Open Repair of Abdominal Aortic Aneurysms and Postoperative Assessment

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CHAPTER 104 Open Repair of Abdominal Aortic Aneurysms and Postoperative Assessment

Most surgeons agree that repair should be considered for abdominal aortic aneurysms (AAAs) larger than 50 to 55 mm in diameter. Open surgical repair was the mainstay of treatment for AAA until the 1990s. This procedure is associated with a low mortality rate in select patients. However, it is also a major operation, with the potential for significant blood loss, stress on the cardiopulmonary system, and a prolonged hospital stay. In particular, patients who have significant comorbidities have a significantly increased mortality risk associated with the procedure. In such patients, endovascular repair may be considered.

A limitation of endovascular repair, however, is that patients with certain types of vascular anatomy are not candidates for the procedure. For example, some length of nonaneurysmal infrarenal aorta (depending on the device used) must be present for placement of the proximal attachment of the endovascular graft. Most operators prefer that the neck have a minimum caliber of 1.5 cm. Aortic neck angles more than 45 degrees are often problematic for proper endograft implantation and may result in excessive stress on the device. Trapezoidal, conical, or thrombus-filled aortic necks may cause device instability. Additionally, the iliofemoral vessels must have a certain (device-dependent) caliber and straightness. In a healthy patient with any of these limitations of anatomy, open surgical repair may be the preferred option.

Open repair of an AAA involves attaching a tube or bifurcated graft within the aneurysm sac. Occasionally, however, the native AAA is excluded from the graft and remains intact posterior to the aortic graft. The transperitoneal or the retroperitoneal approach may be used. In one study, there was no significant difference in mortality rates between the two procedures, and although retroperitoneal repair was associated with less frequent respiratory failure, it was also associated with more frequent wound complications.1

There are no strict anatomic contraindications to open repair of an AAA. However, there are many anatomic variations that must be taken into account. Coexisting aneurysms of the common iliac artery, especially if larger than 3 cm, should undergo exclusion during AAA repair. Attention should also be given to possible aneurysms of the hypogastric and external iliac arteries. The common and external iliac arteries may be severely affected by atherosclerotic disease, and may require arterial bypass grafting.2 Many pararenal aortic aneurysms are now repaired via the open surgical technique because of the frequent lack of a proximal implantation site sufficient for endovascular repair. These aneurysms require greater exposure than infrarenal aneurysms, and are technically more demanding. Repair of juxtarenal, pararenal, or suprarenal aneurysms require suprarenal clamping, which are associated with increased risk for renal damage because of ischemia.

Subsequent sections in this chapter will delineate the postoperative assessment of patients who have undergone open repair of AAAs, postoperative complications that they may encounter, indications and algorithms for imaging these patients, characteristic imaging findings and, finally, postoperative management.

POSTOPERATIVE ASSESSMENT

Early Postoperative Complications

On the first postoperative day after open repair of an AAA, hypotension and cardiac and respiratory dysfunction are the most likely complications to occur. Between days 1 and 3, the most common complications are congestive heart failure, pulmonary embolism, and respiratory failure. Pneumonia occurs most commonly between 4 and 7 days following surgery. The incidence of renal failure peaks within the initial 3 days following surgery and between 1 and 4 weeks postoperatively.2 A midline transabdominal incision is associated with higher postoperative rates of pulmonary complications, persistent ileus, and incisional hernias.

Overall, perioperative complications occur in up to 30% of patients. The organs most commonly affected are the heart, lungs, and kidneys. Cardiac-related complications, including arrhythmia, infarction, and congestive heart failure, occur in about 10% to 15% of patients after elective aneurysm repair. Perioperative renal dysfunction predicts a poorer prognosis and correlates with poor preoperative renal function. Insufficient management of pulmonary disease is also associated with a poorer prognosis.2

