Vascular Graft Infections, Mycotic Aneurysms, and Endovascular Infections: A Scientific Statement From the American Heart Association
2016; Lippincott Williams & Wilkins; Volume: 134; Issue: 20 Linguagem: Inglês
10.1161/cir.0000000000000457
ISSN1524-4539
AutoresWalter R. Wilson, Thomas C. Bower, Mark A. Creager, Sepideh Amin‐Hanjani, Patrick T. O’Gara, Peter B. Lockhart, Rabih O. Darouiche, Basel Ramlawi, Colin P. Derdeyn, Ann F. Bolger, Matthew E. Levison, Kathryn A. Taubert, Robert S. Baltimore, Larry M. Baddour,
Tópico(s)Vascular Procedures and Complications
ResumoHomeCirculationVol. 134, No. 20Vascular Graft Infections, Mycotic Aneurysms, and Endovascular Infections: A Scientific Statement From the American Heart Association Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBVascular Graft Infections, Mycotic Aneurysms, and Endovascular Infections: A Scientific Statement From the American Heart Association Walter R. Wilson, MD, Chair, Thomas C. Bower, MD, Mark A. Creager, MD, FAHA, Sepideh Amin-Hanjani, MD, FAHA, Patrick T. O'Gara, MD, FAHA, Peter B. Lockhart, DDS, Rabih O. Darouiche, MD, Basel Ramlawi, MD, Colin P. Derdeyn, MD, FAHA, Ann F. Bolger, MD, FAHA, Matthew E. Levison, MD, Kathryn A. Taubert, PhD, FAHA, Robert S. Baltimore, MD and Larry M. Baddour, MD, FAHAOn behalf of the American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Surgery and Anesthesia; Council on Peripheral Vascular Disease; and Stroke Council Walter R. WilsonWalter R. Wilson , Thomas C. BowerThomas C. Bower , Mark A. CreagerMark A. Creager , Sepideh Amin-HanjaniSepideh Amin-Hanjani , Patrick T. O'GaraPatrick T. O'Gara , Peter B. LockhartPeter B. Lockhart , Rabih O. DarouicheRabih O. Darouiche , Basel RamlawiBasel Ramlawi , Colin P. DerdeynColin P. Derdeyn , Ann F. BolgerAnn F. Bolger , Matthew E. LevisonMatthew E. Levison , Kathryn A. TaubertKathryn A. Taubert , Robert S. BaltimoreRobert S. Baltimore and Larry M. BaddourLarry M. Baddour and On behalf of the American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Surgery and Anesthesia; Council on Peripheral Vascular Disease; and Stroke Council Originally published13 Oct 2016https://doi.org/10.1161/CIR.0000000000000457Circulation. 2016;134:e412–e460Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2016: Previous Version 1 Vascular Graft InfectionsBackgroundThe use of synthetic material for reconstructive vascular surgery was first reported during the early 1950s. Infection involving vascular graft prostheses is an infrequent but devastating complication of reconstructive vascular graft surgery and is associated with a high morbidity and, in some situations, mortality. Improvements in surgical techniques and graft design, including the use of native venous or arterial tissue, have reduced the frequency of infection and severity of complications from vascular graft infection (VGI). However, these advances have also led to more frequent vascular graft procedures occurring in a patient population with multiple underlying comorbidities that would have previously disqualified them as candidates for vascular reconstructive surgery. Underlying comorbidities, such as diabetes mellitus or immune compromise, increase the risk of infection and serious infection-related complications. The major complications of VGI include sepsis, amputation, disruption of infected anastomotic suture line with rupture or pseudoaneurysm formation, embolization of infected thrombi, reinfection of reconstructed vascular grafts, enteric fistulae to the small or large bowel, bacteremic spread of infection to other sites, and death. VGIs can be categorized broadly into those that occur in an extracavitary location, primarily in the groin or lower extremities, or in an intracavitary location, primarily within the abdomen or less commonly within the thorax.FrequencyThe frequency of VGI depends on the anatomic location of the graft. The infection rate is 1.5% to 2% for most extracavitary grafts and as high as 6% with vascular grafts in the groin.1–9 For intracavitary grafts, the infection rate is ≈1% to 5%.1–6 Graft infection is most common after emergency procedures and after reoperation.1–4,10 Aortic graft erosion or fistulous communication into the duodenum or other areas of the bowel reportedly occurs in 1% to 2% of patients after aortic reconstruction.11,12MicrobiologyThe microbiological cause of VGI has evolved over the years.1 In early published studies, Staphylococcus aureus was the predominant microorganism recovered.1,13 Improvements in surgical technique, administration of prophylactic antistaphylococcal antimicrobial therapy, and other factors have resulted in a changing microbiological epidemiology. Vascular graft surgery performed on patients with multiple underlying comorbidities and the increased frequency of emergency procedures have contributed to the changing spectrum of infection. Other