Thromboembolic and Hematologic

7/26/2019 Thromboembolic and Hematologic

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Hematological andThromboembolic

Disorders inPregnancy

TAGUD, LYZELCSU!ED"C"#E


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#ormal PregnancyHypervolemic statePhysiologic/ Dilutional Anemia

"ncrease $%C!ild thrombocyto&enia

Hypercoagulable state

Diminished 'brinolysis


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Blood volume

HYPERVOE!"#$%A%E


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Plasma Volume


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Red #ell Volume

D"&%"O'A

A'E!"A


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Dilutional/

Physiological AnemiaDe'ned by CDC as(

(( g/d in the 'rst and thirdtrimesters, and

()*+ g/d in the second trimester

lo) hgb le*el

lo) hct le*el


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eu,ocyte #ount

D+ring acti*e labor there may be anothernormal increase, e*en in the absence oinection-.,///0+L


9/105

Platelet #ount

GESTAT"1#AL TH21!%1CYT1PE#"A

Ty&ically de'ned as belo) the -3.th&ercentileor 445,///0+L

&artially d+e to the hemodil+tional e6ectalso d+e to increased &latelet cons+m&tion


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Coag+lation and

7ibrinolysis


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Coag+lation and

7ibrinolysis7ibrinogen, 7actors "", 8"", 9, 9"", and 9""" increase8on $illebrand actor increases

Antithrombin, Protein C, 7actor 8, and 7actor "9le*els remain +nchanged or increased slightly

7ibrinolytic acti*ity is red+ced in normal

&regnancyHYPER#OA-&ABE $%A%E


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HematologicDisorders


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"3 2ED %L11D CELLA3 Anemia

a3 Ac:+ired

b3 Hereditary

%3 Polycythemia

""3 PLATELET D"S12DE2SC3 "nherited Thrombocyto&enia

D3 "TP

E3 Thrombocytosis

73 Thrombotic !icroangio&athies

"""3 "#HE2"TED C1AGULAT"1# DE7ECTSG3 Hemo&hilia

H3 7actor 8"" or "9 "nhibitor Deects

"3 8on $illebrand disease

;3 1ther Coag+lation 7actor Deects


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A'E!"A


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Clinical &ict+reor orms in*ol*es

Fim&aired &rod+ction or instability either o M&e&tide chains @;


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Alpha6 %halassemias

Alpha6 %halassemias


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"n Pregnancy:*Hemoglobin H disease >= 8?

Fcompatible 1ith e4trauterine li0e

FThe neonate a&&ears )ell at birth b+t soonde*elo&s hemolytic anemia3

FAnemia in these )omen +s+ally is )orsenedd+ring &regnancy

Alpha6 %halassemias


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Pregnancy

Hemoglobin Bart DiseaseFdeletion o all o+r Mglobin chain genes@NN0NN

FhomozygousNthalassemia

FHemoglobin %art ( has an a&&reciablyincreased aOnity or oygen

FCa+ses stillbirths


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@6%HAA$$E!"A !AOR OR#OOEY A'E!"A

F Homo=ygo+s

F the neonate is healthy at birth, b+t as thehemoglobin 7 le*el alls, the inant becomes

se*erely anemic and ails to thri*e3F Prognosis is im&ro*ed by iron chelation

thera&y )ith deeroamine


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PlateletDisorders

Platelet Disorders


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"nherited %hrombocytopenias Bernard-Soulier syndrome characteri=ed by lac o &latelet membraneglyco&rotein @GP"b0"9

May-Hegglin anomaly

a+tosomally dominant

characteri=ed by thrombocyto&enia, giant&latelets, and le+ocyte incl+sions

Platelet Disorders


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"mmune %hrombocytopenicPurpura

Also called idiopathic thrombocytopenic purpura(IT!

