Answer: (D) 60% at 5 years

Percutaneous transluminal angioplasty for stenotic lesions in peripheral arteries is considered a viable option for patients thought to be at high risk for surgery. The use of angioplasty instead of vascular bypass avoids the risks and complications of anesthesia, and is associated with shortened hospital stays and more rapid return to normal activities. The overall patency of angioplasty for stenotic lesions is 70% to 80% at 1 year and 50% to 60% at 5 years. Complications specific to angioplasty include vascular dissection, vessel rupture, and distal embolization, which may occur up to 4% of the time.

Answer: (D) Thromboembolic events associated with the popliteal aneurysm

Fifty to eighty percent of patients with popliteal aneurysms present with symptoms most commonly due to ischemia. Ischemia develops due to thrombosis of the aneurysm, distal embolization to the tibial or pedal arteries, or a combination of these. The resulting ischemia may manifest itself in a range from mild claudication to gangrene depending on the extent of thrombosis and embolization. Thromboembolism ultimately occurs in up to 35% of popliteal aneurysms if left untreated.

Less common complications of popliteal aneurysms include venous obstruction and nerve impingement due to local compression by the aneurysm. Popliteal aneurysm rupture is rare, occurring in less than 5% of patients.

Popliteal aneurysms are the most frequent site of peripheral arterial aneurysms. Ninety-five percent are caused by atherosclerosis, and they occur bilaterally 40% to 60% of the time. Of note, there is a high incidence of other concurrent aneurysms, so examination must be inclusive for abdominal, iliac, and femoral artery aneurysms. The incidence of concomitant abdominal aortic aneurysm is approximately 25%.

Diagnosis is initially clinical, with popliteal aneurysms palpable as a pulsatile or, in the case of thrombosis, firm mass. Confirmation of diagnosis on physical examination is made via ultrasound or computed tomography (CT) angiography.

Answer: (C) Intra-arterial site-directed thrombolysis

Thrombolysis is indicated for patients with no or only mild sensorimotor deficits. Furthermore, this technique is useful when complete clot evacuation is unlikely using surgical embolectomy, or when the distal vessels are also occluded preventing inflow patency. A confirmatory angiography should be performed following intra-arterial site-directed thrombolysis.

Arterial narrowing may preclude balloon catheter placement for surgical embolectomy in some patients. In these cases, a guidewire can be passed into and through the clot, followed by an infusion catheter. Arteriography can be performed to confirm the extent of clot and to guide catheter placement. Then, lytic agents can be injected through side holes in the catheter, perfusing the clot from within.

Intra-arterial site-directed thrombolysis allows simultaneous identification of the nature of the lesion via angiography, suggesting stenting or balloon dilation of stenoses. In addition, this allows for the monitoring of progress in thrombolysis. If thrombolysis is not progressing, surgical therapy may be indicated. Thrombolysis should not be used for common femoral artery emboli.

Absolute contraindications to lytic therapy include active internal bleeding, cerebrovascular accident within 2 months, and intracranial disease. Relative contraindications include surgery or trauma within 10 days, likelihood of left heart thrombus, episodes of serious gastrointestinal bleeding within 90 days, hypertension, pregnancy, bacterial endocarditis, and diabetic hemorrhagic retinopathy.

Answer: (D) Percutaneous embolectomy under local anesthesia

The most common cause of peripheral arterial embolization is atrial fibrillation, accounting for 66% to 75% of all cases. The second most common cause (20%) is MI resulting in embolization of left ventricular wall thrombus. Peripheral arterial embolization occurs in 5% of patients with mural wall thrombus, and occurs most frequently between 3 and 28 days after MI.

Treatment for the acutely ischemic limb is guided by category of limb ischemia. Initial workup includes history and physical examination, Doppler ultrasound evaluation of the threatened limb, and prompt initiation of heparin anticoagulation. Current recommendations for unfractionated heparin are an initial bolus of 80 units/kg IV, followed by infusion of 18 units/kg/hr, titrating to a goal aPTT ratio of 2. Determination of the category of limb ischemia is by physical examination and ultrasonography or angiography. Category I is occlusion of a narrowed artery with good collateral perfusion. Treatment is limited to anticoagulation. Category II is a threatened limb that may be salvaged after embolectomy. Category III is a nonsalvageable limb, requiring amputation.

Appropriate management of category II acute limb ischemia is either through emergent surgical embolectomy or intra-arterial site-directed thrombolysis. The risks of thrombolytic agents must be evaluated, especially in patients who have undergone recent cardiopulmonary resuscitation. In addition, thrombolytic agents are not indicated in patients who have sensorimotor deficits. Left heart thrombus is a relative contraindication to lytic therapy.