factors such as changes in hospital flora, surgery in patients with complicated vascular anatomy, and multiple revisions of previous vascular surgery have resulted in a more diverse microbiological spectrum of infection, which includes multidrug-resistant strains, polymicrobial infection, and Candida species. Gram-positive cocci accounts for at least two thirds of VGIs.1,13 Infections caused by coagulase-negative staphylococci are more common than those caused by S aureus. Among S aureus infections, methicillin-resistant S aureus (MRSA) infections are increasing in frequency. Pseudomonas aeruginosa is now the most common cause of gram-negative infections and accounts for at least 10% of VGIs1,14 (Figure 115).Download figureDownload PowerPointFigure 1. Microbiology of prosthetic vascular graft infections. ICD indicates implantable cardioverter-defibrillator; and PPM, permanent pacemaker. Reprinted from Sohail et al15 with permission from the American College of Cardiology Foundation. Copyright © 2007, the American College of Cardiology Foundation.Pathogenesis and Risk Factors for InfectionIntraoperative bacterial contamination of the vascular graft is considered to be the most common cause of VGIs.1,9,10,16,17 The second most common cause of VGIs is a spread of infection from a contiguous site, such as a surgical wound infection or an intra-abdominal or pelvic abscess. As many as 30% of intra-abdominal VGIs occur as a result of erosion of a vascular graft into the duodenum and less commonly into the colon, with development of a fistulous communication between the abdominal aorta and the duodenum or colon. Other causes of VGI include bacterial colonization of a thrombus or direct inoculation of infection during an interventional surgical procedure, such as a percutaneous aspiration or drainage of an abscess or fluid collection.1,9,10,16,17 Less commonly, VGI results from a bacteremia.18 The risk of hematogenous infection of VGI is highest in the early postoperative period (<2 months) and decreases over time because of partial endothelialization of the graft.16,19 Transient bacteremia from a gastrointestinal, genitourinary, or dental procedure can also cause VGI but is a much less common cause than is intraoperative contamination or wound infection.1,18,19Vogel and colleagues20 analyzed risk factors in almost 14 000 patients who had undergone abdominal aortic aneurysm repair. Bacteremia during the index hospitalization for repair was associated (odds ratio [OR], 4.2; 95% confidence interval [CI], 1.5–11.8) with aortic graft infection. In a separate study conducted over a 21-year period, groin infection (OR, 4.1; 95% CI, 1.6–10.7) and wound infection (OR, 5.1; 95% CI, 1.6–16.2) were significant risk factors for VGI.13Clinical PresentationsThe clinical manifestations of VGI are highly variable and relate to whether the location is extracavitary or intracavitary, the pathogenesis of infection, and the duration of time since surgery.ExtracavitaryExtracavitary VGI most often occurs in the groin and much less frequently in the popliteal fossa or more distally in the leg. The clinical manifestations vary depending on whether the infection occurs early, 2 months postoperatively) is less often characterized by signs of systemic sepsis. In these cases, the infection often is indolent, with local stigmata of groin erythema, painful swelling, sinus tract drainage, lack of graft incorporation by surrounding tissue, pseudoaneurysm at the anastomotic site, and erosion of the graft through the skin.The most obvious sign of a graft infection is a draining sinus tract. The clinical presentation of a pseudoaneurysm is variable. There can be little or no localized inflammatory response; a palpable, pulsatile mass; thrombosis of the graft with distal limb ischemia; or hemorrhage. In approximately half of the patients, a pseudoaneurysm at the anastomosis site presents with sudden onset of bleeding or ischemia that can be life- or limb-threatening.1,21 In patients who have undergone extracavitary lower extremity vascular reconstruction, the presence of a painful erythematous swelling in the groin, with or without a draining wound or sinus tract, is highly suggestive of an underlying VGI.Szilagyi and colleagues22 first reported a classification of extracavitary VGI, which was refined and modified by Koenig and von Dongen,23 that shows the widely used modification proposed by Samson et al.24 The Samson modification provides guidance for selection of imaging techniques, options for medical and surgical management, management of complications, and prognosis.The classification of group I through V infection proposed by Samson et al24 might not always be readily apparent clinically, and these groups often overlap. For example, group I VGI can be indistinguishable from group II on physical examination. However, an open wound with