Management of acute and recurrent gout in general practitioner settings

1. Prepared by: Dr. Ahmed Ibrahim Eldesouky Abouelela
Family Medicine Registrar
MMBch, Family Medicine Master degree, MRCGP.int

2. 38 years old male patient with no medical
history presents to your clinic with an
extremely painful and swollen right foot,
which developed over the past 2 days. He has
limited mobility and has just started taking an
over-the-counter non-steroidal anti-
inflammatory drug (NSAID) but has had little
improvement.

3. What relevant questions should
you ask for history taking?

4. History of trauma?
Is this the first time to have such attack?
Analysis of the pain? SOCRATES
Associated constitutional symptoms?
Any gastrointestinal or genitourinary
symptoms, or any recent sexual exposures?
Any conjunctivitis or urethritis?
Any new rash?

5. Does he immunosuppressed?
Has he had any recent surgery/procedures?
Are there any other risk factors such as travel,
alcohol and intravenous drug use?
History of psoriasis or any rheumatic disease?
Family history of psoriasis or any rheumatic
disease?

6. The patient has not had any fevers and there
are no obvious infective foci. He has had
recurrent pain in his right big toe (first
metatarsophalangeal [MTP] joint) in the past 5
years. He has never sought medical attention
for this pain as it generally settles in a few
days. He has no personal or family history of
psoriasis or any autoimmune conditions. He
has a sedentary lifestyle and has been steadily
gaining weight over the past few years.

7. What are the keys aspects of
examination to focus on?

8. Is the patient clinically and vitally stable.
Does the patient in pain or he needs any
painkiller.
Identify whether the pain is from the bone,
joint or soft tissue.
Look, Feel and Move.

9. Warmth and tenderness over the joints
Palpation for soft tissue swelling
Establish the presence of an effusion
Joints assessment for range of motion
Mechanical or degenerative pathology

10.  Enthesitis/dactylitis suggestive of a seronegative
spondyloarthropathy.
 Conjunctivitis, anterior uveitis, episcleritis and
corneal ulcers can be seen in reactive arthritis.
 Skin lesions such as keratoderma blennorrhagica
and erythema nodosum are associated with
reactive arthritis.
 Psoriatic nail changes: nail pits, onycholysis, nail
bed hyperkeratosis points to the possibility of
psoriatic arthritis.

15. On examination, he is well and afebrile. His
body mass index (BMI) is 31 kg/m2. He has a
swollen tender first [MTP] joint with restricted
range of movement due to the pain. There is no
evidence of tophi elsewhere.

16. What are the differential
diagnoses for the patient
symptoms?
What is the most likely cause of
his symptoms?

17.  Crystal arthropathy: gout, pseudogout and
calcium oxalate crystals
 Septic arthritis: Gonococcal infection / Non –
gonococcal infection
 Osteoarthritis
 Monoarthritis as an initial presentation of a
systemic rheumatic condition: Rheumatoid
arthritis, Psoriatic arthritis, reactive arthritis and
inflammatory arthropathy associated with
inflammatory bowel disease

18. In this case, gout is high on the list of
differentials given. Septic arthritis and reactive
arthritis are less likely given the absence of risk
factors but need to be considered

19.  One of the most common forms of inflammatory arthritis.
 Caused by accumulation of excess urate crystals
(monosodium urate) in joint fluid, cartilage, bones,
tendons, bursas, and other sites.
 Patients experience joint swelling and pain during gout
attacks, known as acute gouty arthritis.
 In some patients, the frequency and duration of acute
attacks increase over time and lead to chronic gout, which
may be associated with deposits of uric acid crystals
known as tophi.
 Risk factors for gout include overweight or obesity;
hypertension; alcohol intake; diuretic use; a diet rich in
meat, seafood, and high-fructose food or drinks; and poor
kidney function.

20. How would you investigate the
patient symptoms?

21. The key investigation required to confirm the
diagnosis of gout and to exclude septic arthritis
is joint aspiration for microscopy/culture and
sensitivity, cell count and differential and
crystal analysis

22.  It should be noted that crystal arthropathy can present
in an identical manner to septic arthritis and cannot be
reliably distinguished clinically or by WCC counts,
raised ESR and CRP, or synovial WCC counts.
 Differentiating between the two conditions is
imperative as management is very different and
failure to identify septic arthritis result in rapid,
irreversible joint damage.
 If there is a high clinical suspicion for septic arthritis
the patient should have joint aspiration and then be
given IV antibiotics until septic arthritis is excluded or
confirmed through microbiological testing for
cultures.

23. Full blood evaluation (FBE), electrolytes, liver
function tests (LFTs)
Erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP) levels
Serum uric acid: it may be normal in up to 50%
of patients during an acute episode of gout
Blood cultures: if an infective cause is
suspected
Radiographs to assess if there are gouty
erosions

24. What is the management plan for
this patient?

25. Control the pain, reduce the swelling and
enhance the movement.
Health education for the condition and the
possible differential diagnosis.
Red flags and dangerous signs awareness and
initiating safety netting.
Follow – up with the result of investigations
and further evaluation.

