Diagnostic Tests for Wegener's granulomatosis

Wegener's granulomatosis: Diagnostic Tests

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

• Blood tests
  • White blood cell count
  • Platelet count
  • Sedimentation rate
  • Antineutrophil cytoplasmic antibodies (ANCA) blood test - useful but may also be negative.
• Kidney function tests
  • Kidney urine tests
  • Urine red blood cell casts test
  • Creatinine blood test
  • BUN blood test
• X-rays or scans
  • Chest x-rays
  • Sinus x-rays
  • Sinus CT scans
• Biopsy - the final definitive method looking for vasculitis and granulomas.
  • Sinus biopsy
  • Lung biopsy
  • Kidney biopsy

Home Diagnostic Testing

These home medical tests may be relevant to Wegener's granulomatosis:

• Bladder & Urinary Health: Home Testing:
  • Home Bladder Testing
  • Home Urinary Tract Infection Tests
  • Home Cystitis Tests
  • Home Kidney Tests
  • Home Urine Protein Tests (Kidney Function)
  • Home Prostate Cancer Tests
• Kidney Health: Home Testing:
  • Home Kidney Testing
  • Home Microalbumin Tests (Kidney)
  • Home Urine Protein Tests (Kidney)
  • Home Urinary Tract Infection Test Kits

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/

Diagnostic Tests for Wegener's granulomatosis: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from 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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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

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

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

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.

Testing

A. Initial evaluation. Hematuria is usually detected by dipstick or microscopic examination. The dipstick test relies on detecting hemoglobin and should always be confirmed by microscopic examination of the urine sediment. Some controversy exists about the abnormal number of red blood cells in urine. Most clinicians consider more than three to five red blood cells per high power field (40 × lens) as definitely abnormal. When dipstick testing is positive for blood but urine microscopy reveals no red blood cells, hemoglobinuria or myoglobinuria should be considered. The next step is a urine culture. Baseline blood tests include a renal panel, complete blood count with differential, sedimentation rate, prothrombin time, and partial thromboplastin time.

 B. Further evaluation is highly dependent on the suspected cause. Further blood tests can include serum complement titer (significant if low), antistreptolysin-O titer (high), antinuclear antibody and extended panels with anti-deoxyribonuclease B titer (high), and hemoglobin electrophoresis. A tuberculin skin test or chest x-ray study can be done to detect tuberculosis. Further tests can include imaging studies and cytology. Intravenous pyelogram and abdominal and pelvic ultrasound or computed tomography scanning may detect malignancies of the various anatomic areas as well as benign conditions such as urolithiasis, obstructive uropathy, renal cysts, parenchymal abnormalities, and nonurinary tract lesions. To complete the workup, send the urine for cytology study and proceed with cystoscopy looking for abnormalities of the urethra and bladder. Biopsies of various areas, including kidney and bladder, and invasive vascular studies may be needed. Unless a diagnosis is made, patients will need referral to subspecialists.

Diagnostic assessment

 The key to the diagnosis of hematuria is the clinical history and physical examination. Laboratory and imaging studies only confirm or rule out initial suspicions. The goal is to diagnose a variety of serious illnesses, including malignancies and renal parenchymal diseases. In general, keep in mind that transient hematuria, especially in a young person, is quite common and rarely indicative of significant pathology (4). When present in patients aged more than 50 years, however, transient hematuria always warrants a comprehensive evaluation to rule out malignancy. Similarly, a diagnostic workup should be performed when persistent hematuria is found in patients of any age.

References

1. Froom P, Ribak J, Benbassat J. The significance of microhematuria in young adults. BMJ 1984;288:20–28.

2. Mariani AJ, Mariani MC. The significance of adult hematuria: 1000 hematuria evaluations including a risk-benefit and cost-effectiveness analysis. J Urol 1989;
141:350–355.

3. Messing EM, Young TB, Hunt VB, et al. Hematuria home screening: repeat testing results. J Urol 1995;154(1):57–61.

4. Murakami S, Igarashi T, Hara S, et al. Strategies for asymptomatic microscopic hematuria: a prospective study of 1034 patients. J Urol 1990;144:99–106.

