SURGERY

TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm

OUTLINE HEMOSTASIS
I. Hemostasis  Arrest of bleeding either by
a. Factors Affecting Hemostasis physiological properties of
Response vasoconstriction and coagulation or
b. Vascular Constriction
surgical means.
c. Platelet Function
II. Mechanism of Blood Coagulation  Cessation of blood flow from an
a. Extrinsic Mechanism injured blood vessels.
b. Intrinsic Mechanism  Contraction of blood vessels – first
c. Role of Calcium step in hemostasis due to release of
III. Summary of Blood Clotting Initiation vasoconstrictor substances (e.g.
IV. Conditions That Cause Excessive thromboxane – product of
Bleeding prostaglandin metabolism).
a. Liver disease
b. Hemophilia Factors Affecting Hemostasis Response
c. Thrombocytopenia  Clinical condition of the patient.
V. Tests of Hemostasis and Blood  Nature of the result to the blood
Coagulation vessel.
a. Bleeding Time
 The type of blood vessel injured
b. Rumpel - Leed
c. Platelet Count  Coagulation mechanisms.
d. Prothrombin time  Fibrinolytic activity.
e. Partial Prothrombin Time  Primary hemostasis – formation of
VI. Evaluation of the Surgical Patient as a platelet plug.
Hemostatic Risk  Secondary hemostasis – result in
a. General Considerations intrinsic and extrinsic pathway that
b. Cases of Bleeding during the leads to clot formation.
Operation  Biology of hemostasis
c. Complications of Blood Transfusion
d. Massive Blood Transfusion The four physiologic processes that
VII. Coagulation Factor Deficiencies interrelate to limit blood loss from an injured
a. Classic Hemophilia vessel are:
b. Von WilleBrand Disease  Vascular contrcition
c. Factor IX Deficiency
d. Factor XI Deficiency  Platelet plug formation
e. Acquired - Defibrination Syndrome  Fibrin clot formation
 Fibrinolysis

LEARNING OBJECTIVES
1. To learn about the processes and
mechanism of hemostasis which
involved around Platelet and Clotting
System
2. To know the laboratory tests and
conditions concerning hemostasis
3. To learn about the complications, risk
and considerations about surgery
towards hemostasis
Vascular Constriction
 Vascular constriction is the initial
response to vessel injury. It is more
pronounced in vessels with medial
smooth muscles and is dependent on
local contraction of smooth muscle.
 Vasoconstriction is subsequently
linked to platelet plug formation.
Platelet Function
 Platelets are anucleate fragments of
megakaryocytes. The normal

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
circulating number ranges between o Third Stage
150,000 and 400,000/L.  Conversion of fibrinogen to
 Normally removed by the spleen. fibrin.
 Factor XIII – stabilize the clot
 Ave. life span of 7 to 10 days.
formed.
 Up to 30 percent of circulating Basic theory – balance bet. procoagulants
platelets may be sequestered by and anticoagulants.
spleen.
Steps
Principal mediators in platelet aggregation  Prothrombin activator – is formed in
response to rupture of blood vessels
 ADP or damage to blood itself.
 Serotonin  Prothrombin activator catalyzed
convertion of prothrombin to
Mechanism of Blood Coagulation
thrombin.
 Extrinsic mechanism
 Thrombin acts as enzyme to convert
o Release of tissue thromboplastin
fibrinogen to fibrin to form clot.
(phospholipid and glycoprotein)
from traumatized tissues. Role of calcium
o Contact of blood to damaged  In the absence of Ca clotting will not
endothelial cells or tissue outside occur.
blood vessels.
o Tissue thromboplastin III with Ca Summary of Blood Clotting Initiation
converts to VII to VIIa which in
turn converts X to Xa after which
INTERNATION SYNONYM
extrinsic and extrinsic mechanism
AL NUMBERS
becomes identical.
I Fibrinogen
 Intrinsic mechanism – involves
II Prothrombin
components in the blood. III Thromboplastin
o First Stage IV Calcium
 Two system works V Labile Factor,
simultaneously and initiates Proaccelerin
series of rapid reaction in a VI Activated Labile
cascade fashion. Factor, Accelerin
 Factor XII of Intrinsic System VII Stable Factor,
(IS) is acted upon by foreign Proconvertin
surface (e.g. exposed collagen VIII Antihemophilic
or basement membrane). Factor
 Factor VIII of ES initiate IX Christmas Factor,
activation of Factor X by
Plasma
interaction with tissue juices.
Thromboplastin
 End Point: Activation of Component (PTC)
Factor X.
X Stuart Power
o Second Stage
Factor
 Generation of thrombin from
XI Plasma
prothrombin due to the
Thromboplastin
activation of active X, V, Ca
Antecedent (PTA)
and phospholipid.
XII Hageman Factor
XIII Fibrin Stabilizing
Factor

