Haemostasis in surgery

Surgical hemostasis is one of the pillars of modern surgery. Adequate hemostasis in a surgical patient involves a detailed perioperative clinical evaluation and investigation, and various intra operative techniques and options. Ensuring adequate surgical hemostasis reduces morbidity and mortality by modulating the metabolic response to trauma, decreasing the incidence of post operative anemia, reduces rates of surgical site infection and ultimately improving wound healing

1. HAEMOSTASIS
In Surgery
Dr. Alumona C.

2. OUTLIINE
•INTRODUCTION
–Definition
–Surgical Importance
–Brief History
–Epidemiology
•PHYSIOLOGY OF HAEMSOSTASIS
–Vasoconstriction
–Platelet plug formation
–Coagulation
–Fibrinolysis

3. Outline cont…
•HAEMOSTATIC DEFECTS
–Defective Vasoconstriction
–Defective Platelet Function
–Defective coagulation
•Management of haemostasis in a Surgical Patient
–Pre op Evaluation
•History
•Examination
•Investigations

4. Outline cont…
–Intra Op management
•Surgical technique
•Anesthetic Techniques
•Pharmacological Agents
•Mechanical Techniques
•Blood products
•Post Op Management
•Antibiotics
•Wound care
–Haemostasis in Trauma
•CONCLUSION
•REFRENCES

5. INTRODUCTION
•The process of preventingor terminatingblood loss from an
injured vessel
•Delicate balance between Pro and Anti coagulants
•Congenital and acquired defects result in clinically important
derangements
•Derangements in this process could cause uncontrollable
hemorrhage both spontaneously and on table
•The surgeon has a great role to play

6. Surgical Importance
•Surgical haemostasisis one of the pillars of modern surgery
(others include anaesthesis, antibiotics)
•Adequate surgical haemostasisreduces
morbidity and mortality in post. op patients by
–minimizing blood loss and anemia,
–attenuates the metabolic response to trauma,
–reducing infection and
–improving wound healing.

7. History
•The evolution of modern surgery has followed closely behind
strides in surgical hemostasis
•Ancient medicine men and barber surgeons developed
maneuvers based on intuition to control bleeding in their
patients
•These intuitions informed scientific research and the
elucidation of the hemostatic process and modern
interventions to achieve hemostasis

9. Physiology of Hemostasis
•Involves three (3) interdependent mechanisms
–Initial Vasoconstriction
–Platelet plug formation
–Coagulation/Fibrin formation and Fibrinolysis
•They are interrelated and occur as a
continuum.
•Their products provide multiple
reinforcements.

10. Vaso-constriction
•The initial vascular response to injury.
•Dependent upon local contraction of smooth
muscles.
•Occurs before platelet adhesion to site of injury.
•Effectiveness is dependent on type of vessel,calibre,
perivascular pressure, patternof injury
•Vasoconstrictors: 5-HT, TXA2, bradykinins,
fibrinopeptides, Perivascular pressure

12. Platelet Plug Formation
•Platelets become “sticky” when
exposed to sub-endothelial
collagen to which they become
adherent.
•vWF is necessary for Platelet-
collagen adherence
•The adherent platelets swell,
initiaite a release reaction to
recruit other platelets which
aggregates to form a loose
platelet plug –primary
hemostatic plug

13. Plat. Plug Formation Cont.
•Primary hemostasis
–Forms loose platelet plug
–Reversible and does not involve secretion
–ADP & 5-HT are principal mediators
–Heparin does not interfere with this process
–Aspirin & NSAIDS are both inhibitory
(Aspirin causes irreversible blockade)

14. Plat. Plug Formation Cont.
•Release reaction
–Platelets degranulatesreleasing powerful
mediators
–The Platelet plug becomes compacted to form an
irreversible amorphous plug.
–Mitigated by ADP, platelet factor 4, trace
thrombin, in the presence of Ca2+, Mg2+
–Products include: platelet factor 3 & 4,
thromboglobulin, PDGF, ADP, 5-HT, Ca2+
–Process is inhibited by cAMP

15. Coagulation/Fibrin Formation
•Aims to convert prothrombininto the
proteolytic enzyme thrombin.
•Thrombin cleaves fibrinogenmolecules to
insoluble fibrin
•fibrin provides stability to the platelet plug.
•Involves two pathways:
–Intrinsic Pathways (factors VII, X, II)
–Extrinsic Pathways (factors XII, XI, IX, X and II)

16. Fibrin Formation
& pf3
& Ca
Antithrombin &
plasma protease
inhibitor
Thrombomoduli
n (binds
thrombin
prevents it from
cleaving
fibrinogen)
Protein C (-ve to
fx V&Viii)
FxV acceleartes
thrombin
inhibition

17. Fibrinolysis
•Aim is to maintain patency of blood vessels by
lysisof fibrin deposits
•Initiated from start by circulating kinases, tissue
activators, and kallikrein.
•Dependent on Plasmin which lyses fibrin to
produce fibrin degradation end products
•Smaller products interfere with platelet
aggregation while the larger products
incorporates into the clot resulting in unstable
clots

18. Management of hemostasis In a
Surgical Patient

19. Pre Op Evaluation
•History
–Hx of abnormal bleeding, prolonged bleeding, easy bruising, mucosal
bleeds, menorrhagia
–Hx of coagulation disorder in relatives
–Hx of use of anticoagulant
–Hx of chronic diseases such as CKD, CVDs, CLD, HTN
–Hx of use of drugs eg cytotoxics, anticoagulants
•Examination
–General examination (anemia, jaundice, asterixis, anasarca)
–Skin: ecchymosis, stigmata of cld
–Abd: Hepatomegaly, splenomegaly, ballotable kidneys
–Bed side bleeding time (1-9min, up to 13min in children)

