GOUT

MARISSA P. RUELOS
GOUT
 A disorder that manifests as a spectrum of clinical and pathologic features
built on a foundation of an excess body burden of uric acid.
 Manifested in part by hyperuricemia, which is variably defined as a serum
urate level greater than normal (6.8mg %).
 Chronic heterogenous disorder of urate metabolism.
 Most common form of inflammatory joint disease in men aged >40 years.
 It is derived from the Latin word “guta” means a drop, originally may have
reffered to a drop of poison or evil humor.
 A group of diseases characterized by hyperuricemia and uric acid crystal
formation.
STAGES:

● This disorder can be progressive through 4

stages if untreated:
1. ASYMPTOMATIC HYPERURICEMIA
2. ACUTE GOUT
3. INTERCRITICAL GOUT
4. CHRONIC TOPHACEOUS GOUT
PATIENTS WITH GOUT
PATHOGENESIS:
● 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.
CLINICAL MANIFESTATIONS:

 ACUTE GOUT
• It is a painful 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.
• Fever.
• The attack may go away in a few days, but may return
from time to time.
• Additional attacks often last longer.
• After a 1st gouty attack, half of the people will have no
symptoms. Half of patients may experience another
attack.
CHRONIC GOUT:

● Signs and symptoms include:

 Joint damage
 Loss of motion in the joints
 Joint pain and other symptoms
most of the time, throughout the
day
 Tophi below the skin around
joints or in other places. (Tophi
usually develop only after a
patient has had the disease for
many years
ADVANCED CHRONIC TOPHACEOUS GOUT
● Tophi can be seen clinically, with obvious
deformity demonstrated in hands and foot.
● Tophi may be associated with bony destruction
as seen on x-ray.
● It is characterized by massive deposits of
monosodium urate crystals (Tophi) in articular
cartilage, subchondral bone, synovial
membrane, capsule, tendon sheaths and peri
articular tissues.
● Tophi formation can also occur over eyelids,
nasal cartilage, cornea, tongue, vocal cords and
penis.
● The tophaceous nodules consists of
multicentric disposition of urate
crystals and intra cellular matrix and
foreign body granulomatous reaction.
● As they enlarge in size, calcify, they
can cause pressure symptoms.
● The tophi are firm yellow in color and
occasionally discharge is chalky
material.
TOPHI IN MULTIPLE JOINTS
CRITERIA FOR ACUTE GOUT:

1. More than 1 attack of acute arthritis.

2. Maximum inflammation developed within 1 day.
3. Monoarthritic attack.
4. Redness observed over joints.
5. First metatarsophalangeal joint is painful or swollen.
6. Unilateral first metatarsophalangeal joint attack.
7. Unilateral tarsal joint attack.
8. Tophus (suspected or proven).
9. Hyperuricemia.
10. Asymmetric swelling within joint on xray.
11. Subcortical cysts without erosions in xray.
12. Joint fluid culture negative for organisms during attack.
DIAGNOSTIC EXAM:

 PLAIN RADIOGRAPHY (XRAY)

 SERUM URIC ACID
 SYNOVIALFLUID ANALYSIS (SHOWS URIC
CRYSTALS)
 BUN (BLOOD UREA NITROGEN)
 SERUM CREATININE
 URIC ACID- URINE
RADIOGRAPHIC HALLMARKS OF GOUT

 OVERHANGING
EDGES
 PUNCHED OUT
LESIONS WITH
SCLEROTIC
BORDERS.
 PRESERVATION OF
JOINT SPACE (TILL
LATE).
 DEGENERATIVE
CHANGES.
SYNOVIAL FLUID ANALYSIS:

● THE GOLD
STANDARD
● CRYSTALS
INTRACELLULAR
DURING ATTACKS
● NEEDLE AND RODS
IN SHAPE
● STRONG NEGATIVE
BIREFRINGENCE
BIOCHEMICAL TEST OF GOUT
DIFFERENTIAL DIAGNOSIS:

 PSEUDOGOUT: CHONDRACALCINOSIS,
CPPD
 PSORIATIC ARTHIRTIS
 OSTEOARTHITIS
 RHEUMATOID ARTHRITIS
 SEPTIC ARTHRITIS
 CELLULITIS
GOUT VS CPPD

● SIMILAR ACUTE ATTACKS

● DIFFERENT CRYSTALS UNDER MICROSCOPE:
RHOMBOID , IRREGULAR IN CPPD
GOUT VS RA

● BOTH HAVE POLYARTICULAR, SYMMETRIC ARTHRITIS

● TOPHI CAN BE MISTAKEN FOR RA NODULES
TREATMENT:

