Gouty arthritis

1. SHYAM SHAH MEDICAL COLLEGE,REWA
DEPARTMENT OF
ORTHOPEDIC

2. Gouty Arthritis
• Chronic heterogeneous disorder of urate
metabolism
• Results in deposition of monosodium urate
crystals in the joints and soft tissues, with
accompanying inflammation and degenerative
consequences
• Most common form of inflammatoryjoint
diseasein men aged≥40 years

3. Predisposing Factors
• Purine rich foods – meat, kidney, liver, seafood,
anchovies, oatmeal, certain vegetables (peas, beans,
lentils, mushrooms, cauliflower, spinach),
sweetbreads
• Caffeine
• Drugs– Loop diuretics, NSAIDs,corticosteroids,
Niacin, Sinemet, Cyclosporine, Salicylates,
Ethambutol, Pyrazinamide
• Trauma
• Infection
• Other disease– DM, HTN,vascular dx, renal dx,
thyroid dx, sarcoidosis,etc.

4. Hallmarks of Gout
• Group of conditions which
may be characterized by an
elevation of serum uricacid
(usually)
• Recurrent attacks (flares) of
an acute inflammatory
arthritis with monosodium
urate crystalsdemonstrated
in synovial fluid leukocytes
• Boneand joint destruction
in somecases

5. • Aggregates of uric
acid crystals (tophi) in
and around joints,
soft tissues, and
various organs
• Tophusin bone
leading to erosionsin
some cases
• Kidney diseaseand
stones

7. Hyperuricemia leads to deposit of
urates in the jointfluid, triggering an
inflammatory cascade

8. Stages
Thisdisorder can be progressive through
four stagesif undertreated
Asymptomatic hyperuricemia
Acute gout
Intercritical gout
Chronic tophaceous gout

9. Clinical
Features

10. Acute Gout:
• Acute gout is apainful
condition that typically
affects only one or a
few joints.
• The big toe, knee, or
ankle joints are most
often affected.
• Throbbing, crushing, or
excruciating pain
• Joint appears warm and
red. Fevermay be
there.

12. • Theattack may go away in afew days,but
may return from time totime.
• Additional attacks often lastlonger.
• After afirst gouty attack, half of the people
will have no symptoms. Half of patientshave
another attack.

14. Chronic Gout
• Signsand symptoms include:
• Joint damage
• Lossof motion in thejoints
• Joint pain and other
symptoms most of thetime,
throughout the day
• Tophi below the skinaround
joints or in other places
(Tophi usually develop only
after apatient hashad the
diseasefor manyyears)

15. Advanced Chronic Tophaceous Gout
• Tophi canbe seen
clinically, with
obvious deformity
demonstrated in
hands and foot
• Tophi may be
associated with
bony destruction as
seenon the x-ray

16. • Ischaracterised by massivedeposits of
monosodium urate crystals (Tophi) in articular
cartilage, subchrondral bone, synovial
membrane, capsule, tendon sheaths and peri
articular tissues.
• Tophi formation canalso occur over eyelids,
nasal cartilage, cornea, tongue, vocal cords
and penis

17. • Thetophaceous nodules consists of
multicentric deposition of urate
crystals and intra cellular matrixand
foreign body granulomatous
reaction.
• Asthey enlarge in size,calcify, they
cancausepressure symptoms.
• Thetophi are firm yellow in colour
and occasionally discharge achalky
material.

18. Diagnosis

19. ACRCriteria for Acutegout
Thepresenceof characteristicuratecrystals inthe joint
fluid, or a tophus proved to contain urate crystals by
chemical means or polarizedlight microscopy,or the
presence of 6of the following 12clinical,laboratory, and
radiographic phenomena:
1. More than one attack of acutearthritis
2. Maximum inflammation developed within 1day
3. Monoarthritis attack
4. Rednessobserved over joints

20. 5.First metatarsophalangeal joint painfulor
swollen
6.Unilateral first metatarsophalangealjoint
attack
7. Unilateral tarsal joint attack
8. Tophus(proven or suspected)
9. Hyperuricemia
10.Asymmetric swelling within ajoint onx
ray/exam
11. Subcortical cystswithout erosions on xray
12.Joint fluid culture negative fororganisms
during attack

21. Investigations
• Plain radiographs (may benormal)
• SerumUric acid
• Synovial fluid analyis (shows uricacid
crystals)
• BUN(blood urea nitrogen), Serum
Creatinine
• Synovial biopsy
• Uric acid –urine

22. SYNOVIALFLUIDANALYSIS
(Polarized Light Microscopy)
• TheGold standard
• Crystals
intracellular during
attacks
• Needle & rod
shapes
• Strongnegative
birefringence

23. BIOCHEMICALTESTSFORGOUT:

24. DrugsUsedIn Treatment
• NSAIDs
• Colchicine
• Uricosuric agents
• Allopurinol/ Febuxstat

25. TREATMENTGOALS
1. Rapidly end acute flares
2. Protect against future flares
3. Reducechance of crystalinduced
inflammation
4. Prevent disease progression
5. Lower serum urate to depletetotal
body urate pool
6. Correct metabolic cause

26. Acute Gout - Rx
NSAIDs(unlessCRI,CHF,PUD, etc.)
Corticosteroids (Intra-articular if one
joint, systemicif multiplejoints)
Colchicine (adjust dose in patientsw/
renal insufficiency)
- Most beneficial in first 12-36hours of an
attack
- 1mg initially, then 0.5mg qhr untileither
symptoms relieved or GIside fx
(N/V/diarrhea) or 7mg totalgiven
- Renaldosing:
- If Crclearance<50, dec.dose 50%
- If Crclearance<10, contraindicated.
- Indomethacin 50mg tid
- Naproxen825mg once, then 275q8hr
- Sulindac 200mg bid
- 20-30mg/day if systemicused

27. Prevent DiseaseProgression
• Lower urate to <6 mg/dl :
• Depletes
Total body urate pool
Deposited crystals
• Treatment is lifelong & continuous
• Drug choices :
Uricosuric agents
Xanthine oxidase inhibitor

28. PREVENTION
Maintain the concentration of Uric Acid level within the
normal range.
 Drinking Plenty of Water.
 Balance your weight with proper diet and exercise
 Avoid purine rich foods
 Reducing alcohol consumption
 Avoid Diuretic Drugs.

29.  Foods known to decrease the occurrence of gout include dairy, foods highin
potassium, black cherry juice, blueberries and lemon juice.
 Immediately treating gout will not allow it worse.

31. ThankYou