+s+ally res+lts rom a cl+ster o "gG antibodiesdirected against one or more &lateletglyco&roteins

Antibodycoated &latelets are destroyed&remat+rely in the retic+loendothelial system,es&ecially the s&leen3


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Acute vs* #hronic

Acute "%P #hronic "%P

oten a childhood disease Ad+lts @yo+ng )omen

resol*e s&ontaneo+sly rarely resol*es s&ontaneo+sly

Secondary orms o chronic thrombocyto&eniaa&&ear in association )ith(a3 systemic l+&+s erythematos+sb3 Lym&homasc3 Le+emiasd3 systemic diseases3

Platelet Disorders


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"mmune %hrombocytopenicPurpura

%reatment

Prednisone 4 mg0g0day P1 @or im&ro*ement

Corticosteroid thera&y +s+ally &rod+ces

amelioration3 highdose imm+noglob+lin ( "8

Platelet Disorders


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"mmune %hrombocytopenic

Purpura"n &regnant )omen )ith no res&onse tosteroid or imm+noglob+lin thera&y( o&en or la&arosco&ic s&lenectomy may be

e6ecti*e3 "n late &regnancy, cesarean deli*ery may benecessary or e&os+re3

"ntra*eno+s antiD "gG

There +s+ally is im&ro*ement by 4 to ? days )itha &ea at a&&roimately days3


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9etal and 'eonatal EectsPlateletassociated "gG antibodies cross the&lacenta and may ca+se thrombocyto&enia inthe et+sneonate3

!ay ca+se(7etal death rom hemorrhage

increased ris or intracranial hemorrhage )ithlabor and deli*ery


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%hrombocytosis

>thromocythemia )de'ned as &ersistent &latelet co+nts Q ./,///0L3

+s+ally is asym&tomatic, b+t arterial and *eno+sthromboses may de*elo&

a! secondaryor reacti"e thromocytosis Common ca+ses(

iron de'ciency

inection inRammatory diseases

malignant t+mors

b3 essential thromocytosis


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%hrombocytosis in Pregnancy

#ormal &regnancies ha*e been described in)omen )hose mean &latelet co+nts )ere Q43-. million0L

com&licated by s&ontaneo+s abortion, etaldemise, and &reeclam&sia @#iitty*+o&io andcolleag+es, -//

Treatment d+ring &regnancy incl+des(

as&irin, di&yridamole,

he&arin,

&latelet &heresis, or combinations thereo


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%HRO!BO%"# !"#ROA'-"OPA%H"E$

(*%HRO!BO%"# %HRO!BO#Y%OPE'"#P&RP&RA Pentad o thrombocyto&enia @!oschco)it=

7e*er

#e+rological abnormalities

2enal im&airment

Hemolytic anemia

De'ciency o a *on $illebrand actor clearing &rotease

ADA!TS4?

*HE!OY%"# &RE!"# $Y'DRO!E $ithmore &roo+nd renal in*ol*ement and e)er ne+rological

aberrations

Us+ally d+e to endothelial damage incited by *iral or bacterial

inections



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#"'"#A PRE$E'%A%"O'

Thrombocyto&enia, ragmentation hemolysis, and*ariable organ dys+nction

Preceding *iral &rodrome @/ cases

#e+rological sym&toms de*elo& in +& to / Headache

Altered conscio+sness

7e*er

Stroe

2enal ail+reSe*erity( HUS Q TTP



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%reatment

Plasma&heresis )ith reshro=en &lasmare&lacement not indicated or &reeclam&siaeclam&sia com&licated

by hemolysis and thrombocyto&enia2ed cell trans+sions

Prednisone

7or those )ith mild ne+rological sym&toms

-// mg orally, daily

Plasma echange )ith 77P



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PRE-'A'#Y$evere preeclampsia andecclampsia complicated bythrombocytopenia and overt

hemolysis have been con0used 1ith%%P and vice versaHemolytic anemia is rarely seen in&reeclam&sia, e*en )ith HELLP syndrome

He&atocell+lar necrosis is not described inTTP

Deli*ery does not im&ro*ed TTP



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O'- %ER! PRO-'O$"$

Pregnant 1omen 1ith thromboticmicroangiopathy have a number o0long6term complications.