20. •Investigations
–General: CBC, LFT, EUCr, Abd USS
–Specific -tests of hemostasis
•CT (8-15min)
•PT (VII, X, II) (9.6-11.8sec)
•PTT (XII, XI, IX, X & II) (20-36sec)
•INR, Fx assays, fibrinogen level, Clot elastography and elastometry,

21. Hemostatic Defects

22. Defective Vasoconstriction
•Idiopathic Hemorrhagic Telengiectasia/ Osler
Weber Rendusyndrome
•low perivascular pressure in muscular
dystrophy, ehlers-Danlossyndrom, elderly,
prolonged steriodtherapy

23. Defective Platelet Function
Congenital:
•Bernard Souliersyndrome (GP 1b/IX/V rcptfor
vWF),
•GlanzmanThrombastenia(GP IIb/IIIA)
•Storage pool disease: Dense and αgranules
(occur with partial albinism in Hermansky-
Pudlaksyndrome)
•Trx: DDAVP(desmopressin), platelet
concentrate

24. defective platelet function cont
Acquired platelet disorders.
A.Quantitative Disorders:
1.Failure of production: (related to impairment in
bone marrow functiona):
•Leukemia.
•Myeloproliferativedisorders.
•B12 or folatedeficiencies.
•Chemotherapy or radiation therapy.
•Acute alcohol intoxication
•Viral infections

25. defective platelet function cont
2.Decreased survival.
•Immune-mediated
–Idiopathic thrombocytopenia (ITP)
–Heparin-induced thrombocytopenia
–Autoimmune disorders or B-cell malignancies
–Secondary thrombocytopenia.
•Disseminated intravascular coagulation (DIC)
•Related to platelet thrombi
–Thrombocytopenic purpura(TTP)
–Hemolyticuremic syndrome (HS)

26. defective platelet function cont
3.Sequestration.
•Portal hypertension.
•Sarcoid.
•Lymphoma.
•Gaucher’sDisease.
B.Qualitative Disorders
•Massive transfusion
•Therapeutic platelet inhibitors (aspirin, clopidogrel, prasugrel
dipyridamole, GP IIb/IIIainhibitors)
•Disease states
•Myeloproliferativedisorders
•Monoclonal gammopathies
•Liver disease, ureamia

27. Coagulation Factor Deficiencies
Congenital
–*HaemophiliaA (FxVIII deficiency)
–Von willibrandsDisease (trx: desmopressin& vWF
concentrate)
–*HaemophiliaB (FxIX deficiency/Christmas disease)
–HaemophiliaC (FxXI deficiency) (trx: FFP)
•Acquired
–VitK Deficiency (FxII, VII, IX & X; III, VIII, XI, Protein C,
fibrinogen)
–Ureamia
–Massive Blood Transfusion
–DIC

28. Intra operative Mgt

29. •Anesthetic Techniques
–Posture/Position
–Permissive hypotension
–Intermittent positive pressure ventilation
–Pneumoperitoneum
–Normothermia
–Anaesthetic agent: Regional anesthesia,
L/A+adrenaline, GA: propofol

30. •Pharmacologic methods
–Traxenamic acid
–∑-Aminocaproic acid
–Aprotinin: serine protease inhibitor directly
inhibits free plasmin
–Recombinant factor VIIa (rFVIIa)
–Vit K

31. •Surgical techniques
–Appropriate dissection
–Compression/Pressure and maneuvers
–Vascular clamps and forceps
–Intraluminal balloons
–Arterial ligation
–Diathermy
–Minimal access surgery

32. •Topical agents
–Surgicel (oxidized cellulose)
–Gelfoam (gelatin foam)
–Avitene (microfibrillar collagens)
–Topical thrombin
–Fibrin sealant
–Platelet sealant
–Human recombinant thrombin derivatives

33. •Mechanical Factors
–Digital pressure
–Pringle maneuver
–Preassure packing
–Limb elevation
–Limb exsanguination
–Tourniquets

34. •Blood products
–FFP
–Platelet concentrates
–Factor concentrates

35. Post Op Managementt
–Antibiotics
–Wound care
–Elevation

36. Hemostasis in trauma
•Pre hospital use of traxenamic acid
•PCC
•Damage control resuscitation
–Prompt mechanical or surgical hemorrhage
control
–Permissive hypotension
–Minimalistic crystalloid/ synthetic colloid based
resuscitation
–Early use of blood products in the ration of 1:1:1
of PRBC:FFP:Platelets

37. Conclusion
•It is the responsibility of the surgeon to
preempt surgically important haemorrhage,
employ multiple modalities to prevent it, and
arrest it when it does occur.

38. REFRENCES
•Schwartz: Principles of Surgery, 7/e © 1999 by
The McGraw-Hill Companies, Inc.
•FARQUHARSON’S TEXTBOOK OF OPERATIVE
GENERAL SURGERY 10
TH
EDITION Margaret
Farquharson, James Hollingshead and Brendan
Moran {CRC Press Taylor & Francis Group 6000
Broken Sound Parkway NW, Suite 300 Boca
Raton, FL 33487-2742 © 2015 by Taylor & Francis
Group, LLC}
•Medscape