency. Clinical presentation ranges from pain related to the acute event, collapse due to aortic rupture or pericardial tamponade, or manifestations of organ or limb ischaemia. The purpose of this review was to clarify important clinical issues of AADA management, with a focus on diagnostic and therapeutic challenges. Methods Based on a MEDLINE search the latest literature on this topic was reviewed. Results from the German Registry for Acute Aortic Dissection Type A (GERAADA) are also described. Results Currently, the perioperative mortality rate of AADA is below 20 per cent, the rate of definitive postoperative neurological impairment approaches 12 per cent and the long-term prognosis after surviving the acute phase of the disease is good. Many pathology- and therapy-associated factors influence the outcome of AADA, including prompt diagnosis with computed tomography and better cerebral protection strategies during aortic arch reconstruction. Endovascular technologies are emerging that may lead to less invasive treatment options. Conclusion AADA is an emergency that can present with a wide variety of clinical scenarios. Advances in the surgical management of this complex disease are improving outcomes. Introduction Acute aortic dissection type A (AADA) is a life-threatening vascular emergency. The incidence is estimated to be 2·9 per 100 000 per year1, but may be increasing2. The diagnosis of AADA is challenging because of its varied clinical presentation and because the differential diagnosis includes more common conditions such as myocardial infarction. Management involves complex surgery, perioperative intensive care, and long-term surveillance to detect late dissection-related complications. The study of AADA is hampered by its relatively low incidence, the variability with respect to pathoanatomy and presenting complications, and differences in therapeutic strategies. Several international registries have been established to generate an evidence base that can inform current and future management. The aims of this article were to review the current management of AADA and summarize insights gained from the German Registry for Acute Aortic Dissection Type A (GERAADA). Methods This review was based on a MEDLINE search regarding the term ‘aortic dissection’ combined with other terms of interest. For every subtopic the aim was to include the most valid, representative and contemporary publications. Studies with large patient numbers or meta-analyses of previous series were selected, focusing on series published during the past 15 years (1997–2012) in high-impact journals. For several aspects of AADA, data were included from GERAADA. The registry was initiated by the working group for aortic surgery and interventional vascular surgery of the German Society for Thoracic and Cardiovascular Surgery. Fifty-two cardiac surgery centres in Germany, Austria and Switzerland have contributed data addressing perioperative, demographic, aetiological and follow-up parameters from more than 2500 patients since 2006. Pathology of aortic dissections The initial event in most aortic dissections is the formation of an intimal tear (entry) which allows bleeding within the medial layer of the aortic wall. Pressurized blood cleaves a dissection plane within the media, with propagation to a varying extent along the aorta. The separation of the aortic layers creates two aortic lumens. The true lumen of the aorta remains surrounded by intima and may become compressed by the false lumen, which is surrounded by the intimal–medial dissection flap and a weak medial–adventitia outer wall (Fig. 1)3,4. The dominant direction of propagation of the dissection is antegrade but retrograde propagation also occurs. The weakened false channel may rupture externally or internally owing to additional entry or re-entry tears, which may be multiple, for instance at the intercostal arteries. In a number of dissections, no entry tear is identified (non-communicating dissection)4. Fig. 1 Open in new tabDownload slide a Coronal and b sagittal computed tomography reconstructions showing a dissection membrane in the ascending aorta, aortic arch and descending aorta. c Cross-section of the dissected aorta Aortic dissection most frequently occurs in a previously dilated section of aorta. Once dissection has occurred, acute or chronic dilatation of the false luminal channel follows. Other suspected pathological mechanisms include atherosclerotic intimal destruction and haemorrhage or occlusion of the vasa vasorum with consequent ischaemia5. The most common underlying mechanisms are arterial hypertension and atherosclerosis. Additionally, multiple primary conditions are associated with an increased risk of AADA, among them connective tissue diseases such as Marfans, Loeys–Dietz and Ehlers–Danlos syndromes6, and defects such as bicuspid aortic valves and aortic coarctation. Further risk factors include inflammatory or infective