Gouty arthritis is a form of arthritis that is caused by the buildup of uric acid crystals in the joints. The condition is characterized by sudden and severe attacks of pain, redness, and swelling in the affected joint(s). Gouty arthritis is a chronic condition that can lead to joint damage, disability, and other complications if left untreated. ## Causes of Gouty Arthritis Gouty arthritis is caused by an accumulation of uric acid in the blood, a condition called hyperuricemia. Uric acid is a waste product that is produced when the body breaks down purines, substances that are found naturally in the body and in certain foods. When there is too much uric acid in the blood, it can form sharp, needle-like crystals that accumulate in the joints, leading to inflammation and pain. ## Symptoms of Gouty Arthritis The symptoms of gouty arthritis typically include sudden and severe pain in the affected joint(s), along with redness, swelling, and warmth. The pain is usually most severe during the first 12-24 hours of an attack, and can last for several days to weeks. Over time, gouty arthritis can lead to chronic joint pain, stiffness, and damage. ## Diagnosis of Gouty Arthritis Gouty arthritis is typically diagnosed based on a combination of symptoms, medical history, and laboratory tests. A doctor may perform a physical exam to look for signs of inflammation and check the affected joint(s) for swelling, redness, and warmth. Blood tests may be done to measure the level of uric acid in the blood, and a sample of fluid from the affected joint(s) may be analyzed to look for the presence of uric acid crystals. ## Treatment of Gouty Arthritis The treatment of gouty arthritis typically involves a combination of medications and lifestyle changes. Medications may include nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve pain and inflammation, and corticosteroids or colchicine to reduce the severity and duration of gout attacks. Lifestyle changes may include maintaining a healthy weight, limiting alcohol consumption, and avoiding foods high in purines. ## Prevention of Gouty Arthritis The prevention of gouty arthritis involves making lifestyle changes to reduce the risk of hyperuricemia and gout attacks. This may include maintaining a healthy weight, drinking plenty of water, limiting alcohol consumption, and avoiding foods high in purines, such as red meat, shellfish, and organ meats. ## Conclusion In conclusion, gouty arthritis is a chronic condition that can lead to joint damage and other complications if left untreated. The condition is caused by the buildup of uric acid crystals in the joints.

1. GOUT
Department of orthopaedics

2. GOUT
• Definition : Gout is a hereditary condition of disturbed uric acid metabolism in
which sodium urate crystals are deposited in articular, periarticular and
subcutaneous tissues.
• Gout in full development manifests as :
• A) Hyperuricemia
• B) Recurrent attacks with intervals of freedom from pain
• C) Crystals deposit around joints and extremities leading to crippling deforming
arthritis
• D) Renal diseases involving glomeruli, interstitial tubules & blood vessels
• E) Uric acid Urolithiasis
• F) Cardiovascular lesions

3. GOUTY ARTHRITIS
• It is a metabolic disease associated with deposits of uric acid crystals in the
synovium and the articular surfaces associated with variety of acute and chronic
joint disorders, especially affecting the joints of the feet and legs.

4. ETIOLOGY
• Idiopathic
• Hereditary - many members from the same family may have hyperurecemia
without gout
• Genetic predisposition – it is transmitted as an X linked abnormality of the
enzyme HGPRT which is multifactorial inheritance and runs in family
• Age – it is usually seen b/w 4th and 5th decades of life, if seen in children it is likely
to be rapid, severe, polyarticular and crippling
• Vascular changes – an extremity involving an acute gouty arthritis display
increased rate of blood flow suggesting vascular disturbance as extreme pain
• Disturbed electrolyte equilibrium, suggested marked diuresis
• Decreased urinary 17 ketosteroids levels below 3mg/24hrs is a constant finding

5. ASSOCIATED CONDITIONS
• Obesity
• Atherosclerosis
• Hypertension
• Hyperlipidemia
• Diabetes
• Parenchymal renal disease
• Syndrome X which includes cluster of abnormalities like
• A) resistance to insulin stimulated glucose uptake
• B) hyper insulinemia
• C) hyperlipidemia and dislipoproteinemia

