Infective Endocarditis, Sepsis, Septic Shock, DIC, and the Skin at a Glance
- Infective endocarditis: staphylococcal or streptococcal bacteria most common cause in intravenous drug use setting.
- Sepsis: Gram-positive bacteria most common cause; tenth leading cause of death in the United States.
- Disseminated intravascular coagulation: most commonly from sepsis; results from systemic activation of the coagulation cascade.
- Cutaneous manifestations of these entities include: splinter hemorrhages, Janeway lesions, Osler nodules, erythroderma, cellulitis, purpura, hemorrhage, purpura fulminans, and skin necrosis.
In the United States, the incidence of native-valve endocarditis is 1.7–6.2 cases per 100,000 person-years. The highest rate of infective endocarditis (IE) is seen in intravenous drug users, with an incidence estimated at 150–2,000 per 100,000 person-years. The risk of prosthetic valve IE decreases with time following valve implantation and the cumulative risk is about 2%–3% after 60 months.1
Etiology and Pathogenesis
IE can be subdivided by native valve versus prosthetic valve. The causative organisms in most cases of IE are Staphylococci or Streptococci, implicating skin as the initial site of infection in many cases. Native valve endocarditis occurs most commonly in the setting of valvular disease or in people who use intravenous drugs. Rheumatic valve disease has been replaced by aortic stenosis and mitral regurgitation, as the most common settings in which native valve endocarditis is encountered. At sites of endothelial injury, a sterile thrombus can occur which is particularly susceptible to seeding of bacteria from transient episodes of bacteremia. This can result in the development of valvular vegetations that can cause local tissue destruction and embolic events.
Intravenous drug users are particularly susceptible to IE even though most have no preexisting structural heart disease. More than half of the cases of IE in injection drug users are right sided, involving the tricuspid valve. The most common causative organism is Staphylococcus aureus.
Prosthetic valve endocarditis can be classified as early (in the first 2 months following valve replacement) or late (2 months or later). The newly placed prosthetic valve is particularly susceptible to bacterial colonization because the process of endothelialization does not occur until 2–6 months following surgery. Early prosthetic valve endocarditis is most commonly caused by Staphylococcus epidermidis followed by S. aureus. Late prosthetic valve endocarditis can be due to a variety of organisms including the so-called HACEK organisms (Haemophilus parainfluenzae, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kinsella kinasae).
Most cases of nosocomial endocarditis are secondary to indwelling catheters or to surgical procedures, and are caused by Streptococci. However, nosocomial endocarditis in dialysis patients is most commonly due to S. aureus. Other less common causes of IE include fungi, Pseudomonas, Coxiella burnetii, Bartonella quintana, and Proprionobacteria acnes.