Hoori Hovanessian
Vascular disease is a progressive, degenerative condition that disproportionately affects a subset of patients with other comorbid conditions, such as diabetes and hypertension. When vascular disease progresses despite medical management, surgical treatment often becomes necessary. Although surgery significantly improves quality of life, it is important to realize that the underlying disease continues to progress. These patients are frequent consumers of health care due to disease progression, early or late postoperative complications, or other illness. Knowledge of the pathologic processes that affect the vascular system as well as potential postoperative complications is essential for emergency physicians (EPs).
VASCULAR GRAFTS
Vascular pathology can be subdivided into aneurysmal and occlusive diseases. Aortic aneurysm and aortic dissection have potentially life-threatening consequences. When an aortic aneurysm becomes symptomatic or reaches a predetermined size, aneurysm repair is undertaken with graft replacement. Conventional treatment of aortic dissection involves resection of the damaged segment of the aorta and closure of the entrance into the false lumen. Closure of the lumen can be accomplished by placing sutures or by using biologic glue to seal the layers of the dissected part of the aortic wall. The diseased section of the aorta that is removed is replaced by a prosthetic graft.
Patients with occlusive disease of the vasculature may undergo extra-anatomic and infrainguinal procedures. Extra-anatomic procedures do not conform to the pre-existing anatomy and include femoral–femoral, axillofemoral, and iliofemoral bypasses. Prosthetic grafts are preferred in extra-anatomic reconstruction. Infrainguinal arterial occlusive disease can affect the femoral, popliteal, or tibial arteries. In these cases, autogenous veins are used in below-the-knee reconstructions, whereas both autogenous and prosthetic grafts are used in above-the-knee repairs (1). Polytetrafluoroethylene (PTFE) is the most commonly used synthetic graft. Tissue can grow through the interstices of the graft, incorporating the graft into tissue, theoretically decreasing the chance of thrombosis and infection.
With the advent of endovascular repair techniques, the treatment of aneurysms, dissection and aortoiliac obstructive disease has been undergoing rapid evolution, with endovascular procedures supplanting conventional surgery in many cases. Endovascular aortic aneurysm repair is performed much more frequently than open repair. Thoracic endovascular aortic repair (TEVAR) is now recommended as first-line therapy for thoracic aortic aneurysms (1). TEVAR has been gaining popularity due to decreased perioperative morbidity and mortality compared to open surgical repair (2). Originally utilized as a treatment for aneurysms, its use has expanded to include the treatment of aortic dissections, transections, and penetrating aortic ulcers. Endovascular procedures also outnumber surgical procedures in the treatment of select types of aortoiliac occlusive lesions (3).
It is also important for the EP to be familiar with complications associated with dialysis shunts. Vascular access for dialysis can be obtained through the formation of an arteriovenous fistula (AVF), whereby an artery and vein are anastomosed. Alternatively, a prosthetic graft can be used to join an artery and vein. Common locations for the creation of both native fistula and graft are the radiocephalic (wrist) and brachiocephalic (upper arm) regions. AVFs are currently preferred over prosthetic grafts because of their lower complication rates (less potential for thrombosis and lower infection rate) as well as their overall longevity. Prosthetic grafts may be the only option for patients with failed AVFs and those with poor peripheral veins.
GRAFT COMPLICATIONS
The complications of vascular grafts range in presentation from relatively straightforward to subtle and complex. They can be divided into the following categories: (i) stenosis, thrombosis, and occlusion, (ii) infection, (iii) erosion into contiguous structures with fistulization, (iv) pseudoaneurysm formation, (v) hemodynamic complications (dialysis access grafts), and (f) complications associated with endovascular grafts.
