Diseases » Wegener's granulomatosis » Diagnosis

Diagnosis of Wegener's granulomatosis

Diagnostic Test list for Wegener's granulomatosis:

The list of medical 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

Wegener's granulomatosis Diagnosis: Book Excerpts

• Ask the Following Questions - HEMATURIA
• Differential Diagnosis - Hematuria
• Differential Diagnosis - Hematuria
• Approach to the Diagnosis - HEMATURIA
• Approach to the Diagnosis - AUSCULTATORY SIGNS OF PULMONARY DISEASE
• History and physical examination - Hematuria
• Diagnosis - Acute pyelonephritis
• Diagnosis - Nephrotic syndrome
• Diagnosis - Acute respiratory failure in COPD
• Diagnosis - Infant respiratory distress syndrome
• Diagnosis - Acute poststreptococcal glomerulonephritis
• Diagnosis - Respiratory syncytial virus infection
• Diagnosis - Chronic glomerulonephritis
• Diagnostic tests - Introduction Respiratory Disorders
• Diagnosis - Severe acute respiratory syndrome
• History and physical examination - Hematuria
• History - Hematuria
• History - Solitary Pulmonary Nodule
• Differential Overview - Hematuria
• Diagnosis - Nephrotic syndrome
• Diagnosis - Acute respiratory failure in COPD
• Diagnosis - Respiratory alkalosis
• Diagnosis - Respiratory distress syndrome
• Diagnosis - Respiratory syncytial virus infection
• Diagnosis - Pyelonephritis, acute
• Diagnosis - Respiratory acidosis
• History - Hematuria
• Clinical Features and Diagnosis - Hematuria
• Clinical Features and Diagnosis Respiratory Distress (Neonatal) - Respiratory Distress and Apnea
• History and physical examination - Hematuria
• Approach to the Diagnosis - HEMATURIA
• Approach to the Diagnosis - AUSCULTATORY SIGNS OF PULMONARY DISEASE

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)

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 diagnostis of Wegener's granulomatosis.

HEMATURIA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is there abdominal pain? The presence of abdominal pain with hematuria should first suggest renal calculus, but other causes, such as renal embolism, renal contusion, or laceration, must be considered.
2. Is there dysuria or frequency of micturition associated with the hematuria? The presence of dysuria and frequency with the hematuria should suggest a bladder stone, prostatic disease, or a UTI.
3. Is there fever? The presence of fever with the hematuria would suggest pyelonephritis.
4. Is there a flank mass? The presence of bilateral flank masses with hematuria should suggest polycystic kidneys and hydronephrosis, whereas a unilateral flank mass would suggest a hypernephroma or unilateral hydronephrosis. A solitary cyst or renal vein thrombosis may also present with a flank mass and hematuria.
5. Is there hypertension? The presence of hypertension with the hematuria suggests glomerulonephritis, polycystic kidneys, and collagen diseases.
6. Are there other systemic signs and symptoms? If there are other systemic signs and symptoms, one should be looking for collagen disease, coagulation disorders, leukemia, and sickle cell anemia. When there is no hypertension or other signs and symptoms of systemic diseases, one should be looking for a benign or malignant tumor of the bladder, tuberculosis, or parasitic infection.

DIAGNOSTIC WORKUP

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

• Transient hematuria
  –Urinary tract infection/pyelonephritis
  –Nephrolithiasis (kidney or bladder stones)
  –Exercise
  –Trauma, instrumentation, catheterization, or foreign bodies
  –Endometriosis
  –Transient unexplained
  –Henoch-Schönlein purpura/HUS
  –Coagulopathy and excess anticoagulation
  –Prostatitis, epididymitis

Persistent hematuria
–Sickle cell anemia
–Cancer (prostate, bladder, kidney)
–Benign prostatic hypertrophy
–Polycystic kidney disease
–Intrinsic glomerular disease

Other causes of red or brown urine (pseudohematuria)
–Beeturia (14% population are susceptible after eating beets): Due to excretion of betalaine, a reddish pigment
–Myoglobinuria: Rapidly filtered and excreted; source is usually due to rhabdomyolysis; look for increased elevation of plasma CPK levels
–Hemoglobinuria: Occurs when the filtered load of unbound dimer exceeds resorptive capacity of the proximal tubules, generally at serum levels >100–150 mg/dL

Urethral carbuncle

Urethritis (e.g., Chlamydia)

Porphyria

Phenazopyridine (bladder analgesic): Produces an orange color in urine

Postinfectious glomerulonephropathy

Hereditary (Alport's syndrome)

IgA nephropathy (Berger's disease): Often see gross hematuria without positive family history of disease

Loin pain hematuria syndrome

Thin basement membrane disease (benign familial hematuria): Usually see microscopic hematuria; gross hematuria or renal failure is rare

Hypercalciuria or hyperuricuria

Arteriovenous malformation

Fistula

Others include food dyes, phenolphthalein, rifampin, and porphyrins

Excessive anticoagulation

Trauma

Workup and Diagnosis

• History and physical examination
• Urinalysis in all patients (consider catheterization to distinguish vaginal bleeding from other sources)
  –Blood clots occur with extraglomerular sources
  –Glomerular source of bleeding results in RBC casts, large amounts of protein, dysmorphic RBCs
  –UTI results in pyuria, nitrates, leukocyte esterase
  • Initial labs include BUN/creatinine, electrolytes, calcium, uric acid, CBC, and PT/PTT
  • Centrifuge urine sample: Red sediment only suggests hematuria (RBCs in the urine); heme-negative red supernatant suggests hemoglobinuria; heme-positive clear supernatant suggests myoglobinuria
  • Three-tube test: #1, collect first few mL of urine; #2, midstream; #3, last few mL
    –Hematuria in #1 suggests urethral lesion; in #3, bladder trigone lesion; equally in all three, diffuse lesion
  • IVP (contraindicated in dye allergy), renal ultrasound, or spiral CT to evaluate for stones and renal masses
  • Urine cytology and cystoscopy for patients at risk for bladder cancer (e.g., smoking, cyclophosphamide)
  • Consider C3 level, ANA, ANCA, Anti-GBM, ASO, cryoglobulins, and hepatitis C antibodies
  • Renal biopsy if persistent hematuria with negative workup and evidence of progression (increasing proteinuria, creatinine, and blood pressure)

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Source: In a Page: Signs and Symptoms, 2004

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

• Transient (fever, dehydration, exercise)
• Urinary tract infection
  –Most common cause of gross hematuria
• Hypercalciuria (common)

• Primary glomerulonephritis (GN)
  –Acute poststreptococcal GN: Gross hematuria ±hypertension, oliguria; 5 days to several weeks after Group A strep pharyngitis or pyoderma; can also occur after other infections
  –IgA nephropathy (Berger disease): recurrent gross hematuria occurs at or near onset of a URI
  –Membranoproliferative GN

• GN associated with systemic disease
  –HSP
  –SLE
  –Other vasculitis (rare) e.g.,Wegener
• Other glomerular disease
  –Benign familial hematuria
  –Alport syndrome: Usually X linked, high- frequency deafness, progression to renal failure
  –Glomerular disease (e.g., FSGS) usually presents as nephrotic syndrome
• Tubulointerstitial disease
  –Polycystic kidney disease, interstitial nephritis, papillary necrosis, ATN
• Urinary pelvic junction obstruction
• Urolithiasis/nephrolithiasis
  –Painless in up to 50% of children
• Urethrorrhagia
  –Recurrent gross hematuria (spotting on the underwear)
  –Most common in peripubertal males
• Malignancies (e.g., Wilms tumor)
• Vascular (e.g., renal vein thrombosis)
• Trauma
• Non-urinary tract blood
  –Menses, perineal irritation, pinworms, masturbation, STDs, sexual abuse
• Munchausen/Munchausen by proxy (rare)