renal disease re:+iring dialysis ,trans&lantation, or both

se*ere hy&ertension

trans+sionac:+ired inectio+s diseases

'on6pregnant 1omen 1ho haverecovered 0rom %%P.Persistent cogniti*e deects


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"'HER"%ED #OA-&A%"O'DE9E#%$


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von Cillebrand Disease

Heterogeno+s gro+& o a&&roimately -/ +nctionaldisorders!ost commonly inherited bleeding disorders

&re*alence is as high as 4 to - &ercent

"n*ol*es aberrations o actor 8""" com&le and&latelet dys+nction

!ost *ariants are inherited as a+tosomal dominanttraits

a* %ypes " and "" most common *ariants @Ty&e " acco+ntsor B. o *$D

b* %ype """ most se*ere and is &henoty&ically recessi*e


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Pathogenesis. von CillebrandDisease

Aberrations in vC9

"m&aired &lateletadhesion to

s+bendothelialcollagen

"m&aired ormation oa &rimary hemostatic&l+g at the site oblood *essel in>+ry

"m&aired stabili=ationo the coag+lant&ro&erties o actor 8"""

Bleedingproblems


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#"'"#A !A'"9E$%A%"O'

Characteri=ed clinicallyby (43Easy br+ising

-3E&istais

?3!+cosal hemorrhage

3Ecessi*e bleeding )ithtra+ma, incl+dings+rgery

ABORA%ORY 9EA%&RE$.

Prolonged bleedingtime

Prolonged PTT

Decreased *$7antigen le*els

Decreased actor 8"""imm+nological as )ellas coag+lation&romoting acti*ity

"nability o &latelets in&lasma rom ana6ected &erson toreact to a *ariety ostim+li


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Pregnancy and vCD

'ormal pregnancy!aternal le*els o both actor 8""" as )ell as *) antigen increases

Pregnant 1omen 1ith vCDDe*elo& normal le*els o actor 8""" coag+lant acti*ity as )ell as

*) antigen

"0 0actor V""" activity is very lo1 or i0 there is bleeding.Treatment is recommended

Desmo&ressin by in+sion may transiently increase actor *iii and*) actor le*els, es&ecially in &atients )ith ty&e " disease

Cith signi2cant bleeding4. or -/ +nits or bags o cryo&reci&itate are gi*en e*ery 4- ho+rs

Pregnancy outcomes are generally goodPost&art+m hemorrhage is enco+ntered in +& to ./ &ercent o

cases


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%HRO!BOE!BO"#

D"$ORDER$


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"ntroduction

The ris o *eno+s thrombosis and&+lmonary embolism(

5 higher d+ring the 5rd trimester,

-- higher in the (st7 1,s postpartum @"ultan,

20##, $% "ncidence o thromboembolic e*ents

a*erages a&&roimately 40 4///&regnancies3

DV%is more re:+ent antepartum, Pulmonary embolism is more common in the

2rst 7 1,s postpartum @&acobsen et'al', 200,)or*ay


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Pathophysiology

Predisposing 0actors or thrombosisde*elo&ment that is +rther increasedd+ring &regnancy @+' ircho*(

a*$tasis

!ost constant &redis&osing ris actor

b*ocal trauma

c*Hypercoagulability

%able +6(* $ome Ris, 9actors Associated


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%able + (* $ome Ris, 9actors Associated1ith an "ncreased Ris, 0or%hromboembolism



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%able + (* $ome Ris, 9actors Associated1ith an "ncreased Ris, 0or%hromboembolismObstetrical

CSD

Diabetes

Hemmorrhage K anemia

Hy&eremesis

"mmobility

!+ltietal gestation

!+lti&arity

Preeclam&sia

P+er&eral inection

-eneral

Prior history o0embolism

?. y0o and abo*e

Cancer

Connecti*e tiss+e dse

Dehydration

"mmobility

"nection and inRammatory dse

!yelo&rolierati*e dse

#e&hrotic syndrome

1besity

1ral contrace&ti*e +se

1rtho&edic s+rgery

Para&legia

Sicle cell dse

Smoing

Thrombo hilia

%he most important ris,0actor

(+ < + o all *eno+sthromboembolism casesd+ring &regnancy arerecurrent events @AC1G,-/443



