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Diseases » Rheumatoid arthritis » Diagnosis
 

Diagnosis of Rheumatoid arthritis

Diagnostic Test list for Rheumatoid arthritis:

The list of medical tests mentioned in various sources as used in the diagnosis of Rheumatoid arthritis includes:

Rheumatoid arthritis Diagnosis: Book Excerpts

Tests and diagnosis discussion for Rheumatoid arthritis:

Handout on Health Rheumatoid Arthritis: NIAMS (Excerpt)

Rheumatoid arthritis can be difficult to diagnose in its early stages for several reasons. First, there is no single test for the disease. In addition, symptoms differ from person to person and can be more severe in some people than in others. Also, symptoms can be similar to those of other types of arthritis and joint conditions, and it may take some time for other conditions to be ruled out as possible diagnoses. Finally, the full range of symptoms develops over time, and only a few symptoms may be present in the early stages. As a result, doctors use a variety of tools to diagnose the disease and to rule out other conditions.

Medical history: This is the patient's description of symptoms and when and how they began. Good communication between patient and doctor is especially important here. For example, the patient's description of pain, stiffness, and joint function and how these change over time is critical to the doctor's initial assessment of the disease and his or her assessment of how the disease changes.

Physical examination: This includes the doctor's examination of the joints, skin, reflexes, and muscle strength.

Laboratory tests: One common test is for rheumatoid factor, an antibody that is eventually present in the blood of most rheumatoid arthritis patients. (An antibody is a special protein made by the immune system that normally helps fight foreign substances in the body.) Not all people with rheumatoid arthritis test positive for rheumatoid factor, however, especially early in the disease. And, some others who do test positive never develop the disease. Other common tests include one that indicates the presence of inflammation in the body (the erythrocyte sedimentation rate), a white blood cell count, and a blood test for anemia.

X rays: X rays are used to determine the degree of joint destruction. They are not useful in the early stages of rheumatoid arthritis before bone damage is evident, but they can be used later to monitor the progression of the disease. (Source: excerpt from Handout on Health Rheumatoid Arthritis: NIAMS)

Arthritis: NWHIC (Excerpt)

Blood tests may reveal anemia and the presence of an antibody called rheumatoid factor (RF). However, some people with RF never develop rheumatoid arthritis, and some people with the disease never have RF. (Source: excerpt from Arthritis: NWHIC)

Diagnosis of Rheumatoid arthritis: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Rheumatoid arthritis:

Diagnostic Tests for Rheumatoid arthritis: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Rheumatoid arthritis.


SPLENOMEGALY, ACUTE OR SUBACUTE: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is there fever? The presence of fever should suggest infectious mononucleosis, infectious hepatitis, leptospirosis, acute leukemia, lymphoma, malaria, and bacterial endocarditis, among other things.
  2. Is there a rash? The presence of a rash should suggest thrombocytopenic purpura, acute leukemia, typhoid fever, septicemia, and lupus erythematosus.
  3. Is there jaundice? The presence of jaundice should suggest infectious hepatitis, leptospirosis, malaria, hereditary spherocytosis and other hemolytic anemias, and portal vein thrombosis secondary to chronic liver disease.
  4. Is there lymphadenopathy? The presence of lymphadenopathy should suggest infectious mononucleosis, acute lymphatic leukemia, lymphoma, brucellosis, and reticuloendotheliosis.
  5. Is there a history of trauma? The presence of a history of trauma would suggest a traumatic rupture of the spleen.

DIAGNOSTIC WORKUP

Routine tests include a CBC, platelet count, sedimentation rate, chemistry panel, febrile agglutinins, serum haptoglobins, ANA test, Monospot test, serum protein electrophoresis, tuberculin test, chest x-ray, EKG, and flat plate of the abdomen.

If there is jaundice, a hepatitis profile, red cell fragility test, and blood smear for parasites should be done. If there is fever, serial blood cultures, leptospirosis antibody titer, and smear for malarial parasites should be done. If there is a petechial rash, a coagulation profile should be done. Lymph node biopsies and bone marrow examinations may be necessary. A CT scan of the abdomen and radionuclide scan for liver and spleen size and ratio should be done. The assistance of a hematologist or infectious disease expert should be sought. A surgeon may need to be consulted for an exploratory laparotomy.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

SPLENOMEGALY, CHRONIC: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is it massive? Massive splenomegaly is characteristic of Gaucher's disease, chronic myeloid leukemia, kala azar, and agnogenic myeloid metaplasia.
  2. Is there jaundice? The presence of jaundice with massive splenomegaly would suggest chronic malaria. The presence of jaundice with mild to moderate splenomegaly would suggest alcoholic cirrhosis, chronic hepatitis, and hereditary spherocytosis.
  3. Is there hepatomegaly? The presence of massive splenomegaly and hepatomegaly is characteristic of Gaucher's disease, chronic myeloid leukemia, kala azar, and agnogenic myeloid metaplasia.
  4. Is there pallor? The presence of pallor, of course, suggests anemia and that would make one think of hereditary spherocytosis and other hemolytic anemias, collagen disease, and chronic malaria.
  5. Is there lymphadenopathy? The presence of lymphadenopathy should make one think of chronic lymphatic leukemia, lymphomas, and sarcoidosis.