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

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.

Testing

 The key question is to determine which one of the SPNs is malignant and warrants invasive and immediate action. The following factors can help determine a course of management:

A. Location. Generally, most malignant lesions are found in the upper lobes.

B. Appearance. The smooth margins seen on computerized tomography (CT) scan characterize benign lesions, whereas spiculated, irregular borders are associated with malignant growths.

C. Size. Small size (<2 cm) is most frequently a sign of benignity, although it can be caused by an early, isolated pulmonary metastasis from a primary cancer at another site.

 D. Calcifications. Peripheral, concentric patterns (“bull’s eyes” in granulomas, “popcorn ball” in hematomas) (3) have been associated with benign lesions, but the presence of calcifications has not been found to be a reliable indicator in predicting malignancy, because 14% of cancerous lesions can be calcified.

 E. Aging. The CT scan of the chest is widely available and noninvasive. It accurately measures the nodule and defines its location and morphology.

F. Preliminary results with high resolution computerized tomography with contrast indicate good accuracy in the determination of the nodule malignancy. The MRI is not a preferred imaging tool to analyze a pulmonary nodule but its superior capacity to enhance vascular structures can be useful in the differential diagnosis.

Diagnostic assessment

Controversy exists as to the best way to manage SPN. The decision to observe or to intervene is guided by the following parameters: patient’s age, smoking history, location of the nodule, availability of previous
x-ray studies, and presence and type of calcifications.

 A. Observation. A stable (no growth in 2 years) calcified lesion in a nonsmoker, aged less than 35 years, is almost certainly benign, and can safely be managed by repeat chest x-ray study every 3 months in the first year, then every year for 2 years. The patient’s cooperation and the family physician’s meticulous follow-up are essential to the success of this plan.

 B. Intervention. An irregular, noncalcified lesion, particularly in a smoker or older patient, warrants invasive intervention to obtain a tissue diagnosis.

1. Fiberoptic bronchoscopy is the procedure of choice for centrally located SPNs.

 2. For peripheral lesions, percutaneous needle biopsy is a quick, relatively easy procedure when done by an experienced operator. Its low rate of specificity and potential risks of pneumothorax and bleeding make it a poor choice because the goal is to reach a diagnosis with the least discomfort to the patient.

 3. Thoracoscopic fine-needle aspiration is becoming an alternative to percutaneous needle biopsy. In a small surgical series, it provided an accurate diagnosis in all cases and helped to define the next surgical step (4).

 4. A new surgical technique, video-assisted thoracic surgery (VATS), is fast becoming the diagnostic tool of choice for suspected SPN (5). Its yield is excellent and its capacity allows resectability of benign lesions without thoracotomy; its very low rate of morbidity and mortality are welcome additions to the approach to this difficult problem.

References

1. Turpin S, Maroves H, Costa P, Medeiros F, Ramos M, de Olivera JP. The solitary pulmonary nodule: a retrospective study of 119 cases. Acta Med Port 1998;11(6):
533–538.

2. Swensen SJ, Silverstein MD, Ilstrup DM, Schleck CD, Edell ES. The probability of malignancy in solitary pulmonary nodules. Application to small radiologically indeterminate nodules. Arch Intern Med 1997;157:849–855.

3. Caskey CI, Templeton PA, Zerhouni EA. Current evaluation of the solitary pulmonary nodule. Surg Clin North Am 1990;28(3):511–520.

4. Bousahra M 2nd, Clowry L Jr. Thoracoscopic fine needle aspiration of solitary pulmonary nodules. Ann Thorac Surg 1997;64:1191–1193.

5. Hazelrigg SR, Magee MJ, Cetindag LB. Video assisted thoracic surgery. Chest Surg Clin North Am 1998;8:763–774, vii. >>

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

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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Source: Field Guide to Bedside Diagnosis, 2007

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

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

Hematuria without Proteinuria

Hematuria with Proteinuria

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

Respiratory Distress and Apnea: Diagnostic Approach: Respiratory Distress
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

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

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.

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007