Gout is a metabolic disorder manifesting in primary or secondary forms characterized by hyperuricemia & joint lesions . A metabolic disease characterized by recurrent attack of acute inflammatory arthritis caused by elevated levels of uric acid in the blood (hyperuricemia). Gout: Very painful form of arthritis characterized by the formation of uric acid crystals and severe inflammation. Gout is a metabolic disorder of purine metabolism, characterized by intermittent attacks of acute pain, swelling and inflammation. • It always preceded by hyperuricemia

1. Dr. Niraj Kumar , Pt
Associate Professor Physiotherapy
Dept.
Shri Guru Rai Institute Of
Paramedical Sciences , Dehradun

2. 2640 BC: podagra first identified by the Egyptians
 5th century BC: Hippocrates referred to gout as
“unwalkable disease” and noted links between gout &
lifestyle, demographics & other variables.
 The uric acid crystallizes and deposits in joints, tendons
and surrounding tissues.
 DEFINATION
 Gout is a metabolic disorder manifesting in primary
or secondary forms characterized by hyperuricemia &
joint lesions .
 A metabolic disease characterized by recurrent attack of
acute inflammatory arthritis caused by elevated levels of
uric acid in the blood (hyperuricemia).

3.  Gout: Very painful form of arthritis characterized by the
formation of uric acid crystals and severe inflammation.
 Gout is a metabolic disorder of purine metabolism,
characterized by intermittent attacks of acute pain,
swelling and inflammation. • It always preceded by
hyperuricemia

5. Caused by the deposition of monosodium urate crystals in
tissues
Uric acid is a metabolic by-product of purine catabolism
Purineshypoxanthinexanthineuric acid
Reaction catalyzed by xanthine oxidase, found in the liver
When the balance of dietary intake, synthesis and rate of
excretion are disrupted, hyperuricemia results
Overproduction (10%)
Underexcretion (90%)
Results in arthritis, soft tissue masses, nephrolithiasis and
urate nephropathy

7. Hereditary factors 40-50 age
High Purine Diet (Red Meat, Fatty Poultry, High Fat Dairy,
Seafood)
Alcohol Consumption
Trauma
Osteoarthritis
Surgery
Starvation
Dehydration
Obesity
Drugs (Allopurinol, uricosuric agents, thiazides, loop
diuretics, low dose aspirin)
Renal Impairment
Genetic Mutations (SLC22A9, SLC22A12, ABCG2)

8.  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 inflammatory joint disease in men aged ≥40 years
 This disorder can be progressive through four stages if undertreated
1. Asymptomatic hyperuricemia
2. Acute gout
3. Intercritical gout
4. Chronic tophaceous gout
Image reprinted with permission.
American College of Rheumatology.
ACR Clinical Slide Collection on the Rheumatic Diseases.
Atlanta, Ga.
American College of Rheumatology; 1998.

9.  Group of conditions which may be
characterized by
 An elevation of serum uric acid (usually)
 Recurrent attacks (flares) of an acute inflammatory
arthritis with monosodium urate crystals
demonstrated in synovial fluid leukocytes
 Bone and joint destruction in some cases
 Aggregates of uric acid crystals (tophi) in
and around joints, soft tissues, and
various organs
 Tophus in bone leading to erosions in
some cases
 Kidney disease and stones
1. Image reprinted with permission. American College of Rheumatology.
ACR Clinical Slide Collection on the Rheumatic Diseases. Atlanta, Ga.:
American College of Rheumatology; 1998.
2. http://www.healthinplainenglish.com/health/musculoskeletal/gout/index.htm

10. Biologically significant hyperuricemia (≥6.8 mg/dL) is less than
laboratory defined hyperuricemia (≥8.0 mg/dL)
Underexcretion
Silent
tissue
deposition
Urate
Hyperuricemia ≥6.8 mg/dL
Overproduction
Associated
cardiovascular events
and mortality
Renal
manifestations
Gout
Endogenous
purine synthesis
Dietary
purines
Tissue
nucleic acids
The Hyperuricemia Cascade