Workup and Diagnosis

• History
  –Antecedent illness (including timing)
  –Prior episodes, medication/food exposure
  –Quality of gross hematuria (if present): Color, terminal vs present throughout stream, clots
  –Symptoms: Fever, flank pain, dysuria, rash, hemoptysis, breathing difficulty, joint complaints
  –Family history: Kidney stones, kidney disease, deafness (Alport)
• Physical exam
  –Blood pressure, growth parameters, skin or pharyngeal lesions, cardiac gallop, rales, edema, CVAT, genitourinary exam (external)
  • Labs/studies
    –U/A (dipstick and microscopy), urine culture
    –Dipstick negative =foods, medications
    –Dipstick positive, no RBCs =myoglobin, hemoglobin
    –Dipstick positive, with RBCs =hematuria
    –Macroscopic or microscopic with symptoms (e.g., HTN): Serum chemistries, CBC, ASO, C3, ANA, sickle prep, spot urine calcium/creatinine, STD screen (if sexually active), renal/bladder ultrasound, consider noncontrast helical CT if kidney stones suspected
    –Microscopic hematuria, no symptoms: Repeat U/A two times, 1 week apart; if persists, check serum chemistries, urine culture, sickle prep, spot urine calcium/creatinine and U/As of parents/siblings

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

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

The clinical picture will point to the diagnosis in many cases. If there is a history of abdominal trauma, a contusion or laceration of the kidney or bladder should be suspected. Massive trauma anywhere prompts a tentative diagnosis of crush syndrome. Purpura or bleeding from other sites suggests a coagulation disorder. Severe colicky pain in the abdomen suggests kidney stone. A long history of hypertension tension suggests polycystic kidneys, renal artery stenosis, or glomerulonephritis. A history of fever and rheumatic valvular disease suggests SBE with renal embolism. Painless hematuria in an otherwise healthy looking adult suggests neoplasm, whereas painful hematuria with frequency and dysuria suggests cystitis. Hematuria and a flank mass would make a neoplasm or polycystic kidney likely.

The initial workup should include a CBC, urinalysis, urine culture, chemistry panel, flat plate of the abdomen to assess the presence of stones and kidney size, and personal examination of the urinary sediment. If a renal calculus is suspected, an IVP is ordered immediately and a urologist consulted. A three-glass test will help localized the site of the bleeding. If there is blood in the initial specimen only, the urethra is probably the site of bleeding. If the blood is primarily in the final specimen, the bladder is most likely the site of bleeding. Equal blood discoloration in all specimens points to a renal lesion.

If renal tuberculosis is suspected an AFB smear and culture is done. If collagen disease is suspected an ANA analysis and anti–double strand DNA antibody titer is ordered. If a renal carcinoma is suspected, a CT scan of the abdomen is probably the best study to order but the advice of the urologist ought to be sought. Ultrasonography is useful in differentiating cysts from tumors. If a bladder neoplasm is suspected, cystoscopy will be done. If renal artery embolism or thrombosis is suspected, renal angiography may need to be done to clearly make the diagnosis.

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Source: Differential Diagnosis in Primary Care, 2007

AUSCULTATORY SIGNS OF PULMONARY DISEASE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Clinically, the grouping together of signs provides the best way of narrowing the differential diagnosis.

Rales

1. Bilateral crepitant rales, lack of dullness, and normal breath sounds suggest pulmonary edema or pneumonitis.
2. Focal crepitant rales, reduced alveolar breathing, dullness to percussion, and increased tactile and vocal fremitus suggest lobar pneumonia or pulmonary infarction.
3. Bilateral sibilant and sonorous rales without dullness and with increased bronchial breathing suggest asthma, chronic bronchitis and emphysema, acute bronchitis or bronchiolitis, and cardiac asthma.
4. Focal crepitant rales and amphoric breathing with dullness below and hyperresonance above suggest a lung abscess or cavitation

Hyperresonance

1. Hyperresonance bilaterally with diminished breath sounds bilaterally and sibilant rales suggests pulmonary emphysema or asthma.
2. Focal hyperresonance with diminished or absent breath sounds and no rales suggests pneumothorax.
3. Focal hyperresonance with normal or only diminished breath sounds suggests a large bulla.

Dullness or Flatness

1. Dullness with diminished breath sounds and no rales suggests atelectasis or pleural effusion from empyema, CHF, or pulmonary infarct. In atelectasis, there is no hyperresonance or egophony above the dullness.
2. Dullness with diminished breath sounds and crepitant rales suggests pneumonia or pulmonary infarct. If there is bronchophony as well, there is probably no associated effusion. If there is no bronchophony but hyperresonance and egophony above the dullness, then an associated pleural effusion should be considered.

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Source: Differential Diagnosis in Primary Care, 2007

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

Acute pyelonephritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis requires urinalysis and culture. Typical findings include:

❑ Pyuria (pus in urine): Urine sediment reveals the presence of leukocytes singly, in clumps, and in casts; and, possibly, a few red blood cells.

❑ Significant bacteriuria: Urine culture reveals more than 100,000 organisms/µl of urine.

❑ Low specific gravity and osmolality: These findings result from a temporarily decreased ability to concentrate urine.

❑ Slightly alkaline urine pH.

❑ Proteinuria, glycosuria, and ketonuria: These conditions are less common.

Excretory urography or computed tomography (CT) scan of the kidneys, ureters, and bladder also help in the evaluation of acute pyelonephritis by revealing calculi, tumors, or cysts in the kidneys and the urinary tract. In addition, excretory urography may show asymmetrical kidneys.

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

Nephrotic syndrome: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Consistent proteinuria in excess of 3.5 g/24 hours strongly suggests nephrotic syndrome; examination of urine also reveals increased number of hyaline, granular, and waxy, fatty casts, and oval fat bodies. Serum values that support the diagnosis are increased cholesterol, phospholipids, and triglycerides and decreased albumin levels. Histologic identification of the lesion requires kidney biopsy. Other tests may be done to rule out metabolic causes.

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

Acute respiratory failure in COPD: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Progressive deterioration in ABG levels and pH, when compared with the patient’s “normal” values, strongly suggests ARF in COPD. (In patients with essentially normal lung tissue, pH below 7.35 usually indicates ARF, but patients with COPD display an even greater deviation from this normal value, as they do with PaCO₂ and PaO₂.)

Other supporting findings include:

❑ Bicarbonate — Increased levels indicate metabolic alkalosis or reflect metabolic compensation for chronic respiratory acidosis.

❑ Hematocrit (HCT) and Hb — Abnormally low levels may be due to blood loss, indicating decreased oxygen-carrying capacity. Elevated levels may occur with chronic hypoxemia.

❑ Serum electrolytes — Hypokalemia and hypochloremia may result from diuretic and corticosteroid therapies used to treat ARF.

❑ White blood cell count — Count is elevated if ARF is due to bacterial infection; Gram stain and sputum culture can identify pathogens.

❑ Chest X-ray — findings identify pulmonary pathologic conditions, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, or effusions.

❑ Electrocardiogram — Arrhythmias commonly suggest cor pulmonale and myocardial hypoxia.

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

Infant respiratory distress syndrome: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

CONFIRMING DIAGNOSIS Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest IRDS, a chest X-ray and arterial blood gas (ABG) analysis are necessary to confirm the diagnosis.

❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with IRDS), but 24 hours after birth it will show the characteristic ground-glass appearance and air bronchograms.

❑ ABG analysis shows decreased partial pressure of arterial oxygen; normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).

❑ Chest auscultation reveals normal or diminished air entry and crackles (rare in early stages).

