Preview: Originally Published in Therapeutic Guidelines: Rheumatology, Version 2, 2010

Originally published in
Therapeutic Guidelines: Rheumatology, version 2, 2010
Gout
Clinical presentations
Acute gout
Subacute gout
Chronic gout
Asymptomatic hyperuricaemia
Pathogenesis
Initial assessment
Management
Acute gout
Chronic gout
Copyright 2010 Therapeutic Guidelines Limited Ground Floor, 473 Victoria Street West Melbourne 3003
Preview
version
The complete topic
(8 pages) covers all
the points listed on
the left.
You can view
2sample pages for
free to get an idea
of the scope of the
information you
will receive if you
purchase the topic.
Patients who are in a catabolic state (eg septic) or are dehydrated are at
an increased risk of developing an acute gout attack. This often occurs
during or immediately following a period of hospitalisation.
Subacute gout
Subsequent attacks can involve more joints and have more systemic
features, including fever. These attacks may be of limited severity and
may be separated by long intervals of relatively normal joint function.
Many may not be recognised as gouty attacks, but be presumed to be
due to sprains or other nonarticular (soft tissue) injuries.
Chronic gout
Eventually, recurrent attacks may fail to resolve completely and slowly
lead to a crippling destructive arthritis. Chronic gout may be oligo- or
polyarticular. Gouty tophi are frequently seen at this stage, and are
usually present on the elbows (olecranon bursae), knees (prepatellar
bursae) and peripheral joints such as the toes and fingers.
The symmetrical involvement of the small joints of both hands can
mimic rheumatoid arthritis or psoriatic arthritis. Complicating this
latter situation is the fact that elevated uric acid levels are common in
psoriasis due to increased cell turnover.
Asymptomatic hyperuricaemia
In adults, hyperuricaemia is arbitrarily defined as plasma urate
concentration greater than 0.42 mmol/L for males and 0.36 mmol/L
for females. The prevalence of hyperuricaemia in white males is 5%
to 8%, and is much higher in people of Maori or Pacific Island origin.
Asymptomatic hyperuricaemia may be present from birth in those with
an enzyme deficiency, but otherwise tends to occur in at-risk males from
puberty onwards, and in females after menopause. It may be present for
the life of the individual or lead to an attack of gout or manifestations
of nephrolithiasis.
Sample Page
As gout is rare in children, a diagnosis of gout as the cause of an acutely

inflamed joint in a child is not tenable, unless the individual has a
genetic defect in urate metabolism.
Sample Page (Page 4 of 8)
The patient with suspected gout should have:

plasma urate assay, which may be normal in acute gout
aspiration of an affected joint, bursa or tophus, which is necessary
to obtain a firm diagnosis by detection of urate crystals using
compensated polarised light microscopy because this has
important implications for long-term treatment
a search for secondary causes, including impaired renal clearance
of urate (eg chronic renal disease) and increased cell turnover
(consider underlying malignancy, such as a myeloproliferative
disease) as appropriate.
MANAGEMENT
The management of gout involves providing rapid pain relief for acute
attacks, preventing further attacks, and preventing the complications
of gout such as the formation of gouty tophi and destructive arthritis.
It is important that the health practitioner also manages associated
medical conditions such as excessive alcohol intake, hyperlipidaemia,
hypertension, obesity and glucose intolerance/insulin resistance.
Patient education about the need for therapy, if alcohol and dietary
modification fail to bring about a normal plasma urate, is pivotal to
the management. The emphasis should be on lifelong therapy and
maintaining adherence. The book Getting Rid of Gout may be a useful
adjunct.*
Acute gout
Initially, gout may subside spontaneously in less than a week, but the
patient will usually seek help. The acute treatment should focus on
reducing inflammation and usually has no effect on modifying the
plasma urate concentration. Nonsteroidal anti-inflammatory drugs
(NSAIDs) at the maximum recommended doses reduce inflammation
and pain relatively quickly. An attack will be aborted using:
1
an NSAID orally, at the upper dosing range until symptoms abate

(typically 3 to 5 days), then reduce the dose until signs of joint
inflammation have abated, and then cease (see Table 1, p.5)
OR
* Emmerson B. Getting rid of gout. 2nd ed. Melbourne: Oxford University Press; 2003.
Gout
Therapeutic Guidelines: Rheumatology
Sample Page
Sample Page (Page 2 of 8)

Preview: Originally Published in Therapeutic Guidelines: Rheumatology, Version 2, 2010

Uploaded by

Copyright:

Available Formats

Preview: Originally Published in Therapeutic Guidelines: Rheumatology, Version 2, 2010

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Preview: Originally Published in Therapeutic Guidelines: Rheumatology, Version 2, 2010

Uploaded by

Copyright:

Available Formats

Originally published in

Therapeutic Guidelines: Rheumatology, version 2, 2010

As gout is rare in children, a diagnosis of gout as the cause of an acutely

Sample Page (Page 4 of 8)

The patient with suspected gout should have:

an NSAID orally, at the upper dosing range until symptoms abate

Therapeutic Guidelines: Rheumatology

Sample Page (Page 2 of 8)

You might also like