Gouty arthritis

DEFINITION

Gout is a disease that results from an overload of uric acid in the body. This overload of uric
acid leads to the formation of tiny crystals of urate that deposit in tissues of the body, especially
the joints. When crystals form in the joints, it causes recurring attacks of joint inflammation
(arthritis). Gout is considered a chronic and progressive disease. Chronic gout can also lead to
deposits of hard lumps of uric acid in the tissues, particularly in and around the joints and may
cause joint destruction, decreased kidney function, and kidney stones.

Gout has the unique distinction of being one of the most frequently recorded medical illnesses
throughout history. It is often related to an inherited abnormality in the body's ability to process
uric acid. Uric acid is a breakdown product of purines that are part of many foods we eat. An
abnormality in handling uric acid can cause attacks of painful arthritis (gout attack), kidney
stones, and blockage of the kidney-filtering tubules with uric acid crystals, leading to kidney
failure. The term gout refers the disease that is caused by an overload of uric acid in the body,
resulting in painful arthritic attacks and deposits of lumps of uric acid crystals in body tissues.

Gouty arthritis is typically an extremely painful attack with a rapid onset of joint inflammation.
The joint inflammation is precipitated by deposits of uric acid crystals in the joint fluid (synovial
fluid) and joint lining (synovial lining). Intense joint inflammation occurs as the immune system
reacts, causing white blood cells to engulf the uric acid crystals and chemical messengers of
inflammation to be released, leading to pain, heat, and redness of the joint tissues. As gout
progresses, the attacks of gouty arthritis typically occur more frequently and often in additional
joints

ALTERNATIVE NAMES

Metabolic arthritis

Tophi

Acute hyperurecemia

Disease of kings

Rich man’s disease

History

Anton van Leeuwenhoek described the microscopic appearance of uric acid crystals in 1679.

The word gout was initially used by Randolphus of Bocking, around 1200 AD. It is derived from
the Latin word gutta, meaning "a drop" (of liquid). Gout has however been known since
antiquity. Historically it has been referred to as "the disease of kings"or "rich man's disease".
The first documented description is from Egypt in 2,600 BC. The Greek physician Hippocrates
around 400 BC, also commented on it. Aulus Cornelius Celsus (30 AD) described the linkage
with alcohol, later onset in women, and associated kidney problems:
Again thick urine, the sediment from which is white, indicates that pain and disease are to be
apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very
frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack
eunuchs or boys before coition with a woman, or women except those in whom the menses
have become suppressed... some have obtained lifelong security by refraining from wine, mead
and venery.

The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of
urate crystals in 1679. In 1848 English physician Alfred Baring Garrod realized that this excess
uric acid in the blood was the cause of gout.

INCIDENCE

The prevalence of gout is reported to be less than 1% to 15.3% and it appears to be on the rise.
The incidence increases with age and body mass index. It occurs more commonly in males than
in females.

-Increase with age body mass index

-Occurs in 8.4 of every 1000 people

-Rare in children and young adults

-Men, particularly those between the ages of 40-50 years old are more likely to develop gout
than women, who rarely develop the disorder before menopause.

-People who have had an organ transplant are more susceptible to gout

CAUSES

Gout occurs when urate crystals accumulate around your joint, causing the inflammation and
intense pain of a gout attack. Urate crystals can form when you have high levels of uric acid in
your blood. Your body produces uric acid when it breaks down purines — substances that are
found naturally in your body — as well as in certain foods, such as organ meats, anchovies,
herring, asparagus and mushrooms.

Normally, uric acid dissolves in your blood and passes through your kidneys into your urine. But
sometimes your body either produces too much uric acid or your kidneys excrete too little uric
acid. When this happens, uric acid can build up, forming sharp, needle-like urate crystals in a
joint or surrounding tissue that cause pain, inflammation and swelling.

SIGNS AND SYMPTOMS

>Gout can present in a number of ways, although the most usual is a recurrent attack of acute
inflammatory arthritis (a red, tender, hot, swollen joint).

>The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for
half of cases.

>Other joints such as the heels, knees, wrists and fingers may also be affected. Joint pain
usually begins over 2–4 hours and during the night. The reason for onset at night is due to the
lower body temperature during this time.

>Other symptoms that may occur along with the joint pain include fatigue and a high fever.

>Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology
including hard, non-painful deposits of uric acid crystal known as tophi. Extensive tophi may
lead to chronic arthritis due to bone erosion

>Elevated levels of uric acid may also lead to crystals precipitating in the kidneys resulting in
stone formation. This may result in urate nephropathy
 STAGES

1. Asymptomatic hyperuricemia- the person has elevated levels of uric acid in the blood but
no other symptoms, it does not usually requires treatment
2. Acute gout or arthritis- hyperurecemia has caused the deposits of uric acid crystals in
joint spaces and leads to a sudden onset of intense pain and swelling of joints;
commonly occurs in night.
3. Interval gout- period between acute attacks; person has normal joint function and does
not have any symptoms
4. Chronic tophaceous gout- most disabling stage and usually develops over a long period
as 10 years

RISK FACTORS

 Lifestyle factors. Choices you make in your everyday life may increase your risk of gout.
Excessive alcohol use — generally more than two drinks a day for men and more than
one for women — increases the risk of gout.
 Moderate to heavy drinker
 Medical conditions. Certain diseases and conditions make it more likely that you'll
develop gout.
 untreated high blood pressure (hypertension) and chronic conditions such as
diabetes, high levels of fat and cholesterol in the blood (hyperlipidemia),
narrowing of the arteries (arteriosclerosis) obesity, leukemia, lymphomas, and
hemoglobin disorders.
 Certain medications. The use of thiazide diuretics — commonly used to treat
hypertension — and low-dose aspirin also can increase uric acid levels.
 Family history of gout/genetics. If other members of your family have had gout, you're
more likely to develop the disease.
 Age and sex. Gout occurs more often in men than it does in women, primarily because
women tend to have lower uric acid levels than men do. After menopause, however,
women's uric acid levels approach those of men. Men also are more likely to develop
gout earlier — usually between the ages of 40 and 50 — whereas women generally
develop signs and symptoms after menopause.

Diagnostic examination

-Physical examination

-Polarized light microscopy of the synovial fluid of the involved joint

>identify and characterize crystals

-xray

>show tophi-crystal deposits and bone damage as a result of repeated bouts of

inflammation

-MRI

>use for visualization, Chronic tophaceous gout often presents as juxtarticular soft-tissue
masses, sharply defined erosions, overhanging margin bone, and thickening of the synovium.

-CT scans

>excellent visualization of tophi, Use of CT may assist in differentiating tophi from other
subcutaneous nodules.

-Arthrocentesis

>most reliable test for gout is finding uric acid crystals in a sample of the joint fluid obtained
by joint aspiration
-Blood test

>to measure the uric acid level in your blood

Anatomy and Physiology

Your foot is made up of 3 sections:

1. Forefoot is comprised of 4 smaller toes (phalanges) and 1 big toe (hallux)
2. Midfoot (metatarsal bones) and hindfoot (tarsal bones) make up your foot arches, instep,
heel and ankle; these are responsible for weight bearing and propulsion.

 Arches contain bones, ligaments, muscles and tendons of your foot, which require a lot
of stability and flexibility.

Your foot bones work with your foot muscles to move your foot in 4 directions:

1. dorsiflexion (moving foot upward)

2. plantar flexion (moving foot downward towards sole),
3. abduction (moving foot outward) and
4. adduction (moving foot inward).

Your lower leg muscles muscles and tendons attach on the top of your foot, and your
flexor, abductor and adductor muscles and tendons attach on the bottom of your foot.

Your achilles tendon is the strongest and largest tendon in your body and it connects
your calf muscles (gastrocnemius and soleus) to your heel bone (calcaneus), allowing
your foot to push off when your calf muscles tighten. It is essential for walking, running
and jumping.
 Pathophysiology

Predisposing factors Precipitating factors

age diet
gender lifestyle
family history medications
medical conditions alcohol consumption

Purines are metabolized into

Uric acid

Hyperuricemia

Monosodium urate crystals deposited in tendons, joint, kidneys and other organs

Triggers a local immune mediated inflammatory response, thus inflammation

Signs and symptoms of gouty arthritis

GOUTY ARTHRITIS

If treated: If untreated:
Termination of acute Chronic topaceous
gout
attacks of gout Kidney stones
Normal uric acid level Chronic renal disease
Management
a. Non – surgical management
 Colchine (toxic natural product)
 NSAID (Indomethacin)
 Uricosuric agents (Probenecid) – to correct hyperuricemia, dissolve deposited urate
 Allopurinol – DOC for kidney stones
 Corticosteroids – incase of drug resistance
 Low purine diet
 Lifestyle changes
b. Surgical management
 Incision and drainage of tophi
 Joint replacement
c. Nursing management
 Low purine diet
 Limit/stop alcohol intake
 Pain management
 ROM exercises
 Proper health education
 Immobilize affected part and elevate
 Rest
Discharge Planning

M – Depends on the signs and symptoms exhibited by the client (NSAIDS, Colchicine,
Prednisone)

E – Exercise is vital to reduce the possibility of the attacks of gout

T – cold/warm therapy

H – Assess and monitor flare ups of gout, stress compliance to treatment plan to prevent
complications and to reduce pain

O – Regular visit to the physician to monitor gout attacks and to prevent, treat or diagnose
complications of gout

D – increase oral fluid intake, avoid consumption of alcohol, avoid foods high in purines like
anchovies, asparagus, roasted highland legumes, sardines, grain meats, liver, mackerel

S – Prayer increases patient’s positive attitude toward treatment regimen