HOW TO APPROACH TO A PATIENT WITH BLEEDING DISORDERS
EVALUATION OF THE BLEEDING PATIENT
DEFINITION
• Hemostasis
The arrest of bleeding from an injured blood vessel, involving the combined regulatory activity of vascular, platelet, and plasma factors
Primary Hemostasis
Vessel wall function Platelet functions of Adhesion, Aggregation
Secondary hemostasis
Plasma coagulation factors leading to fibrin deposition ,clot formation
Tertiary hemostasis
Clot retraction Cross link of fibrin clot Fibrinolysis
• Clotting The Coagulation of blood is a complex process by which fluid
form of blood changes to semi solid or solid form.• Bleeding
Extavasation of blood from an ruptured blood vessel to the internal or external tissue.
HEMOSTASIS AND THROMBOSIS
• Dependent on 3 factors:
Vascular endothelium Platelets Coagulation system
1. CLINICAL ASPECTS OF BLEEDING
1. CLINICAL ASPECTS OF BLEEDING
Evaluation of patients with bleeding is a multi-step process:
• Complete history
• Detailed physical exam
• Laboratory evaluation
HISTORY
Is there a personal or family history of bleeding after surgical procedures, dental procedures, childbirth, or trauma?
When the bleeding episode started?
Has the patient received medications that can cause or make worse a bleeding problem?
Many drugs can contribute to bleeding; semisynthetic penicillins cephalosporins
calcium channel blocker dipyridamolethiazides alcohol
quinine, quinidine chlorpromazine, sulfonamides INH, rifampin methyldopa phenytoin, barbiturates, warfarin, heparin, thrombolytic agents NSAIDs, ASA allopurinol
TMP/SMX
PHYSICAL EXAM
1. Assess volume status (correct shock if present)
2. Look for hepatosplenomegaly
3. Do a rectal exam for evidence of GI bleeding
4. Examine oropharynx for evidence of petechiae
HEREDIATARY TELANGECTASIAS
• Mouth: Gum Bleed Gum Hypertrophy Telangectasias Angular stomatitis
SUBCONJUNCTIVAL HAEMORRHAGE
PHYSICAL EXAM
Look for physical signs and symptoms of diseases related to capillary fragility:
Cushing’s syndrome, Marfan syndrome or exogenous steroids
"senile purpura” Petechiae secondary to coughing, sneezing, Valsalva
maneuver, blood pressure measurement
vasculitis ("palpable purpura")
Telangiectasias (Osler-Weber-Rendu syndrome) (HHT)PETECHIAE
VASCULITIS (PALPABLE RASH)
2. HEMATOLOGIC DISORDERS CAUSING BLEEDING
– Platelet disorders
– Coagulation factor disorders
CLINICAL DIFFERENTIATION
PLATELET DEFECTVS
COAGULATION DEFECT
PLATELETS DEFECTS
• Generally have immediate onset of bleeding after trauma
• Bleeding is predominantly in skin, mucous membranes, nose, GI tract, and urinary tract
• Bleeding may be observed as petechiae (<3 mm) or ecchymoses (>3 mm
COMPARISON OF PLATELET AND COAGULAYION DISORDERS
Platelet Disorders Coagulation Factor Disorder
Site of bleeding Skin, mucous membrane and soft tissue
Deep in soft tissues (joints and muscles)
Physical Finding Petechiae, ecchymoses Hematoma, Hemarthrosis
Family History Autosomal dominant Autosomal or X-linked recessive
Bleeding after cuts and scratches
Yes No
Bleeding after surgery and trauma
Immediate, usually mild
Delayed (1-2 days), often severe
CLINICAL ASPECTS OF BLEEDING
COAGULATION DEFECTS
• "Deep" bleeding (in the joint spaces, muscles, and retroperitoneal spaces) is common. Observed on exam as hematomas and hemarthroses.
Hematoma
LABORATORY EVALUATION OF BLEEDING
LABORATORY EVALUATION OF BLEEDING
Platelet function von Willebrand factor vWDBleeding time In vivo test (non-specific)Platelet function analyzer (PFA) Qualitative platelet
disorders
BLEEDING TIME
• 5-10% of patients hospitalized patients have a prolonged bleeding time
• Most of the prolonged bleeding times are due to aspirin or drug ingestion
CBC and smear Platelet count ThrombocytopeniaRBC and platelet morphology TTP, DIC, etc.
