Transcript SCHWARTZ,S PRINCIPLES OF SURGERY 2005 PRESENTED BY:KAMRAN ADHAMI M.D.  A complex process that prevents or terminates blood loss from a disrupted intravascular space  4 major physiologic.

SCHWARTZ,S
PRINCIPLES OF
SURGERY 2005
PRESENTED
BY:KAMRAN ADHAMI
M.D.
 A complex process that prevents or
terminates blood loss from a disrupted
intravascular space
 4 major physiologic events
participate,both in sequence and
interdependently,in the hemostatic
process
 Vascular constriction ,platelet plug
formation,fibrin formation,and fibrinolysis
occur in that general order,but the
products of each of these four processes
are interrelated in such a way that there
is a continuum and multiple
reinforcements
 Injury : vasoconstriction is initial vascular response
to injury .
 Adherence of endothelial cells to adjacent
endothelial cells may be sufficient to cause
cessation of blood loss from the vessel.
 TXA2,from arachidonic acid from platelet
membranes during aggregation (vasoconstrictor)
 Endothelin , serotonin ,5HT,bradykinin,fibrinopeptides
 2 to 4 um in diameter
 150000-400000/uL
 Up to 30% sequestered in the spleen can
release in response to catecholamines
 Average life span 7 to 10 days
 Two pathways:forming a hemostatic plug
and by contributing to thrombin formation
 Injury to the intimal layer in the vascular
wall exposes subendothelial collagen to
which platelets adhere within 15 seconds
of the traumatic event.
 vWF in subendothelium (von willebrand)
 Platelets expand and develop pseudopodal
processes and also initiate a release reaction
that recruits other platelets from the circulating
blood to seal the disrupted vessel
 Primary hemostasis,reversible and is not
associated with secretion
 Heparin does not interfere with this reaction
 In the second wave of platelet
aggregation ,a release reaction occurs in
which several substances including
ADP.ca2+,serotonin,TXA2,and alpha
granule proteins are discharged
 Compaction of the platelets into an
amorphous plug,no longer reversible
 In congenital abnormalities exist,they can
result in abnormal aggregation ,as a
result of effects on either the first wave of
aggregation or the second wave of the
process(granule release)
 Interactions between platelets,vascular
wall,and multiple circulating or membranebound coagulation factors
 Coagulation cascade=2 intersecting
pathways:intrinsic and extrinsic
 Intrinsic because all are intrinsic to the
circulating plasma and no surface is required to
initiate the process
 Extrinsic requires exposure of tissue factor on
the surface of the injured vessel wall to initiate
the arm of the cascade beginning
 PT:VII-X-V-II-fibrinogen
 PTT:XII-XI-IX-VIII-X-V-II-fibrinogenprekallikrein-high molecular weight
kinninogen
 Mixing patient plasma 1:1 with normal
plasma,with and without incubation
for1hour at 37C can distinguish between
factor deficiency and the presence of an
inhibitor
 Regulation:two related process must exist to
balance propagation of the clot before the
entire vascular bed is thrombosed in response
to a local insult.
