27: Vascular Flashcards
Which vessel is diseased in foot claudication?
Distal superficial femoral artery or popliteal disease
[Symptoms occur one level below occlusion]
[UpToDate: Classic claudication is characterized by leg pain that is consistently reproduced with exercise and relieved with rest. The degree of symptoms of claudication depends upon the severity of stenosis, the collateral circulation, and the vigor of exercise. Patients with claudication can present with buttock, hip, thigh, calf, or foot pain, alone or in combination. The usual relationships between pain location and corresponding anatomic site of arterial occlusive disease can be summarized as follows:
- Buttock and hip: Aortoiliac disease
- Thigh: Aortoiliac or common femoral artery
- Upper two-thirds of the calf: Superficial femoral artery
- Lower one-third of the calf: Popliteal artery
- Foot claudication: Tibial or peroneal artery]
During abdominal aortic aneurysm repair, reimplantation of the inferior mesenteric artery should be performed if the back pressure is below what level?
Less than 40 mmHg (IE poor back bleeding)
[Other reasons for implantation include previous colonic surgery, stenosis at the superior mesenteric artery, or flow to left colon appears inadequate]
[UpToDate: Colonic ischemia is uncommon following elective AAA repair. The adequacy of perfusion to the left colon should always be assessed prior to completion of the case, and the inferior mesenteric artery should be reimplanted if there is any question of bowel viability.
In general, if backbleeding from the orifice of the inferior mesenteric artery (IMA) within the aneurysm sac is vigorous, indicating adequate collateral flow, or the vessel is occluded (no backbleeding), reimplantation of the IMA into the aortic graft is not necessary. In one trial, patients with a confirmed patent IMA were randomly assigned to replantation or ligation. There was no significant difference in the incidence of ischemic colitis between the groups (replanted: 6 patients, ligated: 10 patients). However, in patients with prior colon resection or reduced inflow to one or both internal iliac arteries, reimplantation of the inferior mesenteric artery is appropriate.]
A herald bleed (episode of GI hemorrage, often accompanied by abdominal pain, which may precede by hours to weeks a catastrophic GI hemorrage) with hematemesis and then blood per rectum in a patient with a history of abdominal aortic surgery is worrisome for what?
Aortoenteric fistula
[Graft erodes into 3rd or 4th portion of duodenum near proximal suture line]
[UpToDate: Early diagnosis of aortoenteric fistula (AEF) associated with bleeding relies upon recognition of the typical “herald bleed,” which is an episode of seemingly self-limited gastrointestinal bleeding that precedes a later catastrophic episode of hemorrhage. AEF must be kept in mind as a possible etiology of massive gastrointestinal bleeding in patients with prior aortic interventions, no matter how long since the intervention.
The classic triad of gastrointestinal bleeding, abdominal pain, and palpable mass occurs in only 6% to 12% of patients found to have AEFs. When the etiology of AEF is an abdominal aortic aneurysm (AAA), a mass can be palpated in 25% to 70%. The unreliability of clinical findings underscores the need to maintain a high index of suspicion in all cases of gastrointestinal bleeding, especially upper gastrointestinal tract bleeding. Further complicating the matter is the fact that patients with AAA/aortic intervention can have gastrointestinal bleeding due to other causes.
The very low incidence of this condition in the general population puts AEF low in the differential diagnosis of gastrointestinal bleeding.]
95% of patients with aortic dissection present with what?
Severe hypertension
[UpToDate: Hypertension is present in 70% of type B dissections, but only in 25% to 35% of type A dissections. The presence of hypotension complicating a type B dissection is rare, seen in less than 5% of patients, and usually implies rupture of the aorta. By contrast, hypotension may be present in 25% of dissections that involve the ascending aorta, potentially as a result of aortic valve disruption leading to severe aortic regurgitation and/or extravasation into the pericardial space leading to cardiac tamponade. Malperfusion of brachiocephalic vessels by the dissection may falsely depress brachial cuff pressures, usually by involving the left subclavian artery origin in the type B dissection patient.]
What are pulse volume recordings used for?
Used to find significant occlusion and at what level
[UpToDate: Modern vascular testing machines use air plethysmography to measure volume changes within the limb, in conjunction with segmental limb pressure measurement. The same pressure cuffs are used for each test.
Cuffs are placed and inflated, one at a time, to a constant standard pressure. Volume changes in the limb segment beneath the cuff are reflected as changes in pressure within the cuff, which is detected by a pressure transducer and converted to an electrical signal to produce an analog pressure pulse contour known as a pulse volume recording (PVR).
A normal PVR waveform is composed of a systolic upstroke with a sharp systolic peak followed by a downstroke that contains a prominent dicrotic notch. Alterations in the pulse volume contour and amplitude indicate proximal arterial obstruction. The degree of these changes reflects disease severity. Mild disease is characterized by loss of the dicrotic notch and an outward “bowing” of the downstroke of the waveform. With severe disease, the amplitude of the waveform is blunted. Pulse volume recordings are most useful in detecting disease in calcified vessels which tend to yield falsely elevated pressure measurements.
Since the absolute amplitude of plethysmographic recordings is influenced by cardiac output and vasomotor tone, interpretation of these measurements should be limited to the comparison of one extremity to the other in the same patient and not between patients. The dicrotic notch may be absent in normal arteries in the presence of low resistance, such as after exercise.]
What are the 3 most commonly affected arteries in fibromuscular dysplasia?
- Renal
- Carotid
- Iliac
[UpToDate: The most frequently involved arteries are the renal and internal carotid arteries, followed by the vertebral, visceral, and external iliac arteries.
Patients with fibromuscular dysplasia (FMD) have involvement of the renal arteries approximately 75% to 80% of the time and involvement of the extracranial cerebrovascular arteries (eg, carotid and vertebral arteries) approximately 75% of the time. Approximately two-thirds of patients have multiple arteries involved.
Among adults, FMD is more common among females. In most large series, approximately 90% of cases are in women. There does not appear to be a female predominance among children with FMD.
In the past, it was believed that FMD was a disease of young women. However, older individuals account for a large proportion of affected patients in several cohorts. As an example, in the United States FMD Registry, the mean age at diagnosis was 52 years, with a range of 5 to 86 years.]
Venous ulcers of what size often heal without surgery?
Less than 3cm
What is the treatment for varicose veins?
Sclerotherapy
[UpToDate: Chemical ablation involves the introduction of an irritant agent into the vein, causing endothelial damage by either detergent or osmotic action. Liquid sclerosant preparations are typically used to treat telangiectasias, reticular veins, and small varicose veins. Ultrasound-guided sclerotherapy, with the injection of the sclerosant at the level of refluxing perforator veins, has also been used to treat the associated clusters of varicose veins. This technique has been used with good long-term results and without significant complications, but requires an experienced practitioner. Endovenous techniques can also be used to ablate perforator reflux with the use of special probes.
The choice of ablation method depends upon the size of the varicose veins, their location, and presence or absence of venous reflux. Meta-analyses comparing surgery with minimally invasive therapies (sclerotherapy, radiofrequency ablation, laser ablation) have concluded that minimally invasive therapies appear to be at least as effective as surgical excision, with long-term success rates of 78% to 84%. Postoperative pain is generally less and return to work quicker with minimally invasive therapies, compared with surgery. Minimally invasive procedures are generally associated with fewer complications. In one trial, each of the groups showed significant improvements in quality-of-life scores, and 84.3% of treated patients had improved CEAP clinical category following treatment, although vein closure rates varied at one year (highest at 88.5% for endovenous laser ablation, followed by 88.2% for conventional surgery, and 72.2% for foam sclerotherapy).
A later trial involving 798 participants with primary varicose veins compared the outcomes of foam sclerotherapy, laser, and surgery. Clinical success was similar between the groups, but successful ablation of the main trunks of the saphenous vein was less common for foam sclerotherapy compared with surgery. No significant differences were found for quality of life. The frequency of procedural complications was similar for the foam sclerotherapy and surgery groups (6% and 7%, respectively), but was lower in the laser group (1%). The frequency of serious adverse events (approximately 3%) was similar among the groups. A trial comparing saphenous vein high ligation plus phlebectomy with endovenous laser ablation reported follow-up to five years at which time there were no significant differences in rates of recurrent varicose veins or reoperation.
A review of randomized trials comparing ultrasound-guided foam sclerotherapy with endothermal ablation noted that although anatomical success appeared higher with endothermal ablation, clinical success and patient-reported outcome measures were similar. Morbidity and complication rates were very low and not significantly different. Ultrasound-guided foam sclerotherapy was less expensive than endothermal ablation.]
Late swelling following a lower extremity bypass is concerning for what?
Deep vein thrombosis
[UpToDate: We agree with all major society guidelines which recommend long-term aspirin therapy or clopidogrel for all patients with peripheral artery disease.
The 2012 American College of Chest Physicians (ACCP) guideline on antithrombotic therapy for peripheral artery occlusive disease made the following recommendations for the use of antithrombotic agents in patients undergoing infrainguinal vascular surgery:
- Aspirin therapy (75 to 100 mg/day) should begin preoperatively and continue indefinitely in all patients undergoing infrainguinal bypass (to prevent graft failure) or arterial reconstruction. Clopidogrel (clopidogrel 75 mg daily) is an alternative to aspirin in those who cannot take aspirin.
- In patients undergoing below-knee bypass graft surgery with prosthetic grafts, clopidogrel plus aspirin is recommended for a period of one year. For all other patients single rather than dual antiplatelet therapy should be give.]
What is the 1st branch of the external carotid artery?
Superior thyroid artery
[Wikipedia: As the artery travels upwards, it supplies:
- Superior thyroid artery, arising from its anterior aspect
- Ascending pharyngeal artery - arising from medial, or deep, aspect
- Lingual artery - arising from its anterior aspect
- Facial artery - arise from its anterior aspect
- Occipital artery - arising from its posterior aspect
- Posterior auricular artery - arising from posterior aspect
The external carotid artery terminates as two branches:
- Maxillary artery
- Superficial temporal artery]
What are the indications for repair of descending aortic aneurysm?
- Greater than 5.5 cm if endovascular repair is possible
- Greater than 6.5cm if open repair is needed
[UpToDate: For most patients with asymptomatic TAA, we use the following thresholds as criteria for elective repair.
Descending TAA:
- For most average-sized adults: diameter of 6 to 7 cm
- Patient with high surgical risk: diameter ≥7 cm
- For patients with genetically-mediated conditions (syndromic or nonsyndromic), a lower diameter (eg, 5.0 to 6.0 cm depending on the condition) or aortic size index is suggested as an indicator for repair.
- For smaller patients, including many women, a diameter greater than twice the diameter of the nonaneurysmal aorta (normal segment) or aortic size index can be used.
- Rapid expansion ≥10 mm per year for aneurysms <5 cm in diameter. For patients with associated genetically-mediated conditions, a lower expansion rate (eg, >5 mm/year) is suggested as an indicator for repair.]
What is the treatment for median arcuate ligament syndrome?
- Transect median arcuate ligament
- May need arterial reconstruction
[UpToDate: Surgical treatment is the only option for patients with persistent abdominal pain and demonstrated celiac artery compression on imaging studies, since there are no medical therapies. Surgical options include celiac artery decompression alone or surgical decompression combined with celiac artery angioplasty/stent or vascular reconstruction. Surgical decompression involves division of the fibers of the median arcuate ligament and celiac plexus (celiac ganglionectomy). Laparoscopic and robotic-assisted laparoscopic approaches have been reported. With these techniques, a laparoscopic ultrasound probe can be used to confirm patency of the celiac artery once it has been decompressed. Depending on the results of the procedure, secondary celiac stenting can be performed. Regardless of the approach, decompression of the celiac axis does not always relieve symptoms.
The optimal surgical approach remains debated. Celiac artery reconstruction appears to be more commonly performed during open surgical celiac decompression procedures, but a significant number of patients have relief of their symptoms with decompression alone. In a study that compared open and laparoscopic approaches, the distribution of treatments was as follows:
- Open decompression 279/400 (70%)
- With arterial reconstruction (n = 70)
- Without arterial reconstruction (n = 201)
- Laparoscopic decompression 121/400 (30%)
- With percutaneous mesenteric angioplasty (n = 16)
- With open angioplasty/bypass (n = 2)
Celiac artery decompression can be combined with balloon angioplasty/stenting of the celiac, surgical angioplasty, or interposition grafting using an open (eg, open decompression/angioplasty or bypass) or hybrid approach (eg, laparoscopic decompression, percutaneous angioplasty). A primary percutaneous approach without celiac artery decompression is not an option since the underlying problem is extrinsic compression (not intrinsic disease such as that caused by atherosclerosis).]
Which leg is more commonly involved in deep venous thrombosis?
Left leg (Longer left iliac vein)
Following dissection in the groin, what can you do to identify the lymphatic channels supplying a lymphocele if having trouble locating it?
Inject isosulfan blue dye into the foot
What is the second most common pathogen responsible for a mycotic abdominal aneurysms?
Staphylococcus
[#1 is salmonella]
[UpToDate: Blood cultures are positive in 50% to 85% of cases. Organisms have been isolated from aneurysmal tissue in up to 76% of patients. In one case series, multiple organisms were isolated in 8%, and no pathogen was identified in 25% of cases.
Although bacteriologic patterns continue to evolve over time, the organisms with the greatest affinity for the arterial wall, Staphylococcus spp and Salmonella spp, remain the most common. Staphylococcus aureus is the most common pathogen reported in 28% to 71% of cases. In several reports of infected aneurysms, methicillin-resistant S. aureus (MRSA) predominates. In one series of preexisting aneurysms, Staphylococcus epidermidis was the most prevalent organism. Infected aneurysm due to vancomycin-intermediate S. aureus (VISA) has also been described.
Salmonella is reported in 15% to 24% of cases. The diseased aorta appears to be vulnerable to Salmonella, and this pathogen is frequently isolated in infected aneurysms due to bacteremic seeding of atherosclerotic plaque.
Streptococcus pneumoniae was a frequent etiology of infected aneurysms in the pre-antibiotic era but became rare with the advent of penicillin; however, S. pneumoniae may be reemerging as a cause of infected aneurysms.
Other gram-negative organisms are also associated with bacteremic seeding. In one study, although gram-positive organisms predominated, gram-negative organisms were seen in 35% of cases. In this study, gram-negative infections were associated with a higher incidence of aneurysm rupture (84% vs 10%) and mortality (84% vs 50%) compared with gram-positive organisms.
Less common causes of infected aneurysm include Treponema pallidum and Mycobacterium spp. Syphilis (T. pallidum) once caused up to 50% of infected aneurysms. Tuberculosis is a rare cause of infected aneurysms and is most often due to erosion of periaortic lymph nodes into the aortic wall. One review of cases of infected aneurysm caused by Mycobacterium tuberculosis found only 41 cases between 1945 and 1999.]
What percent of patients with abdominal aortic aneurysm rupture die if they reach the hospital alive?
50%
[UpToDate: The mortality associated with ruptured AAA may be as high as 90% when patients who die at home or upon arrival to the hospital are taken into account. In spite of obvious improvements in pre-hospital care, cardiovascular anesthesia, and critical care, surgical mortality following open repair of ruptured AAA has changed very little, remaining about 30% to 50%. Although endovascular aneurysm repair may improve survival following AAA rupture, this has not been definitively established.]
Diarrhea (especially bloody diarrhea) following an abdominal aortic aneurysm repair is worrisome for what?
Ischemic colitis
[UpToDate: Bowel ischemia can affect the small or large intestine. Acute mesenteric ischemia is rare with infrarenal AAA repair. Colonic ischemia is more likely to occur following open repair of ruptured AAA, for which the incidence is between 7% and 27% compared with 0.6% to 13% for elective AAA repair. The incidence varies greatly depending upon the diagnostic algorithm to detect it. When bowel ischemia complicates AAA repair, mortality is increased.
The majority of patients do not have symptoms and only 30% will have bloody diarrhea. Patients with full thickness ischemia are treated with colon resection. The diagnosis and management of colon ischemia is discussed elsewhere.]
Ankle-brachial index (ABI) can be very inaccurate in patients with which condition?
Diabetes
[This is secondary to incompressibility of vessels. Often have to rely on doppler waveforms in these patients]
[UpToDate: The toe-brachial index (TBI) is a more reliable indicator of limb perfusion in patients with diabetes because the small vessels of the toes are frequently spared from medial calcification.
The TBI is obtained by placing a pneumatic cuff on one of the toes. The great toe is usually chosen but in the face of amputation the second or other toe is used. A photo-electrode is placed on the end of the toe to obtain a photoplethysmographic (PPG) arterial waveform using infrared light. The infrared light is transmitted into the superficial layers of the skin and the reflected portion is received by a photosensor within the photo-electrode. The signal is proportional to the quantity of red blood cells in the cutaneous circulation.
Analogous to the ankle and wrist pressure measurements, the toe cuff is inflated until the PPG waveform flattens and then the cuff is slowly deflated. The systolic pressure is recorded at the point in which the baseline waveform is re-established. The ratio of the recorded toe systolic pressure to the higher of the two brachial pressures gives the TBI.
A pressure gradient of 20 to 30 mmHg normally exists between the ankle and the toe, and thus, a normal toe-brachial index is 0.7 to 0.8. An absolute toe pressure >30 mmHg is favorable for wound healing, although toe pressures >45 to 55 mmHg may be required for healing in patients with diabetes. Toe pressures are useful to define perfusion at the level of the foot, especially in patients with incompressible vessels, but they provide no indication of the site of occlusive disease. In addition to measuring toe systolic pressures, the toe Doppler arterial waveforms should also be evaluated.]
What is migrating thrombophlebitis associated with?
Pancreatic cancer
[UpToDate: Unexplained superficial thrombophlebitis, which may be migratory (classic Trousseau’s syndrome), is sometimes present and reflects the hypercoagulable state that frequently accompanies pancreatic cancer. There is a particularly high incidence of thromboembolic events (both venous and arterial), particularly in the setting of advanced disease, and clinicians should maintain a high index of suspicion. Multiple arterial emboli resulting from nonbacterial thrombotic endocarditis may occasionally be the presenting sign of a pancreatic cancer. Thromboembolic complications occur more commonly in patients with tumors arising in the tail or body of the pancreas.]
What is the treatment of nonocclusive mesenteric ischemia?
- Volume resuscitation
- Catheter-directed nitroglycerin can increase visceral blood flow
- Also need to increase cardiac output (dobutamine)
- Resection of infarcted bowel if present
[UpToDate: The treatment of nonocclusive mesenteric ischemia focuses on removing inciting factors (vasoconstrictive medications), treating underlying causes (heart failure, sepsis), hemodynamic support and monitoring, and intraarterial infusion of vasodilators, if necessary.]
Which protein is defective in Marfan syndrome?
Fibrillin (connective tissue elastic fiber)
[UpToDate: Marfan syndrome (MFS) is a highly variable systemic tissue disorder with clinical characteristics similar to a variety of other hereditary disorders from which it should be distinguished. MFS is almost exclusively inherited in an autosomal dominant manner, although rare case reports have described recessive fibrillin 1 gene (FBN1) mutations. While most individuals with MFS have an affected parent, 25% or more of probands have MFS as the result of a de novo mutation.
Most patients with the typical Marfan phenotype harbor mutations involving the gene (FBN1) encoding the connective tissue protein fibrillin-1. However, FBN1 mutations also cause a wide range of milder phenotypes that often show at least some overlap with the classic Marfan phenotype.
In a minority of cases (less than 10%) with typical Marfan phenotype, no mutation in FBN1 is identified. Studies have suggested that at least some of these cases are due to a complete allele deletion, more complex rearrangements, or alterations in regulatory sequences involving the FBN1 gene. In some of these individuals with atypical presentations reminiscent of MFS, an inactivating mutation in a gene encoding for transforming growth factor-beta receptor (TGFBR) may be responsible.]
What is the treatment for a carotid body tumor?
Resection
[UpToDate: Complete surgical resection for cervical (carotid body, vagal, perithyroid) paragangliomas was historically considered the treatment of choice for cervical paragangliomas. Cure rates after complete resection of a benign carotid body tumor are 89% to 100%. Although few data are available, long-term control of disease was reported in 93% of vagal paragangliomas in a systematic review of 211 cases. Cure rates are lower in patients with regional nodal metastases (five-year survival 77% in one series from the National Cancer Database) and adjuvant RT is frequently recommended, although its benefits are unproven.
Resection of carotid body tumors is performed via a transcervical approach. Special care must be taken to avoid injury to the cranial nerves. Especially in Shamblin class III tumors, there is also the potential for injury to the common or internal carotid artery.]
What happens to the ankle-brachial index (ABI) in patients with claudication as they go from resting to walking?
The ABI drops (ABI may be 0.9 but can drop to less than 0.6 with exercise, resulting in pain)
[UpToDate: Some patients with PAD who have a classic history of claudication, and others with atypical extremity pain, have a normal resting ABI (0.91 to 1.30). For these patients, exercise testing is indicated. Abnormal exercise ABIs support a diagnosis of PAD as the etiology of their symptoms.
The study should be performed in a vascular laboratory using a standardized exercise protocol (fixed or graded) and a motorized treadmill to ensure reproducibility of measurements of pain-free walking distance and maximal walking distance.
Exercise treadmill tests are useful for providing the most objective evidence of the magnitude of the functional limitation in patients with claudication, and can also be used to guide the response to treatment.]
What are the 3 indications for repair of an ascending aortic aneurysm?
- Acutely symptomatic
- Greater than or equal to 5.5 cm (> 5.0 cm with Marfans)
- Rapid increase in size (>0.5cm/yr)
[UpToDate: For most patients with asymptomatic thoracic aortic aneurysm (TAA), we use the following thresholds as criteria for elective repair.
Ascending TAA:
- End-diastolic aortic diameter of 5 to 6 cm or aortic size index (aortic diameter [cm] divided by body surface area [m2]) ≥2.75 cm/m2. A body surface area calculator can be found in the link.
- For patients with genetically-mediated TAAD, including syndromic conditions such as Marfan, Loeys-Dietz, vascular Ehlers-Danlos, and Turner syndromes, and nonsyndromic conditions like familial TAAD or bicuspid aortic valve, a lower diameter (eg, 4.5 to 5.0 cm depending on the condition) or aortic size index is suggested as an indicator for repair.
- Non-Turner’s patients undergoing aortic valve surgery: end-diastolic aortic diameter >4.5 cm in diameter at the time of aortic valve surgery.
- Rapid expansion ≥10 mm per year for aneurysms <5 cm in diameter. For patients with associated genetically-mediated conditions, a lower expansion rate (eg, >5 mm/year) is suggested as an indicator for repair.]
What is the most common site of carotid stenosis?
Carotid bifurcation
[UpToDate: The locations most frequently affected by carotid atherosclerosis are the proximal internal carotid artery (ie, the origin) and the common carotid artery bifurcation. Progression of atheromatous plaque at the carotid bifurcation results in luminal narrowing, often accompanied by ulceration. This process can lead to ischemic stroke or transient ischemic attack from embolization, thrombosis, or hemodynamic compromise.]
What is the treatment for superficial thrombophlebitis?
NSAIDS, warm packs, ambulation
[UpToDate: For all patients diagnosed with phlebitis and thrombosis of the lower extremity superficial veins, supportive measures should be instituted and consist of extremity elevation, warm or cool compresses, compression stockings, and pain management.
Risk factors for deep vein thrombosis in those with phlebitis and thrombosis of the lower extremity veins include more extensive thrombosis ≥5 cm, anatomic proximity of thrombus to the deep venous system (≤5 cm from the saphenofemoral or saphenopopliteal junction), and medical risk factors for DVT (eg, prior DVT, thrombophilia, malignancy, estrogen therapy).