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%able + (* $ome Ris, 9actors Associated1ith an "ncreased Ris, 0or%hromboembolismObstetrical

CSD

Diabetes

Hemmorrhage K anemia

Hy&eremesis

"mmobility

!+ltietal gestation

!+lti&arity

Preeclam&sia

P+er&eral inection

-eneral

Prior history o embolism

?. y0o and abo*e

Cancer

Connecti*e tiss+e dse

Dehydration

"mmobility

"nection and inRammatory dse

!yelo&rolierati*e dse

#e&hrotic syndrome

1besity

1ral contrace&ti*e +se 1rtho&edic s+rgery

Para&legia

Sicle cell dse

Smoing

%hrombophilia

%he ne4t most importantindividual ris, 0actor

)6 +) o )omen )ho

de*elo& a *eno+s thrombosisd+ring &regnancy or&ost&art+m ha*e anidenti2able underlyinggenetic disorder@ACOG,20##3

%hrombophilias


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%hrombophilias

"nherited or ac:+ired de'ciencies on&roteins that inhibit coag+lationcascade )hich can lead tohy&ercoag+lability and rec+rrent 8TE3

1bstetrical com&lications associated)ith thrombo&hilias(

Pregnacy loss

Preeclam&sia Placental Abr+&tion

7G2

%hrombophilias


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%hrombophilias

"nherited %hrombophilias.

a3 Antithrombin De'ciency

b3 Protein C De'ciency

c3 Protein S De'ciency

d3 Acti*ated Protein C 2esistanceN 7actor 8Leiden !+tation G-/-4/A

e3 Hy&erhomocystenemia

Ac3uired %hrombophilias(a3 Anti&hos&holi&id antibody

b3 He&arin ind+ced thrombocyto&enia

c3 cancer

"nherited thrombophilias


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Antithrombin De2ciency

%he most thrombogenic o0 theheritable coagulopathies*

2areN 4 in -/// to ./// indi*id+al3

Thrombosis ris d+ring &regnancy )itho+t&ersonal or amily history is ? B3

Thrombosis ris d+ring &regnancy )ith

&ersonal or amily history is 44 /3

Almost al)ays a+tosomal dominant andhomo=ygo+s and is lethal3



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Antithrombin Synthesi=ed in the li*er3

%inds and inacti*ate thrombin and the acti*atedcoag+lation actors "9a, 9a, 9"a, and 9""a3

Accelerated by he&arin3 %YPE " Antithrombin De2ciency

res+lt o reduced synthesis o biologicallynormal antithrombin

%YPE "" Antithrombin De2ciency

Characteri=ed by normal le*els o antithrombin

)ith reduced 0unctional activity3



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Untreated )omen had a ./ ris ostillbirth and 9-R3

!anagement(

a* Heparin or a6ected )omen d+ring &regnancy

)ith or )itho+t &rior thrombosis3

b* Recombinant human antithrombin "anticoag+lation m+st be necessarily )ithheld@s+rgery, deli*ery3

c* Antithrombin concentrate in0usion therapeutic coagulation &regnant )oman)ith antithrombin de'ciency )ho de*elo&edthrombosis d+ring ?rdtrimester3



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Protein # De2ciency

Pre*alence( - to ? &er 4///

7 to ( 0old increased ris or8TE3

Protein # Acti*ated by binding o thrombin to

thrombomod+lin

inacti*ating actor 8a and 8"""a3

Also inhibits the synthesis o&lasminogen acti*ator inhibitor 43

Largely +nchanged in &regnancy3



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Protein $ De2ciency

Pre*alence( - &er 4///

!eas+red antigenically determinedree, +nctional and total S le*els3

All three decline d+ring normalgestation th+s diagnosis is diOc+lt in&regnant )omen

7or screening( meas+re ree S

Protein d+ring -ndor ?rdtrimester3


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Purpura 9ulminans

Associated )ith neonatalhomo=ygo+s &rotein C or SDe'ciency3

Characteri=ed by etensi*e

thromboses in microcirc+lation soonater birth leading to sin necrosis3



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Activated Protein # De2ciency /9actor V eiden !utation

