Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3745_Библиотеки_им_академика_М_И_Перельмана
.pdf
46 Vascular Surgery
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Fig. 5.1.
Chest X-ray demonstrating tortuous and dilated descending thoracic aorta suggestive of a thoracoab-
dominal aorta.
Question 2
Which of the following studies should be performed in this patient in order to plan
therapy?
A. Aortography.
B. Computed tomography (CT) scan of chest.
C. Carotid duplex studies.
D. Cardiac stress test.
E. Arterial blood gas (ABG) analysis.
The CT scans of the chest and aortagram shown in Figs 5.2 and 5.3 were obtained.
Findings were consistent with a thoracoabdominal aneurysm without concomitant
dissection of the aorta. There was no evidence for acute leak or rupture, and the
maximal diameter of the thoracic aorta was 7.3 cm.
Question 3
Briefly describe the Crawford classification system for thoracoabdominal aortic
aneurysms TAAs).

Thoracoabdominal Aortic Aneurysm 47
Fig. 5.2.
CT scan demonstrating aneurysmal dilation of the descending thoracic aorta.
Fig. 5.3.
Aortagram of patient in Fig. 5.2 showing tortuosity of aneurysmal aorta. Note the disparity between
lumen size and aortic diameter, indicating a significant amount of mural thrombus.

48 Vascular Surgery
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
The patient underwent a cardiac stress test, which was normal. Carotid duplex
studies revealed bilateral stenoses of less than 50 per cent. ABG analysis showed pH
7.38, pCO
42 and pO276 on room air.
2
Question 4
Which of the following management schemes seems most reasonable for this
patient?
A. Observation with annual follow-up chest CT.
B. Repair of thoracoabdominal aneurysm after bilateral carotid endarterectomies.
C. Cardiac catheterisation followed by repair of TAA.
D. Elective repair of TAA.
The patient is scheduled for elective repair of his TAA. He expresses concern
about the possibility of complications from the surgery. You explain to him the
most likely complications related to this surgery.
Question 5
List the four most common complications following TAA repair.
The patient seems most concerned about the risk of postoperative paralysis. You
explain to him that there are things you can do to decrease his risk of suffering this
complication, although nothing can eliminate the risk.
Question 6
List four technical modifications that may be beneficial in the prevention of spinal
cord dysfunction following TAA repair.
The patient undergoes repair of TAA and tolerates the procedure well.
Postoperatively, the chest tubes are draining 100–150 cm
3 h. In addition, urine output is steady at 500 cm3/h. The patient has transient drops
in blood pressure to a systolic blood pressure in the 70s, with central venous pressure dropping to 5 mm Hg.
3
blood/hour for the first
Question 7
(a) Describe the initial work-up and potential correction of the bleeding problem
described above in order to prevent a return to the operating room. (b) What fluid
resuscitation approach should be taken to stabilise this patient’s haemodynamic
status?
The patient’s temperature is 34.6°C, international normalised ration (INR) is 1.7
and prothrombin time (PTT) is 50 s (control, 34 s). Platelet count is 33,000. After

Thoracoabdominal Aortic Aneurysm 49
infusion of warm fluids, the use of a warming blanket, and platelet and fresh
frozen plasma (FFP) transfusions, the parameters return to normal and the
drainage from the chest tubes decreases to about 10–20 cm
postoperative day, the patient is noted to have loss of motor function in his lower
extremities.
3
/h. On the second
Question 8
What therapeutic intervention may, if carried out in a timely fashion, restore this
patient’s neurological function partially or fully?
Following appropriate intervention, the patient’s neurological function returns to
normal. The patient’s recovery is otherwise uneventful, and he is discharged on
postoperative day 8 with clean incisions, intact neurological status and adequate
analgesia.
Question 9
What is this man’s approximate predicted 5-year survival?
Commentary
TAAs are less common than infrarenal abdominal aortic aneurysms. One population-based study suggested an incidence of 5.9 TAAs per 100,000 person-years [1].
Although TAAs are more common in males, the male : female ratio of 1.1–2.1 : 1 is
not as weighted as the ratio of abdominal aortic aneurysm (AAA). The aetiology of
TAAs is related to atherosclerotic medial degenerative disease (82 per cent) and
aortic dissection (17 per cent) in most cases [2]. About 45 per cent of TAAs are
asymptomatic and detected during work-up of other systems, usually on chest Xray or cardiac echo exam. Patients tend to be older than AAA patients and therefore
may have more severe comorbidities. When present, symptoms are usually pain
related to compression of adjacent structures by the aneurysm or cough from compression/erosion of airways. Fistulisation into the bronchial tree can lead to massive
haemoptysis, while erosion into the oesophagus can result in upper-gastrointestinal
bleeding. Acute, severe pain may reflect leak, acute expansion or dissection of the
aneurysm and may require more urgent evaluation and treatment. The risk factors
associated with TAA are smoking, hypertension, coronary artery disease, chronic
obstructive pulmonary disease, and disease in other vascular beds. Syphilitic
aneurysms are a rare cause of TAA in this era and usually involve the ascending
aorta. Other causes of vague chest and back pain in a patient such as this include
myocardial ischaemia, pulmonary neoplasm, acute dissection, pneumonia, and
bony metastases. [Q1: C] The clinical and X-ray findings in this particular case argue
against these other possibilities.
The work-up of patients with TAA requires assessment of the aneurysm extent
and size, as well as of the condition of the remaining aorta. [Q2: A, B, C, D, E] Before
any studies are carried out, a thorough history and physical examination, including
vascular assessment, are needed. Currently, aortography remains an important tool