vasculopathies. Iatrogenic causes, such as cardiac catheterization and cardiac surgical procedures requiring aortic cannulation or clamping, are rare causes of AADA3. Classification of aortic dissections In 1965, DeBakey and colleagues7 introduced a classification of aortic dissections, distinguishing three subtypes depending on the location of the entry and extent of the dissection. A few years later, Daily and co-workers8 introduced the more commonly used Stanford classification (Fig. 2). Dissections involving the ascending aorta proximal to the brachiocephalic artery were termed type A, whereas those not involving the ascending aorta were referred to as type B dissections. This classification system disregards the site of primary intimal tear but is clinically more pragmatic than the DeBakey classification, as prognosis and management depend on whether or not the ascending aorta is involved. Fig. 2 Open in new tabDownload slide DeBakey and Stanford classifications of acute aortic dissection Open surgery is nearly always recommended for AADA9. Type B dissections are divided into uncomplicated and complicated courses; uncomplicated cases are treated conservatively, whereas complicated cases are mostly treated by endovascular stenting10. The classification and management of dissections involving the aortic arch but not the ascending aorta is controversial (Stanford type B dissections). Some authors thus prefer the term proximal dissection if the aorta proximal to the left subclavian artery is involved and distal dissection in all other cases9. At least if an intimal tear is found within the arch, the need for immediate surgery is debated. As imaging methods have improved, more subtle lesions of the aortic wall have been identified in patients presenting with a history compatible with dissection. The designation acute aortic syndrome (AAS) was introduced. In addition to classical aortic dissection, AAS includes the entities of intramural haematoma (IMH) and penetrating aortic ulcer (PAU)11. PAU is an intimal lesion caused by rupture of an atherosclerotic plaque, whereas IMH does not necessarily arise from an intimal tear and may result from damage to the vasa vasorum. Both lesions may progress to classical dissection. The European Society of Cardiology differentiates five categories of AAS: classical aortic dissection; intramural haemorrhage/haematoma; subtle/discrete (localized) aortic dissection; plaque rupture/ulceration with subadventitial haematoma; and traumatic/iatrogenic aortic dissection9,12. An aortic dissection is arbitrarily designated acute during the first 14 days; thereafter it is classified as chronic. The present article focuses on acute aortic dissection Stanford type A (AADA). The Stanford terminology has broad acceptance in clinical routine and has implications for subsequent therapy. More than 70 per cent of AADAs involve the aortic arch (DeBakey I), approximately 40 per cent the descending aorta, 30 per cent the abdominal aorta and 30 per cent the supra-aortic vessels13. Clinical presentation of acute aortic dissection type A In addition to acute thoracic and back pain, the clinical presentation of AADA depends on the pathological anatomy and resulting complications. Pericardial tamponade, myocardial ischaemia and acute aortic valve insufficiency (due to detachment of commissures) may each lead to shock. Aneurysm rupture, usually of the ascending aorta, is generally fatal immediately. Cerebral ischaemia may result from obstruction of the supra-aortic branches, low perfusion pressure or thromboembolic events and is a major factor in morbidity. Malperfusion of the spinal cord may result in paraplegia. When the dissection affects the abdominal and iliac arteries, visceral malperfusion syndromes and acute limb ischaemia may occur. The spectrum of clinical presentations ranges from discrete symptoms to severe shock. On admission to hospital, 50 per cent of patients are haemodynamically unstable, approximately 25 per cent have a neurological deficit, over 20 per cent have pericardial tamponade, and 6 per cent have already undergone cardiopulmonary resuscitation13,14. Aortic dissection should always be considered in the differential diagnosis of patients presenting with acute onset of any of the following: chest and back pain, syncope, stroke, paraplegia, limb ischaemia, cardiac failure and abdominal pain15. Symptomatology is often dynamic owing to alterations in the position of the dissection membrane, further antegrade or retrograde propagation, or expansion of the false lumen and subsequent compression of the true lumen. When AADA is diagnosed, immediate surgery is recommended. Historically, the mortality rate was 1–2 per cent per hour for the first 24–48 h from time of symptom onset12,16. In studies of patients with AADA admitted to hospital alive but treated conservatively, the mortality rate approaches 60 per cent17, and is even worse in those who