Diagnostic Tests for Goodpasture syndrome
Goodpasture syndrome: Diagnostic Tests
The list of diagnostic tests
mentioned in various sources as
used in the diagnosis of Goodpasture syndrome
includes:
Goodpasture syndrome Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Goodpasture syndrome:
- Lung & Respiratory Health Tests:
- Bladder & Urinary Health: Home Testing:
- Kidney Health: Home Testing:
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
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Review excerpts from medical books online, free, without registration,
for more information about the diagnostic tests for Goodpasture syndrome.
HEMATURIA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The workup begins with a urinalysis and microscopic examination of the urinary sediment. The physician can easily do this in his office. If there is proteinuria, granular cast, and red cell cast, glomerulonephritis or collagen disease should be suspected. A culture and sensitivity and colony count should be done if a UTI is suspected. A three-glass test may be done. If there is blood in the initial specimen, the cause is most likely in the urethra or male genitalia. If it is in the final specimen, the cause is most likely a bladder lesion. Phase-contrast microscopy may also be helpful in identifying hematuria from a glomerular lesion. If this is negative, an anaerobic culture should be done also and then an AFB smear and culture and guinea pig inoculation to rule out tuberculosis. An intravenous pyelogram will also usually have to be done. A CBC, sedimentation rate, chemistry panel, coagulation profile, and ANA test will help rule out blood dyscrasias, collagen diseases, and other systemic diseases. Ultrasonography may help diagnose a renal cyst.
If the above are not revealing, referral to a urologist is indicated. He will probably do a cystoscopy and retrograde pyelography. He may also want to order a CT scan of the abdomen and pelvis and a renal biopsy. Renal angiography and aortography may be necessary to evaluate renovascular hypertension and renal embolism.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
PURPURA AND ABNORMAL BLEEDING:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
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:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing clots? To rule out artifactitious hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if there’s pain or burning with hematuria episodes.
Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting anticoagulants or aspirin.
Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
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.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Hematuria:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing any clots? To rule out artifactual hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if pain or burning accompanies the episodes of hematuria.
Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting the use of anticoagulants or aspirin.
Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
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:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
should focus on signs of systemic disease (fever, rash, lymphadenopathy, joint swelling, and abdominal or pelvic mass), and underlying medical or renal disease (hypertension, edema). Multiple telangiectasias and mucous membrane lesions indicate hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease). An abdominal mass in children requires exclusion of Wilms tumor.
Testing
A. Initial evaluation. Hematuria is usually detected by dipstick or microscopic examination. The dipstick test relies on detecting hemoglobin and should always be confirmed by microscopic examination of the urine sediment. Some controversy exists about the abnormal number of red blood cells in urine. Most clinicians consider more than three to five red blood cells per high power field (40 × lens) as definitely abnormal. When dipstick testing is positive for blood but urine microscopy reveals no red blood cells, hemoglobinuria or myoglobinuria should be considered. The next step is a urine culture. Baseline blood tests include a renal panel, complete blood count with differential, sedimentation rate, prothrombin time, and partial thromboplastin time.
B. Further evaluation is highly dependent on the suspected cause. Further blood tests can include serum complement titer (significant if low), antistreptolysin-O titer (high), antinuclear antibody and extended panels with anti-deoxyribonuclease B titer (high), and hemoglobin electrophoresis. A tuberculin skin test or chest x-ray study can be done to detect tuberculosis. Further tests can include imaging studies and cytology. Intravenous pyelogram and abdominal and pelvic ultrasound or computed tomography scanning may detect malignancies of the various anatomic areas as well as benign conditions such as urolithiasis, obstructive uropathy, renal cysts, parenchymal abnormalities, and nonurinary tract lesions. To complete the workup, send the urine for cytology study and proceed with cystoscopy looking for abnormalities of the urethra and bladder. Biopsies of various areas, including kidney and bladder, and invasive vascular studies may be needed. Unless a diagnosis is made, patients will need referral to subspecialists.
Diagnostic assessment
The key to the diagnosis of hematuria is the clinical history and physical examination. Laboratory and imaging studies only confirm or rule out initial suspicions. The goal is to diagnose a variety of serious illnesses, including malignancies and renal parenchymal diseases. In general, keep in mind that transient hematuria, especially in a young person, is quite common and rarely indicative of significant pathology (4). When present in patients aged more than 50 years, however, transient hematuria always warrants a comprehensive evaluation to rule out malignancy. Similarly, a diagnostic workup should be performed when persistent hematuria is found in patients of any age.
References
1. Froom P, Ribak J, Benbassat J. The significance of microhematuria in young adults. BMJ 1984;288:20–28.
2. Mariani AJ, Mariani MC. The significance of adult hematuria: 1000 hematuria evaluations including a risk-benefit and cost-effectiveness analysis. J Urol 1989;
141:350–355.
3. Messing EM, Young TB, Hunt VB, et al. Hematuria home screening: repeat testing results. J Urol 1995;154(1):57–61.
4. Murakami S, Igarashi T, Hara S, et al. Strategies for asymptomatic microscopic hematuria: a prospective study of 1034 patients. J Urol 1990;144:99–106.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Petechiae and Purpura:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
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.