drainage of pus or a draining sinus tract strongly suggests that this is not a group I infection. Contrariwise, the absence of an open draining wound or sinus tract does not exclude a group III, IV, or V infection. A visible graft with purulent drainage suggests a group III, IV, or V infection.IntracavitaryIn contrast to extracavitary VGI, intra-abdominal VGI may have no obvious physical findings to suggest infection. Intra-abdominal VGI can present months to years after graft placement.1,4–6 Symptomatic patients with intra-abdominal VGI may have abdominal pain, fever, leukocytosis, failure to thrive, and sepsis. The aortic graft can erode into the third or fourth portion of the duodenum, resulting in intermittent, polymicrobial bacteremia of fecal flora with a combination of aerobic and anaerobic microorganisms. Some blood cultures will contain a mix of enteric microorganisms, whereas other blood cultures contain the same or different microorganisms. These often include Escherichia coli, enterococci, and anaerobic microorganisms including Bacteroides species, fusobacteria, anaerobic cocci, and occasionally Candida species. In a patient who has undergone reconstructive surgery for abdominal aortic aneurysm, the development of sepsis with otherwise unexplained polymicrobial enteric bacteremia is highly suggestive of a VGI with duodenal erosion. Rarely, a VGI can cause a fistulous communication with the colon, with a similar presentation and polymicrobial enteric bacteremia.1,4–6In addition to sepsis, gastrointestinal tract bleeding can occur, which ranges from minimal to massive with potential exsanguination. Depending on the location of the enteric fistula, bleeding can manifest as hematemesis, hematochezia, or melena. A prompt diagnosis of VGI associated with enteric fistula is critical. If untreated, the mortality rate is virtually 100%.1,4,11Intrathoracic VGI often presents differently from intra-abdominal VGI. Intrathoracic VGI that involves the aortic root can present with signs and symptoms similar to those of infective endocarditis (IE) with fever, chills, heart failure, and disruption of the anastomotic suture line of the aortic root. Because intrathoracic VGIs are most often caused by S aureus or coagulase-negative staphylococci, sepsis with a high-grade sustained bacteremia is common with a high-grade sustained bacteremia. If the VGI is associated with surgery for native or prosthetic valve endocarditis, the clinical picture reflects the microbiological cause. Patients with viridans group streptococci or enterococci have a less virulent course than those with infection caused by S aureus or coagulase-negative staphylococci. Infection associated with repair of an aortic aneurysm or aortic dissection usually occurs within 3 months postoperatively and is most often the result of intraoperative contamination with staphylococci or gram-negative microorganisms, including P aeruginosa. Septic emboli can occur in the central nervous system (CNS) or peripherally. Anastomotic rupture can result in sudden massive hemorrhage, which is often fatal.DiagnosisGeneral PrinciplesThe principles for diagnosis of VGI include the following: (1) index of suspicion; (2) recognition of the differences in clinical presentations of extracavitary or intracavitary VGI; (3) time of onset postoperatively; (4) physical findings; (5) laboratory test results including cultures of blood, purulent material from a draining sinus, or aspirates of perigraft fluid and surgical specimens; and (6) imaging. The choice of an imaging modality depends on whether the VGI is extracavitary or intracavitary. In some cases, the diagnosis of VGI requires intraoperative confirmation.General Laboratory Tests and Culture ResultsElevated peripheral white blood cell count and bioinflammatory markers (such as erythrocyte sedimentation rate and C-reactive protein) occur commonly but are not specific for VGI, especially among patients who have multiple underlying comorbidities. Contrariwise, normal inflammatory markers are uncommon in patients with VGI. To assess response to treatment, it can be useful to monitor biomarker levels over time in patients who have undergone medical and surgical therapy or who continue to receive suppressive antimicrobial therapy.Cultures obtained from ultrasound- or computed tomography (CT)–guided aspiration or from intraoperative specimens usually provide an accurate microbiological diagnosis. These results of cultures guide the choice of a specific antimicrobial agent or combination of antimicrobial agents and, when necessary, long-term suppressive therapy. The results of wound swab cultures from a draining sinus, such as from the groin, could represent skin flora or colonization and might not accurately reflect the causative microorganism. The microbiological cause can influence the surgical options. For example, VGIs