are not treated at all18. The International Registry of Acute Aortic Dissection (IRAD) and GERAADA report an in-hospital mortality rate in patients with AADA treated surgically of 28 per cent19 and 17 per cent respectively. Diagnosis Chest pain and heart failure are sensitive but non-specific symptoms. A diastolic murmur on auscultation, a pulse deficit, blood pressure difference and neurological deficit increase the likelihood of AADA in a patient with chest pain15. Electrocardiography may demonstrate myocardial ischaemia (especially in the right coronary territory) or non-specific changes, such as those due to pericardial effusion or left ventricular hypertrophy. Chest X-ray may reveal a widening of the mediastinum (present in 49 per cent of patients in IRAD17), but many emergency radiographs are performed as anteroposterior portable fields, leading to confusion. Some effort has been made to identify biochemical markers, including D-dimer whose absence is useful in ruling out AADA20, and smooth muscle cell myosin heavy chain, which appears to be useful in differentiating AADA from acute coronary syndrome21. However, no marker yet has an established clinical role22. An increase in cardiac troponin level is present in a quarter of cases and is often a further confusing factor. Once clinical suspicion is raised, the diagnosis of an AADA is based on the detection of a dissection membrane in the ascending aorta using specific imaging techniques: transthoracic (TTE) and transoesophageal (TEE) echocardiography, conventional angiography, contrast-enhanced computed tomography (CT) and magnetic resonance imaging (MRI). The sensitivities of MRI, TEE and CT for detecting a dissection are similar at approximately 95 per cent. Although specific, TTE is insensitive (59 per cent) owing to an inadequate window for imaging the ascending aorta. The diagnostic specificity for AADA is highest for MRI (97 per cent), followed by CT (87 per cent)23. Other series have reported even better sensitivity and specificity values for all of the above-mentioned modalities24. Its widespread availability in emergency units and speed make CT the first choice. The pathological anatomy is visualized clearly, together with possible complications including effusions and malperfusion syndromes; it also provides valuable information for treatment planning (Fig. 1). The main drawbacks of CT are its ineffectiveness in detecting the dissection entry site and its inability to provide functional information about the heart. In these regards, MRI and TEE are superior. Many clinicians believe that TEE should be performed routinely after induction of anaesthesia as a further diagnostic aid and as a guide to surgical repair. MRI makes the diagnosis of AADA with the highest sensitivity and specificity; it also detects intimal tears, provides functional information and facilitates multidimensional reconstructions of the aorta. In GERAADA, before surgery over 80 per cent of patients had CT, more than 50 per cent had echocardiography and under 2 per cent received MRI13. The role of preoperative coronary angiography is controversial25. The low rate of concomitant coronary artery disease, the risk of catheter-induced aortic rupture and the delay before surgery are substantial arguments against it. All of the above non-invasive measures are swifter and provide more information than conventional angiography. Angiography may be indicated after operation (or during surgery in the era of the hybrid operating theatre) in patients with visceral malperfusion and dilatation of the descending aorta to guide the appropriate intervention. Perioperative management AADA may present with shock, haemodynamic stability or even hypertensive emergency. Invasive haemodynamic monitoring is mandatory26. Differential blood pressures in the arms may require dual-site arterial blood pressure monitoring; medication should be based on the blood pressure site that best reflects true luminal perfusion. When hypertension is present, reliable blood pressure control is required. Intravenous beta-blockers (such as esmolol) or combined β- and α-receptor antagonists (labetalol) are the first choice9,12 because of the attenuation of the left ventricular pressure rise. Other antihypertensives such as glyceryl trinitrate, sodium nitroprusside, urapidil or clonidine may also be required. Opiates are essential for pain relief and facilitate blood pressure control. Intubation and ventilation may be inevitable in an unstable patient, but should be delayed if possible until reaching the operating theatre because intubation may be followed by rapid haemodynamic deterioration. After surgery patients are usually ventilated for a minimum of several hours. Respiratory dysfunction is not uncommon and prone ventilation often improves oxygenation27. Volume overload due to extracorporeal circulation, renal failure, hypothermia and ischaemia usually necessitates continuous