Gout

A syndrome that occurs from an inflammatory response to the production or

excretion of uric acid resulting in high levels or uric in the blood (hyperuricemia) and
in other part of the body fluids, including synovial fluid .
Gout has an acute onset, usually at night and often involves the first
metatarsophalangeal joint (great toe). The initial acute attack is usually is usually
followed by a period of months or years without manifestations. As the disease
progresses, urates are deposited in various other connective tissues. Deposits in the
synovial fluids cause acute inflammation of the joint (gouty arthritis). Over time,
urate deposits in subcutaneous tissues cause the formation of small white nodules
(tophi). Deposits of crystals in the kidney can form urate kidney stones and result in
kidney failure.
Gout may occur as either a primary or secondary disorder.
*Primary gout- characterized by elevated serum uric acid levels resulting from
either an inborn error of purine metabolism or a decrease in renal uric acid excretion
due to an unknown cause. Impaired uric acid excretion leads to hyperuricemia in
the majority of people with primary gout.
*Secondary gout- HYperuricemia occurs as a result of another disorder or treatment
with certain medications.
The peak age of onset of gout in men is between 40 and 50 years. It is rare in
woman before menopause. The disease is common in Pacific Islanders.

CAUSES
*Primary gout- UNKNOWN
*Secondary gout- treatment with certain medications, disorder associated with rapid
cell turnover such as some malignancies (hemolytic anemia, and polycythemia),
chronic renal disease, hypertension, starvation, diabetic ketoacidosis, ethanol
ingestion.

MANIFESTATIONS and COMPLICATIONS

Hyperuricemia, recurrent attacks of inflammation of a single joint, tophi in and
around the joint, renal disease, and renal stones. Unless treated, its manifestations
appear in 3 stages: asymptomatic, hyperuricemia, acute gouty arthritis, and
tophaceous gout.
STAGES:
1st stage: Asymptomatic Hyperuricemia- serum levels averaging to 9-10 mg/dL.
2nd stage: Acute Gouty Arthritis- acute attack, usually affecting a single joint that
occurs unexpectedly, often beginning at night. This may be triggered by trauma,
alcohol ingestion, dietary excess, or a stressor. It is often precipitated by an abrupt
or sustained increase in uric acid levels. The affected joint becomes red, hot,
swollen, and painful and tender.

3rd stage: Tophaceous (Chronic) Gout- Occurs when hyperuricemia is not treated.
The uriate pool expands, and monosodium urate crystal deposits (tophi) develop in
cartilage, synovial membranes, tendons, and soft tissues.

MANIFESTATIONS OF GOUT

ACUTE GOUTY ARTHRITIS

-Usually monoarticular,
affecting
metatarsophalangeal joint of
great toe, instep, ankle,
knee, wrist, or elbow
- Acute pain
-Red, hot, swollen and
tender joint
-Fever, chills, malaise
-Elevated WBC, and
sedimentation rate

-Tophi evident on joints,

bursae, tendon sheaths,
pressure points, helix of ear
TOPHACEOUS (chronic)
GOUT

-Joint stiffness, limited ROM,

and deformity
-Ulceration of tophi with
chalky discharge

PATHOPHYSIOLOGY
2/3 of the amount produced each day excreted by the kidneys and the rest in
the feces. The serum uric acid level is normally maintained between 3.4-7.0 mg/dL
in men while 2.4-6.0 mg/dL in women. At levels greater than 7.0 mg/dL, the serum
is SATURATED, and monosodium urate crystals may form. It is not known exactly
how crystals form. It is not known exactly how crystals of monosodium urate
crystals are deposited in joints. Several mechanisms may be involved:

Crystals tend t form in peripheral tissues of the body, where lower

temperatures reduce the solubility of the uric acid.
A decrease in extracellular fluid pH and reduced plasma protein binding of
urate crystals are evident.
Tissue trauma and a rapid change in uric acid levels may also lead to crystal
deposition. A rapid increase in uric acid may occur with tissue trauma and
release of cellular components.

The monosodium urate crystals may form in the synovial fluid or in the synovial
membrane, cartilage, or other joint connective tissues. They may also form in the
heart, earlobes, and kidneys. These crystals stimulate and continue the
inflammatory process, during which neutrophils respond by ingesting the crystals.

The neutrophils release their phagolysosomes, causing tissue damage, which

perpetuates the inflammation.

DIAGNOSTIC TEST

Serum Uric Acid is nearly always elevated (usually above 7.5 mg/dL)
and is indicative of hyeruricemia.
WBC count shows significant elevation, reaching levels as high as
20,000/mm3 during an acute attack.
Eosinophil Sedimentation Rate (ESR or sed rate) is elevated during an
acute attack from the acute inflammatory process that accompanies
deposits of urate crystals in a joint.
A 24 hour urine specimen is analyzed to determine uric acid production
and excretion.
Analysis of fluid aspirated from the acutely inflamed joint or material
aspirated from tophus shows typical needle-shaped urate crystals,
providing the definitive diagnosis of gout.

MEDICAL SURGICAL MANAGEMENT

A. Medications
(used to terminate an acute attack, prevent further attacks, and reduce
serum uric acid levels )
- NSAIDs (treatment of choice for an acute attack)
*ex. Indomethacin (Indocin) 50 mg q 8h
- Colchicine (acts by interrupting the cycle of urate crystal deposition
and inflammation in an acute attack of gout)
- Cortecosteroids
- Analgesics
B. Prophylactic Therapy
Clients with high risk for future attacks of acute gout. Prophylactic therapy
plus daily colchicine may be initiated. Prophylaxis is particularly useful
during 1-2 years of treatment with antihyperuremic agents.
C. Dietary Management
- Low purine diet
- obese client should be encouraged to lose weight
- No fasting
- Avoid alcohol

NURSING MANAGEMENT
1. Elevate affected joint
2. Hot or cold compress may be applied for comfort
3. A fluid intake of 2-3 L or more to increase urate excretion and reduce the risk
of urinary stone formation
4. Assess for any side effects especially of each medications
5. Monitor input and output
6. Bed rest to prevent further urate mobilization and joint inflammation
7. Encourage active and passive ROM exercises of joints and muscle-tensing
exercises on unaffected limbs
8. When ambulation required, suggest using a walker or cane as needed