Stenosis, Thrombosis, and Occlusion
Early failure of vein grafts generally indicates a technical problem such as a kink or twist within the graft or incompletely lysed valves when autogenous grafts are used. Later failures are usually a result of intimal hyperplasia at the anastomotic sites (1). Failures that occur beyond 2 years are generally a result of progressive atherosclerosis. Graft thrombosis is the most common complication associated with permanent vascular access. Stenosis is the leading cause of thrombosis, accounting for up to 85% of thromboses. Graft thrombosis may result in a relatively sudden return of the patient’s previous symptoms. These may include claudication or ischemic rest pain that is localized to the forefoot. Pain caused by arterial insufficiency is usually severe unless it is masked by neuropathy. Signs may include skin breakdown with the formation of nonhealing ulcers. Such ulcers may also form between adjacent toes as a result of mild friction. Superinfection of these ulcers as well as osteomyelitis is a well-documented resultant complication. Painful toes that have a cyanotic appearance are suggestive of microemboli.
Dialysis access graft thrombosis is common despite the fact that heparin is used routinely and uremic patients already have an increased bleeding tendency. Complication-free graft use of 51% at 2 years and 39% at 3 years has been reported with polytetrafluoroethylene grafts (4). Thrombosis and occlusion occur secondary to intimal hyperplasia and can be accelerated by hypotension, dehydration, and by excess pressure applied to the graft site (e.g., by bandages or perigraft hematomas). Patients may complain of a sensation of coldness, tingling, or numbness and weakness of the involved extremity.
Because the signs and symptoms associated with vascular graft complications overlap with other more common medical problems, the differential diagnosis is vast. Limb weakness may result from a cerebrovascular accident or a nerve compression syndrome. Embolic events may be caused by atrial fibrillation or endocarditis.
The ED evaluation of the patient with suspected graft occlusion should include a careful examination of distal pulses by palpation, hand-held Doppler, and duplex ultrasonography. Neurosensory examination is less useful in patients with neuropathy but should be attempted. Skin temperature and the color of the affected limb should also be evaluated. The limb may become pale on elevation with a dusky or cyanotic rubor with dependency. Findings in the affected extremity should be compared to findings on the contralateral side. An ankle-brachial index (ABI) measurement can also provide important information. (The technique and interpretation are described in Tables 95.2 and 95.3.) The loss of a previously palpable pulse or a change of 0.15 from a previous ABI requires further evaluation with duplex ultrasonography or angiography. Finally, low cardiac output (hypovolemic or cardiogenic) may enhance thrombosis and accelerate occlusion, resulting in acute limb ischemia. The patient should be evaluated for evidence of volume depletion (blood loss, dehydration), sepsis, or cardiac insufficiency.
The ED management should include optimization of the patient’s volume status. Heparinization to prevent further thrombosis should be counterbalanced against the timing of angiography and the possible use of thrombolytic agents. This decision should be made in conjunction with the vascular surgeon, so consultation should be obtained early. Treatment options include percutaneous or surgical thrombectomy; thrombolytic agents or mechanical dissolution in the case of thrombosis; and angioplasty, endovascular stent placement, or surgical revision in cases of stenosis. Angioplasty has a higher success rate in stenoses involving less than 60% of the lumen. Surgical revision and repair are preferred in cases of high-grade stenosis.
Infection
The incidence of infection after arterial reconstructive surgery with the use of synthetic grafts ranges from 1% (aortic and iliac artery repair) to as high as 5% (in situations wherein the graft is placed in the inguinal area) (5). Infection is a significant problem in patients with prosthetic dialysis access grafts, with an incidence of 3% to 6% (6,7). Risk factors for vascular graft infections include diabetes, renal failure, obesity, use of prosthetic (vs. native) grafts as well as infrainguinal procedures and surgical revisions (especially if done within 30 days of the original operation). The incidence is higher in patients with acquired immunodeficiency syndrome or a history of intravenous drug abuse.
Intraoperative contamination is likely the most common mechanism for early graft infection. Spread of pathogens from contiguous infected or colonized tissue may explain the relatively higher rate of infection in the groin. Other mechanisms may include hematogenous spread of microorganisms as well as erosion of the graft into contiguous bowel lumen, resulting in direct graft contamination.