1. RAPIDLY END ACUTE FLARES

2. PROTECT AGAINTS FUTURE FLARES
3. REDUCE CHANCE OF CRYSTAL INDUCED
INFLAMMATION
4. PREVENT DISEASE PROGRESSION
5. LOWER SERUM URATE TO DEPLETE TOTAL
BODY URATE POOL
6. CORRECT METABOLIC CAUSE
ACUTE FLARES TREATMENT:
ENDING ACUTE FLARES:

● CONTROL INFLAMMATION AND PAIN

TO RESOLVE FLARE
● NOT A CURABLE
● CRYSTALS REMAINS IN JOINTS
● DON’T TRY TOLOWER SERUM URATE
DURING FLARE
ACUTE GOUT TREATMENT
TREATMENT FOR FUTURE FLARES:

● COLCHICINE: 0.5-1.0 mg/day

● LOW-DOSE NSAIDS
● BOTH DECREASE FREQUENCY AND
SEVERITY OF FLARES
● PREVENT FLARES WITH START OF URATE-
LOWERING DRUGS
● BEST WITH 6 MONTHS OF CONCOMITANT
TREATMENT
● NSAIDS:
> INHIBITS PAIN AND INFLAMMATION.
> INHIBITS URATE CRYSTAL PHAGOCYTOSIS BY
DECREASING THE MIGRATION OF GRANULOCYTES INTO
THE INFLAMMATORY AREA.
> INDOMETHACIN, NAPROXEN, KETOROLAC.
● COLCHICINE:
> PRODUCES ITS ANTI-INFLAMMATORY EFFECTS BY
BINDING TO THE INTRACELLULAR PROTEIN TUBULIN,
PREVENTING ITS POLYMERIZATION LEADING TO THE
INHIBITION OF LEUKOCYTE MIGRATION INTO AFFECTED
AREA.
> INHIBITS THE SYNTHESIS AND RELEASE OF
LEUKOTRIENES.
● ALLUPURINOL/ FEBUXOSTAT:
> INHIBITS SYNTHESIS OF URIC ACID BY INHIBITING XANTHINE OXIDASE ENZYME.
GOUT PROGRESSION PREVENTION

● LOWER URATE TO <6 mg/dl

● DEPLETES: TOTAL BODY URATE
POOL DEPOSITED CRYSTALS
● TREATMENT IS LIFELONG AND
CONTINUOUS
● DRUG CHOICES: URICUSORIC
AGENTS; XANTHINE OXIDASE
AGENTS
ASYMPTOMATIC HYPERURICEMIA

● INDICATIONS FOR TREATMENT INCLUDES:

● 24 HOUR URINARY URIC ACID EXCRETION >1100 mg
● SERUM URIC ACID: MEN: >13 mg/dL; WOMEN: >10mg/dL
● NEPHROLITHIASIS
● ANY HISTORY OF SYMTOMS OF GOUT ESPECIALLY
WITH WORSENING RENAL FUNCTION
● PRESENCE OF GOUTY TOPHI IN BONE OR SOFT TISSUES
● RADIOGRAPHIC SIGNS OF GOUTY ARTHIRTIS
● IMPENDING CHEMOTHERAPY OR RADIOTHERAPY FOR
LEUKEMIA OR LYMPHOMA
PREVENTION:
● MAINTAIN THE CONCENTRATION OF URIC ACID LEVEL WITHIN THE NORMAL
RANGE.
● DRINK PLENTY OF WATER.
● BALANCE WEIGHT WITH PROPER DIET AND EXERCISE.
● AVOID PURINE RICH FOODS.
● REDUCING ALCOHOL CONSUMPTION.
● AVOID DIURETIC DRUGS.
 FOODS KNOWN TO
DECREASE THE
OCCURRENCE OF GOUT
INCLUDE DAIRY, FOODS
HIGH IN POTASSIUM,
BLACK CHERRY JUICE,
BLUEBERRIES AND LEMON
JUICE.
 IMMEDIATELY TREATING
GOUT WILL NOT ALLOW IT
WORSE.
NURSING RESPONSIBILITIES:
1. Give pain medication as needed especially during acute attacks.
2. Apply cold packs to inflamed joints to ease discomfort and reduce swelling.
3. Administer anti-inflammatory medication and other drugs, as ordered.
4. To promote sleep, administer pain medication at times that allow maximum rest.
5. Encourage bed rest, but use a bed cradle to keep bed linens off sensitive, in inflamed joints.
6. Encourage the patient to perform techniques that promote rest and relaxation.
7. Provide nutritious diet. Avoid purine rich foods.
8. Before and after surgery, administer colchicines to help prevent gout attacks as ordered.
9. Urge the patient to perform as much self-care as his immobility and pain allow.
10. Urge the patient to drink plenty if fluids 2 liters per day to prevent renal calculi.
11. Discuss the principles of gradual weight reduction with an obese patient.
12. Urge the patient to control hypertension, especially if he has tophaceous renal deposits.
13. Provide emotional support during diagnostic test and procedures.