1. Hemostasis, Surgical Bleeding, and Transfusion
Patrick Chidi Obasi

2. Hemostasis
Complex process that prevents blood loss from disrupted intravascular space.
Major physiologic events:
Primary hemostasis
Vascular constriction
Platelet plug formation
Secondary hemostasis
Fibrin Formation
Fibrinolysis

3. Vascular constriction
Initial vascular response to injury
Linked to platelet plug formation
Thromboxane A2 (TxA2), Serotonin, 5-hydroxytryptamine (5-HT), Bradykinin

4. Platelet Plug Formation
Conversion of cyclooxygenase to TXA2=> stimulates platelet motility and binding (aggregation)
Activated platelets adhere to fibrinogen via GP IIa/IIIb.
Plts adhere to von Willebrand factor on exposed collagen via glycoprotein (GP) Ia/IIa receptor
Adhesion results in the release of agonist like epi, collagen, thrombin, ADP, Serotonin
Platelet cyclooxygenase irreversibly inhibited by ASA and reversibly by NSAIDs

5. Coagulation/Fibrin Formation
Extrinsic pathway
Tissue factor (injured cells) + factor VII
Activates factors X and V
Converts prothrombin to thrombin
Thrombin then converts fibrinogen to fibrin
Elevated PT associated with abnormal extrinsic pathway cascade

6. Coagulation/Fibrin Formation
Intrinsic pathway
All components intrinsic to the circulating plasma
HMW kininogen + factor XII (Hageman factor) bind to exposed collagen
Activation of factors XI, IX + VIII => X+V
Convert prothrombin (factor II) to thrombin
Thrombin cleaves fibrinogen to fibrin
Abnormal measured by a PTT

7. Fibrinolysis
Plasminogen level known to rise as a consequence of exercise, occlusion, and anoxia
tPA-released from endothelium converts plasminogen to plasmin
Plasmin degrades factors V and VIII, fibrinogen and fibrin-leading to lose plt plug

8. Notes on Coagulation Factors
Factor II aka prothrombin
Factor III aka antithrombin
Heparin binds to AT III
Deficiency results in spontaneous thrombosis
Treat def with FFP (has AT-III) and then heparin

9. Notes on Coagulation Factors
Factors V-labile factor
Factor VI – shortest half life. Begins extrinsic pathway
Factor VIII – labile factor
-- only factor not synthesized in liver (made in endothelium)
Factor X – Convergence point for both pathways
Factor XII – aka Hageman factor. Begins intrinsic pathway
Factor XIII – Helps crosslink fibrin

10. Local Hemostasis
Goal is to prevent or interrupt the flow of blood from a disrupted vessel that has been incised or transected
Digital pressure effective and has adv. of being less traumatic
Hemostat, hemoclips, transfixion sutures (prevents slipping)
The adventitia and media constitute the major holding forces in a vessel wall

11. Local Hemostasis
Thermal agents: Harmonic scalpel, electrocautery bovie (causes collagen denaturing leading to coagulation)
Direct cooling with iced saline causes vessels to undergo necrosis by dehydration and destruction of lipid molecules
Chemical agents: epi (induces vasoconstriction), gel foam, surgicel, topical thrombin, fibrin sealant)

12. Heparin Therapy Potentiates action of AT III
Inhibited by admin of protamine (1mg of protamine:100 units of heparin for reversal)
Measured by aPTT
Want PTT between for anticoagulation
Does not cross placental barrier
Stop 4-6 hours before surgery

13. HIT/HITTS
Due to antiplatelet antibodies (IgG) that results in plt destruction
Can cause plt aggregation and thrombosis (“white clot”)
Typically seen 5 to 7 days in first exposure
May occur within 1 to 2 days in re-exposure
Suspected if plt count falls more than 100k or drops by 50% from baseline
LMWH (Lovenox) still at low risk
Tx: stop heparin, start lepirudin/Hirudin, argatroban, dextran

14. Coumadin Therapy
Inhibits cyclo-oxygenation (decarboxylation) step in Vit K synthesis of coag
Effects reversed by Vit K admin
Stop 7 days before surgery
Measured by INR
INR >1.5 – contraind. for surgery
INR >1.3 – contraind. for central line placement, perc. needle bx and eye surgery
Teratogenic

15. Warfarin-induced skin necrosis
Occurs when pt is placed on coumadin without heparin first
Due to short ½ of prot. C and S, which are first to decrease in levels compared with the procoagulants (factors II, VII, IX and X)
Above results in relative hyperthrombotic state
Tx: Heparin if it occurs, prevent by heparinizing first

16. Hypercoagulability Leiden Factor Polycythemia vera
Resistance to activated prot C and S
Spont venous thrombosis
Most commoncongenital hypercoagulability disorder
Tx: heparin, warfarin
Polycythemia vera
Defect in plt function
Can have thrombosis/bleeding
Keep Hct<48 and plts <400 before surgery
Tx: ASA

17. Hypercoagulability AT-III Pts have spont venous thrombosis
Heparin does not work
Tx: AT-III conc, FFP then followed by Heparin

18. Hypercoagulability Lupus Anticoagulant (Procoagulant)
Antiphospholipid antibodies
Prolonged PTT in the face of hypercoag state
Dx: Prolonged PTT not corrected by FFP
Tx: Heparin, coumadin
Acquired hypercoag: Tobacco, malignancy, IBD, infections, post-op state

19. DVT Stasis, venous injury, hypercoagulability
Risk factors include cancer (#1), obesity, varicose veins, history of DVT, immobility
Most common site in post-op pt is the pop vein
Activated prot C resistance due to factor V leiden def is the most common cause of idiopathic recurrence
Dx/Tx:

20. PE
Presents with SOB, tachycardia, hypoxemia, normal or decreased PaCo2
Most common from above knee (iliofemoral region)
Dx/Tx
Indication for surgical procedure
When filters are indicated
Pt who have undergone pulm emboletomy
Pts with contraindication for anticoagulation
PE while on anticoagulant
Free floating above knee DVT

21. PRBC Storage 1 Unit of PRBC has a vol of 250 ml
Storage life is about 35 days
↑K+, ↓ pH, ↓ 2.3-DPG level (↓ O2 del capacity), ↑ IL-1, and IL-6
Each unit expected to raise H/H by 1gm/3%
Fever without hemolysis is the most common transfusion reaction
Acute hemolysis is the most common cause of transfusion related death
Hypotension, shock, dyspnea, bronchospasm, dizziness and flushing are sign of hemolysis
Tx: Supportive