Joint pathologies

HISTORY OF DISEASE
1.
Pai
n.
You should characterize the pain as for any other
pain along the lines of SOCRATES.
Site,onset,character,aggravating
factors,relieving
factors
Pain that worsens with movement and improves
with rest is likely to be non-inammatory.
An acute onset (hours) is consistent with septic
arthritis, gout/pseudogout, and trauma. A more
insidious onset is more common in conditions like
bursitis and tendonitis, where the relevant
anatomical structure becomes inamed with
overuse.
Chronic onset suggests osteoarthritis (note that
some
rheumatologists
prefer
the
term
osteoarthrosis to reect the fact that the
inammation is not the primary pathology).
The severity of pain can usefully be assessed by
asking about joint function for example, can the
patient weight bear?
Associated with swelling
History of night cries(Tb)
History of rest pain
History of morning stiffness(rheumatoid arthritis)
History of easy bruiseability(hemophilia)
2.
Tra
uma.
Sometimes even the slightest of knocks can cause
signicant pain. However, this does not exclude
other diagnoses trauma can precipitate infection
or gout, for example.
Common risk factors for gout. There are many
potential causes of gout, but the more common
ones that you should ask about include use of
thiazide diu- retics, recent heavy alcohol intake,

chronic renal failure, and chemotherapy (high cell

apoptosis, leading to degradation of DNA and
excess urate). A history of renal stones or previous
episodes of gout also makes gout more likely.
Common risk factors for septic arthritis. Again
there are many possible risk factors, but the key
ones are immunosuppression (e.g. diabetes, HIV,
steroid use) and any prosthetic joints.
Risk factors for haemarthrosis. Typically due to a
coagulopathy (e.g. classically haemophilia), although
anticoagulant use is also a risk factor.
3.
Pa s
t medical history
Recent gastrointestinal (GI) or urethral
infection? Reactive arthritis can develop after
either of these types of infection. You should take a
sexual history as a gonococcal infection may be
asymptomatic, and can lead to septic (rather than
reactive) arthritis (via haematogenous spread).
Previous episodes? Think rst of recurrent
conditions like crystal arthropa- thies and overuse
injuries.
Rheumatological disease? This is as relevant for
joint pathology as a past surgical history is for
abdominal pathology.
4.
Oth
er joints.
The involvement of several joints sequentially is
characteristic of gonococcus or rheumatic fever.
The involvement of several joints simultaneously
suggests a rst presentation of a chronic
polyarthritis such as rheu- matoid or psoriatic
arthritis. If you suspect the latter, you should ask
about psoriasis.
5.
Dru
g history.
A variety of drugs (e.g. thiazides, low-dose
aspirin, or ciclosporin) can predispose to gout.
Steroids predispose to osteoporosis, with
subsequent pathological fractures, although
pathological fractures are usually in the spine and
very rarely in the knee.

PHYSICAL EXAMINATION
Conscious
Orientation
Built
Nourishment
GENERAL EXAMINATION
Afebrile
Pallor
Icterus
Cyanosis
Clubbing
Generalized Lymphadenopathy
Pitting pedal edema
VITALS
Heart rate :
BP :
Respiratory Rate :
CVS: s1 s2 heard, No murmurs
RS: Normal vesicular breathing heard over all the lung elds
CNS: No focal neurological decit present
LOCAL

EXAMINATION

You should examine the relevant joint and one

joint above and below, as pain may be referred from these
joints. In this case, this means the knee, hip, and ankle and
the other knee for comparison.
Your joint examination should be based around look, feel, and
move

Inspection: inspect the joint for

erythema,
scars,
swelling,
muscle wasting,
bony deformities.
Make the most of symmetry and compare left with right, as
in some individuals it may be dicult to tell if a joint is
swollen or in some other way abnormal!

Palpation:
f e e l for any eusions;
for tenderness on the bones, ligaments, tendons, or
along the joint line;
for temperature (in case of infection or inammation);
and
for neurovascular status. Checking neurovascular
status is crucial, as a neuropathy or vasculopathy
(either causing the pain or secondary to joint damage)
may rapidly lead to irreversible damage and loss of
function.
Movement: being careful and gentle with the painful
joint,
test the full range of passive and active movement.
Note:
Articular conditions are more likely to present with a
diffusely inamed joint (red, hot, painful) and pain on passive
as well as active motion.
Periarticular conditions tend to have a focal point of
tenderness on palpation (in bursitis this would be over the
bursa; in tendonitis, over the tendon) and pain is usually
much worse on active movement than on passive movement
Following ndings rare in someone presenting with acute joint
pain
Skin:
Tophi: deposits of urate crystals that can be found
anywhere on the body usually around joints and bones. They
are hard lumps that sometimes break through the skin with a
chalky appearance.If present, they suggest chronic gout.