When a cesarean delivery is necessary before 36 weeks’ gestation, amniocentesis enables the determination of the lecithin/sphingomyelin (L/S) ratio and the presence of phosphatidylglycerol. An L/S ratio of more than 2:1 and the presence of phosphatidylglycerol decrease the likelihood of IRDS.

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

Acute poststreptococcal glomerulonephritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis requires a detailed patient history and assessment of clinical symptoms and laboratory tests.

Urinalysis typically reveals proteinuria and hematuria. RBCs, white blood cells, and mixed cell casts are common in urinary sediment. Elevated serum creatinine levels and low creatinine clearance accompany impaired glomerular filtration. Elevated antistreptolysin-O titers (in 80% of patients), elevated streptozyme and anti-DNase B titers, and low serum complement levels verify recent streptococcal infection. A throat culture may also show group A beta-hemolytic streptococcus. Renal ultrasound may show a normal or slightly enlarged kidney. A renal biopsy may confirm the diagnosis or assess renal tissue status.

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

Respiratory syncytial virus infection: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis is usually based on clinical findings and epidemiologic information.

❑Many facilities can perform rapid tests for the virus using fluid obtained from the nose.

❑Cultures of nasal and pharyngeal secretions may show RSV; however, the virus is labile, so cultures aren't always reliable.

❑Chest X-rays help detect pneumonia.

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

Chronic glomerulonephritis: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Patient history and physical assessment seldom suggest glomerulonephritis. Suspicion develops from urinalysis revealing proteinuria, hematuria, cylindruria, and red blood cell casts. Rising blood urea nitrogen and serum creatinine levels indicate advanced renal insufficiency. X-ray or ultrasound shows smaller kidneys. Kidney biopsy identifies the underlying disease and provides data needed to guide therapy.

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

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

Diagnostic tests evaluate physiologic characteristics and pathologic states within the respiratory tract.

Noninvasive tests include:

❑  Chest X-ray shows such conditions as atelectasis, pleural effusion, infiltrates, pneumothorax, lesions, mediastinal shifts, pulmonary edema, and chronic obstructive pulmonary disease (COPD).

❑ Computed tomography scan provides a three-dimensional picture that’s 100 times more sensitive than a chest X-ray.

❑ Magnetic resonance imaging identifies obstructed arteries and tissue perfusion, but movement of the heart and lungs reduces the image’s clarity.

❑ Sputum specimen analysis assesses sputum quantity, color, viscosity, and odor; microbiological stains and culture of sputum can identify infectious organisms; and cytologic preparations can detect respiratory tract neoplasms. Sensitivity tests determine antibiotic sensitivity and resistance.

❑ Pulmonary function tests measure lung volume, flow rates, and compliance. Normal values, individualized by body stature and age, are reported in percentage of the normal predicted value. Static measurements are volume measurements that include tidal volume, volume of air contained in a normal breath; functional residual capacity, volume of air remaining in the lungs after normal expiration; vital capacity, volume of air that can be exhaled after maximal inspiration; residual volume, air remaining in the lungs after maximal expiration; and total lung capacity (TLC), volume of air in the lungs after maximal inspiration. Dynamic measurements characterize the movement of air into and out of the lungs and show changes in lung mechanics. They include measurement of forced expiratory volume in 1 second, maximum volume of air that can be expired in 1 second from total lung capacity; maximal voluntary ventilation, volume of air that can be expired in 1 minute with the patient’s maximum voluntary effort; and forced vital capacity, maximal volume of air that the patient can exhale from TLC. (Peak flow rate, which can be obtained at the bedside, is also a dynamic measurement of pulmonary function.)

❑ Exercise stress test evaluates the ability to transport O₂ and remove CO₂ with increasing metabolic demands.

❑ Polysomnography can diagnose sleep disorders.

❑ Lung scan (ventilation-perfusion or scintiphotography scan) demonstrates ventilation and perfusion patterns. It’s used primarily to evaluate pulmonary embolus.

❑ Arterial blood gas (ABG) analysis assesses gas exchange. Decreased PaO₂ may indicate hypoventilation, ventilation-perfusion mismatch, or shunting of blood away from gas exchange sites. Increased partial pressure of arterial carbon dioxide (PaCO₂) reflects marked ventilation-perfusion mismatch or hypoventilation; decreased PaCO₂ reflects increased alveolar ventilation. Changes in pH may reflect metabolic or respiratory dysfunction.

❑ Pulse oximetry is a noninvasive assessment of arterial oxygen saturation.

❑ Capnography may be used either transcutaneously or in ventilator circuit to determine PaCO₂ trends.

Invasive tests include:

❑ Bronchoscopy permits direct visualization of the trachea and mainstem, lobar, segmental, and subsegmental bronchi. It may be used to localize the site of lung hemorrhage, visualize masses in these airways, and collect respiratory tract secretions. Brush biopsy may be used to obtain specimens from the lungs for microbiological stains, culture, and cytology. Lesion biopsies may be performed by using small forceps under direct visualization (when present in the proximal airways) or with the aid of fluoroscopy (when present distal to regions of direct visualization). Bronchoscopy can also be used to clear secretions and remove foreign bodies.

❑ Thoracentesis permits removal of pleural fluid for analysis.

❑ Pleural biopsy obtains pleural tissue for histologic examination and culture.

❑ Pulmonary artery angiography, the injection of dye into the pulmonary artery, can locate pulmonary embolism. This is considered the gold standard for diagnosing pulmonary emboli.

❑ Positron emission tomography scan uses a short-life radionuclide. Increased uptake of the substance is seen in malignant cells.

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

Severe acute respiratory syndrome: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis of severe respiratory illness is made when the patient has a fever greater than 100.4° F (38° C) or upon clinical findings of lower respiratory illness and a chest X-ray demonstrating pneumonia or acute respiratory distress syndrome.

Laboratory validation for the virus includes cell culture of SARS-CoV, detection of SARS-CoV ribonucleic acid by the reverse transcription polymerase chain reaction (PCR) test, or detection of serum antibodies to SARS-CoV. Detectable levels of antibodies may not be present until 21 days after the onset of illness, but some individuals develop antibodies within 14 days. A negative PCR, antibody test, or cell culture doesn’t rule out the diagnosis.

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

A thorough history is of utmost importance!

A. General aspects

1. Type of hematuria (macro/gross or microscopic).

2. Relationship to urination or timing of hematuria. The three-container method will help to separate the micturition into three portions with an initial, middle, and final portion.

Predominantly, initial hematuria results from anterior urethral disease; final hematuria results from disease of the bladder neck or posterior urethra; and hematuria throughout the stream suggests a disease site higher in the bladder, ureter, or kidney.

 3. Urine color. Color can be affected by the following: Phenazopyridine (orange); nitrofurantoin (brown); rifampin (yellow-orange); l-dopa, methyldopa, and metronidazole (reddish-brown); phenolphthalein in laxatives, red beet and rhubarb consumption, food coloring, and vegetable dyes (red).

 4. Clots, especially wormlike clots, suggest a location above the bladder neck.

 5. Associated symptoms (e.g., recent sore throat, fever, chills, and flulike symptoms) may be the first sign of IgA nephropathy or postinfectious glomerulonephritis. Urinary frequency, dysuria, fever, chills, and urgency point to an infectious process. Diminished urine flow and abdominal pain or flank pain radiating into the groin can indicate the presence of urinary tract obstruction (Chapter 10.5). Vaginal discharge or bowel movement changes may hint at a nonurinary tract cause such as a foreign body (especially in children). A rash, joint pain, photosensitivity, flulike symptoms, and Raynaud’s phenomenon point to a collagen vascular disease.