%he most prevalent o0 the ,no1nthrombophilia syndrome

HeteroFygous inheritance o0 0actor V

leiden is the most common heritablethrombophilia*

Acco+nts or / o 8TE cases in&regnancy

characteri=ed by resistance o &lasma to theanticoag+lant e6ects o acti*ated &rotein C3

Ca+ses(

a3 !issense m+tation in actor 8 gene



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Activated Protein # De2ciency /9actor V eiden !utation

The abnormal actor 8 retains its&rocoag+lant acti*ity th+s &redis&osed tothrombosis3

Diagnosis( D#A analysis



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Prothrombin -)()A !utation

missense m+tation in &rothrombin gene

There is ecessi*e acc+m+lation o&rothrombin )hich can be con*erted tothrombin3

7or hetero=ygo+s carrier )ith history, theris eceeds 4/ 3



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Hyperhomocysteinemia

There is ele*ated le*els o &lasmahomocysteine and is a 1ea, ris, 0actor3

A+tosomal recessi*e

Ca+ses(

C55BT thermolabile mutation o0 +G()6methylene6tetrahydro0olate reductase>!%H9R? the most common cause

De'ciency in the en=ymes in*ol*ed in

methionine metabolism3 #+tritional de'ciencies( olic acid, 8itamin

%5, or 8itamin %4-3

Overvie1 o0 inherited thrombophilias and their eect on coagulation cascade*


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-)(Amutatio

n

c3 Prothrombin le*el

O%HRO!B"' %HRO!B"' #OA-&A%"O


Dec3

thrombinne+trali=ation

9actor Vleiden

!utation

7actor 8

resistant todegradationby &rotein C

"nacti*ates actor8a

"nacti*ates actor

8"""a

Protein

$

Acti*ated &rotein C

Hyperhomocysteinem

ia

Protein C

Protein#

de2ciency

Thrombin binds tothrombomod+linon endothelial

cells

Protein S Protein S

Ac3uired thrombophilias


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Antiphospholipid Antibodies

A+toantibodies directed againstcardioli&in or against &hos&holi&idbinding &roteins s+ch as -glyco&rotein "3

CommonlyN b+t not al)aysN o+nd in&atients )ith SLE

.4- ris o thrombosis d+ring

&regnancy and &+er&eri+m @ACOG,20#23

Ac3uired thrombophilias


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Antiphospholipid Antibodies

De'ned by the ollo)ing eat+res @ACOG,20#2(

43 At least 4 +ne&lained etal death at orbeyond 4/ )s3

-3 At least one &reterm birth beore ? )sbeca+se o &re eclam&sia, se*ereeclam&sia, or &lacental ins+Ociency3

?3 At least ? +ne&lained consec+ti*e

s&ontaneo+s abortion beore 4/ )s3 "n 1omen 1ith this stateG

thromboembolism most commonlyinvolves the lo1er e4tremities*

Deep6 Vein %hrombosis


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Deep Vein %hrombosis

#linical Presentation(most venous thromboses are

con2ned to the deep veins o0lo1er e4tremities*

a3 "lioemoral B/

b3 "liac *ein 4B

c3 Cal *eins 5

!ost cases during pregnancyare le0t sided3

DEEP VE"' %HRO!BO$"$


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#linical Presentation

Abr+&t in onset, )ith &ain and edemao the leg and thigh

2eRe arterial s&asm &ale, cooletremity )ith diminished &+lsations

Homans sign6 cal &ain in res&onseto s:+ee=ing or to Achilles tendonstretching3

?/ 5/ o )omen )ith D8T areasym&tomatic3



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Diagnosis

A*#ompression &ltrasonography

2ecommended by AC1G as initialdiagnostic test

'on6invasive techni3ue that is

currently the most used 2rst line testto detect DV%*

normal 'ndings )ith *eno+s UTZ res+lt donot al1ays e4clude pulmonary

embolism* Thrombosis assoc3 )ith PE d+ring &regnancy

re:+ently originates in the iliac *eins3



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Diagnosis

A* #ompression &ltrasonography

B* !R"

