Obstetric Haematology

Question 1

What are the physiological blood changes in pregnancy?

Answer 1

Mild anaemia
Red cell mass rises (120 -130%)
Plasma volume rises (150%)

Macrocytosis
Normal
Folate or B12 deficiency

Neutrophilia

Thrombocytopenia
increased platelet size

Question 2

What are the demands on blood in pregnancy?

Answer 2

Iron requirement
300mg for fetus
500mg for maternal increased red cell mass
RDA 30mg;
Increase in daily iron absorption:1-2mg to 6mg

Folate requirements increase
Growth and cell division
Approx additional 200mcg/day required

Iron deficiency: may cause IUGR, prematurity, postpartum haemorrhage

Question 3

What does hepcidin do?

Answer 3

It controls the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte-recycling macrophages, and from iron-storing hepatocytes.

Question 4

What does transferrin do?

Answer 4

It regulates the absorption of iron into the blood. TIBC relates to the amount of transferrin in your blood that’s available to attach to iron.

Question 5

What is the iron and folate requirement in pregnancy?

Answer 5

WHO recommends 60mg Fe +400mcg folic acid daily during pregnancy
Cochrane review
Fe/Folate supplements had no effect on measures of maternal or fetal outcome
Maternal Hb higher, Fe reserves higher, fetal ferritin higher

Question 6

What does folate do?

Answer 6

Advise reduces risk of neural tube defects
Supplement before conception and for ≥ 12 weeks gestation
Dose 400μg / day

Question 7

What are the causes of thrombocytopaenia in pregnancy?

Answer 7

Physiological:
‘gestational’/incidental thrombocytopenia
Pre-eclampsia
Immune thrombocytopenia (ITP)
Microangiopathic syndromes
All other causes: bone marrow failure, leukaemia, hypersplenism, DIC etc.

Question 8

What is gestational thrombocytopaenia?

Answer 8

Physiological decrease in platelet count ~ 10%
>50x109/l sufficient for delivery (>70 for epidural)
Mechanism poorly defined
Dilution + increased consumption
Baby not affected
Platelet count rises D2 – 5 post delivery

Question 9

What is Preeclampsia and thrombocytopenia?

Answer 9

50% get thrombocytopenia
Proportionate to severity
Probably due to increased activation and consumption
Associated with coagulation activation
(incipient DIC – normal PT, APTT)
Usually remits following delivery

Question 10

What is ITP?

Answer 10

5% of thrombocytopenia in pregnancy
TP may precede pregnancy
Early onset

Treatment options (for bleeding or delivery)
IV immunoglobulin
Steroids etc.
(Anti-D where Rh D +ve)

Baby may be affected
Unpredictable (platelets <20 in 5%)
Check cord blood and then daily
May fall for 5 days after delivery 
Bleeding in 25% of severely affected (IVIG if low) 
Usually normal delivery

Question 11

What is MAHA?

Answer 11

Film: Fragments
Low platelets
polychromasia

Deposition of platelets in small blood vessels
Thrombocytopenia
Fragmentation and destruction of rbc within vasculature
Organ damage (kidney, CNS, placenta)

Question 12

What has the highest mortality in pregnancy?

Answer 12

VTE

Question 13

How does coagulation change in pregnancy?

Answer 13

Increased thrombin generation
Increased fibrin cleavage
Reduced fibrinolysis
Interact with other maternal factors

Question 14

What Ix are useful in VTE in pregnant women?

Answer 14

Doppler and VQ are safe to perform in pregnancy
D-dimer often elevated in pregnancy
Not useful for exclusion of thrombosis

Question 15

What increases risk of VTE in pregnancy?

Answer 15

Changes in blood coagulation
Reduced venous return
~85% Left DVT
Vessel wall

Variable
Hyperemesis/dehydration
 Bed rest
 Obesity
- BMI>29 3x risk of PE
Pre-eclampsia
Operative delivery
Previous thrombosis/thrombophilia
Age
Parity
Multiple pregnancy
Other medical problems: 
-HbSS, nephrotic syndrome
IVF: ovarian hyperstimulation

Question 16

How do you prevent VTE in pregnant women?

Answer 16

Women with risk factors should receive prophylactic heparin +TED stockings
Either throughout pregnancy
Or in peri-post- partum period
Highest risk get adjusted dose LMWH heparin
Mobilise early
Maintain hydration

Question 17

What is the management of VTE?

Answer 17

Management
LMWH as for non-pregnant
Does not cross placenta
RCOG recommend once or twice daily
Do not convert to warfarin (crosses placenta)
After 1st trimester monitor anti Xa
4 hour post 0.5-1.0u/ml
Stop for labour or planned delivery, esp. for epidural
Epidural: wait 24 hours after treatment dose, 12 hours after prophylactic dose

Question 18

What are the thrombophilia complications in pregnancy?