6. over production of Uric acid
• Primary idiopathic hyperuricemia
• Hypoxanthine guanine phosporibosyl
transferase deficiency
• Phosphoribosyl pyrophosphate
synthetase overactivity
• Hemolytic processes
• Lymphoproliferative disease
• Myeloproliferative diseases
• Polycythemia
• Psoriasis severe
• Acute illness
Decreased excretion of Uric acid
• Primary idiopathic hyperuricemia
• Renal insufficiency
• Polycystic kidney disease
• Diabetes insipidus
• Acidosis
• Hyperparathyroidism
• Hypothyroidism
• Toxemia of pregnancy

7. • Combined mechanism :
• Glucose-6-phosphate dehydrogenase deficiency
• Fructose-1-phosphate aldolase deficiency
• Alcohol
• shock

8. Drugs precipitate gout are
• Diuretic therapy
• IV heparin
• Cyclosporin
• Lead intoxication
• Ethambutol
• Nicotinic acid
• pyrazinamide
Other provocative factors are
• Trauma
• Surgery
• Diet rich in purine
• Haemorrhage
• Infections
• Radiographic therapy
• Venesection

9. URIC ACID METABOLISM
• Uric acid is an end product of purine
metabolism synthesized in the liver, it
is a waste product with no physiologic
role and humans lack the enzyme
which breaks down the uric acid into a
more water soluble product allantoin
• The levels of uric acid are also
determined by the purine
concentration in the body which
further depends on the dietary sources
and biosynthesis of purine.
• The protein rich diet like pulses,
legumes, meat, fish, egg, vegetables
like cabbage, cauliflower, beet root,
sweet potato etc..

10. • In the kidney
• 100% of urate undergoes glomerular filtration
• 98% is resorbed by PCT
• 50% is secreted by distal tubules
• 40% of it undergoes post secretary resorption, hence only about 10% of filtered
urate is excreted in the urine.
• The normal concentration of Sr. Uric acid is 2 – 7mg/dl in males, 2 – 6.5mg/dl in
females, which is irregularly distributed in the body

11. PHYSICAL PROPERTIES
• SOLUBILITY :
• The solubility of uric acid dependant on temperature and pH
• Greater is the temperature and pH, greater is its solubility in water> plasma>
urine.
• CRYSTALLINE FORMS :
• Monosodium urate occurs as a monohydrate and forms crystals in tissue and joint
fluids which are needle or rod shaped and appear negatively birefringent when
seen in polarized light microscope.

12. • HYPERURECEMIA :
• It is a biochemical hallmark of gout, which may be defined as Sr. Urate
concentration greater than 7.0mg/dl.
• Physiochemically it is the concentration of urate in the blood that exceeds the
solubility limits of monosodium urate in plasma (1.0mg/dl )
• In 90% of pts it is due to diminished urate excretion and 10% due to over
production

13. CLASSIFICATION OF HYPERURECEMIA
PRIMARY HYPERURECEMIA
Molecular defects undefined :
• under excretion (90% of prim gout)
• over production (10% of prim gout)
Assoc with specific defects :
• PRPP synthetase overactivity
• HGPRT enzyme parted deficiency
(Kelley seegmiller syndrome)
• HGPRT enzyme complete deficiency
(Lesch Nihan syndrome)
SECONDARY HYPERURECEMIA
Increased catabolism of ATP :
• Glycogen storage diseases
• Tissue hypoxia
• Ethanol, exercises, metabolic myopathy
Increased turnover of uric acids :
• Renal insufficiency
• Intake of Diuretics
• Increased tubular resorption
• Decreased tubular secretion
• Dehydration and Diabetes Insipidus

14. PATHOGENESIS OF ACUTE GOUTY ARTHRITIS
• Central to the pathogenesis of the arthritis is the precipitation of the
monosodium urate crystals in the joint
• As synovium is a poor solvent for urates than plasma, the urates crystallize and
forms microtophi in the synovium and the joint cartilage particularly in the
peripheral joints, where the temperature is <20*C
• Some events like trauma possibly initiate the release of crystals in the synovial
fluids which further initiates cascade of events
• Released crystals are chemotactic to leukocytes and cause the activation of
complement leading to generation of C3a and C5a which causes accumulation of
neutrophils and macrophages in the joints and synovial membrane
• The release of chemokines by fibroblasts and monocytes cause further
accumulation of neutrophils and macrophages in the joint

15. • Phagocytosis of these crystals induce the
release of toxic free radicals leukotrienes
(LTB4) and lysosomal enzymes by
phagocytic cells
• Macrophages and the synoviocytes
secrete variety of mediators which further
intensify the inflammatory reaction and
augment the injury to the articular
surface
• Repeated attacks of acute arthritis lead to
chronic arthritis and formation of tophi in
the inflamed synovial membrane and the
periarticular tissues causing destruction
of the joints and impairing the function.

