Nonvalvular Endovascular Infections
Endocarditis (valvular or mural), myocardial abcess, infected cardiac myxomas, infectious endarteritis, etc.
Endothelial damage Þ Platelet deposition Þ Nonbacterial Thrombotic Endocarditis, Bacteremia Þ Colonization of NBTE Þ Infective Endocarditis Þ Healed Endocarditis
Host factors immunocompetence, local aterial trauma, seeding during surgery, and distant foci of infection.
Microbial virulence factors (Staph, Strep) microbial adhesins, extracellular glycocalyx (slime), colonization factors
Manifestation of systemic infection fever, pallor, weight loss, asthenia splenomegaly.
Intravascular lesion murmur, signs of cardiac failure, Roth spots, Oslers nodes, Janeway lesions, splinter hemmorhages, Storke, Mycotic aneurysm, ischemia or infarction of viscera or extremities: look for localization.
Immunologic problem Arthritis, signs of uremia, vascular phenomena, finger clubbing.
Contiguous Extension valvular endocarditis, prosthetic valve endocarditis (15-45% with abcesses)
Following bacteremia or fungemia prolonged hospitalization, indwelling catheters, and extended courses of antibiotics.
Abnormal myocardium due to previous MI.
Microbiology Staph aureus is most common isolate, (Group F Streptococci, Salmonella, Clostridia, E. coli); Candida and Aspergillus - associated with prolonged hospitalization, post surgery, or immunocompromised host
Clinical Signs insidious onset with or without chest pain; conduction system abnormalities; complications include myocardial rupture, tamponade, and fistulae.
Diagnosis High index of suspicion, multiple blood cultures, and echocardiography especially transesophageal echo.
Treatment/Outcome Contiguous/paravalvular - 75% survival rate. Nonparavalvular -100% mortality due to underlying infection, and delay in diagnosis. Early surgical intervention with resection may improve survival
Infectious Endarteritis and Mycotic Aneurysms
Endarteritis is inflammation of the arterial wall
Epidemiology: 3:1 (M:F), > 65 years old, parallels incidence of atherosclerosis
Risk factors: hematogenous seeding of damaged endothelium; underlying disease like diabetes, cirrhosis, or on steroids (immunocompetency); contiguous extension from adjacent infection; local arterial trauma (IVDA, balloon pumps, catheters, vascular surgery, hemodialysis catheters (29% of cases).
Microbiology Salmonella (cholerasuis and typhimerium) can account for 50%, Staph. Aureus accounts for 30%.
Clinical signs sites are usually aorta (70%) or areas of bifurcation/narrowing. Presenting signs- fever, palpable mass, localized pain, distal emboli. Underlying thoracic or lumbar vertebral osteomyelitis associated with aortic lesions.
Diagnosis frequently after death, positive blood clutures in 50%; CT, ultrasound, labeled white cell scan, and aneurysmal dilation are useful.
Therapy/Management surgical resection and repair or bypass graft of vascular segment. Medical therapy alone uniformly unsuccessful. Complications rupture (75%), fistulae, and distal infection. Parenteral ABs for 4 weeks.
Prosthetic Vascular Graft Infections
Risk factors Epidemiology similar to endarteritis (male predominance, age>65). Adjacent infection, diabetes, surgical factors (revision, emergency repair) Contamination at time of insertion accounts for ~ 95% of infections.
Microbiology Early infection (less than two months) Staph aureus; late infection Staph epi. Mixed infection suggest aortoenteric fistulae. Fungal infection occurs late usually secondary to prolonged antibiotic use
Colonization surgical contamination (95%), hematogenous seeding, contiguous infection.
Immunocompetence diabetes, drug-induced immunosuppression.
Early onset wound infection, sepsis, anastomotic bleeding. Bugs involved - S. aureus, streptococcus, E. coli, Klebsiella, Pseudomonas.
Late onset (>4 mo) upper GI bleed, perigraft infection, false aneurysm, sinus tract (S. epi, E. coli, Klebsiella, Candida)
Clinical presentation Symptoms depend on location of graft. Abscess, thrombosis, sinus tracts, pseudoaneurysms suggest infection. Late complications include hemorrhage, fistulae, septic emboli
Diagnosis Ultrasonography localizes thrombosis, perigraft fluid collections or false aneurysm. CT scan most useful in detecting gas around the graft. Labeled white cell scans showed a diagnostic accuracy of 86% in aortic grafts.
Therapy Removal of graft, debridement and bypass. Postoperative antibiotic therapy for 4-6 weeks is recommended
Infections of Implanted Devices Requiring Venous Access
Subclavian catheters, mediports, pacemakers (1-5% over 3 years), and defibrillators (1-6% in 1 year).
Catheters, mediports emergency insertion, femoral insertion, distant site of infection, thrombosis, parenteral nutrition, IV drug abuse, underlying disease (diabetes, steroid use).
Pacemakers surgical manipulation, postinsertion hematoma, seroma, poor wound healing, underlying diseases including diabetes, skin disorders and steroid use.
Microbiology Staph aureus (50%). S epi predominates in subclavian and mediport infection. S aureus predominates in early pacemaker/ defibrillator infections. Pseudomonas is the most common gram-negative. Candida, Aspergillus are rare causes, usually in association with excessive use of antibiotics or neutropenic patients
Exit site/Pocket infections inflammation, purulent drainage or skin necrosis <2cm of skin from skin exit site.
Tunnel infections inflammation, purulence >2cm from skin exit site.
Intravascular infection - bacteremia with systemic signs of infection
Septic thrombophlebitis - infected thrombus in central veins associated with signs of venous obstruction of arm, neck or face, or septic pulmonary emboli.
Endocarditis-persistent fever, bacteremia; clinical signs of endocarditis lacking
Diagnosis cultures purulent drainage, blood. Quantitative cultures of catheter tip. Imaging CT scan, ultrasonography of neck veins to delineate thrombosis of venous system.
Exit site infection empiric/culture directed antibiotic therapy. Remove if no improvement, progression to tunnel infection or Candida isolated.
Pocket infection like exit site infection, if bacteremia - cure does not require removal of implanted material.
Tunnel infections use empiric/specific antibiotics. Rarely cured with just ABs when Pseudomonas Or Candida.
Intravascular infection Trial antibiotic therapy. Several studies show cure with antibiotic therapy alone in 25-60%. Remove catheter if persistent bacteremia, Pseudomonas, Candida or septic thrombophlebitis. Duration of antibiotic therapy is 2-3 weeks in absence of thrombosis or endocarditis.
Septic thrombophlebitis - removal of catheter (device). Antibiotic and anticoagulation therapy.
Hematogenous seeding of abnormal myocardium - Prolonged hospitalization. Prolonged use of antibiotics.
Contiguous infection - from underlying abscess, at pacemaker attachment sites, mural thrombus, and aneurysms.
Microbiology Staph aureus, viridans Strep, enterococci, candida; Microbiology similar to that for valvular endocarditis.
Diagnosis Nonspecific clinical presentation, Peripheral embolization common and similar to valvular endocarditis
Outcome Mortality rate similar to myocardial abscess especially when complicated by systemic emboli
Infected Cardiac Myxomas
No known predisposing factors
Microbiology same as for mural endocarditis
Clinical presentation FUO, systemic or pulmonary emboli common (88%)
Diagnosis high index of suspicion in patient with presumed valvular infection who fails to respond to appropriate antibiotic therapy
Therapy definitive therapy requires surgical resection of myxoma and postoperative parenteral antibiotics