Septic arthritis of the hip is a potentially devastating condition that can culminate in substantial morbidity and even mortality for the patient. Fortunately, septic arthritis of the adult hip is a rare condition. However, incidence is increased in the elderly and immunocompromised. Diagnosis requires a high index of suspicion and treatment must be early and aggressive to prevent rapid joint degradation. This chapter will discuss the basic tenets of the pathogenesis, clinical presentation, treatment, and outcomes of septic arthritis of the native hip.

Most cases of septic arthritis are monoarticular, involving only one joint, and commonly involve larger joints. The knee accounts for approximately 50% of septic arthritis cases (1). The hip, as mentioned above and the focus of this chapter, is the second most common location, comprising 13% of all septic arthritides (2). Other locations such as the elbow, ankle, and shoulder joints are other likely areas of involvement. Sacroiliac and sternoclavicular joints are locations also seen in intravenous drug users.

Incidence of adult hip septic arthritis is fortunately very low. In the adult population, incidence is particularly increased in the immunocompromised and the elderly. In addition, multiple other risk factors exist and will be discussed in a later section of this chapter.

With regard to age predilection, it is much more common in the pediatric hip as a result of differing blood supply to the hip making it more susceptible to hematogenous inoculation from adjacent osteomyelitis of the metaphysis. After skeletal maturity, the arterial anatomy changes, thus, making the adult hip more resilient to the development of septic arthritis. Excluding pediatric incidence, adult hip joint infection is more common in the elderly.

As in the pediatric population, hematogenous infection is the most common cause of sepsis of the hip joint in the adult. Likely origins include inoculation from pneumonia, endocarditis, diverticulitis, urinary tract infection, and dermatologic infections.

Septic arthritis results from the growth of bacteria within a synovial joint. The pathway begins with bacteria entering the joint and depositing on the synovial membrane (3). The synovial membrane is a highly permeable and vascular connective tissue lining of the joint (4). This synovial lining does not possess a limiting membrane and thus, bacteria can pass easily into synovial fluid via specific collagen receptors (3). It is this absence of a limiting membrane that allows the synovium to be highly permeable, therefore, allowing for an efficient production of synovial fluid as well an easy exchange of nutrients as well as waste removal from the joint (4). However, it is this very phenomenon of high permeability that allows for rapid proliferation of bacteria within the joint after bacterial deposition.

Bacteria deposition on the synovial membrane, in turn, results in an acute inflammatory response. As these bacteria continue to proliferate, they release enzymes and toxins that result in degradation of cartilage. In addition, the normal flow of synovial fluid is altered, which in turn, further enhances the articular degradation as cartilage waste product removal is hindered (4). The vicious cycle escalates as pressure builds within the hip joint, decreasing its blood supply and further enhancing the cartilage destruction. The hip joint capsule becomes involved as well and is weakened by the proteolytic enzymes, therefore, potentially leading to the formation of soft tissue abscesses (4).

Nonpyogenic pathogens, such as fungi and mycobacteria, exert their effects via a different mechanism of action than that of bacterial organisms. The synovium undergoes a granulomatous reaction resulting in a thickened synovium, an effusion, and the production of fibrin “rice bodies” (4). Unlike most bacterial organisms, proteolytic degradation does not take place in these instances. Instead, the cartilage is damaged gradually via chronic granulation tissue infiltration starting peripherally then moving centrally within the hip joint and bone (4). The bone then undergoes caseous necrosis with the possible formation of sinus tracts and soft tissue abscesses (4,5).

Any microbial pathogen can essentially cause infectious arthritis, however, some inciting organisms are more common than others. The most common cause of septic arthritis, in general, is Neisseria gonorrhoeae. N. gonorrhoeae is the most common pathogen in otherwise healthy sexually active adolescents and young adults. Fortunately, it is often less morbid and destructive than other infectious arthritides and responds quickly and well to antibiotic therapy (6,7). Women are two to three times more frequently affected by gonococcal arthritis than men (3,8). The most common location of N. gonorrhoeae inoculation is the knee and rarely affects the hip joint (9,10,11,12).

After N. gonorrhoeae, staphylococci and streptococci are the most common causes of septic arthritis, particularly in the elderly population (13,14). With regard to the hip, Staphylococcus aureus is the most common cause of septic arthritis with reported rates of 40% to 75% (4,15,16). Second to staphylococcus in incidence are the Streptococcus species (5,17,18,19,20).

Gram-negative bacilli-related septic arthritis of the hip is becoming more common with a reported rate of 12% of cases in one series (2,4). These gram-negative bacilli consist of Escherichia Coli, Salmonella species, Pseudomonas species, Klebsiella species, Proteus species, and Enterobacter species (5,21,22,23,24). Septic arthritis of the hip caused by these gram-negative bacilli unfortunately carries a poor prognosis (4). Other bacteria seen in septic arthritis of the hip comprise Listeria species, Haemophilus influenzae, Campylobacter species, and Branhamella species (4,5,25,26,27,28). Such anaerobic species as Bacteroides fragilis and Bacteroides melaninogenicus are being seen with increasing incidence due to improved culturing techniques and an increase in the immunosuppressed population (4,29,30). These make up less than 5% of all cases of septic arthritis of the hip (4,5).

Mycobacterium tuberculosis is increasing in incidence with the increase in pulmonary tuberculosis among immunocompromised individuals (4). Septic hip infections have also been reported with Kingella kingae, Coxiella burnetii, Nocardia asteroides, and Mycoplasma (31,32,33,34,35,36,37).

The organisms Treponema pallidum and Borrelia burgdorferi, involved in syphilis and Lyme disease respectively, have also been cited as causing septic arthritis of the hip (4,5). Neuropathic arthropathy seen with tertiary syphilis can often result in obliteration of the hip joint as well (4,5).

Fungal infections of the hip do occur as well, and these are often due to Candida species (38). Other fungal infections caused by Cryptococcus and Coccidioides have also been reported (5,39).

It is important to know that viruses can cause a synovitis resulting in symptoms mimicking septic arthritis (4). Fortunately, the synovitis is self-limited and no treatment is needed (4,40).

There are multiple risk factors, both local and systemic, that place the patient at increased likelihood of developing septic arthritis. Local disease and systemic disease, or a combination of both, can weaken the ability of the hip joint toward off infection (4).

Rheumatoid arthritis patients are at increased risk for septic arthritis as are patients with artificial joint prostheses (41,42,43). Age over 80 years has also been proposed as a risk factor along with diabetes mellitus (44

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