"mmensely +se+l or diagnosis oilioemoral and &el*ic thrombosis3

#* D6Dimer $creening %ests Their +se in &regnancy is +ncertain b+t

negati*e res+lt is reass+ring3

D* Venography

-old standard to e4clude lo1ere4tremity DV%*

Com&lications( etal e&os+re, thrombosis,

time cons+ming3



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!anagement

Anticoagulation and limited activity During pregnancy( he&arin

@+nractionated0 L!$H is contin+ed

Post- partum ( beg+n sim+ltaneo+sly )ith

)ararin3

#fter symptoms ha"e aated( gradedamb+lation, elastic stocings Kanticoag+lation contin+ed3

Com&ression stocings is contin+ed or -yrs to red+ce incidence o Posthrombotic$yndrome @ chonic leg &aresthesial &ain,intractable edema, sin change, leg +lcer



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!anagement. Anticoagulation

ACCP s+ggest &reerential +se oL!$H d+ring &regnancy beca+se o(

%etter bioa*ailability Longer &lasma hallie

!ore &redictable dose res&onse

2ed+ced riss o osteo&orosis andthrombocyto&enia

Less re:+ent dosing

i l i



90/105


&n0actionated Heparin

Sho+ld be considered initial treatment othromboembolism and in sit+ation in )hichdeli*ery, s+rgery, or thrombosis maybenecessary3

Sae d+ring breasteeding3

!CH

Deri*ati*es o U7H

Cannot cross &lacenta

Acti*ates antithrombin, greater acti*ity againstactor 9a

Sho+ld be a*oided in )omen )ith renal ail+re

i l i



91/105


Car0arin

Generally contraindicated d+ring &regnancy

Used d+ring postpartum together )ithhe&arin

Thera&e+tic doses o U7H0 L!$H aremaintained or . days K +nitl "#2 is maintainedat -? or - consec+ti*e days @ACOG, 20#03

This is to &re*ent the anti &rotein C e6ect o

)ararin leading to &aradoical thrombosisand sin necrosis3

Sae d+ring breasteeding

! A i l i



92/105


During abor

Anticoag+lation sho+ld be con*erted romL!$H to shoter hal lie U7H to a*oid e&id+ralor s&inal hematoma d+ring ne+raial blocade3

ACCP or &lanned deli*ery discontin+e - dailySV U7H or L!H$ - ho+rs beore laborind+ction or CSD3

AC1G ad>+sted dose SV L!$H o U7H can be

discontin+ed -?5h beore labor ind+ction orCSD3

! t A ti l ti



93/105


During abor

AS2AP )ithholding ne+raial blocadeor 4/ 4-h ater last &ro&hylactic dose oL!H$ or -h ater the last thera&e+ticdose3

" labor begins )hile taing U7H,clearance can be *eri'ed by aPTTProtamine s+late3

7or )omen in )hom anticoag+lationthera&y has tem&orarily beendiscontin+ed, &ne+matic com&ressionde*ices are recommended @ACOG, 20##

! t A ti l ti



94/105


During Delivery

He&arin thera&y is generally sto&&edd+ring labor and deli*ery

AC1G and AAP recommend restarting

U7H or L!H$ no sooner than 5h ater*aginal deli*ery, or 54-h ater CSD3

Slo) "8 administration o &rotamines+late generally re*erses the e6ect o

he&arin

! t A ti l ti



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#omplication

Hemorrhage6 most seriouscomplication

Thrombocyto&enia @H"T

1steo&orosisThe latter t)o can be red+ced )ith

L!H$

! t A ti l ti



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Heparin "nduced %hrombocytopenia

T)o ty&es

a3 !ost common nonimm+ne, benign, re*ersiblethat de*elo&s )ithin 4ste) days o thera&y andresol*es W. days )0o thera&y cessation3

b3 Se*ere orm res+lt rom an imm+ne reactionin*ol*ing "gG antibodies direstec againstcom&lees o &latelet actor and he&arin3

