VTE Flashcards

1
Q

What are the three parts of Virchow’s triangle?

How are they affected in pregnancy?

A
  1. Stasis - vasodilation of pregnancy, reduced venous return
  2. Hyper-coagulability - increase in prothrombotic factors, and a reduction anticoagulant factors
  3. Vessel damage - occurs during CS and vaginal birth, and pregnancy is an inflammatory state so endothelial cell are activated
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2
Q

What is the incidence of VTE in pregnancy and the puerperium?

A

2:1000

SOMANZ

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3
Q

What is the relative risk of VTE in pregnancy, compared to the non-pregnant state?

A

RR 4-5 x

SOMANZ

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4
Q

When is the highest risk for VTE

A

Postpartum

  • 30-50% VTE associated with pregnancy occur postpartum
  • 3-5 x risk of antenatal VTE
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5
Q

In women that have PE in pregnancy, what % will have a fatal result?

A

15%

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6
Q

What are the guidance for LMWH VTE prophylaxis in pregnancy for women with a previous Hx VTE?

A
LMWH prophylaxis once pregnancy confirmed, till 6 weeks postpartum if:
- PE in or outside of pregnancy
- Proximal/extensive DVT
- VTE associated with pregnancy or COCP
- Recurrent or unprovoked VTE
 (SOMANZ 2012, 2021)

Previous provoked DVT after surgery/trauma has low association with PA-VTE:

  • No need for antenatal prophylaxis unless addition risk factors
  • Extended 6 week postpartum prophylaxis

Women on long-term oral anticoagulation for any reason: - stop it on diagnosis of pregnancy and commence therapeutic LMWH after 1-3 days, transfer to warfarin postpartum

Therapeutic dose required if previous VTE with:

  • antithrombin deficiency
  • APS
  • Recurrent VTE (intermediate dose)
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7
Q

Should a D-dimer be performed in pregnancy?

A

NO.
Some evidence that higher pregnancy specific levels may be helpful, but not validated at present.
May have some benefit in excluding VTE. BUT poor negative predictive value, up to 40% VTE cases may be missed in pregnancy by using a negative D-dimer for reassurance.

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8
Q

Should the WELLS score / PERC score be used in pregnancy?

A

No

There are currently no validated pretest scoring systems for pregnancy

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9
Q

What is the sensitivity of Serial compression duplex USS in assessing DVT?

A

94%

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10
Q

What is the NPV of Serial compression duplex USS in assessing DVT?

A

99.5%

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11
Q

If a DVT remains untreated, how many patients will develop a PE?

A

15-24%

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12
Q

If suspecting DVT and the Compression Duplex USS is negative, what is the next step?

A

If low clinical suspicion, discontinue LMWH

If high clinical suspicion, discontinue LMWH but REPEAT USS on day 3 and 7

If suspicious for pelvic vein DVT consider MRV.

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13
Q

What ECG changes are seen with a PE?

A
  • Sinus tachycardia
  • T wave inversion
  • S1Q3T3 pattern - deep S wave in lead I, Q wave in III, inverted T wave in III, “classic” finding but is actually low in sensitivity and specificity
  • RBBB
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14
Q

What CXR findings are seen with a PE?

A

Atelectasis, effusion, focal opacities, regional oligaemia, pulmonary oedema, hamptons hump

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15
Q

Is an ABG useful in diagnosing a PE in pregnancy?

A

SOMANZ endorses it use for risk stratification, but

not a sensitive or specific marker for PE and should not be measured by a normal a-a gradient.

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16
Q

Why is breast tissue especially sensitive to radiation exposure during pregnancy?

A

Hormonally increased glandular cavity, increased mitotic rate

17
Q

What is the duration of treatment for a PE / DVT diagnosed in pregnancy?

A

At least 3 months, to 6 months of therapeutic dose LMWH
Can be reduced to a prophylactic dose after this time
Continue until at least 6/52 postpartum

Postnatally, can be offered warfarin if still taking therapeutic doses

18
Q

How do patients present with massive life threatening PE?

A

Shock, refractory hypoxaemia, RV dysfunction on Echo

19
Q

What is the preferred treatment for massive life-threatening PE and why?

A

IV Unfractionated Heparin

  • rapid effect
  • extensive experience in this area
  • can be adjusted more readily if thrombolytic therapy is administered

Thrombolysis can be considered for life threatening PE
- high risk for significant bleeding, miscarriage, still birth

20
Q

What is post-thrombotic syndrome?

