1 anaemia n tcp in pregnancy 2008 dr g kidson
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Anaemia &
Thrombocytopenia inPregnancy
Giselle Kidson-Gerber
Haematology Registrar
Prince of Wales Hospital
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Anaemia in
pregnancy
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Physiological changes in normal
pregnancy RBC dilution with rise in blood volume and
plasma volume
Definition of anaemia in pregnancy
T1, T3 Hb < 110g/L
T2 Hb < 105g/L
Return to normal within 1 week post-partum, if normal iron stores
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Potential consequences of
moderate to severe anaemia Maternal
Fatigue, dyspnoea, syncope, chest pain
Mortality (esp < 50g/L)
Foetal (esp < 60g/L) Impaired mental development if low iron stores
Low birth weight
Preterm labour Perinatal death
Low amniotic fluid volume
Spontaneous miscarriage
Placental Hypertrophy
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Common causes of anaemia in
pregnancyLow MCV Normal MCV High MCV
Iron deficiency Iron deficiency Folate
deficiencyThalassaemia Chronic disease B12 deficiency
Sickle cell
Haemolysis
Bleeding
Infection
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Investigations
FBC, with MCV, blood film
Fe studies: ferritin esp.
Folate (RCF stores) & B12 levels
Reticulocyte count
UEC, LFT, Coagulation studies Haemoglobinopathy screening
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Iron deficiency anaemia
Most common cause in Western countries Increased iron requirements during pregnancy,
especially multiple pregnancies
Replace: Ferrous sulfate 325mg tds (105mg elemental Fe) Anaemia corrects in 4 - 6 weeks Stores replaced in 4 - 6 months
Dietary advice
Once replete Ongoing supplement: 30 - 60mg elemental iron daily
Monitor, including whilst breastfeeding
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Iron therapies
Formulation Elemental Fe(mg)
Folic Acid(mcg)
Ferrous sulfate 105 -
Fefol 87.4 300
FGF 80 300
Elevit 60 800
BlackmoresPregnancy
5 200
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Folic Acid deficiency
2nd most common cause of anaemia in pregnancy
Increased requirements for mother and foetus
Red cell folate: measure more reflective of tissuestores over past months
Supplement all: 200 - 500mcg/d
(greater if haemolysis) Replacement: 1000mcg/d
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Haemoglobinopathies:
Practical significance Major haemoglobinopathy in mother
Rare Specialist obstetric & haematology care
Haemoglobinopathy traits in mother Silent risk: foetus
Transfusion-dependent anaemia or sickle cell disease
Barts disease/hydrops foetalis: maternal & foetal morbidity Dependent on maternal and paternal genotype Importance of appropriate & timely screening
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Difficulties with detection of
haemoglobinopathy traits Patient asymptomatic
Patient unaware of carrier status
Difficult to detect in laboratory: May have normal Hb or MCV
Haemoglobinopathy screening does not
detect all cases Iron deficiency can mask indicator of
thalassaemia trait
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HaemoglobinopathiesGenotype Anaemia MCV Spleen Transfusion
Thalassaemia (2 genes)
Trait +,, 1 abnormal gene None-mild N/ +/- No
Intermedia +, + 2 mildly
abnormal genes
Mild-moderate + Sometimes
Major , 2 abnormal genes Severe + Dependent
Thalassaemia (4 genes)
Trait , 1 missing gene None N - No
2-gene minus ,
,
2 missing genes None-mild N/ +/- No
HbH disease , 3 missing genes Mod - severe + Sometimes
Barts disease , 4 missing genes Incompatible with lifedeath in utero
Sickle Cell (2 genes)
Trait s, 1 abnormal gene None N - No
Disease s, s 2 abnormal genes Mod-severe N/ +/-/ Variable
thal compound s, /+ 2 abnormal genes Variable +/-/ Variable
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Screening
Why? - Detect foetus at risk of majorhaemoglobinopathy
Who? - At risk ethnic groups, ? all(Southern Europe, Middle East, Africa, Asia, Indian subcontinent)
- Mother + partner
When? - Ideally preconception
- Limited timeframe for Ix & intervention
What? - FBC: Hb, MCV
- HbEPG (includes HPLC, HbH bodies)
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Full blood count
Simple Limitations:1. MCV may notdetect - thalassaemia trait
- sickle trait2. Hb may not detect- thalassaemia trait
- thalassaemia trait- sickle trait
Iron deficiency must be excluded as cause oflow MCV
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HbEPG: Hb Electrophoresis
Separates different haemoglobins according to charge
Alkaline & acid gels
Known position of haemoglobin bands
Control
HbE trait
HbE disease
HbS trait
thalassaemiatrait
Normal
HbA
HbF
HbS
HbA2,C,E
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HPLC: High Performance Liquid
Chromatography Separate according to elution time
Quantify % of different haemoglobins present
Iron deficiency lowers HbA2
Normal
HbA predominanthaemoglobin: 88%
HbS trait
HbS band:39%
HbA: 50%
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When to refer or ask for help
Positive result
Unexplained anaemia
Uncertain what investigations to perform Uncertain how to interpret investigations Complex area!
Variation in conditions and test results Specialist services are available: DNA testing
is readily available & should be accessedwhen there is doubt
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DNA testing
Confirm results or clarify unclear results Test mother & partner Foetus
If have a known mutation in both parents Usually gives definitive genotype, although not 100%
predictive of phenotype
Formal genetic counselling prior
Must be organised EARLY in pregnancy- ideally preconception.
