Transcript Venous thrombo-embolism during pregnancy and the puerperium

VTE during pregnancy and the
puerperium
DR MONA YADOLLAHI
CARDIOLOGIST
FACULTY MEMBER OF
RAJAEI HEART CENTER
 VTE (PTE&DVT) represents a significant cause of
pregnancy-related morbidity and mortality.
 Pregnancy and the puerperium increase incidence of
VTE, occurring in 0.05– 0.20% of all pregnancies. (1
in 1600 )
 The risk of VTE is highest in the immediate post-
partum period, particularly after C/S, and returns
to the non-pregnant level after the sixth week
post-partum.
 Case fatality rate is 3.5%.
 In the United States, PE is the sixth leading cause of
maternal mortality, responsible for 20 to 30% of
maternal deaths.
 There are NO clinical signs or symptoms that are
specific for PE.
 NO symptoms to shock or sudden death.
 overlap symptoms, dyspnea occurs in up to 70% of
normal pregnancies.
 Thus, identifying a clinically important PE during
pregnancy is challenging, both over diagnosing and
under diagnosing PE during pregnancy.
 in a study of 38 pregnant women with confirmed
PE:
dyspnea 62%
pleuritic chest pain 55%
cough 24%
sweating 18%
were the four most common presenting features.
 DYSPNEA of normal pregnancy starts during the
first or second trimester, the frequency rises during
the second trimester, and then is reasonably stable
during the third trimester.
 worse when the pregnant woman is in the sitting
position, and is not associated with exercise.
 Is dyspnea of acute or gradual onset?
 Other common findings suggesting pulmonary
embolism are tachypnea, pleuritic chest pain, and
hemoptysis, which do not occur with normal
dyspnea of pregnancy.
 Heart rate may increase above the elevated baseline
rate of normal pregnancy.
 Is cough or wheezing present?
 Acute cough is most commonly due to an acute
respiratory tract infection.
 Other considerations include an acute exacerbation
of underlying chronic pulmonary disease,
pneumonia, and pulmonary embolism.
 Is the chest clear on auscultation?
 Crackles (rales) are indicative of abnormalities
affecting the distal lung parenchyma(interstitial
pulmonary edema or ILD)
 Are other symptoms present?
 Physiologic dyspnea is not accompanied by pain or
other symptoms.
 Thoracic tumors and pulmonary emboli may present
with dyspnea and chest pain, hemoptysis, cough, or
wheezing.
 Is onset early in gestation or near term?
 Women with PPCMP commonly complain of
dyspnea, but onset is rarely before 36 weeks of
gestation, and affected patients usually present
during the first four to five months postpartum.
 Any one or combination
of the symptoms should always
raise alarm and increase the clinical
suspicion for a PE during pregnancy.
 The most significant risk factors for VTE in
pregnancy are a prior history of unprovoked
DVT or pulmonary embolism and thrombophilias.
 From 15% to 25% of VTEs are recurrent events.
 Half of the women who develop a thrombotic event
during pregnancy have either a thrombophilic
disorder or a previous idiopathic VTE.
 On the basis of the type and the total number of risk
factors present in the individual patient, three risk
groups can be identified (high, intermediate, and low
risk groups) and preventive measures applied
accordingly .
 Previous recurrent VTEs and previous VTE—
unprovoked or estrogen related—are considered high
risk factors.
 The exact influence of the other single risk factors or
the summation of several risk factors on total VTE
risk is not known according to ROYAL college.
LABORATORY STUDIES
 ABG, D-dimer levels, and echocardiography are
often performed but are neither sensitive nor specific
as diagnostic or pretest probability tools for the
evaluation of suspected PE during pregnancy.
ABG:
neither sensitive nor specific
A respiratory alkalosis is a very common.
presence of hypoxemia with normal CXR should
raise the clinical suspicion for PE in pregnancy
and prompt further evaluation.
D-dimer
 Increase during the course of a normal pregnancy
and slowly decline postpartum.
 Interpretation of D-dimer levels during pregnancy
and the puerperium is complicated by a lack of
normal reference ranges in this setting.
 Thus, D-dimer levels have limited utility for the
diagnosis of VTE.
 Considering the low sensitivity (high false
negative rate) and specificity (high false positive
rate) of D-dimer in this setting, a high D-dimer is
not diagnostic of PE, and a low D-dimer (even
<500 ng/mL) only modestly lowers the suspicion
but does not effectively eliminate PE from the
differential diagnosis.