volume reduction during the first few postoperative days, often requiring dialysis. Hypotension and hypertension should both be prevented to avoid end-organ ischaemia, bleeding and dissection progression. Systolic blood pressure of 90–110 mmHg, mean arterial pressure of 60 mmHg and central venous pressure of 8–12 mmHg appear adequate both before and after surgery26. Coagulation disorders may result from numerous factors including the preoperative administration of antiplatelet drugs. Additionally, the dissection itself generates activation of inflammatory, coagulation and fibrinolytic cascades. This leads to a profound consumption coagulopathy which is further aggravated by the use of heparin, extracorporeal circulation and hypothermia. Normothermia and a balanced acid–base equilibrium are important goals in the early postoperative phase. Repeated differentiated coagulation analysis can be done with thromboelastography28. AADA surgery is associated with a risk of neurological complications, and early detection facilitates management. Regional or diffuse cerebral ischaemia may lead to cerebral oedema; invasive monitoring of intracranial pressure by a lumbar catheter may be required occasionally29. Surgery for acute aortic dissection type A The main principles of AADA surgery are: resection of the primary intimal tear (entry); stabilization of the aortic wall and prevention of aortic rupture; end-organ (particularly cerebral) protection; and correction/alleviation of complications and malperfusion syndromes. A decade ago, the IRAD survey reported that 28 per cent of patients with AADA reaching hospital alive were treated conservatively17. The in-hospital mortality rate in this group was 58 per cent. Reasons for turning down from surgery were advanced age, co-morbidity and patient refusal. Today the number of patients treated conservatively is probably lower and advanced age is no contraindication to surgery30. Patients with AADA are usually in their fifth or sixth decade, and surgical outcomes correlate closely with age; in a GERAADA analysis the 30-day mortality rate among septuagenarians was 15·8 per cent compared with 34·9 per cent among octogenarians13. In contrast to advanced age, a major preoperative stroke may be a reason for conservative treatment. Ascending aorta The dissection entry is usually found in the ascending aorta, which is dilated and at high risk of rupture. The most conservative procedure for AADA is an isolated supracommissural (sinotubular junction) replacement of the ascending aorta (Fig. 3a). The distal anastomosis can be sutured beneath the aortic cross-clamp during extracorporeal circulation, or it may be constructed during hypothermic circulatory arrest after releasing the cross-clamp (open distal anastomosis). The latter technique allows inspection of the aortic arch and facilitates creation of a very distal anastomosis. In the GERAADA survey, only 5·6 per cent of patients underwent supracommissural replacement of the ascending aorta without circulatory arrest14. Pure ascending aorta replacement is meant to minimize the perioperative risk, but probably increases the risk of later complications such as aneurysmal dilatation of the remaining aorta31. Fig. 3 Open in new tabDownload slide a Supracommissural replacement of the ascending aorta, b hemiarch replacement, c total arch replacement, d trifurcated graft technique and e frozen elephant trunk procedure Aortic root and valve The aortic root is often involved in the dissection, and the aortic valve may be incompetent owing to commissural dehiscence or, rarely, annular dilatation. In GERAADA, aortic regurgitation grade II was found in 40 per cent and grade III in 23 per cent of patients14. Several strategies are available for aortic valve repair or replacement. The displaced intima may be fixed using tissue adhesive. Glue is injected into the false lumen of the dissected sinus and the separated layers are compressed. However, glue can induce necrosis, is prone to cause embolization and risks late redissection32. Consequently, many centres have discontinued the use of tissue adhesive. If the aortic root is dilated and the aortic valve incompetent, the valve must be reconstructed. Several valve-sparing strategies exist (Fig. 4). Usually the native aortic valve is skeletonized by cutting back the sinuses of Valsalva. During the Yacoub procedure, the sinuses of Valsalva are replaced by a mirror image tube graft33, whereas during the David procedure the valve is reimplanted into the graft34. In both cases, the coronary arteries must be reimplanted into the prostheses. Reimplantation is not necessary in the Florida sleeve technique (among others), which completely encases the aortic root with a graft from the outside35. Successful aortic valve reconstruction has even been described for bicuspid valves36. If the aortic valve is sclerotic, stenosed or destroyed, it must be replaced. For combined valve and