Patients with graft infections may present with frank sepsis, an infected wound, or overlying cellulitis. More subtle presentations may include low-grade fever, vague abdominal discomfort, or malaise. Still more complicated presentations may include bleeding, evidence of distal emboli, or the presence of an abdominal mass as a consequence of a false aneurysm. Aortoenteric fistula (AEF) may be the presenting sign in approximately 30% of aortic graft infections (8).
In the ED evaluation of a patient with any type of suspected graft complication, the physician should consider an infectious source, because it may be the underlying cause of graft thrombosis, AEF, or false aneurysm formation. The most common responsible organism is Staphylococcus aureus (with methicillin-resistant staphylococcus aureus (MRSA) becoming increasingly common). Other implicated agents include coagulase-negative staphylococci, enterococci, Pseudomonas aeruginosa, Enterobacteriaceae, and Bacteroides species. Polymicrobial infections occur in 12% to 37% of patients (5). Blood cultures should be obtained, although they may be negative if the lumen is not involved. Computed tomography (CT) scanning may reveal perigraft inflammation or fluid collection, or air adjacent to the graft. Sterile perigraft fluid can be seen on a CT for up to 3 months following graft placement. However, an increase in the volume of the perigraft fluid or persistence of the fluid beyond 90 days may be indicative of infection (9). In the case of grafts that are located close to the skin, the diagnosis is relatively easy in the presence of cellulitic changes, fluctuance, or obvious drainage of pus from the vicinity of the graft site. However, local signs of infection may be absent initially. Graft infection should be considered in any febrile patient, even in the absence of any local findings. Finally, occult infection may be present in old, nonfunctioning dialysis access grafts. The graft may have become seeded from a previous episode of bacteremia or may have become directly inoculated from needle puncture at the time the graft was in use. This source of potential infection should be considered in dialysis patients, as well as in renal transplantation patients, with fever of unclear etiology (10). The diagnosis can be established on an inpatient basis by using indium-111 scanning, which has a sensitivity and specificity over 90% (10).
As with graft thrombosis, the ED management should include optimization of the patient’s fluid status to prevent accelerated graft thrombosis and occlusion secondary to poor perfusion through the graft site. Incision and drainage of suspected abscesses in the vicinity of a graft should not be attempted in the ED, as it can result in catastrophic hemorrhage. Empiric antibiotic therapy should be initiated early. Definitive treatment by a surgeon ranges from local incision and drainage to complete graft removal with debridement of the surrounding infected tissues. Infection in native fistulas can usually be treated with intravenous antibiotics, requiring surgical drainage only in select cases. Therapy should be guided by results obtained from the culture of the infected tissue at surgery following surgical repair. Infections with MRSA and Pseudomonas are associated with higher rates of treatment failure (11,12). Therefore appropriate broad-spectrum antibiotic therapy (such as vancomycin or linezolid for gram-positive coverage and ceftazidime, cefepime, piperacillin-tazobactam, or ticarcillin-clavulanate for gram-negative coverage) should be initiated pending blood culture results.
The rate of endograft infections is low (0.2% to 0.7%) (13). Patients have presented with signs and symptoms of severe sepsis, AEFs, as well as nonspecific symptoms such as malaise (13). Because of the low rates of infection with this relatively new procedure, experience is limited and clear-cut management guidelines are not available. These patients have been managed both conservatively as well as with surgery. Consultation with the vascular surgeon is of paramount importance.
Erosion into Contiguous Structures with Fistulization
Erosions of the prosthetic graft into the bowel can result in the formation of an AEF. Most commonly these occur between an aortic prosthetic graft and the distal duodenum. However, such fistulization has been reported after aortoiliac and aortofemoral procedures as well as after renal vascular graft placement. Fistulization to the bowel at sites other than the duodenum may also occur. Mechanical trauma, prosthetic graft or perigraft infection, and pressure necrosis all contribute to fistulization.