- For patients with phlebitis and thrombosis of the lower extremity veins at low risk for DVT, we suggest oral nonsteroidal anti-inflammatory drugs (NSAIDs) rather than anticoagulation as first-line drug therapy (Grade 2B).
- For patients with SVT (not related to endovenous ablation therapy) who are at increased risk for DVT, we suggest anticoagulation for four weeks over supportive care alone (ie, nonsteroidal antiinflammatory drugs and compression stockings) (Grade 2B). Fondaparinux, low molecular weight heparin, unfractionated heparin, and vitamin K antagonists are equally effective. A decision to anticoagulate the patient when thrombus approaches the deep venous system at other sites (ie, saphenopopliteal junction, perforator veins) should be individualized; either anticoagulation or serial duplex ultrasound may be appropriate.
For patients who present with SVT after radiofrequency or laser vein ablation, we suggest not routinely anticoagulating the patient (Grade 2C). These patients are not at high risk for DVT and are managed initially with supportive care and repeat duplex ultrasound.
For thrombus extending into the deep venous system, the patient is treated according to standard protocols for DVT.]
Pain of sudden onset that is out of proportion to exam and hematochezia are concerning for what?
Superior mesenteric artery embolization (mesenteric ishchemia)
[UpToDate: The typical clinical triad of acute embolic occlusion in an older adult patient with atrial fibrillation (or other source for embolism) and severe abdominal pain out of proportion to the physical examination is present in one-third to one-half of patients. Bowel emptying, nausea, and vomiting are also common, but bloody bowel movements are less common, unless advanced ischemia is present. The patient may be subtherapeutic on previously prescribed antithrombotic therapy. A prior embolic event is present in approximately one-third of patients. It is particularly important in these patients to perform a complete vascular examination examining the carotid, upper extremity, and lower extremity pulses for evidence of reduced perfusion related to synchronous embolism. Over 20% of acute mesenteric emboli are multiple.
For patients with a history of infective endocarditis, most emboli (cerebral most common followed by visceral then lower extremity) occur within the first two to four weeks of antimicrobial therapy and may be more common in patients with mitral valve involvement, larger vegetation size (largest are associated with streptococcus), staphylococcus independent of vegetation size, and increasing vegetation size while on treatment.]
What is the Stanford classification of aortic dissection?
- Class A: Any ascending aortic involvement
- Class B: Descending aortic involvement only
[Based on presence or absence of involvement of ascending aorta]
Which artery is often sacrificed during an abdominal aortic aneurysm repair?
Inferior mesenteric artery
[Can cause ischemia most commonly to the left colon]
[UpToDate: Colonic ischemia is uncommon following elective AAA repair. The adequacy of perfusion to the left colon should always be assessed prior to completion of the case, and the inferior mesenteric artery should be reimplanted if there is any question of bowel viability.
In general, if backbleeding from the orifice of the inferior mesenteric artery (IMA) within the aneurysm sac is vigorous, indicating adequate collateral flow, or the vessel is occluded (no backbleeding), reimplantation of the IMA into the aortic graft is not necessary. In one trial, patients with a confirmed patent IMA were randomly assigned to replantation or ligation. There was no significant difference in the incidence of ischemic colitis between the groups (replanted: 6 patients, ligated: 10 patients). However, in patients with prior colon resection or reduced inflow to one or both internal iliac arteries, reimplantation of the inferior mesenteric artery is appropriate.]
Which nerves and/or arteries travel in the deep posterior compartment of the leg?
- Tibial nerve
- Posterior tibial artery
- Peroneal artery
What are the risk factors for abdominal aortic aneurysm?
- Male gender
- Old age
- Smoking
- Family history
[UpToDate: The risk factors associated with an increased risk of AAA include:
- Smoking (current or past)
- Male gender
- Advancing age
- Caucasian race
- Atherosclerosis
- Hypertension
- Family history of AAA
- Other large artery aneurysms (eg, iliac, femoral, popliteal)
A decreased risk of AAA is associated with:
- Female gender
- Non-Caucasian race
- Diabetes]
All splanchnic artery aneurysms >2cm have a 50% risk for rupture and should be repaired at diagnosis except for which one?
Splenic artery aneurysms
[Only 2% risk of rupture]
[UpToDate: In a large series, rupture was the presenting symptom for splenic artery aneurysm in about 5% of patients, with a mean diameter of 3.5 cm (3.2 cm for males, 2.3 cm for females). The mean diameter of the nonruptured splenic artery aneurysms was 2.2 cm.
The classic presentation of ruptured splenic artery aneurysm is the “double rupture phenomenon.” Initial rupture of splenic artery aneurysm is associated with severe abdominal pain and initial hemodynamic instability, which is compensated for and followed by a period of relative normalization. This latent period is due to containment rupture within the lesser sac and tamponade of the splenic artery aneurysm. If untreated, the lesser sac can give way leading to free rupture into the peritoneal cavity with recurrent hemodynamic instability.
Treatment options for splenic artery aneurysms (SAAs) include open surgical repair, percutaneous intervention with either embolization coils or covered stents, and laparoscopic excision or clipping. Among these, percutaneous intervention of SAA has become increasingly popular due to its high technical success rates and low morbidity.
SAAs are often ideal for coil embolization because of the collateral supply from the short gastric arteries. Reported success rates range from 90% to 100%. For proximal and midvessel SAA, stent-grafts can be used to maintain perfusion in the main artery; however, tortuosity of the artery can complicate stent-graft placement and deployment. Selective splenic artery catheterization and coil embolization of the aneurysm sac are generally recommended for high-risk patients with aneurysm rupture.
As with endovascular treatment, the location of the aneurysm, as well as its presentation, generally dictates the type of open procedure that is performed. Resection with end-end repair can be performed in many cases, especially with proximal and midvessel SAA, owing to the redundancy and tortuosity of the artery. This allows for splenic preservation, which has important implications for the immune system. Splenectomy is performed more commonly in the setting of aneurysm rupture, and may be necessary for aneurysms involving the splenic hilum.
Complications of SAA coil embolization include splenic infarct and reperfusion of the aneurysm, which occurs in 5% to 20% of patients. Splenic infarcts are common occurrences in patients with portal hypertension or hilar SAA, but usually are successfully treated with pain control. In reported series, splenic infarcts occurred in 25% to 40% of the patients treated, but no patient required any further treatment. To evaluate for reperfusion of the aneurysm, annual follow-up with computed tomography (CT) or magnetic resonance imaging (MRI) is necessary.]
What is the treatment for fibromuscular dysplasia?
Percutaneous transluminal angioplasty
[Bypass if that fails]
[UpToDate: In most patients with FMD who are selected for renal revascularization, we suggest percutaneous transluminal angioplasty (PTA) rather than surgery (Grade 2C). However, surgery is preferred if the arterial anatomy is not amenable to PTA, as in patients with small renal arteries (<4 mm), with branch renal artery disease, or with extensive intimal fibroplasia. In addition, patients who fail PTA should have surgical repair.
PTA is typically performed without placement of stent (unlike PTA for atherosclerotic renal artery stenosis). In general, stents are only placed when a dissection results from the performance of PTA or in the rare instance in which a perforation of the renal artery occurs during angioplasty. When PTA is performed, physiologic assessment should be made using a pressure guidewire, with a mean gradient of <5 mmHg across the treated segment suggesting a satisfactory result. It is important to measure pressure gradients both before and after angioplasty to be certain that all of the intraluminal fibrous webs have been adequately disrupted. Post-procedure renal duplex scanning should also be used to assess the adequacy of intervention. In successfully treated patients, the degree of turbulence is less prominent, and velocity elevation in the mid-distal renal artery returns to normal.
If surgery is performed, aortorenal bypass with a saphenous vein graft is the most commonly performed revascularization procedure in patients with renal FMD.
An important limitation of pursuing medical therapy alone is that renal artery stenosis and kidney dysfunction may progress despite good blood pressure control. As a result, every patient with FMD should have periodic measurement of serum creatinine every 6 months and duplex ultrasound every 6 to 12 months. Patients who undergo percutaneous revascularization should have duplex ultrasonography and serum creatinine measurements performed on the first office visit post procedure, then every six months for two years, and then yearly if stable.]
What is the #1 cause of acute death after surgery to repair an abdominal aortic aneurysm?
Myocardial infarction
[UpToDate: Perioperative (30 day) mortality for elective open AAA repair in contemporary series is between 1% and 5%. The cause of death for most patients is multisystem organ failure. For patients who survive open AAA repair, the main cause of death in the long-term is cardiovascular disease. In a study that evaluated 297 patients following open infrarenal/juxtarenal AAA repair, cardiovascular events occurred at a rate of 0.16 cardiovascular events/patient-year. Freedom from cardiovascular events at 1, 5, 10 and 15 years was 94%, 67%, 46%, and 28%, respectively. Survival was 97%, 75%, 51%, and 32%, respectively. The main cause of death was cardiovascular disease (18.2%), followed by cancer (14.5%). Only four (1.3%) deaths were graft-related.
Complications following open AAA repair are similar to other major surgical procedures and are most often related to preexisting medical conditions. Complications include heart failure, myocardial ischemia, acute kidney injury, pulmonary insufficiency and pneumonia. Management of these complications can be found in separate topic reviews. A thorough preoperative evaluation and proper patient selection help to reduce the incidence of these complications.
Perioperative complications related to the aortic procedure include lower extremity ischemia, bowel ischemia, pelvic ischemia, renal dysfunction, and late complications include incisional hernia, anastomotic aneurysm and graft infection/aortoenteric fistula. Late complications of open surgical aneurysm repair were identified in 9.5% of patients in one retrospective review. The mean time between aortic repairs was 11 years. When compared with 993 other patients for whom endovascular repair was the primary aortic repair, late complications following primary open AAA repair occurred in patients who were significantly younger at the time of their first repair (61 vs 74 years), and more patients had a family history of aneurysm (20% vs 7%).
A systematic review identified four trials that included 1532 patients who were considered suitable candidates for endovascular or open repair of nonruptured abdominal aortic aneurysms larger than 5.0 cm in diameter. The 30-day all-cause mortality was significantly lower with endovascular repair (1.6% ves 4.8%). The short-term survival advantage of endovascular repair appears to be much greater when endovascular repair is limited to patients at highest risk for open surgery. This was illustrated in a report of 454 consecutive patients who underwent elective repair (206 endovascular and 248 open surgeries) of an abdominal aortic aneurysm. The overall 30-day mortality rates did not significantly differ for endografting and surgery (2.4% and 4.8%, respectively). However, among patients at highest surgical risk (American Society of Anesthesiologists [ASA] class IV), the 30-day mortality rates were lower for endovascular compared with open repair (4.7% vs 19.2%).]
What causes roughly 50% of visceral ischemia?
Embolic occlusion
[thrombotic occlusion - 25%, nonocclusive - 15%, venous thrombosis - 5%]
[UpToDate: The major etiologies of mesenteric ischemia are mesenteric arterial embolism (50%), mesenteric arterial thrombosis (15% to 25%), mesenteric venous thrombosis (5%), and nonocclusive mesenteric ischemia due to intestinal hypoperfusion (20 to 30%).
Both arterial and venous occlusion can lead to intestinal ischemia from twisting of the bowel (ie, volvulus) around a fixed attachment (ie, adhesion, mesenteric defect) or incarceration and strangulation of intestinal contents within a hernia. Patients with excessive bowel distention from bowel obstruction can get hypoperfusion from increased venous pressure and/or venous thrombosis of the involved segment of intestine.]
What is the most common cause of thoracic outlet syndrome of the subclavian artery?
Compression of subclavian artery usually secondary to anterior scalene hypertrophy (weight lifters)
[Subclavian artery is least common cause of thoracic outlet syndrome]
[UpToDate: Symptoms of arterial compression are the least common type of thoracic outlet syndrome, accounting for only about 1% of cases. Symptoms develop spontaneously unrelated to work or trauma. Arterial TOS (aTOS) is almost always associated with a cervical rib or anomalous rib. It occurs in young patients without typical atherosclerotic risk factors distinguishing it from peripheral artery disease.
Hand ischemia with symptoms of pain, pallor, paresthesia, and coldness is the most common presentation. These symptoms are due to arterial thromboembolization arising from mural thrombus from the subclavian artery or a subclavian aneurysm. In young women, this etiology must be differentiated from the Raynaud phenomenon.
Other presentations include upper extremity pain with activity due to subclavian artery stenosis or occlusion. Rarely, thrombus from the subclavian artery can propagate and embolize retrograde, causing stroke. However, because of the rich collateral circulation around the shoulder, arm ischemia is uncommon.
On physical examination, patients may have a lower systolic blood pressure in the affected arm and distal pulses at the wrist may be diminished or absent. In patients with thromboembolism, finger ischemia or patchy ischemic skin may be present. A bruit or a thrill may be appreciated over the subclavian artery, and in patients who have developed post-stenotic aneurysmal changes, a pulsatile supraclavicular mass may be palpable. In contrast to patients with nTOS, the scalene muscles will not be tender and provocative maneuvers will not elicit any symptoms.]
The two vertebral arteries that supply some of the blood to the head are branches from which artery?
Subclavian artery
Where does adventitial cystic disease (a collection of mucinous material within adventitial wall of the affected vessel) most commonly occur?
Popliteal fossa
[Often bilateral]
[Cleveland Clinic: Adventitial cystic disease is a rare condition in which a cyst forms in an artery and narrows or blocks blood flow. The condition usually affects the popliteal artery, which supplies blood to the knee joint and calf muscles and foot. In rare cases, the condition can cause cysts to form in other arteries.]
[UpToDate: Adventitial cystic disease is a rare entity that can lead to arterial obstruction related to mucoid degeneration of the artery. When it occurs in the femoral or popliteal artery, claudication symptoms are indistinguishable from atherosclerotic popliteal disease. Patients tend to be younger and typical risk factors for cardiovascular disease are often absent.]
What are the indications for an inferior vena cava filter?
- Anticoagulation is contraindicated
- Pulmonary embolism while on coumadin
- Free-floating iliofemoral thrombi
- Following pulmonary embolectomy
[UpToDate: The only widely accepted and validated indications for vena cava filter placement in patients with thromboembolism are an absolute contraindication to therapeutic anticoagulation, complication to anticoagulation, and failure of anticoagulation when there is acute proximal venous thrombosis.
Other possible treatment indications, and prophylactic filter placement, are more controversial. As a result, the use of caval filters varies widely. Although vena cava filters can be placed into the superior vena cava in select situations, the inferior vena cava (IVC) is the standard location for filter placement.
The filter should be placed in a location that will reduce the risk of venous thromboembolism through all the likely venous pathways. With standard anatomy, the filter should be positioned with the tip of the filter just at the inflow of the renal veins, which minimizes the accumulation of thrombus above the filter in the event of filter thrombosis. If the filter thrombosis is substantially below the renal vein inflow, then the dead space between the thrombosed filter and the renal veins would allow a clot to form, potentially leading to pulmonary embolism. IVC filters placed across the renal veins may have no significant effect on renal function, but they may not be stable in a pararenal location due to the inability of fixation mechanisms to fully engage the IVC wall.
If a circumaortic left renal vein is present, then if possible, the filter should be placed inferior to the lower limb of the renal vein. The rationale is that the circumaortic vein can serve as a conduit for thrombus to pass from the lower extremities through the left renal system and into the lungs. This is particularly a concern if a filter above a circumaortic left renal vein thromboses. In some cases, the lower of the renal vein limb is close to the confluence of the iliac veins, and there is not enough room to put the filter below the lower limb and above the confluence. In this case, a decision needs to be made whether to place the filter spanning the lower limb but with the legs of the filter in the IVC above the confluence of the iliac veins (the more common approach), or to place IVC filters in the iliac veins bilaterally. Placement covering the renal veins potentially places veins at risk for damage/thrombosis, but there is no evidence of complications from this approach.
In the setting of duplication of the IVC, a filter should be placed in each of the left and right IVC segments.]
What is the treatment for a type IV endoleak following abdominal aortic aneurysm repair?
Observation
[Can place nonporous stent if that fails. Type IV leak is due to graft porosity.]
[UpToDate: Type IV endoleak is associated with graft porosity and is self-limited, typically resolving in 24 hours. It has not been associated with any long-term adverse events and does not require treatment.]
What is the treatment for hypertension following a carotid endarterectomy (due to injury to the carotid body)?
Nipride to avoid bleeding
[UpToDate: Hypertension – Postoperative hypertension may result in abnormally increased cerebral blood flow because cerebral autoregulation may be disrupted following CEA or CAS. Thus, it is important to strictly control postoperative hypertension, maintaining systolic blood pressure at 100 to 150 mmHg.
Labetalol (5 to 10 mg every 5 minutes), nicardipine (100 to 500 mcg), or esmolol (10 to 50 mg) may be administered in bolus doses. If blood pressure is not controlled with one or more of these bolused medications, intravenous infusion of labetalol (0.5 to 2 mg/minute), nitroprusside (10 to 400 mcg/minute; 0.1 to 4.0 mcg/kg/minute), nitroglycerin (10 to 400 mcg/minute; 0.1 to 4 mcg/kg/minute), nicardipine (initial dose of 3 to 6 mg/hour titrated to a maximum dose of 15 mg/hour), or esmolol (50 to 300 mcg/kg/minute) is administered to control hypertension.
Occasionally, postoperative hypertension is a predecessor of a condition known as cerebral hyperperfusion syndrome. This syndrome is characterized by cerebral edema, petechial or frank intracerebral hemorrhage, and seizures.]
What is the rate of re-stenosis after carotid endarterectomy?
15%
[UpToDate: Restenosis of the carotid artery after carotid endarterectomy (CEA) was reported in up to 20% of patients in early studies, although lower values (2.6% to 10% at five years) have been reported in later studies.
The pathology of the restenotic lesion is related to the time of presentation after initial surgery. Most patients with restenosis are asymptomatic and are identified with routine follow-up carotid imaging.
“Early” restenosis is that which occurs within two to three years after CEA. Patients with early restenosis frequently have highly cellular and minimally ulcerated intimal hyperplasia, similar to that which occurs after angioplasty or with stent placement. As a result, there is a low likelihood of symptomatic embolization.
“Late” restenosis occurs more than two to three years after CEA and generally results from progression of atherosclerotic disease. It is frequently associated with irregular plaques that may serve as an embolic source.]
What is the most common location of a pseudoaneurysm (collection of blood in continuity with the arterial system but not enclosed by all 3 layers of the arterial wall)?
Femoral artery
What is the treatment for temporal arteritis?
- Steroids
- Bypass of large vessels if needed
[No endarterectomy]
[UpToDate: Glucocorticoid treatment should be instituted promptly once the diagnosis of GCA is suspected strongly, often even before it is confirmed. For patients in whom the diagnostic suspicion of GCA is high, especially those with recent or threatened vascular complications such as visual loss, therapy should be started immediately. A temporal artery biopsy should be obtained as soon as possible, but treatment should not be withheld while awaiting the performance or the results of the biopsy.
If the temporal or other artery biopsies reveal no evidence of arteritis but if clinical suspicion of GCA remains strong, glucocorticoid treatment should be continued. Even with optimal bilateral temporal artery biopsy performance, false-negative results occur in at least 9% of GCA cases and probably in even higher percentages in most settings.
Daily dosing is more effective than alternate day dosing, but split dosing (ie, the use of multiple doses during a single day) is no more effective than a single daily dose. This was illustrated in a study of an average daily dose of 45 mg of prednisone given as 15 mg every eight hours, 45 mg once daily, or 90 mg on alternate days. The daily regimens were more effective than the alternate dosing as a result of recrudescence of symptoms on the “off” day.]
What is the treatment of visceral artery aneurysms?
Covered stent is best
[Exclusion with bypass if that fails]
[UpToDate: All visceral artery pseudoaneurysms (VAPAs), symptomatic visceral artery aneurysms (VAAs) and some asymptomatic VAAs that meet criteria for elective repair require treatment to reduce the risk of rupture. The indications for treatment depend upon the natural history of aneurysmal disease.
The goal of treatment of VAA and VAPA is ideally to exclude the aneurysm sac from the systemic circulation while preserving distal blood flow; however, if this cannot be accomplished, the aneurysm can be occluded. Either can be accomplished using an open surgical or endovascular approach.
- For VAA/VAPA affecting vessels that supply an end organ with multiple sources of flow (native or collateral), the aneurysm can be ligated surgically or embolized percutaneously.
- For VAA/VAPA affecting vessels that supply an end organ that does not have multiple sources of flow (native or collateral), blood flow to the organ will need to be preserved either through the aneurysm lumen using a graft or stent graft, or surgical revascularization (eg, bypass).
For patients with ruptured VAA/VAPA, an open approach is often required for rapid control of hemorrhage. However, the ease of open surgical access to the aneurysm depends upon the location of the aneurysm; some difficult-to-access vessels may be better handled with an endovascular approach (eg, pancreaticoduodenal aneurysm). Ligation of the artery proximal and distal to the aneurysm is often adequate. Perfusion to the end organ should be assessed to determine whether or not revascularization is needed.
For elective repair of VAA/VAPA, a percutaneous approach is becoming the first-line treatment for VAAs/VAPAs that are anatomically suitable. The percutaneous approach has high technical success rates, and is associated with decreased lengths of hospital stay.]
What is the appropriate treatment for carotid stenosis in high-risk patients (eg patients with previous carotid endarterectomy and re-stenosis, multiple medicle comorbidities, previous neck XRT)?
Carotid stenting
[UpToDate: Once the diagnosis of restenosis has been made, a decision has to be made about the need for reoperation. This decision is not trivial since reoperative CEA may be associated with a significant incidence of complications, although much of the evidence is retrospective and conflicting, with some authors reporting good outcomes for redo surgery. An additional major concern is that there are no controlled studies of reoperative CEA in patients with restenosis. The presumed benefits of surgery in this group of patients are an extrapolation of the results of trials performed on patients at initial presentation. Because recurrent carotid lesions are typically smooth, nonulcerated intimal hyperplasia with a low risk of thromboembolism, carotid artery stenting is evolving to be the treatment of choice when intervention is deemed appropriate to avoid complications related to redo CEA, but for relatively young patients, re-do CEA with saphenous patching or reconstruction is also appropriate.
A systematic review identified 59 studies involving 4399 patients who underwent redo carotid intervention (surgery or stenting) for restenosis following CEA. There were no significant differences in the perioperative (30 day) rates for mortality, stroke, or transient ischemic attack when comparing redo CEA with CAS performed for restenosis. Patients undergoing redo CEA had significantly increased incidence of cranial nerve injury compared with those undergoing CAS, but most patients recovered within three months. The risk of recurrent stenosis after intervention for restenosis was greater in the CAS patients than in redo CEA patients.]
What is the most likely lower extremity location of a deep vein thrombosis with ankle and calf swelling?
Femoral
Which renal vein can be ligated near the inferior vena cava in emergencies because of collaterals?
The left renal vein (has left gonadal vein and left adrenal vein as collaterals)
[Right renal vein does not have these collaterals]
What is the treatment for hypersensitivity angiitis (often secondary to drug/tumor antigens)?
Calcium channel blockers, pentoxifylline (decreases the viscosity of blood), stop offending agent
[UpToDate: Hypersensitivity vasculitis is a term originally used by Pearl Zeek in 1948 to differentiate small vessel necrotizing vasculitis attributed to a hypersensitivity reaction from the classic polyarteritis nodosa. Distinguishing features included prominent involvement of the skin, and the observation that the condition frequently appeared to be caused by a presumed “hypersensitivity” to serum or drugs. However, this term has fallen out of favor since the Chapel Hill 1994 consensus on the classification of vasculitides excluded the term because of a lack of specificity of clinical (palpable purpura) and histologic presentation (LCV), as well as the inability to describe the precise immune mechanism that caused the small vessel vasculitis. Patients who previously would have been classified as having hypersensitivity vasculitis are now diagnosed with cutaneous small vessel vasculitis if vasculitis is limited to the skin, or with another type of specific small vessel vasculitis if there is evidence of systemic involvement.]