 First,there is a feedback inhibition on the
coagulation cascade,which deactivates the
enzyme complexes leading to thrombin
formation
 Second,fibrinolysis=breakdown the fibrin clot
 A third major mechanism=protein C
system
 thrombin—thrombomodulin---activate
protein C to APC
 Its cofactor protein S
 APC-protein S complex cleaves factors
Va and VIIIa
 FACTOR VIII AND FACTOR IX
 HEMOPHILIA:
 Most frequent are hemophilia A and von
willebrand disease =factor VIII deficiency
 Hemophilia B or christmas disease
=factor IX
 Sex-linked recessive
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Severe=level less than 1%of normal
Moderate=1% to 5%
Mild =5%to 30 %
Severe: severe spontaneous bleeds frequently
into joints,intramuscular
hematoma,retroperitoneal hematomas,and
gastrointestinal and genitourinary bleeding
 Intracranial bleeding and retropharyngeal
bleeding and bleeding from the tongue or
lingual frenulum may be life-threatening
 Mild hemophiliacs don’t bleed
spontaneously
 After major trauma or surgery(platelet
function is normal)
 May bleed several hours later(tooth
extractions or tonsillectomy)
 Treatment:factor VIII or factor IX
concentrate,respectively
Guidelines for replacement:
 CNS and trauma or surgery and
retroperitoneal=hemostatic factor level 100%
initially then 50-100% for 10-14 days
 Retropharyngeal =50-70%
 GI system=50-100%
 Hematuria=40%
 Tooth extraction=50%
 Mouth=30-40%
 Intramuscular=40-50%
 Acute hemarthrosis=30-50%
 Mild to moderate hemophilia A with minor
bleeds is administraction of DDAVP
which induces the release of v WF
raising the levels of v WF and associated
factor VIII
 DDAVP can be given I.V. 0.3ug/kg
daily or by nasal spray one puff
 EACA ,amicar,an inhibitor of
fibrinolysis,especially for bleeding
because of tooth extraction or other oral
bleeding and for urinary tract bleeding
 Low factor VIII
 Autosomal dominant disorder
 2function:1-carrier for factor VIII(v WF level are
low,factor VIII levels are variably decrease of
loss of the carrier protein.)
 2-it is necessary for normal platelet adhesion to
exposed subendothelium and for normal
aggregation under high shear condition
 Characteristic of platelet
disorders;typically easy bruising and
mucosal bleeding.menorrhagia is
common.
 It has 3 types:
 Type I:partial quantitative deficiency
 Type II:qualitative defect
 Type III:total deficiency
 Two options for treatment of it
 Use an intermediate purity factor VIII
concentrate such as humate-P that
contains v WF as well as factor VIII.
 Second option is use of DDAVP, which
raise endogenous v WF levels by release
of the factor from endothelial cells
 In general,type I patients respond well to
DDAVP. Type II patients may
respond,depending on the particular
defect.type III patients usually do not
respond.
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Hemophilia C
Mild bleeding disorder
Autosomal recessive trait
Bleeding may occure after surgery or trauma
Treatment is with fresh-frozen plasma FFP.
Each milliliter of plasma contains 1 unit of factor XI
activity
 Daily infusion is adequate because the half-life is 48h
 DDAVP may also be useful in the prevention of it
 They are rare.autosomal
recessive,significant bleeding in
homozygotes with less than 1%of normal
activity
 Bleeding is treated with FFP.
 FFP contains one unit of activity of X &II
 Factor V activity of plasma is somewhat
less
 Rare.
 Bleeding is uncommon –level less than
3%
 Treatmen with FFP or with recombinant
factor VIIa
 Half-life is very short(2h)
 Half –life of factor VII in FFP is longer
,(4h)
Rare
Autosomal recessive
Bleeding is typically delayed because clots form normally
but are susceptible to fibrinolysis
Umbilical stump bleeding
Intracranial
Spontaneous abortion is usual
Half-life is 9to14 days
Replacement can be accomplished with FFP
,cryoprecipitate ,factor XIII concentrate
Level 1 to 2%

abnormalities of platelet surface
protein

abnormality of platelet granules

enzyme defects

 Srface protein abnormalities :bernard-soulier syndrom
and thrombasthenia(glanzmann,s disease)
 Absence of functional glycoprotein IIb IIIa
 Receptor for fibrinogen and also a receptor for v WF.
 Thrombasthenic patients must be treated with platelet
transfusions
 The bernard-soulier syndrom is caused by a defect in
the GP Ib/IX/V receptor for v WF that is necessary for
platelet adhesion to the subendothelium
 Transfusion of normal platelets is required for bleeding
in these patients
 The most common intrinsic platelet defect is known as
storage pool disease.
 Dense granule deficiency is the most prevalent of
these.
