Hemodynamic Disorders, Thrombosis, and Shock GWAI.pptx

8/10/2019 Hemodynamic Disorders, Thrombosis, and Shock GWAI.pptx

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Hemodynamic Disorders,

Thrombosis, and Shock

Dr. Samadara Siriwardena

BDS, MPhil, PhD, MD Oral Path

Dept of Oral Pathology


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Normal body

compositionWater composes about 60% of total body

mass

3 body compartments containing H2O:Intracellular = 70%

Interstitial = 2%

!lasma = %


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"dema#$e term edemasignies increased &uid in

t$e interstitial tissue spaces'

(luid collections in di)erent body ca*ities are*ariously designated hydrothorax,hydropericardium,or hydroperitoneum+t$e

last is more commonly called ascites,-


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a op ys o ogy oEdema

Hydrostaticpressure

!lasma colloidoncotic pressure

#.o opposingma/or factors

go*erning &uidmo*ement bet.een*ascular andinterstitial space:

natomicstructures .$ic$drain e1cessinterstitial &uidinto *enous blood:

ymp$atics


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"dema

"1udate 5 increased *ascular permeability

in&ammatory edema is a protein5ric$exudate.it$ a specic gra*ity t$at is usually greatert$an -020

#ransudate5 *olume or pressure o*erload orunder conditions of reduced plasma protein istypically a protein5poortransudate;it $as aspecic gra*ity less t$an -02-


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Increased Hydrostatic

!ressureLocalizedincreases in intra*ascular pressure

can result from impaired *enous return

e1- lo.er e1tremity deep *enous t$rombosiscan cause edema restricted to t$e distalportion of t$e a)ected leg-

Generalizedincreases in *enous pressure

.it$ resultant systemic edema occur mostcommonly in congestive heart failurea)ecting rig$t *entricular cardiac function-


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edema

Clinical Signs Most Likely Cause(s)

Bilateral symmetrical edema of skin& subcutis of both legs below kneesin 57-year-old man whose onlycomplaint is shortness of breath

Unilateral edema of one arm in a 60-year-old female with a mastectomy

scar on that side

Increased $ydrostaticpressure in *eins due tocongesti*e $eart failure

ymp$atic obstruction


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8educed !lasma Osmotic !ressure

lbuminis t$e serum protein most responsible for

maintaining intra*ascular colloid osmotic pressure'reduced osmotic pressure occurs .$en albumin isinade4uately synt$esi9ed or is lost from t$e circulation-

n important cause of albumin loss is t$e nephroticsyndrome,in .$ic$ glomerular capillary .alls becomeleay' patients typically present .it$ generali9ed edema-

8educed albumin synt$esis occurs in t$e setting ofdi)use li*er diseases +e-g- cirr$osis', or due to protein

malnutrition-In eac$ case reduced plasma osmotic pressure leads to a

net mo*ement of &uid into t$e interstitial tissues .it$subse4uent plasma *olume contraction-


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ymp$atic Obstruction

Impaired lymp$atic drainage and conse4uentlymphedemais usually locali9ed'

it can result from in&ammatory or neoplasticobstruction- (or e1ample t$e parasitic infection

lariasiscan cause e1tensi*e inguinal lymp$atic andlymp$ node brosis- #$e resultant edema of t$ee1ternal genitalia and lo.er limbs can be so massi*eas to earn t$e appellation elephantiasis.

;ancer of t$e breast can be treated by resectionand


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In&ammatory ymp$aticObstructionilariasis

parasitic infection

.$ic$ leads to lymp$atic

and lymp$ node brosisin t$e inguinal region

resulting in edema of t$e

e1ternal genitalia and

lo.er e1tremity called""!H>#II


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"?"@ 5 ummaryINCREASED

HYDROSTATIC

PRESSURE

Congestive Heart Failure

Ascites

Venous Obstruction

DECREASED

ONCOTIC

PRESSURE

Nephrotic Syndrome

Cirrhosis

Protein Malnutrition

INCREASED

PERMEABILITY

Inflammation

LYMPHATIC

OBSTRUCTION

Inflammatory

Neoplastic

H"8#

IA"8

BI?>"C


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"dema (luidExudate Transudate

Inflammatory igh hydrostati!

pr.

