15. Can carotid endarterectomy be performed on the basis of duplex study alone?

Show answer
The argument for elimination of arteriography in selected cases is persuasive because the carotid arteriogram alone has a morbidity rate > 1%. This rate may represent 25% of the usual total morbidity associated with carotid endarterectomy. However, to realize the benefit of surgery based on duplex ultrasound, the duplex study must have a high positive predictive value (PPV). Fortunately, the PPV is high for severe lesions that meet suitably strict criteria (e.g., peak systolic velocities > 290 cm/sec and end-diastolic velocities > 80 cm/sec).

16. Does duplex ultrasound have a role in the diagnosis of peripheral arterial disease?

Show answer
Its role is limited. Peripheral arterial disease must be assessed functionally, not anatomically. Duplex ultrasound can be used to localize disease that has already been assessed for its functional significance (exercise, not surgery, is typically prescribed for claudication alone).

17. Does transcranial Doppler have a role in the noninvasive diagnosis of cerebrovascular disease?

Show answer
No. Although the technique is widely touted, recent large studies emphasize that the Doppler evaluation of the intracranial arteries does not change the clinical management of any patient.

18. Should D-dimer blood tests be required before patients are evaluated by ultrasound for DVT?

Show answer
D-dimer is a degradation product of cross-linked fibrin. Blood plasma levels of D-dimer are often elevated in patients with DVT. However, DVT is not the only cause of elevated D-dimers and cannot be used instead of ultrasound to diagnose the presence of DVT. Conversely, in selected patient subgroups, a low D-dimer level has a very high negative predictive value and can prevent unnecessary ultrasound testing. The test should be restricted to nonsurgical patients, patients who are not anticoagulated, patients in the outpatient setting, and patients in whom there is a low clinical suspicion of DVT such as a painful limb without swelling or bilateral ankle swelling.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Baker WF: Diagnosis of deep venous thrombosis and pulmonary embolism. Med Clin North Am 82:459-476, 1998. Medline Similar articles
2. Gerlock AJ, Giyanani VL, Krebs C: Applications of Noninvasive Vascular Techniques. Philadelphia, W.B. Saunders, 1988.
3. Moneta GL, Edwards JM, Papanicolaou G, et al: Screening for asymptomatic internal carotid artery stenosis: Duplex criteria for discriminating 60% to 99% stenosis. J Vasc Surg 21:989-997, 1995.
4. Shirit D, et al: Appropriate indications for venous duplex scanning based on D-dimer assay. Ann Vasc Surg 16:304-308, 2002.
5. Zierler RE, Sumner DS: Physiologic assessment of peripheral arterial occlusive disease. In Rutherford RB (ed): Vascular Surgery, 5th ed. Philadelphia, W.B. Saunders, 2000, pp 140-165.

11. What is the primary test for diagnosis of lower extremity ischemia?

Show answer
The ankle brachial index (ABI) or systolic pressure ratio is normally greater than or equal to 1.0. Typically, Doppler ultrasound is used (instead of a stethoscope) as the flow sensor distal to the pressure cuff, but plethysmographic instruments also may be used. Doppler signals are usually monitored at the posterior tibial artery or dorsalis pedis artery.

KEY POINTS: NONINVASIVE VASCULAR DIAGNOSTIC LABORATORY

1. Duplex ultrasound has a sensitivity of 97% in detecting carotid artery disease and an accuracy of 95% in correctly classifying carotid stenoses as > 50% reduction in diameter.
2. The primary test for diagnosis of lower extremity ischemia is the ankle branchial index.
3. The noninvasive test used to diagnose acute DVT is duplex ultrasound.

12. What is gained by measuring pressures at limb levels other than the ankle?

Show answer
Segmental limb pressure (SLP) measurements, performed at the upper thigh, lower thigh, calf, and ankle, localize the arterial segment(s) involved in peripheral arterial occlusive disease.

13. What tests are used for assessing peripheral artery disease in diabetic patients who may have incompressible arteries caused by medial calcification?

Show answer
Pulse volume recording (PVR) is a pneumoplethysmographic technique that tracks the limb volume changes over the cardiac cycle. It measures the segmental pressure changes with pneumatic cuffs as a function of the limb volume changes. The relative PVR amplitudes identify the presence of peripheral artery disease and localize the arterial segment involved. The PVR is unaffected by medial calcification. Great-toe pressure also may be used to diagnose and assess disease severity in diabetic patients because medial calcification rarely affects the digital arteries.

14. How should the patient with suspected intermittent claudication be evaluated?

Show answer
The patient first should be evaluated by obtaining ABIs or segmental limb pressures at rest. The patient with ischemia at rest does not normally need further evaluation. The patient with mild arterial insufficiency at rest or even normal resting pressures should perform an exercise stress test (treadmill walking using either fixed or variable load protocols) followed by ABIs. The distance that the patient is able to walk allows assessment of functional disability, and the postexercise reduction in ankle pressure, or lack thereof, allows assessment of whether the disability is caused by arterial insufficiency rather than musculoskeletal or neurologic pain.

7. What noninvasive test is used to diagnose acute DVT?

Show answer
Duplex ultrasound has replaced venous occlusion plethysmography as the accepted standard. Colorflow duplex is useful because it helps to identify small veins from the muscle and fascial layers. The ultrasound assessment involves the following steps:

1. Examine the vein for echogenic thrombus.
2. Compress the vein, using pressure on the ultrasound probe, looking for complete collapse. Inability to compress the vein suggests thrombosis. Partial compression suggests partial thrombosis.
3. A Doppler signal from the vein that is phasic with respiration suggests no proximal occlusive thrombus. A signal that is spontaneously present but nonphasic suggests flow around an occlusion via small collateral veins. Absence of a Doppler signal in the vein suggests absence of flow.

8. Can duplex ultrasound be used for surveillance in patients at high risk for DVT?

Show answer
Diagnosis of DVT in asymptomatic patients presents a dilemma. The sensitivity of duplex ultrasound is reduced from the reported 95% to < 80% for above-knee detection of DVT in asymptomatic patients. Calf DVT detection is much worse, with sensitivities as low as 20% in many reported series. However, serial contrast venography, although more specific, is not a practical surveillance strategy.

9. Does venous occlusion plethysmography still have a role in the assessment of DVT?

Show answer
Yes. Venous occlusion plethysmography or impedance plethysmography (IPG) has high sensitivity and specificity in detecting occlusive thrombi above the knee, particularly for iliofemoral occlusive thrombi (95%). Because IPG provides functional information about deep venous outflow from the legs, it provides diagnosis of nonvisualized caval or iliac thrombosis, diagnosis of recurrent acute proximal thrombosis superimposed on chronic thrombosis, and functional evaluation of residual or chronic outflow obstruction (venous claudication).

10. What noninvasive tests are useful for evaluation of venous incompetence?

Show answer
Doppler ultrasound can detect venous reflux in the deep veins of the legs and in the greater and lesser saphenous veins. With experience, the test can be done using a simple Doppler (continuous wave versus pulsed Doppler), but duplex ultrasound is often used to facilitate identification of the vein segments and valves and to position a pulsed Doppler sample reliably. Some laboratories measure the duration of reflux during controlled proximal compression as an indicator of severity of valve incompetence, but unless a valvuloplasty or valve transposition is planned for the identified incompetent valve, such specific measures appear to have little clinical utility.