16. MORPHOLOGY
• The distinctive morphological changes seen in gout are :
1. Acute arthritis
2. Chronic tophaceous gout
3. Tophi in various stages
4. Gouty Nephropathy

17. ACUTE ARTHRITIS
• It is characterised by dense neutrophilic infiltration of the synovium and the
synovial fluid
• The synovium appears oedematous, congested and infiltrated with neutrophils,
lymphocytes, plasma cells and macrophages.
• The urate crystals are arranged in cluster can be frequently seen in the cytoplasm
of the neutrophils, which are long slender needle shaped and negatively
birefringent.

18. CHRONIC TOPHACEOUS GOUT
• It occurs due to repetitive precipitation of urate crystals during acute attacks
heavily encrust the articular surfaces and form visible deposits in the synovium.
• The synovium is thickened with inflammatory cells
• It is hyperelastic, fibrotic and forms a panus which destroys the underlying
cartilage, leading to juxta articular bone erosions.
• The subchondral bone is replaced in well circumscribed punched out areas by the
crystalline deposits
• In severe cases it may lead to fibrous or bony ankylosis resulting in partial or
complete loss of joint function.

19. CLINICAL FEATURES
• In the complete development of its course, gout passes through four stages
1. Asymptomatic hyperuricemia
2. Acute gouty arthritis
3. Intercritical period
4. Chronic tophaceous gout

20. 1. ASYMPTOMATIC HYPERURICEMIA
• It is a condition where the serum uric acid level is high but the manifestations of
gout are absent.
• It usually appears around puberty in males and after menopause in females,
though many of them have remained hyperurecemic throughout their life.
• This phase ends with first attack of gouty arthritis or urolithiasis which usually
ranges between 10-40 years with average of 20years.

21. 2. ACUTE GOUTY ARTHRITIS
• First attack usually occurs between 4th and 6th decades and the onset before 25
should raise the suspicion of unusual form of gout
• 85-90% of first attacks affects single joint, most commonly the 1st
metatarsophalangeal joint and in 3-14% the involvement may be polyarticular
• Though any joint may be affected, the decreasing order is great toe, ankle, heels,
knee, wrist, finger and elbows. The rarely affected joints are shoulders, hips,
spine sacro-iliac joint, sternoclavicular and temporomandibular joint.
• These deposits have a predilection for previously damaged joints as in case of
rheumatoid arthritis

22. • In most pts the initial attack may be insidious in onset, usually beginning at night
after the individual has gone to sleep
• Pt experiences intense pain in the affected joint, point becomes hot, dusky red,
swollen and extremely tender, there may be development of lymphangitis which
may be mistaken for cellulitis or septic arthritis.
• The systemic signs include leukocytosis, fever, tachycardia, headache and
elevation of ESR.

23. 3. INTERCRITICAL PERIOD
• Refers to the period once the first attack has resolved and pt is asymptomatic
with joint is normal. In severe cases chronic gouty arthritis develops
• This period usually varies between 1-5yrs although some pts may suffer second
attack as early as 6mnths or as late as 10yrs.
• The second attack usually marks the risk of frequent attacks, the later attacks may
be
1. Less explosive
2. Polyarticular and more severe, it may last long and abate more gradually
• During this period on physical examination there may not be any signs of tophi
there may be development of radiographic changes.