DIAGNOSTIC WORKUP

The diagnostic workup of chronic splenomegaly is similar to that for acute splenomegaly. A splenoportogram may be helpful in diagnosing portal vein thrombosis. Angiography may be helpful in diagnosing a splenic aneurysm. A liver biopsy, splenic aspiration and biopsy, and bone marrow biopsy may all be helpful in diagnosing the reticuloendothelioses such as Gaucher's disease.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Splenomegaly: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Mononucleosis
  • Congestive heart failure
  • Portal hypertension
    –Most often secondary to cirrhosis
  • Hepatitis
  • Hereditary spherocytosis
  • Sickle cell disease
  • Thalassemia major
  • Polycythemia vera
  • Malaria
  • Tuberculosis
  • Other infections: Mycobacterium avium complex, HIV, CMV, RMSF
  • Endocarditis
    • Malignancy (e.g., leukemia, lymphoma, metastases)

    • –Massive enlargement of the spleen usually signifies a lymphoproliferative or myeloproliferative disorder
  • Systemic lupus erythematosus
  • Felty's syndrome (rheumatoid arthritus, splenomegaly, and granulocytopenia)
  • Splenic hemangioma, hamartoma, or cyst
  • Trauma
  • Splenic vein thrombosis
  • Less common causes (“zebras”) include Gaucher's disease, amyloidosis, kala-azar (visceral leishmaniasis), schistosomiasis, rickets, syphilis, babesiosis, typhoid fever, histoplasmosis, and toxoplasmosis

Workup and Diagnosis

  • History and physical examination
    • CBC with differential cell counts
      –Decreases in one or more cell lineages may indicate hypersplenism
      –Neutrophilia suggests infection
  • Examination of the peripheral smear
    –Atypical lymphocytes suggest mononucleosis
    –Spherocytes suggest hereditary spherocytosis
    –Teardrop-shaped RBCs suggest bone marrow invasion
  • Further laboratory studies may include electrolytes, BUN/creatinine, urinalysis, chest X-ray, ANA, rheumatoid factor, HIV testing, and sickle cell prep
  • Abdominal CT or ultrasound better delineate the splenomegaly and may reveal associated abdominal pathology
  • Bone marrow biopsy may be indicated to evaluate for leukemia, myelofibrosis, and/or infection
  • Biopsy, fine needle aspirate, and/or splenectomy may be necessary

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

Arthritis – Multiple Joints: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Infectious
    –Reactive arthritis (postenteric or genital including Reiter syndrome, postviral, poststreptococcal)
    –Acute rheumatic fever (ARF): Migratory, painful; usually affects large joints; diagnosis is based on Jones criteria, which includes five major (arthritis, carditis, Sydenham chorea, erythema marginatum, subcutaneous nodules) and several minor (fever, arthralgia, elevated ESR or CRP, prolonged P-R interval) manifestations
    –Lyme disease: Arthritis is monoarticular or oligoarticular, is rarely symmetric, and is the second most common manifestation of Lyme disease after erythema migrans
    –SBE-related arthritis
    –Septic polyarthritis (unusual)
  • Rheumatic
    –Polyarticular JRA: Arthritis in five or more joints in first 6 months of disease, insidious onset, symmetric involvement, may be RF+ (erosive, similar to adult RA) or RF-
    –Systemic-onset JRA: Presents with severe systemic involvement (fever, rash, serositis), which may precede the arthritis, usually oligoarticular
    –Juvenile ankylosing spondylitis (JAS): Initially affects lower extremity joints; later affects axial skeleton, also affects tendons
    –Psoriatic arthritis
    –Arthritis of IBD: Usually more transient than JRA
    –SLE: May present only with arthritis, may be misdiagnosed as JRA
    –Other connective tissue diseases (scleroderma)
    –Vasculitis (HSP, Kawasaki disease)
  • Malignancy such as leukemia
  • Other systemic disorders: Serum sickness, sarcoidosis, Behçet disease, Ehler-Danlos syndrome, mucopolysaccharidoses, Noonan syndrome, Turner syndrome
  • Medications (minocyline, carbamazapine)
  • Sickle cell disease

Workup and Diagnosis

  • History
    –Acute or chronic; persistent or intermittent; degree of pain, night-time symptoms
    –Systemic symptoms such as fever, weight loss, rash, and fatigue
    –Mouth and/or genital ulcers, abdominal pain, vomiting, diarrhea, bloody stools
    –Past medical history: Birth history, existing medical conditions, surgeries, broken bones, growth and development, any recent URI, genital infection or strep infection, unusual exposures such as tick bites
  • Physical exam
    –Vital signs including growth parameters
    –Musculoskeletal exam for swelling, tenderness, warmth, redness over the joints, range of motion of the joints; asymmetry, muscle strength
    –Lympadenopathy, organomegaly, rash, dysmorphic features, presence of bone pain and neurologic exam (tone, sensory, and reflexes)
  • Labs: CBC, ESR or CRP, RF and ANA; Lyme titers, lupus panel, complement (C3, C4) levels; viral titers (HCV, EBV, parvovirus), LDH, U/A, LFTs
  • Radiology: CXR, X-ray of involved joints, US, MRI, and bone scan to rule out infection, malignancy, and to confirm effusion and tenosynovitis
  • Studies: ECG, echocardiogram, angiogram, UGI/SBF, endoscopy when clinically indicated

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Arthritis – Single Joint: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