root replacements, conduit grafts with tubular vascular prostheses attached to mechanical or biological heart valves are available. The composite graft is anchored in the annulus of the aortic valve, and the coronary arteries must be reimplanted into the graft (Bentall procedure). Experienced surgeons may consider valve-sparing aortic root reconstruction in a subpopulation of young patients with AADA (for example those with Marfan syndrome)37. However, these procedures are technically demanding and time-consuming. Composite grafting should be viewed as the standard strategy. Fig 4 Open in new tabDownload slide Aortic root procedures: a skeletonized aortic valve, coronary buttons, b reimplantation technique (David procedure), c remodelling technique (Yacoub procedure) and d encasing the aortic root (Florida sleeve) In GERAADA, more than 70 per cent of patients received supracommissural ascending aorta replacement, about 20 per cent had a conduit and fewer than 8 per cent underwent aortic valve-sparing root replacement38. Aortic arch The aortic arch is dissected in more than 70 per cent of AADAs. Often the primary intimal tear extends or re-entries are located within the arch39. Aortic arch dilatation or obstruction of the supra-aortic vessels is common in AADA. Arch inspection from inside the lumen is thus required. If no entries or tears are found within the arch, but a dissection membrane is present, the arch may be reconstructed using tissue adhesive. If intimal tears extend into the arch, prosthetic replacement is required. In a proximal arch or hemiarch procedure, the distal anastomosis is fashioned in a transverse manner, replacing the inner curvature which usually contains the tear, but preserving the continuity of the supra-aortic branches. Total arch replacement requires reimplantation of the supra-aortic vessels, which are preferably reinserted as an island of aortic wall (Fig. 3b,c); however, in the event of extreme arch destruction, the vessels must be anastomosed separately. All of these procedures must be done during circulatory arrest and may be associated with an increased risk of death or neurological complications39. Some recommend minimizing the arch procedure in emergency AADA surgery30,40,41. In GERAADA, however, the outcome of extensive arch surgery was not inferior to that of more conservative strategies42. The trifurcated graft technique (Fig. 3d) is an alternative strategy for aortic arch reconstruction that has been reported to be successful in AADA43. After cannulation of the right subclavian artery a short phase of circulatory arrest is employed and the supra-aortic branches are anastomosed to a trifurcated graft. Next, the aortic arch is replaced while the brain is perfused through the graft. This technique enables extensive arch reconstruction with short intervals of44, or even without, circulatory arrest by combining axillary and femoral inflow45. The same principle is used in the strategy of aortic arch debranching46; after ascending aorta replacement, a Y-shaped bypass is interposed between the ascending aorta prostheses and the supra-aortic vessels. In a second step, an endovascular prosthesis is implanted into the aortic arch using the transfemoral route, occluding the native supra-aortic branches (Fig. 5). This procedure has recently been described for AADA47 and may herald a new era of endovascular strategies in the aortic arch. This technique avoids some risks of arch surgery; however, it carries the potential risks of endoleaks and dysfunction of the bypass grafts supplying the supra-aortic branches. Studies in the future will reveal whether these new strategies can compete with the long-term results of conventional arch repair48. Fig. 5 Open in new tabDownload slide Computed tomography reconstruction showing hybrid aortic arch replacement Descending aorta The thoracic and abdominal portions of the descending aorta are involved in 40 and 30 per cent of patients respectively13, but are responsible for just a minority of acute complications. Therefore, the descending aorta itself is not usually treated during emergency surgery for AADA. If all intimal tears are occluded during ascending aorta and arch repair, the descending aorta false lumen may collapse and thrombose. However, in over 70 per cent of patients, the false lumen is perfused chronically, as in a Stanford type B aortic dissection, carrying the risk of further enlargement31,49. Visceral and limb ischaemia may result from dynamic compression of the descending aorta true lumen by the false lumen (true-lumen collapse). Furthermore, the dissection may extend into the aortic branches themselves and thus lead to malperfusion. Finally, the false lumen may thrombose at the level of a branch, causing static compression of the true lumen. The ‘elephant trunk’ is the classical extension of the aortic arch replacement into the descending aorta. During arch replacement, the distal end