50 Vascular Surgery
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
for defining the extent of TAA as well as the status of aortic branches, but CT exam
is the most useful diagnostic test. Helical CT scanning and CT angiography are
rapidly becoming more precise in terms of delineating extent of aneurysm, as well
as diameter, presence of dissection, presence of leak, and involvement of aortic
branches. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) continue to improve and offer benefits over CT such as lack of radiation and non-nephrotoxic contrast agents. MRA has not yet achieved the
resolution of conventional angiography, and its use is contraindicated in unstable
patients. Transoesophageal echocardiography can assess the status of the aortic
valve as well as cardiac function. Significant aortic insufficiency is a contraindication to thoracic aortic cross-clamping unless a shunt or pump is used to bypass
the left heart. In addition to assessment of the aneurysm, the high incidence of
comorbidities in this patient population mandates thorough evaluation of cardiac
as well as pulmonary reserve. Preoperative studies should include EKG and
cardiac stress testing. Further work-up will be dictated by the presence of positive
findings. Screening chest X-ray and preoperative ABG will provide information
regarding pulmonary status. Formal pulmonary function tests should be reserved
for those patients with evidence of significant pulmonary compromise. Since the
risk factors for TAA are the same as those for atherosclerotic disease, a careful
history and physical will dictate whether there is a need to work up disease in
other beds (carotid, mesenteric, renal, lower extremity). Carotid duplex studies
may be done routinely preoperatively and significant stenoses treated before TAA
repair. The status of the patient’s clotting system must be determined and optimised if necessary. In the absence of indications to carry out other operations first,
this patient with a TAA of >6 cm should undergo elective repair of his aneurysm.
[Q4: D] Observation with follow-up imaging studies is dangerous and puts the
patient at risk of death due to aneurysm rupture.
The Crawford classification [Q3] is used to characterise TAAs (Fig. 5.4) [3].
According to this system, aneurysms beginning just distal to the left subclavian
artery and involving the aorta up to but not below the renals are termed type I. Type
II begin aneurysms begin just beyond the left subclavian and continue into the
infrarenal aorta. Type III aneurysms involve the distal half of the thoracic aorta and
varying extents of the abdominal aorta, while type IV refers to those aneurysms
involving the entire abdominal aorta, up to the diaphragm and including the visceral segments. This classification scheme has been useful for predicting morbidity
and mortality following repair of TAAs. In the case of non-dissecting TAA, the four
types occur with approximately equal frequency.
The natural history of TAAs is related to size and growth rate. Understanding
the behaviour of these lesions is of crucial importance when determining treatment. Crawford’s series of 94 TAAs followed for 25 years demonstrated 2-year
survival of 24 per cent, with about half of deaths due to rupture [4]. This series
included dissected as well as non-dissected aneurysms. A more recent series of
non-dissected TAAs revealed rupture rates of 12 per cent at 2 years and 32 per
cent at 4 years; for aneurysms greater than 5 cm in diameter, rupture rates
increased to 18 per cent at 2 years [5]. Rupture is very uncommon in aneurysms
measuring less than 5 cm in diameter. Another risk factor for rupture seems to be
expansion rate, with aneurysms growing more than 5 mm in 6 months at higher
risk than those growing more slowly. Survival in nonoperated patients was 52 per
cent at 2 years and 17 per cent at 5 years. Patients who underwent repair of TAA
had a 5-year survival of 50 per cent. Another series revealed 61 per cent 5-year