  • Septic arthritis
    –Rapid diagnosis critical: Untreated septic arthritis causes irreversible joint and bone destruction
    –Usually presents hyperacutely with very tender, swollen, warm, red joint with severely restricted range of motion
    –Usual pathogens: Haemophilus influenzae type b, Staphylococcus aureus, group B strep in neonates, and Neisseria gonorrhoeae in adolescents; fungal and mycobacterial arthritis are seen rarely, may have chronic course
    • Lyme arthritis
      –Second most common manifestation of Lyme disease (after erythema migrans)
      –Monoarthritis of a knee occurs in about two-thirds of children with Lyme disease
    • Reactive arthritis
      –Probably the most common etiology of childhood rheumatic diseases
      –Transient sterile arthritis following a bacterial GI infection
      –Usually full resolution, but a few children have a chronic course
  • Trauma, overuse, fracture
    –Often acute onset with significant pain
  • Malignancy such as leukemia, neuroblastoma and osteogenic sarcoma
  • Pauciarticular juvenile rheumatoid arthritis (JRA)
  • Spondyloarthropathies (SpA)
  • Congenital hip dysplasia
  • Slipped capital femoral epiphysis (SCFE)
    –Most common adolescent hip disorder
    –Separation of the femoral growth plate
    –More common in obese males
    • Spontaneous osteonecrosis of the joint
      –Mostly in hip (Legg-Calvé-Perthes disease), shoulder, and knee
      –More common in males
    • Internal structural abnormality
      –Discoid meniscus, osteochondritis dissecans, synovial chondromatosis
  • Hemarthrosis due to trauma, bleeding disorder such as hemophilia, or benign tumors such as hemangiomas and pigmented villonodular synovitis
  • Periodic fever syndromes such as familial Mediterranean fever

Workup and Diagnosis

  • History
    –Acute or chronic
    –Mechanical (pain worsens with activities, improves with rest, and usually involves weight-bearing joints)
    –Inflammatory (waxing and waning, symptoms unrelated to use, morning stiffness)
    –History of trauma
    –Night-time symptoms
    –Attempted treatments
    –Systemic symptoms: Fever, rash, pain, fatigue
    –Past medical history: Birth history, existing medical conditions, surgeries, broken bones, growth and development, medications
    –Unusual exposures such as tick bites
    • Physical exam
      –Vital signs, including growth parameters
      –Musculoskeletal exam for swelling, tenderness, warmth, redness, range of motion, asymmetry
      –Muscle strength and neurologic exam (tone, sensory and reflexes)
      –Lympadenopathy, organomegaly, rash, systemic symptoms
  • Radiologic evaluation may include X-ray, US, MRI, and bone scan to evaluate for fracture, infection, tenosynovitis, or internal derangements
  • Lab investigation may include CBC, ESR, CRP, examination of synovial fluid, viral titers (parvovirus), Lyme titers, RF, and ANA

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Neutropenia: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

Extrinsic to bone marrow

    • Acute infection
      –Viral (HAV, HBV, VZV, RSV, EBV)
      –Bacterial (group B strep, typhoid, TB, tularemia), fungal
      –Rickettsial (typhus, RMSF)
      –Protozoal (malaria, toxoplasmosis)
  • Drug-induced
    –Penicillin, sulfonamides
    –Ibuprofen, indomethacin
    –Ranitidine, cimetidine
    –Penicillamine
    –Barbiturates, benzodiazepines
    –Phenothiazines
    –Antithyroid medications
    –Anticonvulsants
  • Environmental toxins (arsenic, benzene)
  • Autoimmune
  • Isoimmune neonatal
    • Splenic or hepatic sequestration
      –Especially with concomitant mild thrombocytopenia or anemia
    • Metabolic disorders
      –Glycogen storage diseases Ib

    Intrinsic to bone marrow or myeloid cell progenitors
  • Chronic benign or idiopathic neutropenia
  • Cyclic neutropenia (autosomal dominant)
  • Marrow replacement with leukemia, lymphoma, or metastatic solid tumors
  • Kostmann syndrome
    –Severe congenital neutropenia
  • Hypo- or dysgammaglobulinemia
  • Myelodysplastic syndrome
  • Myelofibrosis
  • Schwachman syndrome
    • Fanconi anemia
      –May involve neutropenia, anemia, thrombocytopenia, or pancytopenia
      –Associated with absent radius, thumb abnormalities, short stature
  • Cartilage-hair hypoplasia
  • Dyskeratosis congenita
  • Chédiak-Higashi
  • Reticular dysgenesis
  • Myelokathexis

Workup and Diagnosis

    • History
      –Duration (acute or chronic)
      –History and pattern of fever, chronic cough, wheezing
      –Mucositis, aphthous ulcers, “cold sores”
      –Adenitis, signs of malignancy
      –Malabsorption
      –Family history (leukopenia, unusual infections, immunodeficiencies, unexplained early death)
      –Type and frequency of infections
      –Exposure to toxins or drugs
      –Delayed separation of umbilical cord
  • Physical exam: Growth, vital signs, pallor, toxic, phenotypic anomalies, scarred tympanic membranes, allergic shiners, pharyngeal cobblestoning, gingivitis, mucositis/ulcers, lymph nodes, wheeze, chest deformity, splenomegaly, hepatomegaly, rectal abscess, clubbing, cyanosis, skin/nail dystrophies, abnormal thumbs
  • Labs
    –CBC with differential and smear
    –Immunoglobulin levels
    –Cultures (blood, urine, sputum, throat, oral, or skin )
    –Lymphocyte subsets, specific antibody responses
    –Folate level, vitamin B12, metabolic screening
    –HIV, specific infection serologies
    –Exocrine pancreatic function
  • Radiology: Chest X-ray, bone survey
  • Studies: Bone marrow biopsy (neutrophil production), liver biopsy (definitive for glycogen storage diseases)

