Osteo-arthritis

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 Osteo-arthritis (OA)
✓ OA is by far the most common form of
arthritis.
✓ Strongly associated with ageing
✓ A major cause of pain and disability in older
people.

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 Osteo-arthritis (OA)
Characterised by focal loss of articular
cartilage, subchondral osteosclerosis,
osteophyte formation at the joint margin, and
remodelling of joint contour with enlargement
of affected joints.

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 Osteo-arthritis (OA)
➢ Inflammation can occur but is not a
prominent feature.
➢ Joint involvement in OA follows a
characteristic distribution, mainly targeting-
hips, knees, PIP and DIP joints of the hands,
neck and lumbar spine (see Fig. 25.9).

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 Osteo-arthritis (OA)
➢ Inflammation can occur but is not a
prominent feature.
➢ Joint involvement in OA follows a
characteristic distribution, mainly targeting-
hips, knees, PIP and DIP joints of the hands,
neck and lumbar spine (see Fig. 25.9).

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 Osteo-arthritis (OA)
➢ Prevalence of OA rises progressively with age
➢ Estimated that 45% of all people develop knee
OA and 25% hip OA at some point during life.

P
 Osteo-arthritis (OA)
➢ Prevalence of OA rises progressively with age
➢ Estimated that 45% of all people develop knee
OA and 25% hip OA at some point during life.

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 Osteo-arthritis (OA)
▪ Some of these patients are asymptomatic
▪ Lifetime risk of having a total hip or knee
replacement for OA in someone aged 50 is
11% in women
8% in men

P
 Osteo-arthritis (OA)
✓ Symptoms attributable to OA are more prevalent in
women
✓ Except at the hip, men are equally affected

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 Osteo-arthritis (OA)
➢ OA is a complex disorder with both genetic and
environmental components (Fig. 25.14).
➢ Repetitive adverse loading of joints during occupation or
competitive sports is also an important predisposing factor
in farmers (hip OA), miners (knee OA) and elite or
professional athletes (knee OA).

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 Osteo-arthritis (OA)
For most people, however, participation in recreational
sport does not appear to increase the risk of OA,
unless there has been significant joint trauma.

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 Osteo-arthritis (OA)
Congenital abnormalities of the joint, such as
➢ slipped femoral epiphysis, are also associated with a high risk of OA,
due to abnormal load distribution within the joint
➢ increased risk of OA in Paget’s disease of bone
PD- interferes with your body's normal recycling process, in which new bone tissue
gradually replaces old bone tissue. Over time, bones can become fragile and
misshapen. The pelvis, skull, spine and legs are most commonly affected.

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 Osteo-arthritis (OA)
Obesity is another strong risk factor.

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 Osteo-arthritis (OA)
▪ The increased incidence of OA in women has led to
speculation that sex hormones may play a causal role.
▪ No evidence to suggest that circulating sex hormone levels
or reproductive history predispose to OA, some studies
have shown a lower prevalence of OA in women who use
hormone replacement therapy (HRT), as compared with
non-users.

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 Osteo-arthritis (OA)
Genetic factors
• play a key role in the pathogenesis of OA
• family-based studies have estimated that the
heritability of OA ranges between about
43% at the knee
between 60% and 65% at the hip and hand

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 Osteo-arthritis (OA)
▪ Fibrocartilage is produced at the joint margin, which
undergoes endochondral ossification to form
osteophytes.
▪ Bone remodelling and cartilage thinning slowly alter
the shape of the OA joint, increasing its surface
area.

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 Osteo-arthritis (OA)
➢ Patients have higher BMD values at sites distant from the
joint.
➢ This is particularly related to osteophyte formation.

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 Osteo-arthritis (OA)
▪ Synovium undergoes variable degrees of
hyperplasia.
▪ Inflammatory changes may sometimes be observed.
▪ These are much lesser extent than in RA and other
inflammatory arthropathies.

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 Osteo-arthritis (OA)
Clinical features
The main presenting symptoms are:
• pain and functional restriction in a patient over the
age of 45
• but more often over 60 years.

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Osteo-arthritis (OA)
Clinical features
Causes of pain in OA may relate to:
i. increased pressure in subchondral bone (mainly causing night
pain)
ii. trabecular microfractures
iii. capsular distension
iv. low-grade synovitis
v. bursitis
vi. enthesopathy secondary to altered joint mechanics.