of the aortic graft is advanced into the descending aorta. In a second surgical (or interventional) procedure, this prosthesis is then connected to the distal aorta50. This procedure has been refined by the use of stent-graft-reinforced hybrid prostheses which are implanted into the descending aorta in an antegrade fashion during arch replacement (frozen elephant trunk), leading to high false-lumen occlusion rates51,52 (Fig. 3e). Thoracic endovascular aortic repair (TEVAR) has become the standard treatment for several descending aorta pathologies53. TEVAR of type B dissections was studied in the INvestigation of STEnt Grafts in Aortic Dissection (INSTEAD) trial10. The technique is also applicable to complicated AADA. A covered stent-graft is advanced via the femoral arteries into the descending aorta to cover intimal tears, to eliminate compression of the true lumen54, and to prevent or treat aneurysm formation. Indications for TEVAR include: thoracic aorta diameter greater than 5·5 cm, an increase of more than 1·0 cm within 1 year, therapy-resistant hypertension associated with a small true lumen or renal malperfusion, and recurrent episodes of chest/back pain in patients with subacute or chronic aortic dissections and a patent false lumen55. Although TEVAR in the aortic arch with branched stent-grafts is an emerging technique for the treatment of arch aneurysms, endovascular techniques are not yet a substitute for surgical replacement of the primarily diseased ascending aorta and aortic arch48. In malperfusion syndromes resulting from dynamic true-lumen compression through a dead-end false lumen, fenestration of the dissection membrane is a complementary treatment. The rationale of this procedure is to create a connection between the false and true lumens to improve run-off from the false lumen. Consecutive decompression of the true lumen improves distal perfusion. Historically, this procedure was performed surgically56 but it has now been replaced almost totally by interventional fenestration of the dissection membrane. Under angiographic control, a guidewire is advanced from the groin through the true lumen up into the abdominal aorta. Via a long sheath, the dissection membrane is punctured and a balloon catheter is then used to enlarge the window between the true and false lumens57. Today, the method has mostly been replaced by TEVAR, or is combined with TEVAR; however, several modifications of this method remain58,59. Branches narrowed by static compression of the true lumen owing to thrombus in the false lumen may be treated by stenting, as with atherosclerotic lesions. Rarely, interventional revascularization is unsuccessful and conventional peripheral bypass surgery is required to salvage visceral or limb perfusion. Patients presenting with AADA and concomitant critical visceral or peripheral malperfusion represent a therapeutic dilemma. In haemodynamically stable patients, an interventional procedure may be the first choice in order to restore visceral perfusion before cardiac surgery12,60. Arterial cannulation for extracorporeal circulation in surgery for AADA Although venous access for extracorporeal circulation may be established by cannulation of the right atrium or the femoral veins as in elective cardiac surgery, the standard site of arterial cannulation, the ascending aorta, is diseased in AADA. It is important to cannulate the true aortic lumen because false-lumen perfusion may cause progression of the dissection, malperfusion syndromes and aortic rupture. Several strategies have been developed to avoid these problems. Femoral artery cannulation was standard in most centres for many years. Usually, one femoral artery, often the right side, is perfused via the true lumen. However, the embolization of thrombi and the subsequent risk of stroke, as well as pressurization of the false lumen after clamping the ascending aorta, are the main concerns of retrograde perfusion of the dissected aorta4. Contemporary studies suggest worse outcomes after femoral cannulation compared with other strategies61,62; consequently it has lost popularity during recent years. Another site of peripheral cannulation is the right subclavian or axillary artery, which is usually not involved in the dissection. Axillary artery cannulation confers antegrade perfusion of the aortic arch during the initial and final steps of the operation, and allows antegrade cerebral perfusion (ACP) during circulatory arrest via clamping of the brachiocephalic artery. Injury to the brachial plexus and the rather fragile vessel are potential risks during this technique. It remains controversial whether the axillary artery should be cannulated directly, or using the side-graft technique, via an end-to-side tube graft. Axillary cannulation has been shown to be superior to femoral cannulation61,63,64. The carotid arteries have been used for cannulation65, representing a therapeutic opportunity in patients