UBP 5.8 (Short Form): Cardiovascular – Abdominal Aortic Aneurysm

Question 1

What is the difference between an aortic dissection and an aortic aneurysm?

(A 5’6”, 175 pound, 69-year-old male presents to the OR for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm. He has a history of CAD, CHF, HTN, and chronic kidney disease (CKD). He says that he has smoked 2 packs of cigarettes every day for the past 52 years. Medications include atenolol, lisinopril, HCTZ, sublingual NTG, and digoxin. Vital Signs: BP = 165/98 mmHg, HR = 98, R = 17, T = 36.9 C. Lab: Creatinine Clearance = 50 mL/minute.)

Answer 1

An aortic aneurysm is – an abnormal dilation of all three layers of an artery (intima, media, and adventitia) that is 1.5 times the normal diameter, while

an aortic dissection describes – a condition where blood has entered the arterial wall through a tear in the intima, resulting in a blood-filled channel within the aortic wall.

A pseudoaneurysm also describes – a situation in which a defect in the vascular wall results in the formation of an extravascular hematoma (outside the arterial wall, yet contained by surrounding tissue) that remains in free communication with the intravascular space.

Complications associated with an expanding aneurysm include –

• rupture and exsanguination (the most concerning complication);
• dilation of the aortic root, (leading to aortic regurgitation); and
• compression of proximal structures, leading to –
  
  • difficult intubation (tracheal/bronchial compression),
  • superior vena cava syndrome (compression of the superior vena cava), and
  • hoarseness (compression of the left recurrent laryngeal nerve).

Complications associated with the propagation of an aortic dissection include –

• aortic regurgitation (aortic root involvement),
• cardiac tamponade (rupture into the pericardium),
• hemothorax (rupture into the pleura), and
• the occlusion of arteries arising from the aorta.

Question 2

What is a Crawford Type II aortic aneurysm?

Answer 2

• Type II aneurysms, in the Crawford classification system of thoracoabdominal aortic aneurysms,
  
  • originate below the left subclavian artery and extend into the infrarenal abdominal aorta.
• Crawford Type I aortic aneurysms also
  
  • originate below the left subclavian artery, but extend only to involve the celiac axis and mesenteric arteries.
• Type III aneurysms
  
  • originate in the lower descending thoracic aorta and involve the remainder of the aorta (the origin is lower in the descending thoracic aorta than with Type I or Type II – originating below the 6th rib).
• Type IV aneurysms
  
  • originate at the diaphragm and involve the abdominal aorta only.
• Finally, Type V aneurysms
  
  • originate below the 6th rib (lower thoracic aorta) and extend only to the renal arteries.

Type II and III aneurysms are the most complicated to repair,

while the repair of Type II aneurysms carries the greatest risk for paraplegia and renal failure.

Question 3

What are your perioperative concerns in providing an anesthetic for this case?

(A 5’6”, 175 pound, 69-year-old male presents to the OR for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm. He has a history of CAD, CHF, HTN, and chronic kidney disease (CKD). He says that he has smoked 2 packs of cigarettes every day for the past 52 years. Medications include atenolol, lisinopril, HCTZ, sublingual NTG, and digoxin. Vital Signs: BP = 165/98 mmHg, HR = 98, R = 17, T = 36.9 C. Lab: Creatinine Clearance = 50 mL/minute.)