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Osteo-arthritis (OA)
Clinical features
Enthesopathy is a disorder of the entheses, which are the connective tissues
between bones and tendons or ligaments.
Enthesopathy occurs when these tissues have been damaged, due to
overuse, injury or infection.

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Osteo-arthritis (OA)
Clinical features
Enthesopathy is a disorder of the entheses, which are the connective tissues
between bones and tendons or ligaments.
Enthesopathy occurs when these tissues have been damaged, due to
overuse, injury or infection.

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Osteo-arthritis (OA)
Clinical features
▪ Functional restriction of the hands, knees or hips is
an equal, if not greater, problem than pain.
▪ The clinical findings vary according to severity but
are principally those of joint damage.

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Osteo-arthritis (OA)
Clinical features
▪ Pain and disability varies markedly according to site.
▪ It is stronger at the hip than the knee
▪ Poor at most small joints.
▪ Risk factors for pain and disability may differ from
those for structural change.

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Osteo-arthritis (OA)
Clinical features
At the knee, reduced quadriceps muscle strength and
adverse psychosocial factors (anxiety, depression)
correlate more strongly with pain and disability than the
degree of radiographic change.

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Osteo-arthritis (OA)
Clinical features
➢ Radiological evidence of OA is very common in
middle-aged and older people.
➢ Disease may coexist with other conditions, so it is
important to remember that pain in a patient with OA
may be due to another cause.

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Osteo-arthritis (OA)
Clinical features
➢ Radiological evidence of OA is very common in
middle-aged and older people.
➢ Disease may coexist with other conditions, so it is
important to remember that pain in a patient with OA
may be due to another cause.

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Osteo-arthritis (OA)
Clinical features
Generalised nodal OA
Characteristics of this common form
of OA are shown in Box 25.38.

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Osteo-arthritis (OA)
Clinical features
• Some patients are asymptomatic.
• Others develop pain, stiffness and swelling of one or
more PIP joints of the hands from the age of about 40
years onward. 2.5.24

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Osteo-arthritis (OA)
Clinical features
Gradually, these develop posterolateral swellings on
each side of the extensor tendon that slowly enlarge
and harden to become Heberden’s (DIP) and
Bouchard’s (PIP) nodes (Fig. 25.16).

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Osteo-arthritis (OA)
Clinical features
▪ Typically, each joint goes through a phase of episodic
symptoms (1–5 years) while the node evolves and OA
develops.
▪ Once OA is fully established, symptoms may subside
and hand function often remains good.

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Osteo-arthritis (OA)
Clinical features
Affected joints are enlarged as the result of osteophyte
formation and often show characteristic lateral
deviation, reflecting the asymmetric focal cartilage loss
of OA (Fig. 25.17).

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Osteo-arthritis (OA)
Clinical features
• Involvement of the first carpometacarpal joint (CMC)
is also common, leading to pain on trying to open
bottles and jars and functional impairment.
• Clinically, it may be detected by the presence of
crepitus on joint movement, and squaring of the
thumb base.

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Osteo-arthritis (OA)
Generalised nodal OA
Generalised nodal OA has a very strong genetic
component:
▪ Daughter of an affected mother has a 1 in 3 chance
of developing nodal OA herself.
▪ People with nodal OA are at increased risk of OA at
other sites, especially the knee.

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Osteo-arthritis (OA)
Knee OA
Principally targets the patello-femoral and medial
tibio-femoral compartments at this site but
eventually spreads to affect the whole of the joint
(Fig. 25.18).

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Osteo-arthritis (OA)
Knee OA
o It may be isolated or occur as part of generalised nodal OA.
o Most patients, particularly women, have bilateral and
symmetrical involvement.
o With men, trauma is a more important risk factor and may
result in unilateral OA.

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Osteo-arthritis (OA)
Knee OA
▪ Pain is usually localised to the anterior or medial
aspect of the knee and upper tibia.
▪ Patello-femoral pain is usually worse going up and
down stairs or inclines.

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Osteo-arthritis (OA)
Knee OA
• Posterior knee pain suggests the presence of a
complicating popliteal cyst (Baker’s cyst).
• Prolonged walking, rising from a chair, getting in or
out of a car, or bending to put on shoes and socks
may be difficult.