Coagulation PT extrinsic/common pathways
PTT Intrinsic/common pathways
Coag. factor assays Specific factor deficiencies
50:50 mix Inhibitors (e.g., antibodies)
Fibrinogen assay Decreased fibrinogen
Thrombin time Qualitative/quantitative fibrinogen defects
D-dimer Fibrinolysis (DIC)
• Prolonged bleeding time does not predict excess surgical blood loss
• Not recommended for routine testing in preoperative patients
THROMBIN TIME
• Measures rate of fibrinogen conversion to fibrin
• Procedure:– Add thrombin with patient plasma– Measure time to clot
• Variables:– Source and quantity of thrombin
CAUSES OF PROLONGED THROMBIN TIME
• Heparin• Hypofibrinogenemia• Dysfibrinogenemia• Paraprotein• Thrombin inhibitors (Hirudin)• Thrombin antibodies
PLATELETS
APPROACH TO THE THROMBOCYTOPENIC PATIENT• History
– Is the patient bleeding?
2. Are there symptoms of a secondary illness? (neoplasm, infection, autoimmune disease)
3. Is there a history of medications, alcohol use, or recent transfusion?
• History4. Are there risk factors for viral infection?
5.Is there a family history of thrombocytopenia?
6. Do the sites of bleeding suggest a platelet defect?
• Assess the number and function of platelets
– CBC with peripheral smear– Bleeding time – Platelet aggregation study– PFA
CLASSIFICATION OF PLATELET DISORDER
• Quantitative disorders
– Abnormal distribution
– Dilution effect
– Decreased production
– Increased destruction
CLASSIFICATION OF PLATELET DISORDERS• Qualitative disorders
– Inherited disorders (rare)
– Acquired disorders• Immune• Medications• Chronic renal failure• Cardiopulmonary bypass• Liver disease
INHERITED PLATELET DISORDERS
• May-Hegglin : ThrombocytopeniaLarge plateletsNeutrophils – Dohle bodies
.Glazmann’s thrombasthenia: Congenital deficiency or abnormality of GP IIb-IIIa
• Bernard-Solier syndrome: Congenital deficiency or abnormality of GP Ib
ACQUIRED PLATELET DISORDERS• Decreased production: Ineffective thrombopoiesis - MDS
• Increased destruction:ImmuneNon-immune
• Poor aggregationINCREASED PLATELETS DESTRUCTION
ITP IS A DIAGNOSIS OF EXCLUSION !
COAGULATION FACTOR DEFECTS
Inherited Coagulation factor bleeding disorders
– vonWillebrand’s disease
– Hemophilia (A and B)
HEMOPHILIA
Clinical manifestations (hemophilia A & B are indistinguishable)
– Prolonged bleeding after surgery or dental extractions
– Hemarthrosis (most common)
– Soft tissue hematomas
– Other sites of bleedingUrinary tract
CNS, neck (may be life-threatening)
ACQUIRED BLEEDING DISORDERS:
– Vitamin K deficiency– Liver disease – Warfarin overdose– DIC– Inhibitors to CF
VITAMIN K DEFICIENCY
• Source of vitamin K :Green vegetables Synthesized by intestinal flora
• Required for synthesisFactors II, VII, IX ,XProtein C and S
• Causes of deficiency :MalnutritionBilliary obstructionMalabsorptionAntibiotic therapy
DIC
DISSEMINATED INTRAVASCULAR COAGULATION• Sepsis
• Trauma– Head injury– Fat embolism
• Malignancy
PATHOGENESIS OF DICConsumption ofcoagulation factors;presence of FDPs aPTT PT TT Fibrinogen
Presence of plasmin D-dimer
Intravascular clot PlateletsSchistocytes
HEMOSTASIS IN LIVER DISEASE
LIVER DISEASE AND HEMOSTASIS• Decreased synthesis of II, VII, IX, X, XI, and fibrinogen
• Dietary Vitamin K deficiency (Inadequate intake or malabsortion)
• Dysfibrinogenemia
• Enhanced fibrinolysis (Decreased alpha-2-antiplasmin)
• DIC
• Thrombocytopenia due to hypersplenism
MANAGEMENT OF HEMOSTATIC DEFECTS IN LIVER DISEASE
Treatment for prolonged PT/PTT
Vitamin K 10 mg SQ x 3 days - usually ineffective
Fresh-frozen plasma infusion: 25-30% of plasma volume (1200-1500 ml) (immediate but temporary effect)
Treatment for low fibrinogen
Cryoprecipitate (1 unit/10kg body
APPROACH TO BLEEDING DISORDERSSUMMARY
• Identify and correct any specific defect of hemostasis– Laboratory testing is always needed to establish the cause of bleeding
– Screening tests (PT,PTT, platelet count) will often allow placement into one of the broad categories
– Specialized testing is usually necessary to establish a specific diagnosis
• Use non-transfusional drugs whenever possible
• RBC transfusions for surgical procedures or large blood loss
THANK YOU!
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