JOINTS: SEPTIC ARTHRITIS,

RHEUMATOID ARTHRITIS AND

OSTEOARTHRITIS

Leanis Tequia Álvarez - Melissa Arboleda Giraldo

SEPTIC ARTHRITIS

 DIAGNOSIS

The presentation of septic arthritis can vary depending on

the pathogen, underlying medical conditions, or exposures.
Septic arthritis can present in a similar way to other types of
arthritis. More than 50% of patients with septic arthritis
have a history of joint inflammation, joint pain, and fever.
Sweats or chills are less common. Native joint infections
occur most often in the knee, followed by the hip, shoulder,
ankle, elbow, and wrist.

 PHYSICAL EXAM

Physical examination of patients with septic arthritis almost

always reveals a very painful joint with movement, often
including obvious effusion. Presentation is often more subtle
in those with periprosthetic joint infections, small joint
infections, atypical infections (eg, fungal, Lyme disease,
tuberculosis), or immunosuppression.

 LABORATORY EVALUATION

Septic arthritis is diagnosed through laboratory tests, particularly

studies of synovial fluid.
Analysis of synovial fluid obtained by arthrocentesis is necessary to
differentiate septic arthritis from other forms of arthritis and to
determine the causative pathogen. Synovial fluid analysis should
include Gram stain, aerobic and anaerobic cultures, and leukocyte
count with differential.
Elevated levels of white blood cells and CRP in the synovial fluid are
common in both crystalline arthritis and septic arthritis. Synovial
biopsy may be necessary if synovial fluid results are negative and
suspicion of septic arthritis persists.

 IMAGING

No imaging findings are pathognomonic for septic arthritis in

adults. Plain radiography establishes a baseline and can
evaluate fractures. Ultrasound can guide arthrocentesis for
inaccessible joints, such as the hips and small joints. MRI,
preferably with and without contrast, is useful in evaluating
osteomyelitis and soft tissue infections.

 ORGANISMS

Is the most common cause of native joint septic arthritis,

followed by Streptococcus species. Native joint septic
arthritis may be associated with some viral infections, such
as chikungunya, rubella, and parvovirus B19. . In older people,
gram-negative bacteria, especially Escherichia coli, cause
between 23% and 30% of septic arthritis cases. In
adolescents and young adults, Neisseria gonorrhoeae should
be considered.

 TREATMENT

Empirical systemic antibiotics should be started after obtaining

synovial fluid if there is a clinical concern of septic arthritis.
Antibiotic treatment should be based on the results of a Gram
stain of the synovial fluid or the suspicion of a pathogen in the
clinical setting. Gram-negative coverage should be considered for
patients with other risk factors, such as advanced age,
immunosuppression, or bacteremia of urinary or gastrointestinal
origin. Treatment should be individualized based on clinical
response and microbiological results.
The optimal duration of treatment for nongonococcal septic
arthritis is uncertain, but is at least 2 weeks for small joints; at
least six weeks is most commonly prescribed for all joints.

RHEUMATOID ARTHRITIS
 DIAGNOSIS

Rheumatoid arthritis (RA) is a chronic and progressive

inflammatory disorder that manifests as a symmetrical
polyarthritis of small and large joints that can lead to joint
and periarticular structural damage and the consequences of
systemic inflammation.
Routine laboratory studies can help confirm the diagnosis
and establish the presence of inflammation, autoantibodies,
and the risk of damage or erosion.

 PHYSICAL EXAM

The onset of RA peaks between the ages of 40 and 50, but

it is well described in all ages, including children and
adolescents. In addition, the risk of RA increases
considerably after the age of 60.
Diagnosis of RA can be suspected with as little as 2-4 weeks
of joint pain, 6 weeks of demonstrable synovitis in multiple
joints confirms the "chronicity" required for a reliable
diagnosis of RA

 IMAGING

An early diagnosis requires access to medical and diagnostic

services, suspicion based on the initial characteristics, and
judicious use of serologic tests. RA is a clinical and not a laboratory
diagnosis.
RA should be considered in the following settings: Pain, swelling,
and stiffness in multiple joints for 12 weeks or more First-degree
relative of an RA patient with chronic joint symptoms
The required characteristics begin with pain and stiffness in the
joints that improve with activity. Hallmark findings include joint
swelling or effusion and possibly warmth or erythema.