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

Splenomegaly: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

    • Normal variants
      –Palpable spleen tip due to thinner abdominal musculature
      –15–30% of neonates
      –10% of healthy children
      –5% of adolescents
  • Infection/inflammation
    –Acute hepatitis (B or C)
    –Viral (EBV, CMV, HIV)
    –Bacterial (SBE, cat-scratch disease, TB, histoplasmosis, toxoplasmosis, Salmonella)
    –Systemic lupus erythematosus (SLE)
    –Rheumatoid arthritis
    –Inflammatory bowel disease
    –Celiac disease
    –Acidosis
    –Chronic granulomatous disease
    –Serum sickness
    –Protozoal infection (malaria and schistosomiasis are rare in the U.S.)
      • Hemolytic anemias
        –Hereditary spherocytosis
        –Hemoglobinopathies
        –Thalassemia major
        –Nonspherocytic hemolytic anemias (pyruvate kinase deficiency)
    • Malignancy
      –Leukemia, 50% of children with ALL
      –Hodgkin disease, non-Hodgkin lymphoma
      –Metastatic disease
    • Extramedullary hematopoiesis
      –Thalassemia major
      –Osteopetrosis (rare)
      –Myelofibrosis
      • Storage/infiltrative disorders
        –Histiocytosis
        –Lipidoses (e.g., Niemann-Pick, Gaucher)
        –Mucopolysaccharidoses (e.g., Hurler, Hunter)
      • Congestive
        –Chronic congestive heart failure
        –Portal hypertension
             –Portal or splenic venous thrombosis
        –Hepatic fibrosis
        –Cirrhosis
    • Structural
      –Hematoma (trauma)
      –Cysts or pseudocysts
    • Wandering spleen

    Workup and Diagnosis

      • History
        –Fever, LUQ pain, abdominal trauma
        –Ingestion of hepatotoxic substances
        –Acute illness, dyspnea, fatigue, diarrhea
        –Signs of malignancy
        –Pruritus, travel, sexual history
        –Developmental milestones
        –Medical history: NICU stay, umbilical catheter, jaundice, failure to thrive, anemia, heart disease
        –Family history: Early cholecystectomy, gallstones, anemias, ethnic heritage
    • Physical exam
      –Vitals, growth parameters
      –Pallor, jaundice, purpura, petechiae, ecchymoses, excoriated skin, rashes
      –Scleral icterus, cherry red retinal spots, uveitis/iritis
      –New murmur, edema
      –Abdominal distension, ascites, prominent veins, spleen size, tenderness, liver size and texture
      –Lymph node, joint pain or swelling
      • Labs
        –CBC/peripheral smear, ESR or CRP, LFT, PT/PTT
        –EBV/CMV, viral titers, blood culture
        –Autoimmune or rheumatologic tests (ANA, RF)
        –CXR, bone marrow exam
        –immunodeficiency workup, thrombophilia screen
      • Ultrasound: Exclude retroperitoneal tumors or masses, evaluate portal vein flow with Doppler

» READ BOOK EXCERPT ONLINE »

Source: In A Page: Pediatric Signs and Symptoms, 2007

SPLENOMEGALY: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

How does one go about pinning down the diagnosis? There are several clinical clues. One looks in the physical examination for jaundice, lymphadenopathy, a rash, sore throat, hepatomegaly, and a positive Rumpel–Leede test. The combination of symptoms and signs will eliminate certain causes and make others more plausible. For example, splenomegaly with jaundice but no hepatomegaly suggests hemolytic anemia. The size of the spleen is also an important differential feature. If the spleen is very large, it should suggest myeloid metaplasia, chronic myelogenous leukemia, Gaucher disease, and kala-azar.

The laboratory is the principal aid from this point on. Smears for red cell morphology, malaria, and other parasites are invaluable. Blood cultures and a lymph node and bone biopsy may be useful. If a specific disease is strongly suspected, consult the Appendix for appropriate tests.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

Splenomegaly: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

If you detect splenomegaly during a routine physical examination, begin by exploring associated signs and symptoms. Ask the patient if he has been unusually tired lately. Does he frequently have colds, sore throats, or other infections? Does he bruise easily? Ask about left upper quadrant pain, abdominal fullness, and early satiety. Finally, examine the patient’s skin for pallor and ecchymoses, and palpate his axillae, groin, and neck for lymphadenopathy.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Signs & Symptoms (Third Edition), 2006

Osteoarthritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

A thorough physical examination confirms typical symptoms, and absence of systemic symptoms rules out an inflammatory joint disorder. X-rays of the affected joint help confirm diagnosis of osteoarthritis but may be normal in the early stages. X-rays may require many views and typically show:

❑ narrowing of joint space or margin

❑ cystlike bony deposits in joint space and margins and sclerosis of the subchondral space

❑ joint deformity due to degeneration or articular damage

❑ bony growths at weight-bearing areas

❑ fusion of joints. (See Digital joint deformities, page 591.)

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Psoriatic arthritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Inflammatory arthritis in a patient with psoriatic skin lesions suggests psoriatic arthritis.

