Alyana Ellaine S.

Matias, MD
1. Vascular Constriction
2. Platelet Plug Formation
3. Fibrin Formation
4. Fibrinolysis
 initial response to vessel injury

 Contributing factors:
 THROMBOXANE A2 (TXA2)
 ENDOTHELIN
 BRADYKININ AND FIBRINOPEPTIDES
 COAGULATION FACTOR DEFICIENCIES
1. Factor VIII Deficiency (Hemophilia A and von
Willebrand’s Disease)
2. Factor IX Deficiency ( Hemophilia B or Christmas
Disease)
3. Factor XI Deficiency
4. Factor II (Prothrombin Deficiency)
5. Factor VII Deficiency
6. Factor XIII Deficiency
 Sex-linked recessive disorders (Males)
 Plasma factor level:
 SEVERE: <1%
 MODERATE: 1-5%
 MILD: 5-30%

 (+) N platelet function

 TREATMENT:
 Factor VIII or factor IX concentrate
 MOST COMMON congenital bleeding  TYPES:
disorder
1. TYPE I: Quantitative
2. TYPE II: Qualitative
 Defect in vWF, a large glycoprotein
responsible for carrying factor VIII 3. TYPE III: Total Deficiency
and platelet adhesion.

 SYMPTOMS:
 easy bruising
 mucosal bleeding
 Menorrhagia: common in women
 prevalent in the Ashkenazi Jewish population but found in all races.

 RARE spontaneous bleeding,

 but bleeding may occur after surgery, trauma, or invasive procedures

 TREATMENT: FFP
 RARE (AR)  RARE (AR)

 TREATMENT: FFP
 Bleeding is uncommon unless the level is less
 GOAL: 20% to 25% activity. than 3%.

 MC manifestations:
 easy bruising
 RARE (AR)
 mucosal bleeding (epistaxis or oral mucosal
 male-to-female ratio is 1:1. bleeding)
 Delayed bleeding because clots form normally  Postoperative bleeding is also common,
but are susceptible to fibrinolysis reported in 30% of surgical procedures
 Umbilical stump bleeding, Spontaneous
abortion
TRATMENT: FFP or recombinant factor VIIa.
 TREATMENT: FFP, cryoprecipitate, or a factor
XIII concentrate.
1. Thrombasthenia/ Glanzmann 2. Bernard-Soulier syndrome
thrombasthenia

 GP Ib/IX/V receptor for vWF,

 Rare (AR)

 platelet glycoprotein IIb/IIIa (GP IIb/IIIa)  DEFECT: platelet ADHESION to the

complex subendothelium

 DEFECT: platelet AGGREGATION

 NORMAL platetet count  TREATMENT: Platelet Transfusion

 TREATMENT: Platelet Transfusion

 systemic activation of coagulation pathways that result in excessive thrombin
generation and the diffuse formation of microthrombi

 Consumption and depletion of coagulation factors and platelets

 DIAGNOSIS:
1. Thrombocytopenia,
2. Prolongation of the prothrombin time
3. Low fibrinogen level
4. Elevated fibrin markers (FDPs, D-dimer, soluble fibrin mono- mers).
Polycythemia
 excess of red blood cells

 Sequelae:
 increased blood viscosity,
 increased platelet count,
 increased tendency toward stasis

 Thrombocytosis can be reduced by:

 low-dose aspirin
 phlebotomy,
 hydroxyurea.27
 MC abnormalities: Thrombocytopenia and Impaired Humoral Coagulation Function

 Prolonged PT and increase INR

 acidosis, hypothermia, and dilution of coagulation factors

 SHOCK : induces coagulopathy through systemic activation of anticoagulant and

fibrinolytic pathways

 HYPOPERFUSION: causes activation of THROMBOMODULIN on the surface of

endothelial cells.
 Thrombin-TM complexes  induce an anticoagulant state  activation of protein C and
enhancement of fibrinolysis.
 Anticoagulant therapy : Heparin, Warfarin or low molecular weight heparin

 WARFARIN: inhibits Vitamin K epoxide reductase --> interfere with production of

functional Vitamin K dependent clotting and anticlotting factors

Cytochrome Ethanol Cytochrome Isoniazid

P450 Inducers Barbiturates P450 Inhibitors Sulfonamides
Phenytoin Cimetidine
Rifampicin Ketoconazole
Griseofulvin Erythromycin
Carbamazepine Grapefruit huice
St. John’s Wort/ Ritonavir
Smoking Amiodarone
Quinidine
 Bleeding complications manifested as:
 Hematuria
 Soft tissue bleeding
 Intracerebral bleeding
 Skin necrosis
 Abdominal bleeding

 MC complication of Warfarin Therapy: Bleeding into the abdominal cavity

 MC cause of Abdominal Pain in patients receiving anicoagulation therapy:

Intramural Hematoma
 REVERASAL OF HEPARIN THERAPY
NOT indicated when aPTT is <1.3 times the control value
Emergency Surgery Discontinue drug and use of protamine sulfate
for more rapid reversal of anticoagulation
REVERSAL OF WARFARIN THERAPY
Not indicated when the INR is <1.5
Elective Surgery Discontinue drug several days before the OR
with monitoring of prothrombin concentration
Parenteral administration of Vitamin K is
indicated in patients with biliary obstruction
or malabsorption who may be vitamin K
deficient
Low molecular weight heparin should be
administered while the INR is decreasing in
patients with high risk of thrombosis
Emergency Surgery Rapid reversal of anticoagulation can be
accomplished with FFP
 LOCAL HEMOSTASIS

 MECHANICAL HEMOSTASIS

 THERMAL HEMOSTASIS

 TOPICAL HEMOSTASIS
IMPROVEMENT IN OXYGEN CARRYING
CAPACITY
Treatment of Anemica
Volume Replacement
O2 casrrying capacity is a primary fuction
ogf RBC
Threfore transcusion of RBC should
augment o2- carrying capacity
Hgb 9 g/dl
MC INDIDCATION FOR BT IN SURGICAL
PATIENTS IS THE REPLENISHMENT OF THE
BLOOD VOLUME
Estimated blood volume is 7-8% of TBW
Blood loss up to 20%of total blood volume:
replace witg crystalloid solution
Blood loss >20% of total blood volume:
addition of packed RBC and in the case of
massive transfusion, the addition of FFP