Vascular

CHAPTER 24
Vascular


Samuel N. Steerman and Jason Davis


Test Taking Tip


• Vascular emergency questions are asked twice as much as elective vascular reconstruction. Acute ischemia and traumatic injury are favorite topics along with management. If in doubt, perform fasciotomy. Other common topics are risk factor modification, vascular lab testing (ABI), and visceral aneurysm. Endovascular choices are often wrong; be careful not to select an answer just because you don’t fully understand it.


PERIPHERAL ARTERIAL OCCLUSIVE DISEASE


Describe the risk factors associated with atherosclerosis:


Smoking, diabetes, hyperlipidemia, obesity, HTN, sedentary lifestyle


Differentiate between the following:


Arterial ulcers and venous ulcers


Arterial ulcers—painful and usually occur on toes or foot


Venous ulcers—commonly broad-based, shallow at medial malleolus


Claudication and rest pain


Claudication—cramping ischemic muscle pain with exertion that occurs distal to arterial stenosis, associated with 1% risk of limb loss and 5% mortality.


Rest pain—also due to ischemia, arises without exertion and classically wakes patients from sleep (often over distal metatarsals). The pain may resolve with standing or placing foot over side of bed (dependent position, gravity). >50% patients eventually require amputation.


Wet gangrene and dry gangrene


Dry gangrene—dry necrotic “mummified” tissue without signs of infection—not a surgical emergency


Wet gangrene—moist necrotic tissue indicative of active infectious process—requires aggressive debridement or amputation to avoid sepsis


How are ankle brachial index/digital brachial index (ABIs/DBIs) and segmental pressures measured? Pulse volume recordings (PVRs)? What is their significance?


Normal ABI at rest: 1.0 to 1.2, mild arterial insufficiency: 0.7 to 0.9, claudication: 0.5 to 0.7, rest pain and ultimately tissue necrosis: <0.4 (falsely elevated ABIs may be seen in diabetic patients or those with chronic renal disease due to extensive vascular calcification).


PVRs analyze the waveforms at sequential sites along patient’s leg—triphasic or biphasic waveforms, indicates more perfusion than monophasic.


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FIGURE 24-1. Calculating the ankle-brachial index. (Reproduced from Brunicardi FC, Andersen DK, Billiar TR, et al. Schwartz’s Principles of Surgery. 9th ed. www.accessmedicine.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)


What is the half-life of heparin? Intraoperative therapeutic dosing? How is it reversed?


Half-life is 60 to 90 minutes. Intraoperative dosing is 70 to 100 units/kg (activating clotting time of 250 to 350 seconds if measured). Protamine sulfate: 1 mg/100 units of heparin.


What are the 5-year patencies of common and external iliac percutaneous transluminal angioplasty (PTA) without stenting?


Common iliac: 70% to 80%


External iliac: 50% to 60%


What are the classic signs/symptoms of acute arterial occlusion? In what order do they present?


The “6 P’s” include: Paresthesias, Pain, Pallor, Poikilothermia, Pulselessness, Paralysis


What percentage of emboli originate in the heart? First and second most common causes?


80% of peripheral emboli are due to cardiac etiology (First—atrial fibrillation, Second—acute MI)


At what anatomic sites do atherosclerotic lesions most commonly occlude?


Atherosclerosis forms at branch points such as carotid bifurcation, bends, and tethered segments such as superficial femoral artery as it passes through Hunter canal Emboli lodge at arterial bifurcation—that is, femoral bifurcation, brachial bifurcation


How can a peripheral venous embolus cause occlusion in the peripheral arterial circulation?


A “paradoxical embolus” occurs when a peripheral venous thromboembolus crosses into the peripheral arterial circulation through a patent foramen ovale in the heart.


What is the risk of limb loss associated with acute thromboembolic disease? What is the associated mortality?


Risk of limb loss: 8% to 22%


Thromboembolic perioperative mortality: 10% to 17%


Name some of the indications to operate for peripheral arterial occlusive disease:


Tissue necrosis, rest pain, infection, debilitating claudication refractory to nonoperative management (Pentoxifylline, Aspirin, Cessation of smoking, Exercise—PACE pneumonic) NOTE—claudication is not an indication for surgery; it is best treated with supervised exercise training.


What is 5-year patency rate of Fem-Pop vein grafts versus prosthetic grafts


5-year patency of an above-the-knee vein graft is 75% (no difference between in situ or reverse); prosthetic is 40% to 50%.


5-year patency of a below-the-knee vein graft is 65%, prosthetic is 30%.


What do early (<30 day), intermediate, and late (>2 year) bypass graft failures generally represent?


Early—Use of small, poor-quality vein; anastomosis to inadequate outflow artery or technical error (kink/twist of graft; incomplete lysis of valves) at the time of surgery Intermediate—Intimal hyperplasia at anastomotic sites or valve sites within the graft Late—Progression of atherosclerotic disease within the inflow or outflow vessels


Name the 4 calf compartments in order of compartment syndrome probability:


Anterior, lateral, deep posterior, superficial posterior compartment


What is the first sign of compartment syndrome? How long after revascularization is greatest risk?


