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Purpura and Bleeding

Purpura and Bleeding: Excerpt from The Diagnostic Approach to Symptoms and Signs in Pediatrics

Purpura are macular discolorations that donot blanch or disappear with pressure. They include petechiae (<3mm in diameter) and ecchymoses (larger lesions).

Principal Causes of Purpura and Bleeding

1. Lossof vascular integrity
   1. Trauma
   2. Infection
   3. Henoch-Schönlein purpura
   4. Drugs
   5. Langerhans histiocytosis
   6. Ehlers-Danlos syndrome
   7. Vitamin C deficiency
   8. Hereditary hemorrhagic telangiectasia(Osler-Rendu-Weber disease)
2. Thrombocytopenia
   1. Increasedplatelet destruction
      1. Immune-mediated
         1. Neonatal alloimmune thrombocytopenia
         2. Maternal autoimmune thrombocytopenia
         3. Idiopathic thrombocytopenic purpura
         4. Collagen vascular disease
         5. Drug-induced thrombocytopenia
      2. Infection
      3. Hemolytic-uremic syndrome
      4. Thrombotic thrombocytopenic purpura
      5. Wiskott-Aldrich syndrome
   2. Decreased platelet production
      1. Infection
      2. Specific platelet disorders
         1. Congenitalamegakaryocytic thrombocytopenia
         2. Thrombocytopenia–absent radiisyndrome
      3. Bone marrow suppression (generalized)
      4. Bone marrow replacement
      5. Megaloblastic anemia
      6. Platelet sequestration
         1. Hypersplenism
         2. Large hemangiomas
3. Abnormal platelet function
   1. Thrombasthenia(Glanzmann disease)
   2. Giant platelet syndrome (Bernard-Souliersyndrome)
   3. Storage pool deficiency
   4. Drugs
   5. Uremia
4. Coagulation disorders
   1. Factordeficiencies
      1. VonWillebrand disease
      2. Factor VIII deficiency (hemophiliaA)
      3. Factor IX deficiency (hemophilia B,Christmas disease)
      4. Deficiencies of Factors I, II, V, VII,X, XI, and XIII
   2. Vitamin K deficiency
   3. Disseminated intravascular coagulation
   4. Liver disease
   5. Circulating anticoagulants

Clinical Features and Diagnosis

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.

References

1. Behrman RE, et al., eds. Nelson textbookof pediatrics, 16th ed. Philadelphia: WB Saunders, 2000.
2. Beighton P, et al. Ehlers-Danlos syndromes: revisednosology, Villefranche, 1997. Am J Med Genet 1998;77:31–37.
3. Cohen AR. Rash—Purpura. In: Fleisher GR, LudwigS, eds. Textbook of pediatric emergency medicine, 4th ed. Philadelphia:Lippincott Williams & Wilkins, 2000:531–539.
4. Lilleyman JS, et al., eds. Pediatric hematology, 2nded. London: Churchill Livingstone, 1999.
5. McMillan JA, et al., eds. Oski's pediatrics:principles and practice, 3rd ed. Baltimore: Lippincott Williams & Wilkins,1999.
6. Nathan DG, Orkin SH, eds. Nathan and Oski'shematology of infancy and childhood, 5th ed. Philadelphia: WB Saunders,1998.
7. Online Mendelian Inheritance in Man (OMIM). McKusick-NathansInstitute for Genetic Medicine, Johns Hopkins University (Baltimore,MD) and National Center for Biotechnology Information, NationalLibrary of Medicine (Bethesda, MD), 2000. World Wide Web URL: http://www.ncbi.nlm.nih.gov/omim.
8. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.

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Book Source Details

• Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
• Author(s): Paul S. Bellet
• Year of Publication: 2006
• Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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