24. 4. CHRONIC TOPHACEOUS GOUT
• Eventually pt may enter a phase of chronic
polyarticular gout with no pain free inter
critical periods.
• Interval between initial attack to this stage
ranges about 3 – 42yrs with avg 11.6yrs and
average sr. uric acid level is 11mg/dl
• It is characterised by formation of tophi in
various sites helix and anti-helix of ear, ulnar
surface of forearm, myocardium, eyes,
larynx producing saccular distensions of
olecranon bursa or fusiform enlargement of
Achilles tendon

25. • Process of formation of tophi advances progressively, rate of formation correlates
with both degree and duration of hyperurecemia
• Eventually tophi cause
1. Marked limitation of joint movements by direct involvement
2. Large subcutaneous tophi produce grotesque deformities
3. Extensive destruction of the joints particularly hands and feet leading to
degenerative arthritis and crippling deformities
4. Skin over the tophi is thin, shiny and may ulcerate or extrude white chalky or
pasty material composed of urate crystals
5. Nerve compression syndrome
6. Bursa may become distended by urate deposits resulting in sinus or invasion of
underlying bone and tendon.

26. DIAGNOSIS
• The main diagnostic features include :
1. Family history of gouty arthritis
2. Repeated attacks with intervals free from pain
3. Renal disturbance as urate calculus
4. Hyperurecemia
5. Satisfactory response to adequate doses of colchine
• A triad of acute monoarticular arthritis, hyperuricemia and dramatic response to
colchine therapy is presumptive diagnosis of gout

27. INVESTIGATIONS
• Baseline laboratory tests should include a complete blood cell count, ESR, urine
analysis, serum lipids, sr. creatinine, sr. blood urea nitrogen and sr. uric acid
• MUREXIDE TEST
• This test is used to detect uric acid from a tophi by fluid aspirated from joint
• Few drops of nitric acid are added to suspected substance and is evaporated to
dryness, then moistened with ammonium hydroxide.
• It results in purple colour to the presence of uric acid

28. • SYNOVIAL FLUID ANALYSIS :
• During acute attacks the effusion may
appear cloudy due to leucocytes or
may appear thick pasty or chalky due
to presence of crystals.
• The synovial fluid cell count is
increased from 2000 to 60000/cumm
• These crystal may be intracellular or
extracellular when observed under
polarized light microscopy, appears
needle shaped and are negatively
birefringent
•

29. • X- RAY
• Not a diagnostic procedure for initial
attack of gout
• As for bony changes to appear, gout
should be untreated or inadequately
treated for approximately 6 – 12yrs
• Hence radiographic features indicate
chronic gout and is present only in
45% of the pts.

30. • SOFT TISSUE CHANGES :
• Eccentric juxta articular soft tissue
masses ( hand, foot, ankle, elbow,
knee with tendency for extensor
tendons like quadriceps, triceps and
achilles tendon
• Presence of calcific deposit in the
periphery of tophi seen in 50% of the
cases
• Bilateral olecranon bursae
(pathognomonic) and prepatellar
bursae
• Aural calcification

31. • CHANGES IN THE JOINT
• Joint effusion (earliest sign)
• Periarticular or soft tissue swelling in
monoarticular gout
• Preservation of joint space (until late
in disease)
• Absence of periarticular
demineralization
• Eccentric erosion with sclerotic
margins
• Scalloped erosions of the bases of
ulnar metacarpals

32. • CHANGES IN THE BONES :
• Cystic changes
• Erosions which appear as punched out
or lytic bone lesions with or without
sclerosis of margins
• Punched out lytic changes with
overhanging bony edges ( Martel’s
sign) associated with calcified soft
tissue masses.

33. TREATMENT
• Though sr. uric acid concentration may be reduced with non-pharmacologic
therapy by life style changes like weight reduction, decreased alcohol ingestion,
decreased intake of foods with high purine content, control of hyperlipidemia and
hypertension.
• These measures alone play a very minor role, hence necessitating medication is
needed

34. • Drugs used in gout :
• Acute gout - NSAID’S
• - Colchicine
• - Corticosteroids
• Chronic gout
• Uricosuric’s - Probenecid
• - Sulfinpyrazone
• Uric acid synthetase inhibitor - Allopurinol
• - Febuxostat

35. DRUGS IN ACUTE GOUT
• NSAID’S :
• They exhibit their action by inhibiting the chemotactic migration of leukocytes
into the joints
• Commonly used are
• Indomethacin – 25-50mg TDS
• Naproxen sodium or Ibuprofen 825mg once or 275mg TDS
• Sulindac 200mg BD
• They can be continued for 3-4wks while the drugs to control hyperurecemia take
control