"ncidence( X /34

!anagement( sto& he&arin thera&y And

initiate alternati*e anticoag+lation3a3 L!H$

b3 Dana&aroid @AC

c3 7onda&arin+ and argatroban

! t A ti l ti



97/105


Heparin "nduced Osteoporosis

%one loss may de*elo& )ithin 5 monthsor longer o he&arin thera&y and more&re*alent )ith cigarette smoer3

$omen treated )ith any hae&arin sho+ldbe enco+raged to tae 4,.// mg calci+ms+&&lement3

$uper2cial Venous %hrombophlebitis


98/105

Strictly limited to the s+&er'cial *eins o

sa&heno+s system ty&ically seen )ith*aricosities or se:+ela to an ind)elling "8catheter3

He&arin is gi*en )hen D8T is in*ol*ed

Pulmonary Embolism


99/105

y

ca+ses 4/ o maternal death b+t is+ncommon in &regnancy

"ncidence( 4 in B/// &regnancies

?/ 5/ o )omen )ith D8T )ill ha*e

coeisting silent P+lmonary embolism3

#li i l P t ti

P&!O'ARY E!BO"$!


100/105

#linical Presentation

Dys&nea, chest &ain

Co+gh

Synco&e

Hemo&tysis

Tachy&nea, a&&rehension, tachycardia

P+lmonic clos+re so+nd, rales, rictionr+b

ECG( right ais de*iation, T )a*e

in*ersion in anterior chest leads

Al*eolararterial di6erence o Q-/ mmHg

!assive Pulmonary Embolism

P&!O'ARY E!BO"$!


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!assive Pulmonary Embolism

De'ned as embolism ca+singhemodynamic instability3

!ost liely ca+sed by a saddle embolism3

"t is im&ortant to in+se crystalloids

care+lly and to s+&&ort %P )ith*aso&ressor3

1- treatment, ET int+bation and!echanical *entilation are com&leted

&re&aratory to thrombolysis, 'lter&lacement, or embolectomy3

Diagnosis

P&!O'ARY E!BO"$!


102/105

Diagnosis

CT P+lmonary Angiogra&hy

8entilation Per+sion Scintigra&hy L+ngscan

!agnetic 2esonance Angiogra&hy

"ntra*asc+lar P+lmonary Angiogra&hy

There is contro*ersy regarding the bestimaging method to be +sed in &regnancy3

!anagement

P&!O'ARY E!BO"$!


103/105

!anagement

"mmediate treatment is +llanticoag+lation3

Com&lementary &roced+res

a* Vena #aval 9ilters can be +sed in&regnant )omen )ho recently s+6ered PEand m+st +ndergo CSD3

b* %hrombolysis &ro*ide more ra&id lysisthan he&arin3 @eg3 Tiss+e &lasminogenacti*ator

c* Embolectomy stillbirth rate is -//

%hromboprophyla4is


104/105

%hromboprophyla4is

AC1G recommended &lacement o &ne+matic

com&ression de*ices beore CSD or all )omen notalready recei*ing thrombo&ro&hylais3

ACCP recommends ris ad>+sted a&&roach tothrombo&ro&hylais

See table .-

A##P Recommendation 0orthromboprophyla4is 0ollo1ing #$D


105/105

thromboprophyla4is 0ollo1ing #$D

!a>or 2is

actors "mmobility

Post&art+m hemorrhage Q 4 L )ith s+rgery

Pre*io+s 8TE

Thrombo&hilia

Antithrombin De'ciency 7actor 8 leiden

Prothrombin G-/-4/A

!edical condition

SLE

Heart Disease

Sicle Cell Anemia

%lood trans+sion

!inor 2is

7actors %!" Q ?/ g0m-

!+ltietal &regnancy

Post&art+m

hemorrhage Q4L Smoing Q 4/

cigarettes0day

7G2

Thrombo&hilia

Protein C de'ciency

Protein S de'ciency

Documents

Thromboembolic and Hematologic