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Osteo-arthritis (OA)
Knee OA
• Posterior knee pain suggests the presence of a
complicating popliteal cyst (Baker’s cyst).
• Prolonged walking, rising from a chair, getting in or
out of a car, or bending to put on shoes and socks
may be difficult.

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Osteo-arthritis (OA)
Knee OA
Local examination findings may include:
• a jerky, asymmetric (antalgic) gait with less time
weight-bearing on the painful side
• a varus (Fig. 25.19), less commonly valgus, and/or
fixed flexion deformity

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Osteo-arthritis (OA)
Knee OA
▪ • tenderness of the upper medial tibia)
▪ • weakness and wasting of the quadriceps muscle
▪ • restricted flexion/extension with coarse crepitus
▪ • bony swelling around the joint line

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Osteo-arthritis (OA)
Hip OA
Most commonly targets the superior aspect
of the joint (Fig. 25.20).

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Osteo-arthritis (OA)
Hip OA
• Often unilateral at presentation
• Frequently progresses with superolateral
migration of the femoral head
• Poor prognosis

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Osteo-arthritis (OA)
Hip OA
• Lateral hip pain, worse on lying on that side with tenderness
over the greater trochanter, suggests secondary trochanteric
bursitis.
• Common functional difficulties are the same as for knee OA.
• Restricted hip abduction in women may cause pain on
intercourse.

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Osteo-arthritis (OA)
Hip OA
Examination may reveal:
• • an antalgic gait
• • weakness and wasting of quadriceps and gluteal muscles
• • pain and restriction of internal rotation with the hip flexed –
the earliest and most sensitive sign of hip OA
• other movements may subsequently be restricted and painful

P
an antalgic gait an abnormal pattern of
walking secondary to pain that ultimately
causes a limp, whereby the stance phase is
shortened relative to the swing phase.
Osteo-arthritis (OA)
Hip OA
Examination may reveal:
• • an antalgic gait
• • weakness and wasting of quadriceps and gluteal muscles
• • pain and restriction of internal rotation with the hip flexed –
the earliest and most sensitive sign of hip OA
• other movements may subsequently be restricted and painful

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Osteo-arthritis (OA)
Hip OA
• anterior groin tenderness just lateral to the femoral pulse
• fixed flexion, external rotation deformity of the hip
• ipsilateral leg shortening with severe joint attrition and
superior femoral migration
Although obesity is not a major risk factor for development of
hip OA, it is associated with more rapid progression.

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Osteo-arthritis (OA)
Spine OA
The cervical and lumbar spine are predominantly
targeted by OA, then referred to as cervical
spondylosis and lumbar spondylosis, respectively
(Fig. 25.21).

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Osteo-arthritis (OA)
Spine OA
• May occur in isolation or as part of generalised OA.
• Typical presentation is with pain localised to the low back
region or the neck, although radiation of pain to the arms,
buttocks and legs may also occur due to nerve root
compression.
• Pain is typically relieved by rest and worse on movement.

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Osteo-arthritis (OA)
Spine OA
• May occur in isolation or as part of generalised OA.
• Typical presentation is with pain localised to the low back
region or the neck, although radiation of pain to the arms,
buttocks and legs may also occur due to nerve root
compression.
• Pain is typically relieved by rest and worse on movement.

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Osteo-arthritis (OA)
Spine OA
On physical examination
• Range of movement may be limited and loss of lumbar
lordosis is typical.
• Straight leg-raising test or femoral stretch test may be
positive
• Neurological signs may be seen in the legs where there is
complicating spinal stenosis or nerve root compression.

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Osteo-arthritis (OA)
• Early-onset of OA is unusual.
• Typical symptoms and signs of OA may present before the
age of 45.
• In most cases, a single joint is affected and there is a clear
history of previous trauma.
• Specific causes of OA need to be considered in people with
early-onset disease affecting several joints, especially those
not normally targeted by OA, rare causes need to be
considered (Box 25.39).

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Osteo-arthritis (OA)
Kashin– Beck disease
• A rare form of OA that occurs in children, typically between the ages of 7
and 13, in some regions of China.
• Cause is unknown but suggested predisposing factors are selenium
deficiency and contamination of cereals with mycotoxin-producing fungi.
Erosive OA
• This term is used to describe rare patients with hand OA who have a
more prolonged symptom phase, more overt inflammation, more
disability and worse outcome than those with nodal OA.

