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death (25% mortality).

Cerebrovascular accidents are the third leading cause of death in the United States.

Recurrent stroke is the leading cause of death in stroke patients and occurs at the rate of 9% per year.

Causes of cerebrovascular accidents include:

Cerebral artery thrombosis (85% of cases) due to:

Embolization (most common) from a cardiac source or the carotid arteries (Fig. 7-3).

Primary vessel occlusion (due to intracranial atherosclerosis)

Hemorrhage (15% of cases) involving:

Intracerebral hemorrhage (most common)

Subarachnoid hemorrhage (usually due to rupture of an intracranial aneurysm)

Symptoms. Atherosclerosis of the carotid arteries usually involves the origin of the internal carotid artery. Embolization of atherosclerotic debris, fibrin, or platelets from a carotid plaque is the most common cause of ischemic insult to the brain. Alternatively, the stenosis may result in thrombosis of the internal carotid artery, acutely diminishing blood flow distally if collaterals are not well developed.

Transient ischemic attacks (TIA) are episodes of focal neurologic symptoms. The classic TIA syndrome is characterized by abrupt onset, with the maximal symptoms occurring in less than 5 minutes. Rapid resolution usually occurs within 15 minutes but within 24 hours by definition.

Neurologic symptoms correspond to a specific hemispheric arterial distribution. Symptoms include:

Motor deficit contralateral to the involved carotid artery

Sensory deficit contralateral to the involved carotid artery

Aphasia, expressive or global

Amaurosis fugax is transient monocular blindness caused by an embolus to a retinal vessel. Examination of the retina may show a gray or a bright -yellow (Hollenhorst) cholesterol plaque within a retinal artery.

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FIGURE 7-3 Diagram of major extracranial components of cerebral and ocular arterial supply. (Adapted with permission from

Wylie EJ, Ehrenfeld WK. Extracranial Occlusive Cerebrovascular Disease. Philadelphia: WB Saunders; 1970.

)

Cerebrovascular accident, or completed stroke, refers to a neurologic deficit that persists for more than 24 hours. In the case of carotid disease, this again may involve a sensory or motor deficit contralateral to the diseased carotid artery or aphasia.

B Vertebrobasilar artery disease

The vertebrobasilar arteries (Fig. 7-3) comprise the posterior circulation of the brain. Symptoms of vertebrobasilar insufficiency may occur in the form of a TIA or stroke. These symptoms may include:

Loss of vision, diplopia

Indications for surgery center around the patient's presentation and the degree of stenosis determined by preoperative testing.

Symptomatic patients (nondisabling stroke, TIA, or amaurosis) with a 50%–99% stenosis in the ipsilateral carotid artery have a beneficial effect from carotid endarterectomy. The 2-year risk of an ipsilateral stroke is 9% in symptomatic patients with a high-grade stenosis treated with surgery and aspirin. Similar patients treated nonsurgically with aspirin alone have a 26% chance of having an ipsilateral stroke.

Asymptomatic patients with a 60%–99% stenosis may also benefit from carotid repair. An asymptomatic, high-grade carotid stenosis is associated with a stroke rate of approximately 10.6% over 5 years. If the surgery is performed with an operative morbidity and mortality of <3%, the 5-year risk of stroke can be reduced to 4.8%.

Contraindications to carotid repair include:

Disabling stroke, especially with altered level of consciousness

Totally occluded internal carotid artery

Severe medical illness, which will substantially shorten life expectancy

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Carotid endarterectomy is the procedure of choice.

The surgery removes the diseased inner portions of the common, internal, and external carotid arteries.

During the surgery, the artery is clamped, resulting in decreased blood flow to the brain. Cerebral protection, using a shunt, is used routinely by some surgeons and selectively by others. If selective shunting is chosen, the need for shunting can be assessed by:

Measuring the back pressure in the internal carotid artery after clamping the common and external carotid arteries. If the mean arterial pressure is more than 50 mm Hg, shunting is not necessary.

Observing the electroencephalogram for changes after clamping the common and external carotid arteries. If slowing occurs, a shunt should be used.