Numbness of great toe webbing is an early sign of compartment syndrome due to deep peroneal nerve compression (anterior). Greatest risk occurs 4 to 6 hours after revascularization along with release of intracellular ions/proteins/enzymes from damaged sarcolemma.


What is the most common iatrogenic injury during anterior compartment fasciotomy?


Injury to the lateral peroneal nerve in the superior aspect of the incision


Table 24-1 Conditions Qualifying Patients as “High Surgical Risk” for Carotid Endarterectomy


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CEREBROVASCULAR DISEASE


Name the structures that correspond to the following descriptions:


Contents of carotid sheath


Carotid artery, internal jugular vein, vagus nerve, and deep cervical lymph nodes


Vein crosses over carotid at level of bifurcation


Facial vein


Muscle crosses distal carotid arteries


Digastric muscle


Muscle that crosses proximal common carotid artery


Omohyoid muscle


Nerve that is deep to the facial vein and crosses ~1 cm distal to carotid bifurcation


Hypoglossal nerve


Nerve that branches from hypoglossal nerve and can help locate hypoglossal nerve


Ansa cervicalis


Compare and contrast the terms: stroke, TIA, cerebrovascular attack (CVA), and amaurosis fugax.


Stroke refers to acute brain injury with neurologic deficits lasting >24 hours. The neurologic impairment associated with transient ischemic attacks resolves within <24 hours.


CVA indicates permanent ischemic brain damage.


Amaurosis fugax is transient monocular vision loss attributed to ophthalmic artery.


Microemboli can be related to carotid artery stenosis.


What underlying conditions and risk factors predispose strokes?


Atrial fibrillation, atherosclerosis at common carotid artery bifurcation, and HTN


True or False: An audible bruit over the carotid bifurcation indicates significant carotid stenosis.


False—an audible carotid bruit does not correlate well with significant carotid stenosis.


What is the gold standard for identifying carotid artery stenosis? What is the best screening test?


Carotid artery angiography is considered the gold standard to diagnose ICA stenosis. It is, however, invasive (1% risk of stroke) and rarely necessary. Duplex ultrasound is the best test to screen for ICA stenosis. CT angiogram (CTA) or magnetic resonance imaging (MRA) can be used to further characterize.


What are the indications for surgical treatment of cerebrovascular disease?


>50% symptomatic ICA stenosis, <70% asymptomatic ICA stenosis with ulcerated plaque or failure of medical therapy, >80% asymptomatic ICA stenosis, or crescendo TIAs


What are the risks and most common complications of carotid endarterectomy?


0.3% to 1.6% MI, 1% to 4.5% hematoma, restenosis at 2 to 3 years after carotid endarterectomy (CEA) (neointimal hyperplasia) + 3 years after CEA (recurrent atherosclerosis at bifurcation)


Risk of perioperative stroke is 1% for asymptomatic patients and 5% for symptomatic, most often due to a technical defect created at the time of arterial reconstruction (if focal neurologic change occurs in PACU, return to OR for re-exploration)


Cerebral edema +/- headache and/or seizures (due to cerebral hyperperfusion syndrome)


A patient presents with left arm claudication, syncope, and ataxia. What might this be?


More common on the left and due to subclavian or innominate stenosis, subclavian steal syndrome is characterized by upper extremity claudication and signs of vertebrobasilar insufficiency (vertigo, syncopal attacks, confusion, blindness, ataxia, dysarthria)


THORACIC AORTA


What are the branches of the thoracic aorta?


Bronchial, esophageal, intercostal arteries


What artery supplies the lower anterior spinal artery and from where does it originate?


The artery of Adamkiewicz usually originates from an aortic intercostal artery between the 9th and 12th intercostal spaces and can be associated with anterior cord syndrome.


What size defines an aorta as aneurysmal, and at what size is intervention indicated?


Localized or diffuse aortic dilation >50% of normal aortic diameter (1.5–2 cm)


Thoracic aortic aneurysms >7 cm or enlargement >0.5 cm/6 mo warrant surgical intervention (>6 cm for patients with connective tissue disorders).


Name 6 risk factors associated with aneurysm formation.


Age, arteriosclerosis, connective tissue disorder, smoking, HTN, dissection


Differentiate between Crawford stages I to IV of thoracoabdominal aneurysms.


Type I—Involve descending thoracic aorta from left subclavian to suprarenal aorta


Type II—Extend from left subclavian to renal arteries (may continue to aortic bifurcation)


Type III—Mid/distal descending thoracic aorta to most abdominal aorta until bifurcation


Type IV—Includes upper abdominal aorta through all or none of the infrarenal aorta


How is management for Stanford type A aortic dissections different from that for type B?


Dissections involving the ascending aorta (type A) require surgery, whereas dissections not involving the ascending aorta (type B) require tight BP control (Esmolol, etc) in the absence of aortic rupture, intractable pain, malperfusion of branches of aorta, or uncontrollable HTN. Follow-up CT scans are recommended at 1.5, 3, and 6 months, and then annually.