36. • COLCHICINE :
• MOA : it acts by inhibiting the phagocytosis of uric acid and release of
glycoproteins by the phagocytic cells and hence suppresses inflammation
• T/T : 1mg of colchicine given orally followed by 0.25mg 1-3hrly till control of the
attack is achieved (4-12hrs)
• PROPHYLAXIS : colchicine 0.5 – 1.5mg/day can prevent further attacks of gout,
when taken at first symptom of an attack it effectively aborts it
• It can be given intravenously in 1mg dose if oral route is not available or due to
gastrointestinal side effects
• TOXICITY : in overdoses or chronic cases cause CNS depression, intestinal
bleeding, aplastic anaemia, hair loss, bone marrow suppression, hepatic damage,
death may occur due to muscular paralysis and respiratory failure

37. • CORTICOSTEROIDS :
• Monoarthritic gout responds well to corticosteroids given by intra-articular
injection
• Oral prednisolone can be given by 30-50mg/day as the initial dose and tapered
over 5-7days
• A single IV dose of Methylprednisolone or 7mg of Betamethasone or 20-40mg of
Triamcinolone of acetomide are equally effective
• 40-80 IU of ACTH given intramuscularly as single dose or every 12hr for 1-2 days
is effective in pts with acute polyarticular refractory gout
• Systemic corticosteroids can be used only when NSAID’S and Colchicine are not
effective or are contraindicated

38. DRUGS IN CHRONIC GOUT
• URICOSURIC DRUGS : SULFINPYRAZONE
• It acts by inhibiting the tubular resorption of
uric acid
• 100-200mg twice should be started and
gradually can be increased to a maximum
dosage of 800mg/day
• Uricosuric’s are well tolerated and should be
cautiously used in pts with peptic ulcer
• The common adverse effects by them are
rashes and hypersensitivity reactions, these
drugs are not useful in renal diseases and
should not be given during an acute attack

39. • PROBENECID :
• It acts by competitively blocking the active transport of organic acids at all sites,
more prominently in the renal tubules hence it decreases the uric acid
concentration by promoting its excretion
• Started as 0.25mg BD and increased to 0.5 to 1mg bd after a week and pt is
advised to take plenty of oral fluids to prevent crystallization of urate in urinary
tract
• Tophi gradually disappear and joints improve in function, it is the drug of choice
in treating pts with hypertension and on Thiazide
• 70% of pts can be controlled alone with Probenecid, in some NSAID/Colchicine
coverage is advised during 1-2mnths as the fluctuation of plasma urate levels and
acute attack of gout are more frequent.

40. • URIC ACID SYNTHESIS INHIBITOR : ALLOPURINOL
• It reduces the serum uric acid concentration by
inhibiting the enzyme Xanthine Oxidase
• Dose : a dosage of 100mg OD is started which can
be increased to 300mg/day to maximum of
800mg/day.
• Toxic effects : major toxic effects are
hypersensitive reaction, fever, malaise, muscle
pain, gastric irritation, headache, nausea and
dizziness
• It is the best drug to lower serum urate in over
production pts and pts with advanced renal failure

41. • FEBUXOSTAT :
Initiation initiate febuxostat review sUA levels
at 40mg/day after 2-3mnths
Titration target sUA level <6mg/dl reached
Yes No
down titrate febuxostat dose up titrate febuxostat dose
40mg/day to 20mg/day 40mg/day to 80mg/day
Monitoring review or monitor every 6-12mnths
if sUA levels are maintained at 6mg/dl
Maintenance
continue febuxostat therapy at maintenance dose of 20mg/day

42. • PEG – URICASE :
• It is a recombinant porcine like uricase
used for refractory gout
• It metabolises uric acid to allantoin,
which is 5-10times more soluble
• Pegloticase is pegylated to increase its
elimination half life from 8hrs to 10-
12days, hence can be given once in
2weeks around 8mg/ml.
• Given intravenously causes
anaphylactic reactions

43. SURGICAL MANAGEMENT
• The surgical intervention is excision of the lesion to reduce pain, control of
infection and decompression of a nerve
• Surgical principles are :
1. Avoid local anaesthesia – impairs local blood supply
2. Incision parallel with course of blood vessel
3. Sharp dissection
4. Loose suturing to allow escape of liquefied deposits
5. Avoidance of prolonged splinting, which encourages ankylosis