presenting with a cerebral perfusion deficit. In contrast to the peripheral cannulation strategies, many surgeons prefer to cannulate the dissected aorta itself62,66. To guide true-lumen cannulation, direct ultrasonography or transoesophageal ultrasonography and the Seldinger technique are helpful67. Alternatively, the cannula may be placed under direct vision after transecting the tourniquet-controlled distal ascending aorta, allowing very fast cannulation in an emergency68. Others have advocated cannulation via the left ventricular apex69. All these techniques and many modifications coexist38. There is currently no consensus on the superiority of right axillary or aortic cannulation. As the pathoanatomy differs among patients with AADA, so does the optimal cannulation strategy. Cerebral protection in surgery for acute aortic dissection type A Because the integrity of the arch is crucial for perfusion of the brain and lower body during extracorporeal circulation, aortic arch procedures must be completed under circulatory arrest. Owing to the brain's low tolerance of ischaemia, cerebral protection is of the utmost importance. Hypothermia is an effective way of prolonging ischaemic tolerance. During extracorporeal circulation, the body is cooled down. After reaching the desired temperature, extracorporeal circulation is stopped. The arch is opened under hypothermic circulatory arrest (HCA). The optimal temperature for the HCA-alone strategy is controversial. The balance is between better organ protection versus a higher risk of coagulation disorders, systemic inflammatory response syndrome and longer pump times. The Griepp school relies on profound hypothermia of 10–15 °C70, whereas others prefer temperatures of around 20 °C14,71. Several clinical and experimental studies suggest that HCA of less than 30 min at below 20 °C is low risk71–73. In GERAADA, only 22·8 per cent of patients underwent surgery under HCA alone; temperatures between 15 and 20 °C were most commonly employed. Arrest times under 30 min were associated with a postoperative mortality rate of 15·4 per cent. When this threshold was exceeded, the mortality rate rose significantly to 35·7 per cent14. To prolong the safe interval for arch surgery, several cerebral perfusion techniques have been developed. Because the jugular veins and cerebral sinuses have no valves, retrograde cerebral perfusion (RCP) is feasible. This technique can prolong the safe interval for arch surgery by sustained cooling of the brain, but does not seem to meet its metabolic demands74. Although RCP has never been proven to be inferior to antegrade techniques75,76, it has lost popularity. A negligible number (2·2 per cent) of patients actually receive RCP14. ACP has become standard in elective aortic arch surgery; 69·4 per cent of patients with AADA receive ACP14. Independent of the primary cannulation site, the innominate artery and the left common carotid artery may be intubated selectively from inside the aortic arch with balloon-tip catheters (Fig. 6a). This technique allows bilateral cerebral perfusion, but increases the risk of stroke from air embolism or dislodgement of debris. If the right axillary artery is used for arterial cannulation, another approach may be taken (Fig. 6b); after cooling to the desired temperature, pump flow is reduced and the brachiocephalic artery occluded. Henceforth, the brain is perfused selectively via the right carotid and vertebral arteries. This technique avoids manipulation of the carotid arteries and allows uninterrupted cerebral perfusion. Unilateral cerebral perfusion is usually adequate; however, it may be supplemented by an additional cannula in the left carotid artery. ACP extends the safe arch intervention time beyond the threshold with HCA alone. There are numerous reports that cerebral perfusion times of 30–60 min are well tolerated14,77. The optimal ACP approach remains unknown; studies comparing unilateral and bilateral perfusion have generated inconsistent results14,64,78. The optimal cerebral perfusion temperature is also controversial. Experimental studies suggested an advantage with profound hypothermia79,80, but there is no published clinical evidence confirming this. The same holds true for the lower body temperature; although experimental studies support temperatures of approximately 20 °C81, clinical studies have not found any disadvantage for moderate hypothermia (over 25 °C)82. Thus, temperatures vary widely among institutions. In GERAADA, equivalent numbers of patients underwent unilateral and bilateral ACP without relevant differences in outcomes. The spectrum of cerebral perfusion temperatures ranged from below 15° to over 30 °C, 15–20 °C being most common, but not influencing the prognosis14. Fig 6 Open in new tabDownload slide Cerebral perfusion techniques: a selective intubation of the innominate and left carotid arteries, and b primary cannulation of the right subclavian