Differentiate between Debakey types I to III aortic dissections:


Type I—Ascending and descending aorta


Type II—Ascending aorta only, proximal to left subclavian


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FIGURE 24-2. Classification of aortic dissection. DeBakey type I and Stanford type A include dissections that involve the proximal aorta, arch, and descending thoracic aorta. DeBakey type II only involves the ascending aorta; this dissection is included in the Stanford type A. DeBakey type III and Stanford type B include dissections that originate in the descending thoracic and thoracoabdominal aorta regardless of any retrograde involvement of the arch. These are subdivided into subtypes a and b, depending on abdominal aortic involvement. (Reproduced from Cohn LH. Cardiac Surgery in the Adults. 4th ed. www.accesssurgery.com. Copyright © The McGraw-Hill Companies, Inc. All rights reserved.)


Type IIIa—Descending aorta, involves above diaphragm only


Type IIIb—Descending aorta, extends below diaphragm


What genetic defect is most commonly associated with aortic dissections and aneurysms?


Marfan syndrome is caused by a mutation of the fibrillin-1 gene (FBN1).


What are the minimum lengths required distal to the left common carotid artery for the proximal landing zone and proximal to the celiac axis for the distal landing zone when performing a thoracic EVAR (TEVAR)?


Both proximal and distal graft landing zones are required to be 20 mm for TEVAR.


Describe the recommended follow-up for a patient status post-TEVAR:


Lifelong surveillance CTA performed at 1, 6, and 12 months, and yearly thereafter.


Left subclavian revascularization is reserved for which patients during TEVAR with a covered arch?


Patients with a dominant left vertebral artery develop left upper extremity ischemic symptoms, or those who’ve undergone a previous bypass requiring left subclavian flow, some say all nonemergent patients.


What are the 5-year risks of rupture for thoracic aortic aneurysms of 6 cm, 7 cm, and 8 cm?


5-year risks of rupture for thoracic aorta aneurysm (TAAs) are ~31% for 6 cm, ~43% for 7 cm, and ~100% for 8 cm.


What laboratory test should be sent after clamping the supraceliac aorta?


Amylase, lipase, liver function tests


Table 24-2 Annualized Risk of Rupture of Abdominal Aortic Aneurysm (AAA) Based on Size


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INFRARENAL AORTA


Name the following anatomic structures:


Vein that crosses the proximal abdominal aorta


Left renal vein


Vein that runs posterior to the right common iliac artery


Left common iliac vein


Artery with its origin midway along the abdominal aorta, exiting leftward


Inferior mesenteric artery


Can be injured during dissection/clamping along anterior iliac artery near iliac bifurcation?


Ureter and parasympathetic nerve plexus (results in sexual dysfunction)


Place the following aneurysms in decreasing order of frequency: aorta, iliac, femoral, popliteal.


Aorta > Iliac > Popliteal > Femoral artery aneurysms


At what rates do (cm) abdominal aortic aneurysms (AAAs) grow?


The rate of growth for AAAs <5 cm is ~0.32 cm/y, while that for >5 cm is ~0.4 to 0.5 cm/y.


What is the survival rate for ruptured AAAs? What symptoms indicate rupture?


50% of ruptured AAAs reach the hospital, of which only 50% survive (mortality > in winter).


Classic triad of symptoms includes sudden abdominal/flank pain, shock, and pulsatile mass.


What is the best screening test used for AAAs and in what population?


Abdominal ultrasound at age 65 for males who’ve smoked more than 100 cigarettes in their life or anyone with family history.


What are the indications for surgical repair of AAAs, and what is the risk of repair?


AAA diameter >5.5 cm for men or 4.5 to 5.0 cm for women and patients with connective tissue disorders, AAA expansion >0.5 cm/6 mo, AAA symptoms (chronic abdominal/back pain), patient preference for smaller AAA (4.5–5.4 cm) if young low-risk patient, or atypical aneurysms (dissecting, pseudoaneurysm, mycotic, saccular, penetrating ulcers). Mortality risk of open repair is quoted to be <5% (1%–3% for high-volume centers).


What does testicular pain in a patient with abdominal aortic aneurysm classically signify?


Retroperitoneal rupture with ureteral stretch and referred testicular pain


Which bacteria are thought to be an infectious cause of aneurysm formation? Graft infection?


Chlamydia pneumoniae


Staphylococcus aureus (and Staphylococcus epidermidis, usually late)


Describe the early and late complications of open AAA repair? Endovascular aneurysm repair (EVAR)?


Early—Most frequent cause of death after open AAA repair is myocardial dysfunction, but sexual dysfunction (up to 25% males), nonfatal MI, and renal failure are most common.


Late—Upper and lower GI bleed due to aortoenteric fistula (fourth portion of duodenum as it crosses anterior to aorta) can be reduced by wrapping the graft with the aneurysm sac.


EVAR

Aug 13, 2019 | Posted by in ABDOMINAL MEDICINE | Comments Off on Vascular
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