 It may be an isolated defect or occur with partial
albinism in the hermansky-pudlak syndrome.
 Bleeding is primary caused by the decreased released
of ADP from these platelets.
 Mild bleeding may decrease bleeding by DDAVP
 Severe bleeding ,platelet transfusion is required
 PLATELET ABNORMALITIES:
 Qualitative-quantitative-both types
 Quantitative=failure of production,shortened
survival,or sequestration
 Failure of production:general marrow
disorder(leukemia,myelodysplastic
syndrome,severe vitamin B12 or folate
deficiency,chemotherapeutic
drugs,radiation,acute ethanol intoxication,viral
infection
 Platelet transfusion ,with the addition of EACA
 Shortened platelet survival :immune
thrombocytopenia,disseminated intravascular
coagulation, thrombotic thrombocytopenic
purpura and hemolytic uremic syndrome
 Immune thrombocytopenia often presents with
a very low platelet count,petechiae and
purpura,and epistaxis and gum bleeding.large
platelet are seen on peripheral smear.
 Treatment is with corticosteroids(1mg/kg per
day)-or gamma globulin (2g/kg over 2to5 days)
 If the platelet count cannot be maintained
medically with these agents,splenectomy
is indicated and leads to complete or
partial remission in 80%of patients.
 Platelet transfusion is not needed for
splenectomy in patients with ITP.
 DRUGS THAT SHOULD BE
SUSPECTED ARE:
 heparin,quinidine,quinine,gold
salts,sulfonamides,valporic acid,and
chlorothiazide.
HIT:
 Heparin –induced thrombocytopenia is a
special case of drug-induced immune
thrombocytopenia.
 Count fall 5 to 7 days after
 In re-exposure,it may occur within1to2 days.
 Not severe
 Platelet count falls to less than 100000 or it
drops by 50% from baseline.
 in Mild to moderate thrombocytopenia ,this is
characterized by a high incidence of
thrombosis that may be arterial or
venous.(HITTS=heparin –induced
thrombocytopenia –thrombosis syndrome)
 Heparin should be stopped promptly and an
alternative anticoagulant should be instituted
 Lepirudin,argatroban,danaparoid
 Warfarin should not be started in them until
count has recovered to greater than 100000
 TTP=Thrombotic thrombocytopenic purpura
 It is thought that ultralarge v WF molecules
interact with platelets,leading to activation.
 Thrombocytopenia,microangiopathic hemolytic
anemia,renal abnormalities,fever,and
neurologic signs or symptoms
 Treatment is plasmapheresis
 platelet Transfusion should not be used in TTP
unless necessary.
 HUS:Hemolytic uremic syndrom
 Secondary to infection by escherichia coli
0157:H7 or other shiga toxin-producing
bacteria
 Some degree of renal failure,neurologic
symptoms are less frequent
 Thrombocytopenia may occur acutely as
a result of massive blood loss followed by
replacement with stored blood.
 Exchange of 1 blood volume (11 unit in a
75-kg man)decreases the platelet count
from 250000/Ul to 80000/uL.
 ASPIRIN irreversibly inhibits platelet function
.CLOPIDOGREL and ABCIXIMAB have sufficiently
long half-lives,therefore platelet transfusion may be
required if surgery is indicated within a few days of
discontinuing therapy.
 Other
drugs:indomethacin,ibuprofen,phenothiazines,penicillin
s,chelating agents,lidocaine,dextran,betaadrenergic
blockers,nitroglycerin,furosemide,antihistamines
 In general,50000 platelets/u L is adequate for normal
hemostasis,but if there is associated platelet
dysfunction ,there may be a poor correlation between
the platelet count and the extent of bleeding.the
template bleeding time is the most reliable in vivo test
of hemostatic function.
 When thrombocytopenia is present in a patient for
whom an elective operation is being considered,it is
managed on the basis of how much the platelet count
is reduced and the cause of the reduction. A count of
greater than 50000/u L requires no specific therapy.
