Schwartz's Hemostasis, Surgical Bleeding

7/24/2019 Schwartz's Hemostasis, Surgical Bleeding

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Hemostasis, Surgical Bleedingand

Transfusion


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HemostasisHemostasis = to stop bleeding

4 Basic mechanism / phase

Vascular constriction

Platelet plug formation

Fibrin formation

Fibrinolysis


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Vascular ConstrictionInjury to essel contraction smooth muscle

!ediators "

#hrombo$ane %&

at site of injury ia releasearachidonic acid from plateletmembranpotent constrictor smooth muscle

'ndothelinendhothelium(serotonin during

platelet agregation

potent asoconstictors#rombo$ane %& )#*%&+,

Brady-inin, Fibrinopeptides


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Platelet Phase.ource mega-aryocyt marro

%nucleated, normaly remoe by splen,aerage lifespan 0123 day

Integral role hemostasis " forming hemostasisplug and contributing in thrombin formation

Injury intimal layere$poses colagen subendhotelial( factorplatelet adhere )release

%5P(serotonin+recruits other platelet fromcirculating blooddisrupt essel sealed )plateletagregation6brinogen binding the plateletsurface 7 strengthens platelet interactions


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P8%#'8'# I. '*#9'!'8: I!P;9#%


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CoagulationsInteraction endothelium ( platelet (

circulating coagulations factor

Intrinsic

no need for surface e$posure'$trinsic begin once essel is disrupted

Intrinsic(e$trinsic cascade merge into

common pathay on factor *

Prothrombinthrombinchange 6brinogen to6brin

!easurement aP##intrinsic factor, P## e$trinsic factor


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Prothrombin circulating plasma proteins

Vit is re>uired for normal formation of

prothrombin

in lier


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FibrinolysisPreent propagation of clot formation

2? feedbac- inhibition on the coagulation cacscade

&? 6brinolysis

%ims on reconstitution of blood @oInitiated as the same time clotting mechanism

!ain enAyme plasmincleaes 6brin ( degrade

6brinogen

tP% actiates plasminogen more eciently

bound to6brinplasmin is formed selectiely on the clot

Product " '1nodule and 51dimer

mar-er of thrombosis or other conditions in actiation of6brinolysis is present


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Congenital Factor

5e6cienciesCoagulation factor de6ciencyFactor VIII hemo6lia %

Factor I*

hemo6lia B9ecessie autosomal disorders aect in male

Clinical seerity depend on measurable factorVIII or I* in plasma

%? Plasma factor leel D 2E " seereB? 11 2 G E " moderate

C? 11 G 3 E " mild

Platelet function still normal


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Von illebrands disease

Common congenital bleeding disorders

%utosomal dominant disorders, and primarydefect is lo F

platelet disorders mucosal bleeding,easybruising?


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%c>uired hemostatic

defectPlatelet abnormalities could be

Juantitatie or Juantitatie


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%c>uired

hypo6brinogenemia5IC ac>uired syndrome characteriAed by

intraascular actiation of coagulation

Clotting mechanism e$cessie thrombinmicrothrombus formation

Vasculature damage depletion and consumptionof coagulation factor and platelet diusebleeding

Causatie.epsis, trauma, ascular disorder,obstetric complications, malignancy, imunologicdisorder, drugs, sna-e/insect, lier disease,shoc-, massie transfusion


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%nticoagulation and Bleeding

.pontaneous bleeding can be complication ofanticoagulant therapi e$ hematuria,soft tissue

bleeding, intracerebral bleeding, s-in necrosis andabdominal bleeding?

KKKone of the 6srt symptoms of an underlying tumormay be bleeding in patient ith nticoagulation

therapy9apid reersal of anticoagulation can beaccomplished ith FFP in an emergent situation?


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8ocal Hemostasis!echanical prosedurs

digital pressure in pro$imal or oerbleeding site is eectie

#hermal agent

achiees hemostasis by denaturation ofprotein result in coagulation

negatie grounding plate should be placebeneath the patient ti aoid seere s-in burn

#opical hemostasis thrombin deriate product direct te

conersion of 6brinogen to 6brin


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#ransfusion2? Human red cell membrane " least 33

dierent antigen

&? fortunately, only the %B; and the 9h

systems are important in the majority ofblood transfusion

? History

Infection " Hepatitis B,C syphillis HIV12,&

H#8V1I,II


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5ue to surgery or trauma not necessarilyre>uire transfusion

Improement in ;$ygen1Carrying Capacity

#reatment of %nemiaVolume replacement

Belo 0 g/d8 idely accepted


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hole Blood

Ban-ed

9educe of intracelluler %5P 7 &,

disphosphoglycerate decrease o$ygen transport

Clotting factor relatiely stable adantage

'leated lactate, potassium and amonium

Volume replacement

Fresh

%dministered ithin &4 hours of its donation


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Pac-ed 9ed Cells

Choice for most clinical situation

Concentrate suspensions of red blood cells canprepared by remoing most of supernatantplasma after centrifuge reduce reaction byplasma component


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9ed Blood Cells Ideal for patients re>uiring red cells but not

olume replacement

;nly one G Increase ;&carrying

capacity%L' B8;;5 V;8M!'


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By Centrifugation remoing supernatantplasmareduce reaction caused by plasmacomp

;ne unit increse appro$imately 2 g/d8

P9C Formula"

P9C olume = ? $ )Q Hb+ $ B


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Platelet

#he indications thrombocytopenia >ualitatie and

>uantitatie c?b massie bloods loss and replacement ithplatelet1poor products,inade>uate platelet production

R prophylactic " plt?counts belo 23,3331&3,333

R prophylactic preoperatie " plt?counts belo 3,333

R!icroascular bleeding in surgical patient ith platelets

D 3,333R


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FFP9esuscitation trauma1associated

coagulopathy

.ource of the itamin 1dependent factor andis the only source factor V


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Indications for 9eplacement

2? improement in o$ygen1carrying capacity

&? treatment of anemia? olume replacement


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and

Preoperatie 'aluation of hemostasis

Hb leel D 0 gr/dl associated morecomplications

Consider factor " presence cardiopulmonarydisease, type of surgery, li-elihood of surgicalblood loss

I!P;9#%


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'aluation of '$cessie Intraoperatie

Bleeding during or post operatie innefecctie hemostasis,blood transfusion,

undetected hemostasis defect, consumptiecoagulopaty, and or 6brinolysis?

!assie blood tranfusion trombocytopenia

dilutional coagulopaty


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#H%

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Schwartz's Hemostasis, Surgical Bleeding