3. Which noninvasive tests should be used to diagnose extracranial carotid artery disease?

Show answer
Duplex ultrasound has a sensitivity of 97% in detecting carotid artery disease and an accuracy of 95% in correctly classifying carotid stenoses as > 50% reduction in diameter. No other noninvasive test has comparable accuracy.

4. What is duplex ultrasound?

Show answer
Duplex ultrasound uses both image and velocity data (hence the name duplex) in a nearly simultaneous presentation of ultrasound echo images (B-mode ultrasound) and blood velocity waveforms obtained by Doppler ultrasound. The Doppler signals are obtained from a single small region of the blood vessel. Average velocities can be estimated for multiple such regions over a large area of the vessel. By assigning colors to the velocities, blood flow can be visually represented. Such a presentation, called colorflow duplex ultrasound, aids the duplex examination but cannot replace the information obtained from the Doppler velocity waveform.

5. Why is blood velocity important in assessing the degree of carotid artery stenosis?

Show answer

It is often difficult to measure accurately the arterial lumen on a B-mode ultrasound image because the acoustic properties (and hence the image) of noncalcified plaque, thrombus, and even blood may be similar. Arterial narrowing forces blood through a narrower channel, which increases the blood velocity. This velocity can characterize the degree of arterial narrowing. Current practice classifies the degree of internal carotid stenosis based exclusively on the Doppler velocity data.

6. What are the velocity criteria and categorical ranges of carotid artery stenosis?

Show answer
The criteria developed at the University of Washington (Table 73-1) are the most widely accepted. Note that progressive carotid stenosis increases the flow velocity signal as the volume of blood is squeezed through a smaller and smaller orifice. The category > 80% has been termed critical stenosis because of the high rate of disease progression and high incidence of neurologic symptoms for patients in this category.
Table 73-1. UNIVERSITY OF WASHINGTON CRITERIA

1. What is the role of the vascular diagnostic laboratory (VDL) in the assessment and treatment of patients with suspected vascular disease?

Show answer
Although traditional evaluation by an experienced clinician remains the foundation of vascular diagnosis, clinical assessment has its limitations. For example, only one third of cervical bruits are associated with significant carotid artery disease; conversely, as many as two thirds of patients with severe carotid disease present without a cervical bruit. Half of patients with extensive deep venous thrombosis (DVT) of the lower extremity lack signs and symptoms referable to the lower extremities, and more than half of patients presenting with clinical signs of DVT are venographically normal. As many as 40% of diabetic patients have no large-vessel peripheral arterial occlusive disease. The VDL provides objective, quantitative, and functional status data to delineate the severity of extracranial cerebrovascular disease, peripheral arterial occlusive disease, and acute and chronic venous disease.

2. What differentiates the VDL from diagnostic radiology and ultrasound?

Show answer
The VDL provides functional information rather than or in addition to the morphologic data provided by radiology tests and general ultrasound images. This information is particularly important for peripheral arterial occlusive disease, in which anatomic information about the site of stenosis or occlusion is of limited value without knowledge of the functional significance.

1. Where does deep venous thrombosis (DVT) originate?

Show answer
More than 95% of DVTs develop in the deep veins of the lower extremities; the majority originate in the valve sinuses of the calf veins.

2. What is the usual source of a pulmonary embolus?

Show answer
Calf vein thrombosis may propagate proximally into the deep venous system to involve the popliteal, femoral, or iliac veins (or a combination of veins). These proximal DVTs are the culprits in > 90% of pulmonary emboli.

3. What is Virchow’s triad?

Show answer
(1) Hypercoagulability, (2) disruption of an intact venous intimal lining, and (3) stasis of venous blood flow. In most patients with DVT, at least two of these three components are operative.

4. What are the major hypercoagulable syndromes (thrombophilia)?

Show answer
Factor V Leiden mutation, antithrombin III deficiency, protein C deficiency, protein S deficiency, dysfibrinogenemia, lupus anticoagulant, antiphospholipid syndrome, prothrombin 20210A mutation, and abnormalities of fibrinolysis are the major examples. The most common is the factor V Leiden mutation (i.e., activated protein C resistance).

5. What causes venous intimal injury?

Show answer
Venous intimal changes may be secondary to vein wall trauma, infection, inflammation, indwelling catheters, or surgery. Venodilation during anesthesia and surgery may produce microscopic intimal tears as well as stasis. The injured venous intima initiates the release of thromboplastic substances that can activate the coagulation cascade.

6. What causes stasis of venous blood flow?

Show answer
Venostasis is common in surgical patients; it occurs during anesthesia, after certain types of trauma, and with perioperative immobility.

7. What are the usual clinical risk factors for DVT?

Show answer
Risk factors include malignancy (especially pancreatic, genitourinary, stomach, lung, colon, and breast cancer), age older than 40 years, female gender, obesity, history of venous thrombosis or pulmonary embolism, major surgical procedures, pregnancy, limited mobility, hypercoagulable state, and trauma.

8. What signs and symptoms suggest DVT? How can DVT be accurately diagnosed?

Show answer
The signs and symptoms are calf or thigh pain, tenderness, increased skin temperature, swelling, or superficial venous dilatation. None of these signs is specific for DVT. Even the well-known Homan’s sign (i.e., calf pain with dorsiflexion of the foot) is unreliable; its accuracy is only 50%. Doppler ultrasound examination (duplex scanning) detects DVT proximal to the calf veins with > 95% accuracy; unfortunately, it is not as sensitive in detecting calf vein DVT. Ascending venography is still the reference standard.

9. Is there any value to D-dimer testing?

Show answer
Measurement of D-dimer cross-linked fibrin degradation products (FDPs), formed by the action of plasmin on cross-linked fibrin, has been proposed as an alternative to initial noninvasive testing. A sensitivity of 96.8% and a specificity of 35.2% have been reported for the enzyme-linked immunosorbent assay (ELISA) test, making it theoretically possible to limit noninvasive testing to those with positive D-dimer testing. Unfortunately, the ELISA test is time consuming and impractical as a screening test. More rapid (1 hour) ELISA assays are now available. Prospective evaluation of the safety of withholding anticoagulation therapy in patients who are D-dimer negative has been limited. False-positive results are a problem in patients with malignancy, infection, or recent surgery.

10. What methods of perioperative DVT prophylaxis should be used? In which surgical patients?

Show answer
Perioperative DVT prophylaxis is strongly recommended in all high-risk patients who are older than age 40 years and undergoing major general or orthopedic procedures. In general surgical patients, well-applied prophylactic measures decrease the relative risk of DVT by 67%. The best prophylaxis for DVT includes pre- and postoperative walking. Intermittent pneumatic compression stockings and some form of heparin therapy (low-dose unfractionated heparin [LDUH] or low molecular weight heparin [LMWH]) are recommended as the patient’s risk profile increases.
KEY POINTS: VENOUS DISEASE

1. More than 95% of deep vein thromboses (DVTs) develop in the deep veins of the lower extremities; the majority originate in the valve sinuses of the calf veins.
2. Virchow’s triad consists of hypercoagulability, disruption of an intact venous intimal lining, and stasis of venous blood flow.
3. The best prophylaxis for DVT includes pre- and postoperative walking.