What is the treatment for mycotic abdominal aortic aneurysm
Usually needs extra-anatomic bypass (axillary-femoral with femoral-to-femoral crossover) and resection of infrarenal abdominal aorta to clear infection
[UpToDate: There are no randomized trials to guide the management of infected aneurysms. Management strategies are primarily based upon clinical experience guided by case series. The standard treatment of most infected aneurysms is antibiotic therapy combined with surgical debridement with or without revascularization. Revascularization procedures are performed, as needed, depending upon the affected vascular bed and status of distal perfusion. For patients who refuse surgery or who have significant medical comorbidities that preclude surgical intervention, antibiotic therapy alone is an option. Endovascular techniques are emerging as a treatment alternative for infected aneurysm, most commonly for infected aortic aneurysms.
The optimal duration of antibiotic therapy is uncertain and depends on factors, including the immune competence of patient, location of infection, specific bacteria, autogenous versus prosthetic grafts, in situ versus extraanatomic reconstruction, and response to treatment (fever, white count, hemodynamic stability). In general, at least six weeks of parenteral and/or oral antimicrobial therapy is administered for treatment of infected aneurysm. If surgical drainage is performed, this time period commences from the day of surgery. However, there are no data to support a specific duration of antibiotic therapy; in some circumstances, particularly for cases in which autologous vein grafting is used, a shorter duration may be sufficient. A longer duration of treatment may be warranted in the setting of antibiotic-resistant organisms, persistently positive cultures, and/or inflammatory markers that are slow to normalize. Suppressive oral antibiotics following completion of intravenous therapy may be warranted for patients reconstructed with prosthetic graft material in situ during active infection.
Management of infected aneurysms follows the general principles of managing vascular graft infection. The main surgical aim is removal of all necrotic and infected tissue and management of any ensuing ischemia. The decision to pursue vascular reconstruction depends primarily upon the patient’s underlying vascular status and the anatomic site of the aneurysm (which determines the likelihood of ischemia distal to the site following aneurysm excision) but also on the availability of autologous graft material. In many cases, the approach may need to be changed during the course of surgical exploration.]
At what ankle-brachial index (ABI) does someone start to get ulcers?
Less than 0.4
[Usually starts in toes]
[UpToDate: A low ABI is associated with a higher risk of coronary heart disease, stroke, transient ischemic attack, progressive renal insufficiency, and all-cause mortality. The ABI is generally, but not absolutely, correlated with clinical measures of lower extremity function such as walking distance, speed of walking, balance, and overall physical activity. Further evaluation is dependent upon the ABI value.
- The normal ABI is >0.91 to as high as 1.3. Normally, the pressure is higher in the ankle than in the arm. A normal test generally excludes arterial occlusive disease. Mild disease and arterial entrapment syndromes can produce false negative tests. If ABIs are normal at rest but symptoms strongly suggest claudication, exercise testing should be performed.
- An ABI >1.3 suggests the presence of calcified vessels and the need for additional vascular studies, such as pulse volume recordings, measurement of the toe pressures and toe-brachial index, or arterial duplex studies.
- An ABI ≤0.9 is diagnostic of occlusive arterial disease in patients with symptoms of claudication or other signs of ischemia and has 95% sensitivity (and 100% specificity) for detecting arteriogram-positive occlusive lesions associated with ≥50% stenosis in one or more major vessels.
- An ABI of 0.4 to 0.9 suggests a degree of arterial obstruction often associated with claudication.
- An ABI below 0.4 represents multilevel disease (any combination of iliac, femoral or tibial vessel disease) and may be associated with non-healing ulcerations, ischemic rest pain or pedal gangrene.]
What condition is characterized by no femoral pulses, buttock or thigh claudication, and impotence
Leriche syndrome
[Peripheral artery disease with lesion at aortic bifurcation or above]
[UpToDate: Buttock and hip claudication – Patients with aortoiliac disease may complain of buttock, hip, and, in some cases, thigh claudication. The pain is often described as aching in nature and may be associated with weakness of the hip or thigh with walking. Pulses in one or both groins are diminished. Bilateral aortoiliac PAD that is severe enough to cause lower extremity symptoms almost always causes erectile dysfunction in men. Leriche syndrome is the triad of claudication, absent or diminished femoral pulses, and erectile dysfunction.]
What innervates the strap muscles (infrahyoid muscles)?
Ansa cervicalis
[May be injured during carotid endarterecomy but doesn’t cause any serious deficits]
[UpToDate: More distal (cranial) access may be needed. As the internal carotid artery is dissected, the hypoglossal nerve will be seen to cross anteriorly. The nerve is isolated and gently retracted.
The ansa hypoglossus (ansa cervicalis) nerve, which innervates the strap muscles of the neck, is typically seen coursing along the carotid sheath. The ansa can be divided without clinically significant consequence when dissection needs to be carried more cranially. The posterior belly of the digastric muscle can also be divided. Subluxation of the jaw facilitated by nasotracheal intubation, while frequently discussed, is rarely warranted.]
What is the 2nd most common source of cerebral emboli?
Heart
[1st is internal carotid artery]
[UpToDate: Embolism refers to clot or other material formed elsewhere within the vascular system that travels from the site of formation and lodges in distal vessels causing blockage of those vessel and ischemia. The heart is a common source of this material, although other arteries may also be sources of this embolic material (artery to artery embolism). In the heart, clots may form on valves or chambers. Tumors, venous clots, septic emboli, air, and fat can also embolize and cause stroke. Embolic strokes tend to be cortical and are more likely to undergo hemorrhagic transformation, probably due to vessel damage caused by the embolus.
If the infarct and brain symptoms are within the anterior circulation (carotid artery supply), then the extracranial and intracranial carotid arteries, and the middle and anterior cerebral artery branches should be the focus of the examinations.
When the infarct is within the posterior circulation (vertebrobasilar system), the extracranial and intracranial vertebral arteries, the basilar artery, and the posterior cerebral arteries should be the focus of the vascular investigations.]
What is the most common pathogen responsible for an aortic graft infection?
Staphylococcus
[#2 E. coli]
[UpToDate: Aortic graft infection is rare, occurring in about 0.3% of patients undergoing open AAA repair. Extension of the graft into the femoral region increases the incidence to as much as 3%, with an associated mortality as high as 50%.
Aortic graft infection may be the cause or consequence of aortoenteric fistula, which is related to erosion of the proximal aortic graft into the small bowel, usually the third portion of the duodenum.
The incidence of endograft infection ranges from 0.4% to 3%, with an associated mortality rate of about 25%. In one study, 42% of patients diagnosed with graft infection presented within three months of aortic endografting, suggesting contamination during endograft placement.]
What is the treatment for a type I endoleak following abdominal aortic aneurysm repair?
Extension cuffs
[Type I failure is due to flow around the proximal or distal attachment sites.]
[UpToDate: Type I endoleaks are repaired as soon as they are discovered because the aneurysm sac remains exposed to systemic pressure leading to aneurysm growth and rupture. Spontaneous closure of the type I endoleak is uncommon. In one review of patients with endoleaks, aneurysms expanded in a majority of patients. Spontaneous thrombosis of the aneurysm sac, and thus closure of the endoleak, occurred in only 21% of the patients.
Measures to prevent type I endoleak include correcting radiologic parallax during positioning to ensure correct placement and appropriate balloon inflation of the attachment sites once the device is correctly deployed. When a type I endoleak is identified at the time of endograft placement, the initial approach consists of re-ballooning the fixation sites and possibly the reversal of anticoagulation. For proximal type I endoleaks that persist after re-ballooning, the placement of additional aortic cuffs, or a balloon-expandable stentincreases the radial force exerted by the proximal graft and maximizes apposition of the graft to the aortic wall.
For distal type I endoleaks that persist after balloon angioplasty of the distal attachment site, iliac limb extensions are used. If the iliac limb has been undersized, a flared iliac extension limb can be placed to exclude the endoleak. If the distal common iliac artery does not have an adequate length to provide a proper seal, coil embolization of the origin of the hypogastric artery and placement of a limb extension into the external iliac artery may be needed. It is important to maintain pelvic perfusion through the contralateral hypogastric artery to minimize the risk of pelvic ischemia.
The methods discussed above are usually sufficient to repair type I endoleak and exclude the aneurysm. The treatment of late type I leak can be more challenging, but usually involves the same percutaneous strategies.
Conversion to an open surgical repair may be needed in the rare situation in which a type I leak is refractory to percutaneous treatment.]
What is the treatment for deep vein thrombosis?
Heparin, coumadin
[UpToDate: Anticoagulant therapy is indicated for patients with symptomatic proximal DVT, since pulmonary embolism will occur in approximately 50% of untreated individuals, most often within days or weeks of the event.
Initial treatment should be started acutely. Available approved choices include unfractionated heparin, low molecular weight heparin, fondaparinux, rivaroxaban, or dabigatran. If a heparin preparation or fondaparinux is chosen, treatment should be continued for at least five days and oral anticoagulation with a vitamin K antagonist overlapped with one of these agents for at least four to five days. The preferred choice of anticoagulation is discussed in depth separately.
Use of thrombolytic agents or thrombectomy is individualized. Patients with hemodynamically unstable pulmonary embolus (PE) or massive iliofemoral thrombosis and a low bleeding risk are the most appropriate candidates.
Inferior vena caval filter placement is recommended when there is a contraindication to, or a complication of, anticoagulant therapy in an individual with, or at high risk for, proximal vein thrombosis or PE.
The duration of anticoagulation therapy varies with the clinical setting as well as with patient values and preferences.
Patients with a first proximal DVT due to a reversible or time-limited risk factor (eg, trauma, surgery) and those with a first unprovoked or provoked episode of distal DVT should be treated for three months.
Indefinite therapy might be preferred in patients with a first unprovoked episode of proximal DVT or pulmonary embolism who have a greater concern about recurrent VTE and a relatively lower concern about the risks and burdens of long-term anticoagulant therapy.
Most patients with advanced malignancy should be treated indefinitely or until the cancer resolves.]
What is the order of symptoms in Raynaud’s disease?
Pallor -> Cyanosis -> Rubor
[White, blue, red]
[UpToDate: The Raynaud phenomenon (RP) is an exaggerated vascular response to cold temperature or emotional stress. The phenomenon is manifested clinically by sharply demarcated color changes of the skin of the digits. Abnormal vasoconstriction of digital arteries and cutaneous arterioles due to a local defect in normal vascular responses is thought to underlie the disorder.
RP is considered primary if these symptoms occur alone without evidence of any associated disorder. By comparison, secondary RP refers to the presence of the disorder in association with a related illness, such as systemic lupus erythematosus and systemic sclerosis (SSc; scleroderma).]
When should a splenic artery aneurysm be repaired?
- Symptomatic
- Patient is pregnant
- Occurs in woman of childbearing age
- Greater than 3-4cm
[High rate of pregnancy related rupture - usually in the 3rd trimester]
Where is the failure site in a type II endoleak following abdominal aortic aneurysm repair?
Retrograde flow into the aneurysmal sac from patent collaterals (eg parent lumbar, inferior mesenteric artery, intercostals, accesory renal)
[UpToDate: Type II endoleak is due to a patent inferior mesenteric artery or patent lumbar artery branches that allow retrograde flow into the aneurysm sac. Type II endoleaks are the most prevalent type, occurring with all device types with a wide range of reported incidences ranging from 10% to 45% percent. A systematic review identified 1515 type II endoleaks among 21,744 patients who underwent EVAR, for an incidence of 10.2%. The incidence of type II endoleak has been correlated with the number of patent aortic branches prior to endovascular repair of the aneurysm.]
What is the most common variant of fibromuscular dysplasia?
Medial fibrodysplasia
[UpToDate: Medial fibroplasia represents the most common dysplastic lesion, accounting for more than 80% of fibromuscular lesions. Angiographically, medial fibroplasia is characterized by the classic “string of beads” appearance. This appearance is due to alternating fibromuscular webs and aneurysmal dilatation. In areas of dilatation, the internal elastic lamina is absent, which is possibly the primary defect. Total occlusion is uncommon.]
What is the most common late complication after aortic graft placement to repair an abdominal aortic aneurysm?
Atherosclerotic occlusion
[UpToDate: Perioperative (30 day) mortality for elective open AAA repair in contemporary series is between 1% and 5%. Perioperative morbidity and mortality are increased in patients with advanced age, female gender, cardiac, pulmonary, or kidney disease. The cause of death for most patients is multisystem organ failure. For patients who survive open AAA repair, the main cause of death in the long term is cardiovascular disease. Perioperative complications related to the aortic procedure include lower extremity ischemia, bowel ischemia, pelvic ischemia, renal dysfunction, and late complications include incisional hernia, anastomotic aneurysm, and graft infection/aortoenteric fistula.]
What is the most common visceral aneurysm?
Splenic artery aneurysm
[UpToDate: Splenic artery aneurysms are the third most common true aneurysm occurring in the abdomen after aortic and iliac artery aneurysms. Splenic artery aneurysms are more common in women (female: male = 4:1) and in the sixth decade of life, with as many as 80% occurring in patients >50 years of age. Splenic artery aneurysms are associated with intraabdominal aneurysms involving other visceral arteries (3%) and renal arteries (14%). One-third of patients have multiple aneurysms. Splenic artery aneurysms are usually solitary, saccular in shape, and frequently localized to the distal third of the artery, the bifurcation region, and the splenic hilum. False aneurysms of the splenic artery are uncommon but can occur, particularly in association with pancreatitis, but also as a result of instrumentation.]
What percent of patients have hypertension following a carotid endarterectomy?
20%
[UpToDate: Surgical manipulation of the carotid sinus during carotid dissection may result in sympathetic stimulation and resultant hypertension and tachycardia or may increase parasympathetic outflow with resultant bradycardia and hypotension. While injection of local anesthetic, either into the carotid body or into the periadventitial area around the carotid sinus, has been proposed as a method to minimize the bradycardic reflex and reduce hemodynamic lability due to carotid manipulation, there is insufficient data to endorse this practice.
Carotid cross-clamping may precipitate ipsilateral cerebral ischemia due to mechanisms such as decreased carotid blood flow and/or plaque disruption with cerebral embolization. Thus, during cross-clamping, systolic blood pressure should be maintained in a range from the patient’s baseline blood pressure to 20% above that baseline, in order to optimize collateral cerebral perfusion. We prefer to use systolic arterial blood pressure to achieve this goal, although some clinicians prefer to use the mean arterial pressure.
Incision of the carotid artery exposes the baroreceptors in the carotid sinus to atmospheric pressure, which increases sympathetic discharge from the medulla, and may result in vasoconstriction and increased heart rate.
Carotid unclamping and the ensuing period of reperfusion may be complicated by hypotension.]
What percent of blood flow to the brain is supplied by the carotids?
85%
[Wikipedia: Blood supply to the brain is normally divided into anterior and posterior segments, relating to the different arteries that supply the brain. The two main pairs of arteries are the Internal carotid arteries (supply the anterior brain) and vertebral arteries (supplying the brainstem and posterior brain).
The anterior and posterior cerebral circulations are interconnected via bilateral posterior communicating arteries. They are part of the Circle of Willis, which provides backup circulation to the brain. In case one of the supply arteries is occluded, the Circle of Willis provides interconnections between the anterior and the posterior cerebral circulation along the floor of the cerebral vault, providing blood to tissues that would otherwise become ischemic.]
Which nerve is responsible for plantar flexion?
Tibial nerve
[Wikipedia: In the foot, the nerve divides into medial and lateral plantar branches.
Medial plantar nerve - The medial plantar nerve supplies: the abductor hallucis, the flexor digitorum brevis, the flexor hallucis brevis and the first lumbrical. Cutaneous distribution of the medial plantar nerve is to the medial sole and medial three and one half toes, including the nail beds on the dorsum (like the median nerve in the hand). Mnemonic LAFF muscles: L-first Lumbrical, A- Abductor Hallucis, F- Flexor digitorum brevis, F- flexor hallucis brevis
Lateral plantar nerve - The lateral plantar nerve supplies quadratus plantae, flexor digiti minimi, adductor hallucis, the interossei, three lumbricals, and abductor digiti minimi. Cutaneous innervation is to the lateral sole and lateral one and one half toes (like the ulnar nerve).]
What is the most common complication of an aneurysm above the inguinal ligament?
Rupture
[UpToDate: Reported five-year rupture rates for iliac artery aneurysm (IAA) range from 14% to 70%, and as many as 33% of patients with isolated iliac aneurysms present with rupture. The average size of ruptured isolated iliac aneurysms is between 5 and 7 cm. The size of ruptured external IAA may be slightly smaller at 4 cm].
Iliac aneurysm rupture causes acute abdominal, and thigh or groin pain, often accompanied by hemodynamic instability. Retroperitoneal rupture may be contained but intraperitoneal rupture can lead to rapid exsanguination. Rupture into the rectum, ureter, bladder, iliac veins and rectus sheath have all been described. Rupture into adjacent veins can cause high output heart failure.
Mortality from iliac aneurysm rupture is high with a mortality rate of about 30 percent following open repair with reports ranging from zero to 60%. Worse outcomes are related to a delay in diagnosis. Endovascular stent grafting for emergent repair has lowered perioperative mortality rates.
Symptoms related to aneurysm thrombosis or thromboembolism are less common, occurring in 5% to 13% of patients.]
What is the treatment for Raynaud’s disease?
Calcium channel blockers, warmth
[UpToDate: General measures that help to prevent or diminish the severity of attacks of RP include avoiding cold exposure, maintaining warmth of the whole body, smoking cessation, and avoiding sympathomimetic medications and emotional stress.
We recommend use of the slow-release or long-acting preparations of the dihydropyridine calcium channel blockers (CCB), nifedipine (30 to 180 mg/day) or amlodipine (5 to 20 mg/day), in the nonurgent management of RP that has not responded adequately to general measures (Grade 1A). We start with the lowest dose and gradually increase as needed depending upon the response.]
At what ankle-brachial index (ABI) does someone start to get gangrene?
Less than 0.3
[UpToDate: A low ABI is associated with a higher risk of coronary heart disease, stroke, transient ischemic attack, progressive renal insufficiency, and all-cause mortality. The ABI is generally, but not absolutely, correlated with clinical measures of lower extremity function such as walking distance, speed of walking, balance, and overall physical activity. Further evaluation is dependent upon the ABI value.
- The normal ABI is >0.91 to as high as 1.3. Normally, the pressure is higher in the ankle than in the arm. A normal test generally excludes arterial occlusive disease. Mild disease and arterial entrapment syndromes can produce false negative tests. If ABIs are normal at rest but symptoms strongly suggest claudication, exercise testing should be performed.
- An ABI >1.3 suggests the presence of calcified vessels and the need for additional vascular studies, such as pulse volume recordings, measurement of the toe pressures and toe-brachial index, or arterial duplex studies.
- An ABI ≤0.9 is diagnostic of occlusive arterial disease in patients with symptoms of claudication or other signs of ischemia and has 95% sensitivity (and 100% specificity) for detecting arteriogram-positive occlusive lesions associated with ≥50% stenosis in one or more major vessels.
- An ABI of 0.4 to 0.9 suggests a degree of arterial obstruction often associated with claudication.
- An ABI below 0.4 represents multilevel disease (any combination of iliac, femoral or tibial vessel disease) and may be associated with non-healing ulcerations, ischemic rest pain or pedal gangrene.]
What is the most common failure of A-V grafts for dialysis?
Venous obstruction secondary to intimal hyperplasia
[UpToDate: Venous stenosis is the most common cause of late fistula loss, although it does not occur in AVFs with the same degree of frequency as is seen with synthetic grafts. Percutaneous angioplasty is the treatment of choice for these lesions and is associated with a greater than 95% technical success rate. Long-term primary patency rates are reported in the range of 92% at three months, 57% to 77% at six months, and 35% to 69% at one year. The treatment of venous stenosis in AVFs presents no unique problems when compared with lesions seen in association with AV grafts.]
What is the treatment of popliteal entrapment syndrome?
Resection of the medial head of gastrocnemius muscle, may need arterial reconstruction
[UpToDate: Bedside testing is often helpful for assessing pulses. In experienced hands, dynamic Doppler ultrasound has been found to correlate closely with surgical findings and in some institutions is used as a definitive diagnostic test for popliteal artery entrapment. Advanced imaging such as angiography may be needed. The ankle-brachial index is low with significant compromise of arterial flow. Exercise testing may be used to help establish the diagnosis.
During the examination, the popliteal artery should be palpated for an aneurysm. Popliteal aneurysm is extremely rare in young individuals, although pseudo-aneurysms have been associated with trauma to the popliteal fossa and can be delayed in presentation. Popliteal aneurysm is relatively common in older men and in an older athlete with a history and symptoms suggesting popliteal artery entrapment, a careful assessment to exclude aneurysm, possibly including ultrasound, is needed.
Primary care management of popliteal artery entrapment is to have the patient avoid any inciting exercise and to obtain vascular surgery consultation to determine definitive treatment.]
What percent of popliteal artery aneurysms are bilateral?
50%
[UpToDate: As a part of a routine vascular examination, the popliteal fossae bilaterally should be routinely palpated, ideally with the knee slightly flexed. 60% of patients with popliteal aneurysm have a pulsatile popliteal mass which is located at or above the level of the knee joint. Bilateral popliteal artery aneurysms are present in about 50% of patients. A popliteal aneurysm may not be palpable if the aneurysm is small (ie, <2 cm), or if thrombosis has occurred.]
One should only operate on descending aortic dissections under which circumstances?
Visceral or extremity ischemia, or if a contained rupture
[UpToDate: For patients who are hemodynamically stable with uncomplicated type B aortic dissection, we suggest initial medial therapy, rather than intervention (open surgery or endovascular treatment) (Grade 2B). Indications for intervention for type B dissection include occlusion of a major aortic branch leading to end-organ ischemia, persistent severe hypertension or pain, propagation of the dissection (as may be manifested by persistent or recurrent pain), aneurysm expansion, and aortic rupture. Acute distal dissections in patients with Marfan syndrome may also be best treated with surgery.
Repeat surgery is required in up to one-half of patients at 10 years’ follow-up, usually because of extension or recurrence of dissection at the previous site of intervention, localized aneurysm formation remote from the site of repair, graft dehiscence or infection, or aortic regurgitation. The rate of secondary intervention following thoracic stent-grafting due to endoleak or device migration is also high (up to 25%) and depends on the duration of follow-up.
Following treatment of aortic dissection (medical or surgical), the patients should be maintained on anti-impulse therapy to minimize aortic wall stress with a target blood pressure of less than 120/80 mmHg. Predischarge advanced vascular imaging using magnetic resonance (MR) or computed tomographic (CT) angiography should be performed with follow-up examinations at 3, 6, and 12 months, and annually thereafter to detect signs of dissection progression, re-dissection, or aneurysm formation (even if the patient remains asymptomatic). We prefer thoracic MR for younger patients, but chest CT scanning is an alternative; however, CT exposes the patient to ongoing radiation and requires iodinated contrast. Alternating chest CT and thoracic MRI is a reasonable option.]
What is the treatment for renal vascular disease?