Testing
A. Test selection. Initial laboratory: Complete blood count (CBC), platelet count, peripheral smear, prothrombin time (PT), activated partial thromboplastin time (APTT), and possibly a bleeding time (3). If the lesions appear vasculitic, consider a sedimentation rate and C-reactive protein determination. Serum creatinine and urinalysis can be ordered to screen for renal involvement. In vasculitis, the laboratory findings are often nonspecific and a skin biopsy for histology is employed (2).
B. Significance of test results
1. Isolated thrombocytopenia: most often ITP in nonpregnant women. Without atypical features, no follow-up laboratory study is recommended (4).
2. Isolated, increased APTT: low levels of factors VIII, IX, XI. Follow-up studies: factor VIII level and von Willebrand’s factor assay and activity.
A slightly increased APTT and slightly decreased factor VIII are consistent with von Willebrand’s disease. A very prolonged APTT and very low factor VIII is consistent with an acquired factor VIII inhibitor (3).
3. Thrombocytopenia with increased PT, APTT: consider DIC and liver failure. Follow-up study: d-dimer, fibrinogen, fibrin degradation products.
In newborns with purpura, evaluation for sepsis, serologies for the TORCH syndrome (acronym for Toxoplasmosis, Other infections, Rubella, Cytomegalovirus infection, and Herpes simplex), and coagulation factors are also recommended. Proteins C and S activities are also indicated in purpura fulminans (diffuse ecchymoses that become bullous and necrotic); neutropenia or abnormal neutrophils may indicate leukemia. Other laboratory tests when evaluating vasculitis can include complement levels, antinuclear antibody, and cryoglobulins.
Diagnostic assessment (4)
With petechiae resulting from lone thrombocytopenia, ITP may be difficult to differentiate from pregnancy-induced thrombocytopenia (which tends to be milder), viral infection, or drugs. ITP is designated if no other clinically obvious cause is noted.
Thrombotic-thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are seen in many clinical situations, including pregnancy, cancer, infections, chemotherapy, and so on. Signs include the pentad of fever, thrombocytopenia, microangioipathic hemolytic anemia, hemorrhage (including purpura), and neurologic abnormalities. Because of serious consequences, the diagnosis should be considered if thrombocytopenia and fragmented red blood cells are seen on the peripheral smear. TTP-HUS has a normal PT, APTT, and d-dimer as opposed to DIC.
In regard to coagulation factor abnormalities, hemophilia A and B can cause increased bruising and ecchymoses but not nearly as frequently as von Willebrand’s disease. Children being investigated for nonaccidental bruising should be evaluated for coagulation disorders with a CBC, platelet count, PT, APTT, and a bleeding time. With the sudden onset of large ecchymoses and hematomas in an adult with normal platelets, an acquired factor VIII deficiency (autoantibody) should be investigated in cases of a prolonged PT, APTT.
In newborns, a blueberry muffin baby (from extramedullary hematopoiesis) may appear purpuric, and this condition must be differentiated from purpura fulminans secondary to protein C or S deficiency, or sepsis.
Vasculitis causing palpable purpura in children is most common with Henoch–Schönlein purpura. In connective tissue diseases, purpuric lesions are usually a secondary finding.
The causes of purpuric lesions are many. A thorough history and physical examination, along with some basic laboratory studies and an occasional skin biopsy, are all that is needed to establish a likely diagnosis.
References
1. Baselga E, Drolet BA, Esterly NB. Purpura in infants and children. J Am Acad Dermatol 1997;37:673–705.
2. Cuttica RJ. Vasculitis in children: a diagnostic challenge. Curr Probl Pediatr 1997 27:309–317.
3. Loserh JM. Screening and diagnosis of coagulation disorders. Am J Obstet Gynecol 1996;175:778–783.
4. Diagnosis and treatment of idiopathic thrombocytopenic purpura: Recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel. Ann Intern Med 1997;126:319–326.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Solitary Pulmonary Nodule:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
should include a search for evidence of weight loss, chronic obstructive pulmonary disease, and primary or metastatic disease of other organs.
Testing
The key question is to determine which one of the SPNs is malignant and warrants invasive and immediate action. The following factors can help determine a course of management:
A. Location. Generally, most malignant lesions are found in the upper lobes.
B. Appearance. The smooth margins seen on computerized tomography (CT) scan characterize benign lesions, whereas spiculated, irregular borders are associated with malignant growths.
C. Size. Small size (<2 cm) is most frequently a sign of benignity, although it can be caused by an early, isolated pulmonary metastasis from a primary cancer at another site.
D. Calcifications. Peripheral, concentric patterns (“bull’s eyes” in granulomas, “popcorn ball” in hematomas) (3) have been associated with benign lesions, but the presence of calcifications has not been found to be a reliable indicator in predicting malignancy, because 14% of cancerous lesions can be calcified.