"ause

igh #ow Protein !ontent

$%.&'&( )%.&%'( Spe!ifi! gra*ity

+i!h -sent Inflammatory!ells


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ummary"dema is e1tra*asation of &uid from *essels into

interstitial spaces' t$e &uid may be protein poor+transudate, or may be protein ric$ +e1udate,-"demaresults from any of t$e follo.ing conditions:

Increased $ydrostatic pressure caused by areduction in *enous return +as in $eart failure,

?ecreased colloid osmotic pressure caused byreduced concentration of plasma albumin +due todecreased synt$esis as in li*er disease or increasedloss as in idney disease,

ymp$atic obstruction t$at impairs interstitial &uidclearance +as in scarring tumors or certaininfections,

!rimary renal sodium retention +in renal failure,

Increased *ascular permeability +in in&ammation,


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Subcutaneous Edema Edema of the

subcutaneous tissue is

most easily detected

!rossly (not

microscopically)

Push your "nger into it

and a depression

remains

pitting edema


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#ependent Edemais a prominent feature

of ;ongesti*e Heart (ailure' in legs if

standing or sacrum in sleeping patient

Periorbital edemais often t$e initial

manifestation of >ep$rotic yndrome

.$ile late cases .ill lead to generali9ed

edema-

Edema


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Pulmonary Edemais most fre4uently seen in ;ongesti*e Heart

(ailure

@ay also be present in renal failure adultrespiratory distress syndrome +8?,

pulmonary infections and $ypersensiti*ity

reactions


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Normal lung


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Pulmonary Edema


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Pulmonary Edema

Clinical Correlation

@ay cause deathby interfering .it$ O1ygen

and ;arbon ?io1ide e1c$ange

;reates a fa*orable en*ironment for

infection


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$rain Edema#rauma bscess >eoplasm Infection

+"ncep$alitis,


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$rain Edema

Clinical Correlation

(or e1tra &uid $asno space

Herniation into t$e

foramen magnum

leads to deat$


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;linical ;orrelation of "dema

#$e e)ect of edema may be /ust annoying to fatalcondition-

It usually points to an underlying disease-

Ho.e*er it can impair .ound $ealing or clearance

of infection-

;reates a fa*orable en*ironment for infection-

@ay cause deat$ by interfering .it$ O1ygen and

;arbon ?io1ide e1c$ange-


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%emodynamic

terminology%yperemia: locally increased blood

caused by arteriolar dilation .it$augmented in&o. as in a .oring muscleor acute in&ammation

Congestion: locally increased blood due

to impaired *enous out&o. +lungs in $eartfailure,


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%emostasis o&er&ie'Normal hemostasis@aintain blood &uid .it$in *essels

Induce rapid locali9ed plug at in/ury site

hrombosis(ormation of blood clot .it$in *essel

+appropriately or inappropriately,

#$ree components .$ic$ regulate normal$emostasis < t$rombosis:

Aascular .all !latelets ;oagulation cascade


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Hyperemia

Hyperemiaand congestion:/ Dot$ indicate a local increased *olume of blood

in a particular tissue

%yperemia/ an active processresulting from augmented

blood &o. due to arteriolar dilation

/ "1amples: sites of in&ammation

seletal muscle during e1ercise

/#$e a)ected tissue is redder t$an normalbecause of engorgement .it$ o1ygenated blood


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Congestion:apassive processresulting from impaired

*enous return out of a tissue

It may occur: systemically as in cardiac failure

locally resulting from an isolated *enous obstruction

#$e tissue $as a blue5red color (cyanosis): as .orsening congestion accumulation of

deo1ygenated $emoglobin in t$e a)ected tissues


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Congestion (continued)Chronic passive congestion: Is a long5standing congestion

#$e stasis of poorly o1ygenated blood causes:;$ronic $ypo1ia degeneration or deat$ of

parenc$ymal cells subse4uent tissue brosis;apillary rupture small foci of $emorr$age

p$agocytosis and catabolism of t$e eryt$rocytedebrisaccumulations of $emosiderin5ladenmacrop$ages


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i*er .it$ c$ronic passi*econgestion and$emorr$agic necrosis- *,;entral areas are red and

slig$tly depressedcompared .it$ t$esurrounding tan *iableparenc$yma forming aEnutmeg li&erE pattern+so called because itresembles t$e alternatingpattern of lig$t and darseen .$en a .$olenutmeg is cut,- $,;entrilobular necrosis .it$

degenerating $epatocytesand $emorr$age


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%ematoma:/ any accumulation 'ithin tissuet$at results

from a $emorr$age

arge accumulations of blood in body ca*itiesare called +according to location,:

/ Hemothorax

/

Hemopericardium/ Hemoperitoneum

/ Hemarthrosis


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Causes#rauma

t$erosclerosis

In&ammatory erosion of *essels .all

>eoplastic erosion of t$e *essel .all


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Purpura : lig$tly larger +35 to 5mm, $emorr$ages can be associated .it$:

many of t$e same disorders t$at cause petec$iae #rauma vasculitis increased *ascular fragility