11. How does heparin work?

Show answer
Heparin binds to antithrombin III (ATIII), rendering it more active. Low-dose heparin (5000 U administered subcutaneously every 8-12 hours until the patient is fully ambulatory) activates ATIII, inhibits platelet aggregation, and decreases the availability of thrombin.

12. What is LMWH?

Show answer
LMWH is a fragment of heparin produced by chemical breakdown. It exerts its anticoagulation effect by binding with ATIII and inhibiting several coagulation enzymes, principally factor Xa. It has a longer half-life than standard preparation heparin and can be administered once daily. LMWH gives a more predictable anticoagulant response at high doses and thus can be administered without monitoring (it is not necessary to follow the partial thromboplastin time).

13. Should the placement of an inferior vena cava (IVC) filter ever be considered?

Show answer
In patients with a documented, recurrent pulmonary embolism while taking adequate anticoagulation therapy or with an absolute contraindication to anticoagulation, an IVC filter can be placed to prevent embolization or propagation of clot to the lungs. A significant rate of recurrent DVT has been associated with IVC filters.

14. What are the characteristics of chronic venous insufficiency and postphlebitic syndrome?

Show answer
The primary characteristic is venous valvular incompetence with distal ambulatory venous hypertension. After DVT, involved venous segments eventually recanalize to some degree. However, their delicate valves remain scarred or trapped by residual organized thrombus. The loss of valvular function disables the venomotor pump. The vein walls become thicker and less compliant, increasing resistance to proximal blood flow. These factors result in distal venous hypertension. Protein-rich fluids, fibrin, and red blood cells are extravasated and deposited through large pores in the distended microcirculation during periods of venous hypertension. This process leads to inflammation, scarring, fibrosis of the subcutaneous tissues, and discoloration by hemosiderin deposition (”brawny” edema). The resultant inflammatory reaction, scarring, and interstitial edema create a further barrier to capillary flow and diffusion of oxygen; adequate nutrition to the skin is inhibited. These changes may lead to tissue atrophy and ulceration (i.e., venous stasis ulcer).

15. Do all patients with DVT develop postphlebitic syndrome?

Show answer
No. Recent epidemiologic studies suggest that the incidence of venous ulceration is about 5%. As many as one in five post-DVT patients have absolutely no symptoms and maintain normal noninvasive vascular test data. The median time for the appearance of a first venous stasis ulcer is 2.5 years. Of interest, 50% of patients with venous ulcers have no history of DVT (probably because of previous asymptomatic calf vein DVT).

16. How are patients with postphlebitic syndrome treated?

Show answer
With proper patient education and compliance, postphlebitic stasis sequelae can be controlled by nonoperative means in well over 90% of patients, particularly if no residual venous outflow obstruction complicates valvular incompetence. Nonoperative treatment consists of graded elastic compression stockings (or Unna boots) to retard swelling and periodic leg elevation during the day. Patients must be taught to elevate their legs above the heart (”toes above your nose”) at regular intervals (e.g., 10-15 minutes every 2 hours). Compliance is critical.

17. Distinguish between phlegmasia alba dolens and phlegmasia cerulea dolens.

Show answer
Iliofemoral venous thrombosis is characterized by unilateral pain and edema of an entire lower extremity, discoloration, and groin tenderness. A total of 75% of the cases of iliofemoral venous thrombosis occur on the left side, presumably because of compression of the left common iliac vein by the overlying right common iliac artery (May-Thurner syndrome). In phlegmasia alba dolens (literally, painful white swelling), the leg becomes pale and white. Arterial pulses remain normal. Progressive thrombosis may occur with propagation proximally or distally and into neighboring tributaries. The entire leg becomes both edematous and mottled or cyanotic. This stage is called phlegmasia cerulea dolens (literally, painful purple swelling). When venous outflow is seriously impeded, arterial inflow may be reduced secondarily by as much as 30%. Limb loss is a serious concern; aggressive management (i.e., venous thrombectomy, catheter-directed lytic therapy, or both) is necessary.

18. What is venous claudication?

Show answer
When venous recanalization fails to occur after iliofemoral venous thrombosis, venous collaterals develop to bypass the obstruction to venous outflow. These collaterals usually suffice while the patient is at rest. However, leg exercise induces increased arterial inflow, which may exceed the capacity of the venous collateral bed and result in progressive venous hypertension. The pressure buildup in the venous system results in calf pain commonly described as tight, heavy, or bursting (venous claudication). Relief is obtained with rest and elevation but is not as prompt as with arterial claudication.

19. How can one distinguish primary varicose veins from secondary varicose veins?

Show answer
Primary varicose veins result from uncomplicated saphenofemoral venous valvular incompetence and have a greater saphenous distribution, positive tourniquet test result, no stasis sequelae (dermatitis or ulceration), and no morning ankle edema (lymphedema).
Secondary varicose veins are most commonly a consequence of deep and perforator venous incompetence secondary to postphlebitic syndrome.

20. Why do people develop primary varicose veins?

Show answer
The most common cause is congenital absence of venous valves proximal to the saphenofemoral junction. There are normally no valves in the vena cava or common iliac veins and only an occasional valve in the external iliac veins. Thus, the sentinel valve in the common femoral vein just above the saphenofemoral junction is of critical importance. However, anatomic studies reveal that this valve is absent on one or the other side in 30% of patients.

21. How, when, and in whom should varicose veins be treated?

Show answer
Varicose veins that cause discomfort or serious cosmetic embarrassment require treatment. Better results are obtained with early treatment before continuous retrograde pressure and flow down the superficial system and into communicating perforating veins (whenever the patient is standing) cause secondary, irreversible perforator incompetence. High saphenous vein ligation at an early stage can arrest progression of this gravitational process. The distal varicosities can be managed by selective surgical stripping, sclerotherapy, or both.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Clarke-Pearson DL, Dodge RK, Synan I, et al: Venous thromboembolism prophylaxis: Patients at high risk to fail intermittent pneumatic compression. Obstet Gynecol 101:157-163, 2003. Medline Similar articles Full article
2. Franks PJ, Sharp EJ, Moffatt CJ: Risk factors for leg ulcer recurrence: A randomized trial of two types of compression stockings. Age Ageing 24:490-494, 1995. Medline Similar articles
3. Gallix BP, Achard-Lichere C, Dauzat M, et al: Flow-independent magnetic resonance venography of the calf. J Magn Reson Imaging 17:421-426, 2003. Medline Similar articles Full article
4. Geerts W, Heit JA, Clagett GP, et al: Prevention of venous thromboembolism. Chest 119:132s-175s, 2001. Medline Similar articles
5. Ginsberg JS: Management of venous thromboembolism. N Engl J Med 335:1816-1828, 1996. Medline Similar articles Full article
6. Janssen MC, Wollersheim H, Verbruggen B, et al: Rapid D-dimer assays to exclude deep venous thrombosis and pulmonary embolism: Current status and new developments. Semin Thromb Hemost 24:393-400, 1998. Medline Similar articles
7. Philbrick JT, Heim S: The d-dimer test for deep venous thrombosis: Gold standards and bias in negative predictive value. Clin Chem 49:570-574, 2003. Medline Similar articles Full article
8. Sorensen HT, Mellemkjaer L, Steffensen FH, et al: The risk of a diagnosis of cancer after primary deep venous thrombosis or pulmonary embolism. N Engl J Med 338:1169-1173, 1998.

