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Diseases » Goodpasture syndrome » Diagnosis

Diagnosis of Goodpasture syndrome

Diagnostic Test list for Goodpasture syndrome:

The list of medical tests mentioned in various sources as used in the diagnosis of Goodpasture syndrome includes:

Goodpasture syndrome Diagnosis: Book Excerpts

Tests and diagnosis discussion for Goodpasture syndrome:

To diagnose Goodpasture syndrome, doctors can now use a blood test, but a kidney biopsy may be necessary to check for the presence of the harmful antibody. (Source: excerpt from Goodpasture Syndrome: NIDDK)

Diagnostic Tests for Goodpasture syndrome: Online Medical Books

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

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

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.
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.
Is there fever? The presence of fever with the hematuria would suggest pyelonephritis.
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.
Is there hypertension? The presence of hypertension with the hematuria suggests glomerulonephritis, polycystic kidneys, and collagen diseases.
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

PURPURA AND ABNORMAL BLEEDING: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

Is there a petechial rash? The presence of a petechial rash suggests either a thrombocytopenic purpura, which may be idiopathic or secondary to leukemia, aplastic anemia, collagen disease, or drugs. In addition, petechiae may suggest platelet dysfunction, in which case the platelet count will be normal, or vasculitis, such as from collagen diseases, hereditary telangiectasia, scurvy, or drugs.
Is there ecchymosis or bruises? The presence of ecchymosis or bruises would suggest hemophilia, Christmas disease, or other major coagulation defects, but it may also be related to platelet disorders or disseminated intravascular coagulation.
If there is a petechial rash, is the platelet count normal? The presence of a normal platelet count would suggest either thrombocytopathy or vasculitis.
Is there significant mucosal bleeding? The presence of mucosal bleeding along with ecchymosis and bruises suggests platelet disorders or disseminated intravascular coagulation.

DIAGNOSTIC WORKUP

If a coagulation disorder is suspected, consult a hematologist first. Routine diagnostic studies include a CBC, platelet count, sedimentation rate, blood smear for red cell morphology, urinalysis, chemistry panel, coagulation profile, rheumatoid arthritis factor, ANA test, serum protein electrophoresis, VDRL test, EKG, chest x-ray, and flat plate of the abdomen. The coagulation profile should include a platelet count, a bleeding time, a coagulation time, a partial thromboplastin time, and a prothrombin time.

If there is fever, blood cultures should be done. A bone marrow examination and bone marrow culture may be useful. If disseminated intravascular coagulation is suspected, a fibrinogen assay and estimation of fibrin degradation products should be done. Platelet function may be assessed by clot retraction tests. Spleen and liver scans and bone scans may be needed. A CT scan of the abdomen and pelvis may also be necessary. Skin, muscle, and even kidney biopsies are often done to complete the workup.

It can be seen from the above array of diagnostic tests that a hematologist should be consulted at the outset. Various forms of vasculitis may be confirmed by skin or muscle biopsy.

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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

» READ BOOK EXCERPT ONLINE »

Source: In a Page: Signs and Symptoms, 2004

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

Palpable purpura (papules or nodules that are red/purple and do not blanch with pressure)

Leukocytoclastic Vasculitis
–A necrotizing vasculitis of small vessels
–Fever, malaise, fatigue and arthralgias
–Inciting factors include drugs (e.g., NSAIDs, thaizides, and phenothiazines), infection [bacterial (e.g., RMSF, meningococcemia) or viral (e.g., hepatitis)] or, blood abnormalities (e.g., cryoglobulinemia, cryofibrinogenemia)
–Vasculitic injury to kidneys, brain, lung, heart, and GI tract may occur

Collagen vascular diseases
–Systemic lupus erythematosus, Sjögren's syndrome, rheumatoid arthritis
Granulomatous vasculitis (e.g., Wegener's, Churg-Strauss syndrome)
Polyarteritis nodosa
Internal malignancies
–Myeloma, lymphoma, or leukemia
Henoch-Schönlein purpura

Drugs
–Aspirin, NSAIDs, warfarin, heparin
Nonpalpable purpura (flat macules, patches
similar to ecchymoses; or petechiae that do not blanch with pressure)
Trauma
Advancing age (senile purpura)
Actinic changes
Chronic stasis
Coagulopathies (affecting platelet number or function)
–TTP (pentad of fever, microangiopathic hemolytic anemia, thrombocytopenia, renal insufficiency, and neurologic signs)
–ITP
–Drug-induced thrombocytopenia
–Bacteremia and many viral diseases

Scurvy (vitamin C deficiency) can cause hemorrhage and purpura
TORCH infection can cause congenital purpura (“blueberry muffin baby”)
Many systemic diseases (e.g., Cushing's and diabetes have associated nonpalpable purpura)

Workup and Diagnosis

History and physical examination
–History of present illness, past medical history, illness exposure, medication history, and a complete review of systems including systemic symptoms (e.g., arthralgias, myalgias, fever), characteristic spread patterns (e.g., RMSF usually starts peripherally and spreads centrifugally onto the trunk), and CNS symptoms (may suggest SLE or meningococcemia)
–Focused physical examination with complete skin exam and notation of palpable versus nonpalpable rash

Initial laboratory evaluation includes CBC with differential and PT/PTT/INR (to rule out coagulopathy), urinalysis (evaluate for hematuria in HSP), LFTs (to evaluate for hepatitis), BUN/creatinine (evaluate renal insufficiency (which may occur in PAN, HSP, SLE, and many other palpable purpura-inducing diseases), ESR and/or C-reactive protein (to evaluate for collagen vascular disease)
Blood cultures and consider skin cultures by a punch biopsy if the patient is febrile
ANA and rheumatoid factor titers and a viral hepatitis screen may be indicated
Age-appropriate malignancy screening
Punch biopsy is diagnostic for leukocytoclastic vasculitis

» READ BOOK EXCERPT ONLINE »