Thoracoabdominal Aortic Aneurysm 51
Fig. 5.4.
Crawford classification of thoracoabdominal aortic aneurysms, types I–IV.
Reproduced from Morrissey NJ, Hamilton IN, Hollier LH. Thoracoabdominal aortic aneurysms. In: Moore W,
editor. Vascular surgery: a comprehensive review. Philadelphia: WB Saunders, 2001; 417–434, with permission
from Elsevier.
survival following TAA repair. Survival decreased to 50 per cent for patients with
dissecting TAA [6]. [Q9]
Operative repair is usually through a left thoracotomy with a paramedian abdominal extension, depending on the distal extent of the aneurysm. A retroperitoneal
approach to the abdominal segment is used. The distal extent of the aneurysm
determines which intercostal space will be used for a thoracotomy. The incision is
in the fourth or fifth intercostal space for type I or high type II TAA, while an incision in the seventh, eighth or ninth space is appropriate for types III or IV [7].
Careful identification and reimplantation of visceral vessels is important, as is reattachment of intercostal arteries when feasible. Successful repair of TAA results from
careful yet quick technique, as well as maintenance of optimal physiology by the
anaesthesia and surgical teams. Distal aortic perfusion is accomplished either with
left heart bypass and selective visceral perfusion or an axillary-femoral artery
bypass before thoracotomy. Distal aortic perfusion manoeuvres are important for
the prevention of major systemic morbidity following TAA repair.
Patients undergoing TAA repair frequently are older and have significant cardiac,
pulmonary and other vascular comorbidities. These factors, combined with the
magnitude of the operation and extent of aortic replacement, can lead to significant
rates of mortality and serious morbidity. [Q5] Pulmonary complications remain
most common and result from a combination of preoperative tobacco use, chronic
obstructive pulmonary disease (COPD), and the effect of the thoracoabdominal
incision on postoperative pulmonary mechanics. Reperfusion injury may also lead

52 Vascular Surgery
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
to pulmonary microvascular injury and subsequent pulmonary dysfunction [8].
Cardiac complications remain the next most common, in spite of preoperative
cardiac optimisation. Avoidance of hypotension, close monitoring perioperatively
with pulmonary artery catheters, and minimisation of strain on the left ventricle
can help decrease postoperative cardiac dysfunction. Using the bypass circuit to
control ventricular afterload can reduce the risk of cardiac complications [9]. Renal
insufficiency preoperatively increases the risk of postoperative renal failure.
Minimising ischaemic time, selective renal perfusion during cross-clamping, distal
aortic perfusion techniques, and avoidance of hypovolaemia are important in preventing renal failure [10].
Perhaps the most devastating complication following TAA repair is paraplegia.
Despite years of research and development of protective strategies, paraplegia rates
following TAA repair remain between 5 and 30 per cent, with an average of 13 per
cent [6]. Risk factors for postoperative paraplegia include extent of aneurysm,
cross-clamp time, postoperative hypotension, and oversewing of intercostal arteries. Cross-clamp times of less than 30 min are generally safe, while those in the
range of 30–60 min are associated with increasing risk; cross-clamp times of more
than 60 min carry the highest risk for neurological complications (Fig. 5.5).
Minimising cross-clamp time and avoiding hypotension will decrease the risk of
paraplegia. Sequential reperfusion of intercostal vessels by moving the cross clamp
caudally as segments are reimplanted is useful to re-establish flow to these vessels
quickly. In addition, avoiding prolonged mesenteric ischaemia, which may worsen
reperfusion injury to the lungs, heart and possibly spinal cord through release of
cytokines, is beneficial.
Numerous adjuncts have been studied for their ability to prevent paraplegia. [Q6]
The use of cerebrospinal fluid (CSF) drainage to keep CSF pressure at less than
10 mm Hg has been shown to decrease the incidence of postoperative paraplegia
when combined with distal aortic perfusion and/or moderate hypothermia [11].
Fig. 5.5.
Probability of postoperative paraplegia as a function of aortic cross-clamp time.
Reproduced from Svensson L, Loop F. Prevention of spinal cord ischemia in aortic surgery. In: Yao JT, editor.
Arterial surgery. New York: Grune & Stratton, 1988; 273–85, with permission from Elsevier.

