Rheumatoid hands

Published on 02/04/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

Print this page

This article have been viewed 2260 times

[level-membership-for-internal-medicine-category]

127 Rheumatoid hands

Instruction

Examine this patient’s hands.

Salient features

History

• Painful swollen joints

• Morning stiffness.

Examination

• Ask the patient for permission to examine her hands and then ask whether the hands are sore.

Proceed as follows:

• Comment on deformities (Fig. 127.1) such as the following:

• Subluxation at the metacarpophalangeal joint

• Swan-neck deformity

• Boutonnière deformity (hyperextension at the terminal interphalangeal joint and flexion at the proximal interphalangeal joint)

• Z deformity of the thumb

• Dorsal subluxation of the ulna at the carpal joint.

• Comment on the following signs:

• Nailfold infarcts and vasculitic skin lesions

• Palmar erythema

• Wasting of the first dorsal interossei and other small muscles of the hand.

• Test grip and pincer movements. Quickly test for abductor pollicis brevis and interossei, and pinprick sensation over index and little fingers. The median nerve may be involved if there is associated carpal tunnel syndrome.

• Examine the elbow for rheumatoid nodules.

• Ask the patient to perform simple tasks involving hand function, such as unbuttoning clothes or writing.

• Tell the examiner that you would like to examine other joints.

• Highlight the following points:

• Whether terminal interphalangeal joints are spared or affected

• Whether the arthritis is active (if the joints are inflamed) or inactive

• Be prepared to discuss the radiological features.

Fig. 127.1 Deformities of the hands in rheumatoid arthritis.

Diagnosis

This patient has swan-neck deformity of the fingers (lesions) caused by rheumatoid arthritis (aetiology) with marked active arthritis of the interphalangeal joints, and is unable to button her clothes (functional status).

Questions

What is the significance of nodules in rheumatoid arthritis?

The presence of nodules indicates seropositive and more aggressive arthritis (Fig. 127.2).

Fig. 127.2 Hand in seropositive rheumatoid arthritis, showing fixed deformities and gross rheumatoid nodules.

(With permission from Canoso JJ 1997.)

What precautions are necessary before upper gastrointestinal endoscopy or general anaesthesia?

It is prudent to take a cervical spine radiograph to rule out atlanto-axial subluxation.

Which joints are commonly affected in rheumatoid arthritis?

Wrists, proximal interphalangeal joints and metacarpophalangeal joints of the hands, metatarsophalangeal joints and knees.

What is palindromic rheumatoid arthritis?

Palindromic onset is seen in some patients with recurrent episodes of joint stiffness and pain in individual joints lasting only a few hours or days. Hydroxychloroquine may be of value in preventing recurrences.

Advanced-level questions

How would you treat the arthritis?

Prescribe NSAIDs (ibuprofen is the safest at conventional doses) including aspirin. If, after 1 month of NSAIDs, the symptoms persist with no sign of remission then a second-line drug should be added. Second-line drugs include hydroxychloroquine, sulfasalazine and pencillamine. Low-dose methotrexate and gold salts are used to prevent disease progression. Three biologic products that inhibit the actions of tumour necrosis factor-α (TNF-α; infliximab, etanercept and adalimumab) and one that inhibits the action of interleukin-1 (anakinra) produce significant improvement in the severity of arthritis. Etanercept is a fusion protein of the ligand-binding region of the TNF receptor and the Fc portion of human IgG; infliximab is a chimeric (mouse and human) monoclonal antibody against TNF. These TNF inhibitors have surprisingly few side effects. The most common reactions are at the injection site (with etanercept) and hypersensitivity reactions (with infliximab). The TNF-α inhibitors suppress disease activity only during treatment and, consequently, relapses are inevitable once the treatment is discontinued (N Engl J Med 2000;343:1640–1). Alternative agents include lefunomide, a TNF or interleukin-1 blocker; rituximab, an anti-CD20 chimeric monoclonal antibody; and abatacept, which blocks selective costimulation of T cells.

If the patient is known to experience gastric distress with non-steroidal anti-inflammatroy drugs, what precautions would you take while prescribing them?

Prophylaxis for NSAID-associated gastric distress may be attempted with concurrent administration of an H₂-receptor blocker (such as ranitidine), omeprazole or misoprostol. The last is a prostaglandin analogue that has been shown to protect the gastric mucosa.