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
Intrinsic: contact factor XII, Ag-Ab reaction,  Fibrin threads
slow speed o Adsorb thrombin, reducing active
Extrinsic: tissue thromboplastin, thrombin in the plasma.
rapid:immediate
 Antithrombin III
o Antithrombin heparin cofactor -
deactivate thrombin by
combination.
 Heparin
o Secretion of mast cells.
o Combines with antithrombin III
to:
 Inhibit thrombin
 Prevent formation of
intrinsic system

XI and XIII
 Formed only in intrinsic system.
 Produced contact activation product.
 Immediate cause of activation of other
factors I intrinsic system.
 React only when adhered to wettable
surface.
XIII
 Released by platelets.
 Cause across linkage in adjacent fibrin
threads.
 Blood clot
o Network of fibrin threads,
entrapping plasma, platelets, RBC.
 Serum
o Fluid expressed from a clot – clot
retraction.
o Straw colored, fibrinogen and
clotting factors affected.
Plasminogen Activators
 Thrombin
 Activated factor XII
 Lysosomal enzymes from damaged
tissues
 Factors from vascular endothelium
 After 1 to 2 days these activator
usually cause the formation of enough
plasmin – clot dissolution.
 Other plasmiogen activators –
streptokinase
Significance of Fibrinolysis System
 Remove very minute clots from minute
blood vessels.
Conditions That Cause Excessive Bleeding
 Liver Disease – hepatitis, cirrhosis
o Almost all clotting factors are
formed in the liver thus – clotting
factor deficiency.
o Vitamin K deficiency.
o Vitamin K is needed to promote
formation of 4 clotting factors II,
VII, IX, X.
o Synthesized by bacteria in the
GIT.
o Causes:
 Biliary tract obstruction –
decrease blood flow into the
small instine

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
 Severe liver disease.
 Dec factor absorption –
decrease vitamin K trauma.
absorption.
 Hemophilia
o Bleeding tendency that occur
exclusively in males.
o Transmitted genetically by female
chromosome as recessive trait.
o Deficient factor VIII – Hemophilia
A or Classic haemophilia.
 Thrombocytopenia
o Tendency to bleed in small
capillaries.
o Small punctuate hemorrhages –
thrombocytopenic purpura.
o Normal – 150000 to 350000/ cu
mm.
o Bleeding occurs when platelet
count fall below 50,000.
Tests of Hemostasis and Blood Coagulation
 Bleeding Time
o Time required for bleeding to
cease after standard skin incision.
o Time required for compaction of
platelet plug.
o Duke Technique : 2-3mm in
dependent portion of earlobe;
measure time blood flow cease.
o Aspirin ingested within 1 week
will affect result.
o Normal value if platelet count is
>75,000/cu mm.
 Rumpel - Leed
o Tourniquet Test
o Estimate capillary permeability.
o Abnormal in decreased platelet.
o BP cuff upper arm inflated
between systolic and diastolic BP
for 5 minutes.
o POSITIVE if > 2-4
petechiae in circle of 2-5
cm in diameter in
forearm.
 Platelet count
o Normal: 160,000 – 350,000/cu
mm.
o >60,000-70,000/cu mm =
Adequate hemostasis following
 Whole Blood Coagulation
o Lee White Method
o Venous blood from clean
venipuncture.
 Tilt tube for 30seconds
until no flow of blood is
observed.
o Measured intrinsic coagulation
system.
o Normal Value : 9-14 minutes (
Factors XII, XI, IX, VIII)
 Prothrombin Time (Extrinsic
Pathway Integrity)
o One Stage Quick Test
o Measures the time for a gross
clot in a citrated plasma after
calcium and standard
thromboplastin (tissue) is
added.
o Measures the events of the
extrinsic pathway reflecting the
functions of Factors II, V, VII, X
and fibrinogen.
 Preferred method of
controlling anticoagulation
with warfarin.
 Partial Prothrombin Time
(Intrinsic Pathway Intergrity)
o Detects deficiencies in Factors
VIII, IX, XI and XII.
o Screens for intrinsic pathway
abnormalities reflecting the
level of factors VIII, IX, XI, XII in
addition to II, V and X.
o Prolonged by heparin
administration and can be used
to monitor its efficacy.
EVALUATION OF THE SURGICAL
PATIENT AS A HEMOSTATIC RISK
“No single test can detect suspected bleeder,
the best way is by complete history and PE.”
General Considerations
The patient’s history provides meaningful
clues to the presence of a bleeding tendency.