Early postoperative complications also include groin infections (in 2% to 3%), thromboembolism to the kidneys and lower extremities, and hemorrhage. Peripheral ischemia develops in less than 1% of patients postoperatively, but may occur because of damage to diseased arteries during cross clamping, iliac dissection, or peripheral embolization from aortic plaque. Spinal cord ischemia, which may result in paralysis, can occur secondary to a variety of differing factors. The artery of Adamkiewicz may arise below L3 in a minority of patients and ligation of a lumbar artery in the aneurysm sac in such a patient may lead to spinal cord ischemia. An additional cause is suprarenal or supraceliac cross clamping that compromises the spinal cord circulation. Small bowel infarction and colonic ischemia occur in 0.15% and 1% of patients undergoing elective AAA repair, respectively. Colonic ischemia most commonly develops because of ligation of the inferior mesenteric artery.2

Because of the course of the ureter over the iliac vessels, the ureter may be injured during open repair of AAAs. The ureter may have a variant course in patients with renal anomalies such as horseshoe kidney, further raising the likelihood for its injury. Ureteral fistulas with resulting urinomas may occur. Options for repair of ureteral injury include placement of a stent and reimplantation of the injured ureter into the bladder.2

Postoperative Mortality and Survival

The postoperative mortality rate for elective open repair is approximately 5%; it is lower in younger healthier patients and higher in older at-risk patients. Risk factors that increase a patient’s risk of mortality following open aneurysm repair include advanced age, female gender, and any associated comorbidities. Additional factors include the experience of the operating surgeon, need for urgent (rather than elective) repair, and hospital volume (hospitals with higher surgical volumes generally have a lower mortality rate than those with lower volumes).2

Five-year survival of patients after successful elective open AAA repair is 60% to 70% and the 10-year survival rate is approximately 40%. These survival rates are lower than those of matched patients without AAAs, and the increased mortality is mostly to the result of manifestations of atherosclerosis, especially coronary artery disease.3

The few published reports of pararenal aortic aneurysm repair describe mortality rates that vary from 0% to 15.4%. Renal morbidity rates are high in such patients.4 In one study, there was a higher risk of overall perioperative mortality for patients who underwent open repair of juxtarenal and pararenal aortic aneurysms compared with those who underwent open repair of infrarenal aortic aneurysms (12% and 3.5%, respectively; P < .02).5

The mortality for ruptured AAA ranges from 15% to 50%, often caused by hemorrhagic shock, acute renal failure, myocardial infarction, respiratory insufficiency, or multiorgan failure.6 Mortality following open repair of a ruptured AAA is 30% to 40%.

Surgical Conversion from Endovascular Repair

Conversion from endovascular to open repair may be required for a number of reasons (Table 104-1).7 Older age, presence of chronic obstructive pulmonary disease (COPD), wider infrarenal necks, and larger aneurysms have been associated with a higher rate of conversion. In one study, the mortality rate of patients who underwent emergency conversion operations was 40%.8

TABLE 104-1 Reported Reasons for Conversion from Endoluminal Graft (ELG) to Open Repair

Primary Conversion Secondary Conversion
Inability to gain access Persistent endoleak
Aortic rupture Aortic rupture
Failed deployment Sealed endoleak with continued AAA expansion
Irreversible twisting of a nonmodular ELG Apparently successful repair with continued expansion
Migration of ELG causing obstructed flow Infection in the ELG
Endograft thrombosis Renal arteries covered by the endograft

From Myers K, Devine T, Barras C, Self G. Endoluminal versus open repair for abdominal aortic aneurysms 2009. Available at: http://www.fac.org.ar/scvc/llave/interven/myers/myersi.htm. Accessed October 6, 2009.

Clinical Presentation

The vast majority of AAAs are clinically silent. Often, AAAs are detected incidentally during abdominal ultrasonography. AAA rupture should be suspected particularly in patients with known AAAs who present with pain in the low back, flank, abdomen, or groin. On physical examination, a palpable, pulsatile abdominal mass may be detected. Abdominal bruits may reflect renal or visceral arterial stenosis.

Bleeding from a ruptured AAA often leads to hypovolemic shock, the signs of which include hypotension, tachycardia, cyanosis, and altered mental status. Flank ecchymosis (the Grey-Turner sign) may be apparent, and reflects retroperitoneal hemorrhage.