11. Lin et al. J Rheumatol. 2000;27:1045-1050. Campion et al. Am J Med. 1987;82:421-426.
Serum urate levels in 1515 men and 1670
women aged ≥30 in Taiwan 1991-1992
Normative Aging Study:1858 previously healthy men
(average initial age 42) followed for 14.9 years
Cumulativeincidenceofgout,%
0 1 2 3 4 5 6
Years
10
5
15
20
25
30
Initial urate n
≥9.0 94
7.0-8.9 666
<7.0 898
Serum urate, mg/dL
Many patients fit
biological definition
for hyperuricemia
Distribution,%
Urate crystallizes at
a level of 6.8 mg/dL
40
35
30
25
20
15
10
5
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13
Males
Females
Over time, high serum urate levels lead to gout

12.  Over time, untreated, chronic hyperuricemia increases body urate
stores, advancing the severity of the disease
 Flares last longer
 Flares occur more often
 Intercritical segments (flare free periods) decrease
 Persistent pain and stiffness occur
Adapted from Klippel et al, eds. In: Primer on the Rheumatic Diseases. 12th ed. Arthritis Foundation;
2001:313.
Time:
2. Acute flares 4. Chronic
polyarthropathy
with tophus
formation
1. Asymptomatic
hyperuricemia
PainLevels
3. Painless intercritical
segments
Body
Urate
Pool

13.  86% (71/81) of patients who had serum urate <6.0 mg/dL did not
experience an acute flare during the study period
Shoji et al. Arthritis Care Res. 2004;51:321-325.
Average serum urate during the whole investigation period, mg/dL
Incidence of
recurrent
gouty attacks
> 1 year
after each
patient visit, %
5.0 5.5 6.0 6.5 7.0 7.5 8.0 8.5 9.0 9.5 10.0
0.0
10.0
20.0
30.0
40.0
50.0
60.0
70.0
80.0
90.0
100.0
Observed
Logistic regression

14. The victim goes to bed and sleeps in good health. About two o’clock in the
morning he is awakened by a severe pain in the great toe; more rarely in
the heel, ankle, or instep. The pain is like that of a dislocation, and yet the
parts feel as if cold water were poured over them . . . Now it is a violent
stretching and tearing of the ligaments – now it is a gnawing pain, and
now a pressure of tightening. So exquisite and lively meanwhile is the
feeling of the part affected, that it cannot bear the weight of the bedclothes
nor the jar of a person walking in the room. The night is spent in torture.
Sydenham, 1683
Sydenham, T: The Works of Thomas Sydenham, London, New Sydenham Soc. 1850 (translation)

15. Image reprinted with permission. American College of Rheumatology. ACR Clinical Slide Collection on the Rheumatic
Diseases. Atlanta, Ga.: American College of Rheumatology; 1998.

16. Midfoot
Gout can occur
in bursae, tendons,
and joints
Olecranon Bursa
Elbow
Wrist
Knee
Ankle
Subtalar
1st MTP
(eventually affected in ~90%
of individuals with gout)
Fingers

17. Majority experience second acute flare within
1 year of first gout flare
62%16%
6%
5%
4%
7%
Within 1 yr
1-2 yrs
2-3 yrs
3-5 yrs
After 10 yrs
No 2nd in more than
10 yrs
Yu et al. Ann Int Med. 1961;55:179-192

18.  Tophi can be seen clinically, with
obvious deformity demonstrated in
hands and foot
 Tophi may be associated with bony
destruction as seen on the x-ray on right
Images reprinted with permission. American College of Rheumatology. ACR Clinical Slide Collection on the Rheumatic

19. 1) It mostly occur in men in 3rd or 4th decade of life.
2) The metatarsal-phalangeal joint at the base of the big toe is
affected most often,
IN ACUTE STAGE:-
• Sudden onset of joint pain at night in the joint of big toe.
• Swelling & redness in the joint of big toe.
• Tenderness
• Skin may be in red colour and shiny appearance
• Arthritic pain worsen progressively.
• Generally involves one or few joints
• Most common site of initial attack metatarsophalangeal joint.
• Other sites ankle, heel, knee, wrist, elbow and fingers.

