The complication of postoperative retroperitoneal bleeding from the reconstructed right renal artery had to be managed by relaparotomy and single vascular stitches, and clinical recovery was delayed. The patient required 4 months of rehabilitation until she had regained her previous health status. At this point, digestion and renal function had recovered, laboratory findings became normal, and hypertension had to be treated with only one drug (beta-blocker). Postoperative angiographies showed good perfusion of all visceral and renal arteries via the Dacron graft (Fig. 7.4).

7.3  Commentary

The life-threatening aortic dissection starts with an intimal tear (entry) in the ascending aorta (Stanford A, de Bakey I or II) or distally to the left subclavian artery (Stanford B, de Bakey III). De Bakey II dissection affects the ascending aorta only, while de Bakey I and III dissections also involve the descending aorta.1, 2 [Q1: A, C] Most patients with acute aortic dissection present with severe chest pain, which might be misinterpreted as acute MI.3,4

Echocardiography, particularly by the transoesophageal approach, is a reliable and rapid method for diagnosis of aortic dissection and differentiation into Stanford A or B type.5 Nevertheless, the evaluation of organ arteries and their blood flow by ultrasound may be difficult in acute dissection. In our opinion, contrast thoracic and abdominal CT scans, especially using the spiral technique, are appropriate diagnostic methods for determining the extension of dissection and the relation of its dissecting membrane to major branches of the aorta. The perfusion of abdominal organs, and often of their arteries, can be seen easily. In the case of organ malperfusion, angiography may be helpful to determine whether the ischaemia is caused by the dissecting membrane of the aorta or whether the dissection extends into the organ arteries.6 Magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) are effective alternatives in the diagnosis of patients with dissection and renal failure.7 [Q4: A–D]

Without treatment, the prognosis of acute aortic dissection is very poor. In 1958, Hirst et al. reviewed 505 cases of aortic dissection and found that 21% of patients died within 24 h of onset and only 20% survived the first month.3 Causes of death in patients with Stanford A dissection include intrapericardial and free intrapleural rupture, acute aortic valve insufficiency, and, to a minor extent, cerebral and coronary malperfusion. In patients with type B dissections, free rupture of the aorta is less frequent. Dissection of the descending aorta may lead, in about 30% of cases, to obstruction of visceral, renal and extremity arteries, resulting in visceral ischaemia, renal insufficiency and acute limb ischaemia, which may be lethal without prompt and adequate therapy.8–10

[Q3: A, C, E]

To improve the natural course of the disease, in 1955 de Bakey et al. started to treat acute aortic dissections surgically. Within only a few years, they had developed the current principles of operative intervention in acute Stanford A dissection with replacement of the ascending aorta by a graft in cardiopulmonary arrest. Their results were outstanding, with an overall mortality of 21%.1,11

However, the surgical experiences of other workgroups were not so successful. Therefore, Wheat et al. developed a new medical treatment with ganglionic blockers, sodium nitroprusside or beta-blockers to influence the hydrodynamic forces of the bloodstream based on the theory that blood pressure and the steepness of the pulse wave are propagating the dissecting haematoma.12 In 1979, a meta-analysis of 219 patients with acute aortic dissection from six centres revealed that Stanford A patients treated medically had a mortality of 74%, whereas 70% of patients survived after surgical therapy. On the other hand, in patients with acute type B dissection, drug therapy alone had a survival rate of 80%, whereas 50% died after operative intervention.13 Therefore in most centres, current therapy for acute dissection type Stanford A is surgical,14–17 and for uncomplicated Stanford B dissection it is medical.18–22 [Q2: A, D, E]

An acute dissection, involving the ascending aorta, should be considered a surgical emergency. The aim of operative intervention is to prevent or treat dilation or rupture of theaorticroot,andtomaintainaorticvalvefunction.Thefollowingreconstructiveapproach is recommended: in patients in whom the root is not involved by dissection, a tubular graft is anastomosed to the sinotubular ridge. In the presence of commissural detachment, the valve is resuspended before supra-commissural graft insertion. If the aortic valve is affected by congenital or acquired abnormalities, then it is generally replaced.15

Patients with acute uncomplicated Stanford B dissection should be treated medically. Careful monitoring is obligatory, while antihypertensive drugs, such as beta-blockers,23 and analgesics are administered. The aim of treatment is to stabilise the dissected aortic wall within 2 weeks and to prevent further extension of dissection or perforation. Careful clinical and laboratory examinations are necessary to detect symptoms of organ or extremity malperfusion in time. Limb, renal and visceral ischaemia can be observed frequently, but paraplegia due to malperfusion of intercostal arteries is rare.6, 8–10

If peripheral vascular complications occur, several therapeutic strategies are possible. Newer publications describe endovascular procedures, for example emergency aortic stenting to close the “entry” and the false aortic lumen.24–27 Ultrasound-guided endovascular catheter aortic membrane fenestration was performed to restore the blood flow to the aortic branches. Dilation and stenting of dissected organ or iliac arteries were performed to resolve stenosis and restore blood flow.28–30 These new therapeutic methods need to be evaluated in long-term follow-up.

Aortic surgery in the acute stage of aortic dissection is a dangerous procedure. The dissected aortic wall is extremely friable and does not hold sutures well. Therefore we, and many other centres, try to leave the aorta itself untouched and to restore organ or extremity blood flow by extra-anatomical bypass procedures. Extra-anatomical revascularisation also becomes necessary if the aortic branches themselves are dissected.6, 8, 15 Normally, we use one common iliac artery as the donor vessel for extra-anatomical bypass grafting, but the distal lumbar aorta might also be suitable. If only one aortic branch requires revascularisation, then the iliac-visceral bypass is performed with the saphenous vein (Fig. 7.1). If two or more branches are affected, then a Dacron graft is used and the visceral arteries can be implanted into the graft directly or via interposition of the saphenous vein (Fig. 7.4). Blood flow to the legs can be restored with a femoral-femoral crossover bypass or with an axillo-(bi)-femoral graft. If several organ arteries are occluded by the aortic dissecting membrane, and the visceral arteries are undissected, then abdominal aortic fenestration

and membrane resection combined with thrombectomy of the organ arteries can also be performed.31–34 We prefer the latter to treat paraplegia caused by acute aortic dissection.

[Q5: D]

Our only indication for total aortic replacement in the acute stage of dissection is aortic penetration or perforation.

References

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