- Percutaneous transluminal angioplasty
- Place stent if due to atherosclerotic disease
[UpToDate: For patients with unilateral renal artery stenosis who meet one or more of the following four criteria, we suggest revascularization rather than medical therapy alone; revascularization is usually achieved by percutaneous angioplasty with stenting (or surgical revascularization in patients with complex anatomic lesions):
- A short duration of blood pressure elevation prior to the diagnosis of renovascular disease, since this is the strongest clinical predictor of a fall in blood pressure after renal revascularization
- Failure of optimal medical therapy to control the blood pressure
- Intolerance to optimal medical therapy
- Recurrent flash pulmonary edema and/or refractory heart failure
For patients with unilateral renal artery stenosis who do not meet one of the four criteria just listed, we suggest not revascularizing and instead treating with medical therapy alone.
In patients undergoing percutaneous transluminal renal angioplasty (PTRA) for treatment of atherosclerotic renal artery stenosis, we suggest stent placement unless the anatomy precludes stenting.]
Where do the brachial plexus and subclavian artery travel with respect to the 1st rib, anterior scalene artery, and middle scalene muscle?
They pass over the 1st rib posterior to the anterior scalene muscle and anterior to the middle scalene muscle
What is the treatment of a lymphocele following surgery?
Percutaneous drainage (try a couple of times)
[Resection if that fails]
[UpToDate: Lymphoceles are often asymptomatic but can present as pressure or pain, they are often palpable as a rounded smooth mass that can be slightly compressed. They may resolve spontaneously over time, but if there are secondary consequences (pain, lymphedema, etc), they may require image-guided drainage. If drain output continues to be high after several weeks (>50 to 100 mL/day), sclerotherapy with instillation of alcohol, iodine, doxycycline, or talc directly into the cystic collection can be considered. Alternatively, a laparoscopic marsupialization is another option.]
How is abdominal aortic aneurysm rupture diagnosed?
Ultrasound or abdominal CT
[CT shows fluid in retroperitoneal space and extraluminal contrast with rupture]
[UpToDate: Although any imaging study that demonstrates the focal dilation can be used to make a diagnosis, abdominal ultrasound and computed tomography (CT) of the abdomen are the most useful. Each modality is sensitive and specific for establishing a diagnosis of AAA, but recommended under differing clinical circumstances, depending upon the clinical presentation, and the hemodynamic status of the patient.]
What is the treatment for thoracic outlet syndrome of the subclavian vein?
- Thrombolytics initially
- Repair at that admission (cervical rib and 1st rib resection, divide anterior scalene muscles)
[UpToDate: For patients with deep vein thrombosis due to vTOS, thrombolysis and early thoracic outlet decompression are performed to relieve extrinsic vein compression. In properly selected patients, long-term outcomes are excellent following thrombolysis and thoracic outlet decompression.]
What is the most common atherosclerotic occlusion in the lower extremities?
Hunter’s canal (adductor canal)
[Distal superficial femoral artery exits here. The sartorious muscle covers Hunter’s canal]
[Wikipedia: The adductor canal (subsartorial or Hunter’s canal) is an aponeurotic tunnel in the middle third of the thigh, extending from the apex of the femoral triangle to the opening in the adductor magnus, the adductor hiatus.
The canal contains the femoral artery, femoral vein, and branches of the femoral nerve (specifically, the saphenous nerve, and the nerve to the vastus medialis). The femoral artery with its vein and the saphenous nerve enter this canal through the superior foramen. Then, the saphenous nerve and artery and vein of genus descendens exit through the anterior foramen, piercing the vastoadductor intermuscular septum. Finally, the femoral artery and vein exit via the inferior foramen (usually called the hiatus) through the inferior space between the oblique and medial heads of adductor magnus.]
Where do venous ulcers occur?
Above and posterior to the malleoli
[UpToDate: Chronic venous disease is the most common cause of lower extremity ulcers. They are usually located low on the medial ankle over a perforating vein, or along the course of the great or small saphenous veins; they can occur more proximally on the leg if precipitated by trauma, but never in the forefoot or above the level of the knee. The ulcers may be multiple or single, and are exquisitely tender, shallow, exudative and have a granulation base. The ulcer borders are usually irregular but not undermined. They can extend circumferentially around the leg if left untreated.]
Which vasculitis is associated with aneurysms of coronary arteries and brachiocephalic vessels?
Kawasaki’s disease
[UpToDate: Kawasaki disease (KD, previously called mucocutaneous lymph node syndrome) is one of the most common vasculitides of childhood. KD also occurs rarely in adults. It is typically a self-limited condition, with fever and manifestations of acute inflammation lasting for an average of 12 days without therapy. However, complications such as coronary artery (CA) aneurysms, depressed myocardial contractility and heart failure, myocardial infarction, arrhythmias, and peripheral arterial occlusion may develop and lead to significant morbidity and mortality.]
What kind of flow does a normal internal carotid artery have?
Continuous forward flow
[RadioGraphics: The internal carotid artery supplies low-resistance cerebral circulation. The systolic peak in the waveform from this vessel is not as sharp as that in the waveform from the external carotid artery, and a large quantity of forward flow continues throughout diastole.
All intracranial arteries display a low-resistance flow pattern with continuous forward flow during systole and diastole.]
[Picture: Spectrum from the internal carotid artery displays a low-resistance waveform with continuous forward diastolic flow and with a spectral line that ascends farther above the baseline than that from the external carotid artery.]
What is the source of a pulmonary embolism in a patient with a inferior vena cava filter?
- Ovarian veins
- Inferior vena cava superior to filter
- Upper extremity via the superior vena cava
[UpToDate: Small thrombi are capable of passing through patent filters or through collaterals around obstructed filters; furthermore, direct thrombus extension can occur through the filter itself leading to recurrent pulmonary embolism. However, data suggest that recurrent pulmonary embolism is unusual following filter insertion (2% to 4% in most series). Pharmacomechanical thrombolysis is an adjunct that has been used to treat patients with severe symptoms.
The thrombotic complications related to prophylactic IVC filter placement in at-risk populations such as trauma, neurosurgery, oncology, intensive care, and bariatric patients are poorly defined. Data come from diverse studies; in some, pulmonary embolism is specifically sought, in others only clinically documented pulmonary emboli are reported.
One systematic review of retrievable IVC filters estimated an incidence of pulmonary embolism following filter placement of 1.3%. A later randomized trial compared retrievable IVC filters plus anticoagulation with anticoagulation alone in patients with pulmonary embolism and a high risk of recurrence. The rate of symptomatic recurrent pulmonary embolism was 3% in the filter group, which was not significantly different from the control group at 1.5%. Filters were retrieved overall in 85% of patients, and in 93% in whom it was planned and attempted. This study demonstrates that if a patient can be anticoagulated, filter placement will not add any additional protection. In addition, it would suggest that once the patient can be anticoagulated, the filter should be removed since it is not adding any benefit.
A large number of reports on individual filters have been published; however, clearly defined end points and objective criteria for reporting recurrence and mortality rates are lacking.
Other late complications of inferior vena cava (IVC) filter placement are uncommon and include filter migration, which can also occur acutely during filter placement, filter erosion and perforation through the IVC wall, and filter fracture and fragment embolization. Inadvertent misplacements into the right atrium, right gonadal vein, lumbar veins, and even into the aorta have been reported. Most of these complications are reported in individual case studies, and there are otherwise few data to determine the factors that are responsible. In most cases, percutaneous retrieval of the filter is successful.]
What is the correct management of a venous thrombosis with a non-essential central line?
Remove central line and start heparin
[UpToDate: Intravenous catheters cause endothelial trauma and inflammation, which can lead to venous thrombosis. The majority (70% to 80%) of thrombotic events occurring in the superficial and deep veins of the upper extremity are due to the presence of intravenous catheters. The remainder is due to mechanical compression from anatomic abnormalities (ie, venous thoracic outlet syndrome).
Superficial thrombophlebitis due to peripheral catheters is generally self-limited once the catheter is removed. Thrombosis involving the deep veins (ie, subclavian, axillary, brachial) can lead to pulmonary embolism and long-term sequelae in spite of adequate therapy. Pulmonary embolism from upper extremity sources accounts for about 6% of cases.
Superficial phlebitis related to peripheral intravenous catheters should be managed first by discontinuing the intravenous infusion and removing the peripheral catheter. Symptomatic care consists of extremity elevation, warm or cool compresses, and oral nonsteroidal anti-inflammatory drugs (NSAIDs). Excessive pain not controlled with NSAIDs may indicate the presence of a suppurative phlebitis, chemical phlebitis, or extravasation injury.
For patients diagnosed with catheter-induced UEDVT, we suggest anticoagulation (Grade 2B). For uncomplicated cases, three months of anticoagulation therapy should be sufficient. A longer duration of anticoagulation may be warranted if the catheter remains in place, particularly for patients with cancer. The catheter can be left in place if it is functional and there is an ongoing need. For noncancer patients with thrombosis confined to the brachial vein, there is uncertainty about the need for anticoagulation once the catheter has been removed in patients.
For patients diagnosed with catheter-induced UEDVT, we suggest not instituting deep vein thrombolysis as a first line therapy (Grade 2C). Compared with anticoagulation, there is insufficient evidence to suggest that thrombolysis leads to any better outcomes.
For patients with indwelling upper extremity catheters, we recommend not administering prophylactic anticoagulation (vitamin K antagonists, unfractionated heparin, low molecular weight heparin) (Grade 1A). For patients with cancer, we suggest not routinely administering prophylactic anticoagulation (Grade 2A). It may be reasonable to administer prophylactic anticoagulation in high–risk patients when the perceived risk of thrombosis outweighs the risk of bleeding. High-risk factors include previous venous thrombosis, bulky disease, hereditary thrombophilia, or suboptimal catheter tip location.]
What is the definitive treatment of ascending aortic dissection?
Requires open repair, graft is placed to eliminate flow to the false lumen
[UpToDate: Acute type A aortic dissection is a surgical emergency since these patients are at high risk for early life-threatening complications such acute aortic regurgitation, cardiac tamponade, and myocardial infarction. Hemorrhagic stroke is a relative contraindication to urgent surgical intervention. When the aortic valve, sinuses, or arch are involved, the surgical approach involves a full root or hemiarch replacement. Hypothermic circulatory arrest has been used in repairs involving the aortic arch. A hybrid approach to the repair of type A aortic dissection, sometimes referred to as the “frozen elephant trunk repair,” uses an open approach to surgically repair the ascending aorta while using a thoracic endograft to manage the descending aorta.
Repeat surgery is required in up to one-half of patients at 10 years’ follow-up, usually because of extension or recurrence of dissection at the previous site of intervention, localized aneurysm formation remote from the site of repair, graft dehiscence or infection, or aortic regurgitation. The rate of secondary intervention following thoracic stent-grafting due to endoleak or device migration is also high (up to 25%) and depends on the duration of follow-up.
Following treatment of aortic dissection (medical or surgical), the patients should be maintained on anti-impulse therapy to minimize aortic wall stress with a target blood pressure of less than 120/80 mmHg. Predischarge advanced vascular imaging using magnetic resonance (MR) or computed tomographic (CT) angiography should be performed with follow-up examinations at 3, 6, and 12 months, and annually thereafter to detect signs of dissection progression, re-dissection, or aneurysm formation (even if the patient remains asymptomatic). We prefer thoracic MR for younger patients, but chest CT scanning is an alternative; however, CT exposes the patient to ongoing radiation and requires iodinated contrast. Alternating chest CT and thoracic MRI is a reasonable option.]
What is the treatment of venous ulcers?
Unna boot compression (cures 90%)
[UpToDate: For all patients with chronic venous symptoms, we suggest leg elevation (when possible), leg exercises (ankle flexion, walking) to increase calf muscle strength, and compression hosiery (Grade 2C).
For patients who are unable to tolerate, are not compliant with, or in whom compression therapy is contraindicated (eg, occlusive arterial disease), we suggest horse chestnut seed extract (Grade 2B). A typical dose is 300 mg (standardized to 50 mg of escin) twice daily.
Dry skin, itching, and eczematous changes are treated with moisturizers and, if needed, a midpotency topical corticosteroid. We suggest avoiding topical products with common sensitizers (eg, lanolin, neomycin, nickel) (Grade 2C).
For patients with venous insufficiency that is associated with severe edema, weeping, eczema, or ulceration, we recommend compression therapy (Grade 1B). Compression hosiery or compression bandaging systems (elastic or nonelastic) can be used. When choosing compression bandages, we suggest multilayered compression bandages rather than single-layer bandages (Grade 2B). However, multilayered compression bandages are more costly.
Venous ulceration is managed with wound debridement, as needed, barrier creams to protect adjacent skin, and wound dressings tailored to the environment of the wound (eg, absorbent dressings for weeping wounds).
- Topical antibiotics, debriding enzymes, growth factors, and honey are not effective in the management of venous ulceration.
- We suggest aspirin therapy for patients with venous ulceration (Grade 2B). Aspirin appears to accelerate the healing of chronic venous ulcers.
- Patients with slowly healing ulcers, persistent dermatitis, or resistant or recurrent cellulitis should be referred to the appropriate subspecialist.]
Which cranial nerve is most commonly injured during a carotid endarterectomy?
Vagus nerve (secondary to vascular clamping)
[Results in hoarseness because the recurrent laryngeal nerve comes off the vagus]
[UpToDate: Cranial nerve or other nerve injuries occur in about 5% of patients following CEA. The majority of cranial nerve injuries resolve after surgery, and the risk of permanent cranial nerve deficit is low at <1%. Among the 1739 patients who underwent CEA in the European Carotid Surgery Trial (ECST), the rate of motor cranial nerve injuries in the immediate postoperative period was 5.1%, but by hospital discharge, the cranial nerve injury rate declined to 3.7%. In a review of 6878 patients from the Vascular Study Group of New England (VSGNE) database, the overall rate of nerve injury at discharge was 5.6%; 0.7% of patients had more than one nerve affected.
In the VSGNE study discussed above, the hypoglossal nerve was most frequently involved, occurring in 2.7%, followed the facial nerve at 1.9%, and the vagus nerve and glossopharyngeal nerve each at 0.7%. This cited distribution of injuries was similar in the ECST, with injuries involving the hypoglossal nerve (27/1739), marginal mandibular nerve (a branch of the facial nerve) (17/1739), recurrent laryngeal nerve (a branch of the vagus nerve) (17/1739), accessory nerve (1/1739), and sympathetic chain injury leading to Horner syndrome (3/1739). Duration of surgery longer than two hours was the only independent risk factor for cranial nerve injury. In the vascular registry study, patients who suffered a perioperative stroke had a significantly increased risk of cranial nerve injury. Other factors that significantly increased the risk of cranial nerve injury included urgent procedures (odds ration [OR] 1.6, 95% CI 1.2-2.1), immediate re-exploration after closure under the same anesthetic (OR 2.0, 95% CI 1.3-3.0), and return to the operating room for a neurologic event or bleeding (OR 2.3, 95% CI 1.4-3.8). Re-do CEA or prior cervical radiation were not associated with an increased risk.
The vagus nerve, which usually lays posterolaterally in the carotid sheath, may be injured during dissection of the carotid from the internal jugular vein. The vagus nerve may be stretched, inadvertently clamped, or cut at this level leading to hoarseness. The laryngeal nerves are branches of the vagus nerve. The recurrent laryngeal nerve is generally distal to the area of carotid artery dissection; however, a nonrecurrent right laryngeal nerve can occur (<1%; left side even rarer) crossing transversely from the vagus nerve and behind the common carotid artery, increasing its risk for injury during CEA. Injury to the inferior laryngeal nerve results in unilateral vocal cord paralysis. The superior laryngeal nerve is rarely injured during CEA. The internal branch supplies sensation to the larynx, while the external branch innervates the cricopharyngeal muscle. Changes in voice quality may result from superior laryngeal nerve injury.]
When might an emergent carotid endarterectomy be benefitial?
Fluctuating neurologic symptoms or crescendo/evolving transient ischemic attacks
[UpToDate: Early CEA (eg, within two days of TIA or stroke) or emergent CEA for progressing/fluctuating stroke or crescendo TIA may have a high operative risk, as suggested by the following observational reports:
In a meta-analysis of 47 studies (mostly observational or registry studies) published between August 2008 and March 2015 that evaluated early carotid intervention for recently symptomatic stenosis, the following observations were noted:
- The pooled periprocedural stroke and death risk for CEA performed within 48 hours of the index event of stroke was 8.4% (95% CI 5.0-12.7); the corresponding risk for the index event of TIA was 2.8% (95% CI 0.4-7.2)
- The pooled periprocedural stroke and death risk for CEA performed within 15 days of the index event of stroke was 4.9% (95% CI 3.4-6.7); the corresponding risk for the index event of TIA was 1.9% (95% CI 0.8-3.3)
A 2009 systematic review identified 18 nonrandomized studies of CEA for recently symptomatic carotid stenosis that reported data on time from presenting event to CEA, and further stratified CEA into emergent (stroke-in-evolution or crescendo TIA) and nonemergent indications. The rate of perioperative stroke or death was significantly higher with emergent CEA (14%, vs 4% for nonemergent CEA, pooled relative odds 4.6, 95% CI 3.4-63)]
What is the treatment for Leriche syndrome?
Aorto-bifemoral bypass graft
[UpToDate: The 2005 ACC/AHA guidelines, which were produced in collaboration with major vascular medicine, vascular surgery, and interventional radiology societies, made the following recommendations for surgery in patients with aortoiliac (inflow) disease:
- In patients with unilateral disease with acceptable aortic inflow, surgical procedures include aortoiliac bypass, iliac endarterectomy, or iliofemoral bypass.
- For patients with bilateral aortoiliac disease, aortobifemoral bypass grafting is the ideal surgical procedure; however, if the patient is not a suitable candidate, then one of the unilateral procedures listed above or a unilateral percutaneous procedure can be combined with femoral-femoral bypass.
- Axillofemoral bypass should only be used to treat claudication in very limited settings, such as chronic infra-aortic occlusion associated with severe symptoms in a patient who is not a candidate for aortobifemoral bypass or to manage an infected graft in a symptomatic patient.]
Cerebral ischemic events are most commonly from arterial embolization from which artery?
Internal carotid artery
[Heart is the 2nd most common source of cerebral emboli]
[UpToDate: Embolism refers to clot or other material formed elsewhere within the vascular system that travels from the site of formation and lodges in distal vessels causing blockage of those vessel and ischemia. The heart is a common source of this material, although other arteries may also be sources of this embolic material (artery to artery embolism). In the heart, clots may form on valves or chambers. Tumors, venous clots, septic emboli, air, and fat can also embolize and cause stroke. Embolic strokes tend to be cortical and are more likely to undergo hemorrhagic transformation, probably due to vessel damage caused by the embolus.
If the infarct and brain symptoms are within the anterior circulation (carotid artery supply), then the extracranial and intracranial carotid arteries, and the middle and anterior cerebral artery branches should be the focus of the examinations.
When the infarct is within the posterior circulation (vertebrobasilar system), the extracranial and intracranial vertebral arteries, the basilar artery, and the posterior cerebral arteries should be the focus of the vascular investigations.]
What is the treatment for an acute arterial embolism?
Embolectomy, need to get pulses back, postop angiogram (consider fasciotomy if ischemia >4-6 hours)
[UpToDate: Once a diagnosis of acute arterial occlusion has been made by history and physical examination, we initiate anticoagulation with a bolus of intravenous heparin followed by a continuous heparin infusion according to the recommendations of the 2012 American College of Chest Physicians (ACCP) guideline on antithrombotic therapy for peripheral artery occlusive disease and the 2007 Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II) consensus document on the management of Peripheral Artery Disease (PAD). Anticoagulation prevents propagation of thrombus in the arterial and venous systems due to low flow.
- Catheter-based thrombolytic therapy is primarily reserved for patients with acute limb ischemia and a viable extremity. We agree with recommendations made in major society guidelines that catheter-based thrombolytic therapy is effective and beneficial and is indicated in patients with acute limb ischemia of fewer than 14 days duration in those who have a low risk for developing myonecrosis and ischemic nerve damage during the time period required to achieve revascularization. Mechanical thromboembolectomy may be used as an adjunctive therapy in conjunction with pharmacologic thrombolysis. Although many patients treated with thrombolytic therapy will subsequently require surgical or percutaneous revascularization, the magnitude and complexity of the procedure required to revascularize the extremity is frequently less than in those who do not receive prior thrombolytic therapy.
- In spite of advances in care, acute limb ischemia is associated with rates of limb loss as high as 30% and in-hospital mortality rates as high as 20%. Cardiopulmonary complications account for the majority of the deaths, underscoring the severity of the baseline medical condition of these patients.]
What is the treatment of a mal perforans ulcer?
(Mal perforans ulcer is a cutaneous condition of chronic, trophic, ulcerative disease seen on the dependent parts of body in denervating diseases)
- Non-weightbearing
- Debridement of metatarsal head (need to remove cartilage)
- Antibiotics
- Assess need for revascularization
[UpToDate: The treatment of diabetic foot ulcers begins with a comprehensive assessment of the ulcer and the patient’s overall medical condition. Evidence of underlying neuropathy, bony deformity, and peripheral artery disease should be actively sought. The ulcer is classified upon initial presentation and with each follow-up visit using a standardized system to document the examination, treatment plan, and to follow the progress of healing.
- Adequate debridement, proper local wound care (debridement and dressings), redistribution of pressure on the ulcer by mechanical off-loading, and control of infection and ischemia (when present) are important components of treatment for all ulcers, regardless of stage and depth.
- For most patients with diabetic foot ulcers, we suggest surgical (sharp) debridement rather than another method (Grade 2C). If a surgeon with clinical expertise in sharp debridement is not available, we suggest autolytic debridement with hydrogels (Grade 2C). Alternatively, the patient can be referred to a facility with appropriate surgical expertise in the management of diabetic foot problems. Dressings are selected based upon ulcer or postsurgical wound characteristics.
- For managing extensive open wounds following debridement for infection or necrosis, or partial foot amputation, we suggest negative pressure wound therapy (Grade 2A). All necrotic tissue or infected bone (osteomyelitis) first must be removed from the wound.
- Several methods are available to achieve mechanical off-loading, and include total contact casts, cast walkers, wedge shoes, and bedrest. The type of off-loading that is used depends largely on local expertise.
- For patients who present with a diabetic foot ulcer and severe limb ischemia, we recommend early revascularization (Grade 1B). Revascularization should also be performed in patients with a nonhealing ulcer and any degree of limb ischemia.]
What is Buerger’s disease (Thromboangiitis obliterans)?
An inflammation of the arteries, veins, and nerves in the upper and lower extremities, leading to restricted blood flow and gangrene if left untreated
[Highly associated with smoking]
[UpToDate: Thromboangiitis obliterans, also called Buerger’s disease, is a nonatherosclerotic, segmental, inflammatory disease that most commonly affects the small to medium-sized arteries and veins of the extremities. Thromboangiitis obliterans is characterized by highly cellular and inflammatory occlusive thrombus with relative sparing of the blood vessel wall. Patients are young smokers who present with distal extremity ischemia, ischemic digit ulcers or digit gangrene. The disease is strongly associated with the use of tobacco products and smoking cessation is important to decrease the risk for amputation.]
What is the most common acquired hypercoagulable disorder?
Smoking
[UpToDate: Acquired risk factors or predisposing conditions for thrombosis include a prior thrombotic event, recent major surgery, presence of a central venous catheter , trauma, immobilization, malignancy, pregnancy, the use of oral contraceptives or heparin, myeloproliferative disorders, antiphospholipid syndrome (APS), and a number of other major medical illnesses.