Embolectomy with or without revascularization is indicated in patients with sensorimotor deficits. This may be performed percutaneously or surgically. Of note, in patients having suffered recent MI, the risk of intraoperative or postoperative repeat MI is greatly increased; therefore, percutaneous embolectomy under local anesthesia is favored.

Answer: (C) Graft infection

Anastomotic disruption is the cause of delayed hemorrhage in vascular grafts. While the exact cause of disruption is usually unknown, graft infection is suspected in most cases.

Infection by virulent bacteria usually results in graft infections within 4 months of surgery. Patients develop signs of sepsis as well as evidence of local infection. Bacteria contributing to early graft infection include Staphylococcus aureus, Proteus, Klebsiella, Enterobacter, and Pseudomonas, all of which produce proteases and break down the arterial wall adjacent to the anastomosis. This results in separation of the graft from the host artery, creating a pseudoaneurysm. These may rupture, thrombose, or embolize. Less virulent bacteria such as Staphylococcus epidermidis may cause delayed graft infections. Infection of the graft may originate from septic emboli, usually from mitral or aortic valves, or from direct contamination of the graft during initial surgery. Successful treatment of graft infection includes systemic antibiotics and frequently, graft removal and revision.

Poor suture technique has been suspected as a cause of graft failure. However, studies have shown that most cases of anastomotic disruption are due to graft infection. Graft failure due to graft dilation was associated with ultra lightweight knitted Dacron grafts used in the early 1970s. This prosthetic has since been abandoned by manufacturers. Suture failure was previously found with silk sutures in vascular anastomoses. Anastomoses are currently created with more durable suture material such as polypropylene or monofilament expanded polytetrafluroethylene (ePTFE).

In a review of 307 patients who underwent abdominal aortic aneurysm (AAA) repair between 1957 and 1990 at the Mayo Clinic, 9.4% of patients had a graft-related complication. At a mean follow-up of 5.8 years, the rates of complications were as follows: Anastomotic pseudoaneurysm (3%), graft thrombosis (2%), graft-enteric erosion/fistula (1.6%), graft infection (1.3%), anastomotic hemorrhage (1.3%), colon ischemia (0.7%), and atheroembolism (0.3%). In this study, there were no complications attributable to graft failure such as dilation or rupture.

Answer: (E) Staphylococcus epidermidis

S. epidermidis is the most common pathogen associated with infection of implanted medical devices. Characteristically, it causes local chronic infection, but not systemic infection. S. epidermidis produces exopolysaccharides that coat the infected area. This “slime” or “biofilm” protects the bacteria from host defenses and antibiotics, allowing the S. epidermidis to propagate.

Infection by virulent bacteria usually results in graft infection within 4 months of surgery. Bacteria contributing to early graft infection include S. aureus, Proteus, Klebsiella, Enterobacter, and Pseudomonas. Less virulent bacteria such as S. epidermidis may cause delayed graft infections, often presenting over 1 year after surgery. Infection of the graft may originate from septic emboli from mitral or aortic valves, or from direct contamination of the graft during initial surgery.

Patients may present with signs of sepsis, as well as evidence of local infection, including cellulitis, draining tracts, and pulsatile masses (indicating mycotic pseudoaneurysms). Exposed graft should be assumed to be infected. In the case of aortic grafts, patients may present with sentinel gastrointestinal bleeding or major hemorrhage due to an aortoenteric fistula. Alternately, graft-enteric erosion may occur, when the graft erodes into the bowel, but the graft or anastomosis does not rupture. These patients present with chronic anemia, fever, and occult blood positive stool due to ulceration of the bowel.

Blood culture and graft culture may ultimately be positive for the infectious pathogen, but should not delay treatment. Successful treatment of graft infection includes systemic antibiotics and frequently, muscle coverage or graft excision.

Answer: (B) Type I endoleak; urgent endovascular repair

Endovascular aortic aneurysm repair (EVAR) has the advantage of sparing patients a major operation; however, the trade-off is that patients require closer surveillance and more frequent interventions. This is particularly true for patients who develop endoleak, which is defined as the persistent pressurization of the aneurysm sac that permits continued aneurysm growth and potential rupture. Endoleaks can be classified as type I to type IV and endotension, which is sometimes referred to as a type V endoleak. Type I endoleak results from an incomplete seal between the stent graft and the native vessel. Type IA is a proximal leak, while a type IB is a distal leak. Type II endoleak occurs when there is persistent flow through the aneurysm sac via branch vessels, most commonly from the inferior mesenteric artery or lumbar arteries. A separation between stent graft components that permits blood flow into the aneurysm sac is a type III endoleak. Type IV endoleak occurs when blood is able to flow through porous graft material. This type of endoleak is rarely seen with more modern stent graft devices. Endotension refers to persistent pressurization of the aneurysm sac in the absence of radiographic evidence of types I to IV endoleak.

