​Kembara Xtra - Medicine - Pseudogout

​Kembara Xtra - Medicine - Pseudogout 
Autoinflammatory condition brought on by crystallization of calcium pyrophosphate dihydrate (CPPD) in joints
One of numerous illnesses linked to pathologic crystal deposition, mineralization, and ossification
- Chondrocalcinosis (calcification of hyaline or fibrocartilage), pseudogout, and pyrophosphate arthropathy are caused by CPPD crystal deposition.
Gout is caused by the crystallization of monosodium urate.
- Vascular calcification, osteoarthritis, and ankylosing spondylitis are caused by hydroxyapatite deposition.
 If you have arthritis and a pattern of joint involvement that is inconsistent with degenerative joint disease (such as metacarpophalangeal joints or wrists), you should be suspicious of pseudogout.
Broad clinical presentation
- Asymptomatic CPPD (inadvertently discovered on a radiograph, with or without accompanying osteoarthritis abnormalities)
- Acute CPPD arthritis (self-limiting, synovitis, acute onset)
In contrast to MTP in gout, knee is affected in more than 50% of all acute bouts.
 Can be caused by a traumatic event, a medical condition, or surgery (after a parathyroidectomy)
Chronic CPPD crystal deposition may result in a gradual degenerative arthritis in a number of joints, typically big joints, and is most common in elderly people. Symptom onset is typically sneaky.
Identification of CPPD crystals in synovial fluid is necessary for a conclusive diagnosis.
 Endocrine/metabolic; musculoskeletal system(s) affected
Synonyms include CPPD, pyrophosphate arthopathy, chondrocalcinosis, and pseudogout.

Epidemiology 
Prevalence No gender preponderance; thought to affect 4-7% of people in Europe and the United States; 80% of patients >60 years. Women are more likely to present atypically, while men are more likely to present severely.
Only a tiny fraction of persons with chondrocalcinosis who are between the ages of 60 and 75 and 1 in 3 who are beyond 80 develop arthropathy.

Pathophysiology and Etiology 
Acute autoinflammatory response to CPPD crystals in the synovial cavity causes arthopathy. CPPD crystal deposition happens in three stages:
An excessive amount of anionic pyrophosphate (PPi) is produced in the articular cartilage, which causes an inflammatory reaction by binding calcium to generate CCPD crystals. CPPD crystals are engulfed by neutrophils, causing the formation of extracellular traps; increased CPPD crystal deposition results in inflammation and injury.


Genetics 
The majority of instances are sporadic; only 1% of individuals have an uncommon familial pattern with autosomal dominant inheritance.
ANKH gene mutation increases the likelihood of calcium crystal formation.

Risk Elements 
Older age; joint injury


Basic Prevention 

In cases of recurrent CPPD, preventive administration of colchicine 0.6 mg BID may help to lessen the number of episodes.


Gout, hyperparathyroidism, amyloidosis, hemochromatosis, ochronosis, hypothyroidism, Wilson disease, familial hypocalciuric hypercalcemia, X-linked hypophosphatemic rickets, and acromegaly are among the conditions that are associated with it.

Diagnosis: The presentation of pseudogout frequently resembles gout.
Acute CPPD causes discomfort and swelling in one or more joints; the knee is affected 50% of the time; other common joints include the ankle, wrist, toe, and shoulder.
 Proximal joint involvement, often accompanied by tendinous calcifications and tibiofemoral and ankle arthritis (similar to polymyalgia rheumatica).
In 5% of instances, multiple symmetric joint involvement (mimicking RA) may appear following hyaluronic acid injections (Hyalgan, Synvisc).
Chronic CPPD: degenerative arthritis that gets progressively worse with recurrent acute inflammatory attacks

clinical assessment 
Joint effusion, decreased range of motion (ROM), and inflammation (erythema, warmth, and tenderness to the touch) are 50% linked with fever.
DISTINCTIVE DIAGNOSIS
 Gout, septic arthritis, and trauma are among the conditions that might result in acute inflammatory arthritis in one or more joints.
Other acute inflammatory arthritides include acute RA, Lyme illness, and Reiter syndrome.