The time frame for AEF development is wide. Fistulization may occur several days to many years after the initial surgery (14). Clinical presentation is commonly that of gastrointestinal bleeding: hematemesis, hematochezia, melena, or occult blood loss. Patients may present with self-limited herald bleeding several hours to days before exsanguinating hemorrhage ensues. Some patients may have nonspecific symptoms of back or abdominal pain. Because fistulization may be secondary to graft infection, other signs and symptoms may include fatigue and malaise, low-grade fevers, and leukocytosis.
AEF should be considered in the ED evaluation of any patient with gastrointestinal bleeding and a history of aortic repair with graft placement. In the stable patient, workup for other sources of bleeding should be initiated, as other sources of bleeding are more common than AEF. Laboratory studies should include a complete blood count, type and cross, coagulation studies, electrolytes, blood urea nitrogen (BUN), creatinine, and glucose. Endoscopy (upper and lower) is important primarily in evaluating other, more common causes of gastrointestinal bleeding. If endoscopy does not yield a clear-cut answer, abdominal CT with oral and intravenous contrast should be obtained to evaluate for inflammatory changes around the anastomotic sites (14,15).
The ED management should initially focus on stabilization and resuscitation. Unstable patients with suspected AEF require emergency laparotomy to control the bleeding. The patient’s hemodynamic status should be evaluated and blood loss replaced before surgery. Even in stable patients with an AEF, surgical consultation should be obtained early as the treatment is invariably surgical. Occasionally, grafts erode through the skin. These grafts should be considered infected, and the patient should receive antibiotics. A vascular surgeon should be consulted for urgent repair.
Pseudoaneurysm
Disruption of the suture line (dehiscence) at the site of an anastomotic junction may give rise to a false aneurysm (pseudoaneurysm). False aneurysms most commonly occur in femoral artery graft anastomoses. Leaking blood is contained by the adjoining tissues as well as by fibrous scar formation. Infection is an important cause of pseudoaneurysm formation.
Patients with pseudoaneurysms may complain of pain in the groin, back, or abdomen. They may harbor a pulsatile mass in these locations. Other presentations may include hemorrhage (ranging from occult to life-threatening) caused by rupture of the false aneurysm or signs and symptoms associated with distal emboli. False aneurysms occur most commonly in the groin.
Repeated needle puncture for dialysis access can weaken the vessel wall, thereby leading to aneurysm formation. Pseudoaneurysms can form when the graft material is lacerated with the dialysis needle. In both cases, a pulsatile mass may be present. Pseudoaneurysms may expand and eventually rupture, resulting in significant hemorrhage. Pseudoaneurysm expansion can also threaten the viability of the overlying skin, thereby exposing the underlying graft to infection.
The ED evaluation of the patient with a suspected pseudoaneurysm should include imaging by duplex ultrasound, CT, magnetic resonance imaging, or angiography. Ultrasonography can gauge the size of a pseudoaneurysm and determine the presence of any hematoma and the status of the surrounding vasculature.
Surgical consultation is essential, although other management options such as thrombin injection and embolization procedures are currently being evaluated. In addition, antibiotics should be considered if the pseudoaneurysm is thought to have an infectious etiology. Treatment of vascular access graft aneurysms and pseudoaneurysms involves surgical repair.
Hemodynamic Complications of Vascular Access Grafts
Patients with borderline cardiac reserve and an excessive flow rate through their shunt (>500 mL/min) may exhibit signs and symptoms of congestive heart failure. An arterial steal syndrome with resultant distal ischemia may occur in patients with shunts. The incidence is somewhat higher in patients with proximal than those with distal access sites. The steal syndrome occurs when the blood flows from the artery into the low-resistance vein with less arterial blood available distal to the site of the shunt (1). Though surgical correction may be required in severe cases, milder symptoms of paresthesias and coolness to touch can improve gradually with development of collateral blood flow. An alternate complication can occur with high-pressure arterial flow into the low-pressure venous system: Venous hypertension distal to the shunt ensues with swelling of the distal tissue and eventual skin induration and hyperpigmentation (1). Shunt repair may be necessary if the steal syndrome and venous hypertension cause clinical symptoms.