Answer 18

Hypothesis:
An increased tendency to thrombosis is associated with impaired placental circulation 
Resulting in:
Fetal growth restriction (IUGR)
Recurrent miscarriage
Late fetal loss
Abruptio placentae
Severe PET
Biologically plausible but not proven

Antiphospholipid Syndrome (APLS): Recurrent miscarriage + persistent Lupus anticoagulant (LA)/ anticardiolipin antibodies (ACL)
Adverse pregnancy outcome: three or more consecutive miscarriages before 10 weeks of gestation
One or more morphologically normal fetal losses after the 10th week of gestation
One or more preterm births before the 34th week of gestation owing to placental disease.

Question 19

What may be related to thrombophilia complications?

Answer 19

AT, PC,PS deficiency
Factor V Leiden
PTG20210A (high prothrombin)
Hyperhomocysteinemia (HHC)

Question 20

What is fatal bleeding in pregnancy?

Answer 20

MBRRACE 2009 -2011
14 deaths from haemorrhage
placenta praevia
Placenta accreta
principal reason for hysterecetomy

Use of Major Obstetric Haemorrhage protocols
Determine placental site if previous C-Section

Question 21

What is non fatal bleeding in pregnancy?

Answer 21

Post Partum Haemorrhage (PPH) :
> 500 mL blood loss

5% of pregnancies have blood loss >1 litre at delivery.

Requiring transfusion post partum
1% after vaginal delivery
1-7% after C-Section

Question 22

What is the mechanisms of post partum haemorrhage?

Answer 22

major factors are
uterine atony
trauma
haematological factors minor except
dilutional coagulopathy after resuscitation
DIC in abruption, amniotic fluid embolism etc.

Question 23

What is DIC in pregnancy?

Answer 23

Coagulation changes in prenancy predispose to DIC.
Decompensation precipitated by:
Amniotic fluid embolism
Abruptio placentae
Retained dead fetus
Preeclampsia (severe) 
Sepsis

Question 24

What is an amniotic fluid embolism?

Answer 24

‘the most catastrophic event in modern obstetrics’
1 in 20000-30000 births
Sudden onset shivers, vomiting, shock. DIC
86% mortality
16 deaths in last triennium
Presumed due to Tissue Factor in amniotic fluid entering maternal bloodstream
Almost all >25 years
Usually third trimester
Drugs used to induce labour e.g. misoprostol increase risk

Question 25

What is the aims of haemoglobinopathy screening in children?

Answer 25

To avoid birth of children with:
a° thalassaemia (Hb Bart’s, g4)	
Death in utero, hydrops fetalis
b° thalassemia
Transfusion dependent 
HbSS (sickle cell disease)
Life expectancy 43 yrs
Other compound HbS syndromes
Symptomatic, stroke etc.
Some compound thalassaemias
Transfusion dependent, iron overload

Question 26

How do you detect haemoglobinopathies?

Answer 26

Prevalence area:
High ≥ 1.5/10 000 : universal
 Low < 1.5/10 000 : selected 
 Family Origin Questionnaire (FOQ)
FBC: Red cell indices
MCH <27 possible thalassaemia trait
MCH <25 possible α thal trait 
Alpha thal requires DNA analysis*
HPLC
Identifies Hb variants eg: S, C, E
Quantifies Hb A2 (>3.5% → β thal)
Aim to complete by 12/40 (incl partner testing where req’d)

Question 27

What counselling do you do for haemoglobinopathies?

Answer 27

Important disorders are all recessive
Therefore if mother is heterozygous partner should be tested.
Combinations as important as homozygous states
Options
Proceed
Prenatal diagnosis
CVS sampling (10-12 weeks)
Amniocentesis (15-17 weeks), fetal blood sampling
Ultrasound screening for hydrops

Question 28

What is SCD disease in pregnancy?

Answer 28

Hb SS (sickle cell anaemia),
HbS/clinically abnormal Hb e.g. HbC; βthal
~100 pregnancies/year in SCD females in UK
Vaso-occlusive crises become more frequent
Anaemia and existing chronic diseases exaggerated
Complications:
Fetal growth restriction,
Miscarriage, Preterm labour, ? Pre-eclampsia
Venous thrombosis

Question 29

What is the management of SCD in pregnancy?

Answer 29

Red cell transfusion (top up or exchange)
Prophylactic transfusion
reduces number of vaso-occlusive episodes
Not clear whether affects fetal or maternal outcome
Alloimmunisation -extended phenotype: Rh D c E, Kell

Question 30

When is VTE most likely?

Answer 30

6 weeks postpartum