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
 Prolonged bleeding or swelling after
biting the lip or tongue.
 Bruises without apparent injury.
 Prolonged bleeding after dental
extraction.
 Excessive menstrual bleeding.
 Bleeding problems associated with
major and minor operations.
 Medical problems receiving
physician’s attention within the past 5
years.
 Medication including aspirin or
remedies for headache taken within
the past 10 days.
Evaluation of the patient who bleeds
during or after surgical procedures
 Bleeding from surgical wounds
suggest ineffective local hemostasis
except in prostatic bed where
prostate borne plasminogen
activators can be activated by
urokinase.
Cases of Bleeding during the Operation
 Ineffective local hemostasis.
 Complications of blood
transfusions.
o Banked blood 10 units or more in
less than 24 hours – decrease
platelet patients in whom signs of
hemostatic failure develop during
or following operation what large
quantities of blood have been
used should be assumed to be
thrombocytopenic until
demonstrated otherwise.
o Hemolytic transfusion reaction –
hemolyzed RBC is rich in
procoagulant.
 Previously present but
unsuspected hemostatic defect
o Evidence of bleeding e.g. sites of
venipuncture, NGT, catheters.
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 Sepsis
o Endotoxin induced
thrombocytopenia – DIC-
hemolysis leads to defibrillation.
o Meningococcemia, clostridium
welchii, staphylococcal sepsis.
Management
 Local Hemostasis
a o Mechanical procedures
 Direct pressure
 Ligatures
o Thermal agents, Cautery and
Cryosurgery
o Chemical agents (Epinephrine,
Gelatin foam)
 Transfusion of blood
o Background
 June 1667 Jean-Baptiste
Denis and a surgeon,
Emmerez, transfused blood
which cause transfusion
reaction
 In 1990 - Dr.Karl
Landsteiner- identified the
major A, B, and O groups
 In 1939 - Dr.philip Levine
and Dr. Rufus Stetson –RH
grouping
 Replacement Therapy
o Serologic compatibility for A, B, O,
and Rh groups is established
routinely.
o In emergency situations, Type O
negative blood may be transfused
to all recipient - O negative or
type specific blood.
 Autologous Blood Transfusion
o Up to 5 units can be collected.
 Banked Whole Blood
o Once a gold standard, rarely
available, shelf life is now
around 6 weeks.
o At least 70 percent if the
transfused erythrocytes remain
1/9
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
in the circulation for 24 hours  Packed Red Cells and Frozen Red
after transfusion and are viable. Cells
o Blood Preservatives o Concentrated RBC suspension
 ACD –Acid Citrate Dextrose prepared by removing the
supernatant plasma citrate.
 CPD – Citrate Phosphate
o To increase patient’s oxygen
Dextrose carrying capacity.
 Stored at 2 – 4 degree o Treatment of anemia without
Celsius for 21 days. hypovolemia.
 1978 CPDA-1 with Adenine o Decrease incidence of
 Synthesis of ATP, transfusion reactions.
 Platelet Rich Plasma and Platelet
prolonged storage at 2-4
Concentrate
degree Celsius to 35 o Should be used 6 hours after
days. preparation
 Poor source of platelets o Indications.
 Decrease 2,3 DPG  Thrombocytopenia –
 Factors V, VIII secondary to blood loss
and transfusion with
deteriorates in banked
banked blood.
blood  Thrombocytopenia –
 Lactic acid – increase secondary to inadequate
 pH – decrease platelets production and
 K+ - increase – platelet disorders.
precaution in anuric  Concentrates
o Antihemophilic concentrates.
patients.
o Prepared from plasma.
 Ammonia – increase  Cryoprecipitate
 Indication: Hypovolemia o Plasma derivative
secondary to acute o Contains high concentration of
hemorrhage. factor VIII and fibrinogen along
 Typing and with smaller amounts of other
factors.
Crossmatching
o Treatment of Factor VIII
o Major - donor’s deficiency and DIC.
RBC with patient’s
sera Indication for Replacement of Blood or Its
o Minor – donor’s Elements
sera with patient’s  Volume replacement
RBC  Improvement in oxygen carrying
o As a rule: Transfuse capacity – Hb 10
same type specific
 Replacement of clotting factors
blood
 Fresh Whole Blood Complications of Blood Transfusion
o Blood administered within 24h  Hemolytic Reaction
after its donation. o Most common cause of fatal
o Source of Factor X and VIII. hemolytic transfusion reaction is
o Platelets remain useful for the clerical error that results in
first 6 hours. transfusion of the wrong ABO
type of blood.
o Due to incompatibility of ABO
and Rh groups.