Ecchymoses: arger +5 to 25cm, subcutaneous $ematomas +bruises,


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*,!unctate petec$ial $emorr$ages of t$e colonic mucosa a

conse4uence of t$rombocytopenia-

$,(atal intracerebral $emorr$age- "*en relati*ely inconse4uential*olumes of $emorr$age in a critical location or into a closed space +suc$as t$e cranium, can $a*e fatal outcomes-


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20% rapid loss of blood s$oc

Freater loss but slo. may $a*e littleimpact


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Hemostasis and t$rombosis


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%emostasis se+uence Aasoconstriction

!rimary Hemostasis +platelet plug,

% t i -


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%emostasis se+uence -

econdary Hemostasis +brin clot,

#$rombosis and antit$rombotic e*ents


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Platelet response to in0ury!latelets encounter e1tra*ascular matri1

molecules: collagen proteoglycansbronectin

!latelets respond in t$ree p$ases: =

2 =

3 =

d$esion

ecretion +release reaction,

ggregation


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Platelet adhesion and aggregation

?ecient Fpbreceptor on plateletsfor *W(:

?ecient Fp IIb5IIIacomple1:

?ecient *on WillebrandGs factor:

Dernard5ouliersyndrome

Flan9mann

t$rombast$enia

Aon Willebrand disease


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C t l l f th bi


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Central role of thrombin

(unctions:

, (ormation ofbrin

2, Induce plateletaggregation

3, cti*atesendot$elium

, cti*ation oflymp$ocytes monocytes

ibrinolytic system


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y yrestriction of clotting to localsite of in0ury

pplication: abe*idence of ?I;J

+3 non5

morp$ologicabnormalities,

, prolonged !#

2, ele*ated ?5dimer

3, t$rombocytopenia

ig2 34-, Pathologic $asis of

One 8D;morp$ologicabnormalityJ

+not sensiti*e orspecic,

$istocytes

hrombosis a clot 'ithin


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hrombosis a clot 'ithin&esselPredisposing factors 7ircho'8s triad

Endothelial 9n0ury

bnormalblood &o. Hypercoagulability

#raumaat$erosclerosis*asculitis

In$erited orac4uired

t$erosclerosisaneurysms*al*ular $eartdisease

$lood clot


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$lood clot

7enous thrombosis


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7enous thrombosis

@ost common locationJ

@ost serious complicationJ

?eep leg *eins +pel*ic *eins 2nd,

!ulmonary emboli9ation


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#$rombi can $a*e grossly +and microscopically,apparent laminations called lines of :ahn'

t$ese represent pale platelet and brin layersalternating .it$ darer eryt$rocyte5ric$ layers-

uc$ lines are signicant only in t$at t$eyrepresent t$rombosis in t$e setting of &o.ing

blood' t$eir presence can t$erefore potentiallydistinguis$ antemortem t$rombosis from t$ebland nonlaminated clots t$at occur in t$epostmortem state +see also belo.,-

lt$oug$ suc$ lines are typically not asapparent in *eins or smaller arteries +t$rombiformed in sluggis$ *enous &o. usually resemblestatically coagulated blood, careful e*aluationgenerally re*eals ill5dened laminations


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#$rombi on $eart *al*es are called&egetations- Dacterial or fungal blood5borneinfections can cause *al*e damage

subse4uently leading to large t$romboticmasses +infecti*e endocarditis,-

terile *egetations can also de*elop onnoninfected *al*es in $ypercoagulable states

so5called nonbacterial thromboticendocarditis-


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?issolution is t$e result of brinolytic

acti*ation .$ic$ leads to rapid s$rinage ande*en total lysis of recent t$rombi-

Wit$ oldert$rombi e1tensi*e brinpolymeri9ation renders t$e t$rombus

substantially more resistant to proteolysis andlysis is ine)ectual-

#$is is clinically signicant becauset$erapeutic administration of brinolytic

agents +e-g- t5! in t$e setting of acutecoronary t$rombosis, is generally e)ecti*eonly .it$in a fe. $ours of t$rombus formation-


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Older t$rombi become organizedby t$e ingro.t$ ofendot$elial cells smoot$ muscle cells and broblasts

into t$e brin5ric$ clot-;apillary c$annels are e*entually formed-

lt$oug$ t$e c$annels may not successfully restoresignicant &o. to many obstructed *essels

recanali9ation can potentially con*ert a t$rombus intoa *asculari9ed mass of connecti*e tissue-

"*entually .it$ contraction of t$e mesenc$ymal cellsonly a brous lump may remain to mar t$e originalt$rombus site-

Occasionally instead of organi9ing t$e center of at$rombus undergoes en9ymatic digestion presumablybecause of t$e release of lysosomal en9ymes fromtrapped leuocytes and platelets-


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;linical ;orrelationsAenous *ersus rterial #$rombosis

#$rombi are signicant because they causeostruction of arteries and veins and arepotential sources of emoli.