 B. Past medical history should lead to a suspicion of parasites (e.g., Schistosoma heamatobium) if the patient has traveled to endemic areas; of bladder tumor if there was exposure to chemical carcinogens (e.g., aniline dyes), or tobacco smoke. Other causes of hematuria detected in the history include drug ingestion and anticoagulation, and medical problems such as prostatic hypertrophy, diabetes mellitus (nephrosclerosis), analgesic medication abuse (renal papillary necrosis), nephrolithiasis, trauma (including vigorous masturbation), chemotherapy exposure with cyclophosphamide (chemical cystitis), antibiotic use (interstitial nephritis), previous urinary tract malignancies suggesting recurrence, and sickle cell disease (papillary necrosis).

 C. Family history. Delineate any family history of polycystic kidney disease, sickle cell trait and disease, nephrolithiasis, various glomerular diseases, tuberculosis, and benign familial hematuria. The combination of renal failure, deafness, and hematuria suggests Alport’s hereditary nephritis.

Physical examination

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

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

 Obtain a complete history, including smoking, occupational exposure, immigration, and travel. Check previous chest x-ray studies to establish prior presence of a nodule, as well as growth on an existing nodule. An absence of growth over a period of 2 years is generally accepted as a sign of the benign nature of a SPN.

Physical examination

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

Hematuria: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Urinary tract infection

❑ Nephrolithiasis

❑ Anticoagulation

❑ Long distance running

❑ Renal trauma

❑ Bladder cancer

❑ Renal cell cancer

❑ Transitional cell cancer

❑ Glomerulonephritis

❑ Interstitial cystitis

❑ Hemorrhagic cystitis

❑ Hemoglobinuria

❑ Endocarditis

❑ Polycystic kidney disease

❑ Renal artery embolism

❑ Renal vein thrombosis

❑ Endometrial implants

❑ Wegener granulomatosis

❑ Goodpasture syndrome

Diagnostic Approach

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

Nephrotic syndrome: Diagnosis
(Handbook of Diseases)

Consistent proteinuria in excess of 3.5 g/24 hours strongly suggests nephrotic syndrome; examination of urine also reveals an increased number of hyaline, granular, and waxy, fatty casts, and oval fat bodies. Serum values that support the diagnosis are increased cholesterol, phospholipid, and triglyceride levels and decreased albumin levels. Histologic identification of the lesion requires a kidney biopsy.

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Source: Handbook of Diseases, 2003

Acute respiratory failure in COPD: Diagnosis
(Handbook of Diseases)

Progressive deterioration in ABG levels and pH, when compared with the patient’s baseline values, strongly suggests ARF in COPD patients. (In patients with essentially normal lung tissue, a pH less than 7.35 usually indicates ARF, but COPD patients display an even greater deviation from this normal value, as they do with blood Paco₂ and Pao₂.) The following findings further support the diagnosis:

Bicarbonate levels are increased, indicating metabolic alkalosis or metabolic compensation for chronic respiratory acidosis.

Hb levels and hematocrit are abnormally low, which may be due to blood loss, indicating decreased oxygen-carrying capacity.

Serum electrolyte levels may indicate hypokalemia, which may result from compensatory hyperventilation — an attempt to correct alkalosis; hypochloremia is common with metabolic alkalosis.

White blood cell count is elevated if ARF is due to bacterial infection; in certain cases of profound septicemia, the leukocyte count may be decreased. Gram stain and sputum culture can identify pathogens.

Chest X-rays reveal pulmonary pathology, such as emphysema, atelectasis, lesions, pneumothorax, infiltrates, or effusions.

Electrocardiogram reveals arrhythmias, which commonly suggest cor pulmonale and myocardial hypoxia. Large P waves (“p pulmonale”) may indicate a history of right-sided heart failure.

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Source: Handbook of Diseases, 2003

Respiratory alkalosis: Diagnosis
(Handbook of Diseases)

Arterial blood gas (ABG) analysis confirms respiratory alkalosis and rules out respiratory compensation for metabolic acidosis. Findings include a Paco₂ below 35 mm Hg, a pH that’s elevated in proportion to the fall in Paco₂ in the acute stage but that drops toward normal in the chronic stage, and a bicarbonate level that’s normal in the acute stage but below normal in the chronic stage.

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Source: Handbook of Diseases, 2003

Respiratory distress syndrome: Diagnosis
(Handbook of Diseases)

Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest respiratory distress syndrome, the following tests are necessary to confirm the diagnosis:

❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with respiratory distress syndrome) but later shows a fine reticulonodular pattern.

❑ Arterial blood gas (ABG) analysis shows decreased partial pressure of arterial oxygen (Pao₂); normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).

❑ Pulmonary function studies may be necessary.

When a cesarean section is necessary before the 36th week of gestation, amniocentesis allows determination of the lecithin-sphingomyelin ratio, which helps to assess prenatal lung development and the risk of respiratory distress syndrome.

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Source: Handbook of Diseases, 2003

Respiratory syncytial virus infection: Diagnosis
(Handbook of Diseases)

The following clinical findings and epidemiologic information aid in the diagnosis:

❑ Cultures of nasal and pharyngeal secretions may show RSV.

❑ Serum antibody titers may be elevated, but before age 6 months, maternal antibodies may impair test results.

❑ Serology for RSV is positive.

❑ Chest X-rays help detect pneumonia or bronchiolitis.

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Source: Handbook of Diseases, 2003

Pyelonephritis, acute: Diagnosis
(Handbook of Diseases)

Diagnosis requires urinalysis and culture. Typical findings include:

❑ pyuria (pus in urine) — urine sediment reveals the presence of leukocytes singly, in clumps, and in casts; and, possibly, a few red blood cells

❑ significant bacteriuria — more than 100,000 organisms/µl of urine revealed in urine culture

❑ low specific gravity and osmolality, resulting from a temporarily decreased ability to concentrate urine

❑ slightly alkaline urine pH

❑ proteinuria, glycosuria, and keto-nuria — less common.

X-rays also help in the evaluation of acute pyelonephritis. X-ray films of the kidneys, ureters, and bladder may reveal calculi, tumors, or cysts in the kidneys and urinary tract. Excretory urography may show asymmetrical kidneys.

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Source: Handbook of Diseases, 2003

Respiratory acidosis: Diagnosis
(Handbook of Diseases)

❑ The following arterial blood gas (ABG) levels confirm respiratory acidosis: a Paco₂ exceeding the normal level of 45 mm Hg, pH usually below the normal range of 7.35 to 7.45, and a bicarbonate level that’s normal in the acute stage but elevated in the chronic stage.

❑ Chest X-ray, computed tomography scan, or pulmonary function test may help diagnose lung disease.

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Source: Handbook of Diseases, 2003

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

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 artifactitious hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if there’s any pain or burning with 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 any anticoagulants or aspirin.

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

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

Hematuria without Proteinuria

Glomerular Disorders

Acute Postinfectious Glomerulonephritis

Usuallypresents within 1–2 wks after streptococcal pharyngitisor skin infection.

Rare before 3 yrs of age.

Disease spectrum varies from asymptomaticmicroscopic hematuria with normal renal function to acute renalfailure.

Clinical manifestations include fever,abdominal or flank pain, edema, hypertension, and oliguria. Urinecolor is often reddish brown, and red cell casts are usually seen.Proteinuria may or may not occur. In almost all cases, C3 levelis decreased. Supporting evidence of preceding streptococcal infectioncan include positive throat culture, positive streptozyme, or elevatedantistreptolysin O titer.

C3 level should return to normal withinabout 8 wks after onset of illness. Proteinuria can last for 6 mosand microscopic hematuria for 1–2 yrs, but virtually allchildren recover.

Immunoglobulin A Nephropathy

Also knownas Berger disease.

Can occur at any age, but peak incidenceis in adolescence and young adulthood.

Usually presents with recurrent attacksof gross hematuria, which may be associated with upper respiratorytract infections.