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
o Due to: o Tx:
 Administration of wrong  Left side head down to free
blood – clinical or technical the right ventricular outflow
error. tract of air
 Intravascular destruction of  Thrombophlebitis
RBC – hemoglobinuria. o More common in lower
 Tubular necrosis in kidneys – extremities
due to precipitation of Hb.  Overtransfusion and Pulmonary
o SS Edema
 Sensation heat and pain along o SS
the veins into which the blood  Increase CVP
is transfused.  Dypsnea
 Flushing of face, lumbar pains  Rales
and chest pains. o Tx
 Chills, fever, respiratory  Stop transfusion
distress, hypotension,  Diuretics
tachycardia.  Transfusion of diseases
o Tx o Viral hepatitis
 Stop transfusion immediately o AIDS
and discard used blood.  Coagulation Defects
 Insert foley catheter and
monitor vital signs. Massive Blood Transfusion
 Re-crossmatch blood.  It implies single transfusion > than
 Diuretics. 2,500 or 5,000mL/24h
 Alkalinize urine.  Hemostatic failure
 Allergic Reactions  Decrease O2 delivery
o SS
 Acidosis
 Urticaria
 Hyperkalemia
 Fever
 Citrate toxicity
 Anaphylactic shock
o Tx  Hypothermia
 Epinephrine  Pulmonary insufficiency
 Antihistmaines
 Steroids Coagulation Factor Deficiencies
 Sepsis  Inherited deficiencies of all of the
o S/Sx coagulation factors seen
 Chills  Three most frequent are:
 Fever o Factor VIII deficiency
 Cramps (Hemophilia A and Von
 Vomiting Willebrand’s disease)
 Diarrhea o Factor IX deficiency
 Abdominal bleeding (Hemophilia B or Christmas
 Shock dieases)
o Management o Factor XI deficiency
 Blood culture
 O2 Classic Hemophilia
 Antibiotics  Hemophilia A and hemophilia B are
 Stop transfusion immediately inherited as sex-linked recessive
 Air Embolism disorders with males being affected
o SS almost exclusively.
 Dizziness, loss of  Disease of the males, failure to
consciousness synthesize normal factor VII activity.
 Variable clinical presentations.