Performing the surgery using regional cervical block with local anesthesia. This choice allows the neurologic status of the awake patient to be assessed during the case and avoids the risks of general anesthesia. If a change in neurologic status occurs while the artery is clamped, the shunt is inserted.

The blood pressure should be carefully monitored during and after the procedure because these patients are prone to wide pressure swings, which can cause neurologic dysfunction or injury.

Complications of the procedure include stroke; transient cerebral ischemia; bleeding; cranial nerve injury, particularly to cranial nerves X and XII; and those related to other medical conditions, especially myocardial infarction.

Carotid angioplasty and stenting is gaining significant ground in treatment of carotid artery occlusive disease among vascular interventionalists. Currently, clinical trials are investigating the efficacy of

PTA/stenting versus traditional endarterectomy. Although this treatment is considered investigational for de novo lesions, there are accepted indications for using PTA/stenting in the carotid artery:

Reccurent stenosis

Anatomically difficult lesions (high bifurcations)

Irradiated necks

VIII Aneurysms

A Abdominal aortic aneurysms (AAA)

An aneurysm is an abnormal dilatation of the wall of an artery. Generally, an aneurysm is considered significant if its diameter is twice that of the normal proximal artery. An aneurysm of the aorta may rupture and cause death and should be repaired when detected. The cause of AAAs is multifactorial. Age, smoking, hypertension, and family history are all predisposing factors for aneurysm formation. Aneurysms are more common in men (4:1).

Diagnosis. AAAs most often occur below the level of the renal arteries. They are usually discovered on physical examination or during evaluation of an unrelated abdominal condition for which the patient has had a CT scan, ultrasound examination, or abdominal x-rays (incidentaloma).

X -ray. Calcification of part of the abdominal aorta seen on posterior-anterior or lateral abdominal radiograph is present in 60% of patients (“eggshell sign”).

Ultrasonography and CT scan of the abdomen are the most accurate tests for determining aneurysm size (reported as anterior-posterior or lateral diameter). CT is especially useful because it gives details about the relationship of the aneurysm to the renal and visceral vessels and demonstrates venous anomalies, which may be present.

Angiography is useful for patients with hypertension (to evaluate RAS), distal arterial occlusive symptoms, or suspected mesenteric ischemia.

Management. The decision to repair an AAA or to observe it for growth is dependent on aneurysm size and growth rate and the presence of symptoms.

Size. Patients with AAA <5 cm who are without symptoms are followed up with serial ultrasound examinations (every 3–12 months) to determine growth. AAA >5 cm are considered for elective repair depending on the medical condition of the patient.

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Growth rate. The natural history of AAA is growth ranging from 2 to 8 mm/year. Expanding aneurysms with growth >4 mm/year are considered for elective repair.

Symptoms. The vast majority of AAAs are asymptomatic. The presence of symptoms (rupture, unexplained abdominal/back/flank pain, or distal embolization) mandates repair.

Surgical repair

Preoperative evaluation. All patients undergoing elective repair should have careful preoperative medical screening, including a cardiac evaluation. Patients with severe or unstable coronary artery disease should undergo coronary catheterization and, if necessary, aortocoronary bypass preoperatively.

Technique. Surgical repair involves endoaneurysmorrhaphy. This involves opening the aneurysm

sack and suturing a prosthetic graft to the normal aorta within the aneurysm. The aneurysm wall is then wrapped around the graft following repair.

Endovascular repair. New techniques for the exclusion of aneurysms are now being developed. They involve the placement of the graft within the aneurysm via remote sites of access, most commonly the common femoral artery. The need for extensive laparotomy is thus avoided. The long-term results of these procedures are revealing acceptable durability with newer technologies emerging routinely. Currently, it is estimated that over 60% of AAAs worldwide are repaired through endovascular means. Criteria for placement of an endograft for AAA repair is as follows:

Suitable infrarenal neck: 1–1.5 cm with minimal angulation

One adequate common iliac artery: for distal fixation. Unilateral common iliac aneurysms can be excluded by embolizing the hypogastric artery and landing in the external iliac.

B

Ruptured AAA is the eleventh leading cause of death in the United States. The mortality of rupture is reported as high as 75% because many patients will not survive to receive medical care, and those who do undergo repair still have a high perioperative mortality rate.