artery (RSA) Strategies to monitor cerebral protection include electroencephalography, sensory-evoked potentials, jugular bulb venous oxygen saturation, transcranial Doppler and near-infrared spectroscopy, and are reviewed elsewhere in detail83. In elective aortic arch surgery, ACP has become standard. In emergency surgery for AADA, there are arguments for keeping the arch procedure as short as possible30,41. For arch inspection and an open distal anastomosis, surgery under HCA alone may be adequate. If more extensive arch reconstruction (more than 20–30 min) is necessary, ACP should be instituted from the beginning of the arch procedure9,14,72. Follow-up Survivors of surgery for AADA have a favourable prognosis: approximately 90 per cent survival at 1 year, 72–77 per cent at 5 years and 53–56 per cent at 10 years31,49,84. Typical late complications of the aortic root and proximal aorta depend on the nature of the initial intervention, and include redissection, dilatation and aortic regurgitation. With respect to the distal, untreated aorta, aneurysmal dilatation with subsequent rupture remains the main risk. Risk factors include hypertension, a non-resected entry, an enlarged initial aortic diameter, a patent false lumen, lack of beta-blockade and Marfan's pathology. Longitudinal studies demonstrated a risk of further surgical or interventional treatment of 16–25 per cent after 10 years31,49,84. The follow-up of patients with AADA is aimed at early detection of the potential complications. Adequate blood pressure control is paramount. Systolic blood pressure should be consistently below 135 mmHg, and optimally below 120 mmHg9,12,85. Further follow-up includes assessment of the diameter of the entire aorta, behaviour of the anastomoses, endoleaks after TEVAR, and myocardial and aortic valve function. Because MRI avoids radiation, it seems the method of first choice, especially in patients who expect decades of follow-up. However, because of its wider availability, most patients currently undergo repeated follow-up CT. Monitoring aortic diameters by combining TEE and abdominal ultrasonography may be possible in certain patients. Repeated echocardiography is indispensable in monitoring valvular and myocardial function. Patients who have had coronary procedures should undergo regular ergometric monitoring. Follow-up assessment is done at 3, 6 and 12 months after surgery. After this, lifelong annual follow-up is standard12,85, but may vary depending on the course of the disease. Monitoring high-risk patients may help to prevent AADA. Ascending aorta aneurysm with a diameter exceeding 5 cm warrants surgery in younger and otherwise healthy patients. In patients with connective tissue disorders, many experts consider elective ascending aorta replacement at 4·5 cm, whereas in elderly patients diameters of up to 5·5 cm may be treated conservatively9,12,85. In the descending aorta, dilatation exceeding 6 cm usually necessitates intervention55. In each patient, the risk of conservative versus surgical treatment must be balance individually. Present and future advances Improved diagnosis with more widespread use of CT allows faster and better treatment planning for AADA. Surgical techniques have diversified and improved, especially in the field of aortic valve and root reconstruction, and in the field of cerebral protection, which enables more extensive aortic arch surgery. Endovascular strategies are emerging that may lead to less invasive treatment options, especially for complications of the descending aorta. It is likely that endovascular techniques will extend into the arch and the ascending aorta in the future; however, it is questionable whether they can compete with the outcome of conventional surgery. The value of registries in documenting outcome is well known; they could expand to incorporate long-term outcomes, and to provide reliable information not just on survival and major neurological complications but also about functional outcomes in survivors after AADA. Acknowledgements The authors thank Mr Patrick ‘Patty’ Henne (paeddi@live. de) for preparing the drawings. GERAADA is funded by the German Society for Thoracic and Cardiovascular Surgery. Disclosure: The authors declare no conflict of interest. References 1 Mészáros I , Mórocz J, Szlávi J, Schmidt J, Tornóci L, Nagy L et al. Epidemiology and clinicopathology of aortic dissection . Chest 2000 ; 117 : 1271 – 1278 . Google Scholar Crossref Search ADS PubMed WorldCat 2 Olsson C , Thelin S, Ståhle E, Ekbom A, Granath F. Thoracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14 000 cases from 1987 to 2002 . 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TI - Acute aortic dissection type A
JF - British Journal of Surgery
DO - 10.1002/bjs.8840
DA - 2012-09-07
UR - https://www.deepdyve.com/lp/oxford-university-press/acute-aortic-dissection-type-a-4ilh3zX84R
SP - 1331
EP - 1344
VL - 99
IS - 10
DP - DeepDyve
ER -