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Diseases » Wegener's granulomatosis » Tests

Diagnostic Tests for Wegener's granulomatosis

Diagnostic Test list for Wegener's granulomatosis:



The list of diagnostic tests mentioned in various sources as used in the diagnosis of Wegener's granulomatosis includes:

Diagnostic Tests for Wegener's granulomatosis: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review the full text of medical books online, free, without registration, for more information about the diagnostic tests for Wegener's granulomatosis.

HEMATURIA: DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)

The workup begins with a urinalysis and microscopic examination of the urinary sediment. The physician can easily do this in his office. If there is proteinuria, granular cast, and red cell cast, glomerulonephritis or collagen disease should be suspected. A culture and sensitivity and colony count should be done if a UTI is suspected. A three-glass test may be done. If there is blood in the initial specimen, the cause is most likely in the urethra or male genitalia. If it is in the final specimen, the cause is most likely a bladder lesion. Phase-contrast microscopy may also be helpful in identifying hematuria from a glomerular lesion. If this is negative, an anaerobic culture should be done also and then an AFB smear and culture and guinea pig inoculation to rule out tuberculosis. An intravenous pyelogram will also usually have to be done. A CBC, sedimentation rate, chemistry panel, coagulation profile, and ANA test will help rule out blood dyscrasias, collagen diseases, and other systemic diseases. Ultrasonography may help diagnose a renal cyst.

If the above are not revealing, referral to a urologist is indicated. He will probably do a cystoscopy and retrograde pyelography. He may also want to order a CT scan of the abdomen and pelvis and a renal biopsy. Renal angiography and aortography may be necessary to evaluate renovascular hypertension and renal embolism.

 

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

After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing clots? To rule out artifactitious hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if there’s pain or burning with hematuria episodes.

Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting anticoagulants or aspirin.

Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.

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Introduction: Respiratory Disorders: Assessment
(Professional Guide to Diseases (Eighth Edition))

Assessment of the respiratory system begins with a thorough patient history. Ask the patient to describe his respiratory problem. How long has he had it? How long does each attack last? Does one attack differ from another? Does any activity in particular bring on an attack or make it worse? What relieves the symptoms? Always ask whether the patient was or is a smoker, what and how often he smoked or smokes, and how long he smoked or has been smoking. Record this information in “pack years”—the number of packs of cigarettes per day multiplied by the number of smoking years. Remember to ask about the patient’s occupation, hobbies, and travel; some of these activities may involve exposure to toxic or allergenic substances.

If the patient has dyspnea, ask if it occurs during activity or at rest. What position is the patient in when dyspnea occurs? How far can he walk? How many flights of stairs can he climb? Has his exercise tolerance been decreasing? Can he relate dyspnea to allergies or environmental conditions? Does it occur only at night, during sleep? If the patient has a cough, ask about its severity, persistence, and duration; ask if it produces sputum and, if so, what kind. Have the patient’s cough habits and character of sputum changed recently?

Physical examination

Use inspection skills to check for clues to respiratory disease, beginning with the patient’s general appearance. If he’s frail or cachectic, he may have a chronic disease that has impaired his appetite. If he’s diaphoretic, restless, or irritable or protective of a painful body part, he may be in acute distress. Also, look for behavior changes that may indicate hypoxemia or hypercapnia. Confusion, lethargy, bizarre behavior, or quiet sleep from which he can’t be aroused may point to hypercapnia. Watch for marked cyanosis, indicated by bluish or ashen skin (usually best seen on the lips, tongue, earlobes, and nail beds), which may be due to hypoxemia or poor tissue perfusion.

Assess chest shape and symmetry at rest and during ventilation. Increased anteroposterior diameter (“barrel chest”) characterizes emphysema. Kyphoscoliosis also alters chest configuration, which in turn restricts breathing. Assess respiratory excursion and observe for accessory muscle use during breathing. The use of upper chest and neck muscles is normal only during physical stress.

Observe the rate and pattern of breathing because certain disorders produce characteristic changes in breathing patterns. For example, an acute respiratory disorder can produce tachypnea (rapid, shallow breathing) or hyperpnea (increased rate and depth of breathing); intracranial lesions can produce Cheyne-Stokes and Biot’s respirations; increased intracranial pressure can result in central hyperventilation and apneustic or ataxic breathing; metabolic disorders can cause Kussmaul’s respirations; and airway obstruction can lead to prolonged forceful expiration and pursed-lip breathing.

Also observe posture and carriage. A patient with COPD, for example, usually supports rib cage movement by placing his arms on the sides of a chair to increase expansion and leans forward during exhalation to help expel air.