Thoracoabdominal Aortic Aneurysm 53
Reimplantation of intercostal vessels is most likely beneficial in preventing postoperative paraplegia, provided this manoeuvre does not excessively prolong clamp
time [12]. Epidural cooling by continuous infusion of cool saline via a catheter has
been reported to decrease the incidence of paraplegia following TAA repair [13].
Preoperative angiographic localisation of the artery of Adamkiewicz followed by
successful reimplantation of this vessel during surgery has resulted in no neurological sequelae in one series [14]. Patients who did not have preoperative localisation,
or in whom reimplantation was unsuccessful, had a 50 per cent paraplegia rate.
These results have not been reproduced, and angiographic localisation has not
gained widespread acceptance. General anaesthetic agents can also help to prevent
paraplegia, with propofol being the most protective. When left heart bypass is performed using pump techniques, moderate hypothermia can be used to protect the
spinal cord. Other pharmacological adjuncts that may be beneficial include steroids
and mannitol. Free-radical scavengers and inhibitors of excitatory neurotransmitter
pathways have shown benefit experimentally but have not been proven clinically
[15]. At present, the best strategy for preventing spinal cord complications appears
to involve a combination of physiological optimisation of the patient perioperatively, intraoperative use of spinal drainage and some form of distal aortic perfusion, reimplantation of patent intercostal vessels, and minimisation of cross-clamp
time. Other protective adjuncts are used based on surgeon preference and experience. Fig. 5.6 summarises the pathophysiology and prevention of neurological
injury following TAA repair.
Some patients, as in the case we present here, will awake neurologically intact
only to develop paraplegia hours to days later. [Q8] This phenomenon of delayedonset paraplegia may represent reperfusion injury to areas of the spinal cord at
risk from intraoperative hypoperfusion. Avoidance of postoperative hypoperfusion may decrease the incidence of this complication. The epidural catheter is left
in place for 3 days postoperatively. In cases of delayed-onset paraplegia,
maintenance of CSF pressure below 10 mm Hg may permit restoration of function. There are anecdotal reports of reversal of delayed-onset paraplegia by placement of an epidural catheter after onset of paralysis and removal of CSF to
decrease pressure to below 10 mm Hg [16]. Lowering the CSF pressure may
increase cord perfusion pressure enough to rescue the threatened regions of neuronal tissue. Lowering the CSF pressure to below 5 mm Hg may cause intracerebral haemorrhage, therefore the pressure must be monitored closely and
maintained in the safe range.
Repair of a TAA represents a major physiological insult. Excellent anaesthesia
care and monitoring are essential components of a successful operation.
Postoperatively, large volumes of urine output must be replaced on a 1 : 1 basis in
order to avoid hypovolaemia. Use of warmed, balanced electrolyte solutions is preferred. Hypocoagulability in the postoperative period is usually related to incomplete replacement of clotting factors and hypothermia. [Q7] In addition,
supracoeliac aortic clamping has been shown to result in a state of fibrinolysis that
may exacerbate bleeding [17].The aneurysm itself can be responsible for chronic
coagulation factor consumption and a subsequent increased tendency to perioperative hypocoagulability [18]. Ongoing bleeding after TAA repair may require reoperation, and results in an increase in major morbidity and mortality. It is important to
ensure that the PTT and partial thromboplastin times are corrected with plasma
transfusions. Platelets should be replaced if thrombocytopoenia occurs in the face
of ongoing bleeding. Hypothermia is a serious problem and can lead to failure of

54 Vascular Surgery
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
a
b
Fig. 5.6.
aneurysm surgery. Potential preventive interventions are also outlined.
Reproduced from Morrissey NJ, Hamilton IN, Hollier LH. Thoracoabdominal aortic aneurysms. In: Moore W,
editor. Vascular surgery: a comprehensive review. Philadelphia: WB Saunders, 2001; 417–434, with permission
from Elsevier.
Algorithm describing pathophysiology of spinal cord dysfunction following thoracoabdominal