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

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

Vasculitis (palpable purpura)
–HSP: Most common vasculitis, incidence: 0.01%, in 50% follows URI; other triggers are bacterial infection, drugs, vaccines, food, insect bites; lasts 1–2 weeks, age 2–8 (mean 4 years), M > F, IgA-mediated, small vessels
–Polyarteritis nodosa (PAN), Wegener granulomatosis (WG): Rare in children

Hematologic
–ITP: Age 1–5 years; autoantibodies against platelets (platelets destroyed by splenic macrophages); usually 1–6 weeks after viral infection; 70–80% acute self-limited; 10–20% chronic recurrent; <1% associated with intracranial hemorrhage
–Other causes of thrombocytopenia: Wiscott-Aldrich syndrome, aplastic anemia, leukemia, disseminated intravascular coagulation (DIC), thrombocytopenia absent radius (TAR)

Coagulation factor deficiencies:
–Hemophilia A/B (factors VIII/XI): A (1/7,500 male births) four times more common than B; X-linked recessive
–vWD: Prevalence 1%, autosomal dominant, vW factor deficiency or decreased function
–Liver disease: Decreased production of coagulation factors
–Hemorrhagic disease of the newborn: Decreased vitamin K-dependent coagulation factors (II, VII, IX, X)

Infections
–Bacterial/rickettsial: Meningococcemia (MC), Group A strep (scarlet fever), Streptococcus viridans/Staphylococcus aureus (endocarditis), Gonococcus (disseminated), Leptospirosis, Rickettsia rickettsii (Rocky Mountain spotted fever), R. prowazekii (epidemic typhus), Ehrlichiosis
–Viral: Hepatitis B, Dengue hemorrhagic fever, atypical measles

Drugs: Coumadin, heparin, aspirin, thiazide, corticosteroids, penicillins, sulfonamides
Others: Trauma/abuse, scurvy (vitamin C deficiency)

Workup and Diagnosis

Determine location, duration, associated/preceding symptoms, family history of bleeding disorders, social history (for abuse), insect bites, travel history, drugs, easy bruising; meningeal signs; purpura fulminans
HSP: Purpura mostly on buttocks and legs; arthritis, abdominal pain, ±GI hemorrhage, renal disease, self-limited; complications: intussusception, end-stage renal disease <1%; increased platelet/ESR/WBC/IgA
ITP: Sudden petechiae/ecchymoses, epistaxis, or menorrhagia; rare splenomegaly; platelet count usually <20,000; bone marrow exam if other marrow disease is suspected
MC: Septic shock, ±meningitis; culture and Gram stain (blood and CSF)
Hemophilia A/B: Easy bruising, intramuscular hematomas, hemarthroses, B milder than A; mild: 5–30%, moderate: 1–5%, severe: <1% of normal factor level
vWD: Petechiae/ecchymoses, epistaxis, menorrhagia
Endocarditis: Janeway lesions, splinter hemorrhages
PAN/WG: Painful skin nodules, any organ (PAN); skin, kidneys (glomerulonephritis), pulmonary hemorrhage (WG); biopsy; angiography in WG (for aneurysms)
Atypical measles: clinical diagnosis, history of killed vaccine + exposure
DIC: Increased PT/PTT, decreased platelets, increased FDP/D-dimers, hemolysis

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

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

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

Bilateral crepitant rales, lack of dullness, and normal breath sounds suggest pulmonary edema or pneumonitis.
Focal crepitant rales, reduced alveolar breathing, dullness to percussion, and increased tactile and vocal fremitus suggest lobar pneumonia or pulmonary infarction.
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.
Focal crepitant rales and amphoric breathing with dullness below and hyperresonance above suggest a lung abscess or cavitation

Hyperresonance

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

Dullness or Flatness

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.
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.

» READ BOOK EXCERPT ONLINE »

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

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

Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of bleeding disorders or easy bruising? Find out what medications he’s taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Also ask about systemic complaints that may suggest infection, such as a fever. If the patient is female, ask about heavy menstrual flow.

Gender Cue: Purpura is more common in women and particularly in individuals with large areas of subcutaneous fat, such as the breasts, abdomen, buttocks, thighs, and calves.

Inspect the patient’s entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Also inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn’t a cardinal indicator of this condition.

» READ BOOK EXCERPT ONLINE »

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

Goodpasture's syndrome: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Confirmation of Goodpasture’s syndrome requires measurement of circulating anti-GBM antibody by radioimmunoassay and linear staining of GBM and alveolar basement membrane by immunofluorescence.

Immunofluorescence of alveolar basement membrane shows linear deposition of immunoglobulin as well as complement 3 and fibrinogen. Immunofluorescence of GBM also shows linear deposition of immunoglobulin combined with detection of circulating anti-GBM antibody. This finding distinguishes Goodpasture’s from other pulmonary-renal syndromes, such as Wegener’s granulomatosis, polyarteritis, and systemic lupus erythematosus.

A lung biopsy reveals interstitial and intra-alveolar hemorrhage with hemosiderin-laden macrophages. Chest X-ray reveals pulmonary infiltrates in a diffuse, nodular pattern, and renal biopsy commonly shows focal necrotic lesions and cellular crescents.

Creatinine and blood urea nitrogen (BUN) levels typically increase two to three times normal. Urinalysis may reveal red blood cells and cellular casts, which typify glomerular inflammation. Granular casts and proteinuria may also be observed.

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

Allergic purpuras: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

No laboratory test clearly identifies allergic purpura (although white blood cell count and erythrocyte sedimentation rate are elevated). Diagnosis therefore necessitates careful clinical observation, in many cases during the second or third attack. Except for a positive tourniquet test (a test to assess the capillaries’ability to withstand increased pressure), coagulation and platelet function tests are usually normal. Small-bowel X-rays may reveal areas of transient edema; in many cases, tests for blood in the urine and stool are positive. Increased blood urea nitrogen and creatinine levels may indicate renal involvement. Diagnosis must rule out other forms of nonthrombocytopenic purpura.