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Osteo-arthritis (OA)
A plain X-ray of the affected joint should be
performed and often this will show one or more of
the typical features of OA (see Figs 25.17–25.21).

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Osteo-arthritis (OA)
• In addition to providing diagnostic information, X-rays
are used to assess the severity of structural change,
which is useful if joint replacement surgery is being
considered.
• Non-weightbearing postero-anterior views of the
pelvis are adequate for assessing hip OA.

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Osteo-arthritis (OA)
• Patients with suspected knee OA should have standing
antero-posterior radiographs taken to assess tibio-femoral
cartilage loss, and a flexed skyline view to assess patello-
femoral involvement.
• Spine OA can often be diagnosed on plain X-ray, which
typically shows evidence of disc space narrowing and
osteophytes. If nerve root compression or spinal stenosis is
suspected, MRI should be performed.

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Osteo-arthritis (OA)
• Routine biochemistry, haematology and autoantibody
tests are usually normal.
• Synovial fluid aspirated from an affected joint is
viscous with a low cell count.

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Osteo-arthritis (OA)
Unexplained early-onset OA requires additional
investigation, guided by the suspected underlying
condition.

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Osteo-arthritis (OA)
Management
• Treatment follows the principles outlined in Box 25.40.
• Measures that are pertinent in older people are
summarised in Box 25.41.

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Osteo-arthritis (OA)
Education and other general measures
• It is important to explain the nature of the condition fully,
outlining the role of relevant risk factors (obesity, heredity,
trauma) and the fact that established structural changes are
permanent but that pain and function can improve.

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Osteo-arthritis (OA)
Prognosis
The prognosis should also be discussed (good for nodal
hand OA, more optimistic for knee than hip OA), as
should how appropriate action can improve the
prognosis of large-joint OA.

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Osteo-arthritis (OA)
Exercise
• Has beneficial effects in OA, including both strengthening and aerobic
exercise, preferably with reinforcement by a physiotherapist (see Box
25.30).
• Quadriceps strengthening exercises are particularly beneficial in knee
OA.
• Weight loss can have a substantial beneficial effect on symptoms if the
patient is obese and is probably one of the most effective treatments for
reducing pain, particularly in OA of the lower limbs.

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Osteo-arthritis (OA)
• Shock-absorbing footwear
• Pacing of activities
• Use of a walking stick for painful knee or hip OA
• Provision of built-up shoes to equalise leg lengths
can all improve symptoms.

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Osteo-arthritis (OA)
Analgesics and anti-inflammatory drugs
• If symptoms do not respond to non-pharmacological
measures, paracetamol should be given.
• Addition of a topical NSAID, and then capsaicin, for knee and
hand OA can also be helpful.

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Osteo-arthritis (OA)
• Oral NSAID should be considered in patients who remain
symptomatic.
• These drugs are significantly more effective than
paracetamol and can be successfully combined with
paracetamol or compound analgesics such as co-codamol if
the pain is severe.
• Opiates may occasionally be required. For temporary benefit
of moderate to severe pain, intra-articular injection of
corticosteroids can be helpful.

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Osteo-arthritis (OA)
• Local physical therapies such as heat or cold can
sometimes give temporary relief.
• Acupuncture and transcutaneous electrical nerve
stimulation (TENS) have also been shown to be
effective in knee OA.

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Osteo-arthritis (OA)
• Antineuropathic drugs, such as amitriptyline, gabapentin and
pregabalin, are sometimes used in patients with symptoms
that are difficult to control, but the evidence base for their
use is poor.
• Corticosteroid injections Intra-articular corticosteroid
injections are effective in the treatment of knee OA and are
also used for symptomatic relief in the treatment of OA at the
first CMC (carpo-metacarpel) joint.

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Osteo-arthritis (OA)
Surgery
• Surgery should be considered for patients with OA
whose pain, stiffness and reduced function impact
significantly on their quality of life and are refractory
to other treatments.
• Osteotomy can prolong the life of malaligned joints
and relieve pain by reducing intraosseous pressure,
but is performed infrequently.

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Osteo-arthritis (OA)
Surgery
• Total joint replacement surgery is by far the most
common surgical procedure for patients with OA.
• It can transform the quality of life for people with
severe knee or hip OA and is indicated when there is
significant structural damage on X-ray, and pain and
functional impairment are limiting quality of life
despite the use of medical therapy.