Risk factors for rupture include:

Aneurysm size. Approximate rates of rupture in 5 years are:

If less than 4.5 cm in diameter, 9%

If 4.5–7 cm in diameter, 35%

If more than 7 cm in diameter, 75%

Expansion rate of an aneurysm >0.4 cm in diameter per year

The presence of hypertension and chronic obstructive pulmonary disease

Diagnosis of a ruptured AAA involves a triad of clinical findings. For patients who are hemodynamically stable (without any history or suspicion of shock) and in whom the diagnosis is questionable, CT imaging of the abdomen will reveal the presence of an aneurysm and rupture.

Severe pain located in the abdomen, flank, or back

Pulsatile, tender abdominal mass

Shock , presenting with elevated pulse rate, unstable blood pressure, or syncope. Some patients with a small, contained rupture may have a stable blood pressure, but they are at risk for catastrophic decompensation and should be treated urgently.

Management. Surgical repair of a ruptured aortic aneurysm must be performed as soon as the diagnosis is suspected. Patients with the previously noted triad are taken to the operating room without further testing. The technique for repair is similar to that for elective repair, although emergency proximal aortic control is generally obtained in the supraceliac position, just below the level of the diaphragm.

Surgical complications may occur in either elective or emergency aortic surgery. Many of these complications can be minimized by careful management, and if recognized early, some can be successfully treated, preventing major morbidity and mortality.

Postoperative acute renal failure occurs in 21% of cases of ruptured aneurysms and in less than 2% of aneurysms treated by elective surgery. If hemodialysis is required, the risk of mortality increases to approximately 50%.

Ischemic colitis, usually involving the sigmoid colon, may result from ligation of a patent IMA in both elective and emergent surgery. It occurs to some degree in 6% of elective cases but results in full - thickness injury with necrosis in <1% of cases. Ischemic colitis should be

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suspected in any patient with postoperative diarrhea, especially when the stools are heme positive. It can usually be diagnosed with sigmoidoscopy. The mortality rate can reach 50% if diagnosis and treatment are delayed. Treatment consists of resection of necrotic colon, proximal colostomy, and closure of the distal colon (Hartmann's procedure).

Acute leg ischemia can occur postoperatively and is suspected if pulses that were present previously are absent. It is caused by clamp injury to the iliac arteries or distal embolization of the aneurysm thrombus. Treatment is repair of the injury or embolectomy.

Spinal cord ischemia is a rare complication (0.25% of cases) of aortic aneurysm surgery but is most common in cases of ruptured aneurysms. The artery of Adamkiewicz supplies the spinal cord and arises from the aorta usually between thoracic levels 8 and 12; occasionally, however, it arises as low as lumbar level 4. Spinal cord ischemia results from diminished flow through this artery due to systemic hypotension, clamping of the aorta, or ligation of the intercostal/lumbar arteries. The classic anterior spinal artery syndrome is characterized by:

Paraplegia

Rectal and urinary incontinence

Loss of pain and temperature sensation but preservation of vibratory and proprioceptive sensation (due to the independent anterior and posterior circulation of the middle and lower spinal cord)

Aortic graft infection is generally a late complication of repair. It can occur in the body of the graft or at the anastomoses. It may result from bacterial seeding , either at the time of graft implantation or at a later date as a result of bacteremia. The most common infecting organism is Staphylococcus aureus, but Staphylococcus epidermidis is not infrequently found.

Incidence of infection is 1%–4% of all grafts used. It may be decreased significantly by the perioperative use of antibiotics. First -generation cephalosporins (i.e., cefazolin) are the drugs of choice.

Timing. Prosthetic grafts may become infected at any time after implantation, even many years after the surgery.

Presentation. Infected grafts can present in several ways.

Fever accompanied by abdominal discomfort is the usual presentation of infected prostheses contained within the abdomen. If the graft goes to the femoral arteries, the most common presenting sign is an inflammatory mass or draining sinus in the groin.

Gastrointestinal bleeding. Erosion of the graft into the bowel (usually the duodenum) may result in occult bleeding from the bowel wall or massive bleeding if the anastomosis is involved (aortoenteric fistula).