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

Idiopathic thrombocytopenic purpura: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Platelet count less than 20,000/µl and prolonged bleeding time suggest ITP. Platelet size and morphologic appearance may be abnormal; anemia may be present if bleeding has occurred. As in thrombocytopenia, bone marrow studies show an abundance of megakaryocytes and a shortened circulating platelet survival time (hours or days). Occasionally, platelet antibodies may be found in vitro, but this diagnosis is usually inferred from platelet survival data and the absence of an underlying disease.

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

Premature rupture of membranes: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Characteristic passage of amniotic fluid confirms PROM. Physical examination shows amniotic fluid in the vagina. Examination of this fluid helps determine appropriate management. For example, aerobic and anaerobic cultures and a Gram stain from the cervix reveal pathogenic organisms and indicate uterine or systemic infection.

Confirming diagnosis Alkaline pH of fluid collected from the posterior fornix turns Nitrazine paper deep blue. (The presence of blood can give a false-positive result.) If a smear of fluid is placed on a slide and allowed to dry, it takes on a fernlike pattern due to the high sodium and protein content of amniotic fluid.

Staining the fluid with Nile blue sulfate reveals two categories of cell bodies. Blue-stained bodies represent shed fetal epithelial cells, while orange-stained bodies originate in sebaceous glands. Incidence of prematurity is low when more than 20% of cells stain orange.

Physical examination also determines the presence of multiple pregnancies. Fetal presentation and size should be assessed by abdominal palpation (Leopold’s maneuvers).

Other data determine the fetus’s gestational age:

❑ historical: date of last menstrual period, quickening

❑ physical: initial detection of unamplified fetal heart sound, measurement of fundal height above the symphysis, ultrasound measurements of fetal biparietal diameter

❑ chemical: tests on amniotic fluid, such as the lecithin-sphingomyelin (L/S) ratio (an L/S ratio greater than 2 indicates pulmonary maturity); foam stability (shake test) also indicates fetal pulmonary maturity. Presence of phosphatidylglycerol (PG) in the fluid indicates that respiratory distress is unlikely.

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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.

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

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

Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of a bleeding disorder or easy bruising? Find out what medications he’s taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Ask about systemic complaints that may suggest infection, such as fever. If the patient is female, ask about heavy menstrual flow.

Inspect the patient’s entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn’t a cardinal indicator of this condition.

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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

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

A. Have there been any recent illnesses? Henoch-Schönlein purpura is associated with a preceding upper respiratory infection in 60% to 75% of cases (1). Streptococcus pneumoniae is the most commonly cited organism. Various other infections may be responsible for thrombocytopenias and vasculitis.

B. Has there been any recent medication usage? Quinidine, quinine, sulfa, aspirin, and many other medications have been associated with purpuric lesions.

C. Are there any additional symptoms, such as abdominal or joint pain, or gastrointestinal symptoms including changes in stool characteristics? Henoch-Schönlein purpura is associated with all of these; abdominal pain is noted in 40% to 80% of patients (1).

D. Is there a history of heavy menses or mucous membrane bleeding? Coagulation abnormalities such as von Willebrand’s disease (present in 0.5% to 1% of the population) or platelet abnormalities are most likely (3) (Chapter 11.5).

E. Is there a history of prior transfusions or heavy bleeding with previous operations?

F. Are there risk factors for a history of liver disease? There may be impaired synthesis of coagulation factors.

G. Has there been a similar rash in the past? A long history of purpura may be present in idiopathic thrombocytopenic purpura (ITP) as it tends to be a chronic course with an insidious onset in adults.

H. If the patient is a newborn, was there maternal illness, drug exposure, maternal ITP, or was vitamin K given? Hemorrhagic disease of the newborn develops on the second or third day of life. The most common causes of purpura fulminans in the neonatal period are congenital deficiencies of proteins C and S (1).

Physical examination

A. General and vital signs. Does the patient appear toxic or unstable? Considerations would include meningococcemia, Rocky Mountain spotted fever, disseminated intravascular coagulation (DIC), sepsis from Staphylococcus aureus, or thrombotic thrombocytopenic purpura.

B. Skin. Purpura should not blanch or only partially blanch with pressure. Petechiae are generally indicative of a quantitative or qualitative platelet abnormality. These nonpalpable petechiae may be caused by thrombocytopenia, which is either congenital or acquired (Chapter 16.7). The acquired thrombocytopenia can be caused by decreased platelet production as seen with viral infections, B₁₂ or folate deficiency, iron deficiency, or a drug reaction. It is also seen with evidence of platelet destruction as present in ITP, connective tissue disease, leukemia, drugs, DIC, and thrombotic thrombocytopenic purpura. Abnormal platelet function is seen with aspirin ingestion, kidney and liver dysfunction, and in the thrombocytosis seen with myeloproliferative disorders. Significant straining with the Valsalva maneuver can cause petechiae. Lastly, the chronic pigmented purpura are the brown-orange spots occasionally seen on the lower extremities of adults. Schamberg’s disease is the most frequently seen and well known of the group. In these disorders, petechia are often intermixed with the pigmentation.

Ecchymoses are usually associated with coagulation disorders (e.g., in hemophilia, von Willebrand’s disease, anticoagulant usage, DIC, and vitamin K deficiency). Also responsible for ecchymoses are weakened connective tissue with less protection for vessels, as seen in senile purpura; glucocorticoid excess; vitamin C deficiency; and congenital disorders, such as Ehlers–Danlos syndrome.

Palpable purpura are usually secondary to a vasculitis. The causes are many and include hypersensitivity vasculitis to drugs; infections, including viral, rickettsial, and bacterial illnesses; cryoglobulinemias, such as Waldenström’s; and granulomatous causes, such as Wegener’s granulomatosis.