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Osteo-arthritis (OA)
Surgery
• Although surgery should not be undertaken at an early stage
during the development of OA, it is important to consider it
before functional limitation has become advanced since this
may compromise the surgical outcome.
• Patient-specific factors, such as age, gender, smoking and
presence of obesity, should not be barriers to referral for
joint replacement.

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Osteo-arthritis (OA)
Surgery
Only a small proportion of patients with OA progress to
the extent that total joint replacement is required, but
OA is by far the most frequent indication for a total joint
replacement.

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 Osteo-arthritis (OA)
Surgery
Over 95% of joint replacements continue to function
well into the second decade after surgery and most
provide life-long, pain-free function. However, some
20% of patients are not satisfied with the outcome, and
a few experience little or no improvement in pain.

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 Osteo-arthritis (OA)
Surgery
Over 95% of joint replacements continue to function
well into the second decade after surgery and most
provide life-long, pain-free function. However, some
20% of patients are not satisfied with the outcome, and
a few experience little or no improvement in pain.

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 CRYSTAL-INDUCED ARTHRITIS
A variety of crystals can deposit in and around
joints and cause an acute inflammatory arthritis,
as well as a more chronic arthritis associated
with progressive joint damage.

P
 GOUT

SAM RUFUS STORY

p
 GOUT
An inflammatory disease caused by
deposition of monosodium urate
monohydrate crystals in and around synovial
joints.

P
 GOUT
Epidemiology
• The prevalence of gout varies between populations.
• Approximately 1–2%, with a greater than 5:1 male
preponderance.
• Most common inflammatory arthritis in men and in
older women.

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 GOUT
Epidemiology
• Risk of developing gout increases with age and with serum
uric acid (SUA) levels, which are normally distributed in the
general population.
• Levels are higher in men, increase with age and are
associated with body weight.
• Levels are higher in some ethnic groups (such as Maoris and
Pacific islanders).

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 GOUT
• Hyperuricaemia is defined as an SUA level greater
than 2 standard deviations above the mean for the
population.
• More common over recent years in parallel with
increased longevity and the higher prevalence of
metabolic syndrome, of which hyperuricaemia is an
integral component.

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 GOUT
• Hyperuricaemia is defined as an SUA level greater
than 2 standard deviations above the mean for the
population.
• More common over recent years in parallel with
increased longevity and the higher prevalence of
metabolic syndrome, of which hyperuricaemia is an
integral component.

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 GOUT
Hyperuricaemia is an independent risk factor for:
• Hypertension
• vascular disease
• renal disease
• cardiovascular events

P
 GOUT
• Only a minority of hyperuricaemic people develop
gout.
• No evidence to support the use of urate-lowering
therapy in patients with asymptomatic
hyperuricaemia.

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 GOUT
Pathophysiology
• About one-third of the body uric acid pool is derived from
dietary sources and two-thirds from endogenous purine
metabolism (Fig. 25.23).
• The concentration of uric acid in body fluids depends on the
balance between endogenous synthesis, and elimination by
the kidneys (two-thirds) and gut (one-third).

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 GOUT
Pathophysiology
The causes of hyperuricaemia are shown in
Box 25.43.

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 GOUT
Pathophysiology
• Over 90% of patients, the main abnormality is reduced uric
acid excretion by the renal tubules, which impairs the body’s
ability to respond to a purine load.
• In many cases, this is genetically determined and recent
studies have identified polymorphisms in several genes that
are associated with gout, the most important of which is
SLC2A9, which regulates urate excretion by the kidney.

P
 GOUT
Pathophysiology
Impaired renal excretion of urate also accounts for the
occurrence of hyperuricaemia in chronic renal failure,
and for the association between hyperuricaemia and
treatment with thiazide diuretics.

P
 GOUT
Risk factors:
• Metabolic syndrome
• High alcohol intake (beer, which contains guanosine)
• Generalised osteoarthritis
• Diet relatively high in red meat or fructose
• Relatively low in vitamin C or coffee
• Lead poisoning (saturnine gout)

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 GOUT
• Association between OA and gout is thought to be due to
reduction in levels of inhibitors of crystal formation in
osteoarthritic cartilage, predisposing to crystal formation.
• Some patients develop gout because they overproduce uric
acid.
• Mechanisms are poorly understood, except in the case of a
few rare disorders, in which gout is inherited.