Although an initial report from the Leiden group, the ARIC and CHS studies, a Norwegian study, and a meta-analysis found no significant relationship between smoking and VTE, at least six other studies, including an update from the ARIC study, have detected a relationship between the two, with relative risks ranging from 1.3 to 3.3.
- In one study, a high number of pack-years resulted in the highest risk of venous thrombosis among young current smokers (OR for ≥20 pack-years of 4.3; 95% CI 2.6-7.1), when compared with young nonsmokers. In addition, women who were current smokers and used oral contraceptives had an 8.8-fold higher risk (95% CI 5.7-13) than nonsmoking women who did not use oral contraceptives.
- In a Danish case-cohort study, the adjusted hazard ratio for VTE emerging from the combined exposure to the non-O blood type and heavy smoking was 2.98 (95% CI 1.89-4.69), which exceeded the sum of the individual effects.]
Which nerve and/or artery travel in the anterior compartment of the leg?
Deep peroneal nerve, anterior tibial artery
The middle and inferior rectal arteries are branches off of which artery?
Internal iliac artery
[The blood supply enters the rectum posteriorly. The upper rectum is supplied by the superior rectal artery (SRA), a branch of the inferior mesenteric artery (IMA). The middle and lower rectum are supplied by the middle rectal artery and inferior rectal artery, respectively, which branch from the anterior division of the internal iliac artery and/or the pudendal artery.]
What protein is defective in Ehlers-Danlos syndrome?
Collagen (many types of collagen defects identified)
[UpToDate: In most types of Ehlers-Danlos syndrome (EDS), the underlying pathophysiology involves inherited alterations in genes affecting the synthesis and processing of different forms of collagen, which are important in the structure of many tissues and organs, including the skin, tendons, ligaments, vasculature, skeleton, and eyes. A variety of different mutations that may cause an EDS phenotype have been identified for each of the affected genes.]
Popliteal entrapment syndrome is characterized by the loss of pulses with what movement?
Plantar flexion
[UpToDate: The patient with popliteal artery entrapment typically complains of pain deep in the calf that develops only after an intense workout involving repeated ankle dorsiflexion and plantarflexion (eg, cycling, running, marching up and down hills). These symptoms may resemble those of calf claudication. During exercise, the patient may experience paresthesias across the proximal posterior calf while immediately following exercise, he or she may notice a pale, discolored foot and toes. At all other times, the patient typically has no pain, and the examination at rest is normal. Hypertrophied calf muscles may be noted.
Assessment of distal pulses is a key part of the examination for this condition. Palpate the lower extremity pulses (dorsalis pedis and posterior tibialis) to determine whether they are diminished at baseline; it is often helpful to compare the affected and unaffected limbs. Then, palpate the pulses while the patient performs active plantar-flexion and passive dorsiflexion of the ankle, while the knee remains in extension. One helpful examination technique is to have the patient stand on a step in the examination room and perform heel raises, repeatedly raising and lowering his foot above and below the level of the step, while the clinician palpates the distal pulses. The presence of a decreased pulse during such maneuvers suggests the diagnosis.
Bedside testing is often helpful for assessing pulses. In experienced hands, dynamic Doppler ultrasound has been found to correlate closely with surgical findings and in some institutions is used as a definitive diagnostic test for popliteal artery entrapment. Advanced imaging such as angiography may be needed. The ankle-brachial index is low with significant compromise of arterial flow. Exercise testing may be used to help establish the diagnosis.]
What are 3 indications for abdominal aortic aneurysm repair?
- Symptomatic
- Greater than 5.5 cm
- Growth greater than 0.5 cm/yr
[UpToDate: Repair of asymptomatic AAA is generally indicated under the circumstances listed below:
- Asymptomatic AAA ≥5.5 cm
- Rapidly expanding AAA
- AAA associated with peripheral arterial aneurysm (eg, iliac, popliteal) or peripheral artery disease (eg, iliac occlusive disease)]
What is the vascular issue in Ehlers-Danlos syndrome?
Tendency for arterial rupture (especially abdominal vessels) (get aneurysms and dissections)
[UpToDate: Vascular EDS is an autosomal dominant condition that results from mutations in type III procollagen; 50% of cases appear due to de novo mutations. Most of the mutations are in the COL3A1 gene, causing an altered procollagen, which results in a “dominant negative effect.” Since type III collagen consists of a homotrimer, an abnormality in half of the type III procollagen molecules will result in greater than half of the resultant type III collagen molecules being abnormal. Haploinsufficiency mutations that result in half of the normal production of type III procollagen are much rarer; individuals with this type of mutation may have a milder phenotype and may not be diagnosed unless genetic testing is performed because of an affected family member.
Vascular EDS (EDS IV) is potentially life-threatening, and differs from the classic and hypermobility forms most dramatically in the increased risk for these patients of spontaneous vascular or visceral rupture and the absence of large joint hyperextensibility. Small (more distal) joints, however, may exhibit mild hypermobility. The prevalence of the vascular form of EDS is not well studied, but estimates based upon available data suggest a frequency of at least 1 in 100,000, accounting for about 4% of all EDS cases.
Arterial rupture may involve the iliac, splenic, or renal arteries; or the aorta. Preexisting aneurysms are rarely detected prior to a rupture, as the aneurysms are typically pseudoaneurysms. Complications in affected individuals also include significant risk for spontaneous rupture of internal organs (such as the intestine and gravid uterus) and muscles. Maternal mortality during pregnancy is about 12%, although delivery is often uneventful.]
What is the surgical treatment of a popliteal aneurysm?
Exclusion and bypass of all popliteal aneurysms
[25% have complication that requires amputation if not treated. Covered stent not recommended for these]
[UpToDate: Aneurysm exclusion and bypass — With the medial approach, the popliteal artery aneurysm is left in-situ and bypassed using a segment of saphenous vein. The popliteal artery is ligated proximal and distal to the aneurysm to exclude it from the circulation. Ligation of the popliteal artery is performed close to the aneurysm to minimize the loss of collateral vessels.
The conduit of choice for lower extremity bypass is ipsilateral great saphenous vein (reversed or nonreversed). In a study of the Vascunet Registry, vein graft was used in 87% of patients. Below-the-knee prosthetic (polytetrafluoroethylene [PTFE]) grafts have an increased risk of thrombosis and are avoided, whenever possible, for the repair of popliteal artery aneurysm. In one single institution review, primary patency at 24 months for saphenous vein was 95% compared with 79% for PTFE.
The vein graft can be positioned adjacent the popliteal artery (ie, anatomic), or tunnelled subcutaneously along the medial aspect of the knee, depending upon the extent of the bypass, patient anatomy, and operator preference. Anatomic placement allows a straighter graft with less potential for kinking around the knee and may be more suitable for patients with muscular legs; however, the popliteal graft segment may be more difficult to appreciate on ultrasound surveillance.
Extensive aneurysmal degeneration or atherosclerotic disease that affects the superficial femoral artery proximally, or popliteal artery distally (ie, at the origin of the anterior tibial artery) necessitates originating a bypass graft from the common femoral artery or extending the graft distally to one of the tibial vessels, respectively. Aggressive distal bypass to the tibial vessels may be important for optimizing outcomes. In a retrospective review of 51 popliteal aneurysm repairs (37 elective; 14 emergent), overall primary patency rates at one-year and five-years follow-up were 96% and 85%, and secondary patency rates were 100% and 97%, respectively. In this study, the percentage of patients who had a distal infrapopliteal target for lower extremity bypass was particularly high at 57%. However, no significant differences in primary patency were found for popliteal versus more distal bypass targets (84% versus 87% at 5 years).
In-line reconstruction — In-line reconstruction using a posterior approach may be preferred if the aneurysm is focal and confined to the popliteal fossa, especially if the aneurysm is large and compressing adjacent structures. However, this approach limits proximal vascular control, and embolectomy may be incomplete owing to an inability to direct the catheter distally into the individual tibial vessels. As such, most surgeons would not approach a thrombosed popliteal aneurysm posteriorly, particularly if outflow is compromised.
With the posterior approach, a vein or prosthetic graft is used to reconstruct the popliteal artery. In a retrospective review of 571 patients, 45 of whom were managed with a posterior approach, vein graft and PTFE had similar one-year patency rates (85% and 81%, respectively). A ‘lazy’ S-shaped incision is made over the popliteal fossa to minimize problems with scar contracture. After gaining vascular control, the popliteal artery is opened and the graft sutured to normal artery proximally and distally. Upon completion of the repair, the aneurysm sac is closed over the graft, provided enough arterial wall remains (similar to other aneurysm repairs).]
What is the 3rd atherosclerotic stage?
Intimal disruption (From smooth muscle cell proliferation)
[Leads to exposure of collagen in vessel wall and eventual thrombus formation. Fibrous plaques then form in these areas with underlying atheromas]
[UpToDate: The first phase in atherosclerosis histologically occurs as focal thickening of the intima with accumulation of lipid-laden macrophages (foam cells) and extracellular matrix. Smooth muscle cells can also populate the intima, some of which may arise from hematopoietic stem cells, migrate, and proliferate. Lipids accumulate early in fatty streak formation yielding both intracellular lipid and extracellular deposits, which produce the fatty streak. Biglycan, a small dermatan sulfate proteoglycan detected in the intima of atherosclerotic coronary artery segments, can bind and trap lipoproteins, including very low density lipoproteins and low density lipoprotein. The fatty streak can also contain T lymphocytes. Foam cells constitute the hallmark of the early atheroma.
As these lesions expand, more smooth muscle cells accumulate in the intima. The smooth muscle cells within the deep layer of the fatty streak are susceptible to apoptosis, which is associated with further macrophage accumulation and microvesicles that can calcify, perhaps contributing to the transition of fatty streaks into atherosclerotic plaques.]
When do aortoenteric fistulas occur after abdominal aortic surgery?
Greater than 6 months after surgery
[UpToDate: The increased availability of reconstructive vascular surgical procedures for aneurysm repair and reconstruction for severe aortoiliac atherosclerosis gave rise to secondary aortoenteric fistula (SAEF) as a complication of prosthetic reconstruction. The first SAEF was reported in 1953 in a 44-year-old woman three months after aortic repair. Whether or not the incidence of AEF will increase or decrease in the future is uncertain. One might presume that the total number of AEFs will rise because of an increasing life-expectancy and increasing population undergoing vascular repair. On the other hand, it is entirely possible that the incidence will decline owing to improved repair techniques and the development of more durable prosthetic materials, and the decrease in open aortic procedures.
SAEF is far more common than PAEF, but is nevertheless rare. The incidence of SAEF following aortic surgical reconstructions ranges from 0.36% to 1.6%; the incidence of PAEF has been reported to be less than 1%. Because abdominal aortic aneurysms (AAAs) are frequently asymptomatic, it is not possible to determine the percentage of aneurysms that go on to fistulize primarily. Many patients die of AEF before it has been correctly diagnosed, and the incidence may be underestimated. As an example, only four patients were reported from the Dutch literature up to 1996. A study that sought to obtain more realistic figures on the incidence of this condition sent a questionnaire to all surgical clinics in The Netherlands and identified 35 additional cases.
AEF is more common in males compared with females, paralleling the incidence of AAA and aortic surgery. The male to female ratio is 3:1 for PAEF and 8:1 for SAEF. Although AEFs are almost exclusively reported in the adult population, a case of PAEF was reported in a three-year-old child as a result of duodenal perforation after ingestion of a twig.]
What is the most common site of peripheral obstruction from emboli?
Common femoral artery
[UpToDate: Thromboemboli typically lodge where there is an acute narrowing of the artery, such as an atherosclerotic plaque or a vessel branch point; the common femoral, common iliac, and popliteal artery bifurcations are the most frequent locations. In a large series of arterial embolism, for example, the following frequencies were noted:
- Femoral – 28%
- Arm – 20%
- Aortoiliac – 18%
- Popliteal – 17%
- Visceral and other – 9% each
Arterial to arterial embolization of thrombus or plaque originating from aneurysms or atherosclerotic lesions is another well described occurrence and accounts for 20% of peripheral emboli.]
The basilar artery splits into which two arteries?
Posterior cerebral arteries
What is the treatment of subclavian steal syndrome?
Percutaneous transluminal angioplasty with stent to subclavian artery
[Common carotid to subclavian artery bypass if that fails]
[UpToDate: The approach to therapy of subclavian steal associated with symptoms varies with the clinical setting. In many patients, symptoms improve over time without treatment. Interventional treatment is not usually warranted in patients with asymptomatic subclavian stenosis/occlusion. Symptomatic patients with proximal subclavian artery ulcerative occlusive disease complicated by embolization, in the absence of other significant cerebrovascular disease, can be successfully treated by surgical removal or exclusion of the proximal subclavian lesion. Percutaneous angioplasty and stenting (with embolic protection) for embolism related to proximal subclavian artery is appropriate for patients with short stenosis/occlusion at the origin of the subclavian artery. We prefer surgical revascularization if percutaneous treatment will jeopardize the integrity of the vertebral artery. Patients with unacceptable surgical risk or anatomy unfavorable for intervention can be treated with antiplatelet therapy (and possibly oral anticoagulation), but no prospective trials have evaluated the effectiveness of this option.
Extra-anatomic revascularization (eg, carotid-subclavian bypass, carotid transposition) is the most common form of surgical correction for symptomatic subclavian artery stenosis. Overall patency rates of 95% at 1 year, 86% at three years, and 73% at 5 years have been reported. Patency at 5 years is significantly higher for procedures utilizing the common carotid artery as the donor vessel compared with those using the contralateral subclavian or axillary arteries (83% vs 46%, p<0.01). Axillo-axillary bypass is an alternative method for revascularization in patients at high surgical risk.
Although data are limited and no randomized trials are available, retrospective observational studies suggest that percutaneous transluminal angioplasty and stenting is safe in patients with appropriate anatomy (short proximal stenosis or occlusion). The combined stroke and death rate related to percutaneous intervention was 3.6% in one study.
Immediate technical success is achieved in greater than 93% of patients with failures usually related to an inability to cross occlusive lesions. Five-year primary patency rates are about 85%. Sustained resolution of ischemic symptoms is observed in most patients (>95%). Angioplasty alone has inferior outcomes compared with angioplasty and stenting, particularly when recanalizing subclavian occlusions. A systematic review and meta-analysis comparing angioplasty alone with angioplasty and stenting for subclavian artery stenosis found a significantly higher risk of subsequent events for angioplasty alone compared with angioplasty and stenting at one year (odds ratio 2.37, 95% CI 1.32-4.26). Stent placement for treatment of subclavian artery stenosis may be associated with higher rates of technical success, but rates of symptom resolution and long-term outcomes are similar compared with no stent. In-stent restenosis is more likely to develop in younger patients, in patients who were smokers with chronic obstructive disease, and in patients with a baseline vessel diameter ≤7 mm.
Patients with a continuous (compared with intermittent) subclavian and coronary artery steal may have a higher risk of subclavian artery restenosis following endovascular therapy. A retrospective study of 42 patients treated with angioplasty and stenting for coronary subclavian steal syndrome found that the rate of restenosis was higher in patients with a continuous (compared with intermittent) subclavian and coronary steal (41% and 7%). Symptoms due to significant (>70%) recurrent stenosis or obstruction occur in approximately 10% of patients, and are typically treated with repeat angioplasty; however, surgery may be required in up to 5% of patients. A single-center retrospective studied 167 patients scheduled for left internal mammary artery-coronary artery bypass grafting and who underwent stent placement for left subclavian artery stenosis. The left subclavian artery patency rates were 75.2% at 10 years.
Surgical treatment for patients with a subclavian steal and coexisting severe carotid stenosis is more controversial. Because a significant percentage of patients with subclavian steal have concomitant severe extracranial atherosclerotic disease, carotid artery endarterectomy should generally be performed first and may result in symptomatic improvements.]
What findings on CT suggest intestinal ischemia?
- Vascular occlusion
- Bowel wall thickening
- Intramural gas
- Portal venous gas
[UpToDate: For patients in whom the index of suspicion for intestinal ischemia is high, multidetector CT angiography and magnetic resonance (MR) angiography have improved the ability to diagnose acute mesenteric ischemia. The CT scan should be performed without oral contrast, which can obscure the mesenteric vessels, obscure bowel wall enhancement, and can lead to a delay of the diagnosis. The origins of the celiac axis and superior mesenteric artery should also be evaluated for the presence of calcification that indicates an underlying atherosclerotic process as a possible etiology for mesenteric ischemia.
CT is preferred over MR because of its lower costs, speed, and wide availability. However, MR angiography may be more sensitive for the diagnosis of mesenteric venous thrombosis and may be necessary for those with an allergy to iodinated contrast. CT can demonstrate findings consistent with acute ischemia, such as focal or segmental bowel wall thickening, intestinal pneumatosis with portal vein gas, bowel dilation, mesenteric stranding, portomesenteric thrombosis, or solid organ infarction, in addition to ruling out other causes of acute abdominal pain. It is important to note that the bowel wall changes of acute mesenteric ischemia, while sensitive, are not specific. The presence of pneumatosis intestinalis on CT does not necessarily indicate that transmural infarction has occurred, but transmural infarction is more likely in patients with pneumatosis and portomesenteric venous gas. Mesenteric arterial occlusions can be identified as a lack of enhancement of the arterial vasculature with timed intravenous contrast injections. When present, thromboembolic occlusion is specific for the diagnosis; however, the absence of a filling defect is not sufficiently sensitive to rule out acute mesenteric ischemia.
The accuracy of CT was evaluated in a study comparing CT findings in 39 patients who had surgically proven acute mesenteric ischemia with 24 controls in whom suspected acute mesenteric ischemia was disproved at surgery. A single finding of either arterial or venous thrombosis, intramural gas, portal venous gas, focal lack of bowel-wall enhancement, or liver or splenic infarcts had a sensitivity and specificity of 64% and 92%, respectively. In another review, the sensitivity of CT for the diagnosis of mesenteric venous thrombosis was approximately 90%. In a later prospective study of 79 patients with suspected acute mesenteric ischemia evaluated using multidetector CT angiography, a positive predictive value of 100% and a negative predictive value of 94% was found using criteria that required the presence of visualized arterial occlusion, intestinal pneumatosis, portomesenteric venous gas, or bowel wall thickening, in combination with portomesenteric thrombosis or solid organ infarction. The diagnosis was made by the failure to opacify the mesenteric veins with intravenous contrast. Similarly, multidetector CT angiography was used to evaluate 91 patients with suspected acute mesenteric ischemia in another retrospective review. It correctly diagnosed acute mesenteric ischemia in 16 of 18 patients with confirmed acute mesenteric ischemia, while supporting another diagnosis in an additional 38 patients. There were two false negative and two false positive examinations.]
What is the most common site of atheroma embolization?
Renal arteries
[UpToDate: Acute kidney injury is a common manifestation of cholesterol crystal embolism. Acute kidney injury is present in 25% to 50% of cases. Renal disease most often occurs after invasive vascular procedures, but can occur spontaneously. In such patients, the diagnosis may be difficult to establish without biopsy unless other manifestations of crystal embolism are present.
- Because the cholesterol crystal emboli are irregularly shaped and nondistensible, and typically do not completely occlude larger vessels, the renal manifestations are those of distal parenchymal ischemia usually manifested as a bland sediment rather than renal infarction as seen with thromboemboli, which present with flank pain, hematuria that may be gross, and markedly elevated serum lactate dehydrogenase.The characteristics of renal involvement are discussed in detail separately.
- When acute kidney injury occurs after arteriography, the primary differential diagnosis is contrast nephropathy and cholesterol crystal embolism. Unless there are other signs of cholesterol crystal embolism, the two disorders are distinguished by differences in the clinical course. Contrast nephropathy typically begins to recover within three to five days, while cholesterol crystal embolism shows at best an incomplete recovery and there may be a stuttering course with further showers of cholesterol crystals.
- Although not a common manifestation of cholesterol crystal embolism, rhabdomyolysis has been reported in association with massive cholesterol crystal embolism and can lead to heme-pigment-associated acute kidney injury. Rhabdomyolysis presents with elevated serum muscle enzymes (including creatine kinase), red to brown urine due to myoglobinuria if there is persistent renal function, and electrolyte abnormalities. Peak serum creatine kinase levels depend upon the volume of muscle breakdown and the muscle mass of the patient.]
What is Adson’s test for thoracic outlet syndrome of the subclavian artery?
Absent radial pulse with head turned to ipsilateral side
[UpToDate: Compression maneuvers on physical examination (ie, Adson test) may demonstrate a decrease in the radial or ulnar pulse with abduction of the upper extremity overhead. The Adson test is prone to false positive results and the use of duplex ultrasound with these maneuvers has done little to improve its specificity. Thus, the Adson test is of little clinical value and should not be relied upon to make the diagnosis of any of the three types of TOS.]
If performing an aorto-bifemoral repair of an abdominal aortic aneurysm instead of a straight tube graft, you should ensure flow to what?
At least one internal iliac artery (hypogastric artery)
[This is to avoid vasculogenic impotence]
What is the treatment for chronic mesenteric angina?
Percutaneous transluminal angioplasty and stent
[Bypass if that fails]
[UpToDate: For patients diagnosed with chronic mesenteric ischemia, the indication for revascularization is the presence of symptoms, including abdominal pain and weight loss. The aim of intervention is to prevent future bowel infarction. Therapeutic options include open surgical and endovascular revascularization. Provided an endovascular approach is technically feasible, we attempt angioplasty with or without stenting as the initial treatment, rather than using an open surgical approach. Although percutaneous revascularization is associated with a higher rate of restenosis, recurrent symptoms from restenosis can often be successfully managed with repeat angioplasty/stenting.]
What kind of graft is usually used for abdominal aortic aneurysm repair?
Straight tube Dacron graft
[UpToDate: Options for aortic replacement include polyester (eg, Dacron), polytetrafluoroethylene (PTFE) and autogenous vein. The graft diameter should be selected to match the diameter of the aorta. Interestingly, the diameter of an open surgical graft is invariably smaller than the diameter of an endograft used in the same location.
The most widely used material is woven polyester fabric. Although favored by some surgeons for its handling qualities, knitted polyester suffers from high porosity as well as a tendency to dilate over time. Conventional woven polyester, on the other hand, is extremely durable but is somewhat less pliable than knitted fabric. Collagen or albumin coating has eliminated the need to “pre-clot” polyester grafts with whole blood. Most modern grafts employ a hybrid technique that combines the benefits of knitted and woven fabrics (eg, woven double velour), which is easy to handle, durable, and appropriately porous.
PTFE grafts may be more resistant to infection than polyester, although the data supporting this claim are limited. Suture hole bleeding is a problem and may require the use of special large diameter sutures or topical hemostatic agents for control.
Autogenous conduit, such as femoral vein, is usually reserved for the circumstance when gross infection is present. Because of the time needed to harvest the vein, sometimes bilaterally, femoral vein has limited use in the routine open surgical treatment of AAA. Femoral vein may be appropriate in some patients with small iliac or femoral arteries if there is an unacceptable size mismatch between the graft limbs and distal anastomotic site.]
What is the 1st atherosclerotic stage?
Foam cells
[Macrophages that have absorbed fat and lipids in the vessel wall]
[UpToDate: The first phase in atherosclerosis histologically occurs as focal thickening of the intima with accumulation of lipid-laden macrophages (foam cells) and extracellular matrix. Smooth muscle cells can also populate the intima, some of which may arise from hematopoietic stem cells, migrate, and proliferate. Lipids accumulate early in fatty streak formation yielding both intracellular lipid and extracellular deposits, which produce the fatty streak. Biglycan, a small dermatan sulfate proteoglycan detected in the intima of atherosclerotic coronary artery segments, can bind and trap lipoproteins, including very low density lipoproteins and low density lipoprotein. The fatty streak can also contain T lymphocytes. Foam cells constitute the hallmark of the early atheroma.