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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

Purpura/Petechiae/Excessive Bleeding: Differential Overview
(Field Guide to Bedside Diagnosis)

Purpura

❑Trauma

❑Senile purpura

❑Drugs

❑Vasculitis

❑Vitamin K deficiency

❑Psychogenic purpura

❑Cholesterol emboli

❑Warfarin necrosis

❑Scurvy

❑Thrombotic thrombocytopenic purpura

❑Henoch-Schonlein purpura

❑Amyloidosis

Petechiae

❑Autoimmune thrombocytopenia

❑Bacteremia

❑Hypersplenism

Excessive Bleeding

❑Over-anticoagulation

❑Thrombocytopenia

❑von Willebrand disease

❑Circulating anticoagulant

❑Disseminated intravascular coagulation

❑Hemophilia

Diagnostic Approach

A patient with a suspected bleeding disorder should be questioned about response to trauma, past bleeding problems, for example with surgery or dental extractions, history of transfusion, menstrual history and dietary habits. Absence of abnormal bleeding with surgery, significant trauma, or dental extractions makes an inherited bleeding disorder unlikely.

Petechiae are small capillary hemorrhages resulting from platelet or vascular abnormalities. Petechiae on the lower extremities or mucous membranes are usually caused by thrombocytopenia. Tender, elevated petechiae plus abnormalities in other organs suggests vasculitis. Platelet defect disorders produce petechiae and ecchymoses occurring immediately after local trauma. Bleeding is superficial, occurring in the skin, the mucous membranes, the nose, and the gastrointestinal and genitourinary tracts. Bleeding does not occur with normal platelets until the count falls to less than 50,000, and the threshold for important bleeding is 20,000. Oozing blood around catheters suggests DIC, vitamin K deficiency, or platelet abnormalities.

Large-area bruising occurs with vitamin-K–dependent factor deficiency, but not with hemophilia. Plasma protein disorders produce bleeding in deep tissues, such as joints, muscle, and retroperitoneum. The onset of such bleeding can be delayed for hours after trauma.

Palpable purpura is seen with autoimmune or infectious (e.g., meningococcemia, endocarditis) vasculitis. Infectious emboli have an irregular outline, whereas lesions of leukocytoclastic vasculitis are circular.

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Source: Field Guide to Bedside Diagnosis, 2007

Allergic purpura: Diagnosis
(Handbook of Diseases)

No laboratory test result clearly identifies allergic purpura (although the white blood cell count and erythrocyte sedimentation rate are elevated). Diagnosis therefore requires careful observation, usually during the second or third attack. Except for a positive tourniquet test result, coagulation and platelet function test results are usually negative. X-rays of the small bowel may reveal areas of transient edema; test results for blood in the urine and stool are often positive. Increased blood urea nitrogen and serum creatinine levels may indicate renal involvement. The diagnosis must rule out other forms of nonthrombocytopenic purpura.

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Source: Handbook of Diseases, 2003

Idiopathic thrombocytopenic purpura: Diagnosis
(Handbook of Diseases)

Platelet count less than 20,000/µl combined with prolonged bleeding time suggest ITP. Platelet size and morphologic appearance may be abnormal; anemia may be present if bleeding has occurred.

As in thrombocytopenia, bone marrow studies show an abundance of megakaryocytes and a shortened circulating platelet survival time (hours or days). Occasionally, platelet antibodies may be found in vitro, but this diagnosis is usually inferred from platelet survival data and the absence of an underlying disease. The patient’s immunoglobulin G level may also be increased.

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Source: Handbook of Diseases, 2003

Premature rupture of the membranes: Diagnosis
(Handbook of Diseases)

Characteristic passage of amniotic fluid confirms PROM. Physical examination shows amniotic fluid in the va-gina. Examination of this fluid helps determine appropriate management. For example, aerobic and anaerobic cultures and a Gram stain from the cervix reveal pathogenic organisms and indicate uterine or systemic infection. The alkaline pH of fluid collected from the posterior fornix turns nitrazine paper deep blue. (The presence of blood can give a false-positive result.) If a smear of fluid is placed on a slide and allowed to dry, it takes on a fernlike pattern due to the high sodium and protein content of amniotic fluid.

Staining the fluid with Nile blue sulfate reveals two categories of cell bodies. Blue-stained bodies represent shed fetal epithelial cells; orange-stained bodies originate in sebaceous glands. The incidence of prematurity is low when more than 20% of cells stain orange.

Physical examination also determines the presence of multiple pregnancies. Fetal presentation and size should be assessed by abdominal palpation (Leopold’s maneuvers).

Other data determine the fetus’s gestational age:

❑ historic: date of last menstrual period, quickening

❑ physical: initial detection of unamplified fetal heart sound, measurement of fundal height above the symphysis, ultrasound measurements of fetal biparietal diameter

❑ chemical: tests on amniotic fluid such as the lecithin-sphingomyelin (L/S) ratio (an L/S ratio greater than 2.0 indicates pulmonary maturity); foam stability (shake test) also indicates fetal pulmonary maturity.

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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.

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

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

Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of a bleeding disorder or easy bruising? Find out what medications he’s taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Also ask about systemic complaints that may suggest infection, such as fever. If the patient is female, ask about heavy menstrual flow.

CULTURAL CUE:Make sure to ask your patient if he uses any type of folk medicine. Coin rubbing, practiced by cultures such as the Vietnamese, may produce ecchymoses on the back and abdomen; these marks may be misdiagnosed as abuse.

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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

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

Loss of Vascular Integrity

In many bleeding disorders, defective hemostasisoccurs at the site of small vessel injury without any abnormalityof coagulation.

Trauma

May producebleeding into skin. After birth trauma, purpura may occur on presenting part—heador extremity.

Young children commonly have bruiseson lower legs from falls.

Nonaccidental trauma (child abuse)should be suspected if bruises or associated fractures are unexplainedby history. Bruises found on buttocks, back, chest, abdomen, orface or in various stages of resolution or conforming to a beltor cord mark are suspicious of child abuse.

Infection

Most commoncauses of fever and petechiae are viral infections and group A streptococcalpharyngitis. Important to exclude meningococcemia and Rocky Mountainspotted fever because these are life-threatening diseases.

S. pneumoniae and H. influenzae typeb infections can present with septic shock and may be clinicallyindistinguishable from meningococcemia. Purpuric lesions also maybe seen with P. aeruginosa and S. aureus as well as N. gonorrhoeaeinfection.