What are the neurological manifestations of rheumatoid arthritis?

• Peripheral neuropathy: glove-and-stocking sensory loss

• Mononeuritis multiplex

• Entrapment neuropathy, e.g. carpal tunnel syndrome

• Cervical disease or atlanto-axial subluxation may cause cervical myelopathy.

What are the causes of proteinuria in patients with rheumatoid arthritis?

• Drug therapy: gold salts, penicillamine

• Amyloidosis.

What is Sjögren syndrome?

• The association of keratoconjunctivitis sicca (lack of lacrimal secretion) and xerostomia (dry mouth as a result of lack of salivary gland secretion) in association with a connective tissue disorder, usually rheumatoid arthritis. This syndrome may be associated with autoimmune thyroid disease, myasthenia gravis or autoimmune liver disease.

• Anti-Ro (SSA) and anti-SS-B antibodies may be seen in this syndrome.

• Treatment is symptomatic with artificial tears (hypomellose drops or 1% methylcellulose), artificial saliva and NSAIDs for the arthritis.

• The Schirmer filter paper test provides a crude measure of tear production. Filter paper is hooked over the lower eyelid and in normal people at least 15 mm is wet after 5 min, whereas in patients with keratoconjunctivitis sicca it is <5 mm.

What is the role of anti-cyclic citrullinated peptide antibodies?

The presence of autoantibodies to cyclic citrullinated peptide (CCP) is specific to rheumatoid arthritis. Their detection contributes both to the differential diagnosis and to a prediction of the severity of joint destruction, even though the mechanistic significance of these autoantibodies is unclear.

What are the criteria for rheumatoid arthritis?

Patients are definitively diagnosed with rheumatoid arthritis if they score 6 or more points on the following series of assessments:

• Joint involvement:

• 1 medium–large joint: 0 points

• 2–10 medium–large joints: 1 point

• 1–3 small joints: 2 points

• 4–10 small joints: 3 points

• >10 small joints: 5 points.

• Serology:

• Not positive for either rheumatoid factor or anti–citrullinated protein antibody: 0 points

• At least one of these two tests are positive at low titre (more than the upper limit of normal but not higher than three times the upper limit of normal): 2 points

• At least one test is positive at high titre (more than three times the upper limit of normal): 3 points.

• Duration of synovitis:

• Lasting fewer than 6 weeks: 0 points

• Lasting 6 weeks or longer: 1 point.

• Acute phase reactants:

• Neither C-reactive protein nor ESR abnormal: 0 points

• Abnormal C-reactive protein or abnormal ESR: 1 point.

Patients receive the highest point level they fulfill within each domain. For example, a patient with five small joints involved and four large joints involved scores 3 points.

What are the poor prognostic factors?

• Systemic features: weight loss, extra-articular manifestations

• Insidious onset

• Rheumatoid nodules

• Presence of rheumatoid factor >1 in 512

• Persistent activity of the disease for over 12 months

• Early bone erosions.

What are the factors leading to ulnar deviation of the hands?

In the normal grip, the fingers move to ulnar deviation; this is caused by:

• weakening of radial sides of the joint capsule and the radial insertion of the interossei ligaments

• the volar supports of the flexor tendon sheath are weakened by inflammation, allowing the tendon to bow in the direction of the ulna during gripping

• ulnar displacement of the extensor tendons in early deviation makes them slip if the dorsal metacarpophalangeal joint is taut, and this exacerbates the development of ulnar deviation by acting as a bowstring

• joint capsules of metacarpophalangeal joints are weaker on radial sides than on ulnar sides.

What is the role of cadherins in the pathogenesis of rheumatoid arthritis?

Fibroblast-like synoviocytes mediate cartilage damage in rheumatoid arthritis (rheumatoid inflammation causes damage to both articular cartilage and periarticular bone). Cadherin-11 deficiency protects mice from cartilage damage but not from bone erosion, probably because cadherin-11 seems to mediate the migration of fibroblast-like synoviocytes over the articular cartilage and its subsequent damage.

What is the role of phosphatidylinositol 3′-kinase-γ in the pathogenesis of rheumatoid arthritis?