Answer 3

My primary concerns in managing this patient include the risk for:

1. aneurysmal rupture;
2. propagation of the aneurysm (potentially leading to –
   
   • aortic insufficiency and/or
   • cardiac tamponade),
3. myocardial ischemia/infarction (secondary to –
   
   • coronary artery disease,
   • hypertension,
   • congestive heart failure,
   • potential massive blood loss, and
   • perioperative hemodynamic instability);
4. post-operative respiratory complications (secondary to –
   
   • long-term tobacco abuse,
   • surgical manipulation of the diaphragm);
5. paraplegia (secondary to –
   
   • aneurysmal/surgical/stent disruption of radicular arteries supplying the anterior spinal cord,
   • hemodynamic instability, and
   • potential massive blood loss);
6. post-operative acute kidney injury (secondary to –
   
   • pre-existing kidney disease,
   • contrast dye utilization during the procedure,
   • aneurysmal/surgical/stent disruption of the renal arteries,
   • emboli to the renal arteries,
   • hemodynamic instability, and
   • potential massive blood loss);
7. visceral/mesenteric injury (secondary to –
   
   • hemodynamic instability,
   • potential massive blood loss, and
   • aneurysmal/surgical disruption of the superior/inferior mesenteric arteries and/or the celiac trunk);
8. stroke (secondary to –
   
   • embolization of air or thrombotic material,
   • hypertension,
   • hemodynamic instability, and
   • potential massive blood loss);
9. hemorrhage (secondary to –
   
   • aneurysm rupture,
   • vascular injury during graft deployment,
   • coagulopathy, and
   • heparinization);
10. worsening congestive heart failure (secondary to –
    
    • myocardial ischemia,
    • aortic stenosis, and
    • overaggressive fluid administration);
11. difficult airway management (secondary to –
    
    • possible aneurysmal compression of the trachea,
    • lung parenchyma, or
    • superior vena cava –>
      
      • tracheal deviation, rapid desaturation, and airway edema);
12. conversion to an open procedure (secondary to –
    
    • aneurysm rupture,
    • stent migration or malposition, or
    • significant arterial damage when establishing access for device insertion);
13. endoleak (resulting in –
    
    • pressurization of the aneurysm with possible enlargement and/or rupture); and
14. post-implantation syndrome (secondary to –
    
    • endothelial activation by the endoprosthesis).

Question 4

What is post-implantation syndrome?

Answer 4

Postimplantation syndrome is commonly observed after EAR. It is characterized by fever, elevated C-reactive protein levels, and leukocytosis in the absence of an infectious agent. It is usually mild and self-limited, lasting 2–10 days postoperatively, and responds to nonsteroidal antiinflammatory drugs.

Occasionally, an exaggerated response may result in life-threatening distributive shock, respiratory failure, and disseminated intravascular coagulation.

It is hypothesized that EAR induces a significant inflammatory response resulting in endothelial cell activation from intraaneurysmal device manipulation.

Although rare, postimplantation syndrome may manifest as a consumptive coagulopathy.

Endovascular exclusion of a large aortic aneurysm may result in significant thrombus in the excluded aneurysm sac, which can initiate fibrinolysis.

Repeated instrumentation of the aorta, which occurs with difficult endograft placement, may produce endothelial damage resulting in stimulation of a procoagulant response.

Question 5

Would you attempt to lower his blood pressure prior to surgery?

(A 5’6”, 175 pound, 69-year-old male presents to the OR for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm. He has a history of CAD, CHF, HTN, and chronic kidney disease (CKD). He says that he has smoked 2 packs of cigarettes every day for the past 52 years. Medications include atenolol, lisinopril, HCTZ, sublingual NTG, and digoxin. Vital Signs: BP = 165/98 mmHg, HR = 98, R = 17, T = 36.9 C. Lab: Creatinine Clearance = 50 mL/minute.)

Answer 5

I would attempt to lower his blood pressure and reduce his heart rate,

recognizing that hypertension and tachycardia place this patient with a dissecting aneurysm, history of congestive heart failure, and coronary artery disease at increased risk for –

• aneurysmal propagation and/or rupture, (decreasing blood pressure and the force of ventricular contractions reduces aortic wall stress by reducing shear pressure or dP/dT*),
• myocardial ischemia, and
• heart failure.

However, I would be very careful to AVOID hypotension, recognizing that patients with aortic stenosis have increased left ventricular end-diastolic pressures and left ventricular hypertrophy, making them more dependent on normal diastolic aortic pressures to provide adequate coronary perfusion.