CONFIRMING DIAGNOSIS X-rays confirm joint involvement and show:

erosion of terminal phalangeal tufts

“whittling” of the distal end of the terminal phalanges

“pencil-in-cup” deformity of the distal interphalangeal joints

relative absence of osteoporosis

sacroiliitis

atypical spondylitis with syndesmophyte formation. Hyperostosis and paravertebral ossification result, which may lead to vertebral fusion.

Blood studies indicate negative rheumatoid factor and elevated erythrocyte sedimentation rate and uric acid levels.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Rheumatoid arthritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Typical clinical features suggest this disorder, but a definitive diagnosis is based on laboratory and other test results:

❑ X-rays — in early stages, show bone demineralization and soft-tissue swelling; later, loss of cartilage and narrowing of joint spaces; finally, cartilage and bone destruction and erosion, subluxations, and deformities

❑ rheumatoid factor test — positive in 75% to 80% of patients as indicated by a titer of 1:160 or higher

❑ synovial fluid analysis — reveals increased volume and turbidity but decreased viscosity and complement (C3 and C4) levels; white blood cell count usually exceeds 10,000/µl

❑ erythrocyte sedimentation rate — elevated in 85% to 90% of patients (may be useful to monitor response to therapy because elevation commonly parallels disease activity)

❑ complete blood count — usually reveals moderate anemia and slight leukocytosis.

A C-reactive protein test can help monitor response to therapy.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Juvenile rheumatoid arthritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Persistent joint pain and the rash and fever clearly point to JRA. Laboratory tests are useful for ruling out other inflammatory or even malignant diseases that can mimic JRA. Disease activity and response to therapy can also be monitored through laboratory results.

❑ Complete blood count shows decreased hemoglobin levels, neutrophilia, and thrombocytosis.

❑ Erythrocyte sedimentation rate and C-reactive protein, haptoglobin, immunoglobulin, and C3 complement levels may be elevated.

❑ ANA test may be positive in patients who have pauciarticular JRA with chronic iridocyclitis.

❑ RF is present in 15% of JRA cases, compared with 85% of rheumatoid arthritis cases.

❑ Positive HLA-B27 antigens may forecast later development of ankylosing spondylitis.

❑ X-rays in early stages reveal changes, including soft-tissue swelling, effusion, and periostitis in affected joints. Later, osteoporosis and accelerated bone growth may appear, followed by subchondral erosions, joint space narrowing, bone destruction, and fusion.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Septic arthritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Identifying the causative organism in a Gram stain or culture of synovial fluid or a biopsy of synovial membrane confirms septic arthritis. When synovial fluid culture is negative, positive blood culture may confirm the diagnosis.

Joint fluid analysis shows gross pus or watery, cloudy fluid of decreased viscosity, usually with 50,000/µl or more white cells, primarily neutrophils. Synovial fluid glucose is usually more than 40 mg/dl. (See Other types of arthritis, page 584.)

Other diagnostic measures include the following:

❑ X-rays can show typical changes as early as 1 week after initial infection — distention of joint capsules, for example, followed by narrowing of joint space (indicating cartilage damage) and erosions of bone (joint destruction).

❑ White blood cell count may be elevated, with many polymorphonuclear cells; erythrocyte sedimentation rate is increased.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Hypothyroidism in adults: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Radioimmunoassay confirms hypothyroidism with low triiodothyronine (T3) and thyroxine (T4) levels.

Supportive laboratory findings include:

❑ increased TSH level when hypothyroidism is due to thyroid insufficiency; decreased TSH level when hypothyroidism is due to hypothalamic or pituitary insufficiency

❑ elevated levels of serum cholesterol, alkaline phosphatase, and triglycerides

❑ normocytic normochromic anemia.

In myxedema coma, laboratory tests may also show low serum sodium levels, and decreased pH and increased partial pressure of carbon dioxide, indicating respiratory acidosis.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Splenomegaly: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If you detect splenomegaly during a routine physical examination, begin by exploring associated signs and symptoms. Ask the patient if he has been unusually tired lately. Does he frequently have colds, sore throats, or other infections? Does he bruise easily? Ask about left-upper-quadrant pain, abdominal fullness, and early satiety. Finally, examine the patient’s skin for pallor and ecchymoses, and palpate his axillae, groin, and neck for lymphadenopathy.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Splenomegaly: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 A. Presentation. The most common symptom of splenomegaly is a heaviness in the left upper quadrant of the abdomen. The patient may have pain believed to be caused by stretching of the splenic capsule. However, splenomegaly can be entirely asymptomatic. Even rupture of the spleen by trauma or disease process can be without pain.

A history of fevers, night sweats, pain, and fatigue might lead to an infectious cause, whereas alcohol abuse and a history of liver or heart failure would be important in splenomegaly caused by abnormal blood flow.