Aenous t$rombi can cause congestion andedema in *ascular beds distal to an obstructionbut t$ey are most .orrisome for t$eir capacityto emboli9e to t$e lungs and cause deat$-

;on*ersely .$ile arterial t$rombi can emboli9e

and e*en cause do.nstream tissue infarctiont$eir role in *ascular obstruction at critical sites+e-g- coronary and cerebral *essels, is muc$more signicant clinically-


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7enous hrombosis (Phlebothrombosis,

@ost *enous t$rombi occur in t$e supercial ordeep *eins of t$e leg- "g: *aricosities- uc$

supercial t$rombi can cause local congestions.elling pain and tenderness along t$e courseof t$e in*ol*ed *ein but t$ey rarely emboli9e-

>e*ert$eless t$e local edema and impaired

*enous drainage do predispose t$e o*erlyingsin to infections from minor trauma and to t$ede*elopment of varicose ulcers.


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#eep &enous thrombosis can occur .it$ stasis

;ardiac failure is an ob*ious reason for stasis in t$e *enouscirculation- #rauma surgery and burns usually result in reducedp$ysical acti*ity in/ury to *essels release of procoagulantsubstances from tissues and


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;ardiac and rterial #$rombosis!therosclerosisis a ma/or initiator of

t$romboses because it is associated .it$ lossof endot$elial integrity and abnormal *ascular

&o.-"heumatic heart diseasecan cause atrial

mural t$rombi due to mitral *al*e stenosisfollo.ed by left atrial dilation and concurrent

atrial brillation-

Embolism


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Embolism#e"nitiondetac$ed intra*ascular solid

li4uid or gaseous mass carried by blood to asite distant from its origin-ypeshromboembolism:K LL% of all emboli

at or marro': post5trauma to bonesCholesterol: after in*asi*e *ascular procedures

presenting as $ematuria or renal insuMciency dueto multiple renal microinfarctionsumor from neoplasms in*ading *esselsoreign body: intra*enous de*ices< drug abuse

#$romboembolism:


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Pulmonary thromboembolism

Occlusion large pulmonary artery

Occlusion ofsmall arteryresults in.$at type ofinfarctionJ $emorr$agic



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200000 deat$s


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#$e pat$ogenesis of fat emboli syndromeprobably in*ol*es bot$ mec$anical obstructionand bioc$emical in/ury-

(at microemboli occlude pulmonary andcerebral micro*asculature' *ascular occlusionis aggra*ated by local platelet anderyt$rocyte aggregation-

#$is pat$ology is furt$er e1acerbated by freefatty acid release from t$e fat globules

causing local to1ic in/ury to endot$elium-


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ir "mbolism

Fas bubbles .it$in t$e circulation canobstruct *ascular &o. +and cause distalisc$emic in/ury, almost as readily as

t$rombotic masses can-ir may enter t$e circulation during obstetric

procedures or as a conse4uence of c$est .allin/ury-

Fenerally more t$an 00 m of air arere4uired to produce a clinical e)ect' bubblescan coalesce to form frot$y massessuMciently large to occlude ma/or *essels-


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mniotic (luid "mbolismmniotic &uid embolism is a gra*e but fortunately

uncommon complication of labor and t$e immediatepostpartum period + in 0000 deli*eries,-

It $as a mortality rate in e1cess of 20% to 0%-

#$e onset is c$aracteri9ed by sudden se*ere dyspnea

cyanosis and $ypotensi*e s$oc follo.ed by sei9uresand coma- If t$e patient sur*i*es t$e initial crisispulmonary edema typically de*elops along .it$ +in $alft$e patients, disseminated intra*ascular coagulation

+?I;, due to release of t$rombogenic substances from

amniotic &uid-#$e underlying cause is entry of amniotic &uid +and its

contents, into t$e maternal circulation *ia a tear in t$eplacental membranes and rupture of uterine *eins-

Infarction


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Infarctionn infarct is an area of isc$emic necrosis caused by

occlusion of eit$er t$e arterial supply or t$e *enousdrainage in a particular tissue-