In treating his blood pressure, I would FIRST correct any factors that may be contributing to his tachycardia and hypertension, such as – pain, hypovolemia, infection, or anemia.

If this failed to resolve the problem, I would utilize a short-acting B-blocker (i.e., esmolol) and a vasodilator (i.e., nitroprusside) to control his heart rate and blood pressure.

However, before administering a vasodilator, I would ensure adequate B-blockade were established, since failing to do so could lead to increased aortic wall stress and rupture of his aneurysm.

*dP/dT = the change in blood pressure / change in time

Question 6

Are you concerned about his renal function?

(A 5’6”, 175 pound, 69-year-old male presents to the OR for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm. He has a history of CAD, CHF, HTN, and chronic kidney disease (CKD). He says that he has smoked 2 packs of cigarettes every day for the past 52 years. Medications include atenolol, lisinopril, HCTZ, sublingual NTG, and digoxin. Vital Signs: BP = 165/98 mmHg, HR = 98, R = 17, T = 36.9 C. Lab: Creatinine Clearance = 50 mL/minute.)

Answer 6

I am concerned because –

• his pre-existing renal disease (Creatinine clearance < 60 mL/min is an independent predictor),
• increasing age, and
• hypertension –

place him at increased risk for postoperative renal dysfunction, a known complication of endovascular aortic aneurysm repair.

Even in the absence of aortic cross-clamping (which is NOT required during endovascular repair), acute postoperative kidney injury may occur secondary to –

• contrast dye exposure,
• hypoperfusion (secondary to induced hypotension during device deployment,
• temporary aortic occlusion when sealing the proximal and distal ends of the graft to the aortic wall, or significant blood loss),
• stent occlusion of renal vessels, or
• emboli to the renal arteries.
• Men (younger than age 40): 107–139 milliliters per minute (mL/min) or 1.8–2.3 milliliters per second (mL/sec)
• Women (younger than age 40): 87–107 mL/min or 1.5–1.8 mL/sec
• Creatinine clearance values normally go down as you get older (normal values go down by 6.5 mL/min for every 10 years past the age of 20).

Question 7

Would you place a CSF drain?

(A 5’6”, 175 pound, 69-year-old male presents to the OR for aortic visceral debranching followed by endovascular repair of a Crawford Type II thoracoabdominal dissecting aortic aneurysm. He has a history of CAD, CHF, HTN, and chronic kidney disease (CKD). He says that he has smoked 2 packs of cigarettes every day for the past 52 years. Medications include atenolol, lisinopril, HCTZ, sublingual NTG, and digoxin. Vital Signs: BP = 165/98 mmHg, HR = 98, R = 17, T = 36.9 C. Lab: Creatinine Clearance = 50 mL/minute.)

Answer 7

Assuming there were NO contraindications (i.e., coagulopathy), I would place a CSF drain.

Even when aortic cross clamp application is avoided, as is the case with endovascular repair,

the insertion of a lumbar drain to reduce intraoperative and postoperative CSF pressures

(target CSF pressure should be ~8-10 mmHg)

is recommended

for those at increased risk for neurologic injury, such as this patient undergoing visceral debranching and endovascular repair of the thoracic aorta (Class I recommendation).

Other spinal cord preservation strategies that would be employed or considered in this case include –

• Passive hypothermia (32-34 C),
• Avoiding intraoperative hypotension,
• Maintaining normal hematocrit and PaO2,
• Neurophysiologic monitoring (i.e., SSEPs and MEPs),
• Avoiding hyperglycemia,
• Identifying and preserving blood flow to critical intercostal arteries (reattaching them to the aortic graft or some other major vessel), and
• Pharmacologic intervention (i.e., corticosteroids, naloxone, dextrorphan, magnesium, intrathecal papaverine, naloxone, and calcium channel blockers ???).

