Nonvalvular Endovascular Infections

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

Clinical manifestations

Manifestation of systemic infection – fever, pallor, weight loss, asthenia splenomegaly.
Intravascular lesion – murmur, signs of cardiac failure, Roth spots, Osler’s 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.

Myocardial Abcess

Risk factors

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 AB’s 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

Pathophysiology

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).

Risk factors

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

Clinical manifestations

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

Complications

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.

Therapy/ Management

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 AB’s 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.

Mural Endocarditis

Risk Factors

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