 ORGANISMS

The presence of RF and antinuclear antibodies is nonspecific and

is found in patients with infections, malignancies, and rheumatic
diseases. These autoantibodies are present in other diseases,
such as viral hepatitis, systemic lupus erythematosus,
cryoglobulinemia, Sjögren's syndrome, paraproteinemias, bacterial
endocarditis, mycobacterial diseases, syphilis, leprosy, chronic
interstitial lung disease, parasitic infections, and malignancies.
Serum rheumatoid factor is closely related to RA and can confirm
a clinically suspected diagnosis or characterize the severity of the
disease.

 TREATMENT

In early rheumatoid arthritis It is the physician's job to address the

patient's pain, swelling, and stiffness with effective interventions.
There are three modalities that every clinician should address in
early RA: analgesics, corticosteroids, and DMARDs.
Analgesics, the initial goal is to minimize pain, inflammation, and
functional impairment. Analgesic therapy, splints, and physical
therapy should be prescribed liberally soon after onset and used
until a diagnosis is established.

OSTEOARTHRITIS
 DIAGNOSIS

OA is an endemic and debilitating disease, most notable for its effect

on articular cartilage, which is severely degraded over the course of
the disease. Articular cartilage is the smooth cartilage at the end of
the long bones and within the intervertebral discs. It provides a low
friction surface for the joint while being able to transmit heavy loads.
Although the half-life of collagen within cartilage is long, it heals
very slowly, if at all, even with minor injuries. Although the cartilage
has the most marked changes, the entire joint is affected, including
the synovium, articular ligaments, and subchondral bone.
Inflammation, including active synovitis and systemic inflammation,
plays a key role in the pathogenesis of OA.

 PHYSICAL EXAM

Typical joints affected by OA include the knee, hip, distal and

proximal interphalangeal joints, first trapeziometacarpal joints, first
metatarsophalangeal joint, and facet joints of the spine. Other
joints, such as the elbow, wrist, shoulder, and ankle, are less
common. Many clinical features are seen in patients with OA that
may be due to synovial fluid accumulation, active inflammation, or
bony deformity of the joints. Some common clinical findings include
joint line tenderness, reduced passive and active range of motion,
crepitus, joint effusion, and bone swelling and deformity.

 IMAGING

Plain radiography can be useful to confirm the diagnosis and rule

out other pathology. There are certain plain radiographic findings
characteristic of OA. OA often demonstrates joint space narrowing,
osteophyte formation, subchondral sclerosis, and cysts.
The knee joint is usually evaluated using extended knee x-rays,
while the patient is weight bearing. Flexed knee radiographs are
also used to improve intra-articular visualization. Multiple
classification schemes are used to assess joint space narrowing or
osteophyte formation.

 ORGANISMS

It is considered to be polygenetic in nature; there are more

than 80 genes that have been implicated in the
pathogenesis. Some of these genes are for receptors for
vitamin D and insulin-like growth factor 1. OA has also been
associated with a single nucleotide polymorphism in the
growth and differentiation factor gene, which is involved in
the development of healthy bone and cartilage.

 TREATMENT

There is no current cure. Treatment can be broadly categorized into

modifiable risk factor reduction, intra-articular therapy, physical
modalities, alternative therapies, and surgical treatments. There is
also emerging evidence for several novel treatments.
Treatment focuses on reducing pain and stiffness. Subsequently,
treatment focuses on maintaining physical functioning.

 BIBLIOGRAPHY

J. C (2021). Septic Arthritis: Diagnosis
John Scott Earwood, Tyler R. Walker Gregory
and Treatment. American Academy of Family Physicians.

https://eds.s.ebscohost.com/eds/pdfviewer/pdfviewer?vid=21&sid=ec6fa23b-2abe-
464c-8ae2-e40b02ec3f7e%40redis

Rheumatic Disease Clinics of North
John J. Cush. (2022). Rheumatoid Arthritis.
America. Elsevier Inc.https://www-clinicalkey-

es.consultaremota.upb.edu.co/#!/content/playContent/1-s2.0-
S0889857X22000102?returnurl=null&referrer=null
Benjamin Abramoff, Flanklin E. Caldero. (2020). Osteoarthritis. Medical Clinics of
North AmericaElsevier Inc.https://www-clinicalkey-
es.consultaremota.upb.edu.co/#!/content/playContent/1-s2.0-S0025712519301130?
returnurl=null&referrer=null