Microscopic hematuria can occur betweenepisodes of gross hematuria. Mild proteinuria also may occur, particularlyearly in the course. Renal function tends to be normal. Hypertension,nephrotic syndrome, and rapidly progressive course are unusual findings.

Serum concentration of C3 is normal,and this helps to distinguish this disorder from acute postinfectiousglomerulonephritis. Immunoglobulin A is major immunoglobulin inmesangial deposits on renal biopsy.

Henoch-Schönlein Nephritis

Common causeof vasculitis in childhood.

Clinical features include abdominalpain, purpura on buttocks and lower legs, transient arthritis/arthralgiaof large joints, microscopic hematuria, and gastrointestinal bleeding.

Diagnosis is usually clinical.

Renal biopsy is indistinguishable fromimmunoglobulin A nephropathy.

Some children develop chronic nephropathywith progression to end-stage renal disease.

Alport Syndrome

Primaryfeature is recurrent gross hematuria or asymptomatic microscopichematuria. A number of affected children also have sensorineuralhearing loss. Later in life, individuals develop progressive renalinsufficiency.

Usual form of genetic transmissionis X-linked, although autosomal-dominant and autosomal-recessiveforms occur. X-linked phenotype is due to mutation in the gene foralpha-5 chain of basement membrane collagen.

Membranoproliferative Glomerulonephritis

Most commonin the second decade of life. 3 histologic types (I, II, III) havebeen described.

Presentation is variable: gross ormicroscopic hematuria with or without proteinuria or nephrotic syndrome.Hypertension is common, and renal function may be decreased.

Serum C3 level is usually low. C3 nephriticfactor may be present, especially in type II. Different types canonly be distinguished by renal biopsy.

Systemic Lupus Erythematosus

Chronicmultisystem autoimmune disease that is most common in adolescent girls.

Characteristic findings include fever,arthritis, weight loss, and nephritis. Hematuria and proteinuriaare common urinary findings. Antinuclear antibody is usually positiveand serum C3 is usually low.

Antibody to double-stranded DNA isdiagnostic. Renal biopsy usually shows proliferative glomerulonephritiswith immunoglobulin G and C3 deposits.

Familial Benign Hematuria (Thin Basement Membrane Nephropathy)

Autosomal-dominantdisorder in which hematuria is usually microscopic. Positive familyhistory of hematuria and absence of proteinuria suggest diagnosis.Electron microscopy shows thinning of glomerular capillary basementmembrane.

Although thought to be benign, reportby Dische et al. (1985) described thin basement membrane nephropathyin several individuals who developed progressive renal disease.Further study is required to determine whether this disorder isreally benign.

Nonfamilial Benign Hematuria

In many children, diagnostic studies do notreveal the cause of hematuria. These children are categorized ashaving benign nonfamilial hematuria. After months or years, hematuriafrequently disappears. Although this disorder is often benign, somechildren may have slowly developing glomerulonephritis. As longas hematuria exists, these patients should be tested at 6-mo intervalsto determine whether proteinuria develops.

Nonglomerular Disorders

Urinary Tract Infection

Common symptomsare dysuria, frequency, urgency, fever, abdominal pain, flank pain,and vomiting. Microscopic or gross hematuria can occur along withpyuria and bacteriuria.

Positive urine culture confirms thediagnosis.

See Chap.15, Dysuria.

Trauma

Blunt orpenetrating injury to kidney or any portion of urinary tract cancause gross or microscopic hematuria.

With minor trauma and microscopic hematuriain asymptomatic individuals, renal U/S should be performedto search for anatomic abnormality (e.g., hydronephrosis or renalcyst) because minimal trauma rarely causes hematuria in normal kidneys.Otherwise, CT is radiologic study of choice.

Urethral trauma may occur followingcrush-type injury from fractured pelvis or direct injury, and urethrographymay be diagnostic.

Exercise

Vigorous exercise can produce gross or microscopichematuria, which usually resolves within 1–2 days.

Hydronephrosis

In children with hydronephrosis, microscopicor gross hematuria may occur following mild flank or abdominal trauma.Renal U/S may be performed initially.

Renal Vein Thrombosis

Predisposingfactors include perinatal asphyxia, dehydration, septicemia, shock,and coagulopathies (e.g., protein C deficiency).

Gross hematuria usually occurs alongwith palpable unilateral or bilateral flank masses.

Renal U/S with Doppler methodsis diagnostic.

Hemoglobinopathies

HemoglobinopathiesSA, SC, SS, CC, AC, and sickle beta-thalassemia can produce renalbleeding and microscopic or gross hematuria.

Hemoglobin electrophoresis is diagnosticand should be performed in any African-American child with hematuriaof unknown cause.

Idiopathic Hypercalciuria

Microscopicor gross hematuria may occur with increased urinary calcium excretion withoutevidence of urinary stone disease. However, hypercalciuria is riskfactor for development of urolithiasis.

Urine calcium:creatinine ratio (mg:mg)of greater than normal for age can screen for this disorder (Matoset al., 1997). If spot ratio is greater than normal, 24-hr urinecalcium excretion should be measured. Calcium excretion of >4mg/kg/day is indicative of hypercalciuria.

Urolithiasis

Causes inchildren include urinary tract infection, hypercalciuria, hyperuricosuria, cystinuria,and primary hyperoxaluria.

When urinary stone is being passed,abdominal or flank pain (renal colic) and microscopic or gross hematuriaare usual findings.

Diagnostic investigations should includeUA; urine culture; blood urea nitrogen; and serum measurements ofcalcium, phosphorus, uric acid, and creatinine.

CT is recommended to search for underlyingdisease and localize any obstruction.

When calculi are recovered from urine,their biochemical contents should be analyzed. If they are unrecoverablefrom urinary tract, determination of calcium:creatinine ratio inrandom urine specimen should be performed. Ratio greater than normalfor age can screen for hypercalciuria. More precise test is measurementof 24-hr urine calcium excretion.

If these tests are negative, 24-hrurinary excretion of cystine, oxalate, and uric acid should be performed.

Polycystic Kidney Disease

Autosomal-Recessive

Gene hasbeen mapped to chromosome 6.

Common findings in neonates are grossor microscopic hematuria, bilateral flank masses, hypertension,and azotemia.

Renal U/S usually revealslarge echogenic kidneys. Cysts are microscopic and not seen by imaging.

Liver disease is congenital hepaticfibrosis.

Diagnosis is usually clinical and radiologic.

Autosomal-Dominant

Rarely encounteredin childhood.

At least 3 different genetic mutationshave been found.

Gross or microscopic hematuria, unilateralor bilateral abdominal masses, and hypertension are common findings.

Abdominal U/S shows enlargedpolycystic kidneys and hepatic cysts.

Diagnosis is usually based on clinicaland radiographic findings.

Renal Tuberculosis

Usuallydoes not occur until primary disease has been established over several years.

Usually associated with tuberculouscystitis, which can produce suprapubic pain and dysuria.

Gross or microscopic hematuria andpyuria are characteristic.

Mantoux test is usually positive.

Usual urine culture for bacteria isnegative, whereas urine culture positive for acid-fast organismsis diagnostic.

Vascular Malformations

Arteriovenousmalformations of kidney can present with gross hematuria.

Renal U/S and CT may locatemalformation. Renal angiography is definitive.

Foreign Body in Urethra or Bladder

Foreignbody in urethra or bladder usually produces urethral or suprapubicpain, dysuria, and hematuria.

Abdominal radiography may reveal radiopaqueforeign body. Cystoscopy can confirm diagnosis.

It is important to note that a foreignbody in the vagina can produce bleeding that may be mistaken forhematuria.

Neoplasm

A numberof genitourinary neoplasms occur in the pediatric population.

