Approach to Petechiae And Purpura Supervised by:P.H.D.Khaled Khanji Presented by: Salah Eddin Younes Aleppo university hospital medical symposium

Petechiae tiny pin-point hemorrhages in skin or mucous membranes due to not enough platelets to plug up the micro-leaks in small vessels each day.

Purpura hemorrhages larger than petechiae seen in the skin.

Hemostasis Primary hemostasis [ vasoconstriction,platelet plug formation ]. Secondary hemostasis [ activating clotting pathway ].

Laboratory CBC BT PT ( extrinsic & common pathway ). PTT ( intrinsic & common pathway ). TT Peripheral smear. I II V VIII IX XI XII VII X

Laboratory Normal resulttest thousandPlatelet count 4-8 minutesBT secondPT secondPTT secondTT

Causes Hereditary hemorrhagic telangiectasia Blood vessel defect Connective tissue disorder Severe infection drugs Allergic ( HSP ) scurvey Decreased platelet & decreased functionPlatelet defect Hemophillia, VWD Coagulation defect Liver disease, DIC

Thrombocytopenia Excessive destructionImpaired production Immune disorder ( ITP, SLE )Aplastic anemia Hypersplenismmalignancy DICMegaloblastic anemia TTP HUS sepsis Viral infection dilutional

ITP Autoimmune thrombocytopenia. IgG antibody binds to platelets. no systemic illness. Precipitated by viral infection or vaccination. Low PLT, prolonged BT. Corticosteroids, IVIG, Anti-D,splenectomy.

Drug induced thrombocytopenia The most common type of drug induced thrombocytopenia is HIT ( thrombosis ). RifampinAcetaminophen QuinineAcyclovir VancomycinCarbamazepine Trimethoprim/sulfamethoxazoleDiclofenac Phenytoin Hydrochlorothiazide Digoxin Ibuprofen

TTP Microangiopathic hemolytic anemia. Increase in platelet consumption. Thrombocytopenia. Neurologic, renal abnormalities & fever. Low ADAMTS13, elevated LDH. PT & PTT normal. Plasma exchange with FFP.

HUS Microangiopathic hemolytic anemia. Often a prodrome of bloody diarrhea. Low Plt, kidney injury. Absence of neurological abnormalities. Elevated LDH. PT & PTT normal. Self limited.

VWD Family history (AD). The most common congenital disorder of hemostasis. Usually prolonged BT. Normal Plt. Prolonged PTT.

VWD Factor VIII activity Factor VIII antigen BT Decrease or normal Prolonged or normal Type I Decrease or normal ProlongedType IIa Decrease or normal ProlongedType IIb 00ProlongedType III

Hemophilia X-linked Inherited disorder. Factor VIII or IX. Joints bleeding. Prolonged PTT.

Vitamin K deficiency Underlying dietary deficiency or antibiotic use. Prolonged PT more than PTT. II VII IX X

DIC Underlying serious illness. Bleeding & thrombosis. Microangiopathic hemolytic anemia may present. Hypofibrinogenemia, thrombocytopenia. Fibrin degradation product, prolonged PT & PTT. Increased D–dimer. Treat the main cause. Plt, FFP & heparin.

HSP The most common Vasculitis in children. Palpable purpura. Arthralgis & hematuria. Nausea, colic & melena. Self-limited. Corticosteroids.

Qualitative platelet disorders Glanzmann’s thrombasthenia congenital Bernard-soullier syndrome Storage pool disease Myeloproliferative disorders Acquired uremia drugs autoantibody paraprotiens Von Willebrand’s disease

Approach History taking. Physical examination. Laboratory studies.

Why should you ask?Questions to ask Malignancy, infection General health/constitutional symptoms: Fatigue, wt loss, fever ITP, immune-mediatedPrevious/current URTI HUSDiarrhea (bloody), oliguria, edema HUS, ITPInfections contacts, travel history Cause of splenomegalyChronic liver or storage disease Dilutes patient’s own plateletsRecent massive transfusion Small risk of ITP after live vaccine (e.g. MMR)Recent vaccine Adverse drug reactionMedications Hereditary thrombocytopenia (e.g. ineffective thrombopoiesis, short life span), familial TTP Family history

What would this suggest?Physical Findings Infection, malignancy, DIC, TTPGeneral appearance: unwell/toxic Infection, malignancy, DIC, TTP HUS Blood loss Fever,Elevated blood pressure,Hemodynamic instability Increased HR, decreased BP, decreased perfusion Low platelets, risk of anemia Sources of bleeding Skin, mucous membranes,Petechiae, purpura, epistaxis GI tract Hematemesis, melena, frank blood in stools, fecal occult blood MalignancyLymphadenopathy Splenic sequestration of plateletsSplenomegaly HUSRenal failure e.g. edema, HTN Intracranial bleed, TTPAbnormal neuro exam eg. hemiparesis

prolonged BT Vascular defects. Thrombocytopenia. VWD.

Causes of prolonged PT Liver diseases. Vitamin K deficiency. Warfarin therapy. Factor VII deficiency.

Causes of prolonged PTT Factor XII. Factor XI. Factor IX. Factor VIII. Lupus. Heparin.

Causes of prolonged PT & PTT Liver diseases. Vitamin K deficiency. DIC. Heparin. Warfarin. Isolated factor deficiency II,V,X,I.

Normal plt Prolonged PT & PTT noyes Trauma Abuse HSP VWD Qualitative platelet disorders Congenital factor deficiency Liver diseases Vitamin K deficiency VWD Prolonged PT & PTT

Thrombocytopenia Prolonged PT & PTT noyes Sepsis DIC Anemia Peripheral smear Hemolysis no yes ITP Inhireted Thrombocytopenia Malignancy Aplastic anemia Sequestration TTP HUS

conclusion The most important thing is the history & physical examination. CBC & coagulation profile. Thrombocytopenia or not. Anemia.

Clinical case 18 yo boy with leg bruises.he has a history of recurrent furunculosis for which he takes a course of antibiotics for 10 days.3 months ago he started cephalosporin to eradicate his recurrent infection. He is otherwise healthy. Laboratory results : Hb: 13 WBC: 6000 PLT : PTT :74 PT : 21

What treatment is most likely to improve this patient hematologic abnormality ? A.Vitamin K B.Aspirin C.Cryoprecipitate D.FFP E.Heparin

Clinical case 35yo woman with changing mental status.she has had a fever & confusion fo r3 days.prior she was healthy. PE: Pallor,confused,39 and petechia. Laboratory results : Hb: 9 WBC: 6800 PLT : BUN :47 Creatinine : 2.6 PT & PTT normal

Which of the following is the most likely diagnosis ? A.DIC B.TTP C.ITP D.Glanzmann Schistocytosis

Clinical case 10 yo male with history of prolonged epistaxis. PT normal PTT 55 CBC normal BT prolonged

The most likely diagnosis : A.Factor VIII deficiency B.Bernard-soulier C.Vitamin K deficiency D.VWD

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