1. Presence of effusion of unexplained etiology
2. Steroid injection
3. Decompression of a hemorrhagic effusion in traumatized joints
4. Evaluation of abx response in pts w/infectious arthritis
5. Removal of purulent fluid in distended infected joints
Contraindications
1. Cellulitis or broken skin over the intended entry site
2. Coagulopathy
3. Unstable joint
Procedure
1. Palpate the joint and identify the extensor surface (vessels and nerves are less commonly found here).
2. With firm pressure, use a ballpoint pen that has the writing portion retracted to mark the specific area of the joint to be aspirated.
3. Clean the skin w/an antiseptic solution.
4. Use a 25-gauge needle to infiltrate the skin w/1% to 2% lidocaine.
5. Gently insert an 18- or 20-gauge needle connected to a 20- to 30-mL syringe; a slight “pop” may be felt as the needle penetrates the capsule.
6. Apply gentle suction to the syringe to aspirate the fluid.
7. Gently remove the needle, and apply slight pressure to the puncture site.
8. Process the aspirated synovial fluid:
a. Tube 1 (no heparin): viscosity, mucin clot
b. Tube 2 (containing heparin): glucose level
c. Tube 3 (containing heparin): Gram stain, C&S, cytology, CBC w/diff
d. Glass slide: Place a drop of fluid and examine under polarized light.
e. Plate w/Thayer-Martin medium (used in cases of suspected gonococcal arthritis); assessment for Lyme titer, cultures for anaerobes, Mycobacterium tuberculosis, and fungi should be ordered only when clearly indicated.
9. Draw samples for measurement of serum glucose level.
Interpretation of Results
1. Color: Normally it is clear or pale yellow; cloudiness indicates an inflammatory process or presence of crystals, cell debris, fibrin, or TGs.
2. Viscosity is high because of hyaluronate; when fluid is placed on a slide, it can be stretched to a string longer than 2 cm before separating (low viscosity indicates breakdown of hyaluronate [lysosomal enzymes from leukocytes] or the presence of edema fluid).
3. Mucin clot: Add 1 mL of fluid to 5 mL of a 5% acetic acid solution, and allow 1 min for the clot to form; a firm clot (does not fragment on shaking) is nl and indicates the presence of large molecules of hyaluronic acid (this test is nonspecific and infrequently done).
4. Glucose level: nl is approximately = serum glucose level; a difference of >40 mg/dL suggests infection.
5. Total protein concentration is <2.5 g/dL in nl synovial fluid; it is ↑ in cases of inflammatory and septic arthritis.
6. Microscopic examination for crystals:
a. Gout: monosodium urate crystals
b. Pseudogout: Ca2+ pyrophosphate dihydrate crystals
Figure 12-1 is an algorithm for analysis of joint fluid.
FIGURE 12-1 Algorithm for analysis of joint fluid. Examples of inflammatory arthritis are indicated, although many conditions can produce these findings. AS, ankylosing spondylitis; PsA, psoriatic arthritis. (From Goldman L, Schafer AI [eds]: Goldman’s Cecil Medicine, 24th edition. Philadelphia, Saunders, 2012.)
B. Arthritis, Monarticular and Oligoarticular
Septic arthritis (Staphylococcus aureus, Neisseria gonorrhoeae, meningococci, streptococci, Streptococcus pneumoniae, enteric gram(−) bacilli)
Crystalline-induced arthritis (gout, pseudogout, Ca oxalate, hydroxyapatite, and other basic Ca/phosphate crystals)
Traumatic joint injury
Hemarthrosis
Monarticular or oligoarticular flare of an inflammatory polyarticular rheumatic disease (RA, psoriatic arthritis, Reiter’s syndrome, SLE)C. Arthritis, Polyarticular
RA, juvenile (rheumatoid) polyarthritis
SLE, other connective tissue diseases, erythema nodosum, palindromic rheumatism, relapsing polychondritis
Psoriatic arthritis, ankylosing spondylitis
Sarcoidosis
Lyme arthritis, bacterial endocarditis, Neisseria gonorrhoeae infection, rheumatic fever, Reiter’s disease
Crystal deposition disease
Hypersensitivity to serum or drugs
Hepatitis B, HIV infection, rubella, mumps
Other: serum sickness, leukemias, lymphomas, enteropathic arthropathy, Whipple’s disease, Behçet’s syndrome, Henoch-Schönlein purpura, familial Mediterranean fever, hypertrophic pulmonary osteoarthropathyD. Vasculitic Syndromes
See Table 12-1.