Anastomotic Pseudoaneurysms

An anastomotic pseudoaneurysm is a potential late complication after repair of an AAA. It does not contain all the layers normally present in an arterial wall and are at risk for rupture. Anastomotic pseudoaneurysms most commonly result from arterial degeneration or infection.10 They may be aortic, iliac, or femoral. Degenerative anastomotic pseudoaneurysms may present in 0.2% to 15% of patients after AAA repair.1113 One study10 found the most common manifestations of such pseudoaneurysms to be bleeding caused by rupture (30%) and sequelae of chronic limb ischemia (25%). Pseudoaneurysms may also manifest with symptoms caused by compression of adjacent structures or acute limb ischemia, or as an asymptomatic pulsatile mass.

Imaging Indications and Algorithm

Computed Tomography and Computed Tomographic Angiography

In cases of planned open repair of an AAA, a preoperative contrast-enhanced CT scan is usually adequate. Contrast-enhanced CT and, in particular, CT angiography (CTA), are the primary imaging modalities for illustration and evaluation of AAAs and for the postoperative assessment of AAAs. CT and CTA are noninvasive methods that can be used to detect thrombus within the aneurysm, thus making them more accurate in sizing the full extent of AAAs (i.e., wall to wall dimension) than conventional x-ray catheter angiography. Conventional x-ray angiography may yield a falsely low estimate of aneurysm size by demonstrating only the inner luminal diameter of the aneurysm when there is thrombus adherent to the wall of the AAA. CT can demonstrate coexisting aneurysms of the iliac vessels, determine the relationship of an AAA to the renal vessels, reveal venous and renal anomalies (e.g., a retroaortic left renal vein and horseshoe kidney), and demonstrate incidental but perhaps significant intra-abdominal pathology not related to the AAA.

The clinical limitations of CT include its risks related to the use of iodinated contrast (e.g., anaphylactoid contrast reactions, contrast-induced nephropathy) and the need to subject the patient to ionizing radiation exposure. CT of patients with certain metallic implanted devices may also be problematic secondary to metallic artifacts, which may obscure proper visualization of pertinent vascular regions.

Imaging Techniques and Findings

Normal Postoperative Appearance Following Open Surgical Repair

In a patient who has undergone an open surgical repair of an AAA, the graft may be seen as a round, well-demarcated structure within the aneurysmal sac. After intravenous contrast administration on CT, the graft is seen as an enhancing tubular structure surrounded by the native aorta in cases of proximal end-to-end anastomosis (Fig. 104-1). In cases of end-to-side proximal anastomosis, the enhancing graft may be seen running ventral and parallel to the nonenhancing diseased or aneurysmal aorta, which is now collapsed (Figs. 104-2 and 104-3). The graft bifurcation is at a higher level compared with the now occluded native bifurcation in cases of aortic-bi-iliac or aortobifemoral grafts. In cases of more complicated grafts such as combined unilateral aortoiliac with or without femoral to femoral bypass, knowledge of surgical history helps the interpreting physician to follow the graft as an enhancing tubular structure from the site of the proximal to distal anastomosis. MRA (Fig. 104-4) is also well suited for imaging the aortic and iliac graft components after surgery.

Aortic Graft Infection

Aortic graft infection occurs in 1% to 5% of reconstructions.17 This complication has mortality rates of 25% to 75%.18 Aortic graft infection may lead to graft occlusion and anastomotic hemorrhage, which may lead to aortoenteric fistula.

Graft infection may occur from a few days to many years after surgery. CT is considered the imaging modality of choice for the diagnosis of graft infection (Figs. 104-5 to 104-8). One study has shown that CT has a sensitivity of 94% and specificity of 85% for the detection of perigraft infection, with or without associated aortoenteric fistula, when the criteria of perigraft fluid, perigraft soft tissue density, ectopic gas, pseudoaneurysm, or focal bowel wall thickening were used.19 CT-CTA can demonstrate persistent perigraft soft tissue density, fluid, and gas, characteristics associated with graft infection. However, abnormal perigraft soft tissue density may also represent hematoma, fibrosis, and/or postoperative changes. In this regard, MRI may be helpful because it has improved soft tissue contrast resolution and the improved ability to differentiate between subacute and chronic hematomas, thrombus, and fibrosis from perigraft fluid resulting from graft infection (Fig. 104-9).