>early LL% of all infarcts result from t$rombotic orembolic e*ents and almost all result from arterial

occlusion-

Occasionally infarction may also be caused by ot$ermec$anisms suc$ as local *asospasm e1pansion of anat$eroma secondary to intrapla4ue $emorr$age ore1trinsic compression of a *essel +e-g- by tumor,-

lt$oug$ *enous t$rombosis can cause infarction it moreoften merely induces *enous obstruction and congestion-


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@orp$ologyInfarcts are classied on t$e basis of t$eircolor +re&ecting t$e amount of $emorr$age,and t$e presence or absence of microbial

infection-#$erefore infarcts may be eit$er red

+$emorr$agic, or .$ite +anemic, and may beeit$er septic or bland-


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;ed infarctsOccur- .it$ *enous occlusions +suc$ as in o*arian torsion,'

2- in loose tissues +suc$ as lung, t$at allo. blood to collectin t$e infarcted 9one'

3- in tissues .it$ dual circulations suc$ as lung and smallintestine permitting &o. of blood from an unobstructedparallel supply into a necrotic area +suc$ perfusion notbeing suMcient to rescue t$e isc$emic tissues,'

- in tissues t$at .ere pre*iously congested because ofsluggis$ *enous out&o.'

- .$en &o. is re5establis$ed to a site of pre*ious arterialocclusion and necrosis +e-g- fragmentation of an occlusi*eembolus or angioplasty of a t$rombotic lesion,-


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In solid organs t$e relati*ely fe.e1tra*asated red cells are lysed .it$ t$ereleased $emoglobin remaining in t$e form of$emosiderin-

#$us infarcts resulting from arterial

occlusions typically become progressi*elymore pale and s$arply dened .it$ time-

In spongy organs by comparison t$e$emorr$age is too e1tensi*e to permit t$e

lesion e*er to become pale-O*er t$e course of a fe. days $o.e*er it

does become rmer and bro.ner re&ectingt$e accumulation of $emosiderin pigment-


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pleen


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Septic infarctionsoccur .$en bacterial *egetations from a $eart*al*e emboli9e or .$en microbes seed anarea of necrotic tissue-

In t$ese cases t$e infarct is con*erted into anabscess .it$ a correspondingly greaterin&ammatory response

#$e e*entual se4uence of organi9ation

$o.e*er follo.s t$e pattern pre*iouslydescribed-


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(actors #$at In&uence ?e*elopment

of an InfarctAascular occlusion can $a*e no or minimal

e)ect or can cause deat$ of a tissue or e*ent$e indi*idual-

#he ma$or determinants of the eventualoutcome include

%. the nature of the vascular supply,

&. the rate of development of the occlusion,

'. vulneraility to hypoxia,

. and the oxygen content of lood.


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8ate of ?e*elopment of Occlusionlo.ly de*eloping occlusions are less liely to

cause infarction because t$ey pro*ide time fort$e de*elopment of alternati*e perfusion

pat$.ays-


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O1ygen ;ontent of Dlood#$e partial pressure of o1ygen in blood alsodetermines t$e outcome of *ascular occlusion-

!artial &o. obstruction of a small *essel in an

anemic or cyanotic patient mig$t lead totissue infarction

,features


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features

ung acute $emorr$agicinfarction +note .edge5s$ape,

Bidney remote $ealedinfarction +brous scar,

Shock


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?ef-: systemic $ypoperfusion due to reducedcardiac output or reduced e)ecti*e blood *olume-

@a/or causes:;ardiogenic : myocardial pump failure

Hypo*olemic :loss bloodeurogenic : spinal cord in/ury

nap$ylactic : generali9ed Ig"5mediated $ypersensiti*ityresponse .it$ .idespread *asodilation increasedcapacitance increased *ascular permeability


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Septic shock


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p

-6465= mortality rate K00000 deat$s


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ynegati&e sepsis

!roduced by:

!roduced by:

!roduced by:

macrop$ages

macrop$ages

macrop$ages

;linical se4uelae of sepsis


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>O = nitric o1ide

!( = platelet5acti*atingfactor

Stages of shock


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Stages of shockNonprogressi&e phase

8e&e1 mec$anisms acti*ated and perfusion of*ital organs maintained

Progressi&e stage!ersistent tissue $ypoperfusion leads to

.idespread $ypo1ic cell damage metabolicacidosis prolonged *asodilation

9rre&ersible stagee*ere cellular in/ury .it$ multiorgan failure

dominated by renal lungs $eart

Documents

Hemodynamic Disorders, Thrombosis, and Shock GWAI.pptx