SCHWARTZ,S PRINCIPLES OF SURGERY 2005 PRESENTED BY:KAMRAN ADHAMI M.D.

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SCHWARTZ,S PRINCIPLES OF SURGERY 2005PRESENTED
BYKAMRAN ADHAMI M.D.
HEMOSTASIS AND SURGICAL BLEEDING
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BIOLOGY OF HEMOSTASIS

• 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

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• 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

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vascular constriction

• 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 ,5-HT,bradykinin,fibrinopep
  tides

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platelet function

• 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 pathwaysforming a hemostatic plug and by
  contributing to thrombin formation

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• 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)

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• 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

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• 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

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• 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)

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coagulation

• Interactions between platelets,vascular wall,and
  multiple circulating or membrane-bound
  coagulation factors
• Coagulation cascade2 intersecting
  pathwaysintrinsic 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

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• PTVII-X-V-II-fibrinogen
• PTTXII-XI-IX-VIII-X-V-II-fibrinogen-prekallikrein
  -high molecular weight kinninogen

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• Mixing patient plasma 11 with normal plasma,with
  and without incubation for1hour at 37C can
  distinguish between factor deficiency and the
  presence of an inhibitor

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• Regulationtwo 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,fibrinolysisbreakdown the fibrin clot

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• A third major mechanismprotein C system
• thrombinthrombomodulin---activate protein C to
  APC
• Its cofactor protein S
• APC-protein S complex cleaves factors Va and VIIIa

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CONGENITAL HEMOSTATIC DEFECTS
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COAGULATION FACTOR DEFICIENCIES

• 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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• Severelevel less than 1of normal
• Moderate1 to 5
• Mild 5to 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

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• Mild hemophiliacs dont bleed spontaneously
• After major trauma or surgery(platelet function
  is normal)
• May bleed several hours later(tooth extractions
  or tonsillectomy)
• Treatmentfactor VIII or factor IX
  concentrate,respectively

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Guidelines for replacement

• CNS and trauma or surgery and retroperitonealhemo
  static factor level 100 initially then 50-100
  for 10-14 days
• Retropharyngeal 50-70
• GI system50-100
• Hematuria40
• Tooth extraction50
• Mouth30-40
• Intramuscular40-50
• Acute hemarthrosis30-50

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• 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

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• EACA ,amicar,an inhibitor of fibrinolysis,especial
  ly for bleeding because of tooth extraction or
  other oral bleeding and for urinary tract bleeding

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von Willebrand,s disease

• Low factor VIII
• Autosomal dominant disorder
• 2function1-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

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• Characteristic of platelet disorderstypically
  easy bruising and mucosal bleeding.menorrhagia is
  common.
• It has 3 types
• Type Ipartial quantitative deficiency
• Type IIqualitative defect
• Type IIItotal deficiency

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• 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

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• 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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FACTOR XI DEFICIENCY

• 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

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DEFICIENCY OF FACTOR II,V,X

• They are rare.autosomal recessive,significant
  bleeding in homozygotes with less than 1of
  normal activity
• Bleeding is treated with FFP.
• FFP contains one unit of activity of X II
• Factor V activity of plasma is somewhat less

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FACTOR VII DEFICIENCY

• 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)

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FACTOR XIII DEFICIENCY

• 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

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inherited defects

• abnormalities of platelet surface
  protein
• abnormality of platelet granules
• enzyme defects

platelet function defects
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• 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

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• 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

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ACQUIRED HEMOSTATIC DEFECTS

• PLATELET ABNORMALITIES
• Qualitative-quantitative-both types
• Quantitativefailure of production,shortened
  survival,or sequestration
• Failure of productiongeneral 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

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• 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)

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• If the platelet count cannot be maintained
  medically with these agents,splenectomy is
  indicated and leads to complete or partial
  remission in 80of patients.
• Platelet transfusion is not needed for
  splenectomy in patients with ITP.

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• DRUGS THAT SHOULD BE SUSPECTED ARE
• heparin,quinidine,quinine,gold salts,sulfonamides,
  valporic acid,and chlorothiazide.

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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.

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• in Mild to moderate thrombocytopenia ,this is
  characterized by a high incidence of thrombosis
  that may be arterial or venous.(HITTSheparin
  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

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• TTPThrombotic 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.

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• HUSHemolytic uremic syndrom
• Secondary to infection by escherichia coli
  0157H7 or other shiga toxin-producing bacteria
• Some degree of renal failure,neurologic symptoms
  are less frequent

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• 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.

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• 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 drugsindomethacin,ibuprofen,phenothiazines,
  penicillins,chelating agents,lidocaine,dextran,bet
  aadrenergic blockers,nitroglycerin,furosemide,anti
  histamines

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• 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.

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• Sequestration is another important cause of
  thrombocytopenia and usually involves
  sequestration of platelets in an enlarged spleen
  from any cause (portal hypertension,sarcoid,lympho
  ma,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.

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• 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

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• One unit of platelet concentrate contains
  5.51010 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.

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myeloproliferative diseases

• 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.

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• 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.

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COAGULOPATHY OF LIVER DISEASE

• 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.

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• 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.

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hypersplenism

• 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

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anticoagulation bleeding

• 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.

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• 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
  cholesterol-lowering agent clofibrate,anabolic
  steroids,l-thyroxine,glucagons,amidarone,quinidine
  ,and variety of antibiotics(cephalosporins)

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• Present with epistaxis,G I hemorrhage,hematuria,ec
  chymoses,petechiae,hematoma
• Bleeding secondary to anticoagulation therapy is
  not an uncommon cause of rectus sheath
  hematoma,simulating appendicitis,and intramural
  intestinal or retroperitoneal hematoma.

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• 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

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• 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.

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• 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.

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LOCAL HEMOSTASIS

• 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

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MECHANICAL PROCEDURES

• 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.

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• 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 .

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• 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,an
  d vicryl.

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• 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.

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• 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.

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thermal agents

• 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.

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• Advantage of the cautery is that it saves
  timethe 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.

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chemical agents

• 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.

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• Materials are gelatin(gelfoam),oxidized
  cellulose (oxycel),oxidized regenerated cellulose
  (surgicel),and micronized collagen (avitene)

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THANKS FOR YOUR ATTENTION