Palpation of the chest wall detects areas of tenderness, masses, changes in fremitus (palpable vocal vibrations), or crepitus (air in subcutaneous tissues). To assess chest excursion and symmetry, place your hands in a horizontal position, bilaterally on the posterior chest, with your thumbs pressed lightly against the spine, creating folds in the skin. As the patient takes a deep breath, your thumbs should move quickly and equally away from the spine. Repeat this with your hands placed anteriorly, at the costal margins (lower lobes) and clavicles (apices). Unequal movement indicates differences in expansion, seen in atelectasis, diaphragm or chest wall muscle disease, or splinting due to pain.

Percussion should detect resonance over lung fields that aren’t covered by bony structures or the heart. A dull sound on percussion may mean consolidation or pleural disease. (See Characterizing and interpreting percussion sounds.)

Auscultation normally detects soft, vesicular breath sounds throughout most of the lung fields. Absent or adventitious breath sounds may indicate fluid in small airways or interstitial lung disease (crackles), secretions in moderate and large airways (rhonchi), and airflow obstruction (wheezes).

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

After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing any clots? To rule out artifactual hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if pain or burning accompanies the episodes of hematuria.

Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting the use of anticoagulants or aspirin.

Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.

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Hematuria: Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

should focus on signs of systemic disease (fever, rash, lymphadenopathy, joint swelling, and abdominal or pelvic mass), and underlying medical or renal disease (hypertension, edema). Multiple telangiectasias and mucous membrane lesions indicate hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease). An abdominal mass in children requires exclusion of Wilms tumor.

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Solitary Pulmonary Nodule: Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

 should include a search for evidence of weight loss, chronic obstructive pulmonary disease, and primary or metastatic disease of other organs.

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Hematuria: Diagnostic Approach
(Field Guide to Bedside Diagnosis)

A reasonable cutoff for discriminating benign from serious causes of hematuria is 10 RBCs/HPF. The urine dipstick detects as few as 1 to 2 RBCs/HPF. Analysis of the urine sediment is crucial. White cells and bacteria are indicative of cystitis whereas white cell casts are seen in pyelonephritis. Red cell casts and dipstick proteinuria indicate glomerulonephritis. Red cells from a glomerular source tend to be distorted. A positive dipstick for hemoglobin but no RBCs in the urinalysis suggests the presence of myoglobin or free hemoglobin derived from intravascular hemolysis. Menstrual blood contamination needs to be considered in the differential of microscopic hematuria.

Initial hematuria suggests a urethral source; terminal hematuria, the prostatic urethra, trigone, or base; and total hematuria, the kidney, ureter, or bladder. Massive hematuria is usually associated with bladder neoplasm, benign prostatic hypertrophy, or trauma. Bright red urine suggests a lower urinary source. Passage of bulky disc-like or fragmented clots implies the bladder as source, long shoestring clots suggest a ureteral origin, and pyramidal clots are from the renal pelvis. Glomerular sources virtually never produce clots (due to the presence of tissue plasminogen activators in the glomeruli and tubules). With a presentation of painless total hematuria, a urinary tract cancer is found in 20%.

Flank pain associated with hematuria may result from the passage of stones or clots. Hypertension suggests renal disease. Rash, fever, arthralgia/arthritis, or hemoptysis suggests a connective tissue disease or vasculitis. Beets, blackberries, and rhubarb, as well as pyridium, rifampin, phenothiazines, and anthracyclines, can produce red urine without blood.

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Hematuria: Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.

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Hematuria: Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

  • First stepin diagnosis is to determine whether there is blood in urine. Althoughblood may produce pink, red, or brownish color of the urine, othersubstances also may produce same type of urinary discoloration.
  • Urine dipstick detects hemoglobin containedin red cells as well as free Hgb. It can detect as few as 1 or 2red cells per high-power field in uncentrifuged specimen. Microscopydetermines whether red cells are in urine and thus the presenceof hematuria.
  • Urine sample that tests positive ondipstick but negative on microscopy indicates presence of hemoglobinor myoglobin. Serum is pink in color with hemoglobinuria and normalin color with myoglobinuria.
  • Best way to distinguish myoglobin fromHgb is immunochemically. Red, orange, or brownish urine that isdipstick negative for blood indicates that certain foods (blackberries,beets), food dyes, urate crystals, or drugs (pyridium, desferoximine)are coloring urine. Urine containing porphyrin initially has normalcolor but changes to red on standing; dipstick is negative, andno red cells are seen on microscopy.

