Obstetric Haematology Flashcards
What are the physiological blood changes in pregnancy?
Mild anaemia
Red cell mass rises (120 -130%)
Plasma volume rises (150%)
Macrocytosis
Normal
Folate or B12 deficiency
Neutrophilia
Thrombocytopenia
increased platelet size
What are the demands on blood in pregnancy?
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
What does hepcidin do?
It controls the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte-recycling macrophages, and from iron-storing hepatocytes.
What does transferrin do?
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.
What is the iron and folate requirement in pregnancy?
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
What does folate do?
Advise reduces risk of neural tube defects
Supplement before conception and for ≥ 12 weeks gestation
Dose 400μg / day
What are the causes of thrombocytopaenia in pregnancy?
Physiological:
‘gestational’/incidental thrombocytopenia
Pre-eclampsia
Immune thrombocytopenia (ITP)
Microangiopathic syndromes
All other causes: bone marrow failure, leukaemia, hypersplenism, DIC etc.
What is gestational thrombocytopaenia?
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
What is Preeclampsia and thrombocytopenia?
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
What is ITP?
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
What is MAHA?
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)
What has the highest mortality in pregnancy?
VTE
How does coagulation change in pregnancy?
Increased thrombin generation
Increased fibrin cleavage
Reduced fibrinolysis
Interact with other maternal factors
What Ix are useful in VTE in pregnant women?
Doppler and VQ are safe to perform in pregnancy
D-dimer often elevated in pregnancy
Not useful for exclusion of thrombosis
What increases risk of VTE in pregnancy?
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
How do you prevent VTE in pregnant women?
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
What is the management of VTE?
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
What are the thrombophilia complications in pregnancy?
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.
What may be related to thrombophilia complications?
AT, PC,PS deficiency
Factor V Leiden
PTG20210A (high prothrombin)
Hyperhomocysteinemia (HHC)
What is fatal bleeding in pregnancy?
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
What is non fatal bleeding in pregnancy?
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
What is the mechanisms of post partum haemorrhage?
major factors are
uterine atony
trauma
haematological factors minor except
dilutional coagulopathy after resuscitation
DIC in abruption, amniotic fluid embolism etc.
What is DIC in pregnancy?
Coagulation changes in prenancy predispose to DIC. Decompensation precipitated by: Amniotic fluid embolism Abruptio placentae Retained dead fetus Preeclampsia (severe) Sepsis
What is an amniotic fluid embolism?
‘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
What is the aims of haemoglobinopathy screening in children?
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
How do you detect haemoglobinopathies?
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)
What counselling do you do for haemoglobinopathies?
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
What is SCD disease in pregnancy?
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
What is the management of SCD in pregnancy?
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
When is VTE most likely?
6 weeks postpartum