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
 Spontaneous bleeding when there is o Cryoprecipitates – 9.6 units/mL
no FVIII in plasma. o Factor VIII Concentrates
 Sex linked recessive mode of
inheritance. Von WilleBrand Disease
 Bleeding usually appear in early (Pseudohemophilia)
childhood.  Transmitted as autosomal dominant.
 Hemarthrosis is the most  Male and Female equally affected.
characteristic orthopedic problem:  Von Willebrand’s diseases (vWD), the
o Treatment: most common congenital bleeding
 Factor VIII therapy disorder, is characterized by low levels
 Bed rest of factor VIII.
 Apply cold packs  Primary defect is a low level of vWF, a
o May lead to equines deformity large glycoprotein responsible for
or Volkman’s contracture of carrying factor VIII and platelet
forearm. adhesion.
o Fasciotomy is contraindicated  Patients with vWD have bleeding that is
 Epistaxis, hematuria and intracranial characteristic of platelet disorders (i.e.,
bleeding may occur easy bruising and mucosal bleeding).
 Retroperitoneal or intramural  Associated with variable deficiency in
intestinal bleeding may produce Factor VIII and qualitative failure of
abdominal sympromatology. platelets to aggregate.
 Plasma factors:  Bleeding manifestations are milder than
o Less than 1% of the normal  classic haemophilia.
Severe  Treatment
o 1-5%  moderately severe o Cryoprecipitated plasma which
o 5-30%  mild disease contains Factor VIII and R:WF
 Severe (von Willebrand Factor).
o Have spontaneous bleeds o Fresh Frozen Plasma
frequently into the joins. o Factor VIII concentrate such as
 Patients with severe hemophilia have: Humate-P that contains vWF as
o Severe spontaneous bleeding well as factor VIII.
into joints which leads to o Desmopressin acetate, which
crippling arthropathies, raises endogenous vWF levels
intramuscular and by triggering release of the
retroperitoneal hematomas, GI factor from endothelial cells.
and retropharyngeal bleeding.
 Patients with moderately severe Factor IX Deficiency (Christmas Factor
haemophilia. Disease)
o Have less spontaneous bleeding  Sex linked recessive mode of
but are likely to bleed severely transmission.
after trauma or surgery  Mild bleeding.
 Patients with mild disease. Factor XI Deficiency (Rosenthal’s Disease)
o Do not bleed spontaneously and  Autosomal dominant
frequently. Have only minor  Minor bleeding episode
bleeding after major trauma or  Treatment
surgery. o Replacement therapy
 Treatment
o Fresh whole blood
o 1 unit of F VIII activity – amount
present in __ or plasma
o Fresh frozen plasma – 0.6
units/mL

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)
 SURGERY
TRAUMA
HEMOSTASIS, BLEEDING AND TRANSFUSION
Dr. Roberto Lozada; 09/20/2019, 11:30 am -1:30 pm
Acquired
Defibrination Syndrome – Consumption
Coagulopathy or Disseminated
Intravascular Coagulation
 Triggered by introduction of potent
thrombogenic material into
circulation --- malignant tumors from
prostate, pancreas, lungs,
intravascular hemolysis.
 Crushing injuries – release of fat –
retain of dead tissues.
 Sustained intravascular coagulation
and fibrinolysis – depletion of clotting
factors – spontaneous bleeding
(viscious cycle).
Other Causes:
o Severe infection usually gram (-)
o Severe and sustained
hypoperfusion with serious
tissue damage
o Ischemic injuries of the liver

These conditions causes:

 Release of thromboplastic material
 Endotoxin – activation of Factor XII
and reaction of platelets

 Treatment

o Correct primary cause

o Heparin
o Transfuse platelets
o Fresh frozen plasma

TAKE NOTE!
High Plasma to RBC ratio 1: 1.4

1/9
TG9: I Domingo, Ezer, Garingo, Magarse, Salvador, Rios I
Editor/s: Magarse (09212671763/3368004)