A
Chronic persistent leg swelling
Pain
Feeling of heaviness
Dependent cyanosis
Telangiectasis
Chronic pigmentation
Eczema
Associated varicose veins
Venous ulceration (most severe cases)
21
Q

What are risk factors for post-thrombotic syndrome?

A
Smoking
Maternal age > 33
Obesity
Proximal postnatal thrombosis
Recurrent ipsilateral DVT
22
Q

What are INTRAPARTUM risk factors for VTE

A
CS (particularly EmCS)
Prolonged labour > 24h
PPH > 1L / requiring RBC
Stillbirth
Mid-cavity / rotational operative delivery
PTB
23
Q

What are PRE-PREGNANCY and ANTENATAL risk factors for VTE?

A
PRE-PREGNANCY: 
Previous VTE
Previous 1st degree relative with VTE
Inherited Thrombophilia ( high risk and low risk)
APS
Age > 35
Parity > 3
Smoker
Medical comorbidities (T1DM with nephropathy, cancer, etc)
Gross varicose veins
ANTENATAL:
Hyperemesis
OHSS
ART
Admission or immobility
Surgery e.g. appendicectomy 
Sepsis
APH
Multiple pregnancy 
PET
24
Q

What are medical comorbidites that increase risk for VTE?

A
Cancer
Active SLE, IBD or inflammatory polyarthropathy
Nephrotic syndrome
T1DM with nephropathy 
Heart failure
IVDU
Sickle cell disease
25
Q

What are contraindications to LMWH?

A
Active bleeding
Allergy
Severe renal / liver disease
Thrombocytopenia, Plt < 75
Known bleeding disorder
Acute stroke in previous 4 weeks (Haemorrhagic / ischaemia)
Uncontrolled HTN
26
Q

What are the advantages of UFH compared to LMWH?

A

Shorter half life
- required interval between prophylactic UFH and regional anaesthesia is less ( 4 hours c.f. 12 hours with LMWH)
More complete reversal with Protamine sulphate
Less concern regarding neuraxial haematomas

27
Q

What are the risks of Warfarin in pregnancy

A

Crosses placenta
Embryopathy in approx 5% of fetuses exposed between 6-12/40
Dose dependent, higher incidence if >5mg/ day

C-ongenital heart defects
H-ypoplasia of nasal bridge
V-entriculomegaly
A-genesis of corpus callosum
S-tipple epiphysis
Other adverse effects
Miscarriage
Stillbirth
Neurological impairment
Fetal and maternal haemorrhage
28
Q

What is the guidance around a family Hx of VTE?

A
  • Significant family Hx is only for 1st degree relatives
  • Correlated with increased risk of VTE in pregnancy/postpartum
  • Risk stratified to high risk and low risk thrombophilias

LOW RISK

  • Antenatal LMWH not usually required
  • Extended LMWH postpartum should be considered if other risk factors

HIGH RISK

  • factor V leiden homozygous, protein c or protein s deficiency, multiple inherited thrombophilias
  • consider antenatal prophylactic LMWH AND prolonged 6 week postpartum course
  • Antithrombin (factor Xa) deficiency particularly high risk therefore consider intermediate/therapeutic dose antenatally and for 6 weeks postpartum
    (SOMANZ)
29
Q

What is the guidance around inherited thrombophilias?

A
  • The majority of inherited thrombophilias have minimal increased risk of VTE
  • The high risk conditions: antithrombin deficiency, factor V leiden homozygous, protein c and protein s deficiency, >1 thrombophilic marker

Low risk thrombophilia
- no need for antenatal or extended postnatal LMWH
High risk thrombophilia and no FHx VTE
- extended 6 week postnatal prophylaxis only
High risk thrombophilia and positive FHx VTE
- consider antenatal prophylaxis
- extended 6week postnatal prophylaxis

Antithrombin deficiency

  • The most high risk thrombophilia, 11% risk antenatal VTE and 29% risk postnatal VTE, which increases significantly if FHx of VTE
  • Antenatal prophylaxis with intermediate of therapeutic dose LMWH
  • extended 6week postnatal prophylaxis

(SOMANZ)

30
Q

Compare V/Q, Q-only and CTPA scanning for diagnosis of PE in pregnancy.