caused by MRSA, P aeruginosa, or other multidrug-resistant microorganisms are managed surgically differently from VGIs caused by more susceptible microorganisms as discussed below.Role of Imaging and Interventional Techniques for the Diagnosis of VGIGeneral PrinciplesThe choice of an imaging modality depends in part on the site of infection. For intracavitary VGI, a combination of imaging modalities might be necessary. Computed tomographic angiography (CTA) is most often used for diagnosis and to define anatomy for subsequent revascularization. Sinograms can be useful in highly selected patients, but other imaging modalities have diminished their utility. In addition, there is a risk of introducing pathogens into a perigraft area with high-pressure instillation of contrast material. Invasive angiography is rarely useful for the diagnosis of VGI. The choice of an imaging modality is best determined by consultation among experts in vascular surgery, infectious diseases, vascular medicine, and radiology.Extracavitary VGIEven when clinical or microbiological findings strongly suggest a VGI, imaging, most often ultrasonography or CTA, is used to support the diagnosis, determine the extent of the infection, identify a fluid collection for aspiration for culture, or detect a pseudoaneurysm or bleeding at the site of the anastomosis. A CTA is useful to define vascular anatomy to help guide medical and surgical treatment. Figure 2 shows an algorithm for the diagnosis of Samson I to V VGIs using a combination of clinical findings, ultrasonography, or other imaging modalities, and surgery.Download figureDownload PowerPointFigure 2. Extracavitary vascular graft infection: diagnosis using Samson classification. CT indicates computed tomography; I&D, irrigation and débridement; and MRI, magnetic resonance imaging.It is reasonable to consider ultrasonography as the initial imaging procedure.1,25,26 Ultrasonography is used primarily, but not exclusively, in patients with extracavitary VGI. Compared with other imaging modalities, ultrasonography is less expensive, can be done quickly, including at the bedside, and does not expose patients to the potential risk of contrast-associated kidney injury. Pseudoaneurysm formation can be detected by ultrasonography. Ultrasonography can also identify a subcutaneous or perigraft fluid collection that could be aspirated for analysis, culture, cell count, and other studies used to differentiate a noninfected seroma from bleeding. A sinogram can demonstrate extension of a sinus tract to the graft, which might involve an anastomotic site. A potential risk of sinograms is that an infection can be introduced during the procedure by the high-pressure instillation of contrast material into the perigraft area.In selected patients with suspected or established extracavitary VGI and indeterminate findings on ultrasound, it is reasonable to perform CTA or magnetic resonance imaging (MRI) to identify perigraft fluid collection not attributable to recent (≤3 months) graft implantation; an increase in the size, location, and the consistency of the fluid; or an anastomotic pseudoaneurysm.27 CT-guided aspiration of fluid can be useful diagnostically instead of or in combination with ultrasound-guided aspiration. CT or MRI is useful to define the extent of infection preoperatively in patients with established extracavitary VGI.1 Positron emission tomography (PET)/CT imaging has been reported in patients with intracavitary VGI, but there are few reports regarding its utility. Some studies reported that PET/CT was useful in the diagnosis of extracavitary VGI.28–32 Until more data are available with PET/CT for extracavitary VGI diagnosis, other imaging modalities may be considered before a PET/CT is obtained. An indium-labeled white blood cell study can be considered, most often in combination with other imaging techniques in patients with indeterminate findings on ultrasonography, CTA, or MRI. Indium scans used alone were not useful to identify VGI in patients with no findings to suggest VGI.28–32 Indium scans can be falsely positive in the early postoperative period and have decreased sensitivity in patients who are receiving current or recent antimicrobial therapy.1,33–36Recommendations for Imaging in Diagnosis of Extracavitary VGIIt is reasonable to consider ultrasonography as the initial imaging procedure of choice (Class IIa; Level of Evidence B).It is reasonable to consider CTA or MRI when extracavitary graft infection is suspected and there are indeterminate findings on ultrasonography (Class IIa; Level of Evidence B).A PET/CT or indium-labeled white blood cell study scan may be considered when extracavitary graft infection is suspected and ultrasonography, CTA, or MRI findings are indeterminate (Class IIb; Level of Evidence B).Intra-Abdominal VGIFigure 3 shows an algorithm for the diagnosis of