Abdominal Aortic Aneurysm

Description

The normal aortic diameter is approximately 20 mm (2 cm). The aorta is considered widened, dilated, or aneurismal when it increases to 1.5 times the normal diameter.
Patients may present perioperatively for aneurismal repair as well as for nonvascular surgeries with a known (or unknown) diagnosis of an abdominal aortic aneurysm.

Epidemiology

Incidence

12–19% of patients with an AAA have a first-degree relative with a history of AAA.
Total incidence in the adult population: 2–4%

Prevalence

Approximately 90% of AAAs that are found incidentally on screening are <3.5 cm.
Most common age 65–75 years
Male:female 7:1
Infrarenal aneurysms comprise ~90% of AAAs.

Mortality

Mortality: Ruptured AAA is the 13th leading cause of death in the US, causing an estimated 15,000 deaths per year.
AAA rupture is usually fatal (70–80%) and only 50% present to the hospital alive.

Etiology/Risk Factors

Chronic smokers (4 times more likely than nonsmokers) (1)
Male gender
Atherosclerosis
Hypertension
Marfan syndrome, Ehlers–Danlos syndrome, syphilis, trauma, mycotic infection (rare causes)

Physiology/Pathophysiology

The extracellular matrix is comprised of elastin and collagen, which provides tensile strength. Tensile strength is defined as the maximum stress that a material can withstand while being stretched or pulled before being deformed or broken. Thus, they provide a necessary function to the aorta—to endure the pulsatile, high pressures of blood being ejected from the left ventricle.
The pathogenesis of aneurysms involves alterations in the connective tissue of the aortic wall. It has been proposed that adventitia elastin degradation is a primary, and hallmark, event that leads to AAA formation; collagen disruption is the ultimate cause of rupture.
Inflammation is believed to play a role with macrophages and T lymphocytes capable of:
- Producing proteolytic enzymes that can cause protein degradation
- Causing smooth muscle apoptosis
- Releasing pro-inflammatory cytokines
Degradation that results in weakening of the aortic wall and aneurysmal development can result from a number of different causes:
- Arteriosclerosis most commonly affects the abdominal aorta (compared to the thoracic). It is also more likely to result in aneurysm (compared to stenosis in the infrarenals).
- Infection
Laplace's law states that T = (R × P)/H, where T is tension, R is radius, P is change in pressure, and H is wall thickness. Thus, vessel diameter widening, increased arterial pressures, and decreased wall thickness result in increased tension; the increased tension can serve to further exacerbate the size of the aneurysm.
Morphology: A fusiform aneurysm has a fairly uniform shape, with symmetrical dilation that involves the full circumference of the aortic wall. Saccular aneurysms have a localized dilation that appears as an outpouching of only a portion of the aortic wall. A pseudoaneurysm is not an aneurysm, but instead, is a well-defined collection of blood and connective tissue outside the vessel wall.

Anesthetic Goals/Guiding Principles

Patients with a diagnosis of AAA often have comorbid cardiovascular conditions such as cerebrovascular, coronary, or renal disease.
Both the size and rate of growth of aneurysm are important when determining the need for intervention.

Diagnosis ⬆ ⬇

Symptoms

Usually asymptomatic
Expanding AAA may present with abdominal or back pain (due to pressure on surrounding tissues) or pain in the legs (due to disturbed blood flow).
Ruptured AAA: Classic triad (hypotension, back pain, pulsatile abdominal mass) presents in only 1/2 of patients.

History

How and when the AAA diagnosed; any change in size, current plan of treatment
Risk factors
Comorbid conditions; patients are considered "vasculopaths" and disease in other vessels should be considered until proven otherwise.

Signs/Physical Exam

Presence of an abdominal bruit or lateral propagation of the aortic pulse wave offers subtle clues and may be more frequently found than a pulsatile mass.

Medications

No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs. There may be some protective effects with ACE inhibitors, beta-blockers, and statins.
- Beta-blockers can reduce cardiac morbidity and mortality and should be continued perioperatively. HR control and decreased contractility result in less systolic pressure generated against the aneurysm wall.
- Statins’ pleiotropic effects have been shown to decrease postoperative cardiac, cerebral, and renal morbidity in patients undergoing major vascular surgery; should be continued perioperatively.

