This document discusses hemostasis in surgical patients. It begins by defining hemostasis as the state of fluid equilibrium within blood vessels. It then describes the two mechanisms of hemostasis - primary hemostasis involving vasoconstriction and platelet plug formation, and secondary hemostasis involving activation of the coagulation cascade and formation of a fibrin clot. The document outlines the coagulation cascade and its natural inhibitors. It discusses various defects of hemostasis, preoperative screening tests for bleeding risk, and strategies to achieve surgical hemostasis including direct pressure, cauterization, packing, topical hemostats, and fibrin glue.

1. Hemostasis in the Surgical
Patient
Amr Aborahma , MD
Lecturer of Vascular Surgery

2. WHAT ARE YOUR EXPECTATIONS ?

4. Hemostasis in the Surgical Patient
Is It An Important Topic ?

5. From your point of view !!

6. Does All bleeding (eventually)
stops ?

7. Bleeding Clotting
Hemostasis
Under normal conditions, blood circulates
through the intact vasculature without
thrombus formation or haemorrhage

8. Hemostasis
State of fluid equilibrium within the blood vessels
Vessels
Coagulation
Proteins Platelets
Fibrinolysis/ Inhibitors

9. Hemostasis
A process which causes bleeding to stop
Primary Hemostasis
Arteriolar vasoconstriction
Formation of platelet plug
Secondary Hemostasis
Activation of coagulation cascade
Formation of permanent plug

11. Constriction of vessels
There are 2 mechanisms for vessel
constriction:
– Local smooth muscle contractile response
– Thromboxane A2 release from endothelium

12. Formation of platelet plug
Exposure of the subendothelial layers cause platelets
to adhere.
They release ADP and TxA2, inducing further platelet
aggregation and activation
Adhesion requires von Willebrand factor (vWf) from
the subendothelial layers.

13. The time taken for platelet plug to form
(Bleeding Time - BT) gives a non-specific
indication of:
• The state of the vascular endothelium
• The number of platelets in the circulation
• The platelets are functioning correctly (can
release granules and produce pseudopodia)
• Demonstrates the presence of vWF

14. Coagulation Factors
Factor I Fibrinogen
Factor II Prothrombin
Factor III Tissue Thromboplastin
Factor IV Calcium Ions
Factor V Labile Factor, Proaccelerin
Factor VII Stable Factor, Proconvertin
Factor VIII Antihemophilic Factor
Factor IX Christmas Factor
Factor X Stuart-Prower Factor
Factor XI Plasma Thromboplastin Antecedent
Factor XII Hageman Factor
Factor XIII Fibrin Stabilizing Factor
All coagulation factors are made in the
liver, except for vWF

15. Clotting cascade
Intrinsic Pathway
– All factors occur from within the circulation
– in vivo, the pathway is triggered by exposure of "contact factors"
to collagen or basement membrane at the site of injury or a
foreign substance such as a prosthetic device
Extrinsic Pathway
– Requires tissue thromboplastin to be released from damaged
cells (outside the circulation)
Both pathways lead to the activation of prothrombin
(factor II)
Final common pathway converts fibrinogen to fibrin

16. Clotting cascade

17. Natural inhibitors of the coagulation cascade
 Thrombomodulin
 Antithrombin III
 Tissue factor pathway inhibitor
 Protein C
 Protein S

18. Which is moving?

19. Natural inhibitors of the coagulation cascade
 Antithrombin III is a large protease inhibitor that inhibits
thrombin and factors IXa, Xa, XIa, and XIIa but does not
inhibit thrombin within clots
 Heparin accelerates the reaction time of
antithrombin III 1000 fold

20. Natural inhibitors of the coagulation cascade
 Protein C and Protein S
 Vitamin K-dependent serine proteases synthesized
in the liver
 Circulate as inactive forms (zymogens)
 Protein C
 inhibits the activity of factors Va and VIIIa
 Protein S
 cofactor that potentiates the action of Protein C

21. Take A Break !!!
Watch this video

23. Defects of Hemostasis
Congenital disorders
Hemophilia A,B
von Willebrand disease
Acquired disorders
Hepatic disorders
DIC
Vitamin K defeciency
Anticoagulants
Massive blood transfusion
Platelet disorders

25. Preoperative screening for bleeding risk
 Complete history and physical
Eckman et al. Ann Intern Med Vol 138, No 5

26. Preoperative screening for bleeding risk
 Incidence of a significant hereditary deficiency of a
coagulation factor is low (1 per 10,000-40,000)
 approximately 1/3 of these are asymptomatic
 Acquired deficiencies of factors should be suspected in the
presence of advance hepatic disease, malabsorption, or
malnutrition

27. Hemostasis Screening Tests
• Bleeding Time
• Clotting Time
-Vascular
Platelet Count -Platelet
PT -Coagulation factors
-Fibrinolysis
APTT
TT
Euglobulin Clot Lysis Time
D = Dimer

28. Clinical testing and preoperative screening
 Prothrombin time (PT)
 measure extrinsic and common pathways
 affected by low concentrations of fibrinogen, prothrombin
and factors II, V, VII, X
 Activated partial thomboplastin time (aPTT)
 measures intrinsic and common pathways
 deficiencies in all clotting factors except factors VII and
XIII may prolong the aPTT

29. Surgical hemostasis

30. Stopping the bleeding
Direct pressure.
More direct pressure. Pack. Pack. Pack.
Electrocautery.
Ligate vessel

31. Methylcellulose
Gelfoam
– Absorbable
– Liquefies in 2-5
days
– Serves as a
scaffold for
coagulation

32. Oxidized regenerated cellulose
Surgicel
– Binds platelets and chemically precipitates
fibrin

33. Microfibrillar collagen
Decellularized bovine source
Stimulates latelet adhesion
Stops venous ooze
Absorbed in 90 days

34. Thrombin + Gelfoam + CaCl
Thrombin for cleavage/activation
Gelfoam as matrix
Very useful in vascular surgery

35. Fibrin glue
Tiseel
FDA approved in 1998
Concentrated fibrinogen and f VIII
Thrombin and calcium
Aprotinin to prevent clot dissolution
Takes time to prepare
Good for diffuse oozing, needle punctures,
parenchymal injuries

36. Questions

37. What is your feedback?

39. Thank You
Email: amr.aborahma@gmail.com