Septic Arthritis


Ovid: Adult Reconstruction

Editors: Berry, Daniel J.; Steinmann, Scott P.
Title: Adult Reconstruction, 1st Edition
> Table of Contents > Section
II – Knee > Part B – Evaluation and Treatment of Knee Disorders >
20 – Septic Arthritis

20
Septic Arthritis
M. Wade Shrader
David J. Jacofsky
Acute bacterial infection of a joint, known as acute
septic arthritis, is a serious, and can be a life-threatening,
infection. Septic arthritis occurs primarily through three mechanisms:
(a) direct inoculation through an open wound or penetrating object
(including surgery); (b) spread from adjacent infected tissue, such as
a soft tissue infection or local osteomyelitis; or (c) hematogenous
seeding from bacteremia. Even with appropriate, aggressive intervention
and treatment, septic arthritis can cause substantial morbidity, and a
delay in diagnosis or treatment can make the consequences even more
serious.
Septic arthritis most commonly affects small children
and the geriatric population. Patients with any immune system
compromise are especially at risk, including those patients with
diabetes, rheumatoid arthritis, malnutrition, and chronic renal or
liver failure. Patients using intravenous drugs and those with chronic
indwelling intravenous catheters are at higher risk. Vascular
insufficiency may increase the risk of infection by compromising host
immune defenses and also can impair the treatment of infection by
decreasing delivery of antimicrobial agents to infected tissues.
Pathogenesis
The incidence of septic arthritis in the general
population has been estimated to be 2 cases per 100,000, although the
incidence is much higher in immunocompromised populations. In patients
with rheumatoid arthritis, the incidence has been estimated to be
between 30 and 70 cases per 100,000. The most commonly affected joint
is the knee.
The most common source of infection is hematogenous
spread. Joints are at risk for hematogenous seeding because of the lack
of basement membranes in the synovial tissues. Thus, bacteria that are
present in the blood vessels have relatively easy access to the joint
space without the barrier of the basement membrane.
The most common infectious agent in adult septic arthritis is Neisseria gonorrhea.
This infection often occurs in sexually active young adults, is
typically polyarticular, and may be associated with a papular rash.
Gonococcal septic arthritis can be successfully treated with
antibiotics and is the only type of joint infection that does not
require surgical debridement.
The most common cause of nongonococcal septic arthritis in adults is from Staphylococcus aureus.
Patients typically have monoarticular involvement, and bacteria are
usually spread hematogenously. The hip and knee are the most common
joints involved, although infections of the shoulder, elbow, wrist, and
ankle also may be seen. Methicillin-resistant strains of staphylococcus
(MRSA) are becoming more prevalent, with three out of four positive S. aureus cultures being methicillin-resistant in some centers.
Other infectious agents may be responsible for septic
arthritis, depending on the patient population and the environment.
Streptococci, Salmonella, and Pseudomonas are all frequently encountered organisms.
Diagnosis
The clinician must maintain a high level of suspicion
for septic arthritis because of the serious consequences of a missed
diagnosis. Patients typically present with a swollen, red, painful
joint. They often will not be able to bear weight on the affected lower
extremity and will complain of decreased joint motion secondary to
pain. Fevers and chills are sometimes present. Often, however, all of
these complaints are not present, and the severity of the symptoms can
be quite variable. A thorough history should be elicited, specifically
considering any recent infections, immune compromise, social history,
travel history (to exclude tick bites), and a complete sexual history.
Musculoskeletal infections caused by mycobacterial or fungal organisms
do not typically present with the acute, dramatic inflammatory response
seen in bacterial infections. The diagnosis in these cases often is
made based on a high index of suspicion of the health care provider.