Diagnostic Tests & Interpretation

Labs/Studies

Electrolytes, CBC, BUN/CR, PT/PTT
12-lead EKG
Echocardiography, stress testing, and coronary angiography may be indicated to evaluate the myocardium.
Carotid ultrasound if bruits are present, especially if history of stroke or TIA.
Ultrasound report should be reviewed even in patients presenting for nonvascular surgery.
CT scan with contrast or MRA is typically performed when patients present for repair; provides information on the position, diameter, and involvement of the mesenteric vessels.
Type and crossed units for open AAA repair

Concomitant Organ Dysfunction

Aortic disease is indicative of other atherosclerotic diseases including coronary, cerebral, peripheral vascular, and renal diseases.
Chronic obstructive pulmonary disease
Diabetes mellitus

Circumstances to Delay/Conditions

In patients presenting for nonvascular surgery, symptomatic and large aneurysms (i.e., >5.5 cm in diameter) as well as growth >1 cm/year should be considered for endovascular or surgical repair.
Acute coronary or cerebral event

Classifications

There are many classification systems in determining the risk of AAA rupture which take into account the rate of increase, size, comorbid factors, etc (2).
Biggest predictors of risk of rupture (annually) are diameter of the aneurysm and rate of expansion.
- <4.0 cm in diameter = <0.5%
- 4.0–4.9 cm in diameter = 0.5–5%
- 5.0–5.9 cm in diameter = 3–15%
- 6.0–6.9 cm in diameter = 10–20%
- 7.0–7.9 cm in diameter = 20–40%
- >8.0 cm in diameter = 30–50%

Treatment ⬆ ⬇

PREOPERATIVE PREPARATION

Premedications

Anxiolytics as needed; anxiety may increase BP and the risk of AAA rupture.
Beta-blockers may be titrated to heart rate goals, particularly if taking chronically.
Perioperative statin therapy initiation may be indicated for their pleiotropic effects.

INTRAOPERATIVE CARE

Choice of Anesthesia

Non vascular procedures: Based on the type of surgery, patient comorbidities, and physical exam
Open AAA repair: Neuraxial techniques may be appropriate; however, traumatic placement may necessitate the delay of surgery (patients are heparizined intraoperatively).

Monitors

Standard ASA monitors
Non vascular procedures: Additional monitoring depends on the surgery and patient comorbidities.
Open AAA repair:
- 2 large-bore peripheral IVs or a central introducer sheath for possible rapid fluid and blood administration
- Arterial line to assess rapid hemodynamic changes and the potential for hypotension and MI; may be placed pre-induction.
- Pulmonary artery catheter may be indicated when pulmonary vascular resistance, cardiac output, and mixed venous oxygen saturation can help guide therapy.
- TEE may be indicated to evaluate myocardial function and detect regional wall motion abnormalities.

Induction/Airway Management

A slow, controlled induction is necessary to ensure an adequate depth of anesthesia and minimize hemodynamic changes. Hypotension can impair perfusion, while hypertension can result in aneurysmal rupture (transluminal pressures, coughing, bucking, etc.).
Short-acting agents, such as esmolol and nitroglycerin, may be necessary to blunt the patient's response to tracheal intubation and the subsequent increased tension against the aneurysmal wall that could result in rupture.

Maintenance

Maintenance agents (non vascular and AAA repairs): Balanced volatile or intravenous techniques may be utilized.
Hemodynamics (non vascular and AAA repairs): Close titration of intravenous and inhalation agents with an emphasis on reducing tension against the aneurysmal wall. Maintaining HR and MAP within 20% of baseline is generally appropriate (3).
- Short-acting drugs permit a rapid termination of effect, if desired, and allow for enhanced titration.
- Opioids, beta-blockers, and vasodilating drugs can be used to control pain and BP. Esmolol has ultra-short action and organ-independent elimination making it particularly useful.
Aggressive fluid replacement may cause dilutional and hypothermic coagulopathy. This can result in secondary clot disruption from increased blood flow, increased perfusion pressure, and decreased blood viscosity thereby exacerbating bleeding.

Extubation/Emergence

Standard extubation criteria; special attention to blood loss, hemodynamics, and normothermia. Consider postoperative intubation in complicated AAA repairs or with significant comorbidities.
Smooth extubation (avoid coughing and bucking)
Control of hypertension and tachycardia is important; consider beta-blockers and/or vasodilators.

Follow-Up ⬆ ⬇

Bed Acuity

Non vascular repair: Depends on surgery, comorbidities, intraoperative course
AAA repair: ICU or monitored setting, given the high risk of cardiac complications. (MI occurs more frequently postoperatively than intraoperatively). The postoperative period is marked by increased myocardial oxygen demand, increased catecholamine levels, hypoxia, hypercoagulability, and large fluid shifts. Consider supplemental oxygen (nasal cannula, face mask), incentive spirometry and deep breathing, and early mobilization.

Complications

In AAA procedures, cardiac complications, such as myocardial ischemia or infarction are most commonly seen. Additionally, hemorrhage or coagulopathy, peripheral embolization, and aortocaval or aortoduodenal fistula can occur.

section name header

Basics ⬇