Wilms tumor, most common renal tumorin children, usually presents as abdominal or flank mass that doesnot cross midline unless it is very large. Gross hematuria occursin small number of cases. Renal U/S or CT shows renal massthat distorts collecting system.

Renal hemangioma is rare lesion thatcan present with recurrent gross hematuria. Diagnosis is confirmedby renal angiography.

Renal carcinoma is rare in pediatricpopulation, but renal U/S can demonstrate mass lesion.

Bladder tumors are exceedingly rarein children, but suprapubic mass is sometimes palpable. Most commonbladder tumor is rhabdomyosarcoma, which can present with hematuriaor acute urinary retention. Abdominal U/S, CT, and cystoscopyare useful in locating and defining extent of tumor.

In all cases of genitourinary tractneoplasms, histologic diagnosis is definitive.

Bleeding Disorders

Although gross or microscopic hematuria mayoccur with bleeding disorders (hemophilias, thrombocytopenia, disseminatedintravascular coagulation), it is uncommon to have isolated hematuriaas only manifestation. See Chap.53, Recurrent Infection.

Drugs

A number of drugs (penicillins, sulfonamides,cephalosporins, rifampin, tetracycline, cisplatin, lithium) maycause gross or microscopic hematuria. Cyclophosphamide may causehemorrhagic cystitis.

Hematuria with Proteinuria

Hematuriawith proteinuria may occur with several glomerular renal disordersas discussed previously:

Acute postinfectious glomerulonephritis

Immunoglobulin A nephropathy

Henoch-Schönlein nephritis

Alport syndrome

Membranoproliferative glomerulonephritis

Systemic lupus erythematosus

Other glomerular renal diseases thatusually present with hematuria and proteinuria are discussed inthis section.

Membranous Nephropathy

Most commonduring second decade of life and usually presents with nephroticsyndrome. Microscopic hematuria is more common than gross hematuria.

Renal biopsy confirms diagnosis.

Glomerulonephritis of Chronic Infection

Disordersassociated with glomerulonephritis of chronic infection includeendocarditis and ventriculoatrial shunt infections.

Clinical features are those of acuteglomerulonephritis, namely edema, hypertension, and renal insufficiency.Serum C3 is often decreased.

Idiopathic Rapidly Progressive Glomerulonephritis

Uncommondisease in children; often preceded by viral illness.

Affected children have acute onsetof hematuria, proteinuria, oliguria or anuria, and azotemia.

Serum C3 level is normal or mildlydecreased. Many children progress to end-stage renal disease withina few weeks or months without treatment.

Renal biopsy and clinical course arediagnostic.

Hemolytic-Uremic Syndrome

Typicalform follows prodromal illness consisting of fever, vomiting, abdominal pain,and, often, bloody diarrhea. This is followed in 5–10 daysby hemolytic anemia with fragmented red cells, thrombocytopenia,and acute renal injury with hematuria, proteinuria, and often oliguriaor anuria.

Most common pathogen is E. coli 0157:H7.

Polyarteritis Nodosa

Necrotizingvasculitis that affects small and medium-sized arteries. Althoughcause is unknown, it may follow viral URI, streptococcal infection,or chronic hepatitis B infection.

Characteristic findings include fever,abdominal pain, hematuria, hypertension, purpura, arthritis, andstroke.

Lab findings include increased sedimentationrate, anemia, leukocytosis, proteinuria, and hypergammaglobulinemia.In some cases, antineutrophil cytoplasmic antibody is found.

Biopsy demonstrating the vasculitisis diagnostic.

Antiglomerular Basement Membrane Disease (Goodpasture Disease)

Associationof pulmonary hemorrhage and glomerulonephritis in which antibodies againstlung and glomerular basement membrane can be demonstrated.

Characteristic findings are hematuria,proteinuria, hemoptysis, and progressive renal failure. Serum C3level is normal.

Renal biopsy shows linear stainingof immunoglobulin G along glomerular basement membrane.

Focal Segmental Glomerulosclerosis

Clinicallyindistinguishable from minimal change nephrotic syndrome but shouldbe suspected when there has been inadequate response to standardcorticosteroid therapy.

Microscopic hematuria and occasionallygross hematuria may occur.

Renal biopsy is diagnostic.

Wegener Granulomatosis

Disorderof unknown cause characterized by vasculitis that affects upperand lower respiratory tract and kidneys.

Fever, malaise, weight loss, hemoptysis,dyspnea, hematuria, and proteinuria are characteristic findings.

Antineutrophil circulating antibodiesthat bind to proteinase 3 are specific for this disorder. Sinus,airway, lung, or kidney biopsy that shows necrotizing granulomatouslesions and presence of specific antineutrophil circulating antibodiesthat bind to proteinase 3 confirm the diagnosis.

Diagnostic Approach

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

Respiratory Distress and Apnea: Clinical Features and Diagnosis: Respiratory Distress (Neonatal)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Upper Respiratory Tract Obstruction

Disorders that cause upper respiratory tractobstruction are discussed in Chap.63, Stertor, Stridor, and Airway Obstruction.

Lower Respiratory Tract Disorders

Transient Tachypnea of the Newborn

Delayedresorption of lung fluid or mild immaturity of surfactant systemare most probable explanations for this disorder, which usuallyoccurs in term infants soon after birth.

Respiratory rate is commonly 60–80breaths/min but sometimes is >100 breaths/min.Mild intercostal retractions and expiratory grunting also may occur.

Characteristic chest radiographic findingsare prominent perihilar markings, hyperaeration, widening of interlobarfissures, and evidence of interstitial and pleural fluid.

Most infants require <40% supplementaloxygen. Tachypnea usually resolves in 3 or 4 days.

Respiratory Distress Syndrome (Hyaline Membrane Disease)

Respiratorydistress syndrome, which is most common cause of respiratory distress inpreterm infants, is due to inadequate amount of surfactant. Someinfants experience intrapartum asphyxia and fail to expand theirlungs at birth, whereas others develop tachypnea and expiratorygrunting within first 1–2 hrs of life.

Spectrum of disease varies from mild(tachypnea and minimal oxygen requirement) to severe (apnea andrespiratory failure). Crackles may be heard on chest exam.

Characteristic chest radiograph showsdiffuse reticulogranular infiltrates, atelectasis, and air bronchograms.

Diagnosis is clinical and radiographic.

Meconium Aspiration and Other Aspiration Syndromes

Neonateswho aspirate meconium are usually those who have had intrapartumasphyxia.

Thick meconium in upper airway andmeconium staining of skin and nails are usual findings. Airway obstruction,pneumonia, and respiratory failure can occur.

Chest radiography shows irregular distributionof coarse, patchy infiltrates and hyperaeration.

Clinical and radiologic findings arediagnostic.

Aspiration of feedings sometimes occursin normal infants but is more frequent in those with sucking andswallowing disorders (see Chap.65, Sucking and Swallowing Difficulty).

Pneumonia

Pneumoniamay be caused by infections acquired transplacentally, during birthprocess, and postnatally. Viral infections transmitted by transplacentalroute include enteroviruses, adenoviruses, influenza viruses, rubellavirus, varicella-zoster virus, herpes simplex virus, cytomegalovirus,and HIV. Transplacental bacterial infections caused by L. monocytogenes,M. tuberculosis, or T. pallidum are less common than viral infections.

Neonatal pneumonia is most commonlyacquired during birth process. Group B Streptococcus is most commonpathogen; other pathogens (e.g., gram-negative enteric bacteria)are less common. Most common viral agents acquired during birthprocess are herpes simplex virus and cytomegalovirus. C. trachomatisis also acquired during delivery and usually presents at 2–8wks of age with staccato cough and wheezing. History of conjunctivalinfection may or may not exist.

Inadequate hand washing and exposureto respiratory equipment or humidified incubators may contributeto infection, especially with S. aureus and gram-negative entericbacteria.