 B. Family history may give clues to inherited red blood cell disorders and inherited disorders of metabolism.

Physical examination

The diagnosis of splenomegaly is made by palpation of a mass in the left upper quadrant. Harrison’s Textbook of Medicine cites that a spleen is palpable in 3% of normal college freshmen, whereas in tropical countries, the incidence of splenomegaly may reach 60% (1). Percussion is also used to delineate the size of the spleen. Percussion is only approximately 60% accurate in most studies, with palpation about 50% accurate. To palpate the spleen, the patient is in the supine position with the knees flexed to decrease abdominal muscle tone. Begin the examination by palpating the right lower quadrant and move upward across the abdomen as the patient breathes in deeply. Beginning the examination low in the abdomen, allows the lower edge of a markedly enlarged spleen to be detected.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Arthritis/Dermatitis: Differential Overview
(Field Guide to Bedside Diagnosis)

❑Lyme disease

❑Erythema nodosum

❑Rheumatoid arthritis

❑Systemic lupus erythematosus

❑Psoriatic arthritis

❑Disseminated gonococcemia

❑Sarcoidosis

❑Scleroderma

❑Dermatomyositis

❑Reiter syndrome

❑Rheumatic fever

❑Behçet syndrome

❑Still disease

❑Hypersensitivity vasculitis

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Acute Monoarticular Arthritis: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Injury

❑ Gout

❑ Osteoarthritis

❑ Lyme disease

❑ Gonococcal arthritis

❑ Seronegative spondyloarthropathy

❑ Septic arthritis

❑ Pseudogout

❑ Septic bursitis

❑ Avascular necrosis

Diagnostic Approach

Ascertain that arthritis (joint inflammation) is present by eliciting pain on joint motion. A hot, swollen joint with constitutional symptoms such as fever, weight loss, and malaise suggests infection. The skin may hold clues to psoriasis, systemic lupus, viral exanthems, Lyme disease, and others. Erythema nodosum occurs with sarcoidosis or inflammatory bowel disease. Urethritis suggests gonorrhea or Reiter syndrome. A monoarticular presentation of a polyarticular disease may be rarely seen in rheumatoid arthritis, Reiter syndrome, ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease, and sarcoidosis.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Polyarticular Arthritis: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Osteoarthritis

❑ Rheumatoid arthritis

❑ Lyme arthritis

❑ Systemic lupus erythematosus

❑ Psoriatic arthritis

❑ Polyarticular gout

❑ Viral arthritis

❑ Scleroderma

❑ Reiter syndrome

❑ Inflammatory bowel disease

❑ Gonococcal arthritis

❑ Ankylosing spondylitis

❑ Systemic vasculitis

❑ Sarcoidosis

❑ Pseudogout (CPPD)

❑ Acute rheumatic fever

❑ Still disease

Diagnostic Approach

Ascertain that the pain is articular; that is, it is exacerbated by the function of the joint. Detecting synovitis limits the differential to inflammatory arthridites and systemic rheumatic diseases. Findings of synovitis include palpable soft tissue bogginess around a joint, warmth over a joint, or effusion. Involvement of the wrists, elbows, or metacarpophalangeal joints implies inflammatory disease rather than osteoarthritis. Morning stiffness persisting for as long as 1 to 2 hours, relieved by NSAIDs, is typical for inflammatory arthritis, as is a history of a red joint.

Differentiating features include the following: Erythema nodosum: sarcoidosis, inflammatory bowel disease-related arthritis, or Behçet disease. Rash: lupus, Still disease, vasculitis, dermatomyositis, endocarditis, disseminated gonorrhea, or Behçet disease. Fever greater than 40˚C: Still disease, bacterial arthritis, or lupus. Fever preceding arthritis: viral arthritis, Lyme, reactive arthritis, Still
desease, or bacterial endocarditis. Spiking fever: bacterial infection or Still
disease. Splenomegaly: rheumatoid arthritis and lupus. Raynaud: scleroderma, mixed connective tissue disease, or lupus. Oral ulcers: lupus, Behçet disease, or viral arthritis. Dry eyes and mouth: Sjögren syndrome, mixed connective tissue
disease, or lupus. Ocular findings: lupus, Behçet disease, sarcoidosis, or reactive arthritis. Migratory arthritis: gonococcemia, rheumatic fever, meningococcemia, viral arthritis, lupus, acute leukemia, or Whipple disease. Episodic recurrences: Lyme, crystal-induced arthritis, inflammatory bowel disease, Still disease, or lupus. Morning stiffness: rheumatoid arthritis, polymyalgia rheumatica, Still
disease, or viral arthritis. Symmetric small-joint synovitis: rheumatoid arthritis, lupus, or viral arthritis.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Osteoarthritis: Diagnosis
(Handbook of Diseases)

A thorough physical examination confirms typical symptoms, and the absence of systemic symptoms rules out an inflammatory joint disorder. X-rays of the affected joint help confirm diagnosis of osteoarthritis but may be normal in the early stages. X-rays may require many views and typically show:

❑  narrowing of joint space or margin

❑  cystlike bony deposits in joint space and margins

❑  sclerosis of the subchondral space

❑  joint deformity due to degeneration or articular damage

❑ bony growths at weight-bearing areas

❑  fusion of joints.

No laboratory test is specific for osteoarthritis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Psoriatic arthritis: Diagnosis
(Handbook of Diseases)

Inflammatory arthritis in a patient with psoriatic skin lesions suggests psoriatic arthritis. X-rays confirm joint involvement and show:

❑ marginal erosion at interphalangeal joints with areas of thin, “fluffy” new bone formation

❑ “whittling” of the distal end of the terminal phalanges

❑ “pencil-in-cup” deformity of the distal interphalangeal joints

❑ relative absence of osteoporosis

❑ sacroiliitis

❑ atypical spondylitis with syndesmophyte formation, resulting in hyperostosis and paravertebral ossification, which may lead to vertebral fusion.

