ABSITE REVIEW Review Session #12 September 21, 2006

CARDIAC/VASCULAR (Primary Contributor: Keith Cavaness)

1. What are the indications for carotid endarterectomy, and what clinical trials show this? Schwartz's Principles of Surgery - 8th Ed. (2005)

Both trials (NASCET and ECST)showed that carotid endarterectomy conferred significant benefit in symptomatic patients with a 70 to 99% stenosis. Although the NASCET trial observed a small but significant benefit in patients with 50 to 69% stenoses, the ECST trial found no evidence of benefit in patients with lesser degrees of disease. The Asymptomatic Carotid Atherosclerosis Study (ACAS) trial was a prospective study that randomized 1600 patients with asymptomatic stenosis of 60% or greater to either carotid endarterectomy and aspirin or aspirin alone. This study was interrupted because of a significant benefit identified in patients undergoing carotid endarterectomy. At the time of interruption of the study, a relative reduction in stroke rate by 50% was observed by patients undergoing carotid endarterectomy.

2. What are the four types of acute mesenteric vascular insufficiency and how are they treated? Schwartz's Principles of Surgery - 8th Ed. (2005)

(1) Acute embolic mesenteric ischemia – This is an acute obstruction of the superior mesenteric artery by an embolic clot, generally from the atrium. Usually the proximal jejunum is spared as the embolus lodges after the first branch. The primary goal of surgical treatment in embolic mesenteric ischemia is to restore arterial perfusion with removal of the embolus from the vessel. The abdomen is explored through a midline incision, which often reveals variable intestinal ischemia from the mid-jejunum to the ascending or transverse colon. Once the proximal SMA is identified and controlled with vascular clamps, a transverse arteriotomy is made to extract the embolus, using standard balloon embolectomy catheters. (2) Acute thrombotic mesenteric ischemia - These patients generally have a thrombosis at pre-existing mesenteric artery atherosclerosis. Often they require a reconstructive procedure to the distal SMA to bypass the proximal occlusive lesion and restore adequate mesenteric flow. Exploration in patients with thrombotic mesenteric ischemia often reveals a much more extensive intestinal necrosis than in patients with embolic mesenteric ischemia, due to the extensive atherosclerotic process; often the proximal jejunum is involved. Either saphenous vein or prosthetic graft may be used and different authors have advocated each; factors that decide that are availability of saphenous vein, convenience and degree of contamination. (3) Mesenteric Vein Thrombosis: Certain conditions such as cirrhosis of the liver predispose to acute thrombosis of the mesenteric veins, which

clinically presents similar to other forms of acute mesenteric vascular insufficiency. This should be suspected if the arteriogram is normal, but signs of reduced blood flow or bowel wall edema is present. The venous phase of the arteriogram may show the thrombosis. CT scan may also make the diagnosis, and the thrombus can often be seen in the vessel. Treatment is celiotomy and resection followed by anticoagulation if peritonitis is present, anticoagulation alone if it is not. (4) Nonocclusive mesenteric ischemia - The treatment of nonocclusive mesenteric ischemia is primarily pharmacologic if no signs of peritonitis are present, with selective mesenteric arterial catheterization followed by infusion of vasodilatory agents such as tolazoline or papaverine. Once the diagnosis is made via mesenteric arteriography, intra-arterial papaverine is given at a dose of 30 to 60 mg/h. This must be coupled with the cessation of other vasoconstricting agents. Concomitant intravenous heparin should be administered to prevent thrombosis in the cannulated vessels.

3. What are the differing etiologies of a pulseless lower extremity? ACS Surgery: Principles & Practice (2006)

The characteristic signs and symptoms of acute limb ischemia (ALI) may be summarized as the six Ps: Pulselessness, Pain, Pallor, Poikilothermia, Paresthesia, and Paralysis. The etiology of ALI can be divided into two distinct categories: thrombosis and embolism.