Echocardiography
 NOT routinely performed in the diagnostic
evaluation of a pregnant patient suspected of having
a PE.
 excludes CMP or to evaluate the size of the RV in a
patient with confirmed PE.
 However, the prognostic value of RV dilation by
echocardiogram has not been formally evaluated in
pregnancy.
 PE cannot be definitively diagnosed
without confirmatory imaging.
 The two most common modalities for imaging are
lung scintigraphy [V/Q] and (CTPA).
 although contrast-enhanced pulmonary angiography
was the gold standard, neither test is commonly used
in the pregnant population.
 Employing strategies that use compressive
ultrasound (CUS) to avoid the radiation exposure
of V/Q and CTPA have been described, but CUS is
not definitively diagnostic of PE.
 The evidence to support choosing one imaging
modality over another is weak in the pregnant
population
CXR
 Despite its poor diagnostic accuracy, a CXR should
be performed in every pregnant patient in whom a
PE is suspected. This both evaluates for alternative
diagnoses and allows the accurate interpretation
of V/Q scan results.
 For those with a normal CXR, V/Q scanning remains
the test of choice for the diagnosis of PE in
pregnancy .
 A positive V/Q scan demonstrates a definitive
pattern of mismatch between the ventilation and
perfusion images of the lung.
 In general, only normal or very low probability scans
and high probability scans are considered diagnostic.
 Unlike the general population, pregnant women
have a relatively low likelihood of
indeterminate V/Q scans and a high likelihood of
diagnostic V/Q scans.
 CTPA has a high negative predictive value for ruling
out the diagnosis of PE in pregnancy .
 However, compared to that reported in the general
population, it may have a slightly higher rate of
nondiagnostic studies during pregnancy, particularly
when the chest radiograph is abnormal.
 CTPA is diagnostically useful when V/Q scanning is
not available or is indeterminate (eg, when the chest
radiograph is abnormal) or when an alternate
pathology is being considered.
Contrast-enhanced pulmonary angiography
it is rarely performed in this population.
it is less sensitive than CTPA for the detection of
emboli.
Most of the thrombi missed on contrast angiography
were sub segmental .
 The Wells score has limited value in the pregnant
population, probably due to the high prevalence of
baseline tachycardia and the low likelihood of certain
risk factors (eg, malignancy or recent surgery) that
are listed on the scoring system.
 The International Commission of Radiologic Protection
suggests that the radiation doses delivered in utero by
imaging tests (such as those performed in the diagnosis
of PE) present no measureable increased risk of fetal
death or developmental abnormalities over the
background incidence of these entities.
 The National Council of Radiation Protection and
Measurements considers the risk of radiation-associated
abnormalities to be negligible, at less than 50 mGy when
compared with other risks of pregnancy.
 The danger threshold for injury to the fetus is considered
to be 50 mSv (50 000 mGy)
prophylaxis
 LMWH has become the drug of choice for the prophylaxis and
treatment of VTE in pregnant patients. It causes less bone loss
than UFH, and the osteoporotic fracture rate is lower (0.04%
of pregnant women treated with LMWH).
 The dose of LMWH for thrombo prophylaxis is based on the
booking weight. There are no data to guide appropriate doses
of LMWH for pregnant women who are obese or puerperal.
 It is agreed that women of higher weights should receive
higher doses, but there are no studies available on the optimal
dose and weight ranges.
 Patients at high risk for VTE should receive the usual
prophylactic dose of 0.5 IU /kg body weight of enoxaparin or
50 IU/kg body weight dalteparin twice daily.
 LMWH has also become the drug of choice for the
treatment of VTE in pregnancy and puerperium.
Treatment
 recurrent VTE 1.15%.
 major bleeding 1.98%.
 HIT 0.04%.
 In clinically suspected DVT or pulmonary embolism,
treatment with LMWH should be given until the
diagnosis is excluded by objective testing.
Dosage
 The recommended therapeutic dose is calculated
on body weight (e.g. enoxaparin 1 mg/kg body
weight twice daily, Dalteparin 100 IU/kg body
weight twice daily) aiming for 4–6 h peak anti-Xa
values of 0.6–1.2 IU/mL
Monitoring
 The necessity to monitor anti-Xa values regularly in
patients with VTE is still controversial.