 Sequestration is another important cause of
thrombocytopenia and usually involves
sequestration of platelets in an enlarged spleen
from any cause (portal
hypertension,sarcoid,lymphoma,Gaucher,s
disease)
 Total body platelet mass is essentially normal
in patients with hypersplenism ,but a much
larger fraction of the platelets than normal are
in the enlarged spleen.
 Platelet transfusion doesnot increase the
count as much as it would in a normal
person because the transfused platelets
will end up in the spleen.
 Splenectomy is not indicated to correct
the thrombocytopenia of hypersplenism
caused by portal hypertension
 One unit of platelet concentrate contains
5.5*10^10 platelets and would be expected to
increase the circulating platelet count by about
10000/u L in the average 70-kg person.hence
a transfusion of 4 to 8 pool platelet
concentrates should raise the count by 40000
to 80000/u L and should provide adequate
hemostasis,as documented by bleeding time
and control of the hemorrhagic manifestations.
 The polycythemic patient,particularly with
marked thrombocytosis,is a major surgical risk.
 If possible,the operation should be deferred
until medical management has effected normal
blood volume,hematocrit level,and platelet
count.
 Spontaneous thrombosis is a complication of
polycythemia vera and can be explained in part
by increased blood viscosity,increased platelet
count,and an increased tendency toward
stasis.
 TREATMENT:
 Hydroxyurea or anagrelide
 Elective surgical procedures should be delayed
weeks to months after institution of treatment.
 HCT less than 48%, platelet count under
400000/u L
 In emergency procedures,phlebotomy and
replacement of the blood removed with
lactated Ringer,s solution.
 All of the coagulation factors are synthesized
by hepatocytes,although factor VIII level
behave differently from those of other factors
with hepatic insufficiency.
 Levels of the vitamin K –dependent factors and
factor V decrease progressively
 Fibrinogen and factor VIII levels tend to be
elevated with mild liver disease.
 Fibrinogen levels decrease with progression
from COOK,s class A to B to C cirrhosis.factor
VIII is low only with very severe liver disease.
 Thrombocytopenia is seen in patients with
cirrhosis who have hypersplenism.
 Treatment of bleeding in patients with
coagulopathy caused by liver disease usually
done with FFP
 If the fibrinogen is less than 100mg/dL,
administration of cryoprecipitate(8to 10
bags)may be helpful.
 Platelet sequestration
 Total body platelet mass is essentially normal
in patients with hypersplenism,but a much
larger fraction of the platelets than normal are
in the enlarged spleen.
 Platelet transfusion does not increase the
platelet count as much as it would in a normal
person because the transfused platelets will
end up in the spleen
 Spontaneous bleeding may be a complication
of anticoagulant therapy with either
heparin,warfarin,or one of the newer
anticoagulants,low molecular weight heparins
 It is reduced with a continuous infusion
technique,regulating the a PTT between 1.5
and 2.5 times the upper limit of normal.
 Therapeutic anticoagulation is more reliably
achieved with low molecular weight
heparin,and laboratory testing is not routinely
used to monitor dosing of these agents.
 Effect of the warfarin is reduced in receiving
barbiturates
 Increase warfarin requirements have also been
documented in patients taking contraceptives,other
estrogen-containing compounds,corticosteroids,and
adrenocorticotropic hormone(ACTH)
 Medications known to increase the effect of oral
anticoagulants include phenylbutazone,the cholesterollowering agent clofibrate,anabolic steroids,lthyroxine,glucagons,amidarone,quinidine,and variety of
antibiotics(cephalosporins)
 Present with epistaxis,G I
hemorrhage,hematuria,ecchymoses,pete
chiae,hematoma
 Bleeding secondary to anticoagulation
therapy is not an uncommon cause of
rectus sheath hematoma,simulating
appendicitis,and intramural intestinal or
retroperitoneal hematoma.