20. CHRONIC STAGE:-
• Formation of gouty tophi:- Deposition of urate salts
(sodium urate monohydrate) in the periarticular
tissues of involve jt. . These lumps are called gouty
tophi. Patients may develop large subcutaneous tophi
(Stones) in pinna of external ear, eyelids, nose and
around joints
• Frequency of attacks increases, continuous deposit
leads to damage joints and chronic pain .
• The ureate crystals in kidney leads renal disease.
• Articular cartilage may be destroyed result in joint
deformities

21. • Joint fluid aspiration
• Blood test (Serum uric acid levels)
• X-rays- Shows degeneration, gouty tophi, joint
space narrow and sclerosis.

22. 1. Pseudo gout ,
2. RA,
3. neoplasm
4. septic arthritis
5. infectious arthritis
6. acute rheumatic fever
7. juvenile RA
8. acute fracture
9. palindromic rheumatism.

23. GOALS:-
1. Prevent acute attack
2. Reduce pain & inflammation
3. prevent complications
• destructive arthropathy
• tophi
• renal stones

24. ACUTE GOUT:- Treat patients with uric-acid-lowering
medications such as:-
1) Allopurinol:- Allopurinol is well tolerated by most people, but in
some people, it can cause an allergic rash.
2) Colchicine (Colcrys) can cause signs and symptoms such
as nausea, diarrhea, and rarely muscle weakness.
3) Probenecid is generally well tolerated but should not be used in
patients who have uric acid kidney stones, as it can worsen the kidney
stones and potentially harm the kidneys in these patients.
4) Febuxostat (Uloric) can cause liver abnormalities, nausea and rash.
5) NSAIDs can cause irritation of the stomach and ulcers in some cases.
The liver and the kidneys are periodically monitored in patients taking
NSAIDs over the long term.
6) Corticosteroids
7) Vitamin C. Vitamin C may help lower uric acid levels.

25. Uric acid is formed when proteins in the food we eat, called
purines, are broken down. The primary dietary goal for gout
is to avoid intake of foods with high amounts of purine in
them. Foods considered high in purine content include:
Foods considered high in purine content include:
Some fish, seafood and shellfish, including anchovies,
sardines, mackerel, scallops, herring, mussels, codfish, trout,
and haddock
Some meats such as bacon, turkey, veal, venison, liver, beef
kidney, brain, poultry, pork, and lamb, Crab, lobster, oysters,
shrimp and sweetbreads
Alcoholic beverages

26. Foods considered moderate in purine content
include:
Meats such as beef, veal, poultry, pork, and lamb
Crab, lobster, oysters, and shrimp
Vegetables such as asparagus, spinach, green peas,
mushrooms, and cauliflower
Kidney beans, lentils, and lima beans

27. 1) Weight loss. Being overweight increases the risk of developing gout,
and losing weight lowers the risk of gout also lessen the stress on joints.
2) Complex carbs:- Eat more fruits, vegetables and whole grains, which
provide complex carbohydrates. Avoid foods such as white bread, cakes,
candy, sugar-sweetened beverages and products with high-fructose corn
syrup.
3) Water:- Keep yourself hydrated by drinking water. An increase in water
consumption has been linked to fewer gout attacks. Aim for eight to 16
glasses of fluids a day with at least half of that as water.
4) Fats:- Cut back on saturated fats from red meats, fatty poultry and high-
fat dairy products.
5) Proteins:- Limit daily proteins from lean meat, fish and poultry to 4 to 6
ounces (113 to 170 grams). Add protein to your diet with low-fat or fat-free
dairy products, such as low-fat yogurt or skim milk, which are associated
with reduced uric acid levels.

28. 1. Physical therapist should focus on reinforcement of
management program and splinting, orthotics, or other
assistive devices to protect the affected joint
2. Stretching exercise to help increase circulation and reduce
stiffness around the joint areas.
3. Strengthening exercise
4. Physiotherapist may also use modalities such as ultrasound
or laser in the acute phase.
5. Maintenance of ROM, strength, and function.
6. Massage
7. Endurance exercise
8. Cardio exercise
9. Muscle massage

29. Septic Arthritis.
Pseudogout,
Rheumatoid Arthritis,
Psoriatic Arthritis,