 Given the need for dose increase as pregnancy
progresses to maintain a certain therapeutic anti-Xa
level, it seems reasonable to determine anti-Xa levels
also during pregnancy in patients with VTE.
 A simple guide is dose adjustment
according to increasing weight
during pregnancy.
‫موارد منع مصرف هپارين با وزن مولكولي كم‬
‫خونريزي فعال در طي بارداري و يا پس از زايمان‬
‫احتمال خونريزيهاي شديد (جفت سر راهي)‬
‫بيماريهاي خوني مثل وون ويل براند يا هموفيلي يا اختالالت انعقادي اكتسابي‬
‫ترومبوسيتوپني (شمارش پالكت كمتر از ‪ 75‬هزار)‬
‫سكته مغزي حاد در ‪ 4‬هفته اخير ( ايسكميك يا هموراژيك)‬
‫بيماريهاي شديد كليوي ) ‪GFR‬كمتر از ‪ 30‬ميلي ليتر در دقيقه )‬
‫بيماري شديد كبدي ) ‪PT‬بيشتر از حد طبيعي يا واريسهاي شناخته شده)‬
‫فشار خون باالي كنترل نشده‬
‫(فشار خون سيستوليك باالتر از ‪ 200‬يا فشار خون دياستوليك بيشتر از ‪120‬‬
‫ميليمتر جيوه)‬
 No LMWH when the patient thinks that she is in labour
 LMWH should be discontinued 24 hours prior to
planned delivery
 Regional anaesthetic should not be used until at least 24
h after last dose of therapeutic LMWH
 LMWH should not be given for 4 h after spinal
anaesthesia
 Epidural catheter should not be removed within 12
hours of the most recent injection
UFH
 It is favored in patients with renal failure and when
urgent reversal of anticoagulation by protamine is
needed, as well as in the acute treatment of massive
pulmonary emboli.
 In patients with acute pulmonary embolism with
hemodynamic compromise, i.v. administration of
UFH is recommended (loading dose of 80 U/kg,
followed by a continuous i.v infusion of 18 U/kg/h).
 The dose is then titrated to achieve a therapeutic
aPTT, defined as the aPTT that corresponds to an
anti-Xa level of 0.3–0.7 IU/mL.
 When hemodynamic are improved and the patient is
stabilized, UFH can be switched to LMWH in
therapeutic doses and maintained during pregnancy.
 LMWH should be switched to i.v. UFH at least 36 h
before the induction of labor or caesarean delivery.
 UFH should be discontinued 4–6 h before
anticipated delivery, and restarted 6 h after delivery
if there are no bleeding complications.
 Neither UFH nor LWMH is found in breast milk in
any significant amount and they do not represent a
contraindication to breastfeeding.
Thrombolysis
 Thrombolytics are considered to be relatively
contraindicated during pregnancy and peripartum
and should only be used in high risk patients with
severe hypotension or shock.
 The risk of haemorrhage, mostly from the genital
tract, is 8%.
 Fetal loss of 6% and 6% pre-term delivery were
reported.
 Both thrombolytics do not cross the placenta in
significant amounts.
 When thrombolysis has been given, the loading dose
of UFH should be omitted and an infusion started at
a rate of 18 U/kg/h.
 After stabilization of the patient, UFH can be
switched to LMWH for the residual duration of
pregnancy.
Fondaparinux
 There are very few studies on fondaparinux in
pregnancy.
 one has shown minor transplacental passage of
fondaparinux.
 Because of the scarce data, the drug should not be
used in pregnancy .
Rivaroxaban
 Rivaroxaban crosses the placental barrier and has
therefore not been evaluated, and is not
recommended in pregnant patients.
Vena cava filters
 Indications for vena cava filters are the same as in
non-pregnant patients. However, the risk associated
with the procedure may be increased.
 In patients with recent PTE, pre-partum heparin
treatment should be restarted 6 h after a vaginal
birth and 12 h after a caesarean delivery, if no
significant bleeding has occurred, with subsequent
overlap with vitamin K antagonists for at least 5
days.
Post-partum management
 Vitamin K antagonists may be started on the second
day after delivery and continued for at least 3
months or for 6 months if pulmonary embolism
occurred late in pregnancy.
 The INR should be between 2 and 3 and needs
regular monitoring, ideally once every 1–2 weeks.
Vitamin K antagonists do not enter the breast milk in
active forms and are safe for nursing mothers.
Thanks for your tolerance & attention