Other causes of postnatal infectionsinclude respiratory syncytial virus, parainfluenza viruses, influenzaviruses, herpes simplex virus, cytomegalovirus, and fungi (C. albicans).

Infants with pneumonia present withrespiratory distress. Chest radiography shows interstitial or alveolarinfiltrates or consolidation. With suspected bacterial pneumoniain newborns, blood and spinal fluid cultures should be performed,and treatment begun immediately while awaiting culture results.

Diagnosis of viral infections is discussedin other chapters.

Pulmonary Air Leaks

Extrapulmonaryair can accumulate in interstitial spaces of lung (pulmonary interstitialemphysema), mediastinum (pneumomediastinum), pleural space (pneumothorax),and pericardium (pneumopericardium).

Common cause of pulmonary interstitial emphysemais positive-pressure mechanical ventilation.

Pneumomediastinum results from dissectionof air from interstitial space into mediastinum.

Pneumothorax results from mediastinalair rupture into pleural space or rupture of air blebs on surfaceof lung. Most common causes of pneumothorax are respiratory distresssyndrome, meconium aspiration, and high-pressure mechanical ventilation.

Pneumopericardium is produced fromdissection of mediastinal air into pericardium.

Clinical presentation depends on sizeand location of air leak. Significant unilateral pneumothorax collapsesipsilateral lung and shifts heart and mediastinum to opposite sidewith diminished breath sounds on affected side. Significant pneumopericardiummay compromise cardiac filling and cause diminished cardiac output.

Chest radiography is diagnostic ofdifferent types of air leak.

Pulmonary Hemorrhage

Predisposingfactors in neonatal period include perinatal asphyxia, septicemia,and mechanical ventilation, especially in those with respiratorydistress syndrome.

Accompanying respiratory distress isbloody fluid, which oozes from nose, mouth, or endotracheal tube.

Depending on how severe bleeding is,chest radiography may show spectrum of findings ranging from patchyinfiltrates to opacification of lungs.

Bronchopulmonary Dysplasia

This form of chronic lung disease developsin neonates treated with prolonged oxygen therapy and positive-pressureventilation for primary lung disorders. Most infants improve duringfirst 1–2 yrs of life, and with time chest radiograph becomesnormal. However, some of these children continue to have abnormalpulmonary function in childhood. Others with severe disease developcor pulmonale and succumb to their illness.

Congenital Malformations of Lungs, Bronchi, Diaphragm, andRib Cage

Lung Agenesis and Aplasia

Lung agenesisis complete absence of lung or lobe and its branches, whereas lung aplasiais complete absence of lung tissue except for presence of smalllobar bronchus.

Respiratory distress often occurs atbirth with decreased breath sounds on affected side.

Chest radiography shows opaque hemithoraxwith displacement of mediastinum and normal lung toward involvedside.

Bronchoscopy shows absence of mainbronchus in agenesis and presence of small bronchus in aplasia.

Pulmonary Hypoplasia

Pulmonaryhypoplasia refers to smaller than normal lungs. Can be isolatedmalformation or occur in association with space-occupying lesionsof thorax (congenital diaphragmatic hernia, cystic adenomatoid malformation,large pleural effusion), oligohydramnios (renal agenesis, polycystickidney disease), and thoracic and abdominal wall abnormalities (asphyxiatingthoracic dystrophy, large omphalocele).

Respiratory distress, chronic cough,and recurrent infection may occur with unilateral hypoplasia. Thoraxis asymmetric because of underdevelopment of 1 side.

Chest radiography shows small hemithoraxwith displacement of mediastinum toward affected side. When bilateralhypoplasia occurs as isolated malformation, respiratory distressoccurs at birth and chest radiography shows small but clear lungfields.

Pulmonary Sequestration

Mass ofnonfunctioning pulmonary tissue that receives its blood supply fromsystemic circulation.

May occur within or outside a lobe.Intralobar sequestration usually occurs in lower lobe of eitherlung, whereas extralobar sequestration usually occurs just aboveor below diaphragm on left side. Whereas intralobar sequestrationis usually isolated malformation, extralobar sequestration is commonly associatedwith other malformations (e.g., diaphragmatic hernia and pulmonaryhypoplasia).

Clinical findings include respiratorydistress, hemoptysis, and recurrent pneumonia.

Chest radiography shows mass lesion.

Chest CT or MRI is usually diagnostic.

Lobar Emphysema

Overdistensionof lobe of lung (usually upper lobe). Usually congenital but alsomay be acquired secondary to extrinsic or intrinsic airway obstruction.

Respiratory distress occurs with decreasedbreath sounds and hyperresonance on involved side.

Chest radiography shows large distendedlobe or lobes with displacement of mediastinum to opposite sideand compression of contralateral lung. Extension of pulmonary vesselsto periphery of hyperexpanded lung almost always distinguishes lobaremphysema from lung cyst or pneumothorax.

Cystic Lung Lesions

Bronchogenic Cyst

Abnormalbudding or branching of tracheobronchial tree produces bronchogenic cysts,which are found incidentally or because they are infected. Locationcan be above or at carina or adjacent to 1 of main lobar bronchi.

They usually do not communicate withtracheobronchial tree and are usually fluid-filled, but if theycommunicate with airway or esophagus, they may contain air. Airwayor lung compression can cause respiratory distress.

CT or MRI is usually diagnostic.

Congenital Cystic Adenomatoid Malformation

Usuallyconsists of multiple cysts, frequently within 1 lobe of lung.

Size of lesion determines age of presentationand degree of respiratory distress.

Chest CT is usually diagnostic.

Intrapulmonary Cysts

Can be singleor multiple and involve ≥1 lobes of lung.

Respiratory distress may occur duringneonatal period. Older children may develop chronic cough or persistentinfiltrate.

Chest radiography usually shows ovalor round translucent area or areas within pulmonary parenchyma containingair or combination of fluid and air.

Chest CT usually confirms diagnosis.

Congenital Pulmonary Lymphangiectasia

Is the dilatationof lung lymphatics. Can occur as isolated defect, with congenital heartlesions that cause obstruction of pulmonary venous drainage, orwith generalized lymphangiectasia.

Respiratory distress usually beginsat birth.

Chest radiography shows reticular appearanceof lungs with nodular infiltrates and hyperinflation.

Localized form of this disorder, whichis less common, may only involve 1 or 2 lobes of lung and presentlater in life with mild respiratory distress or abnormal chest radiograph.

Lung biopsy confirms diagnosis.

Chylothorax

Presenceof chylous fluid in the thorax. Usually attributed to trauma fromdelivery or congenital abnormalities of thoracic duct system.

Lymph does not become chylous untilingestion of formula or breast milk. If large amount of chyle accumulates,respiratory distress occurs, with decreased breath sounds over affectedthorax.

Chest radiography shows large fluidcollection and shift of mediastinum.

Thoracentesis reveals chyle, whichappears milky and has high protein and fat content.

Bronchial Malformations

Bronchialstenosis usually involves main bronchus with narrowing just distalto carina. Narrowing of lobar bronchus usually results in recurrentinfection or atelectasis of involved lobe. Usual presenting featuresare respiratory distress and recurrent lung infection.

Chest radiography may show hyperinflationof involved lung and evidence of recurrent infection or atelectasis.

Chest CT or bronchoscopy is usuallydiagnostic.

Diaphragm Lesions

Congenital Diaphragmatic Hernia

Congenitaldefect in diaphragm allows herniation of abdominal organs into hemithorax,producing varying degrees of lung hypoplasia. Nearly 90% areon left side.

Severe respiratory distress beginsat birth.

Diagnostic chest radiograph shows air-filledloops of bowel and occasionally liver in thoracic cavity.

