Introduction

Blood travels from the heart to the rest of the body through blood vessels called
arteries, and returns back to the heart through other blood vessels called veins.
Veins are either superficial or deep. The former are close to the surface of the body,
and the latter is deep in the body and are almost always beside an artery of the same
name, eg the iliac vein is adjacent to the iliac artery.
Arteries and veins are structurally different. The former have muscular walls,
unlike the latter, which also contain valves. Blood clots can form in an artery or a vein
(thrombosis). Arterial thrombosis leads to a compromise of the blood flow to the body
part served by the artery. The term venous thromboembolism (VTE) is used to refer to
thrombosis in the veins. VTE can occur in any vein in the body. The common sites are
the veins in the legs and/or pelvis (leading to deep vein thrombosis DVT) and the
lungs (leading to a pulmonary embolism PE).
The most serious complication of a DVT is PE, which is life-threatening. PE
results from a thrombus breaking off (embellishing) and travelling to the lungs where it
can get stuck, leading to a compromise in the blood flow to the affected part of the
lungs. The likelihood of DVT is increased during pregnancy, and in the first six weeks
after childbirth. The risk is one in 500, which is 10 times the risk of a non-pregnant
woman of the same age.
The highest risk of DVT and/or PE is in the immediate period after childbirth.
However, it is important to remember that DVT and/or PE can occur at any time during
pregnancy, even in the first three months. About 10 to 20% of VTEs are PEs, which is a
common cause of maternal deaths in developed and developing countries, including
Malaysia.
There are several risk factors, some of which are inherited, while others are
acquired. These risk factors are identified in about 80% of those affected. It is not
uncommon for a person to have more than one risk factor. The inherited risk factors
include Factor V Leiden mutation, Prothrombin gene G20210A mutation, Antithrombin
III deficiency, Protein C or S deficiency, disorders of plasminogen and plasminogen
activation, and a strong family history (mother, father, brother or sister who has had a
DVT).
The risk factors related to pregnancy are maternal age of 35 years or more,
multiparity (have had three or more babies), previous DVT, high blood pressure,
dehydration, medical conditions like heart disease, lung disease or arthritis, multiple
pregnancy (twins or more), and hospitalisation.The risk factors related to delivery are
prolonged labour, instrumental vaginal delivery, Caesarean section, post-partum
haemorrhage, and blood transfusion.
The risk of VTE may increase or decrease. It may increase if other factors
develop in addition to the initial risk factors, eg complications during delivery in an
obese mother. It may decrease with smoking cessation.The obstetrician and the
midwife will assess a pregnant womans risk at the time of pregnancy, when changes
occur during pregnancy, at admission to hospital, and after delivery.

Objectives
i) To give a good information about DVT involving pregnant women which can be used
as references or guidance in handling patients with suspected DVT.
ii) As a tool in helping to develop an implementation and evaluation plan for DVT patient
and can be used as guideline in the workfield as a midwife.












Central Points
Thrombosis can affect anyone, but being pregnant makes your blood more likely
to clot. Doctors believe that the changes in clotting of the blood are designed to reduce
bleeding at the time of normal delivery.When youre carrying a baby there is a dramatic
reduction in the speed of blood flow in your veins, which carry the blood from your legs
back to the heart. Doctors think that this is due to the effect of pregnancy hormones on
the veins and also because of the womb getting bigger as the pregnancy advances.
The reduction in blood flow becomes obvious in pregnancy by 16 weeks and is at
its most sluggish closer to full-term as your body gets ready for the actual delivery. The
blood flow does not return to normal until six weeks after delivery. This sluggish flow in
the veins is why many women get some swelling of the legs when they are pregnant.
It is this reduction in blood flow, combined with the increased clotting tendency while
pregnant that can result in a clot in the leg. This condition can be prevented, and if it
does occur, can be treated.Also, at the time of delivery, as the baby presses on the
veins in the pelvis, minor damage can occur to these veins leading to an increased risk
of having a clot for up to six weeks after delivery.In Malaysia, PE is the third cause of
maternal mortality according to the report on Confidential Enquiries into Maternal
Deaths from 1991 to 1996.

Literature Review
Pregnant women are more susceptible than non-pregnant women to forming
blood clots in their veins (venous thrombosis). When these clots occur in the deep leg
veins, the clot can break up and fragments (emboli) move to the lungs where they may
block the blood flow to the lungs (pulmonary embolism). This can have serious
consequences.





Deep vein thrombosis (DVT) is a serious problem in the antenatal and postpartum
period of pregnancy. Thromboembolic complications are the leading cause of both
maternal and fetal morbidity and mortality (Greer 2002). The incidence of venous
thromboembolism during normal pregnancy is sixfold higher than in the general female
population of childbearing age (Holmes 2005).
During normal pregnancy there are substantial changes in the hemostatic
system, many of which are procoagulant and are thought to be in preparation for the
hemostatic challenge of delivery. Normal homeostasis requires a balance between
coagulation and fibrinolysis to maintain the integrity of the vascular. The complex
physiological changes evident during pregnancy appear to ensure a constant
coagulation-fibrinolysis balance. The balance is maintained, at least partly, by an
increase in fibrinolytic activity, but decreases in other factors such as factor XI, and
monocyte tissue factor expression may also serve to counterbalance procoagulation
changes.
The causal link between pregnancy and VTE is best explained by Virchows triad,
a framework that categorizes elements of the pathophysiology of VTE into three broad
categories: venous stasis,vascular damage, and hypercoagulability (Figure 1). Venous
stasis,which begins in the first trimester and peaks at 36 weeks (Macklon NS 1997) is
thought to be caused by progesterone-induced venodilation, pelvic venous compression
by the gravid uterus, and pulsatile compression of the left iliac vein by the right iliac
artery.The latter may lead to the marked propensity for left-leg DVT in pregnancy (over
80%)(Ray JG 1999).DVT in pregnancy appears to more commonly arise from proximal
veins (iliac and femoral) rather than calf veins, the usual location in nonpregnant
patients, leading to a higher propensity for isolated iliac vein thrombosis and ileofemoral
thrombosis in pregnant patients with DVT (Chan WS 1990).As a consequence of the
latter, pregnancy associated DVT is more likely to be associated with long term post-
phlebitic syndrome (Bergqvist A,1990). Vascular damage to the pelvic vessels can
occur during pregnancy due to venous distension, as well as after normal vaginal,
assisted vaginal, or cesarean deliveries.Hypercoagulability occurs as the hemostatic
system is progressively activated to prepare the pregnant women for the hemostatic


challenges of delivery. This hemostatic challenge is illustrated by the fact that
peripartum hemorrhage remains the leading cause of maternal mortality in the
developing world, and has likely been the leading cause of maternal mortality
throughout human evolution.( Khan KS 2006).

Figure 1











References:
1. Oral Rivaroxaban for Symptomatic Venous Thromboembolism. New England
Journal of Medicine. December 2010.
2. Spencer FA, Emery C, Lessard D, et al. The Worcester Venous
Thromboembolism Study : A population-based study of the clinical epidemiology
of venous thromboembolism. Journal of General Internal Medicine 2006; 21:722
727.