Neurovascular problems associated with vascular access include pain, weakness, muscle atrophy, and paresthesias. These hemodynamic and neurovascular complications are more problematic with fistulas but do occur with prosthetic grafts as well.
Complications Associated with Endovascular Grafts
Several early complications have been described in this emerging area of vascular repair. Limb ischemia or occlusion may require subsequent extra-anatomic (femoral–femoral) bypass, thrombectomy and angioplasty, or thrombolysis. These complications may occur intraoperatively (during endovascular graft placement) or over a year later (16). These complications are a result of vascular trauma as well as underlying peripheral vascular disease. Endoleaks, which complicate 10% to 20% of repairs, are defined as incomplete exclusion of the aneurysm with persistent leakage of blood into the aneurysmal sac (17). This can result in enlargement of the sac and/or increased pressure in the sac, ultimately leading to aneurysmal rupture. Several types of endoleaks have been defined including those that occur at the site of attachment of the graft to the aorta (from incomplete seal of the endograft) or through the stent graft itself (via a tear or fracture) (18). Other potential complications include distal embolization, graft occlusion, kinking, migration or prolapse into the aneurysm, and infection. Device migration may occur intraoperatively or over time. Device manufacturers are addressing this problem. Migration of the stent graft may present as an endoleak. Stent graft erosion into the esophagus has also been reported (19). More commonly observed complications of TEVAR include spinal cord ischemia and stroke. The incidence of paraplegia or paraparesis after TEVAR with stent grafts varies from 0% to 8% and typically extends from the lumbosacral to the high thoracic cord levels (20). The incidence of stroke due to embolization of atheroma or thrombus formation after instrumentation and disruption of plaques varies from 2.3% to 8.2% (21).
Endovascular repair continues to evolve with advances in the design of endografts. Research is also ongoing in the design of more complex endografts, intended for situations where aortic pathology involves branch vessels. Long-term complications remain unknown given the relative infancy of this field. In general, however, endovascular procedures have been associated with lower complication rates, shorter hospital stays, as well as lower costs.
CRITICAL INTERVENTIONS
• The patient’s hemodynamic status should be evaluated and fluid losses replaced.
• In patients with massive gastrointestinal hemorrhage and an intra-abdominal graft, emergent vascular consultation should be obtained and the patient readied for surgery.
• Empiric antibiotic therapy should be initiated in any febrile or septic-appearing patient with a fever of unknown etiology and the presence of a vascular graft, whether functioning or nonfunctioning. Given the higher complication rates with MRSA and Pseudomonas infections, antibiotic coverage should be provided for these organisms.
DISPOSITION
Most graft complications require surgical consultation and management in a hospital setting. After diagnosis and initial measures such as the initiation of antibiotic therapy and replenishment of fluid and blood loss, stable patients should be admitted and managed by a vascular surgeon. Unstable patients require resuscitation prior to emergent surgical intervention.
Diagnostic and management decisions should ideally be made in conjunction with a vascular surgeon as well as an interventional radiologist skilled in these relatively novel procedures.
Common Pitfalls
• Failure to consider graft thrombosis when a patient with a vascular graft has a recurrence of claudication, rest pain, skin breakdown, or nonhealing ulcers
• Failure to exclude infection when evaluating patients for any type of graft complication
• Failure to evaluate the ABI and compare it to the previously obtained values
• Failure to consider AEF in any patient with gastrointestinal bleeding and a history of aortic repair
• Failure to consider a pseudoaneurysm in patients with a history of vascular repair and complaints of abdominal or groin pain, hemorrhage, or pulsatile mass
• Failure to appreciate that low-flow states may contribute to vascular access thrombosis
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