Option of prenatal genetic diagnosis with IVF
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Take home message
Evaluate anaemia PRIOR to pregnancy
Determine cause of low MCV
Replace iron, if deficient
Low threshold for haemoglobinopathyscreening and referral
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Thrombocytopenia
in pregnancy
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Thrombocytopenia
Physiological thrombocytopenia in normal pregnancy
Average decrease in platelet count of 10%
Occurs mostly in 3rd trimester
Due to haemodilution or accelerated destruction
Normalises 24 -72 hours post-partum
Complicated Thrombocytopenia
Up to 10% of pregnancies
Mild - 100 - 150 x 109/L
Moderate - 50 - 100 x 109/L
Severe - < 50 x 109/L
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Causes of Thrombocytopenia in
Pregnancy Pregnancy-specific
Increased destruction:
Gestational
Preeclampsia
HELLP
Acute Fatty Liver ofPregnancy
Disseminated intravascular
coagulopathy
Non-pregnancy-specific
Increased destruction:
Idiopathic thrombocytopenic purpura(ITP)
Microangiopathies: TTP, HUS, DIC
SLE, Antiphospholipid syndrome
Drug-induced
Viral infections: HIV, HCV, EBV, CMV
HypersplenismDecreased production:
Bone Marrow Disease
Nutritional deficiency
Liver disease
Congenital thrombocytopenia
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Causes of Thrombocytopenia in
Pregnancy Pregnancy-specific
Increased destruction:
Gestational
Preeclampsia
HELLP
Acute Fatty Liver ofPregnancy
Disseminated intravascular
coagulopathy
Non-pregnancy-specific
Increased destruction:
Idiopathic thrombocytopenic purpura(ITP)
Microangiopathies: TTP, HUS, DIC
SLE, Antiphospholipid syndrome
Drug-induced
Viral infections: HIV, HCV, EBV, CMV
HypersplenismDecreased production:
Bone Marrow Disease
Nutritional deficiency
Liver disease
Congenital thrombocytopenia
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Causes of Thrombocytopenia in
Pregnancy Pregnancy-specific
Increased destruction:
Gestational
Preeclampsia
HELLP
Acute Fatty Liver ofPregnancy
Disseminated intravascular
coagulopathy
Non-pregnancy-specific
Increased destruction:
Idiopathic thrombocytopenic purpura(ITP)
Microangiopathies: TTP, HUS, DIC
SLE, Antiphospholipid syndrome
Drug-induced
Viral infections: HIV, HCV, EBV, CMV
HypersplenismDecreased production:
Bone Marrow Disease
Nutritional deficiency
Liver disease
Congenital thrombocytopenia
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Causes of Thrombocytopenia in
Pregnancy Pregnancy-specific
Increased destruction:
Gestational
Preeclampsia
HELLP
Acute Fatty Liver ofPregnancy
Disseminated intravascular
coagulopathy
Non-pregnancy-specific
Increased destruction:
Idiopathic thrombocytopenic purpura(ITP)
Microangiopathies: TTP, HUS, DIC
SLE, Antiphospholipid syndrome
Drug-induced
Viral infections: HIV, HCV, EBV, CMV
HypersplenismDecreased production:
Bone Marrow Disease
Nutritional deficiency
Liver disease
Congenital thrombocytopenia
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Clinical approach
Symptoms, bleeding history
Prenatal platelet count
Gestation
Previous pregnancies
Associated features
Co-morbidities
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Gestational Thrombocytopenia
Occurs in 5-8% of all pregnancies
75% of all pregnancy-associated
thrombocytopenia
? Mechanism: haemodilution, accelerated plt turnover, trapping ordestruction at placenta
Maternal haemorrhage risk: not increased
Foetal thrombocytopenia risk: not increased
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Gestational Thrombocytopenia
Clinically - asymptomatic- normal pre-natal platelet count- occurs in late T2 & in T3- normalises post-partum
Mildthrombocytopenia: Platelet count > 70 x109/L (usually > 100)
Anti-platelet antibodies do not reliablydistinguish from ITP
Diagnosis of exclusion
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Idiopathic Thrombocytopenic
Purpura (ITP) 5% of pregnancy-associated thrombocytopenia,
0.1% of pregnancies
Concern: maternal and foetal haemorrhage Clinically - any trimester
- prenatal thrombocytopenia
- bleeding history Especially likely to be ITP if
Platelet count
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Idiopathic Thrombocytopenic
Purpura (ITP) Maternal haemorrhage riskincreased,
relates to platelet count Platelet count < 20: risk of spontaneous bleeding
Platelet count > 50: aim for NVD Platelet count > 70: for epidural (variable, anaesthetist preference)
Foetal thrombocytopeniadue to trans-placental passage of maternal IgG: 10-20% platelet count < 50 x109/L
5% platelet count < 20 x109/L: 25-50% develop bleeding Best predictor: sibling
Check cord platelet count at delivery, nadir day 2-3.
Therapeutic options: monitor only, IVIg, prednisone,(splenectomy)
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Summary of approach to
thrombocytopenia in pregnancy Exclude pre-eclampsia syndromes
BP, UA, symptoms, FBC, UEC, LFT, Uric Acid
Exclude non-pregnancy-related medical causes,usually have specialist involved already
When to refer:
Known history of ITP
Unknown cause & platelet count is
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Thank-you
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