1. What is an abdominal aortic aneurysm (AAA)?

Show answer
A ≥ 50% increase in normal aortic diameter. Normal infrarenal aortic diameter is 2.0 cm for men. A definition of AAA as an aorta ≥ 3.0 cm in diameter is appropriate.

2. What is the incidence of AAA?

Show answer

* 3% in unselected adult patients screened with ultrasound
* 5% in patients with known coronary artery disease
* 10% in patients with known peripheral vascular disease

3. What is the etiology of AAA?

Show answer
Elastin is the primary load-bearing element of the aorta. In the normal human aorta, there is a gradual reduction in the amount of elastin present in the distal compared with the proximal aorta. Elastin fragmentation and degeneration are observed histologically in AAA walls. These observations help explain the predilection of AAAs in the infrarenal aorta. Absence of vasa vasorum in the infrarenal aorta has led to the suggestion of a nutritive deficiency. The degradation of aortic media in aneurysmal disease implies a disrupted balance between proteolytic enzymes and their inhibitors.

4. Do AAAs have a genetic component?

Show answer
Multiple reports describe a familial subgroup of AAAs. Therefore, screening of AAA patients’ first-degree relatives who are 50 years old and older makes sense. Two prospective studies demonstrated that approximately 30% of these relatives also harbor an AAA. The proposed genetic defect has been linked to abnormal type III collagen.

5. Are patients with AAA prone to aneurysms in other vascular beds?

Show answer
Yes. Forty percent of patients with a popliteal artery aneurysm harbor an AAA. Seventy-five percent of patients with a femoral artery aneurysm also have an AAA. Patients with thoracic aneurysms have a 20% chance of having a simultaneous AAA. Five percent of patients develop aortic aneurysms proximal to their graft at ≥ 5 years after infrarenal AAA repair.

6. Can AAAs reliably be detected on physical examination?

Show answer
No. The aortic bifurcation is at the level of the umbilicus. Therefore, the pulsatile mass of an AAA is located in the epigastrium. Thus, only relatively large AAAs can be detected in thin patients.

7. Can AAAs be detected by radiography?

Show answer
Plain abdominal or lumbar spine radiographs can detect occult AAA in about 20% of cases. A thin rim of calcification identifies the aneurysmal aortic wall. The majority of AAAs contain insufficient calcium to be visualized by radiography.

8. Which imaging method is the best for screening patients for AAA?

Show answer
Abdominal ultrasound (US) permits measurement accuracy within 0.3 cm and data in both cross-sectional and longitudinal dimensions.

9. What is the best single imaging modality to plan AAA repair?

Show answer
The contrast-enhanced computed tomography (CT) scan is the best one. Diameter measurements are accurate within 0.2 cm. Venous anomalies (i.e., retroaortic or circumaortic left renal vein, inferior vena cava duplication, and left-sided inferior vena cava) that dramatically alter the operative approach are well visualized on CT. Although CT is excellent at detecting aneurysmal rupture or leak (92% accuracy and 100% specificity), it is less useful for predicting suprarenal aneurysm involvement (sensitivity, 83%; specificity, 90%; positive predictive value, 48%).

10. What is the manifestation of a symptomatic AAA?

Show answer
Acute low back pain is the most common presenting symptom (82%), but only one third of AAAs are diagnosed before rupture. A hypotensive elderly man with acute onset of low back pain has a leaking AAA until proven otherwise.

11. What is the appropriate management of a patient suspected of a ruptured AAA?

Show answer
Just before emergent surgical exploration, patients who are hemodynamically unstable with a pulsatile abdominal mass should have an electrocardiogram to rule out myocardial infarction.

12. Should all patients presenting with AAA rupture undergo repair?

Show answer
Patients in profound shock or cardiac arrest at the time of presentation have little chance of survival. Extreme age, dementia, metastatic cancer, and other severe end-stage medical problems should force you to reassess this allocation of medical resources.

13. Do all patients with ruptured AAAs make it to surgery?

Show answer
Approximately half of patients with a ruptured AAA die before reaching the hospital. One fourth of those who make it to the hospital die before they can be brought to the operating room. Therefore, only 25% of patients make it to surgery.

14. How is a ruptured AAA treated operatively?

Show answer
The patient should not be anesthetized until completely prepped and draped and ready for immediate incision because the blood pressure may decrease dramatically upon induction of anesthesia. Rapid proximal aortic control is the key to successful outcome of operations for ruptured AAA. This can be at the diaphragm (in an unstable patient, with free intraperitoneal bleeding or a retroperitoneal hematoma that extends proximal to the left renal vein) or at the infrarenal aortic segment (in a stable patient with a lower retroperitoneal hematoma). Intraluminal balloon occlusion of the aorta is an option with free intraperitoneal rupture. As soon as control is obtained, the patient is resuscitated and clamps are moved to the more standard infrarenal location. Distal control can also be obtained with balloons or packs to prevent iliac venous injury.
KEY POINTS: ABDOMINAL AORTIC ANEURYSM

1. An AAA is defined as a ≥ 50% increase in normal aortic diameter.
2. Forty percent of patients with a popliteal artery aneurysm harbor an AAA.
3. CT is the single best imaging modality to plan an AAA repair.
4. AAA should be repaired electively when the size reaches 5.5 cm in diameter.

15. How should patients with symptomatic nonruptured AAAs be managed?

Show answer
Symptomatic AAAs are rapidly expanding and at high risk for rupture. Therefore, most vascular surgeons agree that symptomatic but intact AAAs should be repaired expeditiously (as early as is conveniently possible).
16. Are there any alternatives to open surgical repair for ruptured AAA? Show answer
Endovascular prosthetic grafts have been successfully placed in high-risk patients with symptomatic AAAs or contained ruptures both in the aortic and aortoiliac position.

17. What are the rupture rates of AAAs?

Show answer
A 5-cm diameter AAA has an annual rupture risk of < 1%. The risk of AAA rupture increases with size. Annual rupture risk is 10% for a 6-cm AAA and 30% for AAAs > 7 cm.

18. How fast do AAAs enlarge?

Show answer
The average expansion rate of all AAAs is 0.4 cm/year. However, 20% of all AAAs demonstrate no change in size over time. Conversely, 20% expand at a rate > 0.5 cm/year. Rapid expansion (0.5 cm/6 months) is considered to be predictive of rupture and an indication for repair.