As these lesions expand, more smooth muscle cells accumulate in the intima. The smooth muscle cells within the deep layer of the fatty streak are susceptible to apoptosis, which is associated with further macrophage accumulation and microvesicles that can calcify, perhaps contributing to the transition of fatty streaks into atherosclerotic plaques.]
What is popliteal entrapment syndrome?
Loss of pulses with plantar flexion due to medial deviation of the popliteal artery around medial head of the gastrocnemius
[Patients present with mild intermittent claudication]
[UpToDate: Popliteal artery entrapment occurs most often due to a congenital anomaly that causes the medial or lateral gastrocnemius head to shift toward the popliteal artery during knee flexion, thereby compressing the artery. It is seen primarily in young active men (mean age 30 years) and therefore is not associated with an increased risk of cardiovascular disease. Multiple case reports document this condition in bicyclists, military personnel in active training, and runners. The cause appears to be repetitive overuse that gradually causes pathological thickening of vessel walls in the popliteal artery as a response to excessive pressure from the muscle belly. In bicyclists, the injury appears to be associated with repetitive knee flexion during extended rapid pedaling.
The patient with popliteal artery entrapment typically complains of pain deep in the calf that develops only after an intense workout involving repeated ankle dorsiflexion and plantarflexion (eg, cycling, running, marching up and down hills). These symptoms may resemble those of calf claudication. During exercise, the patient may experience paresthesias across the proximal posterior calf while immediately following exercise, he or she may notice a pale, discolored foot and toes. At all other times, the patient typically has no pain, and the examination at rest is normal. Hypertrophied calf muscles may be noted.]
Which symptoms would manifest during an anterior cerebral artery event?
Mental status change, release, slowing
[Frontal release signs are primitive reflexes traditionally held to be a sign of disorders that affect the frontal lobes. Conceptually, these reflexes are “hard-wired” before birth and are therefore able to be elicited in the newborn. As the brain matures, certain areas (usually within the frontal lobes) exert an inhibitory effect thus causing the reflex to disappear. When disease processes disrupt these inhibitory pathways the reflex is “released” from inhibition and elicitable once again, hence the term “frontal release sign”.]
[Wikipedia: Some frontal release signs and their role in infancy:
- Palmar grasp: Baby naturally grabs objects.
- Palmomental reflex: stroking on the thenar eminence of the hand causes contraction of sub mental muscles .
- Rooting reflex: Baby finds breast to suckle.
- Sucking reflex: Baby sucks breast / bottle teat to get milk.
- Snout reflex: Involved in suckling.
- Glabellar reflex: May protect eyes in certain situations.]
Where is abdominal aortic aneurysm most likely to rupture?
Left posterolateral wall, 2-4 cm below renals
[UpToDate: AAA rupture typically produces acute, severe abdominal pain and other manifestations that are determined by the location of the rupture, and whether the rupture is contained, ruptures freely into the peritoneum, or ruptures into an adjacent venous structure causing a fistula (eg, aortocaval, aortoiliac). Autopsy studies have found that abdominal aortic aneurysm rupture occurs most commonly in the posterior aorta, which correlates to the levels of highest stress in mechanical modeling studies.
- Proximal aortic rupture near the renal arteries leads to severe back/flank pain, whereas distal rupture near the iliac bifurcation causes low abdominal/pelvic pain and may cause pain that radiates to the groin or thigh due to lumbar nerve irritation.
- Posterior aortic wall rupture is likely to be initially contained within the retroperitoneum leading to retroperitoneal hematoma. The initial rupture is associated with a severe, often focal pain. If the hematoma stabilizes, the pain may subside. Patients with posterior rupture may attribute the initial pain to another cause, and delay seeking medical attention.
- Rupture of the anterior aortic wall may be contained for a brief period of time. The initial clinical manifestation will be abdominal pain, but rupture is likely to progress quickly to free intraperitoneal rupture with profound hemodynamic instability. Many of these patients succumb before they are able to be transported to the hospital.]
What test should be performed in a patient with chronic mesenteric angina?
Lateral visceral vessel aortography to see origins of celiac and superior mesenteric arteries
[UpToDate: Demonstration of stenosis of the major mesenteric vessels is a requirement for a diagnosis of chronic mesenteric ischemia. Calcification of mesenteric vessels seen on plain abdominal films (often obtained in an initial evaluation) may be a clue to the diagnosis of mesenteric atherosclerosis, but is not specific. For patients with suggestive symptoms, we agree with the American College of Radiology consensus opinion that recommends computed tomography (CT) of the abdomen as the initial imaging study, since it reliably identifies or excludes the presence of atherosclerotic vascular disease as the most likely etiology, and simultaneously rules out other abdominal pathologies as the source of symptoms. Conventional arteriography is indicated for diagnostic confirmation when the results of noninvasive testing are equivocal, and for therapeutic intervention when clinically appropriate.
Computed tomographic (CT) angiography has sensitivities and specificities exceeding 90% for the diagnosis of chronic mesenteric ischemia due to atherosclerosis. High-grade mesenteric vascular stenoses in at least two major vessels (celiac, superior mesenteric, or inferior mesenteric) must be established. Evidence for collateral formation to compensate for the reduced main arterial flow is typically present. Contrast-enhanced magnetic resonance (MR) angiography is also highly sensitive for detecting arterial stenoses at the origins of the celiac or mesenteric arteries; however, the technique is much less reliable for detecting more distal lesions. Quantification of postprandial flow on MR angiography may prove useful as a diagnostic modality.
Duplex ultrasonography of the mesenteric vessels has also been advocated as a reasonably accurate screening modality for the detection of high-grade celiac and superior mesenteric artery stenosis. For patients who are initially seen in an office setting, a duplex ultrasound is a reasonable first study. Sensitivity exceeding 90% has been reported in patients with more than a 50% stenosis of the superior mesenteric or celiac arteries.
Because the negative predictive value of duplex ultrasonography approaches 99%, it is justifiable to pursue other etiologies of abdominal pain after a negative study. However, the number of patients who have been studied using this technique is limited, and technical considerations, including the expertise of the examiner, large body habitus, intraintestinal gas, and prior abdominal surgery, should be considered in assessing the results. Duplex ultrasound can also be used to diagnose the median arcuate ligament syndrome. With inspiration, the celiac artery moves inferiorly and becomes more vertical. This leads to decompression of the celiac artery from the median arcuate ligament of the diaphragm, which is manifested by increased flow velocities.]
What is the mortality rate within 3 years of leg amputation?
50% mortality within 3 years of leg amputation
[UpToDate: Long-term survival following major lower extremity amputation in patients with peripheral artery disease has improved, but remains significantly lower than age-matched controls. In one study, the overall survival after above-knee amputation was 78% at one year and 55% at 3 years.
Long-term survival is worse for patients with more proximal amputation, diabetes, and renal dysfunction, but does not appear to be related to previous revascularization procedures, gender, or a history of hypertension. Whether there are any ethnic or racial differences remains unsettled.
- One-year survival is 50% to 60% following above-knee amputation, and 65% to 80% for below-knee amputation.
- Long-term survival for patients with diabetes is generally worse compared with patients without diabetes. In a review of 788 patients, five-year survival for patients with diabetes was 31% compared with 51% for patients without diabetes. In another study, the median time to death was 27 months in patients with diabetes compared with 47 months following amputation.
- In a review of 788 patients who underwent major amputation, one-year survival was 52% for dialysis-dependent patients compared with 75% in patients with normal renal function. For patients who were not dialysis dependent but had a preoperative serum creatinine >2 mg/dL, one-year survival was not significantly different (56% vs 52%) compared with dialysis-dependent patients.]
Early swelling following a lower extremity bypass is concerning for what?
Reperfusion injury and compartment syndrome
[Wikipedia: Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. The inflammatory response is partially responsible for the damage of reperfusion injury. White blood cells, carried to the area by the newly returning blood, release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage. The restored blood flow reintroduces oxygen within cells that damages cellular proteins, DNA, and the plasma membrane. Damage to the cell’s membrane may in turn cause the release of more free radicals. Such reactive species may also act indirectly in redox signaling to turn on apoptosis. White blood cells may also bind to the endothelium of small capillaries, obstructing them and leading to more ischemia. Another hypothesis would be that normally, tissues contain free radical scavengers to avoid damage by oxidizing species normally contained in the blood. Ischemic tissue would have a decrease function of these scavengers because of cell injury. Once blood flow is reestablished, oxygen species contained in the blood will damage the ischemic tissue because the function of the scavengers is decreased.]
What is the treatment for Buerger’s disease?
Stop smoking or will require continued amputations
[UpToDate: or patients diagnosed with thromboangiitis obliterans, we recommend smoking cessation (Grade 1A). Smoking cessation reduces symptoms and decreases the risk for major amputation. Continued smoking is associated with an overall amputation rate of 40% to 50%.
Other treatments used to manage pain associated with critical ischemia include iloprost infusion, sympathectomy and spinal cord stimulation. Calcium channel blockers and intermittent pneumatic compression indirectly improve pain by increasing blood flow.
Surgical revascularization is usually not indicated due to the distal nature of occlusive disease and because most patients do well with smoking cessation. Bypass surgery may be considered in select patients with severe ischemia and suitable distal target vessels. Although the long–term patency rates are inferior to those seen with peripheral artery disease due to atherosclerosis, limb salvage rates are generally greater than 90% and may be more correlated to smoking cessation.]
What is the 1st choice treatment for an isolated iliac lesion (peripheral arterial disease)?
Percutaneous Transluminal Angioplasty (PTA) with stent
[If that fails, consider femoral-to-femoral crossover]
[UpToDate: Percutaneous transluminal angioplasty (PTA) of uncomplicated iliac stenosis has high initial technical success rates generally >95%. Five-year primary patency rates are about 75%. Assisted primary and secondary patency rates are >95%.
Intravascular stents can be used primarily or as an adjunct to manage a suboptimal angioplasty result. Selective stenting is supported by a study that randomly assigned 279 patients with intermittent claudication due to iliac artery stenosis to primary stenting, or PTA with adjunctive stenting for a residual mean pressure gradient >10 mmHg. Initial hemodynamic success and complication rates were similar for primary and adjunctive stenting, and no differences in outcome, including quality of life, were apparent at two years or at five years. Although stents have been shown to improve patency, restenosis due to fibrointimal hyperplasia is a frequent occurrence. Mechanical and pharmacological techniques to reduce restenosis are actively being investigated. A small feasibility study has used one such device comprised of a drug-eluting (everolimus) bioresorbable vascular scaffold to treat iliac or femoral artery lesions. At one and two years follow-up, binary restenosis rates (>50%) were 12.1% and 16.1%, respectively, and freedom from target lesion revascularization was 91.2% and 88.2%, respectively. There were no procedure-related amputations or deaths at two years follow-up. Although these result are encouraging, direct comparisons with drug-eluting balloons and drug-eluting polymer coated metal stents are needed.
In addition to its benefits in focal iliac stenosis, PTA with or without stenting can also produce long-term outcomes similar to surgery in patients with complex or long-segment disease and bilateral iliac occlusions. Some authors advocate primary stenting under these conditions. To evaluate the influence of lesion severity on outcomes of PTA and stenting, a multicenter study in Europe (BRAVISSIMO study) prospectively studied 325 patients undergoing percutaneous intervention of TASC A, B, C, or D aortoiliac lesions. The primary endpoint was primary patency at 12 months, defined as a target lesion without a hemodynamically significant stenosis on Duplex ultrasound (>50%, systolic velocity ratio ≥2.0), and without target lesion revascularization (TLR) within 12 months. The overall primary patency rate was 93.1%. The one-year primary patency rates were 94% for TASC A lesions, 96.5% for TASC B lesions, 91.3% for TASC C lesions, and 90.2% for TASC D lesions. There were no significant differences between the TASC groups.
PTA and stents have also been used to treat stenosis of the aortic bifurcation. To avoid displacement of plaque across the aortic bifurcation during balloon angioplasty or embolization of debris down the contralateral iliac artery, a technique that uses two (“kissing”) balloons positioned simultaneously across both limbs of the aortic bifurcation and inflated in unison can be used. This technique is usually followed by the placement of kissing stents. In one study, stent insertion was successful in all 20 patients; symptoms were improved in 19, 12 of whom became asymptomatic. In a study of 80 patients with stenosis of the aortic bifurcation, primary and assisted primary patency rates at five years were 64.5% and 81.8%, respectively.]
Where does the subclavian vein travel with respect to the 1st rib, anterior scalene muscle, and clavicle?
It passes over the 1st rib anterior to the anterior scalene muscle and then behind the clavicle
Where does the right renal artery run in relation to the inferior vena cava?
Right renal artery runs posterior to the inferior vena cava
At what ankle-brachial index (ABI) does someone start to get claudication?
Less than 0.9
[Typically occurs at same distance each time]
[UpToDate: A low ABI is associated with a higher risk of coronary heart disease, stroke, transient ischemic attack, progressive renal insufficiency, and all-cause mortality. The ABI is generally, but not absolutely, correlated with clinical measures of lower extremity function such as walking distance, speed of walking, balance, and overall physical activity. Further evaluation is dependent upon the ABI value.
- The normal ABI is >0.91 to as high as 1.3. Normally, the pressure is higher in the ankle than in the arm. A normal test generally excludes arterial occlusive disease. Mild disease and arterial entrapment syndromes can produce false negative tests. If ABIs are normal at rest but symptoms strongly suggest claudication, exercise testing should be performed.
- An ABI >1.3 suggests the presence of calcified vessels and the need for additional vascular studies, such as pulse volume recordings, measurement of the toe pressures and toe-brachial index, or arterial duplex studies.
- An ABI ≤0.9 is diagnostic of occlusive arterial disease in patients with symptoms of claudication or other signs of ischemia and has 95% sensitivity (and 100% specificity) for detecting arteriogram-positive occlusive lesions associated with ≥50% stenosis in one or more major vessels.
- An ABI of 0.4 to 0.9 suggests a degree of arterial obstruction often associated with claudication.
- An ABI below 0.4 represents multilevel disease (any combination of iliac, femoral or tibial vessel disease) and may be associated with non-healing ulcerations, ischemic rest pain or pedal gangrene.]
What is the treatment for a type V endoleak following abdominal aortic aneurysm repair?
Repeat EVAR or open repair
[Type V endoleak is endotension, in which the aneurysmal sac increases in size without a definite visualization of a leak on imaging studies.]
[UpToDate: Type V endoleak was more commonly associated with semiporous graft materials (first generation expanded polytetrafluoroethylene [ePTFE] endografts), in which sac enlargement was associated with exudation of a protein rich material across the wall of the endograft. A change in the graft design appears to have resolved this problem, confirming the source of this type of endoleak. Treatment consisted of relining the existing endograft with a newer, lower porosity graft, or explantation of the graft.]
What is the most common location of a mal perforans ulcer (a cutaneous condition of chronic, trophic, ulcerative disease seen on the dependent parts of body in denervating diseases)?
2nd metatarsal-phalangeal joint
[UpToDate: The physical examination may reveal several abnormalities that result from diabetic neuropathy, such as claw toes and Charcot arthropathy (also called diabetic neuropathic arthropathy). Chronic motor neuropathy often affects the small intrinsic muscles of the feet so that the action of the larger muscles in the anterior tibial compartment is unopposed. This leads to subluxation of the proximal interphalangeal-metatarsal joints, resulting in a claw toe appearance. One consequence of this abnormality is increased pressure on the metatarsal heads, which are a common site of ulcer development.]
What is the vascular issue in Marfan syndrome?
Aortic root dilatation
[UpToDate: Aortic root disease, leading to aneurysmal dilatation, aortic regurgitation, and dissection, is the main cause of morbidity and mortality in the Marfan syndrome (MFS). There can be poor correlation between the severity of the cardiovascular and the ocular or skeletal manifestations. Although dilated, the aorta in MFS tends to be stiffer and less distensible than in controls, and these changes increase with age.
Dilatation of the aorta is found in approximately 50% of young children with MFS and progresses with time. Approximately 60% to 80% of adult patients with MFS have dilatation of the aortic root (with normal range adjusted for patient body surface area and age) by echocardiography, often accompanied by aortic regurgitation. Importantly, all patients diagnosed with MFS using the revised criteria must have aortic root dilatation, a family history of aortic root dilatation, or an FBN1 mutation previously associated with aortic root dilatation, highlighting the strong predisposition for emergence of vascular disease. Dilatation may also involve other segments of the thoracic aorta, the abdominal aorta, the root of the pulmonary artery or even the carotid and intracranial arteries, although this is much less frequent than observed in LDS.]
Which symptoms would be manifested during a middle cerebral artery event?
Contralateral motor and speech (if dominant side), contralateral facial droop
Thoracic outlet syndrome of the subclavian vein usually presents as?
Effort-induced thrombosis of subclavian vein that is acutely painful, with swollen, blue limb
[Paget-von Schrotter disease, baseball pitchers]
[UpToDate: Symptoms of venous compression are the second most common clinical finding of TOS, accounting for about 3% of cases. Venous TOS (vTOS) typically occurs in individuals who perform vigorous repetitive exertion of the upper extremities, usually with the arms above shoulder level. Forearm fatigue within minutes of using the arm may be present in vTOS.
Swelling can be accompanied by pain and cyanosis of the affected extremity; paresthesias in the fingers are common but are a manifestation of swelling in the hand rather than nerve compression. Collateral venous patterning may be seen in the skin overlying the ipsilateral shoulder, neck, and chest wall and indicates compensatory superficial venous flow due to subclavian vein stenosis or occlusion.
Upper extremity edema due to varying degrees of venous compression or overt deep vein thrombosis is the hallmark of vTOS. Upper extremity venous thrombosis due to thoracic outlet compression is termed “spontaneous” to distinguish it from instrumentation-related or “catheter-induced” venous thrombosis. Spontaneous upper extremity venous thrombosis is historically referred to as Paget-Schroetter syndrome or “effort” thrombosis. Spontaneous upper extremity venous thrombosis is discussed elsewhere.]
What kind of flow does a normal external carotid artery have?
Triphasic flow
[RadioGraphics: This artery supplies the high-resistance vascular bed of the facial muscles. The normal spectrum in this location rises sharply during systole and falls rapidly, approaching zero or descending transiently below the baseline, in diastole. Normal value ranges in adults include a PSV of 57–87 cm/sec, an EDV of 11–21 cm/sec, and an RI of 0.72–0.84.]
[Picture: Spectrum from the external carotid artery shows a high-resistance waveform with reversal of flow in early diastole.]
What is the gold standard for diagnosing thoracic outlet syndrome of the subclavian vein?
venography but duplex ultrasound makes the diagnosis and is quicker to get
[UpToDate: The predominant clinical symptoms and signs direct the nature of further evaluation depending on the type of TOS.
For arterial and venous TOS, the diagnosis is supported by the demonstration of stenosis or occlusion of the corresponding subclavian vessel in a patient with an appropriate clinical history. Diagnostic tests are often negative or equivocal in neurogenic thoracic outlet syndrome (nTOS), and further imaging is primarily used to exclude other conditions, such as degenerative cervical disk or spinal column disease, shoulder disease, and various forms of intracranial disease.
Imaging studies can help confirm a suspected diagnosis of thoracic outlet syndrome. Chest x-rays are important to identify bony abnormalities such as cervical ribs, long transverse cervical processes, or rib/clavicular fracture calluses. Because more than 90% of aTOS patients will have a bony abnormality, the absence of rib abnormalities nearly eliminates a diagnosis of aTOS.
Ultrasonography is the initial imaging test to evaluate aTOS or vTOS because it is inexpensive and noninvasive. Duplex ultrasound is a highly sensitive and specific test for venous stenosis or occlusion when performed by an experienced vascular ultrasound technician. A positional test can be easily performed to assess patency of the involved vessels with provocative maneuvers. For aTOS, duplex ultrasonography may demonstrate an increased flow velocity in the subclavian artery at the site of a stenosis or aneurysmal degeneration of the artery distal to a stenosis. These findings in a patient with a typical clinical history and no risk factors for atherosclerosis support a diagnosis of aTOS. Equivocal duplex studies are followed up with additional imaging.
In many centers, conventional arteriography has been supplanted by CT angiography for the diagnosis of aTOS; however, arteriography may still be needed for patients who have signs and symptoms of acute arterial insufficiency or ischemia, and to plan surgical reconstruction. The advantage of arteriography and venography is the ability to obtain dynamic studies in which the patient performs upper extremity maneuvers during imaging to assist in identifying arterial or venous compression, or to initiate thrombolytic therapy, if indicated. Although contrast venography is not always needed to establish a diagnosis of vTOS, early intervention with catheter-based thrombolytic therapy appears to be associated with improved outcomes.
The role for computed tomographic or magnetic resonance imaging is evolving and provides important diagnostic information especially when ultrasound results are equivocal. ]
What is the #1 preventative agent for atherosclerosis?
Statins (IE lovastatin)
[UpToDate: Currently available statins include lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin, and, in some countries, pitavastatin. These agents are competitive inhibitors of HMG CoA reductase, the rate-limiting step in cholesterol biosynthesis. They occupy a portion of the binding site of HMG CoA, blocking access of this substrate to the active site on the enzyme.
A reduction in intrahepatic cholesterol leads to an increase in LDL receptor turnover that results from an enhanced rate of hepatic LDL receptor cycling. Statins also reduce VLDL production, via an effect mediated by hepatic apo B secretion, and it is associated with a diminished rate of recovery of HMG CoA reductase activity after drug treatment.
Most of the statins have modest HDL-cholesterol (HDL-C) raising properties (about 5%), although rosuvastatin has a larger effect. Triglyceride concentrations fall by an average of 20% to 40% depending upon the statin and dose used. The reduction in plasma triglycerides is due to a decrease in VLDL synthesis and to clearance of VLDL remnant particles by apo B/E (LDL) receptors.]
How do renovascular hypertension due to renal atherosclerosis and fibromuscular dysplasia (FMD) differ in terms of laterality, location, and gender?
- Renal atherosclerosis occurs most often on the left side, proximal 1/3, and in men
- Fibromuscular dysplasia (FMD) occurs most often on the right side, distal 1/3, and in women
[UpToDate: Both atherosclerosis and FMD may cause renal artery stenosis and carotid artery disease. Patients with atherosclerosis are usually older and have typical cardiovascular risk factors such as dyslipidemia, diabetes mellitus, and a history of tobacco use, whereas individuals with FMD are usually younger and have fewer cardiovascular risk factors. However, given that FMD can occur in older patients, age alone does not exclude the diagnosis.
Atherosclerosis usually involves the ostial or proximal segment of the arteries, whereas FMD involves the middle or distal segment. In addition, the “string of beads” appearance is unique to FMD. Thus, atherosclerotic disease and FMD can typically be distinguished radiographically.]
Where is the failure site in a type IV endoleak following abdominal aortic aneurysm repair?
Graft wall porosity or suture holes
[UpToDate: Type IV endoleak is associated with graft porosity and is self-limited, typically resolving in 24 hours. It has not been associated with any long-term adverse events and does not require treatment. Type IV leak can obscure more serious type I or III leaks and can be quite disconcerting to see at completion angiography.]
What treatment is best for short stenoses and excellent for common iliac artery stenosis?
Percutaneous transluminal angioplasty (PTA)
[Intima usually ruptured and media stretched, pushes plaque out]
[UpToDate: In our practice, we use a combination of angioplasty and stenting, depending upon the lesion morphology and location.
