Sepsis background

Shoulder sepsis can have a devastating impact on shoulder function, particularly if diagnosis and treatment are delayed or inadequate. The general principles in the pathogenesis of shoulder sepsis are similar to those pertaining to all intra-articular infections. There are three fundamental pathways for pathogens to enter a joint:

1.

Spontaneous hematogenous seeding via the synovial blood supply
2.

Contiguous spread from adjacent metaphyseal osteomyelitis via the intra-articular portion of the metaphysis
3.

Penetration of the joint by trauma, therapy, or surgery

Susceptibility to infection is determined by the adequacy of the host defenses. Spontaneous bacteremia, trauma, and surgery present opportunities for inoculation of the joint, particularly if local or systemic conditions are favorable for infection to develop. However, shoulder sepsis is relatively uncommon due to the normal defense mechanisms, a good local blood supply, and the use of antibiotic prophylaxis.

Certain patient groups with immune system depression or aberrations are at increased risk for infection. Patients with rheumatoid disease can manifest a spontaneous and somewhat cryptic sepsis in joints. ^, Infants, children, the elderly, patients with vascular disease, diabetes, or drug abuse, and patients with human immunodeficiency virus infection have an increased susceptibility to specific organisms, as have patients with hematologic dyscrasias or neoplastic disease.

Joint infection requires a threshold inoculum of bacteria and can be facilitated by damaged tissue, foreign body substrata, and the acellularity of cartilage surfaces. Total joint arthroplasties are at potential risk of infection because of the presence of metal and polymer biomaterials and the decreased phagocytic ability of macrophages in the presence of methylmethacrylate. Biomaterials and adjacent damaged tissues and substrates are readily colonized by bacteria in a polysaccharide biofilm that is resistant to macrophage attack and antibiotic penetration. ^, With antibiotic prophylaxis, infection rates of total joint arthroplasty have been reported to be low, at 1% to 5% depending on the device and the location. ^, However, once infected, biomaterials and damaged tissues are exceedingly resistant to treatment, such as those implicated with Cutibacterium acnes (formerly Propionibacterium acnes ), a common commensal skin flora organism that triggers an immune response and promotes biofilm adhesions. ^, This is essential to consider and diagnose when treating prosthetic joint infections.

Clinical infection in immunosuppressed patients involves the maturation of an inoculum of known pathogens (e.g., Staphylococcus aureus or Pseudomonas aeruginosa ) or the transformation of nonpathogens (e.g., Staphylococcus epidermidis ) to a septic focus of adhesive virulent organisms. This transformation can occur in the presence of, and be potentiated by, the surface of biomaterials, ^, damaged tissue, and defenseless cartilage matrix surfaces.

History

The work of outstanding scientists such as Louis Pasteur (1822–1895), Joseph Lister (1827–1912), and Robert Koch (1843–1910) in the last quarter of the 19th century ushered in the modern age of bacteriology and an early understanding of intra-articular sepsis. Koch’s experiments with culture media at the Berlin Institute for Infectious Disease verified the role of the tubercle bacillus in musculoskeletal infection.

In the latter part of the 19th century, the concept of antisepsis was developed. Lister maintained that sepsis was the main obstacle to significant advances in surgery. He documented a dramatic reduction in cases of empyema, erysipelas, hospital gangrene, and surgical infection through the use of antiseptic techniques. Although the popularization of antiseptic techniques in the surgical theater greatly reduced the rate of complications resulting from infection, it was not until the 1930s that specific antimicrobial therapy was discovered. In 1935 a German bacteriologist, Gerhard Domagk, discovered that sulfonamides protected mice against fatal doses of hemolytic staphylococci. Sulfonamides were soon used for infections in patients, with excellent results.

Although the history of bacteriology, antiseptic techniques in surgery, and the development of antibiotics is well documented, very little of the early literature relates specifically to infections about the shoulder. In Codman’s book, The Shoulder , first published in 1934, infections of the shoulder and, in particular, osteomyelitis of the proximal humerus were considered to be very rare lesions. Codman cited a report by King and Holmes in 1927 in which a review of 450 consecutive symptomatic shoulders evaluated at the Massachusetts General Hospital revealed five cases of tuberculosis of the shoulder, one luetic infection of the shoulder, three unspecified shoulder infections, and two cases of osteomyelitis of the proximal humerus. The rarity of tubercular lesions of the shoulder was documented through the results of four large series of tuberculosis involving the musculoskeletal system (Townsend, 21 of 3244 cases; Whitman, 38 of 1833 cases; Young, 7 of 5680 cases; and Billroth, 14 of 1900 cases). As microbial culturing and identification techniques developed in the early 20th century, streptococcal and staphylococcal species were more often identified as the causative agents in shoulder infection.

Septic anatomy

Anatomic relationships are intimately linked to the pathogenesis of joint sepsis and osteomyelitis. The vascularity of the proximal humerus and periarticular structures (particularly the synovium) and the intricate system of bursae about the shoulder are critical factors.

Classically, the age-dependent presentations of hematogenous osteomyelitis and septic arthritis of the shoulder (and of other large joints, such as the hip and knee) have been attributed to the angiogenic development of the growth plate and epiphysis. The most detailed studies of the formation of blood vessels in this area have been completed for the proximal femur but are analogous to the same development about the proximal humerus. Experimental work by Trueta demonstrated that before 8 months of age, there are direct vascular communications across the growth plate between the nutrient artery system and the epiphyseal ossicle. This observation was believed to account for the frequency of infection involving the epiphyseal ossicle and subsequent joint sepsis in infants. At some point between 8 and 18 months of age (an average of 1 year), the growth plate forms a complete barrier to direct vascular communication between the metaphysis and epiphysis. The last vestiges of the nutrient artery turn down acutely at the growth plate and reach sinusoidal veins. At this point the blood flow slows down, creating an ideal medium for the proliferation of pathogenic bacteria.

In the adult shoulder, the intra-articular extent of the metaphysis is located in the inferior sulcus and is intracapsular for approximately 10 to 12 mm. An infection of the proximal metaphysis, once established, can gain access to the shoulder joint via the haversian and Volkmann canals at the nonperiosteal zone ( Fig. 46.1 ). With the obliteration of the growth plate at skeletal maturity, anastomoses of the metaphyseal and epiphyseal circulation are again established.