19. When are angiograms helpful in the diagnostic workup for AAA?

Show answer
Traditionally, angiography has been indicated in patients when there is concern regarding the extent of the proximal neck, concomitant visceral occlusive disease, renal artery anomalies, a prior colectomy with need to visualize the visceral circulation, or lower extremity occlusive or aneurysmal disease.

20. What is the difference between extraperitoneal and transabdominal approach?

Show answer
Elective aortic graft placement can be carried out equally well via a transperitoneal or extraperitoneal approach. The former provides better pelvic exposure. The extraperitoneal approach provides superior exposure of the suprarenal aorta and facilitates postoperative pulmonary management.

21. What are endografts? Are they durable?

Show answer
Endovascular grafts are graft-covered stents that are placed via the femoral artery by interventional (i.e., radiographic) methods to exclude the aneurysm without the need for an abdominal incision or cross clamping the aorta. Multiple different series of successful endovascular AAA repair have been reported. Successful endograft placement has been reported in a wide variety of high-risk operative candidates. Many vascular surgeons and interventionalists are making aortic endograft placement their preferred treatment for patients with AAAs. The major drawbacks are late leaks or rupture from the graft, the cost of the procedure, and the need for long-term patient follow-up.

22. At what size should asymptomatic AAAs be repaired electively?

Show answer
They should be repaired electively when the AAA reaches 5.5 cm in diameter. The only benefit for repair of an asymptomatic AAA is to prevent subsequent rupture and death. Therefore, all candidates for elective repair must expect to live at least 5 years.

23. What are the technical aspects of AAA surgery?

Show answer
The two important decisions are the location of arterial clamps and the type of graft to place. The majority of cases can be managed by placing the arterial clamp below the renal arteries. This avoids prolonged ischemia to the kidneys. The aneurysm is opened after clamping proximally and distally. Lumbar artery orifices are oversewn to prevent bleeding from collateral arteries. The inferior mesenteric artery is often occluded, but when it is patent and not vigorously backbleeding, it may require reimplantation.

24. What are the major noncardiac complications of AAA repair?

Show answer
Renal failure (elevation in creatinine) and intestinal ischemia (bloody diarrhea).

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Barry MC, Burke PE, Sheehan S, et al: An “all comers” policy for ruptured abdominal aortic aneurysms: How can results be improved? Eur J Surg 164:263-270, 1998.
2. Boyle JR, Thompson MM, Nasim A, et al: Endovascular abdominal aortic aneurysm repair in the “hostile abdomen.” J Royal Coll Surg Edinb 43:283-285, 1998.
3. Hill BB, Wolf YG, Lee WA, et al: Open versus endovascular AAA repair in patients who are morphological candidates for endovascular treatment. J Endovasc Ther 9:255-261, 2002. Medline Similar articles Full article
4. Holzenbein TJ, Kretschmer G, Dorffner R, et al: Endovascular management of “endoleaks” after transluminal infrarenal abdominal aneurysm repair. Eur J Vasc Endovasc Surg 16:208-217, 1998. Medline Similar articles
5. Killen DA, Reed WA, Gorton ME, et al: 25-year trends in resection of abdominal aortic aneurysms. Ann Vasc Surg 12:436-444, 1998. Medline Similar articles Full article
6. Lawrence PF, Wallis C, Dobrin PB, et al: Peripheral aneurysms and arteriomegaly: Is there a familial pattern? J Vasc Surg 28:599-605, 1998. Full article
7. Lederle FA, Johnson GR, Wilson SE, et al: Rupture rate of large abdominal aortic aneurysms in patients refusing or unfit for elective repair. JAMA 287:2968-2972, 2002. Medline Similar articles Full article
8. Lederle FA, Wilson SE, Johnson GR, et al: Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med 346:1437-1444, 2002.

29. What is the role of CEA?

Show answer
Although CEA remains the standard of care for carotid artery disease, percutaneous angioplasty with stenting has been investigated as an alternative. The underlying rationale is to decrease morbidity, hospital costs, and anesthetic risks and to improve long-term patency. Reported rates of success, morbidity, and mortality run the gamut from stroke and death rates comparable to CEA (2.4%) to significantly higher neurologic risk (stroke rate, 8.8%) and higher cost. One randomized trial is currently under way in Great Britain, and applications for two other studies are being considered in the United States. Carotid angioplasty has no apparent benefit compared with CEA.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Barnett HJM, Taylor DW, Eliasziw M, et al, for the North American Symptomatic Carotid Endarterectomy Trial Collaborators: Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 339:1415-1425, 1998. Full article
2. Beebe HG: Scientific evidence demonstrating the safety of carotid angioplasty and stenting: Do we have enough to draw conclusions yet? J Vasc Surg 27:788-790, 1998. Full article
3. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study: Endarterectomy for asymptomatic carotid artery stenosis. JAMA 273:1421-1429, 1995.
4. Jordan WD, Voellinger DC, Fisher WS, et al: A comparison of carotid angioplasty with stenting versus endarterectomy with regional anesthesia. J Vasc Surg 28:397-402, 1998. Medline Similar articles
5. Mansour MA, Kang SS, Baker WH, et al: Carotid endarterectomy for recurrent stenosis. J Vasc Surg 25:877-883, 1997. Medline Similar articles
6. Moore WS, Kempszinski RF, Nelson JJ, Toole JF, for the ACAS Investigators: Recurrent carotid stenosis: Results of the asymptomatic carotid atherosclerosis study. Stroke 29:2018-2025, 1998. Medline Similar articles
7. North American Symptomatic Carotid Endarterectomy Trial Collaborators: Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. N Engl J Med 325:445-453, 1991.
8. Yadav JS, Roubin GS, Iyer S, et al: Elective stenting of the extracranial carotid arteries. Circulation 95:283-381, 1997.

1. What diseases affect the carotid arteries?

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Atherosclerosis is by far the most common (accounting for 90% of lesions in the Western world). The carotid also can be affected by fibromuscular dysplasia, inflammatory arteriopathies (e.g., Takayasu’s arteritis), extrinsic compression (e.g., neoplasm), and trauma.

2. What are the most common symptoms of carotid artery disease?

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* Transient ischemic attack (TIA)
* Reversible ischemic neurologic deficit (RIND)
* Cerebrovascular accident (CVA)
* Amaurosis fugax

3. Define TIA, RIND, and CVA.

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These clinical terms describe a spectrum of cerebral ischemic syndromes. A TIA is a neurologic deficit that lasts < 24 hours. Most TIAs last only 15-30 seconds. RIND lasts longer than 24 hours and completely resolves within 1 week (usually within 3 days). CVA, or acute stroke, is a stable neurologic deficit that may show gradual improvement over a long period.

4. Define amaurosis fugax.

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It is an episode of transient (minutes to hours) monocular blindness, often likened to a window shade pulled across the eye. It is caused by decreased blood flow through or embolization into the ophthalmic artery.

5. What are Hollenhorst plaques?

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They are bright yellow plaques of cholesterol, usually at a branch point in the retinal vessels, that have embolized from the carotid bifurcation. Clinically, this finding indicates that the atheromatous plaque in the carotid is quite friable. Further embolization may occur with manipulation at the time of surgery.