Although the normal graft has surrounding fat attenuation in the early postoperative period, there should be less than 5 mm of soft tissue attenuation between the aneurysm wall and underlying graft. Persistent fluid or soft tissue attenuation around the graft may persist for up to 3 months after surgery. Similarly, pockets of gas around the graft may be present for up to 10 days after surgery, but persistence after about 4 weeks postsurgery suggests infection.20

Duplex ultrasound or CTA can confirm the occlusion and also reveal perigraft fluid, consistent with infection. MRI, however, has higher specificity for differentiating thrombus and fibrosis from fluid related to infection and can be used in difficult cases.

A recent study has shown that positron emission tomography (PET)-CT has a sensitivity of 93%, specificity of 91%, positive predictive value of 88% and negative predictive value of 96% for the diagnosis of vascular graft infection.21 PET alone, although highly sensitive, has low specificity and limited anatomic localization.

Aortoenteric Fistula

Secondary aortoenteric fistula is a rare but severe complication after abdominal aortic surgery, with mortality rates approaching 100%. This type of fistula accounts for most aortoenteric fistulas. They often result from infection near the proximal anastomosis between the aorta and prosthesis. It is estimated that 80% of secondary aortoenteric fistulas involve the duodenum; typically, its third and fourth parts are affected. These fistulae may occur at any time between 2 weeks and many years after surgery. The annual incidence ranges from 0.6% to 2%.18

Although contrast-enhanced CT using a CTA protocol (Figs. 104-10 and 104-11) is the favored diagnostic modality,22 its sensitivity and specificity vary (from 40% to 90% and 33% to 100%, respectively). CT conducted with oral water-soluble contrast before and after contrast-enhanced CTA is preferred for patients who are not actively bleeding to delineate the fistula from the overlying duodenum (see Fig. 104-10). Prior to intervention, other modalities (e.g., endoscopy, radionuclide studies, angiography) may be needed to arrive at the diagnosis. Conventional x-ray catheter angiography may be combined with embolization and/or stent placement for therapy.

Many other entities, such as retroperitoneal fibrosis, infected aortic aneurysm, aortitis and, most commonly, perigraft infection, may mimic aortoenteric fistula. Features that suggest aortoenteric fistula include periaortic or intra-aortic gas, breach of the aortic wall, loss of fat planes, extravasation of aortic contrast agent into the bowel lumen or para-aortic space, retroperitoneal hematoma, and hematoma in the bowel wall or lumen. Perigraft air is more often seen in association with aortoenteric fistula than with aortic graft infection alone. The most specific feature of aortoenteric fistula is extravasation of intravenously administered contrast agent from the aorta into the bowel lumen.19 Similarly, extravasation of oral water-soluble contrast from the bowel into or around the aortic graft is a specific feature of aortoenteric fistula. Ectopic gas should not persist after 3 to 4 weeks postsurgery, which suggests infection and/or fistula formation to bowel.19

POSTOPERATIVE MANAGEMENT

Most patients are followed postoperatively in the surgical intensive care unit. The patient’s hemodynamic profile is monitored continuously. Coagulation studies, complete blood count (CBC) and serum chemistries, and electrocardiograms are typically assessed. Patients with high or intermediate risk factors have troponin I levels drawn at 24 hours postprocedure and again at 96 hours postprocedure, or prior to discharge. Deep venous thrombosis and gastric ulcer prophylaxis are also typically initiated following surgical repair.2

Anastomotic Pseudoaneurysms

Surgical repair of anastomotic aortic pseudoaneurysms involves resection followed by placement of an interposition graft or vascular bypass. Endovascular repair is a good alternative,27 particularly for patients with multiple comorbidities. Some patients are not candidates for stent graft placement because of unusual anatomy or technical limitations of the stent graft.

KEY POINTS

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