Thoracoabdominal Aortic Aneurysm 55
coagulation. Since hypothermia is often used intraoperatively as a spinal cord protective measure, it may persist as a problem postoperatively. Aggressive correction
with warm fluids, blood products and warming blankets is needed to restore normothermia and proper function of coagulation as well as other enzymatic systems.
Reoperation is reserved for ongoing significant bleeding following correction of
coagulopathy and hypothermia. Reoperation for bleeding results in mortality rates
of 25 per cent or greater in these patients [19].
References
1. Bickerstaff LK, Pairolero PC, Hollier LH, Melton LJ, Van Peenen HJ, Cherry KJ, et al. Thoracic aortic
aneurysms: a population based study. Surgery 1982;92:1103–8.
2. Panneton JM, Hollier LH. Nondissecting thoracoabdominal aortic aneurysms: part I. Ann Vasc Surg
1995;9:503.
3. Crawford ES, Crawford JL, Safi HJ, Coselli JS, Hess KR, Brooks B, et al. Thoracoabdominal aortic
aneurysms: preoperative and intraoperative factors determining immediate and long term results of
operations in 605 patients. J Vasc Surg 1986;3:389–404.
4. Crawford ES, DeNatale RW. Thoracoabdominal aortic aneurysm: observations regarding the natural
course of the disease. J Vasc Surg 1986;3:578–82.
5. Cambria RA, Gloviczki P, Stanson AW, Cherry K, Bower TC, Hallet JW, Pairolero PC. Outcome and
expansion rate of 57 thoracoabdominal aortic aneurysms managed nonoperatively. Am J Surg
1995;170:213–17.
6. Panneton JM, Hollier LH. Dissecting descending thoracic and thoracoabdominal aortic aneurysms:
part II. Ann Vasc Surg 1995; 9:596–605.
7. Hollier LH. Technical modifications in the repair of thoracoabdominal aortic aneurysms. In:
Greenlagh RM, editor. Vascular surgical techniques. London: WB Saunders, 1989; 144–51.
8. Paterson IS, Klausner JM, Goldman G, Pugatch R, Feingold H, Allen P, et al. Pulmonary edema after
aneurysm surgery is modified by mannitol. Ann Surg 1989;210:796–801.
9. Hug HR, Taber RE. Bypass flow requirements during thoracic aneurysmectomy with particular
attention to the prevention of left heart failure. J Thorac Cardiovasc Surg 1969;57:203–13.
10. Kazui T, Komatsu S, Yokoyama H. Surgical treatment of aneurysms of the thoracic aorta with the aid
of partial cardiopulmonary bypass: an analysis of 95 patients. Ann Thorac Surg 1987;43:622–7.
11. Safi HJ, Hess KR, Randel M, Iliopoulos DC, Baldwin JC, Mootha RK, et al. Cerebrospinal fluid
drainage and distal aortic perfusion: reducing neurologic complications in repair of thoracoabdominal aortic aneurysm types I and II. J Vasc Surg 1996;23:223–9.
12. Safi HJ, Miller CC 3rd, Carr C, Iliopoulos DC, Dorsay DA, Baldwin JC. Importance of intercostal
artery reattachment during thoracoabdominal aortic aneurysm repair. J Vasc Surg 1998;27:58–68.
13. Cambria RP, Davison JK, Zannetti S, L’Italien G, Brewster DC, Gertler JP, et al. Clinical experience
with epidural cooling for spinal cord protection during thoracic and thoracoabdominal aneurysm
repair. J Vasc Surg 1997;25:234–43.
14. Webb TH, Williams GM. Thoracoabdominal aneurysm repair. Cardiovasc Surg 1999;7:573–85.
15. Wisselink W, Money SR, Crockett DE, Nguyen JH, Becker MO, Farr GH, Hollier LH. Ischemia-reperfusion of the spinal cord: protective effect of the hydroxyl radical scavenger dimethylthiourea. J Vasc
Surg 1994;20:444–50.
16. Hollier LH, Money SR, Naslund TC, Proctor CD Sr, Buhrman WC, Marino RJ, et al. Risk of spinal
cord dysfunction in patients undergoing thoracoabdominal aortic replacement. Am J Surg
1992;164:210–14.
17. Gertler JP, Cambria RP, Brewster DC, Davison JK, Purcell P, Zannetti S, et al. Coagulation changes
during thoracoabdominal aneurysm repair. J Vasc Surg 1996;24:936–45.
18. Fisher DF, Yawn DH, Crawford ES. Preoperative disseminated intravascular coagulation caused by
abdominal aortic aneurysm. J Vasc Surg 1986;4:184–6.
19. Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 patients undergoing
thoracoabdominal aortic operations. J Vasc Surg 1993;17:357–70.
Соседние файлы в папке Библиотека им академика М.И. Перельмана