6. What mechanisms produce neurologic deficits?

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* Embolization from atherosclerotic arteries or the heart
* Reduced blood flow
* Occlusive disease with thrombosis
* Intracranial hemorrhage

7. What is the natural history of a TIA?

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The natural history of a TIA is defined by the pathology of the ipsilateral carotid artery. In patients with severe stenosis (> 70%), the risk of ipsilateral stroke within 24 months is 26%. For those with moderate disease (50-69%), the risk is 22% at 5 years. With minimal stenosis (< 30%), the risk is 1% at 3 years (see Required Reading in Chapter 1).

8. What is the effect of aspirin on TIAs?

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Acetylsalicylic acid is a cyclooxygenase inhibitor that decreases platelet stickiness and lowers the incidence of both TIAs and stroke.

9. What does a carotid bruit signify?

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Unfortunately, a carotid bruit is a general marker for atherosclerosis and is specific for very little; it is more predictive of a cardiac event than a neurologic event. Although a carotid bruit indicates increased risk of neurologic events, it is just as likely to occur on the contralateral side as on the side of the bruit.

10. Does the sound of a bruit correlate with the degree of stenosis?

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No. As a stenosis progresses, the bruit should actually diminish and disappear as flow decreases.

11. What test should be ordered to evaluate a cervical bruit?

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Duplex scanning.

12. When is surgery indicated for symptomatic carotid artery disease?

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Surgery is strongly indicated for symptomatic carotid artery disease associated with > 70% stenosis. The absolute risk reduction of stroke is 17% at 2 years. Recent data also suggest a smaller benefit in patients with symptomatic stenoses of 50-69% (6.5% risk reduction at 5 years). Patients with stenosis of < 50% do not benefit from surgery.
KEY POINTS: CAROTID DISEASE

1. The symptoms of carotid disease include transient ischemic attack, reversible ischemic neurologic deficit, cerebrovascular accident, and amaurosis fugax.
2. A carotid bruit is a general marker for atherosclerosis and is specific for very little; it is more predictive of a cardiac event than a neurologic event.
3. Surgery is strongly indicated for symptomatic carotid artery disease associated with > 70% stenosis.

Show answer
The absolute reduction in risk of stroke is 6% over a 5-year period in asymptomatic patients with > 60% stenosis who undergo carotid endarterectomy (CEA) plus aspirin versus patients treated with aspirin alone (5.1% versus 11%). Thus, CEA should be performed for asymptomatic carotid disease when the patient is expected to live at least 3 years and when the CEA can be performed with a combined stroke and mortality rate of < 3%.

14. What are the complications of carotid endarterectomy?

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* TIA or stroke (approximately 2%)
* Hematoma
* Cranial nerve injury
* Hypertension
* Hypotension

15. Which cranial nerves (CNs) may be injured during CEA? What are the clinical signs of injury?

* Facial nerve (CN VII): injury to the marginal mandibular branch may cause droop of the ipsilateral corner of the mouth
* Glossopharyngeal nerve (CN IX): difficulty in swallowing both solids and liquids
* Vagus nerve (CN X): hoarseness, loss of effective cough
* Superior laryngeal nerve (branch of the vagus): voice fatigue, loss of high-pitch phonation
* Hypoglossal nerve (CN XII): deviation of the tongue to the ipsilateral side, difficulty with speech and chewing

16. What is the danger of wound hematoma after surgery?

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The main danger is airway compromise, which may necessitate emergent decompression by opening of the wound. Whether vacuum drains prevent this complication is not clear.

17. What are the possible causes of postoperative hypertension?

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* Denervation of the carotid sinus
* Cerebral rennin, norepinephrine production, or both
* Preexisting hypertension
* Central neurologic deficit

18. When do neurologic events occur during CEA?

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* Dissection: dislodgement of material from the arterial wall with embolization
* Clamping: ischemic infarct
* Postoperatively: intimal flap, reperfusion, external carotid artery clot

19. What is a shunt? When is it used?

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A shunt is a small plastic tube that diverts blood flow around the surgically opened carotid artery while endarterectomy is performed. A shunt is used to ensure adequate cerebral blood flow and to avoid intraoperative cerebral ischemia. Many surgeons routinely use shunts, but others use them selectively, if at all. The decision to use a shunt is based on intraoperative assessment, including temporary clamping of the carotid under local anesthesia, measurement of stump pressure, intraoperative electroencephalography, or transcranial Doppler. None of these methods is 100% accurate.

20. What is stump pressure?

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Stump pressure is the back pressure of the internal carotid artery after clamping. It is used to assess the adequacy of cerebral perfusion. The “safe” pressure varies from author to author, but is probably around 40 mmHg.

21. Does stenosis recur after carotid endarterectomy?

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Yes. The reported incidence has been quite variable and ranges from < 2% to as much as 36%. During the first 24 months after operation, restenosis is thought to be secondary to myointimal hyperplasia. Beyond this time, it is caused by progression of disease (atherosclerosis). The incidence is lower when the arteriotomy is closed with a vein patch angioplasty.

22. What is the most common complication associated with reoperation endarterectomy?

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Cranial nerve injury (reported incidence = 2-20%). Most injuries are transient, however.
23. In which layer of the artery is the carotid endarterectomy performed? Show answer
The outer layers of the tunica media.

24. What anatomic landmark is useful in identifying the level of the carotid artery bifurcation?

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The facial vein.

25. How many branches of the internal carotid artery are located in the neck?

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None.

26. When the internal carotid artery is occluded, which branches of the external carotid artery form collaterals and reestablish circulation in the circle of Willis?

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The periorbital branches of the external carotid artery form communications with the ophthalmic artery, a branch of the internal carotid.

27. What are the functions of the carotid sinus and the carotid body?

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Both are located at the carotid bifurcation and are innervated by the glossopharyngeal and vagus nerves, respectively. The function of the carotid sinus is regulation of blood pressure. Hypertension stimulates efferent impulses to the vasomotor center in the medulla, inhibiting sympathetic tone and increasing vagal tone. The carotid body regulates respiratory drive and acid-base status via chemoreceptors. It also induces bradycardia when manipulated (this is your target during carotid massage for cardiac dysrhythmias).

28. When was the first successful surgical procedure of the extracranial carotid artery performed? Who is credited with it?

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In 1954 by Eastcott.

1. Describe claudication and its physiology.

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Intermittent claudication consists of reproducible lower extremity muscular pain induced by exercise and relieved by short periods of rest. It is caused by arterial obstruction to affected muscular beds, which restricts the normal exercise-induced increase in blood flow, producing transient muscle ischemia. Studies have shown that more than half of patients with intermittent claudication have never complained of this symptom to their physicians, assuming that difficulty with walking is a normal consequence of aging.

2. List the different nonoperative therapies for intermittent claudication.

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Risk factor modification, exercise, and pharmacologic therapies. Smoking cessation reliably doubles walking distances, and the need for eventual amputation in patient’s with lower extremity arterial occlusive disease decreases after smoking cessation. Exercise (defined as walking until onset of leg pain, resting, and then resuming walking) for 30-60 minutes, 3 days per week for 6 months has also been demonstrated in multiple randomized trials to increase walking distance by more than 100%. Currently, the only Food and Drug Administration (FDA)-approved drugs for the treatment of claudication are pentoxifylline (minimally effective) and cilostazol (appears more effective).