P
 GOUT
Severe hyperuricaemia can also occur in patients with
leukaemia undergoing chemotherapy due to increased
purine turnover.

P
 GOUT
Clinical features
The classical presentation is with an acute mono-
arthritis, which in over 50% of cases affects the first
MTP joint (Fig. 25.24).

P
 GOUT
Clinical features
Other common sites are:
Ankle Midfoot
Knee Small joints of hands
Wrist Elbow
The axial skeleton and large proximal joints are rarely involved.

P
 GOUT
Clinical features
Other common sites are:
Ankle Midfoot
Knee Small joints of hands
Wrist Elbow
The axial skeleton and large proximal joints are rarely involved.

P
 GOUT
Typical clinical features
• Rapid onset
• Reaching maximum severity in 2–6 hours
• Often waking the patient in the early morning
• Severe pain, often described as the ‘worst pain ever’

P
 GOUT
Typical clinical features
• Extreme tenderness
• Unable to wear a sock or to let bedding rest on the
joint
• Marked swelling with overlying red, shiny skin
• Self-limiting over 5–14 days, with complete resolution

P
 GOUT
Typical clinical features
• Joint shows signs of marked synovitis, swelling and
erythema.
• Accompanying fever, malaise and even confusion, especially
if a large joint such as the knee is involved.
• As the attack subsides, pruritus and desquamation of
overlying skin are common.
(Peeling skin (desquamation) occurs when the top layer of skin peels to

P replace itself.)
 GOUT
Typical clinical features
• Joint shows signs of marked synovitis, swelling and
erythema.
• Accompanying fever, malaise and even confusion, especially
if a large joint such as the knee is involved.
• As the attack subsides, pruritus and desquamation of
overlying skin are common.
(Peeling skin (desquamation) occurs when the top layer of skin peels to

P replace itself.)
 GOUT
• Main differential diagnosis is septic arthritis, infective
cellulitis or reactive arthritis.
• Acute attacks may also manifest as bursitis,
tenosynovitis or cellulitis, which have the same
clinical characteristics.
• Many patients describe milder episodes lasting just a
few days.

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 GOUT
• Some have attacks in more than one joint.
• Others have further attacks in other joints a few days
later (cluster attacks), the first possibly acting as a
trigger.
• Simultaneous polyarticular attacks are unusual.
Some people never have a second episode after an
acute attack.

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 GOUT
• In others, several years may elapse before the next
attack.
• In many, however, a second attack occurs within 1
year
• May progress to chronic gout, with chronic pain and
joint damage
• Occasionally severe deformity and functional
impairment.
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 GOUT
• Patients with uncontrolled hyperuricaemia who suffer
multiple attacks of acute gout may also progress to chronic
gout.
• Crystals may be deposited in the joints and soft tissues to
produce irregular firm nodules called tophi.
• These have a predilection for the extensor surfaces of
fingers, hands, forearm, elbows, Achilles tendons and
sometimes the helix of the ear.

P
 GOUT
• Tophi have a white colour, differentiating them from
rheumatoid nodules (Fig. 25.25).
• Tophi can ulcerate, discharging white gritty material
• Become infected or induce a local inflammatory
response
• With erythema and pus in the absence of secondary
infection.

P
 GOUT
• Usually a feature of long-standing gout but can
sometimes develop within 12 months in patients with
chronic renal failure.
• Occasionally, tophi may develop in the absence of
previous acute attacks, especially in patients on
thiazide therapy who have coexisting OA.

P
 GOUT
• In addition to causing musculoskeletal disease, chronic
hyperuricaemia may be complicated by renal stone formation
• If severe, renal impairment due to the development of
interstitial nephritis as the result of urate deposition in the
kidney.
• This is particularly common in patients with chronic
tophaceous gout who are on diuretic therapy.

P
 GOUT
Investigations:
• Diagnosis of gout can be confirmed by the
identification of urate crystals in the aspirate from a
joint, bursa or tophus.
• In acute gout, synovial fluid shows increased
turbidity due to the greatly elevated cell count (> 90%
neutrophils).

P
 GOUT
• In chronic gout, the appearance is more variable but
occasionally the fluid appears white due to the high
crystal load.
• Between attacks, aspiration of an asymptomatic first
MTP joint or knee may still reveal crystals.