    • Hematuria without Proteinuria

  • Microscopichematuria without proteinuria is most commonly due to urinary tractinfection, trauma, acute postinfectious glomerulonephritis, immunoglobulinA nephropathy, familial benign hematuria, or nonfamilial benignhematuria.
  • Following history and physical exam,these tests should be performed initially: UA of child and familymembers (to diagnose familial benign hematuria), urine culture,serum creatinine, blood urea nitrogen, C3, calcium:creatinine ratio,and renal U/S. If results of these tests are normal, andproteinuria is consistently absent, most causes of hematuria havebeen excluded and further diagnostic studies (e.g., cystoscopy andrenal biopsy) are usually unnecessary.
  • Children categorized as having nonfamilialbenign hematuria because they have normal evaluation and no recognizablerenal disease may prove to have transient hematuria, but as longas hematuria occurs, these children should be followed for possibleoccurrence of proteinuria. Those with familial benign hematuriaalso should be followed.
  • In addition to above tests, diagnosticevaluation of gross hematuria should include CBC, platelet count,antistreptolysin O or streptozyme titer, and Hgb electrophoresis(in African-American children). Renal angiography may be necessaryif vascular malformation is suspected. If proteinuria occurs whenhematuria subsides, renal biopsy may be indicated.

    • Hematuria with Proteinuria

  • Glomerulonephritisshould be suspected in every child with hematuria and proteinuria.
  • Presence of red cell casts indicatesglomerular bleeding.
  • Results of tests for urinary protein(urine dipstick, sulfosalicylic acid test) are usually positivewith gross hematuria. Although dipstick protein reading of 3+ to4+ may signify glomerular disease with gross hematuria,lower reading may have diagnostic significance. See Chap. 50, Proteinuria, forprotein concentrations corresponding to dipstick readings.
  • To more reliably detect proteinuriaassociated with glomerular disease, urine should be tested whengross hematuria subsides.
  • Renal biopsy is required for specificdiagnosis unless there is evidence of unequivocal acute postinfectiousglomerulonephritis or family history of Alport syndrome. Biopsymay be necessary with acute postinfectious glomerulonephritis ifserum C3 level does not become normal within 2 mos, if proteinuriapersists for >6 mos, or to distinguish it from idiopathicrapidly progressive glomerulonephritis if presentation is that ofacute renal failure.

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

    After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing clots? To rule out artifactitious hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if there's pain or burning with hematuria episodes.

    Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting anticoagulants or aspirin.

    Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.

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    Tests and diagnosis discussion for Wegener's granulomatosis:

    To treat people with Wegener’s granulomatosis most effectively, doctors must diagnose the disease early in its course. There are no blood tests that a doctor can use to diagnose Wegener’s granulomatosis, but blood tests are important to rule out other causes of illness and to determine which organ sites may be affected. Most blood tests are nonspecific and can only suggest that a person has an inflammatory process. Anemia (low red blood cell count), elevated white blood cell count and platelet count, and an elevated sedimentation rate are commonly found in people with Wegener’s granulomatosis. If the kidneys are involved, red blood cells and structures called red blood cell casts are visible in the urine when viewed under a microscope, and the blood tests measuring kidney function (creatinine and BUN) may show abnormalities.

    X-ray results can be very helpful in diagnosing Wegener’s granulomatosis. People with lung involvement will have abnormal chest x-rays, which may show one or many fluffy infiltrates, solid nodules, or cavities. Sinus x-rays or computed tomography (CT) scans in people with sinus involvement may show thickening of the sinus lining.

    Many patients with active Wegener's granulomatosis have a blood test that reveals the presence of a specific type of antibody called antineutrophil cytoplasmic antibodies (ANCA) (an antibody is a disease-fighting protein). Although a positive ANCA test is useful in supporting a suspected diagnosis of Wegener’s granulomatosis, in most instances it is not used by itself to make a diagnosis of this disorder. The ANCA test may be negative in some patients with active Wegener’s granulomatosis.

    Currently, the only definite way to diagnose Wegener’s granulomatosis is by performing a biopsy of an involved organ site (usually the sinuses, lung, or kidney). The tissue is examined under the microscope to confirm the presence of vasculitis and granulomas (a specific type of inflammation), which together are diagnostic features of the disease. A biopsy is very important both to confirm the presence of Wegener’s granulomatosis and also to assure the absence of other disorders that may have similar signs and symptoms.

    Treatment

    With the appropriate treatment, the outlook is good for patients with Wegener’s granulomatosis. In a study of 158 patients who were treated at the National Institutes of Health (NIH), 91 percent of them markedly improved. After 6 months to 24 years of follow-up, 80 percent of the patients survived.

