Prosthetic joint infection

Source: Wikipedia, the free encyclopedia.
Prosthetic joint infection
Antibiotics
FrequencyApproximately 2% of hip and knee replacements

Prosthetic joint infection (PJI), also known as peri-prosthetic joint infection (PJI), is an acute, sub-acute or chronic infection of a

necrotic tissue and local antibiotics applied to the joint space. The bacteria that usually cause prosthetic joint infections commonly form a biofilm
, or a thick slime that is adherent to the artificial joint surface, thus making treatment challenging.

Signs and symptoms

The most common symptom of periprosthetic joint infections is

sinus tract, or a tract connecting the joint space to the external environment, is more common in chronic PJI, and is definitively diagnostic of PJI.[3] Fever may be present in PJI, but is uncommon.[2]

Cause

Prosthetic joint infections can occur any time after a joint replacement. Early infections (occurring within 4 weeks of a joint replacement) are usually due to Staph aureus,

strep viridans being the most common causative organism.[4]

The most common causes of PJIs are aerobic, gram positive bacteria, including staph aureus and coagulase negative staphylococcus (such as

Propionibacterium acnes is the most common cause of shoulder PJIs.[3]

Risk factors for PJI include diabetes, immunosuppression, smoking, obesity, chronic kidney disease, the presence of a soft tissue infection, or an infection in another part of the body or increased fat tissue around the replaced joint.[1] Surgical factors that may lead to an increased risk of PJIs include wound dehiscence (unplanned opening of the surgical wound after the surgery) and hematoma (collection of blood) formation.[1]

The presence of multiple artificial joints,

MRSA PJIs, rheumatoid arthritis or bacteremia place people at risk for multiple PJIs (either concurrent or subsequent infections).[2]

Prolonged operative times, in which the joint is left open to the external environment, determined as greater than 90 minutes in a single study, also increases the risk for PJIs.[2]

Pathophysiology

Prosthetic joint infections are generally difficult to treat as most causative organisms form a biofilm, or a thickly adherent membrane, against the artificial joint surface. The bacteria secrete

phagocytic activity encountering the biofilm, also allowing the bacteria to persist.[2]

Diagnosis

The presence of a PJI is confirmed when one of the proposed major diagnostic criteria are met:[4]

Polymerase chain reaction testing of the joint fluid or sonification fluid may aid in the diagnosis.[4]

Skin swabs, sinus tract swabs, swabbing of the artificial joint surface during surgery is not recommended due to the high risk of contaminants and low diagnostic yield (including the risk of contaminants rather than the pathologic organism being cultured).[4][2]

Blood cultures are positive in approximately 25% of cases of PJIs, especially in acute PJI, however, the organism isolated from blood culture does not always correlate to the organisms isolated from the joint fluid, and therefore blood cultures are not diagnostic of PJIs.[2]

Routine blood work attempting to identify infection including elevated white blood cells on a complete blood count, elevated inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) or procalcitonin are not sensitive nor specific in diagnosis PJIs.[4]

PET scan may help to identify hypermetabolic areas consistent with infection and aid with the diagnosis.[4]

Magnetic resonance imaging is specific to soft tissue infections, with metal artifact reduction sequence (MARS) MRIs having great utility to aid in the diagnosis of PJIs.[4]

Treatment

Antibiotic treatment alone, without surgical debridement, usually results in treatment failure.[2] Acute infections (in which the biofilm is thought to be immature) are usually treated using the DAIR technique; debridement, systemic and local antibiotics, and implant retention (the implant is not removed).[4][2] However, the mobile, easily interchangeable components of the implant are often replaced in the DAIR approach.[4] DAIR is contraindicated if there is a sinus tract, loosening of the prosthesis, or the surgical wound cannot be closed.[2] The microbial cure rate of DAIR is 74%, 49% and 44% in early, sub-acute and late infections respectively.[2]

Antibiotic loaded polymethylmethacrylate (PMMA) which are placed in the joint are helpful, however these non-resorbable beads may themselves be colonized by bacteria with an associated biofilm, therefore bio-absorbable local antibiotic carriers (calcium sulfate beads, resorbable gentamicin sponges) are preferred.[4]

Chronic PJIs may be treated using 1 stage revisions, where the artificial joint is replaced with a new one during the same surgical procedure, or with a 2-stage revision; in which the infected joint is removed and an antibiotic spacer is placed, this is followed by a second surgery in which a new artificial joint is placed.[4] Two step revisions are associated with increased morbidity, longer hospital stays, longer immobilization time, worse functional outcomes and higher costs.[4] Therefore, for intact, or mostly intact bone and soft tissue, and without a history of joint replacement revisions; a 1 step exchange is the treatment of choice.[4]

Negative pressure wound therapy is not recommended as the sponges used are often themselves colonized by the biofilm or by new organisms from the environment (including multi-drug resistant organisms).[4]

An extended course of antibiotics is required in PJIs, usually 6–12 weeks of antibiotic therapy.

ampicillin-sulbactam or amoxicillin with clavulanic acid with vancomycin added in cases of MRSA is a commonly employed empiric antibiotic treatment strategy.[4]

If surgery fails or the PJI persists despite optimal antibiotic therapy, resection arthroplasty of the hip with a pseudarthrosis (Femoral head ostectomy) is sometimes done.[2] Or in cases of knee PJIs failing treatment; an arthrodesis (artificial induction of ossification of the knee joint) is done.[2] These are considered last line therapies due to significant disability.[2]

Prevention

cephalosporins) is believed to reduce the risk of acute PJIs.[2][1]

Screening for and eradication of MRSA carriage and chlorhexidine wipes or soap and water skin cleansing prior to surgery may possibly decrease the risk of PJIs.[2]

According the American Dental Association: in patients with prosthetic joint implants, prophylactic antibiotics prior to routine dental procedures are generally not recommended in the prevention of PJI. However specific circumstances placing patients at higher risk, as determined by the dentist or other physicians, may warrant antibiotic prophylaxis.[5]

Prognosis

The 5-year mortality after hip PJIs is 21%, which is 4 times that of age adjusted controls.[2] And the 10 year mortality after hip PJIs was 45%, as compared to 29% in people with non-infected hip replacements.[2] 25% of people with PJIs have an unplanned re-operation within 1 year of PJI treatment.[2] Hospital stays are longer in those with knee and hip PJIs as compared to un-infected knee and hip replacement controls; at 5.3 vs 3 days (knee) and 7.6 vs 3.3 days (hip).[2]

Epidemiology

PJIs are the most common cause of knee replacement failures, and the third most common cause of hip replacement failures.[1] As of 2017, 2.1% of hip and 2.3% of knee replacements will at some time develop a PJI.[2] The incidence of PJIs have more than tripled in the last 20 years, with the incidence expected to further increase in the future. This increase is believed to be due to the much greater number of hip and knee arthroplasties being performed presently.[2]

References