SURGERY: HEMOSTASIS SGD

AUTHOR: RUO

1. What are the major physiologic responses in the 5. Explain the “Y” diagram of coagulation cascade.
hemostatic process?  Coagulation:
 Primary hemostasis o Results in the cleavage of fibrinogen to
 Fibrin formation insoluble fibrin that stabilizes platelet
 Removal of fibrin plug
o Intrinsic pathway:
2. Vasoconstriction is the initial vascular response to injury.  Initiated by exposure of
What are the mediators of vasoconstriction? coagulation factors to
 Vasoconstriction: subendothelial collagen at
o Begins prior to platelet adherence as a site of vascular damage
reflex response to various stimuli o Extrinsic pathway
o Linked to platelet plug and fibrin  Activated by tissue factors
formation (glycoproteins)
o Vasoconstrictors: TXA2, serotonin o The intrinsic and extrinsic pathways
 Released during platelet converge at activation of FactorX
aggregation (factor Xa) which cleaves prothrombin
o Extent and orientation of injury to blood to thrombin
vessel influence the degree of bleeding o All coagulation factors except
thromboplastin, factor VIII and calcium
3. Explain the role of platelets in hemostasis. are synthesized in the liver
 Primary hemostasis: o Factors II, VII, IX and X are vitamin K
o Reversible process not affected by dependent
heparin administration
o Platelets adhere to subendothelial 6. What are the commonly used laboratory tests to detect
collagen of disrupted vascular tissue abnormalities in the intrinsic and extrinsic pathway?
o Requires von Willebrand Factor Platelet count  Assess adequacy of platelets which can
o Platelets expand and initiate release provide hemostasis following trauma or
reaction recruiting additional platelets, surgical procedure if other hemostatic
aggregation forms plug sealing factors are normal
disrupted vessel
 Fibrinogen-dependent degranulation Bleeding time  Assess interaction between platelets and
o Irreversible damaged blood vessels and formation of
o Platelet factor 3 is released platelet plug
o Platelet derived mediators also  Deficiencies in platelet number, formation
influence subsequent fibrinolytic or some coagulation factors will yield
process prolonged bleeding time
4. What are the mediators and inhibitors of platelet adhesion
and aggregation? Prothrombin  Measure extrinsic pathway
Time (PT)  Thromboplastin is added with calcium to
Mediators ADP, TXA2, serotonin aliquot of citrated plasma
Inhibitors (vasodilates) Prostacyclin, EDRF, PGE2  Detects deficiencies in F II, VII, X or
fibrinogen
Partial  Measure intrinsic clotting pathway
Thromboplastin  Determine abnormalities in factors VIII,
Time (PTT) IX, XI and XII