A novel inhibitor of phosphatidylinositol 3′-kinase has been shown to be effective in blocking inflammation and joint destruction in mouse models of rheumatoid arthritis.

AB Garrod coined the term rheumatoid arthritis in 1858.

HSC Sjögren, a Swedish ophthalmologist, described this condition in 1933.

A Caplan, a British physician, was an industrial officer in the Welsh coal mines.

In 1931 Philip S Hench (1896–1965) of the Mayo Clinic observed that arthritic pain temporarily decreased in pregnant women. He then studied the phenomena for the next 8 years, finding that allergic conditions such as asthma, hay fever and food sensitivity were also lessened in the presence of jaundice or pregnancy. He reasoned that a steroid hormone may be responsible, since levels of steroid hormones are high in the blood during pregnancy. (Hench PS. A reminiscence of certain events before, during and after the discovery of cortisone. Minn Med 1953;36:705–710).

Edward Kendall (1886–1972), Chief of the Division of Biochemistry, suggested the name ‘corsone’ on a piece of paper but Hench amended this to ‘cortisone’, and thus the steroid hormone was ‘baptized’. The 1950 Nobel Prize for Medicine was jointly awarded to Kendall, Hench and Tadeus Reichstein (1897–1996) of Basel University, Switzerland, for their discoveries relating to the hormones of the adrenal cortex, their structure and biological effects (Lancet 1999;353:1370).

Sir John Vane, showed that inhibition of prostaglandin synthesis was central to both the actions and side effects of aspirin (Proc R Coll Phys Edinb 2000;30:191–8).

[/level-membership-for-internal-medicine-category][not-level-membership-for-internal-medicine-category]

127 Rheumatoid hands

Instruction

Examine this patient’s hands.

Salient features

History

• Painful swollen joints

• Morning stiffness.

Examination

• Ask the patient for permission to examine her hands and then ask whether the hands are sore.

Proceed as follows:

• Comment on deformities (Fig. 127.1) such as the following:

• Subluxation at the metacarpophalangeal joint

• Swan-neck deformity

• Boutonnière deformity (hyperextension at the terminal interphalangeal joint and flexion at the proximal interphalangeal joint)

• Z deformity of the thumb

• Dorsal subluxation of the ulna at the carpal joint.

• Comment on the following signs:

• Nailfold infarcts and vasculitic skin lesions

• Palmar erythema

• Wasting of the first dorsal interossei and other small muscles of the hand.

• Examine the elbow for rheumatoid nodules.

• Ask the patient to perform simple tasks involving hand function, such as unbuttoning clothes or writing.

• Tell the examiner that you would like to examine other joints.

• Highlight the following points:

• Whether terminal interphalangeal joints are spared or affected

• Whether the arthritis is active (if the joints are inflamed) or inactive

• Be prepared to discuss the radiological features.

Fig. 127.1 Deformities of the hands in rheumatoid arthritis.

Diagnosis

Questions

What is the significance of nodules in rheumatoid arthritis?

The presence of nodules indicates seropositive and more aggressive arthritis (Fig. 127.2).

Fig. 127.2 Hand in seropositive rheumatoid arthritis, showing fixed deformities and gross rheumatoid nodules.

(With permission from Canoso JJ 1997.)

Where are nodules found?

Flexor and extensor tendons of the hand, sacrum, Achilles tendon, sclera, lungs and myocardium.

What are the skin lesions in rheumatoid arthritis?

Vasculitis, nailfold infarcts.

What are the causes of anaemia in rheumatoid arthritis?

• Anaemia of chronic disease

• Megaloblastic anaemia from folate deficiency or associated pernicious anaemia

• Felty syndrome

• Drugs: NSAIDs causing iron-deficiency anaemia, gold causing bone marrow suppression.

What factors have been implicated in anaemia of chronic disease?

• Decreased production of red blood cells:

• Inadequate iron: impaired absorption and transport, failure to release iron stores

• Decreased concentration or marrow resistance to erythropoietin.

• Ineffective erythropoiesis

• Abnormal development of erythroid progenitor cells

• Increased destruction of red cells.

What is Felty syndrome?

Buy Membership for Internal Medicine Category to continue reading. Learn more here

[/not-level-membership-for-internal-medicine-category]

250 Cases in Clinical Medicine

Recent Posts

Categories

Search Engine

Rheumatoid hands