READ & REVIEW info on this.

Question 8

The resident working with you asks you to explain the various types of endoleaks. What would you say?

Answer 8

The failure to completely isolate the aneurysmal sac from arterial blood flow is termed an endoleak.

This complication is concerning because of the potential for – pressurization of the aneurysmal sac (endotension) leading to aneurysm enlargement and rupture.

There are five types of endoleaks described.

• Type I endoleak – occurs with failure of the seal between the stent-graft and the aortic wall at the proximal or distal attachment site.
• Type II endoleak – results when retrograde flow from intercostal arteries results in filling of the aneurysm sac.
• Type III endoleak – is the result of structural failure of the stent-graft results in flow into the aneurysmal sac (usually results with inadequate overlap and seal between modular components of the graft).
• Type IV endoleak – results secondary to excessive porosity of the graft itself.
• Type V endoleak – describes a situation in which pressurization of the aneurysmal sac occurs despite the absence of an identifiable leak on imaging.

Type II and IV endoleaks are generally considered benign, rarely requiring any intervention (although type II endoleaks may lead to aneurysm enlargement).

Type I and III endoleaks, on the other hand, require urgent intervention since they are associated with an increased risk of aneurysmal rupture.

Type V endoleaks also require intervention if they lead to aneurysmal expansion.

• type 1: leak at graft ends (inadequate seal) - most common after repair of thoracic aortic aneurysms 4
  
  • 1a: proximal
  • 1b: distal
  • 1c: iliac occluder
• type 2: sac filling via branch vessel (eg lumbar or inferior mesenteric artery)
  
  • most common after repair of abdominal aortic aneurysms 4 (80%)
  • sometimes referred to as a “retroleak”
  • enthusiastic examiners sometimes ask for the eponymous name of the large collateral artery between the IMA and SMA = Riolan’s arch.
  • most spontaneously resolve and require no treatment.
    
    • 2a: single vessel
    • 2b: two vessels or more
• type 3: leak through a defect in graft fabric (mechanical failure of graft)
  
  • 3a: junctional separation of the modular components
  • 3b: fractures or holes involving the endograft
• type 4: a generally porous graft (intentional design of graft)
• type 5: endotension

Endotension also referred to as a type V endoleak, is not a true leak but is defined as continued expansion of the aneurysm sac greater than 5mm, without evidence of a leak site.

It is a poorly understood phenomenon but thought to be formation of a transudate due to ultrafiltration of blood by the graft membrane or unidentified leak.

Some centres are trialling the use of an endovascular relining technique to reduce aneursym expansion due to endotension, or stent reinforcement can be performed.

Question 9

What is a pseudoaneurysm?

Answer 9

It describes a situation in which a defect in the vascular wall results in the formation of an extravascular hematoma (outside the arterial wall, yet contained by surrounding tissue) that remains in free communication with the intravascular space.

Question 10

Complications associated with an expanding aneurysm?

Answer 10

• rupture and exsanguination (the most concerning complication);
• dilation of the aortic root, (leading to aortic regurgitation); and
• compression of proximal structures, leading to –
  
  • difficult intubation (tracheal/bronchial compression),
  • superior vena cava syndrome (compression of the superior vena cava), and
  • hoarseness (compression of the left recurrent laryngeal nerve).

Question 11

Complications associated with the propagation of an aortic dissection?

Answer 11

• aortic regurgitation (aortic root involvement),
• cardiac tamponade (rupture into the pericardium),
• hemothorax (rupture into the pleura), and
• the occlusion of arteries arising from the aorta.

Question 12

What is visceral debranching?

Answer 12

http://vasculareducation.com/wp/visceral-debranching-of-the-abdominal-aorta-for-the-treatment-of-type-ii-taaa-using-hybrid-prothesis-for-renal-arteries/

Visceral debranching of the abdominal aorta for the treatment of Type II TAAA using hybrid prosthesis for renal arteries