 Certain surgical procedures should not be
performed in the face of anticoagulation .(CNS
–eye)
 Because of the added problem of local
fibrinolysis,prostatic surgical treatment should
not be carried out in a patient on
anticoagulants
 Blind needle introduction should be avoided
 Discontinuation of heparin may be
sufficient if the operation can be delayed
for several hours,for more rapid
reversal,1 mg of protamine sulfate for
every 100 units of heparin most recently
administered is immediately effective.
 Parenteral administration of vitamin K also is
indicated in elective surgical treatment of
patients with biliary obstruction or
malabsorption who may be vitamin K-deficient.
 The drug should result in a normal PT or
INR.By contrast ,if low levels of factors
II,VII,IX,X are a result of hepatocellular
dysfunction,vitamin K administration is
ineffective
 Vitamin K therapy should not be prolonged
over 1 week if no response is noted.
 Significant surgical bleeding is usually caused
by ineffective local hemostasis.
 The goal of local hemostasis is to prevent or
interrupt the flow of blood from a disrupted
vessel that has been incised or transected.
 Hemostasis may be accomplished by
interrupting the flow of blood to the involved
area or by direct closure of the blood vessel
wall defect.
 The techniques are classified as
MECHANICAL,THERMAL,CHEMICAL
 The oldest mechanical method of effecting
closure of a bleeding point,or of preventing
blood from entering the area of disruption,is
digital pressure.
 Tourniquet
 Pringle maneuver ,which occludes the hepatic
artery and portal vein in the hepatoduodenal
ligament as a method of controlling bleeding
from a transected cystic artery or the raw
surface of the liver.
 The most obvious disadvantage of digital pressure is
that it cannot be used permanently.
 A ligature or a hemoclip replaces the hemostat as a
permanent method of effecting hemostasis of a single
disrupted vessel.
 When a small vessel was transected ,a simple ligature
is sufficient .
 For large arteries with pulsation and longitudinal
motion,a transfixion suture to prevent slipping is
indicated.
 When the bleeding is from a lateral defect in a large
vessel,sutures are required .
 The adventitia and media constitute the
major holding forces in a vessel wall,and
multiple fine sutures or small hemoclips
are preferable.
 Nonabsorbable sutures,such as
silk,polyethylene ,and wire,evoke less
tissue reaction than absorbable material
such as catgut,polyglycolic,and vicryl.
 Diffuse bleeding from multiple small
vessels can be controlled by pressure
applied directly over the bleeding
area,and this is now deemed preferable
to the prolonged use of a proximally
placed tourniquet because the latter is
associated with a greater danger of
tissue necrosis.
 Direct pressure applied by means of pack
affords the best method of controlling diffuse
bleeding from large areas.
 Unless the heat is so great as to denature
protein,it can actually increase
bleeding,whereas cold packs promote
hemostasis by inducing vascular spasm and
increasing endothelial adhesiveness.
 Bleeding from cut bone can be controlled by
packing beeswax on the raw surface to effect
pressure.
 Heat achieves hemostasis by
denaturation of protein that result in
coagulation of large areas of tissue.
 When electrocautery is employed ,the
amplitude setting should be high enough
to produce prompt coagulation,but not so
high as to set up an arc between the
tissue and the cautery tip.
 Advantage of the cautery is that it saves
time;the disadvantage is that more tissue is
necrosed than with precise ligature.
 Local cooling has been applied to control
bleeding from the eroded mucosa of the
esophagus and stomach.
 Direct cooling with iced saline is effective and
acts by increasing the local intravascular
hematocrit and by causing vasoconstriction of
the arterioles.
 Epinephrine ,injected locally or applied
topically ,induces vasoconstriction and
can reduce bleeding.
 The drug is generally used for an oozing
site such as the tonsillar bed or for a
bleeding duodenal ulcer that is
concurrently cauterized.
 Materials are gelatin(gelfoam),oxidized
cellulose (oxycel),oxidized regenerated
cellulose (surgicel),and micronized
collagen (avitene)