E. Systemic Lupus Erythematosus (SLE)
Chronic multisystemic disease characterized by production of antibodies and protean clinical manifestations
TABLE 12-1
Systemic Vasculitis∗
| Large-Vessel | Pathophysiology | Clinical Features/Dx | Management |
| Giant Cell Arteritis (Temporal Arteritis) |
Affects large-caliber vessels that contain internal elastic membranes Multinucleated giant cells w/in vessel wall or adventitia Age >50 yr Women 2:1 |
New-onset headache (temporal or occipital) in pt >50 yr Visual changes/loss (ischemia of optic nerve ± inflammation of ophthalmic artery) Jaw claudication (± ischemia of masseter or temporalis mm) PMR (pain in hip/shoulder girdle) UE limb claudication, subclavian steal Aortic regurgitation Dx: ↑↑↑ ESR and CRP Anemia + thrombocytosis Established via temporal artery bx |
Prednisone 1 mg/kg/day gives rapid response Treat immediately when dx is suspected; temporal artery biopsy findings will not change w/steroid administration until at least 4 wk Taper prednisone over 4-6 wk, guided by ESR and CRP Flares commonly occur during tapering and are managed by increasing the prednisone dose by 10 mg over dose that initially controlled the disease Low-dose aspirin to ↓ risk of CVA |
| Polymyalgia Rheumatica | Pain and stiffness in the proximal limbs associated w/elevated acute phase reactants Associated w/giant cell and late-onset RA |
Pain, stiffness, and limitation in passive ROM of the shoulder and hip girdle muscles No peripheral joint swelling Dx: ↑ ESR and CRP Mild normochromic, normocytic anemia |
Low-dose prednisone Tapered over a 6-mo period Can use MTX as steroid-sparing agent |
| Takayasu Arteritis | Affects aorta and its major branches, pulmonary arteries 2nd-4th decade of life Women 8:1 |
Inflammatory Phase Fever, arthralgias, myalgias, malaise, wt loss for several months Audible bruits over carotid, subclavian, renal, iliac vessels Pulseless Phase UE/LE claudication ± vascular insufficiency Pulse deficits and differential systolic BP’s HTN ± RAS Dx: ↑ ESR and CRP CTA or MRA or aorta and branches to show narrowing |
Inflammatory Phase High-dose corticosteroids Can use MTX of TNF-α blockers as corticosteroid-sparing agents Pulseless Phase Difficult to Rx because active vessel inflammation may be absent => Look for inflammation w/contrast MRI and PET scans Low-dose aspirin Treat lipids aggressively to prevent atherosclerosis |
| Medium-Vessel | Pathophysiology | Clinical Features/Dx | Management |
| Polyarteritis Nodosa | Inflammation and necrosis of medium-sized and small muscular artery walls Age of onset: 40-60 yr 50% cases associated with Hep B |
Fever, arthralgia, myalgia, abd pain, wt loss Peripheral nerve: mononeuritis multiplex HTN ± renoarteriolar involvement Testicular pain, painful cutaneous nodules/skin ulcers/palpable purpura/livedo reticularis Spares lungs Dx: P-ANCA Necrotizing arteritis on bx specimens of involved skin, sural nerve (do not use kidney given risk of hemorrhage) Aneurysms and stenoses on CTA |
High-dose corticosteroids × several weeks w/slow taper following Use cyclophosphamide in patients who do not respond In hep B(+) patients, give short course (1-2 wk) of steroids w/antiviral Rx (entecavir) (>50% HBeAg(+) Pts w/polyarteritis nodosa respond w/resolution of arteritis and seroconversion to hep B e-antibody positivity |
| Kawasaki’s Disease | Usually occurs in children Seen in adults w/HIV |
Fever >5 days + nonexudative conjunctivitis, erythema of oral mucosa Edema of extremities w/desquamation ACS or peripheral vascular occlusion Coronary aneurysms (MC in children) Dx: made by clinical features |
High-dose salicylates and early administration of IVIG TTE to r/o coronary artery aneurysm |