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 Thrombin Time  Screen abnormalities in fibrinogen and
(TT) will detect circulating anticoagulants and
inhibitors of anticoagulation
Tests for  Measures fibrin degradation
fibrinolysis products
 False (+): in liver, kidney
diseases, thromboembolitic disorders and
pregnancy
7. What are the indications of blood replacement therapy?
 Volume replacement
o Most common indication for blood
transfusion
o Hematocrit can be used to estimate
blood loss
o In normal persons, normal reflex allow
the body to accommodate up to
moderate size blood losses
o Significant hypotension develops only
up to about 40% loss of blood
 Improvement in oxygen carrying capacity
o Whole blood substitute, fluosol –DA
provides oxygen carrying capacity in
the absence of blood products
 Replacement of clotting factors
o Supplemental platelets or clotting
factors required in the treatment of
certain hemorrhagic conditions
 Massive transfusion
o Refers to a single transfusion of greater
than 2500 or 5000 ml over a 24-hour
period
8. What are the different banked blood preparations and
components and when are they used?
Fresh whole blood Improve outcomes in patients with
trauma-associated coagulopathy
Provides greater coagulation activity
than equal units of component
therapy
Packed RBC Used for patients who are known to
have been previously sensitized
Fresh frozen plasma Replace labile factors in patients
with coagulopathy and documented
factor deficiency
Leukocyte reduced and Profound granulocytopenia with
leukocyte washed RBC evidence of infection unresponsive
to antimicrobials
Platelet concentrates Thrombocytopenia
Cryoprecipitate Hemophelia A, vWF disease,
hypofibrinogenemia
Hemostasis
9. What are the congenital coagulation factor deficiencies?
Classical Hemophelia  Sex-linked recessive disorder
(Factor VIII deficiency)  Significant bleeding is usually first
noted when subject is toddler
 Hemarthrosis is most
characteristic orthopedic problem
 Retroperitoneal bleeding or
intramural intestinal hematoma
may also occur
Christmas disease  Clinically indistinguishable from
hemophelia A
(Factor IX deficiency)
 Inherited X-linked recessive
disease
Von Willebrand  Autosomal dominant trait
disease  Characterized by abnormal vWF
and decrease in the level of factor
VIII:C (procoagulant)
 Prolonged bleeding time
 Spontaneous bleedings often
limited to skin or mucus membrane
 Epistaxis and menorrhagia are
also common
10. What are the blood products used for the treatment of each
type?
Classical Hemophelia  Cryoprecipitate concentrates of
(Factor VIII deficiency)
factor VIII
Christmas disease  All patients require substitution
therapy when major or minor
(Factor IX deficiency)
surgery is performed
 Treatment should be directed to
achieving levels of 20-50% of
normal for first 3-5 days and then
maintain plasma level of 20% for
approximately 10 days
Von Willebrand  Only cryoprecipitate is effective
disease (10-40 units/kg q12h)
 Should start 1 day before surgery
11. What are the acquired hemostatic defects?
Platelet abnormalities  Most common abnormality of
hemostasis in the surgical patient
(Thrombocytopenia)
 Uremia: affects bleeding time and
platelet aggregation
 thrombocytopenia due to acute
alcoholism, drug effect or viral
infection generally will correct within
1-3 weeks
 severe thrombocytopenia may be
due to vitamin B12 or folate
deficiency may be responsive to
nutrient therapy
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  idiopathic thrombocytopenia or o Seen with a retained dead fetus,
lupus erythematosus may respond separation of the placenta and amniotic
to steroid therapy fluid embolism
o Defibrination has been observed in
Acquired  accompanied by deficiency in association with extracorporeal
Hypofibrinogenemia – factors II, VI, VIII and platelets circulation, disseminated carcinoma,
Defibrination  most patients with acquired lymphoma and a variety of infections
Syndrome hypofibrinogenemia suffer from DIC o Prolonged TT, PTT and PT
(Fibrinogen  prolonged TT, PTT and PT o
Deficiency)  low platelet count, (+) plasma
protamine test, reduced fibrinogen
and increased FDP is highly
suggestive of this syndrome
 if there
Pathologic  reduction in fibrinogen and factors
Fibrinolysis V and VII is seen
 can be seen in patients with
metastatic prostatic carcinoma,
shock, sepsis, hypoxia, neoplasia,
cirrhosis and portal hypertension
 treat by giving EACA, and inhibitor
of fibrinolysis
Myeloproliferative  hemorrhage is the most common
diseases complication in this group followed
by thrombosis and infection
 preoperative use of antiplatelet
agents and anticoagulants has
been suggested in these patients
Liver disease  advanced liver disease may result
in decreased synthesis of
coagulation factors II, V, VII, X and
XIII
 there may also be increased
fibrinolysis due to failure of liver to
clear plasminogen activators

12. Explain the process of fibrinolysis and its end products.

 Fibrinolysis
o Lysis of fibrin deposists and
antithrombin III which maintains
patency of blood vessels
o Fibrinolysis depends on plasmin which
is derived from precursor plasmin
protein plasminogen
o Plasmin lyses fibrin which interfere with
platelet aggregation
13. What are the inhibitors of fibrinolysis?
 Inhibitors:
o PAI-1
o Alpha2-antiplasmin
14. What is disseminated intravascular coagulopathy?
 DIC:
o Caused by introduction of
thromboplastic material into the
circulation

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