Diagnosis

If gastrointestinal bleeding is present, endoscopy of the esophagus, stomach, and duodenum should be done to search for bleeding sites, such as an ulcer. The distal duodenum should be visualized because the aortoenteric fistula may be visible in this location.

CT scan may demonstrate air or fluid around an infected graft or may show a false aneurysm.

An indium -tagged white blood cell scan may localize the area where the graft is infected.

An aortogram may demonstrate a false aneurysm and also will guide the surgeon regarding vessels available for reconstruction at surgery.

A sinogram , which outlines the graft, is diagnostic if a draining sinus is present.

Treatment. Traditional surgical treatment involves total graft excision (via a laparotomy) and extra-anatomic bypass . In hemodynamically stable patients, the extra-anatomic bypass may be performed prior to graft excision and generally involves an axillobifemoral bypass.

Sexual dysfunction. The sympathetic nerves controlling ejaculation cross the left common iliac artery near the aortic bifurcation. Injury during aortic repair may result in retrograde ejaculation. Additionally, disturbance of pelvic blood flow during aortic reconstruction may

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result in vasculogenic impotence. Perfusion of at least one hypogastric artery should be maintained in planning the method of graft placement.

C Atypical aneurysms of the abdominal aorta

Inflammatory aneurysms are characterized by a dense fibrotic reaction primarily involving the anterior and lateral walls of the aneurysm and the surrounding tissues.

The duodenum is often densely adherent to the aneurysm wall and can be severely injured if attempts are made to mobilize the aneurysm. The aneurysm is repaired by dissecting the neck above the area of inflammation for proximal control, frequently above the duodenum near the renal vein. Control of the iliac vessels is often obtained after the aneurysm has been opened by using balloons to occlude the lumens from within.

If the diagnosis is suspected preoperatively, a retroperitoneal approach may be used.

The inflammatory reaction frequently recedes after the aneurysm is repaired.

Mycotic AAAs are caused by bacterial inflammation of the arterial wall. In the infrarenal aorta, the most common organism found is Salmonella.

Mycotic aneurysms usually are saccular, occur in atypical locations, and lack calcification of the wall.

Patients present with fever, elevated white blood cell counts, and positive blood cultures. Evidence of septic embolization may also be present.

Treatment begins with culture and sensitivity -directed antibiotics. The aneurysm is then surgically

symptoms predominate, with sparing of the thumbs. Vasospasm may be associated with collagen vascular disease, atherosclerosis, trauma, and embolism from peripheral arterial lesions or may be without an identifiable associated disease.

A

Raynaud's phenomenon is episodic vasoconstriction, most commonly of the fingers but occasionally of the feet. It is usually initiated by cold exposure or emotional stimuli and occurs mainly in women.

The affected digits may go through a classic sequence of color changes, including:

Pallor due to severe vasospasm in the dermal vessels

Cyanosis due to sluggish blood flow and resultant marked blood desaturation

Rubor due to the reactive hyperemia

Symptoms begin with numb discomfort that is usually localized in the fingers. The prognosis is guarded because patients may then develop small vessel occlusions, leading to digital ulceration or gangrene.

Associated local or systemic disease. Raynaud's phenomenon is considered a disorder that occurs secondary to other diseases, most commonly scleroderma and collagen vascular diseases.

Management of Raynaud's phenomenon includes a number of different modalities.

Cold should be avoided. Hands should be protected by gloves or hand warmers in extremely cold weather.

Tobacco should be avoided because it stimulates vasoconstriction.

Calcium channel blockers, such as nifedipine, are the drugs of choice. Use of phenoxybenzamine for alpha blockade may be therapeutic.

Cervical sympathectomy is not recommended in these patients unless digital ulceration is present.

B

Raynaud's disease is similar to Raynaud's phenomenon; however, the condition shows no association with a systemic disease. The prognosis is benign, without significant threat of tissue loss. Seventy percent of patients are young women who usually have bilateral and symmetrical symptoms. Treatment is similar to that for Raynaud's phenomenon. Sympathectomy is not indicated.