Blood studies indicate negative rheumatoid factor and elevated erythrocyte sedimentation rate and uric acid levels.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Rheumatoid arthritis: Diagnosis
(Handbook of Diseases)

Typical signs and symptoms suggest RA, with a firm diagnosis supported by laboratory and other test results:

X-raysin early stages show bone demineralization and soft-tissue swelling; later, loss of cartilage and narrowing of joint spaces; and finally, cartilage and bone destruction and erosion, subluxations, and deformities.

RF is positive in 75% to 80% of patients, as indicated by a titer of 1:160 or higher.

Synovial fluid analysisshows increased volume and turbidity but decreased viscosity and elevated white blood cell counts (often greater than 10,000/µl).

Serum protein electrophoresis may show elevated serum globulin levels.

Erythrocyte sedimentation rate and C-reactive protein are elevated in 85% to 90% of patients (may be useful to monitor response to therapy because elevation typically parallels disease activity).

Complete blood count usually shows moderate anemia, slight leukocytosis, and thrombocytosis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Juvenile rheumatoid arthritis: Diagnosis
(Handbook of Diseases)

Persistent joint pain, rash, and fever clearly point to JRA. Laboratory tests are useful for ruling out other inflammatory or even malignant diseases that can mimic JRA and for monitoring disease activity and response to therapy.

Complete blood count shows decreased hemoglobin levels, neutrophilia, and thrombocytosis.

Erythrocyte sedimentation rate, complement (C)-reactive protein, haptoglobin, immunoglobulin, and C3 levels may be elevated.

❑ Test results may be positive for ANAs in patients who have pauciarticular JRA with chronic iridocyclitis.

RF is present in 15% of patients with JRA, as compared with 85% of patients with RA.

❑ Positive HLA-B27 test may forecast later development of ankylosing spondylitis.

❑ Early X-ray changes include soft-tissue swelling, effusion, and periostitis in affected joints. Later, osteoporosis and accelerated bone growth may appear, followed by subchondral erosions, joint space narrowing, bone destruction, and fusion.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Hypothyroidism in adults: Diagnosis
(Handbook of Diseases)

Radioimmunoassay confirms hypothyroidism with low triiodothyronine (T3) and thyroxine (T4) levels.

Supportive laboratory findings include:

❑ increased TSH level when hypothyroidism is due to thyroid insufficiency; decreased TSH level when hypothyroidism is due to hypothalamic or pituitary insufficiency

❑ elevated levels of serum cholesterol, alkaline phosphatase, and triglycerides

❑ normocytic, normochromic anemia.

In myxedema coma, laboratory tests may also show low serum sodium levels as well as decreased pH and increased partial pressure of carbon dioxide, indicating respiratory acidosis.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Splenomegaly: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

If you detect splenomegaly during a routine physical examination, begin by exploring associated signs and symptoms. Ask the patient if he has been unusually tired lately. Does he frequently have colds, sore throats, or other infections? Does he bruise easily? Ask about left upper quadrant pain, abdominal fullness, and early satiety.

Physical examination

Begin the physical examination by performing a complete abdominal assessment, including palpation of the spleen. Examine the patient’s skin for pallor and ecchymoses, and palpate his axillae, groin, and neck for lymphadenopathy. (See Splenomegaly: Causes and associated findings, pages 280 and 281.)

» READ BOOK EXCERPT ONLINE »

Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Splenomegaly: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Begin by exploring associated signs and symptoms. Ask the patient if he has been unusually tired lately. Does he frequently have colds, sore throats, or other infections? Does he bruise easily? Ask about left-upper-quadrant pain, abdominal fullness, and early satiety.

» READ BOOK EXCERPT ONLINE »

Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Splenomegaly: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Infection

  • In neonates,septicemia is most common cause of enlarged spleen. Usual pathogens aregroup B Streptococcus and E. coli.
  • Most common cause of enlarged spleenin infants, children, and adolescents is acute viral infection,especially with Epstein-Barr virus or cytomegalovirus.
  • Other causes are bacterial (septicemia,endocarditis, cat scratch disease, tularemia, brucellosis, tuberculosis,splenic abscess, leptospirosis, Lyme disease, syphilis); fungal(histoplasmosis, candidiasis); rickettsial (Rocky Mountain spottedfever); and parasitic (malaria, toxoplasmosis, visceral larva migrans,schistosomiasis).
  • Hemolytic Anemia

    Any hemolytic anemia may give rise to splenomegaly.See Chap. 45, Pallor (Anemia).

    Cardiac Failure

    Splenomegaly may occur with cardiac failure.See Chap. 7, Cardiac Failure.

    Trauma

  • Automobile,bicycle, and sled-riding accidents as well as falls are common causesof acute splenic injury. Splenic contusion or hematoma may producesplenic enlargement and tenderness.
  • Abdominal U/S and CT can locateand define extent of injury.
  • Neoplasia

  • Benign splenictumors include hemangioma, lymphangioma, and hamartoma. Spleen isenlarged and asymmetric. Abdominal U/S and CT define locationand extent of mass lesion.
  • Common malignancies involving spleenare acute lymphoblastic leukemia, acute myeloid leukemia, Hodgkindisease, and non-Hodgkin lymphoma. See Chap. 38, Lymphadenopathy.
  • Portal Hypertension

  • Any causeof portal hypertension may cause enlarged spleen. Major causes areliver disease (cirrhosis, hepatitis, extrahepatic biliary atresia);cavernous transformation of portal vessels; and portal or splenicvein thrombosis.
  • In many cases, abdominal U/Swith Doppler methods can define portal venous anatomy.
  • Metabolic Disorders

