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Diagnosis of Immune Thrombocytopenic Purpura

Diagnostic Test list for Immune Thrombocytopenic Purpura:

The list of medical tests mentioned in various sources as used in the diagnosis of Immune Thrombocytopenic Purpura includes:

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

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


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

  1. What is the WBC count? Thrombocytopenia with a high white count suggests leukemia or myeloid metaplasia. Thrombocytopenia with a normal white count suggests idiopathic thrombocytopenic purpura or drug reaction. Thrombocytopenia with a low white count suggests lupus erythematosus, aplastic anemia, myelofibrosis, drugs, myelophthisic anemia, or pernicious anemia.
  2. What is the ANA? A positive ANA in the face of thrombocytopenia and a low white count suggests lupus erythematosus.

DIAGNOSTIC WORKUP

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

  1. 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.
  2. 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.
  3. If there is a petechial rash, is the platelet count normal? The presence of a normal platelet count would suggest either thrombocytopathy or vasculitis.
  4. 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.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

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
>>>>

» READ BOOK EXCERPT ONLINE »

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

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

Disorders of increased destruction

  • Immunologic platelet consumption
    –Immune thrombocytopenic purpura (ITP)
    –Drug-induced (antiepileptics, septra)
    –Infection (EBV, CMV, malaria, Parvovirus, HIV, other viral illnesses)
    –Autoimmune disease (SLE)
    –Evans syndrome: ITP with immune hemolytic anemia
    –Allergy or anaphylaxis
    –Posttransplant
    • Nonimmunologic
      –Chronic microangiopathic hemolytic anemia
      –Hemolytic-uremic syndrome (HUS)
      –Thrombotic thrombocytopenic purpura
      –Shear (catheters, cardiopulmonary bypass, congenital or acquired heart disease)

    Disorders of decreased production
  • Bone marrow infiltration: Leukemia, neuroblastoma, histiocytosis, osteopetrosis
  • Marrow failure: Aplastic anemia, congenital microangiopathic anemia, thrombocytopenia with absent radii (TAR), Fanconi anemia, myelodysplasia, amegakaryocytic thrombocytopenia
  • Abnormal platelet size or morphology
    –Bernard-Soulier
    –May-Hegglin
    –Gray platelet
    –Wiskott-Aldrich
    • Severe nutritional deficiency
      –B12, folate

    Combined disorders
    • DIC, Kasabach-Merritt syndrome, storage diseases, renal disease, pre-eclampsia

    Sequestration
    • Hypersplenism/portal hypertension, thrombosis, cavernous transformation of portal vein, hypothermia

    Neonatal
  • Congenital anomalies (trisomy 13 or 18)
  • Maternal causes: ITP, SLE, HELLP syndrome, DIC, hyperthyroidism, viral illness, drug use
  • NEC

Workup and Diagnosis

  • History: Recent illness, diet history; bleeding (nose, gum, stool, urine, skin, duration, amount); bone pain, fever, lethargy or crankiness, limp; HIV risk factors, diet history; exposure to toxins or radiation
  • Medical history: Congenital anomalies; bleeding with previous surgery or trauma, menorrhagia; frequent infections, congenital cyanotic heart disease
  • Family history: Thrombocytopenia; autoimmune or collagen vascular diseases; blood dyscrasias, hematologic malignancies; storage diseases
  • Physical exam
    –General appearance, growth
    –Petechiae, purpura, ecchymoses, eczema, pallor
    –Jaundice, nail dystrophy
    –Lymph node chains
    –Splenomegaly, hepatomegaly, bruit, masses
    –Caput medusae or spider hemangiomas
    –Palatal petechiae, gum bleeding, leukoplakia
    –Absent radii, thumb anomalies, joint abnormalities
  • Studies
    –Bone marrow exam
    –Abdominal ultrasound; chest X-ray
  • Labs
    –All patients: CBC/diff with peripheral smear
    –Selected patients: direct and indirect Coombs, LDH, DIC panel (PT/PTT, fibrinogen, D-dimers), blood culture, HIV, ANA, urinalysis, renal function, CMV and EBV titers, hepatitis B and C serologies

» READ BOOK EXCERPT ONLINE »

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

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

The laboratory workup will provide the best means of diagnosing the cause of thrombocytopenia. If there is pancytopenia, the most likely cause is aplastic anemia or bone marrow invasion. Collagen disorders such as lupus erythematosus would cause a similar picture. If only the platelets are affected, autoimmune disorders would be more likely the cause. The initial workup should include a CBC, blood smear for morphology, sedimentation rate, serum B12 and folic acid levels, chemistry panel, ANA, serum haptoglobins, red cell survival, and protein electrophoresis. A hematologist should be consulted.

» READ BOOK EXCERPT ONLINE »

Source: Differential Diagnosis in Primary Care, 2007

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

Thrombocytopenia: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Diagnosis is based on the results of the patient history (especially a drug history), physical examination, and laboratory tests. Coagulation tests reveal a decreased platelet count (in adults, less than 100,000/µl), prolonged bleeding time, and normal prothrombin time and partial thromboplastin time. If increased destruction of platelets is causing thrombocytopenia, bone marrow studies will reveal a greater number of megakaryocytes (platelet precursors) and shortened platelet survival (several hours or days rather than the usual 7 to 10 days).

» READ BOOK EXCERPT ONLINE »

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.

» READ BOOK EXCERPT ONLINE »

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.

» READ BOOK EXCERPT ONLINE »

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

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: 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.

» READ BOOK EXCERPT ONLINE »

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

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.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Thrombocytopenia: Diagnosis
(Handbook of Diseases)

To diagnose thrombocytopenia, obtain a patient history (especially a drug history), a physical examination, and the following laboratory tests:

❑ Coagulation tests reveal a decreased platelet count (in adults, < 100,000/µl), prolonged bleeding time, and normal prothrombin time and partial thromboplastin time. Platelet-associated antibodies may be present.

❑ If increased destruction of platelets is causing thrombocytopenia, bone marrow studies will reveal a greater number of megakaryocytes (platelet precursors) and shortened platelet survival (several hours or days rather than the usual 7 to 10 days). >

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

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.

» READ BOOK EXCERPT ONLINE »

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.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Chronic fatigue and immune dysfunction syndrome: Diagnosis
(Handbook of Diseases)

The cause and nature of CFIDS are still unknown, and no single test unequivocally confirms its presence. Therefore, the diagnosis is based on the patient’s history and the CDC criteria. Because the CDC criteria are admittedly a working concept that may not include all forms of this disease and are based on symptoms that can result from other diseases, diagnosis is difficult and uncertain. Considerable overlap exists between CFIDS and fibromyalgia syndrome, with many patients having features of both.

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Source: Handbook of Diseases, 2003

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

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

    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

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

    The laboratory workup will provide the best means of diagnosing the cause of thrombocytopenia. If there is pancytopenia, the most likely cause is aplastic anemia or bone marrow invasion. Collagen disorders such as lupus erythematosus would paint a similar picture. If only the platelets are affected, autoimmune disorders would be more likely the cause. The initial workup should include a CBC, blood smear for morphology, sedimentation rate, serum B12 and folic acid levels, chemistry panel, ANA, serum haptoglobins, red cell survival, and protein electrophoresis. A hematologist should be consulted.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007


     » Next page: Signs of Immune Thrombocytopenic Purpura

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