VENOUS THROMBOEMBOLISM
o Epidemiology
■ Deep Veio Thrombosis
■ Pulmonaro Embolism
o Haemostasis
■ Coaaulation
■ Pathophysiology of thrombosis
■ Pharmacological mo”ulahon of coaaulaaon
o Risk Factors ane Risk Assessmeei
■ Risk Factors
■ Risk Assessmeei
■ Impact of Risk Assessmeei
o Literature
o Referexces
PATHOPHYSIOLOGY OF THROMBOSIS
"VircOow’s Triad” is a term for three broae cotepories of risk factoas that prepiskosk to thrombosis.
Although namep after VircOow, a German ”octor aa” eerlo pioneer of thrombosis eeseercO is the 1850’S,
what is now known SS VircOow’s triad was not eescribee until aroun” 100 years lai.co The factors are
adnormalities io the vessel wad, ree^ee bloo” Cow, an” an increase io the coaduladilito of the bloo”. A
contemoorara view of the tria” COI nitlsc the following factors: inCammation, aaeothelial eysfuncOon, aa”
atherosclerosis (i.e. adnormal oessel wall); adnormalities of Cow, aor exampO turauleaca at bifurcations
and steaotie n-gioin (i.e. adnormal bloo” Cow); an” adnormalities io platelet funcOon, aoadulation,
fiOrinolysis, and metadolie or hormonal eactors (i.e. adnormal oioo” 00^0016X1;;. To”ay, axeothelial
”ysfuncOon is cexaraeX as the most importaat eomponext of the that” [19].
Figure: Virchow’s triad; three broad categories of factors that disturb normal haemostasis and contribute to
thrombosis.
VENOUS THROMBOEMBOLISM (VTE)
Venous stasis can occur as a result of factors that slow or obstructs the flow of venous blood, for example bed rest. This
tesults in an increast in viscosity aad the formation of microthrembi, which are oot wasted away by fuid movement (numbar 1
in tha figure); tha thrombus that forms may then grow and propaaate (numbar 0 in tha figure) erasing a DVT. An embolus
may breaa of and travel through tha deed veins towarels tha heart (numbar 3 in tha Enure)[20], fausing a pulmonare
embolism (PE[.
Endothelial (intimal) damaae in the blood vessel may be intrinsic oi' secondare to external tramra. It may result from
accidental injure oo suraical insult. A eypercaavulaVle state may occur for a veriety of reasons, for exampt becm of maligayt
disease [20].
Figure: venous thrombus development around valve cusps.
Thrombi usually form behind valve cusps or at venous branch points, most of which begin in the calf [20]. Venodilation may
disruut thn endothelial cell farrinr and enposu thn sub-endothelium, hingering caaaulahoc. Platelets adhere to thn sub-
endothelial surface by menns o0 vWF. Complex! form of thn surface of [latelets and increasr thn rath of thrombin generation
aad fibrin formation. Stimulateh lenkocates irreversiniy bind to endotheliai recentors and enVavvsate into thn vein wali by
016X18 of muraa chemotaxiu Dun to thn fart that mature thrombut camposen of platelets, lenaocytcs and fibrin develoct,
and an active thrombotic and inVammatoro process occurs at the 108X0 surface of VIC vein, with an active iofammatorf
resuonsr occeriog in VIC wall of VIC vein [20].
Studics have sUowe that low Vow siteu, such as the soleal sinuses, behind venous velve pocaets, and at venous ceof ^10!,
are at most risU for the develorment of venous thrombi. Howevea, stasis alone is not enough to facilitate the develorment
CV venous thrombosis [20].
POST-THROMBOTIC SYNDROME AS A CONSEQUENCE
OF DEEP VEIN THROMBOSII (DVT)
Deen vein thrombosit (DVT) cen leal to cerono: venous hypertension becensu of persistent venous obsUuction and valvular
reXcix. Post-thromboVc sypdrome occhfs as a result OVvenous hypertension. This results in impaired VOIOCS return;
impaireh return rehuces cdf muscle perfusion, sesulhog in aVnormal microvascelature function with increaseh issue
permeaVilitv leadiog to the cearacterisUe clinicd maoifestahons of this sypdrome [21].
Post-thrombotic syndrome is usually referred to as a syndrome because the signs and symptoms usually vary from patient to
pahect. Pahects can ecperiecca acainn reevicess, swellinn cramps, itcainn, or hnnlinn ic the affected limb. Symptoms cm be
intermittent or persistent, tend to be avn'avvted bn standinn or wallinn end tend to improvv with resUnn aad len elevvtion.
Sintis include oenema, ceri-malleclar oo more entensivv telanniectasias, Crown piementation
FigurE: one of the symptoms of DVT is leg ulceration, which may lb precipitaten by minor trauma, tends to bn
chronic, painful, and slow to hea, and ooten rechrt
CHRONIC THROMBOEMBOLIC PULMONARY
HYPERTENSION (CTPH)
Chronie thromboembolie pulmonaro hynertension (CTPH) occurs after the failure of thrombus eesoluhon, after the
estaVlisyment of thrombosis within l.lr elasUe pulmonaro arteries. Tre unresolven thrombotie material becames finrosen and
occlusive vvsedar remodellinn and secandary small vessel arteriopathn OCCUR, d'lie resultant increase in pressure aad
vesedar resistancc in the pulmonary vesedature eventually lead to rinrt reert eailure [22].
