Hem Onc

1. Hem Onc Anemia Acquired Bleeding Disorders Transfusion Therapy

2. Anemia • Category of Causes • Analyzing Indices • Approach & Treatment

3. Biggest Takeaway Anemia is a sign, not a diagnosis

7. Category of Causes • 1) Blood Loss • 2) Decrease RBC Production • 3) Increased RBC Destruction*more than one can occur in one person

8. Category of Causes • 1) Blood Loss - Principles of Hemorrhage Management • 2) Decrease RBC Production • 3) Increased RBC Destruction*more than one can occur in one person

9. Principles of Hemorrhage Management • Volume Resuscitation • Balanced, minimal crystalloids • Permissive Hypotension • Source Control • GI (Upper, Lower) • Ob/GYN (Ectopic, Abruption, Post-Partum, Non-Pregnancy) • ICH • AAA • Hemoptysis • Nasal • GU/Retroperitoneal • Trauma (Bones/Compartments, Peritoneal, Hemothorax) • Adjuncts • Reverse Coagulopathy • Lethal Triad

10. Category of Causes • 1) Blood Loss - Principles of Hemorrhage Management • 2) Decrease RBC Production- Nutritional deficiency (iron, folate, B12) - Aplastic or myelodysplastic • 3) Increased RBC Destruction*more than one can occur in one person

11. Category of Causes • 1) Blood Loss - Principles of Hemorrhage Management • 2) Decrease RBC Production - Nutritional deficiency (iron, folate, B12) - Aplastic or myelodysplastic • 3) Increased RBC Destruction - Sickle-Cell Disease - Drug-induced autoimmune Hemolytic Anemia*more than one can occur in one person

12. Anemia Indices • MCV • RDW • Ferritin • Reticulocyte Count • Peripheral Blood Smear • Direct/Indirect Coombs Test

20. Category of Causes • 1) Blood Loss - Principles of Hemorrhage Management • 2) Decrease RBC Production - Nutritional deficiency (iron, folate, B12) - Aplastic or myelodysplastic • 3) Increased RBC Destruction - Sickle-Cell Disease - Drug-induced autoimmune Hemolytic Anemia • Hemodilutional*more than one can occur in one person

21. Approach & Management • Assess for acute blood loss • Transfuse those who are: - Symptomatic - Hemodynamically unstable - Evidence of tissue hypoxia - Limited cardiopulmonary reserve Liberal transfusion not recommended • Replace nutritional deficits

22. Acquired Bleeding Disorders • Platelet Defects • Coagulation Disorders

23. Biggest Takeaway Always consider bleeding disorders when managing hemorrhagic shock/bleeding catastrophes

25. Acquired Bleeding Disorders • Platelet Defects • Thrombocytopenia - ITP - Drug-Induced - Nonimmune • Functional Platelet Disorders • Coagulation Disorders

26. Thrombocytopenia • Production • Destruction • Loss • Splenic sequestration

29. ITP • Antiplatelet antibodies that attack surface glycoproteins (glycoprotein Iib/Iia) leading to platelet destruction, some impaired production • Idiopathic/Primary or Secondary to medical condition (AI, infections) & Drugs • Primary: at any age, typically more female ages 30-60, typically resolves <6mo (viral #1) • Treatment: typically not needed in asymptomatic patients until <30k (supportive care) - Prednisone 1mg/kg/d for 4 weeks; IVIG 1g/kg/d; Rhogam; Monoclonal Abs - Life-threatening: IV Steroids (Dexamethasone) & IVIG, Platelets 2-3x nl, emergent splenectomy

31. Drug Induced Thrombocytopenia • Presentation similar to ITP • Typically 5-14d after initiation of drug (sooner if re-exposure) • Chronic alcohol use is a common cause • Typically normalizes after cessation of causative agent • Heparin-induced Thrombocytopenia: paradoxical hypercoagulable platelet activation

34. Nonimmune (Non-Drug) Thrombocytopenia • TTP • HUS • Heparin-Induced Thrombocytopenia (HIT) • DIC • Viral • HELLP/Pre-Eclampsia/Gestational Thrombocytopenia • Liver disease +/- Chronic Alcohol • Excessive Hemorrhage • Hemodialysis, extracorporeal circulation • Splenic sequestration (SCD, Cirrhosis)

35. Functional Platelet Disorders

40. Functional Platelet Disorders • Consider transfusing active bleeding patients who have functional platelet disorders to raise levels >50k • Macroglobulinemia – high viscosity can impair platelet function, may need plasmapheresis to reduce protein level to correct hemostatic function

41. Acquired Bleeding Disorders • Platelet Defects • Thrombocytopenia - ITP - Drug-Induced - Nonimmune • Functional Platelet Disorders • Coagulation Disorders • Liver Disease • Renal Disease • DIC

42. Liver Disease Coagulopathy • Hepatocytes synthesize all coagulation factors and regulatory proteins (except factor VIII and vWF) - Diseases affecting hepatic parenchyma can result in decreased synthesis of these factors - Includes Vit K dependent factors (also affected by malabsorption, cholestasis, etc.) - PT prolongation common for decompensated hepatic function (poor predictor of bleeding severity) • Concomitant decrease in anticoagulant proteins >> at risk of both bleeding and thrombosis- Twice as likely to develop unprovoked DVT! Higher incidence portal vein thrombosis • Treatment: balanced transfusion as normal, however caution plasma (can precipitate thrombosis, worsen portal hypertension/severity of variceal bleeding); F7 and PCC not shown beneficial, Vit K?

43. Renal Disease Coagulopathy • Early renal disease: tendency for thrombosis relating to increased production of procoagulant factors, decreased tissue plasminogen activator • Advanced renal disease: platelet dysfunction, decreased ability to adhere to damaged endothelium and aggregate; uremic toxins and impaired drug elimination • Risk for minor (mucosal, cutaneous) and major bleed (ICH, GI) • PT, PTT, platelet numbers normal, bleeding time prolonged • Treatment:Desmopressin (DDAVP) 0.3 mg/kg IV/SC for uremic platelet dysfunction, increases serum vWF and enhances platelet aggregation ; Cryoprecipitate, Conjugated Estrogen, Erythropoiten; Hemodialysis; platelets not helpful (quickly defective)

44. DIC • Inappropriate widespread activation of coagulation system, thrombin generation, small vessel thrombosis, consumption of clotting factors/platelets • Concomitant activation of fibrinolytic system, fibrin clots, subsequent bleeding

50. Transfusion Therapy • PRBCs • Platelets • Coagulation Factors/Plasma • Complications