intra-abdominal VGI in patients with or without associated gastrointestinal bleeding. Patients with suspected VGI and aortoenteric fistula should undergo CTA, an esophagogastroduodenoscopy, followed by vascular imaging as soon as the patient is stable enough to tolerate the procedure.1,4,8,11,27 An esophagogastroduodenoscopy can demonstrate subtle or obvious erosion or a thrombus, which usually is located in the third or fourth portion of the duodenum overlying the abdominal aortic aneurysm graft. The ulcer or thrombus should not be manipulated, because this can cause sudden massive bleeding.Download figureDownload PowerPointFigure 3. Intra-abdominal vascular graft infection: algorithm for diagnosis. CTA indicates computed tomographic angiography; EGD, esophagogastroduodenoscopy; GI, gastrointestinal; IN, indium; MRA, magnetic resonance imaging; MRI, magnetic resonance angiography; and PET, positron emission tomography. *Combination of imaging tests is often necessary; see Table 2 for advantages and disadvantages of the different imaging modalities.The imaging modalities most widely used for the diagnosis of intra-abdominal VGI are CT, MRI, indium scanning, and PET/CT.1,28–32 Invasive angiography is rarely helpful for the diagnosis and has been replaced by CTA to determine anatomy for revascularization. Table 1 shows the utility, advantages, and disadvantages of specific imaging modalities for the diagnosis of intra-abdominal VGI.1Table 1. VGIs: Imaging Advantages and DisadvantagesModalityAdvantagesDisadvantagesUltrasoundMost useful for extracavitaryCan be performed at bedsideInexpensiveNo contrast kidney injuryAspiration for analysis, cultureDetect pseudoaneurysmLimited use for intracavitary VGICannot discriminate seroma, hematoma, abscessCTSensitivity 85%–100%; specificity 85%–94%Rapid resultLess expensive than MRI, PET/CTAspiration for analysis, cultureCTA useful for surgical planningContrast kidney injuryNoncontrast with renal disease less diagnosticMight not differentiate hematoma from inflammation, especially low-grade inflammationImages degraded by metallic clips, spinal hardwareMagnetic resonanceSensitivity 68%–85%; specificity 97%–100%Use when CT nondiagnosticNo contrast kidney injuryDifferentiate hematoma, inflammation, infectionGood soft tissue resolutionMRI/MRA can detect mycotic aneurysm, bleeding, enteric fistulaMore expensive than CTNo guided aspirationLimited use in patients with intracardiac devicesGadolinium fibrosing dermopathy in renal diseaseIndium-labeled WBC scan (In-scan)Sensitivity 67%–73%; specificity 87%No contrast kidney injuryUse when CT, MRI nondiagnosticResults take ≥24 hDecreased sensitivity with recent antimicrobial therapyFalse-positive result in early postoperative periodUse in combination with other imagingPETSensitivity 78%–96%; specificity 70%–93%No contrast kidney injuryLess experience than with other imagingDoes not identify specific anatomic locationExpensiveUse in combination with other imagingCT indicates computed tomography; CTA, computed tomography angiography; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; PET, positron emission tomography; VGI, vascular graft infection; and WBC, white blood cell study.Modified from Sohail et al1 with permission from the publisher. Copyright © 2007, Elsevier.It is reasonable to consider CT imaging as the initial imaging procedure in patients with suspected intra-abdominal VGI. In the absence of recent manipulations, the presence of perigraft air is highly suggestive of VGI. CT findings often suggestive of infection include perigraft fluid with fat stranding, lack of fat plane between graft and bowel, and anastomotic leakage or aneurysm. Perigraft fluid is usually reabsorbed within 3 months postoperatively, and perigraft air is usually absorbed within the first week or so, although it can persist for as long as 2 months postoperatively.1,28,37–39 Intra-abdominal VGI can occur many months to years after surgery and might not have the CT findings typically seen in early infection.28,39,40 In these patients, MRI can be considered if the CT findings are inconclusive.1,40–42 MRI can be superior to CT to identify subtle perigraft inflammatory changes when CT images are degraded by metallic clips in the abdomen, and it can differentiate hematoma from inflammatory changes in the perigraft area.40 However, the role of MRI used alone for the diagnosis of VGI is not defined. In one study, the sensitivity was relatively low at 68%, but the sensitivity was high (97%).40 MRI combined with an indium scan can be considered in patients with inconclusive MRI or CT findings.40 Used alone, indium scans have lower sensitivity and specificity than other imaging techniques.1,33–35Several studies have reported that PET/CT is useful for the diagnosis of intra-abdominal VGI.1,28–32,42–46 Three recent studies summarized the role of PET/CT for the