Common iliac artery stenoses are first angioplastied. If there is a satisfactory result, we stop. However, if there is a flow-limiting dissection or persistent high-grade stenosis associated with a pressure gradient, we recommend the use of stents to improve the long-term patency. Balloon-expandable bare metal stents (eg Palmaz) or covered stents (eg, iCast), are typically used to treat lesions at the origins of the common iliac arteries. Self-expanding bare metal stents (eg, nitinol) or covered stents (eg, Viabahn) are generally preferred for longer segments and for lesions that involve the external iliac arteries. The choice of stent is largely a matter of personal choice based on personal experience and local availability, given the wide range of stent materials, geometric designs, delivery systems, and coatings.
Calcified lesions should be treated with balloon-expandable stents, particularly in the external iliac artery. Covered stents should be used for heavily calcified lesions.]
Which nerve and/or artery travel in the lateral compartment of the leg?
Superficial peroneal nerve
What is the treatment for thoracic outlet syndrome of the subclavian artery?
- Cervical rib and 1st rib resection
- Divide anterior scalene muscle
- Possible bypass graft if artery is too damaged or aneurysmal
[UpToDate: Patients with aTOS are treated according to the nature of their symptoms and initial presentation. Patients with signs and symptoms of upper extremity thromboembolism undergo thoracic outlet decompression in conjunction with embolectomy, thrombolytic therapy, or anticoagulation. Arterial TOS is nearly always associated with a correctable anatomic bony abnormality, and, without decompression, the rate of recurrent thromboembolism is high. The supraclavicular approach offers direct access to the subclavian artery. Occasionally, arterial reconstruction (ie, surgical bypass) may be needed.]
What is subclavian steal syndrome?
Proximal subclavian artery stenosis resulting in reversal of flow through ipsilateral vertebral artery into the subclavian artery
[UpToDate: The term “subclavian steal” refers to a phenomenon of flow reversal in the vertebral artery ipsilateral to a hemodynamically significant stenosis or occlusion of the subclavian artery. In most cases, subclavian steal is asymptomatic, does not warrant invasive evaluation or treatment, and represents an appropriate physiological response to proximal arterial disease. Subclavian steal syndrome implies the presence of significant symptoms due to arterial insufficiency in the brain (ie, vertebrobasilar insufficiency) or upper extremity which are supplied by the subclavian artery.
Subclavian artery occlusion or a hemodynamically significant stenosis proximal to the origin of the vertebral artery results in lower pressure in the distal subclavian artery. As a result, blood flows from the contralateral vertebral artery to the basilar artery, and may flow in a retrograde direction down the ipsilateral vertebral artery, away from the brainstem. Reversed vertebral artery flow, although it may have deleterious neurologic effects, serves as an important collateral artery for the arm in this setting.]
What is the DeBakey classification of aortic dissection?
- Type I: Ascending and descending
- Type II: Ascending only
- Type III: Descending only
[Based on the site of tear and extent of dissection]
Communication between the internal and external carotid arteries occurs via which two arteries?
- Ophthalmic artery (from the ICA)
- Internal maxillary artery (from the ECA)
What is the treatment for Kawasaki’s disease?
Steroids (possible coronary artery bypass grafting)
[UpToDate: In patients with KD, we recommend a single dose of intravenous immune globulin (IVIG; 2 g/kg) administered over 8 to 12 hours (Grade 1A). It is preferable that IVIG be administered within the first 10 days of illness, before aneurysms typically develop, but IVIG should be administered even beyond this 10-day window in patients with evidence of persistent vasculitis or systemic inflammation (eg, persistent fever).
In patients with KD, we suggest that aspirin be administered in the acute phase of illness (Grade 2C). The American Academy of Pediatrics (AAP) and American Heart Association (AHA) recommend high-dose aspirin (80 to 100 mg/kg/day), but it is not clear that this dose is more effective than the lower doses used in some clinical trials (30 to 50 mg/kg per day). The total daily aspirin dose of 30 to 50 mg/kg per day is administered in four divided doses (maximum dose 4 g per day). The dose of aspirin is decreased to 3 to 5 mg/kg per day 48 hours after the resolution of fever. Aspirin is continued until laboratory markers of acute inflammation (eg, platelet count and erythrocyte sedimentation rate [ESR]) return to normal, unless coronary artery (CA) abnormalities are detected by echocardiography.
Glucocorticoids may more rapidly reduce the level of inflammatory markers and fever and decrease the rate of initial treatment failure in certain high-risk patients. However, the addition of glucocorticoids to initial IVIG therapy does not impact the overall rate of CA aneurysms. Thus, we do not recommend routine use of glucocorticoids for initial therapy of KD (Grade 1B).]
Do deep lymphatics have valves?
Yes
[Wikipedia: The lymph capillaries drain the lymph to larger contractile lymphatics, which have valves as well as smooth muscle walls. These are called the collecting lymphatics. As the collecting lymph vessel accumulates lymph from more and more lymph capillaries in its course, it becomes larger and is called the afferent lymph vessel as it enters a lymph node. Here the lymph percolates through the lymph node tissue and is removed by the efferent lymph vessel. An efferent lymph vessel may directly drain into one of the (right or thoracic) lymph ducts, or may empty into another lymph node as its afferent lymph vessel. Both the lymph ducts return the lymph to the blood stream by emptying into the subclavian veins
The functional unit of a lymph vessel is known as a lymphangion, which is the segment between two valves. Since it is contractile, depending upon the ratio of its length to its radius, it can act either like a contractile chamber propelling the fluid ahead, or as a resistance vessel tending to stop the lymph in its place.]
Where is the failure site in a type I endoleak following abdominal aortic aneurysm repair?
Proximal or distal graft attachment sites
[Type I failure is due to flow around the proximal or distal attachment sites.]
[UpToDate: Type I endoleak is due to an incompetent seal at the proximal or distal attachment sites. It occurs in 0% to 10% of endovascular aortic aneurysm repairs.
Type I leak can occur immediately after device placement or can develop over time. Immediate proximal type I endoleak is typically due to incomplete apposition of the stent-graft to the aortic neck. Contributing factors include mural thrombus, aortic neck calcification, angulation, a short aortic neck, reverse tapering of the neck, and incorrect device sizing. Immediate distal type I endoleak is usually due to incorrect sizing of the iliac limbs, or inadvertent deployment of the endograft limb, often because of excessive iliac tortuosity, within the more proximal, larger iliac vessel. Late type I endoleaks can develop as a result of aneurysmal degeneration of the aortic neck or iliac arteries, severe angulation at the fixation sites or graft migration.]
What is the surgical treatment for an aortic graft that erodes into bowel and forms an aortoenteric fistula?
Bypass through non-contaminated field (eg axillary-femoral bypass with femoral-to-femoral crossover), resect graft, and then close hole in the duodenum
[UpToDate: Treatment of aortoenteric fistula (AEF) includes initial resuscitation and hemodynamic support, antimicrobial therapy, and aortic repair (which requires graft removal in the case of secondary aortoenteric fistula [SAEF]). Without treatment, AEF is nearly uniformly fatal. The type and timing of repair is individualized, taking into account the clinical presentation (severity of bleeding or infectious process), type of AEF (primary or secondary), patient comorbidities, and aortic anatomy, among other factors. The initial care and resuscitation of the patient with gastrointestinal bleeding and hypovolemic shock are discussed separately.
Antimicrobial therapy based on the sensitivity of the organisms recovered should be continued for a minimum of three months. Ideally, comanagement with an infectious disease service is recommended. Longer-term antimicrobial therapy may be recommended when only a portion of a prosthetic graft has been removed (ie, portions that were not involved by the AEF).
Open repair of AEF is often complicated, requiring a patient with sufficient cardiac and respiratory reserve to tolerate the procedure. For patients who are not deemed fit for open repair, an endovascular approach has been suggested as a less invasive method to temporarily or definitively (often along with long-term antimicrobial therapy) manage the AEF. Some have suggested using an aortic occlusion balloon at, or above, the level of the AEF for rapid control of the aorta.]
Which vessel is diseased in calf claudication?
Common femoral artery or proximal superficial femoral artery disease
[Symptoms occur one level below occlusion]
[UpToDate: Classic claudication is characterized by leg pain that is consistently reproduced with exercise and relieved with rest. The degree of symptoms of claudication depends upon the severity of stenosis, the collateral circulation, and the vigor of exercise. Patients with claudication can present with buttock, hip, thigh, calf, or foot pain, alone or in combination. The usual relationships between pain location and corresponding anatomic site of arterial occlusive disease can be summarized as follows:
- Buttock and hip: Aortoiliac disease
- Thigh: Aortoiliac or common femoral artery
- Upper two-thirds of the calf: Superficial femoral artery
- Lower one-third of the calf: Popliteal artery
- Foot claudication: Tibial or peroneal artery]
What is the most common peripheral aneurysm?
Popliteal artery aneurysm
[UpToDate: Popliteal artery aneurysms are the most common true peripheral aneurysm, occurring more frequently than femoral artery aneurysms, but less frequently than abdominal aortic aneurysm. The prevalence of popliteal aneurysm in the general population is difficult to determine, but appears to be increasing possibly due to more common use of imaging modalities and an aging population.
A screening study of 1074 men identified popliteal artery aneurysm in 1%. In another screening study of men between the ages of 65 and 74, abdominal aortic aneurysms were identified in 4.9% of patients. Of these patients, 6.8% had femoral artery aneurysms and 9.6% had popliteal artery aneurysms.
Men are more commonly affected than women and present at a younger age. In one study of hospitalized patients, the incidence of femoral or popliteal artery aneurysms was 7.4 per 100,000 males and 1.0 per 100,000 females.]
What are the surgical indications for treating a popliteal artery aneurysm?
- Symptomatic
- >2cm
- Mycotic
[UpToDate: For patients with acute lower extremity ischemic symptoms due to popliteal aneurysm (any size), we recommend emergent popliteal aneurysm repair due to the high risk of limb loss without treatment. We suggest thrombolytic therapy prior to repair for patients with absent or limited distal runoff; restoration of outflow improves the long-term patency of revascularization. Lytic agents can be administered intraoperatively or using catheter-based techniques depending upon the clinical scenario. The patient should be anticoagulated with intravenous heparin while awaiting repair.
For patients with patent popliteal aneurysm ≥2.0 cm, we suggest elective repair of the aneurysm over conservative management for patients at low risk for perioperative surgical morbidity (Grade 2B). Elective aneurysm repair is associated with a lower long-term risk of limb-threatening ischemia and limb loss.
Patients with popliteal aneurysm <2.0 cm are typically observed. However, the presence of mural thrombus may increase the propensity for artery expansion and risk of thromboembolic complications. The role of antiplatelet and anticoagulant therapy in the conservative management of small popliteal artery aneurysms, and particularly those with mural thrombus, has not been defined. As such, some clinicians prefer to repair popliteal aneurysm <2.0 cm when they are associated with significant thrombus.
We perform serial physical examination and duplex ultrasonography every 6 to 12 months for patients who are managed conservatively. The time interval between examinations depends on the patients’ risk factors for expansion.]
What presents as a painless neck mass, usually near the carotid bifurcation, that is highly vascular and composed of neural crest cells?
Carotid body tumor
[UpToDate: Carotid body tumors typically present as painless, gradually enlarging masses located in the upper part of the neck below the angle of the jaw. In later stages, dysphagia, deficits of cranial nerves VII, IX, X, XI and XII, and hoarseness or a Horner’s syndrome may result from pressure on the vagus or sympathetic nerves. Physical examination discloses a rubbery non-tender mass in the lateral neck that is more freely movable in the horizontal plane than vertically, referred to as a positive Fontaine’s sign. There may be a carotid bruit or the tumor may be pulsatile.]
What is median arcuate ligament syndrome?
Chronic, recurrent abdominal pain related to compression of the celiac artery by the median arcuate ligament
[Bruit near the epigastrium, chronic pain, weight loss, and diarrhea]
[UpToDate: Celiac artery compression syndrome (also referred to as celiac axis syndrome, median arcuate ligament syndrome, and Dunbar syndrome) is defined as chronic, recurrent abdominal pain related to compression of the celiac artery by the median arcuate ligament. It is an uncommon disorder that is characterized clinically by the triad of postprandial abdominal pain, weight loss, and sometimes an abdominal bruit. The diagnosis is often one of exclusion, given the nonspecific symptoms which overlap with other forms of chronic intestinal ischemia. Treatment may involve surgical decompression of the celiac access; however, patient selection can be challenging because success cannot be guaranteed.
Celiac artery compression syndrome was initially described in the 1960s and is defined as abdominal pain related to compression of the celiac artery by the median arcuate ligament. The syndrome is also referred to as celiac axis syndrome, median arcuate ligament syndrome, and Dunbar syndrome.
The median arcuate ligament is a fibrous arch that traverses the aorta just cephalad to the origin of the celiac artery, and bridges the crura of the diaphragm. Adjacent to the median arcuate ligament is the celiac plexus (or ganglion), which originates from preganglionic splanchnic nerves, somatic branches from the phrenic and vagus nerves, parasympathetic preganglionic nerves, and sympathetic postganglionic fibers.]
What is the 1st branch of the internal carotid artery?
Ophthalmic artery
[Wikipedia: Branches include - Ophthalmic, anterior choroidal, anterior cerebral, middle cerebral and posterior communicating artery.]
Where are the two watershed areas of the bowel?
- Griffith’s = splenic flexure
- Sudak’s = upper rectum
What test is indicated if pulse volume recordings suggest significant peripheral arterial disease?
Arteriogram
[Gold standard for vascular imaging]
[UpToDate: Conventional arteriography provides the reference standard for arterial vascular imaging and involves the intravascular injection of a contrast agent during planar radiographic imaging. The base images are enhanced by background subtraction of a precontrast frame using a digital technique (ie, digital subtraction arteriography [DSA]) allowing only the opacified arterial system to be seen on the image. DSA provides superior contrast resolution with lower doses of intravenous contrast compared with non-digital techniques. DSA also has the benefit of image magnification and imaging the vessels in real-time while also offering the option for simultaneous intervention. However, conventional arteriography has potential serious side effects related to arterial puncture, and higher doses of ionizing radiation compared with other imaging methods, and potential for nephrotoxicity (related to intravenous contrast, particularly in patients with pre-existing renal impairment), and allergic reactions to the contrast agent.]
At what ankle-brachial index (ABI) does someone start to get rest pain?
Less than 0.5
[usually across the distal arch and foot]
[UpToDate: A low ABI is associated with a higher risk of coronary heart disease, stroke, transient ischemic attack, progressive renal insufficiency, and all-cause mortality. The ABI is generally, but not absolutely, correlated with clinical measures of lower extremity function such as walking distance, speed of walking, balance, and overall physical activity. Further evaluation is dependent upon the ABI value.
- The normal ABI is >0.91 to as high as 1.3. Normally, the pressure is higher in the ankle than in the arm. A normal test generally excludes arterial occlusive disease. Mild disease and arterial entrapment syndromes can produce false negative tests. If ABIs are normal at rest but symptoms strongly suggest claudication, exercise testing should be performed.
- An ABI >1.3 suggests the presence of calcified vessels and the need for additional vascular studies, such as pulse volume recordings, measurement of the toe pressures and toe-brachial index, or arterial duplex studies.
- An ABI ≤0.9 is diagnostic of occlusive arterial disease in patients with symptoms of claudication or other signs of ischemia and has 95% sensitivity (and 100% specificity) for detecting arteriogram-positive occlusive lesions associated with ≥50% stenosis in one or more major vessels.
- An ABI of 0.4 to 0.9 suggests a degree of arterial obstruction often associated with claudication.
- An ABI below 0.4 represents multilevel disease (any combination of iliac, femoral or tibial vessel disease) and may be associated with non-healing ulcerations, ischemic rest pain or pedal gangrene.]
How does the risk of mortality or paraplegia following descending aortic aneurysm repair compare between the open and endovascular approach?
- 2-3% for endovascular approach
- 20% for open repair
[UpToDate: The choice of approach to repair (open versus endovascular) for descending thoracic aortic aneurysm (TAA) should take into account the etiology (sporadic, genetically-mediated), location in the descending aorta, and extent of the aneurysm, and the patient’s expected survival (short-term and long-term), which depends upon the patient’s age and medical comorbidities.
Thoracic aortic aneurysm/dissection can be sporadic or related to genetically-mediated disorders (nonsyndromic or syndromic). The etiology of descending aneurysmal disease determines the preferred approach to repair.
- For patients with sporadic (degenerative) descending TAA (asymptomatic, symptomatic) that does not involve the visceral segment, and anatomy that is otherwise suitable for endovascular repair, we use an endovascular rather than open surgical approach to repair. Endovascular repair is associated with reduced perioperative morbidity and mortality; however, the long-term durability of endovascular TAA repair compared with open surgical repair remains uncertain. Endovascular repair combined with a debranching procedure may still be an option for distal TAA but cannot generally be performed in an urgent setting given the need for customized endovascular devices.
- For patients with syndromic descending TAA, we use an open surgical approach to replace the descending thoracic aorta, rather than endovascular stent-graft placement. Unfavorable late aortic remodeling at the site of stent-graft placement has been reported likely related to the persistent radial force of these devices against the abnormal aortic tissue. However, some feel that stent-grafting may be justified in emergencies as a “bridging” method to later definitive surgical repair. The approach for those with nonsyndromic TAA is less well-defined, but either approach may be appropriate depending on the extent of repair needed, patient age, and other comorbidities.]
Where is the failure site in a type III endoleak following abdominal aortic aneurysm repair?
Either failure at the overlap sites when using multiple grafts or it is failure due to a graft fabric tear
[Essentially a type III endoleak is graft malfunction or disruption.]
[UpToDate: Type III endoleaks are due to a junctional leak or disconnect of the endograft components (IIIA) or holes in the endograft fabric (IIIB). Type III endoleak is as serious as type I endoleak because it pressurizes the aneurysm sac.]
What is the most commonly diseased intracranial artery?
Middle cerebral artery
[UpToDate: Studies performed in the 1960s first established the importance of atherosclerotic intracranial large artery occlusive disease as a cause of stroke. One of the largest, the Joint Study of Extracranial Arterial Occlusion, evaluated 3788 patients (84% of whom were white) with signs and symptoms of ischemic cerebrovascular disease using four vessel angiography. Stenotic lesions were found in 7.7% of basilar arteries, 4.4% of intracranial vertebral arteries, 6.7% of intracranial carotid arteries, 3.8% of middle cerebral arteries (MCA), 3.2% of anterior cerebral arteries (ACA), and 2.6% of posterior cerebral arteries (PCA). Isolated intracranial occlusive disease was observed in 6.1% of all patients.]
Which cell type mediates reperfusion injury?
Polymorphonucleocyte (PMN)
[Wikipedia: Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. The inflammatory response is partially responsible for the damage of reperfusion injury. White blood cells, carried to the area by the newly returning blood, release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage. The restored blood flow reintroduces oxygen within cells that damages cellular proteins, DNA, and the plasma membrane. Damage to the cell’s membrane may in turn cause the release of more free radicals. Such reactive species may also act indirectly in redox signaling to turn on apoptosis. White blood cells may also bind to the endothelium of small capillaries, obstructing them and leading to more ischemia. Another hypothesis would be that normally, tissues contain free radical scavengers to avoid damage by oxidizing species normally contained in the blood. Ischemic tissue would have a decrease function of these scavengers because of cell injury. Once blood flow is reestablished, oxygen species contained in the blood will damage the ischemic tissue because the function of the scavengers is decreased.]
What is the treatment of adventitial cystic disease?
Resection of cyst
Cleveland Clinic: Surgery is recommended for symptomatic patients. This involves resection of the cyst and reconstruction of the section of the blood vessel, if necessary. Resection is associated with low rates of recurrence. Aspiration of the cyst has been used in rare cases but the risk is of recurrence is higher if the cyst is aspirated.]
Compartment syndrome is most likely to occur in which compartment of the leg?
Anterior compartment of the leg
[Results in foot drop]
[UpToDate: The anterior compartment of the leg is the most common site for acute compartment syndrome (ACS). It contains the four extensor muscles of the foot, the anterior tibial artery, and the deep peroneal nerve. Signs of ACS affecting the anterior compartment include loss of sensation between the first (ie, great) and second toes and weakness of foot dorsiflexion. Late sequelae include foot drop, claw foot, and deep peroneal nerve dysfunction.]
What is the medical treatment for homocystinuria?
Folate and B12
[Homocystinuria can increase the risk of atherosclerosis]
[UpToDate: Homocysteine is an intermediary amino acid formed by the conversion of methionine to cysteine. Homocystinuria or severe hyperhomocysteinemia is a rare autosomal recessive disorder characterized by severe elevations in plasma and urine homocysteine concentrations. Clinical manifestations of homocystinuria include developmental delay, osteoporosis, ocular abnormalities, thromboembolic disease, and severe premature atherosclerosis.
There is no high quality evidence from trials with clinical endpoints to support treating patients who do not have severe hyperhomocysteinemia (homocystinuria).
The majority of hyperhomocysteinemia is caused by low levels of folate and vitamin B12 in patients with or without the thermolabile variant of MTHFR. Correcting nutritional inadequacy of folic acid, vitamin B12, and choline (betaine) will lower homocysteine levels. A diet rich in fruits, vegetables, and low-fat dairy products and low in saturated and total fat also can lower fasting serum homocysteine.
In patients who are treated beyond diet, the treatment varies with the underlying cause, but generally involves vitamin supplementation with folic acid, vitamin B12, and vitamin B6.]
[Wikipedia: No specific cure has been discovered for homocystinuria; however, many people are treated using high doses of vitamin B6 (also known as pyridoxine). Slightly less than 50% respond to this treatment and need to take supplemental vitamin B6 for the rest of their lives. Those who do not respond require a Low-sulfur diet (especially monitoring methionine), and most will need treatment with trimethylglycine. A normal dose of folic acid supplement and occasionally adding cysteine to the diet can be helpful, as glutathione is synthesized from cysteine (so adding cysteine can be important to reduce oxidative stress).
Betaine (N,N,N-trimethylglycine) is used to reduce concentrations of homocysteine by promoting the conversion of homocysteine back to methionine, i.e., increasing flux through the re-methylation pathway independent of folate derivatives (which is mainly active in the liver and in the kidneys). The re-formed methionine is then gradually removed by incorporation into body protein. The methionine that is not converted into protein is converted to S-adenosyl-methionine which goes on to form homocysteine again. Betaine is, therefore, only effective if the quantity of methionine to be removed is small. Hence treatment includes both betaine and a diet low in methionine. In classical homocystinuria (CBS, or cystathione beta synthase deficiency), the plasma methionine level usually increases above the normal range of 30 micromoles/L and the concentrations should be monitored as potentially toxic levels (more than 400 micromoles/L) may be reached.]
Where is the failure site in a type V endoleak following abdominal aortic aneurysm repair?
Expansion of aneurysm without evidence of leak
[UpToDate: Type V endoleak, also referred to as endotension, is defined as continued aneurysm sac expansion without a demonstrable endoleak on any imaging modality. The phenomenon is poorly understood. It was more commonly associated with semiporous graft materials (first generation expanded polytetrafluoroethylene [ePTFE] endografts), in which sac enlargement was associated with exudation of a protein rich material across the wall of the endograft. A change in the graft design appears to have resolved this problem, confirming the source of this type of endoleak.]
What percent of patients suffer aortic insufficiency as a result of aortic dissection?
70%
[Caused by annular dilatation or when aortic valve cusp is sheared off]
Which nerve and/or artery travel in the superficial posterior compartment of the leg?