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Physical Exam
The physical exam should focus on determining if any
signs of infection are present. Vital signs, including temperature,
should be obtained. The joint should be examined for effusion,
erythema, and tenderness to palpation. The most specific sign of septic
arthritis is pain with passive range of motion, which should be
determined in any physical exam of the extremities. In the knee, septic
arthritis may be differentiated from septic prepatellar bursitis by
determining if pain with range of motion is seen only in deeper flexion
(bursitis) or can be elicited at near full extension as well.
Radiographic Features
Plain radiographs are recommended for most
musculoskeletal complaints of the extremities. Plain films should be
scrutinized to determine if there are any fractures, dislocations, or
other pathologic bony processes that might explain the patient’s
symptoms. Plain radiographs may not always be helpful in the diagnosis
of septic arthritis, although in more chronic cases erosive changes can
be seen. Soft tissue swelling, loss of soft tissue planes, or effusions
may be the only findings on radiographs of patients with septic
arthritis. Chronic or neglected infections can progress to adjacent
osteomyelitis, which often can be detected on plain radiographs.
Magnetic resonance imaging (MRI) can be helpful in some
circumstances. MRI views will definitely show effusion and fluid
collections that may be infectious. MRI also may demonstrate other
reasons for joint swelling, such as ligament rupture or meniscal tear.
Nuclear imaging with technetium bone scan or indium-tagged white blood
cell scan also can be used, but often are not necessary to confirm the
diagnosis.
Laboratory Workup
Screening laboratory values should be obtained in all
patients, both to assist in the diagnosis of the septic arthritis and
to follow the indices after treatment. A complete white blood count
with differential, erythrocyte sedimentation rate (ESR), and C-reactive
protein should be obtained if infection is suspected, although
inflammatory disorders alone can lead to false-positive results.
The gold standard in diagnosis of septic arthritis
remains arthrocentesis (joint fluid aspiration). The joint should be
aspirated with a large-bore needle, and this should be done before
empiric antibiotic treatment is begun. Fluoroscopy can be used to aid
in the aspiration, if necessary for some joints (e.g., hip). The fluid
should immediately be sent for Gram stain, cell count, culture, and
crystal analysis. Cultures from superficial sites such as draining
fistulas should be avoided, as the organisms colonizing these sites may
not be the same as the deeper infecting organism. Joint fluid cultures
are positive in about 85% of nongonococcal septic arthritis, but only
in about 25% of cases in which gonococcus is the infecting agent.
A joint fluid aspirate analysis that shows a nucleated white blood cell count >100,000/mm3 is indicative of septic arthritis, and counts between 50,000/mm3 and 100,000/mm3
are inflammatory but not necessarily infectious. The white blood cell
differential count also provides valuable information to aid in the
diagnosis. A differential count with an unusually high proportion of
polymorphonuclear cells (>90%) is also highly suggestive of septic
arthritis, whereas <50% neutrophils is unlikely to be an acute
infection.
Joint fluid analysis must be performed in a timely,
urgent fashion to allow treatment that will prevent the systemic spread
of infection and preserve the health of the articular cartilage.
Intra-articular lysosomal enzyme release, including metalloproteases
and collagenases, can digest glycosaminoglycans and cause articular
cartilage cell death. The release of these enzymes is mediated by
cytokines such as interleukin-1 (IL-1). Cartilage softening and
fissuring can be seen secondary to glycosaminoglycan depletion within 7
days from the onset of infection. Laboratory investigations in animal
models have shown that joint debridement and lavage decrease the rate
and magnitude of collagen breakdown, probably through the removal of
leukocytes and associated destructive enzymes.
Treatment
The three classic principles in management of the acute
septic joint are as follows: (a) thorough joint drainage and synovial
debridement, (b) appropriate antibiotic therapy, and (c) joint rest in
a stable position. All three of these treatment principles are crucial
in the successful treatment of septic arthritis.
There are three techniques to drain a septic joint: (a)
open drainage, lavage, and debridement; (b) arthroscopic drainage,
lavage, and debridement; and (c) serial aspirations, lavage, and
drainage. Controversy remains over which method is the most appropriate
way to treat a septic joint. The gold standard remains an open
arthrotomy, which allows for adequate drainage and lavage and provides
the opportunity for a thorough synovial debridement, a factor that many
surgeons feel is key to successful treatment. Experienced
arthroscopists argue that they can provide equally efficacious drainage
and lavage through the arthroscope. Proponents of arthroscopic
debridement also argue that they can actually perform a more thorough
synovial debridement by using posterior portals to allow for
debridement of the posterior compartment of the knee. Although its
indications and use are limited, serial aspirations and lavage also can
be successful in treating the native septic joint, particularly if the
infection is <72 hours old and the patient is not immunocompromised.
It is critical, however, that if the patient does not show significant
improvement within 24 to 48 hours with repeated aspirations, surgical
irrigation and debridement should be performed. In general, closed
suction drainage for 24 to 48 hours after operation is recommended.
The initial antibiotic should be chosen based on the
patient risk factors, patient history and clinical signs, and the
initial Gram stain. Culture results should dictate change to the most
appropriate antibiotic, based on sensitivity data.

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Typically,
intravenous antibiotics are continued for 4 to 6 weeks. When nonviable
tissue is encountered in the joint and when a clinical response to
treatment is not seen, a “second-look” surgery and repeat debridement
may be indicated.

The joint should be kept immobilized for the first 48 to
72 hours of treatment. However, once clinical improvement is noted, the
patient should begin rehabilitation, including range-of-motion and
strengthening exercises. Some surgeons advocate the use of continuous
passive motion (CPM) devices to minimize the possibility of forming
postinfectious intra-articular adhesions. Dynamic splints, passive
motion exercises, and joint manipulations are used as needed but are
rarely necessary.
After the septic arthritis has been successfully
treated, the joint involved may develop arthritis, or suffer from
decreased loss of motion. Any subsequent surgical treatment aimed at
that joint (for example: capsular release, osteotomy, arthroplasty)
must take into account the possibility of residual infection.
Suggested Readings
Canale ST, ed. Campbell’s Operative Orthopedics. 9th ed. St. Louis, MO: Mosby—Year Book; 1998.
Dubost JJ, Soubrier M, Sauvezie B. Pyogenic arthritis in adults. Joint Bone Spine. 2000; 67(1):11-21.
Kohli R, Hadley S. Fungal arthritis and osteomyelitis. Infect Dis Clin North Am. 2005; 19:831-851.
Koval KJ, ed. Orthopedic Knowledge Update 7, Home Study Syllabus. Rosemont, IL: American Academy of Orthopedic Surgeons; 2006.
Leirisalo-Repo M. Early arthritis and infection. Curr Opin Rheumatol. 2005; 17(4):433-439.
Morrissy RT, Weinstein SL. Lovell and Winter’s Pediatric Orthopedics. 4th ed. Philadelphia: Lippincott-Raven Publishers; 1996.
Perry CR. Septic arthritis. Am J Orthop. 1999; 28:168-178.
Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect Dis Clin North Am. 2005; 19:853-861.
Ross JJ. Septic arthritis. Infect Dis Clin North Am. 2005; 19:799-817.
Smith JW, Chalupa P, Shabaz Hasan M. Infectious arthritis: clinical features, laboratory findings and treatment. Clin Microbiol Infect. 2006; 12(4):309-314.
Zimmermann B III, Mikolich DJ, Ho G Jr. Septic bursitis. Sem Arth Rheum. 1995; 24:391-410.

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