Purpura fulminans, a severe form ofbleeding caused in part by loss of vascular integrity, is characterizedby large ecchymoses and gangrene of extremities. It is often foundin association with disseminated intravascular coagulation (DIC)and may accompany meningococcemia as well as septicemia from otherpathogens.

Henoch-Schönlein Purpura

Vasculitischaracterized by symmetric purpuric rash on buttocks and lower legs.Abdominal pain, arthritis of large joints, and blood in stools arefrequent findings. Hematuria with or without proteinuria also mayoccur.

Platelet count is normal.

Diagnosis is usually clinical.

Drugs

Several drugs (e.g., penicillins and sulfonamides)may cause increased capillary fragility and purpura. Corticosteroidsmay cause purpuric striae.

Langerhans Histiocytosis

Scaly rashwith papules and vesicles that also may be purpuric may occur. Othermanifestations include lymphadenopathy, hepatosplenomegaly, anemia,and thrombocytopenia.

Skin biopsy is diagnostic.

Ehlers-Danlos Syndrome

Caused bymutations in genes that code for collagen, collagen-modifying enzymes, andpossibly other extracellular matrix components.

Beighton et al. (1998) revised classificationin which 6 major types are now described. Most common types areknown as classical, hypermobility, and vascular types. Genetic transmissionis autosomal-dominant.

Classical type is characterized by skin hyperextensibility,joint hypermobility, atrophic scars that widen with age, and easybruising.

Hallmarks of hypermobility type aregeneralized joint hypermobility, hyperextensibility of skin, andchronic joint and limb pain.

Vascular type is characterized by extensivebruising, thin translucent skin, small joint hypermobility, andarterial/intestinal/uterine rupture.

Vitamin C Deficiency

Scurvy israre in U.S.

Occurrence is due to lack of ascorbicacid (vitamin C) in diet.

Characteristic findings include purpura,especially on lower extremities, gingival and soft tissue bleeding,and leg pain and swelling.

Clinical and radiographic findingsalong with low serum vitamin C level are diagnostic.

Hereditary Hemorrhagic Telangiectasia (Osler-Rendu-WeberDisease)

Autosomal-dominantdisorder characterized by multiple telangiectasias of skin and bleedingfrom respiratory and GI tracts. Gene locus of most frequent formhas been mapped to chromosome 9q34.1.

Epistaxis, GI bleeding, and skin bruisingare common findings.

Diagnosis is usually clinical.

Thrombocytopenia

May be due to increased platelet destruction,decreased platelet production, or platelet sequestration. More than1 mechanism may be responsible for thrombocytopenia, especiallywhen considering effects of infection and drugs.

Increased Platelet Destruction

In disorders that cause increased plateletdestruction, large platelets may be seen on blood smear. Exam ofbone marrow usually reveals normal or increased number of megakaryocytes.

Immune-Mediated

Neonatal Alloimmune Thrombocytopenia

About 98% ofpopulation have PL-A1 antigen on platelet surface. When maternal plateletslack this antigen, fetal platelets crossing placenta stimulate productionof maternal antibody, which results in their destruction.

Diffuse purpura usually occur at orsoon after birth.

Maternal platelet count is normal.Platelet typing of parents confirms diagnosis.

Maternal Autoimmune Thrombocytopenia

Maternalantibody crosses placenta, binds to infant's platelets,and destroys them. Maternal platelet count is usually low, whereasinfant platelet counts vary from near normal to <10,000/mm³.

Other than presence of generalizedpetechiae, these infants appear well.

Self-limited and usually resolves by3 mos of age.

Idiopathic Thrombocytopenic Purpura

Often followsonset of viral infections, with peak incidence at 2–6 yrsof age.

Hallmark is presence of purpura, whichcan vary from pinpoint petechiae to large ecchymoses in random distribution.

Antibodies against common plateletglycoproteins bind to platelet membrane, causing platelets to beremoved by tissue macrophages in the spleen. CBC is normal exceptfor marked thrombocytopenia. Platelet count is usually <50,000/mm³ andoften <10,000/mm³.

Bone marrow exam is unnecessary unlessleukemia is suspected.

Presence of epistaxis, gross hematuria,or bloody stools indicates more significant bleeding problem. Intracranialbleeding is most serious complication and is associated with plateletcount of <10,000/mm³.

Association of autoimmune hemolyticanemia or neutropenia with idiopathic thrombocytopenic purpura iscalled Evans syndrome.

Collagen Vascular Disease

Collagen vascular diseases (e.g., systemiclupus erythematosus) may produce immune-mediated thrombocytopenia.In some women with systemic lupus erythematosus, antiplatelet antibodiescross placenta, producing transient neonatal thrombocytopenia.

Drug-Induced Thrombocytopenia

Immune-mediated thrombocytopenia may be dueto drugs (e.g., sulfonamides, phenytoin, valproic acid, acetazolamide,carbamazepine, and quinidine). Purpura usually appear within 24hrs of exposure and begin to disappear after discontinuation ofthe drug.

Infection

Infection with several pathogens (see previoussection) may trigger onset of thrombocytopenia with or without DIC.

Hemolytic-Uremic Syndrome

Often aconsequence of diarrheal illness caused by E. coli 0157:H7.

Usual clinical findings include hemolyticanemia, thrombocytopenia, and renal failure.

Blood smear shows fragmented red cells(schistocytes).

Thrombotic Thrombocytopenic Purpura

Similarin many respects to hemolytic-uremic syndrome. However, usuallyoccurs in adults and tends to be chronic and relapsing.

Characterized by thrombocytopenic purpura,microangiopathic hemolytic anemia, and widespread thrombotic occlusionsin microcirculation, primarily in brain and liver.

Wiskott-Aldrich syndrome

Thrombocytopenic purpura, eczema, and impairedcell-mediated immunity with increased susceptibility to infectioncharacterize this X-linked recessive disorder. Platelet count usuallyis <50,000/mm³. See Chap. 53, Recurrent Infection.

