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					We know that during pregnancy, women have a five-
fold risk of VTE as compared to non-pregnant
women.
Absolute risk of group VTE during pregnancy is
between 0.5-3/100 women, based on studies using
Radiographic documentation.
As we know that PE is one of leading cause of
maternal death in U.S. The prevalence and severity of
this condition warrant consideration of anticoagulant
therapy in pregnancy for women at risk for VTE.
Numerous changes in the coagulation system
account for the hypercoagulation state associated
with pregnancy.
Virchow’s triad  factor (Fibrinogen, we will
brand, Ristocetin co-factor activity) anticoagulant
(AI, UI, S,C) marked mean term and post delivery.
Recently, it has been recognized that up to ½ of
women who have thrombotic events during
pregnancy possess an underlying congenital or
acquired thrombophilia.
Most common thrombophilias in occasion:
– FSLM – prevalence of 5% of this population.
– PGM – 2% of 5% of this population.
In approximately 50% of patient with hereditary
thrombophilia, the initial thrombotic event occurs
in the presence of an additional risk factor e.g.
pregnancy ocp orthopedic trauma, and major
surgery.
Traditionally, it was believed that the risk of VI was
greatest in the 3rd trimester and immediately
postpartum.
Most recent studies have found that antepartum DVT is at
least as common as postpartum and occurs with equal
frequency in all 3 trimester.
However, PE is a common postpartum.
Recurrence: Women with history of TE have an risk of
recurrence when they become pregnant.
The estimate recurrence 7.5 – 12% were based only on 2
random secondary trials.
But no studies differentiated between the risk of
recurrence based on underlying risk factor (but most of the
estimate of recurrence are based on women who had their
initial event day OCP use).
? Other familial hypercoagulation state
 These are some of the clinical consideration and
 recommendation that might assure some of these
 question which we needed in our clinical practice.
 How should be tested?
1.   Hx of thrombosis esp. if it will affect man.
2.   Family hx of thrombosis without personal but strong family hx of
     thrombosis. History of thrombosis  control, e.g. first degree
     relative with AT deficiency homozygous factor 5LM or PGM.
     May benefit from testing, e.g. – antepartum prophylaxis. – They
     are more likely to have multiple inherited risk factors with risk
     of thrombosis (4-40%), e.g. 15% C + 39% S  positive FSLM
     with markedly risk of thrombosis.
APS  (pt with history of T, RDL, early or severe PET or
unexplained IUGR)  prophylactic anticoagulation may
improve the pregnancy outcome.
Hereditary thrombophilia C, S, AT, FSL, PGM, Meth.
THFR.
Severe early PET, unexplained fetal loss or still birth
Abruption  No RCT supporting the efficacy of
anticoagulation Rx in preventing these conditions.
So, it is important to discuss with the patient the
implication of Positive test and to determine whether the
patient management would be altered during pregnancy
or not.
3. Also test AT, PC&S with extensive ____,
   Warfarin and Heparin use – may result in falsely
   low valves.
4. DNA test for FSLM, PGM, THFR are reliable in
   pregnancy.
So after we identified our patient
candidate for Rx, what are the type of
anticoagulation.
 What test should we order?
 These are the test that we order to evaluate the risk of
 thromboembotic events in female with history of
 thrombosis FHx 1st degree relative with specific
 mutation.
1.   Given the law prevalence of AT-III and consideration should
     variable pathogenicity of Protein C & S) be given to test only
     when all other studies have yielded with negative results.
     Normal physiological changes in pregnancy result in marked
     alteration.
2.   In Prot S & C, so the test should be deferred until after
     pregnancy, e.g. Prot S  by 40% in pregnancy.
HEPARIN
–  in pregnancy   p. volume
                      R. clearance
                     in Heparin binding Protein
                     Heparin deg. by the placenta
          Bioavailability of Hep.
No prospective trials that have determined adequate
prophylactic doses in pregnancy.
Still the major concerns with use of Heparin during
pregnancy are not fetal but maternal  include
      OST, Bleeding, skin necrosis
- 2 P.T. of pregnant women exposed to Heparin
  confirmed a mean bone loss of 5%, complete
  reversability of this process has not been clearly
  established nor the dose response relationship.
- Some found that selected patient with FHx of
  osteoporosis, smoker – p. evaluation of bone density
  may have therapeutic implication.
                          HIT
      BNIT                                  IT
•   Common                        -   Less common
•   Reversible                    -   >severe
•   Less severe                   -   D 5-14 of full dose
•   Occur in 1st few days of Rx         of Heparin
•   Not require cessation of Rx   -   3% of patient may
                                        have wide spread
                                        thrombosis
DVT and PE are the most frequent presentation
Rx should discontinue
It is recommended to measure Platelets on Day 5
and periodically for the 1st 2 weeks of treatment.
                         LMWH
1. Advantages over standard Heparin
   – It may reduces the 3 complications associated
     with standard Heparin – (Bleeding,
     Osteoporosis, HIT).
   – It crosses the placenta into fetal circulation.
   – It has better bio-availability over the standard
     Heparin because of H binding process.
   – It can be restricted to once or twice daily dosing.
2. Dose   same reason  R. clearance and p.
   volume.

3. No need for laboratory monitoring but peak
   antifactor – Q4-6 weeks should be utilized
   especially in patient receiving twice daily dose.
Relatively C.I. in pregnancy, because it crosses the
placenta into fetal circulation.

It is use mainly pp and antipartum should be
restricted to selected patient – RhD, vulv. HD, AF –
those with prolonged high dose Heparin Rx is
contraindicated.
After we knew the type of anticoagulant, what do we
use for them?
Adjusted dose not frequently used mainly used in
selected patient those with vulvular heart disease
and AF.
Certain high risk condition that require dosage
adjustment to achieve higher therapeutic level.
               REGIMEN
Because of the absence of adequate prospective
trials, number of different prophylactic regimen was
offered by various consensus panel.
One study determined that during pregnancy, a
doubling of the dose of Heparin was required to
achieve same anticoagulant response of non-
pregnant patient – Taley 5u 2t/d.
Pregnant ladies who require adjusted dose
prophylactic, may benefit from higher bio-
availability of LMWH.
          ACUTE THROMBOSIS

After 3 months of therapeutic heparinization,
experts differ as to what should be done for rest
of the pregnancy.
Some recommend using L.D. of S.C. Heparin
and others in continuing therapeutic
anticoagulant for the rest of prgnancy.
LMWH may be an alternative Rx for acute
event but actual dose is not clear yet.
    INTRAPARTUM & POSTPARTUM

  Intrapartum care is complicated, and Rx
  approaches vary.
  It is helpful to consult with personnel who have
  expertise in the intrapartum management of
  such patient.

Low dose – varies widely, although all agree that
  the postpartum period is one of high risk.
                    ANALGESIA
The use of spinal or epidural in patient may receiving
thromboembolic prophylaxis is controlled.
Safety of LMW, or oral anticoagulant – before the
procedure is unclear (because no studies addressing
anticoagulant in pregnancy relative to use of conduction
anesthesia).
Although, FDA – reported cases of
Finally, the American Society of _______ anesthesia
has recommended.
MAJOR CONCERN
       6-12 Wks.              Mid Trimester
- Skeletal embryopathy     - optic atrophy
- Stippled epiphysis       - microcephaly
- Nasal & limb hypoplasia - developmental delay

Bleeding and fetal loss may occur at anytime.

				
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