P
 GOUT
Biochemical screen-
• Renal function
• Uric acid level
• Glucose
• Lipid profile
Although hyperuricaemia is usually present, this does not
confirm the diagnosis.

P
 GOUT
Biochemical screen-
• Renal function
• Uric acid level
• Glucose
• Lipid profile
Although hyperuricaemia is usually present, this does not
confirm the diagnosis.

P
 GOUT
• Normal uric acid levels during an attack do not
exclude gout, as serum urate falls during the acute
phase response.
• Elevated ESR and CRP and a neutrophilia are typical
of acute gout, and they return to normal as the attack
subsides.
• Tophaceous gout may be accompanied by a modest
but chronic elevation in ESR and CRP.

P
 GOUT
• Radiographs are usually normal in acute gout but
well-demarcated erosions may be seen in patients
with chronic or tophaceous gout (Fig. 25.26).
• Tophi may also be visible on X-rays as soft tissue
swellings.
• In late disease, destructive changes may occur
similar to those in other forms of advanced
inflammatory arthritis.

P
 GOUT
Management
• Oral NSAIDs are effective for pain relief in the acute attack
and are the standard treatment, but have to be prescribed
with caution in old age.
• Local ice packs can also be used for symptomatic relief.
• Patients with recurrent episodes can keep a supply of an
NSAID and take it as soon as the first symptoms occur,
continuing until the attack resolves.

P
 GOUT
Management
• Oral colchicine, which works by inhibiting microtubule
assembly in neutrophils, is also very effective.
• Usually given in doses of 0.5 mg twice or 3 times daily.
• Most common adverse effects are nausea, vomiting and
diarrhoea.
• Joint aspiration can give pain relief, and may be combined
with an intraarticular steroid injection if the diagnosis is clear
and infection can be excluded.
P
 GOUT
Management
• Short course of oral or intramuscular corticosteroids
can also be highly effective in treating acute attacks.
• Patients who have more than one acute attack within
12 months and those with complications should be
offered urate-lowering therapy (Box 25.44).

P
 GOUT
Management
• Long-term therapeutic aim is to prevent attacks
occurring by bringing uric acid levels below the level
at which monosodium urate monohydrate crystals
form.
• A therapeutic target of 360 µmol/L (6 mg/dL) is
recommended.

P
 GOUT
Management
• Allopurinol is the drug of first choice.
• Recommended starting dose is 100 mg daily, or 50 mg in
older patients and in renal impairment.
• Dose of allopurinol should be increased by 100 mg every 4
weeks (50 mg in the elderly and those with renal impairment)
until the target uric acid level is achieved, side-effects occur
or the maximum recommended dose is reached (900
mg/day).
P
 GOUT
Management
• Acute flares of gout often occur following initiation of
urate-lowering therapy. The patient should be warned
about this and told to continue therapy, even if an
attack occurs.
• The risk of flares can be reduced by administration of
oral colchicine (0.5 mg twice daily) or NSAID therapy
for the first few months.
P
 GOUT
Management
• In the longer term, annual monitoring of uric acid
levels is recommended.
• In most patients, urate-lowering therapy needs to be
continued indefinitely.

P
 GOUT
Management
• Febuxostat is a xanthine oxidase inhibitor that is useful in
patients who fail to respond adequately to allopurinol, and
those in whom it is contraindicated or has been poorly
tolerated.
• It undergoes hepatic metabolism and so no dose adjustment
is required for renal impairment. It is more effective than
allopurinol at reducing uric acid levels and, as a result,
commonly provokes attacks at the recommended starting

P dose (80 mg daily).

 GOUT
Management
• Uricosuric drugs, such as probenecid or sulfinpyrazone, can
be effective but require several doses each day and
maintenance of a high urine flow to avoid uric acid
crystallisation in renal tubules.
• Salicylates antagonise the uricosuric action of these drugs
and should be avoided.
• Uricosurics are contraindicated in overproducers, those with
renal impairment and in urolithiasis (they increase stone
P formation).
 GOUT
Management
• Patients should be advised to lose
weight where appropriate and to
reduce excessive alcohol intake,
especially beer.
• Thiazide diuretics should be
stopped if possible

P
 GOUT
Management
Patients should be advised to avoid large amounts of
seafood and offal, which have a high purine content, but
a highly restrictive diet is not necessary.

SAM RUFUS STORY

P
Thank
you
Dr. Prafulla C. Deka