A

CTPA

  • NPV 100%, sensitivity 83%
  • Higher dose of radiation and therefore higher risk for future breast cancer (1/2000 lifetime risk - though likely lower now with modern radiology techniques)
  • Useful in detecting other lung pathology
  • More widely available, less delay in diagnosis
  • Can continue breast feeding after
  • Can lead to over diagnosis - More sensitive to detecting SSPE - but these are of little clinical significance with no increase in mortality or recurrence if treated or not

V/Q

  • NPV 100%, sensitivity 100%
  • Nuclear imaging not as widely available
  • Lower dose of radiation and lower risk of future breast cancer (1/40,000 lifetime risk - though likely lower with modern radiology techniques)
  • Lower rate of non-diagnostic studies, particularly in the third trimester
  • Must avoid breast feeding for at least 12 hours due to increased passage of radioactive contrast in breast milk

Both studies give negligible doses of radiation to the fetus (<1mSv), well below the threshold (10mGy) for increased risk of miscarriage, genetic damage or congenital malformation. Even if this threshold is exceeded the risk of additional childhood cancer is roughly 2/1000.

Perfusion only scanning is generally not recommended due to the relatively low levels of radiation and risks associated.

  • NPV 83%, sensitivity 60%
  • If abnormal perfusion scan, then need to do a ventilation scan after
  • 1/4 - 1/2 studies are inconclusive

(SOMANZ 2021)

31
Q

What is the sensitivity and NPV of CTPA and V/Q scanning?

A

CTPA
- NPV = 100%, sensitivity 83%
V/Q
- NPV = 100%, sensitivity 100%

32
Q

What is the current guidance regarding the best modality of scanning in suspected PE?

A
  • Do not avoid doing necessary scan due to concerns about radiation - the radiation exposure is minimal with both CTPA and V/Q scanning and is far outweighed by the potential risks of PE.
  • Both CTPA and V/Q are safe and acceptable options
  • In clinically stable women with a normal CXR - preference is for V/Q scan
  • If clinically unstable women or with CXR abnormalities, a CTPA is preferred

Others:

  • Echo can be considered in unstable women to assess evidence of right heart strain and aid risk stratification
  • If multiple scans are performed calculate the breast and fetal radiation exposure
  • If radiation contraindication non-gadolinium MRA can be considered if available
33
Q

What steps can be taken to reduce breast tissue exposure in CTPA?

A
  • Choose V/Q scan instead or perfusion-only
  • bismuth protective shield for breasts ( reduces by 50%)
  • Reduced contrast monitoring component of CTPA
34
Q

What is the public health importance of PE?

A
  • Most common cause of direct maternal death in Aus

- 3rd most common cause of direct maternal death in NZ

35
Q

How long before birth/CS, epidural placement, epidural removal should PROPHYLACTIC dose LMWH be stopped?
And for UFH?

A

LMWH

  • 12 hours CS
  • 12 hours epidural placement or removal
  • Can restart 4 hours after epidural removal
  • Can restart 6-12 hours after delivery

UFH

  • 4-6 hours CS
  • 4-6 hours epidural placement or removal
  • Can restart 1 hour after epidural removal
36
Q

How long before birth/CS, epidural placement, epidural removal should THERAPEUTIC dose LMWH be stopped?
And for UFH?

A

LMWH

  • 24 hours CS
  • 24 hours epidural placement or removal
  • Can restart 4 hours after epidural removal
  • Can restart 12-24 hours after delivery

UFH

  • 24 hours CS BUT 4-6 if given IV
  • 24 hours epidural placement BUT 4-6 if given IV
  • 4-6 hours before removal
  • Can restart 1 hours after epidural removal
37
Q

What additional steps should happen if woman is on therapeutic LMWH or UFH and needs urgent delivery.

A
  • All routine care and work-up
  • Senior obs review and senior anaesthetic review
  • Stop anticoagulation
  • Decision re. timing - can delivery be delayed till reversal of thromboprophylaxis
  • Ensure IV access, FBC and G&H
  • Measure anti-Xa levels for LMWH, and APTT for UFH
  • Liase with haematology and Consider administration of protamine (more effective for reversal of UFH)
  • Ensure plan in place for recommencing anticoagulation postpartum
38
Q

What is the mechanism of action for heparin?

A

Binds to antithrombin causing structural change and increasing its activity, thus:

  • inhibits factor Xa cleavage of prothrombin to thrombin (factor IIa), and acts directly to inhibit thrombin
  • which is required for cleavage of fibrinogen to fibrin involved in stable clot formation.