| Small-Vessel | Pathophysiology | Clinical Features/Dx | Management |
| Wegener’s Granulomatosis (Granulomatosis w/Polyangiitis) | Involvement of small to medium-sized arteries and can be associated w/a “pauci-immune” (no immune complexes) GN | Upper airway disease (70%): sinusitis, epistaxis, and nasal septal perforation/saddle nose deformity ± cartilage erosion Pulmonary: cough, hemoptysis, pleurisy, multifocal infiltrates or nodules on CXR Ocular symptoms: scleritis, uveitis, keratitis Purpura, ulcers on skin Pauci-immune GN (80%) Dx: C-ANCA Established by kidney or lung bx Antiproteinase-3 Abs’ |
High-dose corticosteroids w/3-6-mo course of cyclophosphamide B-cell depletion Rx w/rituximab has been shown to be equally as effective as cyclophosphamide Following remission: steroids are tapered and cyclophosphamide is stopped => Rx is continued for 18 mo w/azathioprine or wkly MTX (90% achieve remission, relapses are frequent w/MTX) Bactrim for PCP prophylaxis |
| Small-Vessel | Pathophysiology | Clinical Features/Dx | Management |
| Microscopic Polyangiitis | Necrotizing vasculitis that predominantly affects the lungs and kidneys Age of onset: 30-50 yr |
Fever, arthralgia, purpuric skin rash, mononeuritis multiplex Rapidly progressive GN or pulmonary hemorrhage Dx: P-ANCA Antimyeloperoxidase Ab (60%-80%) Confirm w/bx of affected tissue (skin, lung, kidney): lung: pulmonary capillaritis; kidney: pauci-immune or diffuse necrotizing GN similar to Wegener’s; skin: necrotizing arteritis of arterioles |
High-dose corticosteroids + cyclophosphamide OR rituximab Following remission, those treated w/cyclophosphamide should transition to azathioprine or wkly MTX |
| Churg-Strauss Syndrome | Systemic vasculitis in the spectrum of hypereosinophilic disorders | Most often occurs in setting of antecedent asthma, allergic rhinitis, sinusitis Eosinophilia (>10%) Migratory pulmonary infiltrates Fever, arthralgias, myalgias, purpura Dx: P-ANCA (50%); usually have pauci-immune GN and mononeuritis Established by bx and confirmed eosinophilic tissue infiltration |
High-dose corticosteroids allow full remission in 80-90% Oral or IV cyclophosphamide is recommended in pts w/neuro, GI, renal, or cardiac involvement Maintenance Rx w/azathioprine or MTX for 12-18 mo following remission |
| Henoch-Schönlein Purpura | “Systemic” IgA nephropathy Usually occurs in children In men >50 yr old, look out for association w/solid tumors or MDS |
Palpable purpura affecting distal LEs Abdominal pain, arthritis Hematuria/proteinuria Usually self-limiting Dx: Confirm w/bx of affected tissue (skin, lung, kidney): skin: shows presence of leukocytoclastic vasculitis w/IgA deposits; kidney: GN w/IgA deposition |
Short course of moderate-dose steroids (20-40 mg/day of prednisone) Decreases duration and severity of skin and joint symptoms associated w/HSP In patients w/proliferative GN give high-dose steroids and monthly cyclophosphamide |
| Small-Vessel | Pathophysiology | Clinical Features/Dx | Management |
| Essential Cryoglobulinemic Vasculitis | Immunoglobulins that precipitate from serum in the cold Type I cryoglobulins: monoclonal, self-aggregate, associated w/Waldenström’s and MM; associated w/hyperviscosity Type II cryoglobulins: monoclonal IgM or IgA rheumatoid factors that bind to Fc of IgG, associated w/hep C and HIV Type II cryoglobulins: seen in setting of autoimmune disorders (SLE, Sjögren’s, RA) |
Palpable purpura, mononeuritis multiplex LAD, HSM Renal failure ± GN Dx: ↓ C3, C4 (immune-complex GN) 80% of type-II cryoglobulinemic vasculitis is associated w/hep C |