3. Define critical limb ischemia.

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Critical limb ischemia potentially threatens the viability of the limb. Symptoms include rest pain (e.g., foot pain at rest) typically occurring at night when the patient is supine and the gravity contribution to foot arterial pressure is no longer present. This pain is relieved with foot dependency or short periods of ambulation. Poor tissue circulation does not heal minor skin breakdown caused by incidental trauma. These ischemic ulcers are frequently painful and can progress to gangrene.

4. What is the ankle brachial index (ABI)?

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ABI is the highest ankle pressure (anterior tibial or posterior tibial artery) divided by the higher of the two brachial pressures. The normal ABI is slightly > 1 (1.10). An ABI of 1.0-0.5 is typical of patients with claudication. Patients with rest pain have an ABI < 0.5, and patients with tissue necrosis often have an ABI much lower.

5. Describe the natural history of claudication.

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Multiple natural history studies have documented the benign nature of claudication. The cumulative 10-year amputation rate is 10%. One third of patients experience symptom deterioration, and half of these patients require some sort of revascularization. Continued smoking and diabetes are major risk factors for progression.

6. Describe the natural history of critical limb ischemia.

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In the past, it was commonly believed that chronic ischemic rest pain or necrosis inevitably led to either reconstruction or major amputation. This is both simplistic and inaccurate. Clearly, continuous ischemic rest pain or progressive gangrenous changes are unstable conditions that require therapy. However, the control groups from several pharmacologic trials for critical limb ischemia noted improvement over time in 40%. Vascular disease is a systemic disease, and 50% of patients with critical limb ischemia succumb to cardiac disease within 5 years.

7. What are segmental limb pressures? How are they used?

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Just as the ABI is recorded at the ankle, cuffs at the high thigh, above knee, and below knee level can record pressures. Noting the location of decreases in arterial pressure can determine the level of the vascular obstruction.

8. Describe the natural history of graft occlusions.

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Although bypass grafts can dramatically improve lower extremity circulation, they have a limited life expectancy. When these grafts fail, the limb involved is frequently in worse circulatory trouble than before the bypass. This is because of division of major arterial collateral pathways during the operation and thrombus propagation or embolization to occlude distal arteries at the time of graft occlusion.

9. What is the prognosis of young patients with vascular disease?

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Significant atherosclerosis in young patients (age < 40 years) is infrequent. These patients are almost exclusively heavy smokers with a high incidence of hypercoaguable states (defective fibrinolysis, anticardiolipin antibodies, homocysteinemia, or deficiencies in natural anticoagulants). Those with limb-threatening conditions frequently progress to limb loss despite attempts at revascularization. Reconstructive procedures have limited longevity and require frequent revision in this population.

10. Describe the anatomic distribution of vascular disease in diabetes.

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Diabetic patients are unique. They have a predilection for calcification of the arterial wall, rendering diagnostic studies (ankle pressure, ABI) unreliable because of false elevation. The digital arteries are usually spared, and the great toe pressure can be used to approximate the ankle pressure. The inflow arteries (i.e., aorta, iliacs, common femorals) are usually spared. Intermittent disease is often present in the superficial femoral and popliteal arteries. Significant occlusive disease most commonly affects the profunda femoris, posterior and anterior tibials, and pedal arteries, with relative sparing of the peroneal artery.

11. What are the implications of renal failure on outcomes?

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Patients with end-stage renal failure who have critical limb ischemia are at the end of life, with 3 year survival rates < 30%, similar to patients with metastatic cancer. In addition, the healing potential for partial foot amputations after successful revascularization is limited. Reconstructions in these patients are technically difficult because of calcified distal targets. The combination of these problems has caused many vascular surgeons to discourage vascular reconstructions in these patients.

12. Discuss the concept of inflow versus outflow.

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The limb is thought of as a separate circulation network when planning revascularization procedures. Adequate leg circulation requires blood to enter the leg from the heart (inflow) and reach the foot from the thigh (outflow). In the normal limb, the inflow to the leg is via the aorta and iliacs, and common and deep femoral arteries. The normal outflow to the foot is the popliteal and three tibial arteries (anterior, posterior, and peroneal). For bypasses to work, they need adequate inflow (i.e., blood coming into them) and outflow (i.e., a vascular bed to supply).

13. What are the choices for autogenous conduits?

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The success of infrainguinal bypass is highly dependent on the conduit (what the graft is made of). The best choices for conduit in order of preference would be a single segment greater saphenous vein, spliced pieces of saphenous vein, spliced lesser saphenous veins, arm veins, spliced arm veins, and prosthetic material with a distal vein cuff. Cryopreserved cadaver veins are expensive and are generally of limited durability. Prosthetic grafts are best used for above-the-knee popliteal targets, because the bend at the knee joint and the size mismatch at more distal arteries decrease their longevity in these positions markedly.

14. What are the indications for arteriography?

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Arteriography is only performed in order to plan future operations or interventions. Diagnostic arteriography without intervention is rarely used in lower extremity occlusive disease. Arteriography is expensive and carries a finite risk of bleeding, arterial injury with thrombosis, and renal failure from contrast agent toxicity (combined 3%).

15. What are the patency rates of inflow procedures?

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The durability of vascular reconstructions is measured by patency. Patency has three types, all measured via a life table method, which accounts for the moderate number of deaths (primarily cardiac origin) occurring in vascular patients over time. Patency can be primary (the graft has remained functioning without any intervention), assisted primary (the graft has never thrombosed but has required some intervention to keep it functioning), or secondary patency (the graft has thrombosed, but an intervention has reopened it and it is again functioning). The four most common procedures to improve inflow are iliac angioplasty, aortofemoral bypass, femorofemoral bypass, and axillofemoral bypass. The most durable is the aortofemoral bypass, which has a 10-year primary patency of 80%. Five-year primary patency rates for iliac angioplasty, axillofemoral, and femorofemoral bypass are 65%, 70%, and 70%, respectively.

16. What are the patency rates of infrainguinal bypass procedures?

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Infrainguinal bypasses include grafts to the above-knee popliteal, below-knee popliteal, the tibials, and the pedal arteries. Five-year primary patency rates for above-knee popliteal grafts with saphenous vein and prosthetic are 80% and 65%, respectively. Five-year primary patency rates for below-knee saphenous vein popliteal grafts are 75%. Five-year primary patency rates for tibial bypasses are 65%. Five-year primary patency rate for pedal bypass is 50%.

17. Name the primary cause of perioperative mortality.

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The majority (> 90%) of all peripheral vascular disease patients have underlying coronary artery disease. Because of the ambulatory limitations of their peripheral vascular disease, most of these patients have no overt coronary symptoms. The most common cause of perioperative mortality in vascular surgery is myocardial infarction. The decision to work-up and revascularize (surgically or with angioplasty and stenting) coronary artery disease in these patients before the vascular operation is an area of ongoing controversy.