The endoleak classification schema helps determine treatment and urgency. The type of endoleak is typically confirmed by digital subtraction angiography as this allows real time assessment of flow. Types I and III, because of the risk of aneurysm growth and rupture, typically require urgent intervention. Balloon angioplasty may help approximate the graft to the vessel wall in the case of type I endoleak. If not, a Palmaz balloon expandable stent can be placed proximally to complete the seal. Alternatively, an extension aortic cuff (type IA) or iliac extension limb (type IB) may be deployed. Type III endoleaks are repaired by deploying a stent within the current stent or utilizing a cuff if the endoleak is in the distal aspect of the stent graft. The management of type II endoleak is controversial—some have advocated a conservative approach because of the low risk of aneurysm rupture. More recent research suggests that persistent type II endoleaks (>6 months) in the presence of aneurysm sac expansion require treatment via embolization of the offending vessels or, rarely, via open ligation. Type IV endoleak typically resolves with the discontinuation of anticoagulation and is rare in the modern era of EVAR. Endotension is rarely encountered and is typically treated with either open surgical repair or deploying another stent graft into the current one if symptoms of aneurysm growth are present. For all types of endoleak, continued aneurysm growth or symptoms, such as back or abdominal pain, mandate treatment. In this question, the patient has type IA endoleak with aneurysm growth, mandating urgent intervention.

Answer: (B) Accelerated atherosclerosis

While acute graft rejection is the most common cause of death within the first year after cardiac transplantation, accelerated atherosclerosis leading to myocardial infarction is the most common cause of death thereafter.

CMV infection is associated with accelerated atherosclerosis, but itself is not the cause of death. Fungal infections occur in 7% to 15% of cardiac transplantations, characteristically within the first few months. The death rate from ventilator-associated pneumonia early after transplant is approximately 20% to 30% in ventilated patients.

Answer: (B) Daily use of 81-mg aspirin indefinitely

Aspirin has demonstrated efficacy in maintaining graft patency following infrainguinal prosthetic bypass in multiple randomized clinical trials. In addition, statins may enhance graft patency following bypass surgery. Anticoagulation with warfarin should be reserved for patients at high risk for clotting, while the use of clopidogrel after prosthetic grafting remains undefined. Preliminary data suggest that aspirin in combination with clopidogrel may provide superior patency results, though further studies are necessary.

The multicenter, prospective Dutch Bypass Oral Anticoagulants or Aspirin (BOA) trial randomized 2,690 lower-extremity bypass patients to anticoagulation to INR 3 to 4.5 or 80-mg aspirin daily. In subgroup analysis for prosthetic grafts, patients receiving aspirin had improved graft patency compared with patients receiving anticoagulation. Conversely, vein graft patients fared better in the anticoagulation arm. In combined analysis for both prosthetic and vein, the patency rates were not significantly different for the two therapies. A Veterans Affairs Cooperative trial compared aspirin to aspirin and warfarin (goal INR 1.4 to 2.8), and found no improvement in those receiving the additional warfarin. Predictably, patients receiving warfarin in both studies suffered twice as many hemorrhagic events. Statins were found to decrease the risk of vein graft failure by 3.2 times in a retrospective study of 172 patients.

Five-year patency rates for infrainguinal bypass are inferior to those seen with aortofemoral bypasses, ranging from 15% for bypasses to the tibial artery using prosthetic graft, to 80% for bypasses to the popliteal artery using saphenous vein.

Answer: (E) Thoracic outlet syndrome (TOS)

All of the symptoms described in the question are due to TOS. TOS is a constellation of neurovascular symptoms attributed to compression of the subclavian artery and vein, as well as the brachial plexus and sympathetic chain as they run over the first rib. The structures that may cause compression include the scalenus anticus and medius, pectoralis minor, and subclavius muscles, costocoracoid ligament, costoclavicular membrane, and cervical ribs.

Symptoms are attributed to nerve compression, arterial compression, sympathetic compression, and/or venous compression. Ninety-five percent of patients present with pain and paresthesias, of which most involve the ulnar nerve. Arterial compression may present as an incidental finding, and is associated with aneurysm proximal to the outlet compression. Alternately, patients may present with thrombosis and distal embolization, requiring surgical intervention. Sympathetic compression results in chest, neck, shoulder, arm, and hand pain. This often simulates angina pectoris, and is termed “pseudoangina.” Additional potential symptoms resulting from sympathetic compression include Raynaud phenomenon and reflex sympathetic dystrophy. Venous compression (Paget-Schroetter Syndrome) is rare, results in effort thrombosis of the axillary subclavian vein, and occurs due to repetitive muscular activity or trauma.

Initial treatment of neurologic symptoms entails conservative measures including physical therapy. Failure of conservative treatment in the face of persisting symptoms necessitates surgery. Patients with neurologic complaints should undergo nerve conduction velocity (NCV) studies of the ulnar or median nerve across the thoracic outlet. Normal values are greater than 85 m/sec. Patients with values of 60 to 85 m/sec should respond to conservative therapy consisting of physical therapy; however, patients with NCVs less than 60 m/sec usually require surgery.