Diaphragmatic Eventration

Abnormalhigh position of diaphragm or portion of diaphragm, which is dueto congenital defect of muscularization of diaphragm.

Most children are asymptomatic, butmild respiratory distress can occur.

Diagnosis is usually made by chestradiography or fluoroscopy.

Diaphragmatic Paralysis or Paresis

Occurrenceis usually due to phrenic nerve injury from thoracic surgery.

Respiratory distress and asymmetricchest movement can occur.

Fluoroscopy or U/S that showsparadoxic movement of affected hemidiaphragm during respirationis diagnostic.

Rib Cage Anomalies

Thoracicrib cage anomalies that reduce amount of intrathoracic volume maycause respiratory distress. These include asphyxiating thoracicdystrophy, thanatophoric dysplasia, achondrogenesis, and chondroectodermaldysplasia.

Structural anomalies of rib cage andthorax usually are obvious on physical exam.

Physical exam, chest radiograph, andskeletal survey are usually diagnostic of specific disorder.

Persistent Fetal Circulation

Is the persistenceof high pulmonary vascular resistance after birth with resultinghypoxemia and cyanosis. Affected infants are usually near term,and many have history of perinatal asphyxia.

Soon after birth, respiratory distressoccurs. Hyperoxia test with exposure to 100% oxygen for5–10 mins shows small, if any, increase in partial pressureof arterial oxygen (P_aO₂)(<20 mm Hg). Simultaneous preductal-postductal measurementsof P_aO₂ inright arm and umbilical artery reveal P_aO₂ inright arm that is >15 mm Hg higher than in umbilical artery,which is consistent of right-to-left shunt across patent ductusarteriosus

2-D echocardiogram with Doppler methodsshould be performed to rule out any form of structural cardiac disease.

Cardiac Disorders

Disorders that cause cardiac failure or cyanosismay produce respiratory distress. See Chap.7, Cardiac Failure, and Chap. 12, Cyanosis.

Hematologic Disorders

Anemia

Severe acute or chronic anemia may causerespiratory distress. Pallor usually is evident. Low Hct or Hgbconfirms presence of anemia. Diagnostic approach to anemia is discussedin Chap. 45, Pallor (Anemia).

Polycythemia

Common occurrence in infants who have haddelayed clamping of umbilical cord or in infants of diabetic mothers.Venous Hct is greater than 65%, and mild respiratory distressmay occur.

Metabolic Disorders

Hypothermia

May occur in preterm low-birth-weight infantswho are otherwise normal, or in ill newborns who have bacterialmeningitis, septicemia, or intracranial hemorrhage. Oxygen consumptionis significantly increased, and hypoxemia as well as metabolic acidosismay occur.

Hypoglycemia

Irregularrespirations, apnea, seizures, and alteration of consciousness mayoccur in infants with hypoglycemia.

Low blood glucose is diagnostic (see Chap. 59, Seizures).

Metabolic Acidosis

Increase in minute ventilation is compensatoryresponse to metabolic acidosis and lowered blood pH. Normal aniongap with reduced bicarbonate may occur with diarrhea or renal tubularacidosis. Increased anion gap with accumulation of fixed acid occurswith lactic acidosis (lactate), diabetic ketoacidosis (beta-hydroxybutyrate,acetoacetate), and organic acidemias (organic acids).

Neurologic and Muscle Disorders

Brain Disorders

Respiratory distress and apnea may occurwith intracranial hemorrhage or cerebral edema as consequence ofperinatal asphyxia or birth trauma. Other causes of depressed respirationand apnea include cerebral malformations (Chiari, Dandy-Walker),bacterial meningitis, viral encephalitis, and brain tumors.

Spinal Cord Injury

Injury tospinal cord in neonates may occur with vaginal breech delivery orshoulder dystocia.

Fractures of vertebrae with transectionof the cord may result in irregular respirations and apnea, as wellas absence of spontaneous movements.

Neurologic findings depend on locationand severity of lesion.

Neuromuscular Disorders

Disorders affecting neuromuscular system(spinal muscular atrophy, myasthenia gravis, congenital myopathies)may produce slow and shallow respirations with hypoventilation andrespiratory failure (see Chap.33, Hypotonia and Weakness).

Drugs

Drugs (e.g., magnesium sulfate, morphine,and meperidine) that are given to some mothers during labor cancause neonatal respiratory depression. Neonatal drug withdrawalsyndrome may produce tachypnea as 1 of its manifestations. >>

» READ BOOK EXCERPT ONLINE »

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

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

The clinical picture will point to the diagnosis in many cases. If there is a history of abdominal trauma, a contusion or laceration of the kidney or bladder should be suspected. Massive trauma anywhere prompts a tentative diagnosis of crush syndrome. Purpura or bleeding from other sites suggests a coagulation disorder. Severe colicky pain in the abdomen suggests kidney stone. A long history of hypertension suggests polycystic kidneys, renal artery stenosis, or glomerulonephritis. A history of fever and rheumatic valvular disease suggests SBE with renal embolism. Painless hematuria in an otherwise healthy looking adult suggests neoplasm, whereas painful hematuria with frequency and dysuria suggests cystitis. Hematuria and a flank mass would make a neoplasm or polycystic kidney likely. The initial workup should include a CBC, urinalysis, urine culture, chemistry panel, flat plate of the abdomen to assess the presence of stones and kidney size, and personal examination of the urinary sediment. If a renal calculus is suspected, an IVP is ordered immediately and a urologist consulted. A three-glass test will help to localize the site of the bleeding. If there is blood in the initial specimen only, the urethra is probably the site of bleeding. If the blood is primarily in the final specimen, the bladder is most likely the site of bleeding. Equal blood discoloration in all specimens points to a renal lesion. If renal TB is suspected, an acid-fast bacillus (AFB) smear and culture is done. If collagen disease is suspected, an ANA analysis and anti–double-strand DNA antibody titer is ordered. If a renal carcinoma is suspected, a CT scan of the abdomen is probably the best study to order, but the advice of a urologist ought to be sought. Ultrasonography is useful in differentiating cysts from tumors. If a bladder neoplasm is suspected, cystoscopy will be done. If renal artery embolism or thrombosis is suspected, renal angiography may need to be done to clearly make the diagnosis.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

AUSCULTATORY SIGNS OF PULMONARY DISEASE: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Clinically, the grouping together of signs provides the best way of narrowing the differential diagnosis.

Rales

1. Bilateral crepitant rales, lack of dullness, and normal breath sounds suggest pulmonary edema or pneumonitis.
2. Focal crepitant rales, reduced alveolar breathing, dullness to percussion, and increased tactile and vocal fremitus suggest lobar pneumonia or pulmonary infarction.
3. Bilateral sibilant and sonorous rales without dullness and with increased bronchial breathing suggest asthma, chronic bronchitis and emphysema, acute bronchitis or bronchiolitis, and cardiac asthma.
4. Focal crepitant rales and amphoric breathing with dullness below and hyperresonance above suggest a lung abscess or cavitation.

Hyperresonance

1. Hyperresonance bilaterally with diminished breath sounds bilaterally and sibilant rales suggests pulmonary emphysema or asthma.
2. Focal hyperresonance with diminished or absent breath sounds and no rales suggests pneumothorax.
3. Focal hyperresonance with normal or only diminished breath sounds suggests a large bulla.

Dullness or Flatness

1. Dullness with diminished breath sounds and no rales suggests atelectasis or pleural effusion from empyema, CHF, or pulmonary infarct. In atelectasis, there is no hyperresonance or egophony above the dullness.
2. Dullness with diminished breath sounds and crepitant rales suggests pneumonia or pulmonary infarct. If there is bronchophony as well, there is probably no associated effusion. If there is no bronchophony but hyperresonance and egophony above the dullness, then an associated pleural effusion should be considered.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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