  • Splenomegalymay occur with a number of metabolic diseases:

  • Amino acid disorders (tyrosinemia)
  • Carbohydrate disorders (galactosemia,hereditary fructose intolerance)
  • Mucopolysaccharidoses (Hurler and Huntersyndromes)
  • Lipidoses (Gaucher disease, Niemann-Pickdisease, GM-1 gangliosidosis type I)
  • Glycoprotein disorders (sialidosistype II, fucosidosis)
  • See Chap.13, Developmental Delay, and Chap. 36, Jaundice, fordiscussion of these disorders.
  • Other

  • Splenomegalyalso may occur with

  • Splenic cysts
  • Connective tissue diseases (systemiclupus erythematosus, juvenile rheumatoid arthritis, systemic vasculitis)
  • Inflammatory bowel disease
  • Sarcoidosis
  • Histiocytoses
  • Drug hypersensitivity reactions
  • See other chapters for discussion ofthese disorders.
  • Diagnostic Approach

  • The findingof splenomegaly is usually made on physical exam.
  • Most common causes of enlarged spleenin pediatric population are viral infection, trauma, hemolytic anemia,cardiac failure, and malignancy.
  • History and physical exam provide cluesfor diagnosis and any subsequent investigation.

  • CBC providesinformation about hematologic, infectious, and inflammatory processes.
  • Finding of pancytopenia may indicatebone marrow dysfunction or portal hypertension with hypersplenism.
  • Increased sedimentation rate suggestsinfectious, inflammatory, or neoplastic process.
  • Bacterial, fungal, and other culturesmay be performed with suspected infection.
  • Bone marrow exam is useful in diagnosisof histiocytoses, lysosomal storage disorders, and some infections(e.g., disseminated histoplasmosis).
  • Liver function tests and abdominalU/S with Doppler methods should be performed with suspectedportal hypertension.
  • Abdominal U/S and CT locateand define extent of splenic masses.
  • » READ BOOK EXCERPT ONLINE »

    Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

    Splenomegaly: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If you detect splenomegaly during a routine physical examination, begin by exploring associated signs and symptoms. Ask the patient if he has been unusually tired lately. Does he frequently have colds, sore throats, or other infections? Does he bruise easily? Ask about left upper quadrant pain, abdominal fullness, and early satiety. Finally, examine the patient's skin for pallor and ecchymoses, and palpate his axillae, groin, and neck for lymphadenopathy.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    SPLENOMEGALY: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    How does one go about pinning down the diagnosis? There are several clinical clues. One looks during the physical examination for jaundice, lymphadenopathy, a rash, sore throat, hepatomegaly, and a positive Rumpel–Leede test. The combination of symptoms and signs will eliminate certain causes and make others more plausible. For example, splenomegaly with jaundice but no hepatomegaly suggests hemolytic anemia. The size of the spleen is also an important differential feature. If the spleen is very large, it should suggest myeloid metaplasia, chronic myelogenous leukemia, Gaucher disease, and kala-azar. The laboratory is the principal aid from this point on. Smears for red cell morphology, malaria, and other parasites are invaluable. Blood cultures and a lymph node and bone biopsy may be useful. If a specific disease is strongly suspected, consult Appendix A for appropriate tests.


    SPLENOMEGALY
    Increased Increased  
    ProductionNeoplasiaDestructionObstructionInfiltration
    Red Cells
    Aplastic anemia Myelophthisic anemia
    Polycythemia
    Hemolytic anemia Lupus erythematosus Pernicious anemia
    White Cells
    Myeloid metaplasia Infection
    Leukemia Agranulocytosis
    Platelets
    Idiopathic thrombocytopenic purpura
    Lymph Tissue
    Infectious mononucleosis
    Hodgkin lymphoma Lymphangioma
    Supporting Tissue
    Metastatic carcinoma (rare)
    Lupus erythematosus Collagen disease
    Hemochromatosis Reticuloendotheliosis Hurler disease Amyloidosis Sarcoidosis
    Arteries Embolism Aneurysm
    Veins Hemangioma
    Congestive heart failure Cirrhosis Thrombosis Banti disease Carcinoma of the tail of the pancreas

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    Splenomegaly: Splenomegaly - DIAGNOSIS
    (The 5-Minute Pediatric Consult)

    General goal is to determine the etiology of the large spleen:

    • Phase 1: Establish the presence of enlarged spleen, not a palpable spleen that is pushed down by inflated lungs.
    • Phase 2: Rule out common causes such as a viral infection, bacterial infection, or anemia.
    • Phase 3: Rule out malignancy or storage disease or other rare causes of large spleen.

    » READ BOOK EXCERPT ONLINE »

    Source: The 5-Minute Pediatric Consult, 2008

    Fever and Neutropenia: Diagnosis
    (Pediatric Infectious Disease)

    Due to the risk for life-threatening infection in the patient with fever and neutropenia, current practice suggests that patients meeting the above definitions be admitted to the hospital.

    Cultures of the blood, urine, and if possible, induced sputum should be obtained. Chest radiographs are also suggested, especially if respiratory symptoms are present.

    » READ BOOK EXCERPT ONLINE »

    Source: Pediatric Infectious Disease, 2004


     » Next page: Signs of Rheumatoid arthritis

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