Diagnostic Tests for Immune Thrombocytopenic Purpura
Immune Thrombocytopenic Purpura: Diagnostic Tests
The list of diagnostic tests
mentioned in various sources as
used in the diagnosis of Immune Thrombocytopenic Purpura
includes:
Immune Thrombocytopenic Purpura Tests: Book Excerpts
Home Diagnostic Testing
These home medical tests may be relevant to Immune Thrombocytopenic Purpura:
Immune Thrombocytopenic Purpura Diagnosis: Book Excerpts
Tests and diagnosis discussion for Immune Thrombocytopenic Purpura:
The physician will take a medical history and
perform a thorough physical examination. A careful review of medications
the patient is taking is important because some drugs can be associated
with thrombocytopenia. A complete blood count will be done. A low platelet
count will establish thrombocytopenia as the cause of purpura. Often the
next procedure is a bone marrow examination to verify that there are
adequate platelet-forming cells (megakaryocyte) in the marrow and to rule
out other diseases such as metastatic cancer (cancer that has spread to
the bone marrow) and leukemia cancer of the blood cells themselves).
Another blood sample may be drawn to check for other conditions sometimes
associated with thrombocytopenia such as lupus and infection.
(Source: excerpt from Immune Thrombocytopenic Purpura (ITP): NIDDK)
Diagnostic Tests for Immune Thrombocytopenic Purpura: Online Medical Books
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for more information about the diagnostic tests for Immune Thrombocytopenic Purpura.
THROMBOCYTOPENIA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
The diagnostic workup should include a CBC, blood smear, sedimentation rate, urinalysis, serum B
12
, chemistry panel, ANA, serum haptoglobins, red cell survival, liver spleen scan, CT scan of the abdomen, and a hematology consult for bone marrow study.
» READ BOOK EXCERPT ONLINE »
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
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
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.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
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.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
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.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 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.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
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. >
» READ BOOK EXCERPT ONLINE »
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
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
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