Arterial compression should be confirmed with ultrasonography and arteriography. Patients with aneurysms should
undergo first or cervical rib resection, and thrombectomy and/or embolectomy, aneurysm repair, and dorsal sympathectomy as necessary.

In diagnosing sympathetic compression resulting in “pseudoangina,” workup includes ruling out coronary artery disease via coronary angiogram. First rib resection for neurovascular symptoms usually resolves pain and other associated symptoms from sympathetic compression.

Treatment of venous compression is resection of the first rib, costoclavicular ligament medially, and the scalenus anticus muscle.

Answer: (E) Percutaneous transluminal angioplasty (PTA) under local anesthesia

COPD is the fifth leading cause of death in the United States. It is associated with multiple perioperative complications, including failure to extubate postoperatively and prolonged postoperative mechanical ventilation.

Patients with iliac arterial occlusion present with absent pulses in the ipsilateral leg, as well as claudication-type pain. Diagnosis is confirmed with arteriography. While a bypass graft may be indicated in a healthier patient, it would be prudent to avoid an operation necessitating intubation in this scenario.

PTA under local anesthesia, with or without placement of a stent into the artery, would be a viable option here. The average success rate of PTA for treatment of total occlusion of the iliac artery is 65% with a 2- to 4-year patency rate of 75% to 100%.

Anticoagulation using intravenous heparin is inadequate definitive therapy for the occlusion of the iliac artery. Aortobifemoral artery bypass with PTFE graft would be indicated in a patient with occlusive disease of the abdominal aorta and/or bilateral iliac arteries. In this example, aortobifemoral artery bypass would not be the best option given the patient’s comorbidities and the limited extent of disease.

Answer: (E) Position the patient in left lateral decubitus Trendelenburg position

Venous gas embolism (VGE) occurs when gas is introduced into the systemic venous circulation. This requires that the pressure gradient be such that air entry into the vessel is promoted over the egress of blood. A rare occurrence, VGE is typically iatrogenic, and while room air is the most common agent, any gas used medically can be causative (CO₂, NO₂, N₂, etc.).

Once in the venous circulation, the gas embolism travels to the right heart and enters the pulmonary arterial circulation, leading to impaired gas exchange, dysrhythmias, and pulmonary hypertension. The latter can cause acute right heart strain and subsequent heart failure. The classic scenario in which VGE occurs is in the placement or use of central venous or hemodialysis catheters, though it can be seen in a variety of other situations, including trauma, childbirth, and craniotomy. Auscultation may demonstrate the classic finding of a churning murmur (“mill-wheel” murmur) that is present throughout systole and diastole. Other signs include jugular venous distension, dyspnea, chest pain, mental status changes, and cardiovascular collapse.

In the instance of mental status changes or any neurologic signs, it must be assumed that the patient developed a paradoxical embolism, most commonly through a patent foramen ovale, with conversion of the VGE to an arterial gas embolism (AGE). While treatment for both involves prevention of further embolization, supportive care, resuscitation, intubation, 100% oxygen administration, and a possible role for hyperbaric oxygen therapy, the immediate positioning of the patient differs based on whether or not the embolism is venous or
arterial in nature. VGE patients should immediately be placed in the left lateral decubitus and Trendelenburg (head down) position, with the goal of maintaining the embolus in the right ventricle and preventing it from traveling into the pulmonary circulation. Because arterial flow is stronger, this position will not prevent AGE from traveling distally to the heart and brain where it will disrupt flow. The Trendelenburg position may also exacerbate cerebral swelling associated with AGE to the brain; accordingly, the preferred position for AGE is in the flat supine position.

Isolated case reports and some animal experiments have suggested that for patients with VGE, evacuation of the embolism may be possible through a central venous catheter, though this is typically only done if the patient already has a catheter in place; rarely is the volume evacuated sufficient to achieve clinical improvement.

Answer: (D) HR >120, decreased blood pressure, very decreased pulse pressure, respiratory rate 30 to 40, urine output 5 to 15 mL/hr

This patient is in stage III hypovolemic shock, having lost 30% to 40% of his blood volume. A 70-kg man is estimated to have 4,900 mL of blood volume, or 70-mL blood per kg of ideal body weight. The hypovolemic shock classification helps guide treatment and prognostication.

Other types of shock include neurogenic, cardiogenic, and vasogenic shock. At the cellular level, shock is characterized by insufficient oxygen delivery (inadequate end-organ perfusion). An adrenergic response ensues within minutes, leading to tachycardia, vasoconstriction (i.e., decreased pulse pressure), and decreased renal blood flow (leading to low urine output).