26. Reducing inflammation and pain is the focus of
gout management in the acute setting.
Drugs used to treat an episode of acute gout
include NSAIDs, glucocorticoids, colchicine
and animal-derived corticotropin.

27. Recommendation 1:ACP recommends that
clinicians choose corticosteroids, non –
steroidal anti-inflammatory drugs (NSAIDs),
or colchicine to treat patients with acute gout.
(Grade: strong recommendation, high-
quality evidence).

28. NSAIDs are very effective and, in the absence
of contraindications, they reduce symptoms
rapidly.
Particularly when given in the upper dosing
range and initiated early.
All NSAIDs, including cyclooxygenase-2
(COX-2) inhibitors, are effective in acute gout.

29. Intra-articular steroid injection is an effective
option for relieving the symptoms.
Oral corticosteroids can be considered.
The current Australian Therapeutic
Guidelines recommend prednisolone at doses
of 15–20 mg daily, typically for 3–5 days,
Then be weaned to cessation over 2 weeks.

30.  Colchicine can also be effective in the acute
setting.
 Guidelines recommend that patients be
commenced on 1 mg of colchicine, followed by
500 μg 1 hour later.
 No further colchicine is to be taken for 72 hours.
 There is no benefit in administering higher doses.
 Colchicine must be used carefully in people with
renal impairment.
 Increasingly, colchicine is used for prophylaxis
against flares of gout as urate-lowering therapy is
introduced.

31. Recommendation 2:ACP recommends that
clinicians use low-dose colchicine when using
colchicine to treat acute gout.
(Grade: strong recommendation, moderate-
quality evidence)

32. Initial blood tests reveal leukocytosis with
neutrophilia. Kidney and liver function tests
are within range and blood cultures are
negative.
ESR: 26 mm/hour.
CRP: 17 mg/L.
Serum uric acid: 0.56 mmol/L.
X-ray of his right foot shows erosion at his first
MTP joint.

33. Referral the patient to a rheumatologist for
further management of suspected gout. A joint
aspirate found to have a white cell count
(WCC) of 51,000 x 106/L; 70% of this
represents polymorphs. Needle – shaped
intracellular and extracellular crystals that
exhibit negative birefringence are seen. Testing
for microbial cultures remains negative.

34. Normal Non-
inflammatory
Inflammatory
(crystalline)
Inflammatory
(non-
crystalline)
Septic
(gonococcal)
Septic
(non-
gonococcal)
Transparency Transparent Transparent Translucent –
opaque
Translucent –
opaque
Opaque Opaque
Color Clear Straw Yellow Yellow Yellow–green Yellow–green
Viscosity High High Low Low Variable Variable
White cell
Count
<200 x 106/L 200–2000 x
106/L
2000–100,000 x
106/L
2000–100,000 x
106/L
34,000–68,000
x
106/L
>50,000 x
106/L
(>100,000 x
106/L is
more specific)
Polymorph
Cell count (%)
<25 <25 ≥50 ≥50 ≥75 ≥75
Gram stain Negative Negative Negative Negative Variable
(<50%)
Positive (60–
80%)
Culture Negative Negative Negative Negative Positive (25–
70%)
Positive
(>90%)
Crystals Negative Negative Positive Negative Negative Negative

35. The patient asks you whether
anything needs to be done to
prevent his gout from recurring.
How would you advise him?

36. Preventive interventions should include non-
pharmacological and pharmacological
strategies.

37. Weight reduction is important for management.
Referral to a dietitian should be considered for
target patients.
Good control hypertension if present.
Avoid alcohol intake and diuretic use.
Avoid diet rich in meat, seafood, and high-
fructose food or drinks.

38. Evidence was insufficient for gout-specific
dietary advice or therapies (such as reduced
intake of red meat, fructose, and alcohol) to
improve symptomatic outcomes.
Lifestyle changes alone are unlikely to be
sufficient in achieving the target SUA.
It is well documented that lifestyle changes
alone rarely lead to more than 10–18%
reduction in serum urate.

39. The main aim is to achieve a sustained level of
serum urate below the threshold for saturation
of urate, which will promote spontaneous
dissolution of monosodium urate crystals to
prevent further attacks, joint/bone damage and
deposition of tophi in other tissues and organs.
 Urate-lowering therapy does not reduce the
risk for acute gout attacks in the first 6 months
in patients with gout.