Sural nerve
[Wikipedia: The sural cutaneous nerve consists of the fusion of the medial sural cutaneous nerve (MSCN) which is a terminal branch of the tibial nerve and the lateral sural cutaneous nerve (LSCN) which is one of the terminal branches of the common fibular nerve. These two branches, MSCN and LSCN, are connected by the sural communicating branch and form the sural nerve. How the two branches fuse, the contribution of the fibular and tibial branch, the location of the connection, and differences between the two lower extremities contribute to variability of this nerve.
From the mid calf down to the ankle the nerve courses subcutaneously along a line drawn from the mid-posterior popliteal fossa to just posterior to the lateral malleolus and thence under the malleolus and forward along the lateral aspect of the foot. It supplies sensation to the skin of the lateral foot and lateral lower ankle.]
Which nerve is responsible for eversion of the foot and lateral foot sensation?
Superficial peroneal nerve
[Wikipedia: The superficial peroneal nerve or superior fibular nerve, innervates the peroneus longus and peroneus brevis muscles and the skin over the antero-lateral aspect of the leg along with the greater part of the dorsum of the foot (with the exception of the first web space, which is innervated by the deep peroneal nerve).
It passes forward between the peroneus muscles and the extensor digitorum longus, pierces the deep fascia at the lower third of the leg, and finally divides into a medial dorsal cutaneous nerve and an intermediate dorsal cutaneous nerve. In its course between the muscles, the nerve gives off muscular branches to the peroneus longus and peroneus brevis muscles and cutaneous filaments from the integument of the lower part of the leg.
Injury to the nerve can result in an inability to evert the foot and loss of sensation over the dorsum of the foot (with the exception of the first web space between the great toe and the second toe, where the inferior fibular nerve innervates).]
What is the Arc of Riolan?
An important collateral between the Superior mesenteric artery and inferior mesenteric artery
[UpToDate: The meandering mesenteric artery is an inconstant communication between the SMA and IMA that is variably described, and is also referred to as the central communicating artery, and historically referred to as the Arc of Riolan.]
[Radiopaedia: The arc of Riolan (AOR), also known as the mesenteric meandering artery (of Moskowitz) or central anastomotic mesenteric artery, is an arterio-arterial anastomosis between the superior and inferior mesenteric arteries.]
Which vessel is diseased in mid-thigh claudication?
External iliac
[Symptoms occur one level below occlusion]
[UpToDate: Classic claudication is characterized by leg pain that is consistently reproduced with exercise and relieved with rest. The degree of symptoms of claudication depends upon the severity of stenosis, the collateral circulation, and the vigor of exercise. Patients with claudication can present with buttock, hip, thigh, calf, or foot pain, alone or in combination. The usual relationships between pain location and corresponding anatomic site of arterial occlusive disease can be summarized as follows:
- Buttock and hip: Aortoiliac disease
- Thigh: Aortoiliac or common femoral artery
- Upper two-thirds of the calf: Superficial femoral artery
- Lower one-third of the calf: Popliteal artery
- Foot claudication: Tibial or peroneal artery]
The two vertebral arteries that supply some of the blood to the head, join to form which artery?
Basilar artery
What vessel type does not contain a basement membrane?
Lymphatic vessels
[Wikipedia: The general structure of lymphatics is based on that of blood vessels. There is an inner lining of single flattened epithelial cells (simple squamous epithelium) composed of a type of epithelium that is called endothelium, and the cells are called endothelial cells. This layer functions to mechanically transport fluid and since the basement membrane on which it rests is discontinuous; it leaks easily. The next layer is that of smooth muscles that are arranged in a circular fashion around the endothelium, which by shortening (contracting) or relaxing alter the diameter (caliber) of the lumen. The outermost layer is the adventitia that consists of fibrous tissue. The general structure described here is seen only in larger lymphatics; smaller lymphatics have fewer layers. The smallest vessels (lymphatic or lymph capillaries) lack both the muscular layer and the outer adventitia. As they proceed forward and in their course are joined by other capillaries, they grow larger and first take on an adventitia, and then smooth muscles.]
Which test is used to confirm aortic dissection
Chest CT with contrast
[UpToDate: CT is the most common initial choice, due to its widespread availability, particularly in the emergency department setting. More than one study is often needed to obtain all the necessary information to fully guide treatment. In one IRAD review, patients had an average of 1.83 studies per patient. The initial study was CT in 61%, TEE in 33%, aortography in 4%, and MR in 2%. The availability of some studies may be limited, and accuracy depends upon the performance and interpretation of the test by skilled individuals, and as such, the studies chosen may differ from institution to institution.
CT scanning has a reported sensitivity of 83% to 95% and specificity of 87% to 100% for the diagnosis of acute aortic dissection. The chief limitation of imaging is the ascending aorta, where the sensitivity may drop to <80%, as contrast enhancement can be dependent on timing of the injection. As an example, a CT scan to evaluate for initially suspected pulmonary embolus as a source of chest pain may or may not time correctly for assessment of the ascending aorta. The accuracy of CT may be substantially improved with spiral (helical) CT and perhaps with multidetector (multislice) CT. Spiral CT may be more accurate than MR or TEE for the detection of aortic arch vessel involvement. A potential limitation is a spiral CT artifact that can simulate an aortic dissection flap in patients if performed without echocardiogram (ECG) gating. Advantages of CT include ready availability at most hospitals, even on an emergency basis, and identification of intraluminal thrombus and pericardial effusion. Two disadvantages of standard CT are that the intimal flap is seen in less than 75% of cases and that the site of entry is rarely identified. In addition, potentially nephrotoxic iodinated contrast is required, and there is no capability to assess for aortic insufficiency. If the CT is equivocal, or further delineation of the dissection is needed, MR angiography or TEE is indicated.
The diagnosis of aortic dissection by CT scanning requires the identification of two distinct lumens; the intimal flap may or may not be demonstrated. In most cases, the true lumen may be localized by its continuity with an undissected proximal or distal segment of the aorta. The presence of intraluminal thrombus is a good marker of the false lumen, but in patients with a concomitant degenerative aneurysm, thrombus may be present in the true lumen. In the majority of cases, the false lumen is larger than the true lumen. A compressed true lumen is the key radiographic finding, which should substantially raise the index of suspicion for renal/visceral/lower extremity malperfusion syndrome. Curving of the dissection flap into the true lumen is seen in 63% of acute type B dissections, but only 25% of chronic dissections. Indeed, it may be appropriate, if open surgical intervention is chosen as the revascularization procedure, to proceed directly to surgery after CT alone in circumstances where the clinical and/or laboratory signs dictate the need for urgent revascularization, as in evidence of bowel ischemia or vascular rupture.]
What is the treatment for a type II endoleak following abdominal aortic aneurysm repair?
Observation most of the time, percutaneous coil embolization if pressurizing aneurysm
[Type II endoleak is failure due to retrograde flow into the aneurysmal sac from patent collaterals (IE patent lumbar, IMA, intercostals, accessory renal).]
[UpToDate: The significance and management of type II endoleaks are controversial. Most investigators argue that careful follow-up imaging to detect changes in aneurysm sac diameter and morphology is preferred, since spontaneous resolution occurs in many cases. In the systematic review, 35.4% resolved spontaneously over a range of three months to four years. If an increase in the diameter of the aneurysm sac is detected, the endoleak should be repaired. Residual aneurysm sac expansion is considered significant when a diameter increase of 5 to 10 mm is documented. Repair is also indicated for persistent endoleaks (>6 to 12 months duration), because the natural history is not completely benign. However, there is no consensus regarding treatment of type II endoleaks that are not associated with aneurysm sac enlargement. In the systematic review, among 14 patients (<1%) with isolated type II endoleak who ruptured, six patients were not known to have any aneurysm expansion.
The approach to the repair of type II endoleaks is most commonly endovascular, consisting of transarterial embolization of the feeding vessels or translumbar embolization of the aneurysm sac. In the systematic review, there were 393 interventions for 1515 type II endoleaks, of which 71.5% were technically successful. Among studies that reported outcomes of intervention, translumbar embolization (n = 57) had a higher initial success rate (81% vs 63%) and fewer recurrent endoleaks (19% vs 36%) compared with transarterial embolization (n = 120). Transarterial embolization also had a higher rate of complications (9.2% vs 0%).
Other approaches include laparoscopic clipping of the involved branch vessels, or surgical conversion.]
How do you expose the superior mesenteric artery (SMA) during embolectomy to treat mesenteric ischemia?
Divide ligament of Treitz, SMA is to the right of this near the base of the transverse colon mesentery
[UpToDate: Open superior mesenteric artery (SMA) embolectomy remains a good option and should be performed in those with indications for open surgical intervention. Mesenteric embolectomy is performed through a midline abdominal incision that allows full inspection of the bowel. The proximal superior mesenteric artery can be exposed at the root of the mesentery by retracting the transverse colon cephalad, mobilizing the distal duodenum, and palpating the SMA in the root of the mesentery.
A transverse arteriotomy is made, through which 3 Fr or 4 Fr Fogarty embolectomy catheters can be introduced to extract the clot. The catheters should be advanced distally as well as proximally. Absence of additional thrombus with multiple passes and restoration of pulsatile inflow confirms clearance of the artery. The vessel is flushed with heparin and the arteriotomy repaired primarily. If arterial inflow cannot be obtained, repeat mesenteric arteriography may be necessary. If inflow cannot be restored, bypass from the aorta or other location can be necessary.]
What is the treatment for a type III endoleak following abdominal aortic aneurysm repair?
Secondary endograft to cover overlap site of tear
[Type III endoleak is either failure at the overlap sites when using multiple grafts or it is failure due to a graft fabric tear.]
[UpToDate: Type III leak is treated to prevent aortic rupture typically by deploying additional stent-graft components to seal the fabric defect or bridge the disconnected components.]
What is the most common cause of acute arterial emboli?
Atrial fibrillation
[Other common causes are recent MI with left ventricular thrombus, myxoma, aorto-iliac disease]
[UpToDate: The majority of arterial emboli that travel to the extremities originate in the heart, with the lower extremities affected more frequently than the upper extremities. Potential sources of emboli from the heart include atrial thrombus formation due to atrial fibrillation, left ventricular thrombus formation following myocardial infarction or left ventricular dysfunction, and debris from prosthetic valves and infected cardiac valves (septic emboli).]
Which symptoms would be manifested during an posterior cerebral artery event?
- Vertigo
- Tinnitus
- Drop attacks
- Incoordination
Which vessel is diseased in buttock claudication?
Aortoiliac disease
[Symptoms occur one level below occlusion]
[UpToDate: Buttock and hip claudication – Patients with aortoiliac disease may complain of buttock, hip, and, in some cases, thigh claudication. The pain is often described as aching in nature and may be associated with weakness of the hip or thigh with walking. Pulses in one or both groins are diminished. Bilateral aortoiliac PAD that is severe enough to cause lower extremity symptoms almost always causes erectile dysfunction in men. Leriche syndrome is the triad of claudication, absent or diminished femoral pulses, and erectile dysfunction.]
What are the initial steps of treating claudication?
- ASA
- Smoking cessation
- Exercise until pain occurs to improve collaterals
[UpToDate: Claudication is associated with an increased risk of coronary, cerebrovascular, and renovascular disease, and peripheral artery disease (PAD) is considered to be a coronary heart disease risk equivalent. To reduce the risk for cardiovascular disease progression and complications, we recommend a secondary prevention strategy that includes antiplatelet therapy (aspirin 75 to 162 mg/day or clopidogrel 75 mg/day), smoking cessation, control of blood sugar and blood pressure, lipid-lowering therapy, and dietary modification (as needed) to achieve the goals set in national guidelines. We do not use dual antiplatelet therapy in patients with claudication in the absence of other indications (eg, drug-eluting stent, prosthetic distal lower extremity bypass).]
Which vasculitis affecting medium arteries, is characterized by weight loss, rash, arthralgias, hypertension, and kidney dysfunction, and is associated with aneurysms that thrombose or rupture (renals most commonly involved)?
Polyarteritis nodosa
[UpToDate: Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis that typically affects medium-sized muscular arteries, with occasional involvement of small muscular arteries. Unlike some other vasculitides (eg, microscopic polyarteritis, granulomatosis with polyangiitis [Wegener’s]), polyarteritis nodosa is not associated with antineutrophil cytoplasmic antibodies (ANCA).
Patients typically present with systemic symptoms. The kidneys, skin, joints, muscles, nerves, and gastrointestinal tract are commonly involved, usually in some combination and sometimes all at once by the time of diagnosis. PAN can affect virtually any organ but has a striking tendency to spare the lungs. Clinical variants or subsets of PAN include single-organ disease and cutaneous-only PAN.
The spectrum of disease known as PAN has evolved and narrowed substantially due to the identification and classification of other forms of vasculitis that had previously been considered PAN. Most importantly, the establishment and acceptance of microscopic polyangiitis as a distinct disease, and the routine availability and recognition of ANCA testing as critical to diagnosing vasculitides other than PAN, have led to more patients with vasculitis being classified as not having PAN. Patient cohorts of PAN included in case series and other research studies published prior to the 1990s almost certainly included a mixture of the newer definition of PAN with microscopic polyangiitis and possibly other forms of vasculitis. Thus, case series of PAN published after this time period that specifically exclude patients with MPA provide important updated information about this disease.]
Which nerve injury is rare but can occur with a really high carotid dissection during carotid endarterectomy?
Glossopharyngeal nerve injury
[Cranial nerve IX]
[UpToDate: The glossopharyngeal nerve is more cephalad than the extent of the typical neck dissection during CEA. A branch of this nerve, the nerve of Hering, is clinically important since it innervates the carotid sinus and is responsible for the bradycardic and hypotensive responses that can be seen with manipulation of this structure. Excessive dissection in the carotid bifurcation can injure this nerve.]
What is the 2nd atherosclerotic stage?
Smooth muscle cell proliferation
[Caused by growth factors released from macrophages and results in wall injury]
[UpToDate: The first phase in atherosclerosis histologically occurs as focal thickening of the intima with accumulation of lipid-laden macrophages (foam cells) and extracellular matrix. Smooth muscle cells can also populate the intima, some of which may arise from hematopoietic stem cells, migrate, and proliferate. Lipids accumulate early in fatty streak formation yielding both intracellular lipid and extracellular deposits, which produce the fatty streak. Biglycan, a small dermatan sulfate proteoglycan detected in the intima of atherosclerotic coronary artery segments, can bind and trap lipoproteins, including very low density lipoproteins and low density lipoprotein. The fatty streak can also contain T lymphocytes. Foam cells constitute the hallmark of the early atheroma.
As these lesions expand, more smooth muscle cells accumulate in the intima. The smooth muscle cells within the deep layer of the fatty streak are susceptible to apoptosis, which is associated with further macrophage accumulation and microvesicles that can calcify, perhaps contributing to the transition of fatty streaks into atherosclerotic plaques.]
Which nerve is responsible for dorsiflexion and sensation between the 1st and 2nd toes?
Deep peroneal nerve
[Wikipedia: In the leg, the deep peroneal nerve supplies muscular branches to the anterior compartment of extensor muscles in the leg which include the tibialis anterior, extensor digitorum longus, peroneus tertius, and extensor hallucis longus (propius), and an articular branch to the ankle-joint. After its bifurcation past the ankle joint, the lateral branch of the deep peroneal nerve innervates the extensor digitorum brevis and the extensor hallucis brevis, while the medial branch goes on to provide cutaneous innervation to the webbing between the first and second digits.
Damage to the deep peroneal nerve, as is possible with traumatic injury to the lateral knee, results in foot drop. The deep peroneal nerve is also subject to injury resulting from lower motor neuron disease, diabetes, ischemia, and infectious or inflammatory conditions. Injury to the common peroneal nerve is the most common isolated mononeuropathy of the lower extremity and produces sensory problems on the lateral lower leg in addition to foot drop.]
What is the most common congenital hypercoagulable disorder?
Resistance to activated protein C (Leiden factor)
[UpToDate: Factor V Leiden (FVL) results from a single point mutation in the factor V gene (guanine to adenine at nucleotide 1691), which leads to a single amino acid change (replacement of arginine with glutamine at amino acid 506); hence the names factor V R506Q and factor V Arg506Gln. This abolishes the Arg506 cleavage site by aPC in factor V and factor Va. This defect was initially termed “aPC resistance” because the anticoagulant activity of aPC was reduced in a modified activated partial thromboplastin time (aPTT) assay.
aPC-mediated cleavage of factor V and Va have different consequences for protein function. aPC cleavage of the procoagulant factor Va causes factor Va degradation, whereas aPC cleavage of the anticoagulant factor V enhances factor V function. FVL is insensitive to both of these cleavages because it lacks the Arg506 cleavage site. Thus, the FVL mutation simultaneously increases coagulation by creating two distinct changes in the coagulation cascade:
- Enhanced procoagulant role of factor Va – aPC destroys factor Va in a series of sequential cleavages. The first cleavage at Arg506 exposes additional cleavage sites at Arg306 and Arg679. Since activated FVL cannot be cleaved at Arg506, these other sites remain buried in the protein, resulting in 20-fold slower degradation of activated FVL. The extended presence of activated FVL results in continued thrombin generation.
- Reduced anticoagulant role of factor V – aPC cleavage of unactivated factor V at position 506 enhances its ability to act as a cofactor in the degradation of factors Va and VIIIa. Since unactivated FVL cannot be cleaved at Arg506, it is less effective as a cofactor for aPC, resulting in reduced degradation of factors Va and VIIIa.
Heterozygosity for the FVL mutation is the most common inherited thrombophilia in unselected Caucasian populations, accounting for 40% to 50% of cases. A study involving 1690 unrelated individuals from Europe found a prevalence of approximately 4%, and a study involving 356 individuals from Canada found an incidence of approximately 5%. In a series of 4047 men and women participating in the Physicians’ Health Study and the Women’s Health Study (both in the United States), the following frequencies for FVL heterozygosity were found:
- Caucasians – 5.3%
- Hispanic Americans – 2.2%
- Native Americans – 1.2%
- African Americans – 1.2%
- Asian Americans – 0.45%]
The tongue deviates to the side of injury to which nerve?
Hypoglossal nerve (CN XII)
[Can occur during carotid endarterectomy]
[UpToDate: The hypoglossal nerve supplies motor function to the tongue. It is routinely identified during CEA. Injury to this nerve is one of the more frequent cranial nerve injuries associated with CEA and can result from inadvertent retraction or, rarely, transection. On physical examination, hypoglossal nerve injury is manifested as tongue deviation toward the side of injury (ie, ipsilateral to the CEA).]
Why do 20% of patients have hypertension following a carotid endarterectomy?
Injury to the carotid body
[Tx: nipride to avoid bleeding]
[UpToDate: Surgical manipulation of the carotid sinus during carotid dissection may result in sympathetic stimulation and resultant hypertension and tachycardia or may increase parasympathetic outflow with resultant bradycardia and hypotension. While injection of local anesthetic, either into the carotid body or into the periadventitial area around the carotid sinus, has been proposed as a method to minimize the bradycardic reflex and reduce hemodynamic lability due to carotid manipulation, there is insufficient data to endorse this practice.
Carotid cross-clamping may precipitate ipsilateral cerebral ischemia due to mechanisms such as decreased carotid blood flow and/or plaque disruption with cerebral embolization. Thus, during cross-clamping, systolic blood pressure should be maintained in a range from the patient’s baseline blood pressure to 20% above that baseline, in order to optimize collateral cerebral perfusion. We prefer to use systolic arterial blood pressure to achieve this goal, although some clinicians prefer to use the mean arterial pressure.
Incision of the carotid artery exposes the baroreceptors in the carotid sinus to atmospheric pressure, which increases sympathetic discharge from the medulla, and may result in vasoconstriction and increased heart rate.
Carotid unclamping and the ensuing period of reperfusion may be complicated by hypotension.]
Damage to which nerve affects the corners of the mouth (smile)?
Mandibular branch of the facial nerve
[May be injured during carotid endarterecomy]
[UpToDate: The facial nerve exits the stylomastoid foramen and courses along the inferior portion of the ear. The most common branch affected during CEA is the marginal mandibular branch, which may be damaged during improper or prolonged retraction. The resulting paresis of the lateral aspect of the orbicularis oris muscle ipsilateral to the CEA may be identified during bedside examination as an asymmetric smile.]
What is the #1 source of emboli leading to superior mesenteric embolism?
Heart (Atrial fibrillation)
[UpToDate: The majority of arterial emboli originate from the heart. Cardiac embolism can be related to arrhythmia, valvular disease, ventricular aneurysm, or poor cardiac function. Cardiac dysfunction can lead to peripheral hypoperfusion, and the treatment of certain conditions may involve the use of medications that cause vasoconstriction, leading to nonocclusive ischemia. Cardiopulmonary bypass during cardiac surgery can lead to underperfusion of the intestines, showering of microemboli, release of vasoactive substances, and alterations in coagulation.]
What is the most common site of upper extremity stenosis?
Subclavian artery
[UpToDate: The subclavian arteries provide blood flow to the upper extremities. On the left, the subclavian artery originates directly from the aorta distal to the left common carotid artery. On the right, blood flows first through the innominate artery, which divides into the right common carotid artery and right subclavian artery. The anatomy of the aortic arch can vary and may include an anomalous origin of the subclavian arteries. Retroesophageal subclavian vessels may compress the esophagus causing dysphagia, but the vessel may also be compressed leading to upper extremity ischemia.
The vertebral arteries most often arise bilaterally as the first branch of the subclavian artery. In approximately 6% of patients, the vertebral artery, especially the left, may originate directly from the aortic arch. The subclavian artery passes over the first rib posterior to the anterior scalene muscle and becomes the axillary artery at the lateral margin of the first rib. The axillary artery becomes the brachial artery at the lower margin of the teres major muscle. The brachial artery passes between the biceps and triceps muscles accompanied by the ulnar and median nerves adjacent to the humerus and supplies the soft tissues of the arm. In the antecubital fossa, the brachial artery divides into the radial, interosseus, and ulnar arteries to supply soft tissues of the forearm. Distally at the wrist, the ulnar artery and radial artery supply the hand.
The collateral circulation around the shoulder is usually sufficient such that flow around a focal area of stenosis in the subclavian artery is well-compensated. When the proximal subclavian artery is occluded, blood flow is maintained to the arm via connections between the superior and inferior thyroid arteries; vertebral arteries, intercostals, superior epigastric, and internal thoracic arteries; profunda cervicis and descending branch of the occipital artery; scapular branches of the thyrocervical trunk and the branches of the axillary artery; and the thoracic branches of the axillary artery with the aortic intercostals.]
What is amaurosis fugax?
Occlusion of the ophthalmic branch of the internal carotid artery causing transient visual changes like a shade coming down over the eyes
[Hollenhorst plaques on ophthalmic exam]
[UpToDate: Amaurosis fugax (from the Greek “amaurosis,” meaning dark, and the Latin “fugax,” meaning fleeting) refers to a transient loss of vision in one or both eyes. Varied use of common terminology may cause some confusion when reading the literature. Some suggest that “amaurosis fugax” implies a vascular cause for the visual loss, but the term continues to be used when describing visual loss from any origin and involving one or both eyes. The term “transient monocular blindness” is also often used but is not ideal, since most patients do not experience complete loss of vision with the episode. “Transient monocular visual loss” (TMVL) and “transient binocular visual loss” (TBVL) are preferred to describe abrupt and temporary loss of vision in one or both eyes, since they carry no connotation regarding etiology.
Transient visual loss, either monocular or binocular, reflects a heterogeneous group of disorders, some relatively benign and others with grave neurologic or ophthalmologic implications. The task of the clinician is to use the history and examination to localize the problem to a region in the visual pathways, identify potential etiologies, and, when indicated, perform a focused battery of laboratory tests to confirm or exclude certain causes. Therapeutic interventions and prognostic implications are specific to the underlying cause.]