E. Aging. The CT scan of the chest is widely available and noninvasive. It accurately measures the nodule and defines its location and morphology.
F. Preliminary results with high resolution computerized tomography with contrast indicate good accuracy in the determination of the nodule malignancy. The MRI is not a preferred imaging tool to analyze a pulmonary nodule but its superior capacity to enhance vascular structures can be useful in the differential diagnosis.
Diagnostic assessment
Controversy exists as to the best way to manage SPN. The decision to observe or to intervene is guided by the following parameters: patient’s age, smoking history, location of the nodule, availability of previous
x-ray studies, and presence and type of calcifications.
A. Observation. A stable (no growth in 2 years) calcified lesion in a nonsmoker, aged less than 35 years, is almost certainly benign, and can safely be managed by repeat chest x-ray study every 3 months in the first year, then every year for 2 years. The patient’s cooperation and the family physician’s meticulous follow-up are essential to the success of this plan.
B. Intervention. An irregular, noncalcified lesion, particularly in a smoker or older patient, warrants invasive intervention to obtain a tissue diagnosis.
1. Fiberoptic bronchoscopy is the procedure of choice for centrally located SPNs.
2. For peripheral lesions, percutaneous needle biopsy is a quick, relatively easy procedure when done by an experienced operator. Its low rate of specificity and potential risks of pneumothorax and bleeding make it a poor choice because the goal is to reach a diagnosis with the least discomfort to the patient.
3. Thoracoscopic fine-needle aspiration is becoming an alternative to percutaneous needle biopsy. In a small surgical series, it provided an accurate diagnosis in all cases and helped to define the next surgical step (4).
4. A new surgical technique, video-assisted thoracic surgery (VATS), is fast becoming the diagnostic tool of choice for suspected SPN (5). Its yield is excellent and its capacity allows resectability of benign lesions without thoracotomy; its very low rate of morbidity and mortality are welcome additions to the approach to this difficult problem.
References
1. Turpin S, Maroves H, Costa P, Medeiros F, Ramos M, de Olivera JP. The solitary pulmonary nodule: a retrospective study of 119 cases. Acta Med Port 1998;11(6):
533–538.
2. Swensen SJ, Silverstein MD, Ilstrup DM, Schleck CD, Edell ES. The probability of malignancy in solitary pulmonary nodules. Application to small radiologically indeterminate nodules. Arch Intern Med 1997;157:849–855.
3. Caskey CI, Templeton PA, Zerhouni EA. Current evaluation of the solitary pulmonary nodule. Surg Clin North Am 1990;28(3):511–520.
4. Bousahra M 2nd, Clowry L Jr. Thoracoscopic fine needle aspiration of solitary pulmonary nodules. Ann Thorac Surg 1997;64:1191–1193.
5. Hazelrigg SR, Magee MJ, Cetindag LB. Video assisted thoracic surgery. Chest Surg Clin North Am 1998;8:763–774, vii. >>
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Hematuria:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
A reasonable cutoff for discriminating benign from serious causes of hematuria is 10 RBCs/HPF. The urine dipstick detects as few as 1 to 2 RBCs/HPF. Analysis of the urine sediment is crucial. White cells and bacteria are indicative of cystitis whereas white cell casts are seen in pyelonephritis. Red cell casts and dipstick proteinuria indicate glomerulonephritis. Red cells from a glomerular source tend to be distorted. A positive dipstick for hemoglobin but no RBCs in the urinalysis suggests the presence of myoglobin or free hemoglobin derived from intravascular hemolysis. Menstrual blood contamination needs to be considered in the differential of microscopic hematuria.
Initial hematuria suggests a urethral source; terminal hematuria, the prostatic urethra, trigone, or base; and total hematuria, the kidney, ureter, or bladder. Massive hematuria is usually associated with bladder neoplasm, benign prostatic hypertrophy, or trauma. Bright red urine suggests a lower urinary source. Passage of bulky disc-like or fragmented clots implies the bladder as source, long shoestring clots suggest a ureteral origin, and pyramidal clots are from the renal pelvis. Glomerular sources virtually never produce clots (due to the presence of tissue plasminogen activators in the glomeruli and tubules). With a presentation of painless total hematuria, a urinary tract cancer is found in 20%.
Flank pain associated with hematuria may result from the passage of stones or clots. Hypertension suggests renal disease. Rash, fever, arthralgia/arthritis, or hemoptysis suggests a connective tissue disease or vasculitis. Beets, blackberries, and rhubarb, as well as pyridium, rifampin, phenothiazines, and anthracyclines, can produce red urine without blood.
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Source: Field Guide to Bedside Diagnosis, 2007
Purpura/Petechiae/Excessive Bleeding:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
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
Hematuria:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Purpura:
Physical assessment
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
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.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Hematuria:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
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:
Diagnostic Approach
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
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. >
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Hematuria:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing clots? To rule out artifactitious hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if there's pain or burning with hematuria episodes.
Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting anticoagulants or aspirin.
Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.
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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.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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