Decreased Platelet Production

In disordersthat cause decreased platelet production, platelets in peripheralblood tend to be normal in size or small. Bone marrow exam showsabsence or decreased number of platelets.

In addition to conditions discussedin this section, infection also causes decreased platelet production.

Specific Platelet Disorders

Congenital Amegakaryocytic Thrombocytopenia

Rare disorder characterized by nonimmunethrombocytopenia with decreased marrow megakaryocyte counts. Redcells are macrocytic and fetal hemoglobin levels are increased.Pancytopenia and even leukemia may occur in some cases.

Thrombocytopenia–Absent Radius Syndrome

Neonatal thrombocytopenia and bilateral absenceof radii with presence of both thumbs characterize this autosomal-recessivedisorder.

Bone Marrow Suppression (Generalized)

Drugs, radiation,and infection including septicemia may cause bone marrow suppressionand thrombocytopenia.

Many cancer chemotherapeutic agentscause thrombocytopenia, including cytosine arabinoside, cyclophosphamide,methotrexate, and doxorubicin.

Chloramphenicol may cause dose-dependentreversible bone marrow suppression or dose-independent irreversiblemarrow aplasia.

Aplastic anemia and Fanconi anemiaare discussed in Chap. 45, Pallor(Anemia).

Bone Marrow Replacement

Normal bone marrow may be replaced by leukemiaof all types, metastatic neuroblastoma, and histiocytoses. The resultis platelet destruction and thrombocytopenia. See Chap. 38, Lymphadenopathy.

Megaloblastic Anemia

Folic acid and vitamin B₁₂ deficienciesmay be associated with thrombocytopenia and neutropenia due to inadequateproduction or increased destruction in bone marrow. See Chap. 45, Pallor (Anemia).

Platelet Sequestration

Hypersplenism

Can leadto platelet sequestration and thrombocytopenia.

Common causes include portal hypertensionand storage diseases.

Spleen is enlarged and firm. Plateletcount in such disorders usually is 50,000–100,000/mm³;therefore, significant bleeding is unusual.

Large Hemangiomas

Hemangioma-thrombocytopenia (Kasabach-Merritt)syndrome is autosomal-dominant disorder characterized by large hemangiomas,thrombocytopenia, microangiopathic hemolytic anemia, and consumptionof coagulation factors.

Abnormal Platelet Function

Qualitative platelet disorders should besuspected when platelet count is normal and bleeding time is prolonged.

Thrombasthenia (Glanzmann Disease)

Absenceor deficiency of glycoprotein IIb-IIIa complex is responsible forthis disorder of platelet aggregation. Genetic transmission is usuallyautosomal-recessive, but autosomal-dominant form has been described.Gene locus has been mapped to chromosome 17q21.32.

Usually presents in infancy or childhoodwith multiple bruises and purpura. Recurrent epistaxis and menorrhagiaare also common findings. Platelet count is normal, bleeding timeis prolonged, and platelet aggregation is absent on blood smear.

Assay of glycoprotein IIb-IIIa complexin platelet membrane establishes diagnosis.

Giant Platelet Syndrome (Bernard-Soulier Syndrome)

In thisautosomal-recessive disorder, glycoprotein Ib is absent from plateletmembrane. Also, glycoproteins IX and V have been shown to be deficientin this syndrome.

Characteristic features are easy bruisingand severe bleeding, especially at time of injury or surgery. Mildthrombocytopenia, giant platelets, prolonged bleeding time, anddefective in vitro platelet agglutination with ristocetin are usualfindings.

Demonstration of absence of glycoproteinIb in platelet membrane confirms diagnosis.

Storage Pool Deficiency

Deficiencyin number and contents of dense granules, alpha granules, or both,impairs platelet aggregation.

These rare disorders usually presentin childhood or adolescence with easy bruising and prolonged bleedingfrom minor cuts, epistaxis, or menorrhagia.

Electron microscopy of platelets isdiagnostic.

Drugs

Acetylsalicylic acid (aspirin) causes defectin second phase of platelet aggregation, and bleeding time is prolonged.NSAIDs, valproic acid, and high-dose penicillins also may causeplatelet dysfunction.

Uremia

Purpura as well as mucous membrane and GIbleeding can occur with uremia. Exact cause of platelet defect inuremia is unknown, but in vitro platelet aggregation is abnormaland platelet adhesion is decreased.

Coagulation Disorders

Factor Deficiencies

von Willebrand Disease

Caused byquantitative or qualitative decrease in von Willebrand factor (vWF),which is carrier protein for coagulation factor VIII. Gene for vWFhas been mapped to chromosome 12p13.3.

Superficial bruising, epistaxis, prolongedoozing from minor wounds, and prolonged heavy menstrual periodsmay occur.

Screening tests usually reveal prolongedactivated partial thromboplastin time (aPTT) and bleeding time.

Diagnosis can be confirmed by measuringvWF antigen and vWF ristocetin cofactor. The latter test is measureof vWF functional activity.

Factor VIII Deficiency (Hemophilia A)

Caused bymutations in Factor VIII gene, which has been mapped to Xq28.

Characteristic manifestations includebleeding into joints and muscle as well as prolonged bleeding fromwounds. Excessive bleeding may occur after circumcision; however,evidence of bleeding may not occur until a child begins to walk,when excessive bruising may be noted after frequent falls.

Risk of intracranial bleeding aftereven mild head trauma is always serious concern.

Prolonged aPTT is only abnormal coagulationscreening test, whereas decreased Factor VIII assay confirms diagnosis.

Factor IX Deficiency (Hemophilia B, Christmas Disease)

Factor IXgene has been mapped to Xq27.

Clinical presentation is indistinguishablefrom that of Factor VIII deficiency.

Screening coagulation tests revealprolonged aPTT. Decreased Factor IX assay confirms diagnosis.

Deficiencies of Factors I, II, V, VII, X, XI, and XIII

Clinicalpicture in Factor I deficiency is similar to that of platelet disorders,with bruising, epistaxis, and mucous membrane bleeding. Intracranialor joint bleeding is rare. Prothrombin time (PT), aPTT, and bleedingtime are prolonged. Prolongation of either thrombin time or reptilasetime or both should suggest this disorder. Very low or absent serumfibrinogen confirms diagnosis.