Hep C–associated cryoglobulinemia responds to antiviral therapy w/interferon alfa + ribavirin Short course of corticosteroids In patients with renal failure, digital gangrene, neuro disease, 2-3-wk course of plasma exchange recommended |
| Cutaneous Leukocytoclastic Vasculitis | Seen in pts w/connective tissue diseases and as a reaction to drugs/viruses 40% idiopathic 60% ± autoimmune disease (SLE), drugs, infection, hematologic malignancy |
Palpable purpura, tender nodules, persistent urticaria, or shallow ulcers Lesions seen most commonly on distal LEs Dx: Neutrophils and mononuclear cells invading the walls of dermal capillaries, arterioles, and venules seen on bx |
Removal of offending drugs or treatment of the infectious etiology Favorably responds to NSAIDs, colchicine, or dapsone Manage urticarial lesions w/combining antihistamines (H1 and H2 blockers) |
∗ Vasculitis: Inflammation of blood vessel walls that causes vessel narrowing/occlusion, aneurysm, or rupture.
Etiology
The exact etiology and pathogenesis are uncertain.
Genetic susceptibility to lupus is likely inherited as a polygenic trait. Multiple genetic linkages including 1q23, 2q35-37, 6p21-11, and 12q24 show strong associations with SLE. Environmental factors such as ultraviolet light exposure and Epstein-Barr virus infection may have a triggering role. Autoantibodies can be present years before the diagnosis of SLE. Evidence supports the improper processing of nuclear proteins and nucleic acid from programmed cell death. This leads to the presentation of self-DNA to plasmacytoid dendritic cells. Plasmacytoid dendritic cells propagate antibody and immune complex production and other arms of specific autoimmunity.Diagnosis
H&P
Constitutional: unexplained fever, fatigue, malaise
Skin: malar rash sparing nasolabial folds (acute cutaneous lupus), annular or papulosquamous rash (subacute cutaneous lupus), raised erythematous patches with subsequent edematous plaques and adherent scales (discoid cutaneous lupus); alopecia, nasal, or oropharyngeal ulcerations; Raynaud’s phenomenon; petechiae, palpable purpura, skin ulceration, or digital ischemia (vasculitis); livedo reticularis or livedo racemosa (secondary antiphospholipid antibody syndrome)
Musculoskeletal: arthritis (tenderness, swelling, effusion) typically affecting peripheral joints; myositis
Cardiac: pericardial rub (pericarditis), heart murmur (Libman-Sachs endocarditis and other valvular heart disease), congestive heart failure (myocarditis), premature atherosclerotic heart disease
Pulmonary: pleuritis, pneumonitis, diffuse alveolar hemorrhage
Gastrointestinal: abdominal pain, intestinal vasculitis, ascites
Neurologic: headache, psychosis, seizure, acute confusional states, peripheral or cranial neuropathy, transverse myelitis, CVA, chronic cognitive impairment
Hematologic: anemia (hemolytic, anemia of chronic disease, aplastic anemia), thrombocytopenia, leukopenia, lymphadenopathy, secondary antiphospholipid antibody syndrome
Renal: ARF, proteinuria, nephritic syndrome, nephrotic syndromeW/Up
The diagnosis of SLE is suspected when any four or more of the following 1997 American College of Rheumatology criteria are present:• Malar rash
• Discoid rash
• Photosensitivity (recurrence of unusual skin rash in sun exposed areas)
• Oral or nasopharyngeal painless ulceration
• Arthritis
• Serositis (pleuritis, pericarditis)
• Renal disorder (persistent proteinuria >0.5 g/day, or 3+ on dipstick if quantitation not performed; cellular casts)
• Neurologic disorder (seizures, psychosis [in absence of offending drugs or metabolic derangement])
• Hematologic disorder:
• Hemolytic anemia with reticulocytosis
Buy Membership for Internal Medicine Category to continue reading. Learn more here