40.  Recommendation 3:ACP recommends against
initiating long-term urate-lowering therapy in most
patients after a first gout attack or in patients with
infrequent attacks.
(Grade: strong recommendation, moderate-quality
evidence)
 Recommendation 4:ACP recommends that clinicians
discuss benefits, harms, costs, and individual
preferences with patients before initiating urate-
lowering therapy, including concomitant prophylaxis, in
patients with recurrent gout attacks.
(Grade: strong recommendation, moderate-quality
evidence)

41. Two strategies are present for urate-lowering
therapy
First: monitoring serum urate levels and
targeting therapy to achieve a specific urate
level (treat to target) reduces acute gout attacks
and subsequent joint damage.
Second: bases the intensity of urate-lowering
treatment on the goal of avoiding recurrent
gout attacks (“treat to avoid symptoms”), with
no monitoring of urate levels.

42.  American college of physician (ACP) does not recommend
against a "treat-to-target approach" but advised that there is
insufficient evidence to determine whether the benefits of
increase urate – lowering therapy to reach a target uric acid
level exceed the harms associated with repeated monitoring
and increased medication.
 American College of Rheumatology (ACR) guideline in
2012 recommends a target serum urate level below 6 mg/dL
(357 µmol/L) at a minimum, with some patients faring
better when the serum urate level is below 5 mg/dL (297
µmol/L).
 European League Against Rheumatism (EULAR)
guideline released in 2016 includes the same
recommendation.
 The current Australian Therapeutic Guidelines
recommend lowering SUA levels to ≤0.3 mmol/L.

43.  Allopurinol, a hypouricaemic drug, remains the
first-line treatment for lowering serum urate.
 Allopurinol should be prescribed at a starting dose
of 100 mg daily (in patients with renal
impairment, the initial dose should be 50 mg daily
or less).
 The dose can be titrated up every 4 weeks in
increments of 100 mg (or 50 mg for patients with
renal impairment) until the target SUA level is
reached.

44. Failure to titrate the dose of allopurinol to
achieve the target SUA level results in the poor
management of a treatable condition.
Most prescriptions are for 300 mg daily or less.
However, it has been shown that only 21% of
patients achieved an SUA <0.36 mmol/L on a
dose of 300 mg/day.

45. Alternatives to allopurinol, for patients who are
allergic to, or intolerant of, allopurinol, include
probenecid.
Probenecid can be used in patients with
adequate renal function.
Febuxostat can be considered in allopurinol
intolerant patients with poor renal function.

46. The rheumatologist started the patient on
allopurinol 100 mg daily in conjunction with
low-dose colchicine 500 μg daily to reduce the
risk of a gout flare triggered by the
introduction of allopurinol.
The increased risk of gout flares associated
with the introduction of allopurinol is due to
monosodium urate shedding into the joint
synovial fluid as the serum urate level
decreases.

47.  The rheumatologist provides recommendations to
increase his allopurinol dose in increments of 100
mg per month until the SUA target is reached.
 The rheumatologist also advises that colchicines
be continued until he has been free of gout for 1–3
months on the therapeutic dose of allopurinol (ie
the dose at which the SUA target has been
achieved).
 The rheumatologist advises the patient to follow
up with his GP.

48. What will you do with the
patient in his follow – up visits?

49. Assess and reinforce compliance to allopurinol.
Provide advice for lifestyle changes.
Monitor SUA levels and adjust the dose of
allopurinol if required.
Arrange monthly FBE, kidney function tests
and LFTs to monitor for adverse effects until
stable, after which the frequency of monitoring
can be decreased.

50.  The Gout and Uric Acid Education Society has an
interactive quiz on gout, patient education kit and a video
library, www.gouteducation.org
 Arthritis Australia provides general disease and treatment
information, and support services,
www.arthritisaustralia.com.au/images/stories/
documents/info_sheets/2015/Condition%20specific/Gout.pd
f; www.
arthritisaustralia.com.au/images/stories/documents/info_she
ets/2015/ General%20management/Goutanddiet.pdf
 The American College of Rheumatology,
www.rheumatology.org/practice/
clinical/patients/diseases_and_conditions/gout.asp
 National Institute of Arthritis and Musculoskeletal and
Skin Diseases, www.niams.nih.gov

51.  Rheumatology Expert Group. Crystal deposition
disease. Gout. In Therapeutic guidelines:
Rheumatology. Melbourne: Therapeutic Guidelines
Limited; 2010, www.tg.au/?sectionid=117
 The Royal Australian College of General
Practitioners. Clinical guidelines for the diagnosis and
management of early rheumatoid arthritis, www.
racgp.org.au/your-
practice/guidelines/musculoskeletal/rheumatoidarthritis/
 Australian Rheumatology Association,
www.rheumatology.org.au
 Arthritis Australia is recommended for general disease
and treatment information, as well as support services,
www.arthritisaustralia.com.au

52. ‫ت‬‫س‬‫لا‬‫ا‬‫ن‬‫س‬‫خ‬‫ي‬‫ل‬‫ع‬‫ا‬‫ز‬‫ي‬‫خ‬‫لله‬‫ا‬‫م‬‫ك‬‫ا‬‫ز‬‫ج‬‫و‬‫اع‬‫م‬