Factor II, V, VII, and X deficienciesmay present with easy bruising or prolonged bleeding after trauma,surgery, or dental work. Prolonged PT occurs and diagnosis is confirmedby factor assay. aPTT is normal with Factor VII deficiency, whereasboth PT and aPTT are prolonged with Factor II, V, and X deficiencies.

In Factor XI deficiency, mild bleedingincluding epistaxis or menorrhagia may occur. aPTT is prolongedand specific factor assay is diagnostic.

Easy bruising, prolonged umbilicalcord bleeding, and sometimes GI bleeding occur with Factor XIIIdeficiency. Screening coagulation tests are normal. Specific factorassay is diagnostic.

Vitamin K Deficiency

Resultsin failure of vitamin K–dependent coagulation factors (II,VII, IX, and X) to develop calcium-binding sites, which are necessaryfor effective coagulation function.

Because newborns have low vitamin Kstores, failure to give vitamin K immediately after birth may causegeneralized bleeding between 2 and 4 days of age. Hematochezia,melena, hematemesis, or bleeding from other sites also may occur.

History of failure to give vitaminK at birth; normal platelet count; normal or prolonged bleedingtime; prolonged PT and aPTT; decreased Factors II, VII, IX, andX; and reversal of prolonged PT and aPTT with decreased subsequentbleeding after vitamin K administration confirm diagnosis.

In infancy, childhood, and adolescence,causes of vitamin K deficiency include liver disease with cholestasisand fat malabsorption, prolonged antibiotic usage, and cystic fibrosis.Some clinical findings are easy bruising and ecchymoses as wellas mucous membrane and visceral hemorrhage. PT and aPTT are prolonged,whereas coagulation factors II, VII, IX, and X are decreased.

Disseminated Intravascular Coagulation

More commoncauses are septicemia, shock, and massive trauma.

Bleeding is secondary to consumptionof coagulation factors and platelets. Bruising, oozing from venipuncturesites, mucous membrane bleeding, and purpura may occur.

Certain lab findings confirm diagnosis:decreased platelet count; prolonged PT, aPTT, and bleeding time;decreased serum fibrinogen; increased fibrin split products; anddecreased Factors V and VIII.

Liver Disease

Coagulationabnormalities in acute liver failure include decreased synthesisof coagulation factors (the liver is site of synthesis of all coagulationfactors except Factor VIII); vitamin K malabsorption and decreasedactivity of Factors II, VII, IX, and X secondary to cholestasis;thrombocytopenia secondary to hypersplenism; production of abnormalfibrinogens; and DIC.

Bleeding as well as purpura may occur.

Lab findings usually show thrombocytopenia;prolonged PT, aPTT, and bleeding time; low serum levels of prothrombinand fibrinogen; and decreased serum levels of Factors V, VII, IX,and X.

Circulating Anticoagulants

May be associated with viral infections,malignancy, and collagen vascular disease. Usually prolonged aPTTfails to correct after adding normal plasma in test tube. In affectedindividuals, bleeding is uncommon, especially those with lupus anticoagulants.

Diagnostic Approach

Age, clinical findings, family history, andscreening tests (CBC with differential, platelet count, analysisof blood smear, PT and aPTT, and standardized Ivy bleeding time)are either diagnostic or narrow diagnostic possibilities in individualspresenting with purpura and bleeding.

Age

Neonates,especially preterm infants, have some features that may predisposeto purpura and bleeding. They have increase in capillary fragilityand decrease in platelet aggregation. Concentrations of vitaminK–dependent clotting factors are lower than adult normalvalues.

Diagnostic approach to purpura andbleeding depends on whether neonate is well or ill and whether plateletcount is normal or decreased.

In well neonate with normal platelet count,most common disorders that cause bleeding are trauma, vitamin Kdeficiency, Factor VIII or IX deficiency, and in utero exposureto drugs taken by mother (e.g., acetylsalicylic acid, phenytoin,or coumadin).

In well neonate with decreased plateletcount, most common disorders are alloimmune thrombocytopenia andmaternal autoimmune thrombocytopenia.

In ill neonate, common causes of bleedingand purpura are severe birth trauma, septicemia, and DIC. Othercauses include congenital infection (herpes simplex, cytomegalovirus,rubella, toxoplasmosis, syphilis), congenital leukemia, and osteopetrosis.

In infancy, childhood, and adolescence,most common causes of purpura and bleeding are accidental trauma,child abuse, Henoch-Schönlein purpura, idiopathic thrombocytopenicpurpura, leukemia, infection, and Factor VIII and IX deficiencies.

Clinical Findings

Typically,individuals with loss of vascular integrity have superficial bleedingwith purpura. Diagnosis of loss of vascular integrity depends onclinical recognition of vascular disorder and absence of plateletor coagulation disorder.

Individuals with thrombocytopenia orplatelet dysfunction usually have purpura and superficial bleedingof mucous membranes including epistaxis and GI tract bleeding. Alsomay have hematuria, menorrhagia, and intracranial bleeding. Normalplatelet count with prolonged bleeding time suggests qualitativeplatelet defect.

Individuals with Factor VIII or IXdeficiency, which are most common coagulation disorders, have recurrentbruising and bleeding into joints and muscle.

Family History

Positivefamily history may help confirm diagnosis.

As general rule, genetically transmitteddisorders usually have their onset in infancy with appearance ofrecurrent purpura and bleeding.

Acquired disorders are usually acute,variable in time of onset, and typically associated with infection,drug reactions, malignancy, or immunologic disorders.

Screening and Diagnostic Tests

A plateletcount of <150,000/mm³ isabnormal. Bleeding is rare with platelet count of >30,000/mm³.Large platelets are usually seen on blood smear in disorders inwhich thrombocytopenia is due to increased platelet destruction.Normal-sized platelets are usually seen in disorders in which thrombocytopeniais due to decreased production. When thrombocytopenia is associatedwith neutropenia or pancytopenia, bone marrow aspirate should beperformed searching for evidence of aplastic anemia, leukemia, orother malignancies.

