Q.1:-What do we mean by the
term venous thromboembolism (VTE)
& is prevalence ?? Ans: VTE encompasses deep vein
thrombosis (DVT) and pulmonary
embolism (PE). The incidence of VTE ranges from 0.76 to 2.0 episodes
per 1,000 pregnancies and varies from country to county. Fortunately in our
country VTE is relatively uncommon though DM & HTN are rampant. Admittedly,
many cases remain undiagnosed and are treated as Resp distress (in post op
period particularly), Moreover minor pulm embolism can often be self limiting.
VTEs account for 9% of all maternal deaths in the United States.
Q.2: When VTE is more common & when
PE is more common both being the expression of same pathology?? Ans:-Approximately 80%
of all VTEs express as DVT in pregnancy period
and 20% of all VTE are manifested
as PE . But PE occurs
more frequently postpartum. .
Approximately half of all VTEs occur in the antepartum period though Cesarean
delivery imparts a three to five times greater risk than a vaginal delivery.
Ans: Pregancy:--Pregnancy is considered a
hypercoagulable state. Normal pregancy changes favours a hypercoagulable
state e.g. due to rise of 1) Fibrinogen,
2) other coagulation factors, 3) and plasminogen activator inhibitor-1 (PA1-1)
levels. All such components are raised.
By contrast natural anticoagulants
are decreased like A) free protein S levels, and B) fibrinolytic
activity.
Q.4: What may be other top up conditions to promote VTE in preg?? Ans:-One of the most significant risk factors
is 1) a personal history of VTE. 2) Medl disorders like heart disease, lupus, obesity, diabetes, and hypertension
increase risk of thrombosis. 3) Recent surgery, 4) family history of VTE, 5) bed
rest or prolonged immobilization, 6) smoking, 7) age older than 35 years, 8) multiple
gestations, 9) preeclampsia, and 11) postpartum infection also promotes
thrombus formation.
The following associated conditions
are now considered not an important cause of accelerated rate of VTE!! Such are
Fetal death in utero, severe IUGR, abruption, and severe early-onset
preeclampsia have been correlated with underlying thrombophilias that affect
uteroplacental circulation. However, these are still controversial and recent studies fail to
reliably establish causal links between thrombophilias and these adverse
pregnancy outcomes.
Q. 6 Kinds of thrombophilias
??
Thrombophilias may be
inherited or acquired. Pregnancy may trigger an event in women with an
underlying thrombophilia.
What goes
wrong with her sice birth?? Causes of congenital / Inherited thrombophilias
Inherited
thrombophilias are present in
over half of all maternal thrombotic events. The causative congenital factors
are 1) Antithrombin deficiency and 2) Homozygosity for factor V Leiden mutation
are the most potent of the inherited thrombophilias. Double or compound heterozygosities
(for both factor V Leiden and 3) prothrombin G20219A) are also at greater risk
of VTE. The prevalence at USA are as follows which hover do not match with our country
Factor V Leiden Homozygosity
|
34.4
|
Prothrombin G20210A Homozygosity
|
26.4
|
Factor V Leiden heterozygous
|
8.3
|
Prothrombin G20210A heterozygous
|
6.8
|
Protein C deficiency
|
4.8
|
Antithrombin deficiency
|
4.7a
|
Protein S deficiency
|
3.2
|
Methylenetetrahydrofolate
reductase (MTHFR)
|
0.74
|
C677T homozygote
|
|
Factor V Leiden +
prothrombin G20210A (compound
|
88.0
|
heterozygosity)
|
|
Antiphospholipid
antibody syndrome
|
15.8
|
Acquired thrombophilias:
Include A) persistent antiphospholipid
antibody syndromes (APS) (lupus anticoagulants or Anticardiolipin antibodies).
APS is present in 15% to 17% of women with recurrent pregnancy loss.
Routine screening for
thrombophilias is not recommended in all pregnant women and screening
indications are controversial. ACOG no longer recommends thrombophilia testing in women
with recurrent fetal loss, placental abruption, IUGR, or preeclampsia but such work up may be
needed in following conditions:- A) Personal or family history of
VTE (first-degree relative with VTE before age 50 years in absence of other
risk factors). B) APS
screening may be appropriate for women with repeated fetal losses (three
losses <10 weeks’ gestation or one loss >10 weeks’ gestation of a morphologically
normal fetus).
1) VTE during pregnancy
(workup to be done after delivery) or VTE associated with a nonrecurrent risk
factor such as prolonged immobilization. Over 70% of DVTs in pregnancy develop in the iliofemoral veins, which
are more likely to embolize, and the majority are on the left side.
A)
Clinical Diagnosis of DVT is difficult in pregnancy because expected changes
in pregnancy may mimic the symptoms of DVT. Additionally, many patients are
asymptomatic. If symptoms exist, the most common include calf or lower
extremity swelling, pain or tenderness, warmth, and erythema. Homan sign (calf
pain with passive dorsiflexion of the foot) is present in <15% of cases, and
a palpable cord is present in <10% of cases. Symptoms of an iliac DVT
include abdominal pain, back pain, and swelling of the entire leg. In pregnant
women with clinical suspicion of DVT, diagnosis is confirmed in <10%.
B)
Venous duplex imaging, including compression ultrasound, color,
and spectral Doppler sonography, has replaced contrast venography as the gold standard and is the most
commonly available noninvasive diagnostic method, with a sensitivity of 97% and
specificity of 94% in symptomatic proximal DVT. If the deep venous system is normal,
the presence of a clinically significant thrombus is unlikely. Limitations
include poor sensitivity for asymptomatic disease and difficulty in detecting
iliac vein thromboses
C) Magnetic resonance imaging (MRI):
Studies in nonpregnant patients show a sensitivity of 100% and specificity of
98% to 99% for pelvic and proximal DVTs while maintaining a high accuracy in
detecting below-the-knee DVTs.
D)
D-Dimer test is a sensitive but nonspecific test for DVT; However, its use in pregnancy is limited, as D-dimer
normally increases with gestational age. A normal D-dimer result may be reassuring
if clinical suspicion is low.
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