diagnosis of VGI.30–32 Although there were variables in imaging techniques and patient selection among these studies and other studies, the sensitivity and specificity of PET/CT were similar to those reported with standard CT for the diagnosis of VGI28–32,39,43–46 (Table 11). PET/CT may be less precise than conventional CT to identify the anatomic location of VGI. A linear, diffuse, homogenous uptake over a blood vessel is not indicative of VGI, whereas a focal uptake over a blood vessel on PET/CT is highly suggestive of VGI.32Sah et al31 reported that the use of a 5-point visual grading score increased the accuracy of PET/CT for the diagnosis of VGI. The administration of antimicrobial therapy before PET/CT decreased the sensitivity and specificity of the diagnosis of VGI.31 There are currently no published studies that demonstrate a clear benefit of serial PET/CT to follow the response to antimicrobial therapy for VGI.32 The use of PET/MRI for the diagnosis of VGI is being evaluated.32 PET/CT alone or in combination with other imaging modalities can be considered if the results of standard CT studies are inconclusive for the diagnosis of VGI.28–32,43–46 On the basis of the published studies, it is reasonable to use standard CT as the initial imaging modality for the diagnosis of VGI.30–32Intrathoracic VGIImaging studies are necessary to confirm the diagnosis and define the extent of infection and vascular anatomy. Diagnostic tests including CTA or MRI with or without an indium scan should be used in combination with blood culture results and echocardiography findings.1 Echocardiography alone cannot diagnose infection but can define anatomy, valvular dehiscence, graft anastomotic disruption, fistulae, or aneurysm formation. There are few published data for the use of PET/CT for the diagnosis of intrathoracic VGI. Angiography is not helpful for the diagnosis of VGI. It is used rarely to define complex anatomy before resection or revascularization.Recommendations for Diagnosis of Intracavitary VGIIn patients with gastrointestinal tract bleeding and suspected intra-abdominal VGI, an esophagogastroduodenoscopy and CTA are recommended (Class I; Level of Evidence B).In patients with suspected intra-abdominal VGI, it is reasonable to obtain a CTA as the initial imaging procedure (Class IIa; Level of Evidence B).In patients with suspected intra-abdominal VGI and indeterminate CTA findings, an MRI, PET/CT, or indium white blood cell study scan may be considered (Class IIb; Level of Evidence C).In patients with suspected intrathoracic VGI, echocardiography, CTA, and MRI used in combination with clinical findings and blood culture results are recommended for diagnosis (Class I; Level of Evidence B).Management of VGIsGeneral PrinciplesA multidisciplinary approach that includes specialists in cardiology, vascular medicine, vascular and cardiovascular surgery, radiology, infectious diseases, and in selected cases, plastic surgery is recommended for the successful management of VGI. The care team should also include specialists who assist in management of diabetes mellitus, smoking cessation, obesity, lower extremity ulcerations, lymphedema, vascular stasis, and other conditions that impair wound healing and increase the risk of infection.The selection and duration of antimicrobial therapy depend on the causative microorganisms, the location and type of graft infection, and other factors that are discussed below in the sections on management of specific VGIs.Recommendation for Management of VGIs: General PrinciplesA multidisciplinary team approach including specialists in vascular and cardiovascular surgery, vascular medicine, cardiology, infectious diseases, and radiology is recommended (Class I; Level of Evidence B).ManagementExtracavitary VGIThere is no widely accepted procedure of choice nor standardized surgical therapy for management of extracavitary VGI. The choice of a specific surgical procedure should be individualized for each patient.The Samson classification (Figure 4) helps define the extent and type of VGI, guides the selection of medical and surgical options, and determines prognosis.Download figureDownload PowerPointFigure 4. Extracavitary vascular graft infection: algorithm for management. I&D indicates irrigation and débridement; MRSA, methicillin-resistant Staphylococcus aureus infection; and VAC, vacuum-assisted closure device.Samson I and II VGIs.Antimicrobial therapy alone, with or without débridement, is reasonable for patients with Samson class I or II VGI (Figure 5). These infections should be treated as soft tissue infection that does not involve the graft. Unless there is recovery of a causative microorganism from cultures of wound drainage from purulent material or fluid from ultrasound-guided aspiration, antimicrobial therapy usually is emp
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