Native artery thrombosis is usually the end stage of a long-standing disease process of atheromatous plaque formation at specific sites in the arterial tree. In patients with native conduits, intimal hyperplasia and valvular hyperplasia are the two leading causes of graft failure. The situation is different in the prosthetic graft population, where the inherent thrombogenicity of the graft material and kinking of the graft from crossing joints are the leading causes. Peripheral arterial embolization results in the sudden onset of extreme ischemia as the absence of collateral vessels compounds the reduction in flow to the extremity. The heart is by far the predominant source of spontaneous arterial emboli. MI is the next most important cause of peripheral emboli. Tumors (e.g., atrial myxomas) are occasional sources of peripheral emboli. Cardiac vegetations from bacterial or fungal endocarditis should be considered as possible sources of peripheral emboli when I.V. drug abuse is suspected in a patient with no previous

Differentiation of Embolism from Thrombosis Variable Embolism Thrombosis

Identifiable source Frequently detected None

Claudication Rare Frequent

Physical findings Proximinal and contralateral pulses normal

Evidence of ipsilateral and contralateral peripheral vascular disease

Angiographic findings Minimal atherosclerosis; sharp cutoff; few collaterals; multiple

occlusions

Diffuse atherosclerotic disease; tapered and irregular cutoff; well-developed collateral

circulation

history of cardiac disease. Foreign objects (e.g., missiles) can also embolize if they gain access to the arterial tree. Finally trauma can cause pulselessness by direct injury to the vascular structures or by injury to muscles causing compartment syndrome.

4. What are some complications of open abdominal aortic repair?

ACS Surgery: Principles & Practice (2006) Overall morbidity after elective aneurysm repair ranges from 10% to 30%. The most common complication is myocardial ischemia, and MI is the most common cause of postoperative death. Mild renal insufficiency is the second most frequent complication, occurring after 6% of elective aneurysm repairs; however, severe renal failure necessitating dialysis is rare in this setting. The third most common complication is pulmonary disease; the incidence of postoperative pneumonia is approximately 5%. [NB: a classic ABSITE question is the patient s/p aneurysm repair who becomes acutely oliguric. Such patients need invasive hemodynamic monitoring to discern the cause of lack of perfusion to the kidneys] Postoperative bleeding may occur as well. Common sources of such bleeding include the anastomotic suture lines, inadequately recognized venous injuries, and coagulopathies resulting from intraoperative hypothermia or excessive blood loss. Any evidence of ongoing bleeding is an indication for early exploration. Lower-extremity ischemia may occur as a result of either emboli or thrombosis of the graft and may necessitate reoperation and thrombectomy. So-called trash foot may also develop when diffuse microemboli are carried into the distal circulation. Colon ischemia develops after 1% of elective aneurysm repairs. Patients usually present with bloody diarrhea, abdominal pain, a distended abdomen, and leukocytosis. Diagnosis is confirmed by sigmoidoscopy, which reveals mucosal sloughing. In cases of transmural colonic necrosis, colon resection and exteriorization of stomas are warranted. Paraplegia is rare after repair of infrarenal AAAs: the incidence is only 0.2%. Most instances of paraplegia occur after repair of a ruptured aneurysm or when the pelvis has been devascularized. The majority of patients recover at least some degree of neurologic function. Late complications − such as pseudoaneurysms at the suture lines, graft or graft limb thrombosis, and graft infection − may occur but are extremely rare. Graft infection may be associated with graft-enteric fistula and is notoriously difficult to diagnose and treat.

5. What are the different types of leaks encountered after endovascular repair?

ACS Surgery: Principles & Practice (2006) On occasion, endovascular AAA repair fails to exclude blood flow from the aneurysm sac completely. This condition, known as endoleak, may arise from an incomplete seal at the site where the endograft is affixed to the aortic neck or the iliac arteries (type I endoleak), from retrograde flow into the aneurysm from the inferior mesenteric artery or the lumbar arteries (type II endoleak), or from the graft or modular junction site (type III endoleak). Type I and type III endoleaks call for secondary treatment to prevent possible aneurysm rupture. The

significance of type II endoleaks is less certain. There is no clear evidence that type II endoleaks lead to aneurysm rupture; however, most such endoleaks are treated if they are associated with aneurysm enlargement.