18. Name the primary cause of perioperative morbidity.

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Wound complications occur in ≤ 25% of patients undergoing lower extremity bypass for critical limb ischemia. Postoperative lymphedema, ischemic neuropathy, and prolonged (often measured in months rather than weeks) wound healing are all important issues for these patients.

19. What are the causes of graft failure?

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Early failure (within 30 days) is caused by technical problems with the operation (graft kinking or twisting, narrowing of the anastomosis, bleeding, infection, intimal flaps, or embolization). Graft failure at months 2 through 18 is most often caused by fibrointimal hyperplasia at distal anastomoses or venous valve sites within the graft. Late graft failure (> 18 months) is most frequently caused by recurrent atherosclerosis. Hypercoaguable states are an unusual cause of graft failure.

20. What therapeutic options are available for graft failure?

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If a vein graft fails immediately postoperatively, the correct approach is to explore the distal anastomosis and to fix the presumed technical problem. If a graft fails weeks to months after implantation, the correct course is somewhat controversial. Exploring the graft to mechanically remove thrombus and repair any stenoses has a poor success rate and is not recommended. Using thrombolytic therapy to open the graft and then repair any underlying stenoses seems attractive, but the longevity of grafts treated in this manner has been poor, with < 50% remaining patent at 1 year. Replacing the vein graft with a new bypass provides the most durable alternative providing it is technically possible and the patient is an operative candidate. Inflow grafts that occlude are usually managed with operative thrombectomy and revision of the distal anastomotic stenosis.
KEY POINTS: ARTERIAL INSUFFICIENCY

1. Ankle-brachial index (ABI) is the highest ankle pressure divided by the higher of the two brachial pressures.
2. Critical limb ischemia potentially threatens the viability of the limb.
3. Patients with end-stage renal failure who have critical limb ischemia are at the end of life, with 3-year survival rates < 30%.
4. If a vein graft fails immediately postoperatively, the correct approach is to explore the distal anastomosis and to fix the presumed technical problem.

21. What method of graft surveillance should be used?

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Because of the limited options for occluded vein bypass grafts, ultrasound studies are used to detect stenoses within the graft before occlusion. Various criteria have been championed to accurately detect > 50% narrowing within the graft or native inflow and outflow arteries. Natural history data indicate that grafts with > 50% stenoses left untreated have high intermediate-term failure rates. Recurrent symptoms and changes in the ABI are too insensitive to detect these lesions.

22. What therapeutic options are available for graft stenoses?

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The majority of vein graft stenoses are caused by fibrointimal hyperplasia of sclerotic portions of the graft or valve sites. These lesions are a firm rubber consistency and less amenable to long-term success with percutaneous angioplasty. Open techniques (resection and interposition vein grafting or vein patch angioplasty) are more durable but also cause more patient morbidity.

23. What is the role of iliac angioplasty and stenting?

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Iliac artery atherosclerotic lesions that respond best to balloon angioplasty are of short length (< 3 cm) and are confined to the common iliac artery. Nondiabetic patients fare better than diabetic patients. Current reports of initial success is > 90%, which has improved with the usage of stents to treat iatrogenic arterial dissections (splitting the arterial wall at the intima or media layers), but their effect on long-term success is still unproven.

24. How is viability determined in cases of acute ischemia?

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The five P’s of acute ischemia are pain, pallor, pulselessness, paresthesia, and paralysis. Early findings with acute ischemia include absent pulse, pain, and pallor. Paresthesia and paralysis are later findings. Classical teaching states irreversible muscle ischemia after 6 hours. However, in clinical practice, there are many overlaps. Perhaps the most sensitive finding that indicates limb nonviability is muscle rigor in the calf. The vast majority of ischemic limbs can be managed with initial heparin therapy followed by angiography and surgery or thrombolysis the next day(s).

25. How is thrombus distinguished from embolus in acute ischemia?

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The diagnosis of acute thrombotic versus embolic lower extremity arterial occlusion is complicated. Findings suggestive of embolus include no history of vascular disease, normal contralateral leg circulation, no history of cardiac arrhythmia or recent myocardial infarction, and no known cardiac thrombus. Patients with embolus frequently have rather profound leg ischemia because of the proximal nature of the occlusion (aortic or femoral bifurcation) and the absence of any developed collaterals. Occasionally, arteriography is required to differentiate between the two.

26. When is thrombolysis indicated?

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Thrombolytic therapy requires a patient without contraindications (bleeding risks) and a thrombus that can be crossed with a guidewire. The lytic medication (urokinase, streptokinase, or tissue plasminogen activator) needs to be placed directly within the thrombus. Acute native arterial occlusions should not have evidence of patent outflow arteries (e.g., a thrombosed popliteal artery aneurysm). Arterial embolus in an extremity that is not severely ischemic and can tolerate the time course of successful thrombolysis (frequently multiple hours of intra-arterial infusion and repeat trips to the angiography suite for angiograms to help determine optimal catheter repositioning for complete thrombus lysis). The use of thrombolytic therapy for graft occlusions is more controversial because of the relatively poor long-term durability of these grafts after flow is restored.

27. What is compartment syndrome?

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Reperfusion after acute ischemia can lead to profound tissue swelling in the involved extremity. Edema of the involved muscle can increase the pressure within the fascia bound muscle compartments (i.e., anterior, lateral, deep posterior, and superficial posterior) to a level that exceeds the capillary perfusion pressure (> 30 mmHg). Muscle death is then inevitable unless the pressure is relieved by opening the compartments surgically, a procedure known as fasciotomy. Patients complain of intense pain and swelling, with associated paresthesia. Pedal pulses can remain palpable.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. Carter SA: The challenge and importance of defining critical limb ischemia. Vasc Med 2:126-131, 1997. Medline Similar articles
2. Faries P, Morrissey NJ, Teodorescu V, et al: Recent advances in peripheral angioplasty and stenting. Angiology 52:617-626, 2002.
3. Gahtan V: The noninvasive vascular laboratory. Surg Clin North Am 78:507-518, 1998. Medline Similar articles
4. Lau H, Cheng SW, Hui J: Eighteen-year experience with femoro-femoral bypass. Aust N Z J Surg 70:275-278, 2000. Medline Similar articles Full article
5. Nehler MR, Hiatt WR: Exercise therapy for claudication. Ann Vasc Surg 13:109-114, 1999. Medline Similar articles Full article
6. Nehler MR, Taylor LM Jr, Moneta GL, Porter JM: Natural history, nonoperative treatment, and functional assessment in chronic lower extremity ischemia. In Moore W (ed): Vascular Surgery: A Comprehensive Review. Philadelphia, W.B. Saunders, 1998, pp 251-265. Full article
7. Ouriel K, Veith F: Acute lower limb ischemia: Determinants of outcome. Surgery 124:336-342, 1998. Medline Similar articles
8. Pomposelli FB Jr, Arora S, Gibbons GW, et al: Lower extremity arterial reconstruction in the very elderly: Successful outcome preserves not only the limb but also residential status and ambulatory function. J Vasc Surg 28:215-225, 1998. Medline Similar articles