    In most cases, standard therapy consists of a combination of a glucocorticoid drug that reduces inflammation and a cytotoxic drug that interferes with the abnormal growth of cells.

    Prednisone is the most common glucocorticoid drug (a steroid) that is used. Prednisone is similar to hydrocortisone, the natural glucocorticoid hormone produced by the body. It is chemically different from the anabolic steroids that have been used by athletes and is given in doses much higher than the body normally produces. Prednisone is usually administered as a single morning dose in an attempt to imitate how the body normally secretes hydrocortisone. When the person’s illness improves, the prednisone dose is gradually decreased and converted to an every other day dosing schedule, usually over a period of 3 to 4 months. With further improvement in the disease, the prednisone is very gradually decreased and discontinued completely after approximately 6 to 12 months. When prednisone is taken by mouth, the body stops making its own natural hydrocortisone. As the prednisone dose is gradually reduced the body will resume making hydrocortisone again. It is extremely important that prednisone never be stopped suddenly because the body requires prednisone (or hydrocortisone) for its function and may not be able to immediately make what it needs.

    Cyclophosphamide (CytoxanÔ) is the most commonly used cytotoxic drug. Cyclophosphamide is taken once a day by mouth. It is important for a patient to take the drug all at once in the morning followed by drinking a large amount of fluid. Although the initial dose of cyclophosphamide is based on the patient’s weight and kidney function, the doctor may adjust the dosage based on the blood counts, which are monitored closely to be sure that the white blood cell count is maintained at a safe level. Cyclophosphamide is continued for a full year beyond that point at which the disease has become quiet (is in remission). The dose of cyclophosphamide is then decreased gradually and eventually discontinued.

    Cyclophosphamide and prednisone are both powerful drugs that suppress the immune system. Although these medications are beneficial in treating Wegener’s granulomatosis, patients and their doctors should be aware that the drugs potentially have serious side effects. Careful monitoring by the doctor is very important. Because these drugs suppress the immune system, they can affect the body’s ability to fight off infection. Patients should report immediately any symptoms of infection and, specifically, any fever to their doctors. Prednisone can cause weight gain, cataracts, brittle bones, diabetes, and alterations in mood and personality. Cyclophosphamide can cause bone marrow suppression (lowering of blood counts), sterility, hemorrhagic cystitis (bleeding from the bladder) as well as other serious side effects.

    Approximately half of people with Wegener’s granulomatosis may experience a return (relapse) of their disease. This occurs most frequently within two years of stopping medication, but potentially can occur at any point both during treatment or after stopping treatment. Thus, it is extremely important that patients continue to see their physicians regularly, both while they are on these medications, as well as after the medications have been stopped. Even while on medication, many patients are able to lead relatively normal lives and will remain in remission after therapy has been stopped completely.

    Research

    Since the 1970s, research physicians at the National Institute of Allergy and Infectious Diseases (NIAID), a component of NIH, have been interested in Wegener’s granulomatosis. NIAID scientists first introduced the combination of a glucocorticoid with cyclophosphamide for treating people with this disease. This dramatic breakthrough remains the standard of treatment. Despite this, researchers realize that these medicines have serious side effects and cannot be tolerated by all people. Therefore, NIH researchers continue to study Wegener’s granulomatosis to understand the causes of the disease and to develop new treatments. NIAID is conducting several studies to investigate new treatment regimens. These studies each have individual entry criteria but are open to patients who have a definitive diagnosis of Wegener’s granulomatosis and who have active disease.

    Further Information

    For information about enrolling in an NIAID clinical study at NIH's facility in Bethesda, Maryland, the patient's personal physician should call or write to:

    Dr. Michael C. Sneller
    Head, Immunologic Diseases Section
    or
    Dr. Carol A. Langford
    Immunologic Diseases Section
    Laboratory of Immunoregulation
    National Institute of Allergy and Infectious Diseases
    National Institutes of Health
    Building 10, Room 11B-13, MSC 1876
    10 Center Drive
    Bethesda, MD 20892-1876
    301/496-1124

    For more information on patient support groups, contact:

    Wegener's Foundation, Inc.
    Attention: Ms. Linda Baltrusch
    3705 South George Mason Drive
    Suite 1813 South
    Falls Church, VA 22041
    703/931-5852

    Wegener's Granolomatosis Support Group, Inc. (International)
    P.O. Box 28660
    Kansas City, MO 64188-8660
    800/277-WGSG (9474)
    http://www.wgsg.org/

    (Source: excerpt from Wegener's Granulomatosis, NIAID Fact Sheet: NIAID)

     » Next page: Diagnosis of Wegener's granulomatosis

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