6. What are the options to treat a patient with an infected aortic graft? ACS Surgery: Principles & Practice (2006)

Before definitive reconstruction, all infected graft material must be debrided, along with any grossly infected vascular tissue and surrounding soft tissue. Once debridement is complete, there are several options for reconstruction, including (1) extra-anatomic bypass, (2) use of an arterial allograft, (3) placement of vascular prostheses treated with or soaked in antibiotic solutions, and (4) in situ replacement with a femoral-popliteal vein (FPV) graft. The choice among these options is made on the basis of the specific clinical situation present.

7. What are the indications for postoperative intra-aortic balloon pumps? How do they work? Schwartz's Principles of Surgery - 8th Ed. (2005) The most frequent indications for use of IABP are to provide hemodynamic support during or after cardiac catheterization, cardiogenic shock, weaning from cardiopulmonary bypass, and for preoperative use in high-risk patients and refractory unstable angina. A balloon catheter is inserted through the femoral artery and advanced into the thoracic aorta. With electronic synchronization, the balloon is inflated during diastole and deflated during systole. Coronary blood flow is increased by improved diastolic perfusion, and afterload is reduced. The cardiac index typically improves after insertion, and the preload decreases. Total myocardial oxygen consumption is diminished by approximately 15%. Generally, the IABP is used for a few days with minimal morbidity.

8. What is the superior vena cava syndrome? Griffith's 5-Minute Clinical Consult - 14th Ed. (2006) Partial or complete obstruction of the superior vena cava, 90% extrinsic, 70% from neoplasm (most frequently bronchogenic carcinoma), also thrombosis, fibrosis, invasion and aneurysm causing suffusion, varying degrees of airway obstruction and/or cyanosis of the face, neck, arms and occasionally chest and upper abdomen. Usual course - acute; (usually 28 days from onset of symptoms to diagnosis).

9. What is atrial natriuretic factor? Taber's® Cyclopedic Medical Dictionary - 20th Ed. (2005)

A peptide secreted by the atrial tissue of the heart in response to an increase in blood pressure. It influences blood pressure, blood volume, and cardiac output. It increases the excretion of sodium and water in urine, thereby lowering blood volume and blood pressure and influencing cardiac output. Its secretion rate depends on glomerular filtration rate and inhibits sodium reabsorption in distal

tubules. These actions reduce the workload of the heart. Also called atrial natriuretic hormone or atrial natriuretic peptide.

10. What are the types and treatments of acute thoracic aortic dissection? There are two traditional classification schemes that remain in common use: the DeBakey classification and the Stanford classification.

In their current use, both of these methods describe the segments of aorta that are involved in the dissection, rather than the site of the initial intimal tear. The main drawback of the Stanford classification is that it does not distinguish between patients with isolated ascending aortic dissection and patients with dissection involving the entire aorta; both patients would be classified as type A, despite the fact that their treatment, follow-up, and prognosis are substantially different. Borst and associates advocated a more simplified, descriptive classification of aortic dissection instead of the traditional DeBakey and Stanford schemes. In this system, the proximal aortic segment (ascending and transverse arch) and distal aortic segment (descending thoracic and thoracoabdominal) are considered independently. This is useful because treatment strategies are based on which segments are involved. For example, patients with isolated proximal aortic dissections often undergo emergent operation. In contrast, when only the distal aorta is involved, the initial treatment is usually medical; surgery is reserved for patients who develop complications. Patients with dissections that involve both the proximal and distal segments often undergo surgical repair of the proximal segment, followed by aggressive medical treatment for the remaining distal dissection.