Laboratory Results 

Initial examinations (lab, imaging)
Analysis of synovial fluid reveals an inflammatory effusion:
Neutrophil predominance (80-90%) and a cell count of 2,000 to 100,000 WBCs/mL
Polarized microscopy reveals a modest number of positively birefringent crystals; high false-negative rate; >50,000 WBC count increases chance of septic arthritis; >100,000 WBCs/mL; Take into account the following to rule out underlying disease:
- Serum magnesium, calcium, and phosphorus
- Alkaline phosphatase in serum
- Serum ferritin, total iron-binding capacity, and parathormone (i-PTH) levels - Serum iron and thyroid-stimulating hormone (TSH) levels
Radiographic findings in pseudogout are neither sensitive nor specific, according to a plain radiograph.
- Fibrocartilage calcifications that are punctate and linear, especially in the knees, hips, symphysis pubis, and wrists
Ultrasound: joint effusion, synovial thickening, and hyperechoic deposits - May be more helpful than plain radiography for the diagnosis of pseudogout in peripheral joints, with a positive predictive value of 92% and a negative predictive value of 93%. Chronic CPPD: subchondral cysts and loose bodies in joints not typically affected by degenerative joint disease.Chondrocalcinosis is visible on MRI as hypointense lesions, especially in the knee men.isci


Procedures for Diagnosis/Other 
ALERT

Aspiration may aid in the relief of symptoms and hasten the resolution of the condition. Synovial fluid analysis with proof of CPPD crystals is required for the diagnosis.
Interpretation of the test CPPD crystal deposition in synovium, ligaments, and tendons

Management 

Rest and elevating the afflicted joint(s) will help reduce inflammation and target symptom reduction.
 Apply cool compresses or ice to the injured joints.
 Avoid exerting weight on the aching joint; use crutches or a walker.

First Line of Medicine
Ice packs, rest, and joint aspiration with or without steroid injection are recommended for acute attacks. Oral NSAIDs and/or colchicine are recommended for preventative treatment of chronic CPPD.Oral NSAIDs: Naproxen 500 mg PO BID with food and Ibuprofen 600 to 800 mg PO TID-QID with food; not to exceed 3.2 g/day. Although indomethacin has greater complication rates than ibuprofen (RR = 1.2) and other NSAIDs (relative risk [RR] = 2.2], other NSAIDs are still effective.
Indications not to use:
Avoid if you have a history of aspirin or NSAID hypersensitivity, active peptic ulcer disease, or recurrent upper GI lesions.
- Serious GI bleeding can happen suddenly; the patient should be informed of the signs and symptoms. administer misoprostol 200 mg PO every other day (QID) or a proton pump inhibitor (PPI) to individuals at risk for stomach ulcers brought on by NSAIDs.
- Use caution if you have cardiovascular illness, especially if you have heart failure or difficult-to-control hypertension. - Avoid taking aspirin and an anticoagulant at the same time.
1.2 mg at the first symptom of a flare, followed in one hour; oral colchicine, 0.5 mg up to 3–4 times day, with or without a 1 mg initial dosage; intra-articular steroid injection, prednisolone sodium phosphate 4–20 mg or triamcinolone diacetate 2–40 mg with local anesthetic
 Supportive methods for immobilization and symptomatic alleviation (application of cold or cool packs).
Next Line
Prednisone used orally: 30 to 50 mg daily for 7 to 10 days
Consider referring individuals with extensive, space-occupying tophaceous lesions for surgical removal. IM triamcinolone acetonide 40 mg; repeat if necessary in 1–4 days.
Alternative treatments for chronic CPPD include ethylenediaminetetraacetic acid (EDTA), hydroxychloroquine, infliximab, probenecid, and anakinra (anti-IL-1). Studies on a large scale are required to gauge effectiveness.


Alert 
Methotrexate had no discernible effect in a recent randomized trial of patients with chronic-recurrent CPPD.


Referral 

If the patient or the infected joint is not responding, you might want to consider seeing an orthopedist or rheumatologist.

Further Treatments 

Isometric exercises are used in physical therapy to maintain muscle strength throughout the acute phase.
As the swelling and pain decrease, start performing joint ROM exercises.
Restart weight bearing once the pain has subsided.

Surgical Techniques 

Analyze the joint fluid and do arthrocentesis.

Admission 
If: Synovial fluid WBC count >50,000/mL; Treat with appropriate antibiotics pending culture findings; consider hospitalization for septic arthritis.

Patient Follow-Up Monitoring
48 to 72 hours after starting therapy, reevaluate your reaction, and after a week, reevaluate again as necessary.

Diet 
There is no established link to diet

Changes in Lifestyle: Rest the injured joint; Symptoms normally go away in 7 to 10 days.

The prognosis for an acute attack's remission is excellent; it typically lasts for 10 days.
Patients who endure recurring attacks may develop progressive joint degeneration and functional limitations.

Complications 
Osteoarthritis and recurrent acute episodes of  pseudogout 


 Geriatric considerations
A loading dose of colchicine is not necessary in older patients using NSAIDs because of the high prevalence of renal insufficiency in this population, who also require careful monitoring and are more likely to experience GI bleeding and acute renal insufficiency.

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