Gouty tophi.
Rheumatoid nodules: subcutaneous nodules,
classically found on elbows and ears, which are
pathognomonic of rheumatoid arthritis.
A variety of rashes are seen in conditions that can
also cause arthritis
e.g.
psorias
is, systemic lupus erythematosus (SLE).
Nails: look for pitting, subungual hyperkeratosis, and
onycholysis all signs of psoriasis, associated with
psoriatic arthritis.
Uveitis (inammation of the middle layer of the eye),
evidenced by a painful red eye with diminished vision, and
sometimes an irregularly shaped pupil. This is often
associated
with
HLA-B27-positive
inammatory
arthropathies.
Mouth ulcers which may be evidence of inammatory
bowel disease (par- ticularly Crohns disease), itself
associated with arthropathy.
Lung signs suggestive of brosis (e.g. clubbing, late
inspiratory crackles), as pulmonary brosis is a
complication sometimes seen in various inammatory
arthropathies.

Do not overly focus on these, as beyond the skin and nail signs
these are relatively rare in someone presenting with acute
joint pain.

PROVISIONAL DIAGNOSIS

articular

Peri articular

Non-articular

Trauma (resulting in,e.g.,

fracture, meniscal
tear,haemarthrosis)

Ligament injury

Nerve

Tendonitis

entrapment

Bursitis

Bone malignancy

Fasciitis

Osteomyelitis

Epicondylitis

Neuroma

Gout
Pseudogout
Septic arthritis
Seronegative

Periostitis

spondyloarthropathy
Transient synovitis
First presentation of
chronic mono- or
polyarthritis (e.g.
rheumatoid arthritis)
Sarcoidosis
Amyloidosis
Vasculitis
SLE
Rheumatic fever
SPECIAL INVESTIGATION

The diagnosis is still not clear despite the history and

examination both septic arthritis and crystal arthropathies
remain equally likely.You will want to perform microscopy (cell
count and crystals), Gram stain, and culture on the joint uid
aspirate. There are several possible ndings:
Crystals. Present in gout (urate crystals negatively
birefringent and needle shaped) and pseudogout (calcium
pyrophosphate crystals positively bire- fringent and
rhomboid shaped). Detected by microscopy.
Infection. Cloudy aspirate with elevated white blood cell
count, a high neu- trophil component, and bacteria visible on
microscopy, with positive cultures a few days later, indicate
septic arthritis. Note, however, that the white cell count may
also be elevated in crystal arthropathies. Also note there is a
false negative rate of about 2025% in gonococcal septic
arthritis. If you suspect gonococcus, you should request
additional tests (below).
Blood. Haemarthrosis is seen in trauma with or without a
fracture. If fat globules are present, it strongly suggests a
fracture (the fat comes from the bone marrow).
White cells. In the absence of crystals, blood, and infection
(all of which cause inammation as well), inammation as
evidenced by white cells could be due to reactive arthritis
(Reiters syndrome), enteric arthropathy (due to inammatory bowel disease), rheumatoid arthritis, psoriatic arthritis,
and rheumat- ic fever. Non-inammatory aspirate (clear and
with a normal white cell count) usually suggests trauma or
osteoarthritis.
Cultures: take swabs of skin lesions, or of throat, urethra,
cervix, and rectum if gonococcal arthritis is a possibility.
Blood cultures should be requested if there is a clinical
suspicion of sepsis, although results may be negative in
early infection.
Bloods:
Complete blood count (FBC), C-reactive protein (CRP),
and erythrocyte sedi- mentation rate (ESR): these will
reveal any widespread inammatory and/ or infectious
process. Osteomyelitis will also result in deranged inammatory markers (e.g. ESR and CRP) but not always a raised
white cell count and APTT, PT

If
you suspect rheumatoid disease, you may want to
request rheumatoid factor, anticyclic citrullinated peptide
(anti-CCP) antibodies, antinuclear antibody (ANA), and other
autoantibodies.
Serum urate: Patients who develop gout have often had
hyperuricaemia
for years, although during acute gout their serum urate is
often normal or low. For this reason it should not be ordered
in the acute setting. Also note that asymptomatic
hyperuricaemia is fairly common in the population and thus
a nding of elevated urate is not very helpful in diagnosis.
Imaging:
X- R AY
imaging rarely contributes anything to the diagnosis of nontraumatic, acute monoarthritis. As with serum urate, it may
occasionally be misleading as pathology unrelated to the
acute monoarthritis may be picked up, e.g. osteoarthritis.
However:
Radiographs are useful if there has been trauma as they
identify fractures
and, depending on the site, some effusions (e.g. elbow).
Magnetic resonance imaging (MRI) is the imaging of
choice for soft tissue injuries and other extra-articular
pathology, e.g. osteomyelitis. If you have excluded
intra-articular pathology, MRI can be very helpful.