With normal platelet count but abnormalbleeding time, most likely diagnoses are von Willebrand disease,aspirin ingestion, qualitative defect in platelet function, anduremia. Tests for renal function, vWF antigen, vWF ristocetin cofactor,and platelet function should be considered.

Possible causes of prolonged PT includeFactor VII deficiency, mild vitamin K deficiency, and liver disease.

Prolonged aPTT may be caused by FactorVIII, IX, XI, and XII deficiencies; von Willebrand disease; andpresence of circulating anticoagulant. There is no clinical bleedingwith Factor XII deficiency.

Possible causes of prolonged PT andaPTT include liver disease, DIC, vitamin K deficiency, congenitalfactor deficiencies (II, V, and X), and fibrinogen disorders (afibrinogenemia,hypofibrinogenemia). Liver function tests should be performed withsuspected liver disease. Otherwise, thrombin time, serum fibrinogen,fibrin split products, and assays for Factors II, V, and X shouldbe performed as indicated. Serum fibrinogen is decreased in congenitalafibrinogenemia, DIC, and sometimes in severe liver disease.

>>>>>>

» 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)

» READ BOOK EXCERPT ONLINE »

Source: Nursing: Interpreting Signs and Symptoms, 2007

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

Ask the patient when he first noticed the lesion and whether he has noticed other lesions on his body. Does he or his family have a history of bleeding disorders or easy bruising? Find out what medications he's taking, if any, and ask him to describe his diet. Ask about recent trauma or transfusions and the development of associated signs, such as epistaxis, bleeding gums, hematuria, and hematochezia. Also ask about systemic complaints that may suggest infection, such as a fever. If the patient is female, ask about heavy menstrual flow.

Inspect the patient's entire skin surface to determine the type, size, location, distribution, and severity of purpuric lesions. Also inspect the mucous membranes. Remember that the same mechanisms that cause purpura can also cause internal hemorrhage, although purpura isn't a cardinal indicator of this condition.

» 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

Bilateral crepitant rales, lack of dullness, and normal breath sounds suggest pulmonary edema or pneumonitis.
Focal crepitant rales, reduced alveolar breathing, dullness to percussion, and increased tactile and vocal fremitus suggest lobar pneumonia or pulmonary infarction.
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.
Focal crepitant rales and amphoric breathing with dullness below and hyperresonance above suggest a lung abscess or cavitation.

Hyperresonance

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

Dullness or Flatness

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.
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

» Next page: Signs of Goodpasture syndrome

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Diagnosis of Goodpasture syndrome

Diagnostic Test list for Goodpasture syndrome:

Goodpasture syndrome Diagnosis: Book Excerpts

Tests and diagnosis discussion for Goodpasture syndrome:

Diagnostic Tests for Goodpasture syndrome: Online Medical Books

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

DIAGNOSTIC WORKUP

PURPURA AND ABNORMAL BLEEDING: Ask the Following Questions: (Algorithmic Diagnosis of Symptoms and Signs)

DIAGNOSTIC WORKUP

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

Workup and Diagnosis

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

Workup and Diagnosis

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

Workup and Diagnosis

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

Workup and Diagnosis

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

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

Rales

Hyperresonance

Dullness or Flatness

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

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

Goodpasture's syndrome: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Allergic purpuras: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Idiopathic thrombocytopenic purpura: Diagnosis (Professional Guide to Diseases (Eighth Edition))

Premature rupture of membranes: Diagnosis (Professional Guide to Diseases (Eighth Edition))

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

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

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

Physical examination

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

Physical examination

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

Physical examination

Hematuria: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

Purpura/Petechiae/Excessive Bleeding: Differential Overview (Field Guide to Bedside Diagnosis)

Diagnostic Approach

Allergic purpura: Diagnosis (Handbook of Diseases)

Idiopathic thrombocytopenic purpura: Diagnosis (Handbook of Diseases)

Premature rupture of the membranes: Diagnosis (Handbook of Diseases)

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

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

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

Hematuria without Proteinuria

Glomerular Disorders

Acute Postinfectious Glomerulonephritis

Immunoglobulin A Nephropathy

Henoch-Schönlein Nephritis

Alport Syndrome

Membranoproliferative Glomerulonephritis

Systemic Lupus Erythematosus

Familial Benign Hematuria (Thin Basement Membrane Nephropathy)

Nonfamilial Benign Hematuria

Nonglomerular Disorders

Urinary Tract Infection

Trauma

Exercise

Hydronephrosis

Renal Vein Thrombosis

Hemoglobinopathies

Idiopathic Hypercalciuria

Urolithiasis

Polycystic Kidney Disease

Autosomal-Recessive

Autosomal-Dominant

Renal Tuberculosis

Vascular Malformations

Foreign Body in Urethra or Bladder

Neoplasm

Bleeding Disorders

Drugs

Hematuria with Proteinuria

Membranous Nephropathy

Glomerulonephritis of Chronic Infection

Idiopathic Rapidly Progressive Glomerulonephritis

TREATMENTS &
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Dr. Huntley's
Diagnosis
Checklist

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

PURPURA AND ABNORMAL BLEEDING: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

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

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

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

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

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

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

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

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

Goodpasture's syndrome: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Allergic purpuras: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Idiopathic thrombocytopenic purpura: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Premature rupture of membranes: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

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

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

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

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

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

Hematuria: Differential Overview
(Field Guide to Bedside Diagnosis)

Purpura/Petechiae/Excessive Bleeding: Differential Overview
(Field Guide to Bedside Diagnosis)

Allergic purpura: Diagnosis
(Handbook of Diseases)

Idiopathic thrombocytopenic purpura: Diagnosis
(Handbook of Diseases)

Premature rupture of the membranes: Diagnosis
(Handbook of Diseases)

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

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

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

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

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

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

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

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