Obstetric haematology Flashcards by Emily Southall

how does the full blood count change in pregnancy

mild anaemia:
* red cell mass rises (120-130%)
* plasma volume rises more than red cell mass (150%) expansion complete by end of 2nd trimester

macrocytosis
* normal
* or B12/folate def

neutrophilia - cells are normally more marginalised come into the circulation.

thrombocytopenia: Fall in plt count -> increase in plt turnover -> earlier plts released -> increase in plt size.

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iron requirement in pregnancy

300mg for fetus
500mg for maternal increased red cell mass
in diet - 30g
normally absorb 1-2mg from 30mg, in preg absorb 6mg

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consequence of iron deficiency in pregnancy

IUGR
prematurity
postpartum haemorrhage

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folate requirements in pregnancy

increase

growth and cell division
approx additional 200mcg/day required

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summarise the iron cycle - including the changes in pregnancy

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RCOG recommendations with folate supplements

supplement before conception and for >= 12 wks gestation
400ug/day

reduces risk of neural tube defects

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definition of anaemia in pregnancy

Hb<110 1st trimester
<105 2nd and 3rd
<100 postpartum

reduction in threshold due to dilutional effect

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things to dx iron deficiency anaemia

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summarise how the platelet count changes in pregnancy

Due to increased clearance - mainly in 3rd trimester
Shift in normal distribution to L

Platelet clumping - so if low plt count correlate with film

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causes of thrombocytopenia in pregnancy

physiological - gestational/incidental thrombocytopenia
PET
ITP
MAHA
bone marrow failure, leukaemia, hypersplenism, DIC etc

when plts <150 - most will be gestational
<100 - splite gestational and ITP
<70 - mostly ITP, more PET than gestational

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summarise gestational thrombocytopenia

physiological decrease in plt count - approx 10%
>50 is sufficient for delivery
>70 for epidural (spinal haematoma)
mechanism - unknown. dilution and increased consumption
baby not effected
plt count rises day 2-5 post delivery

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summarise preeclampsia and thrombocytopenia

50% get thrombocytopenia - propirtionate to severity
due to increased activation and consumption
associated with coag activation (incipient DIC - normal PT and APTT, high factor 8) 1st thing that happens in insipient DIC )

mx is delivery

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summarise immune thrombocytopenia in pregnancy

accounts for 5% of thrombocytopenia in pregnancy
can precede pregnancy
Rx - IVIG, steroids, azathioprine

baby can be effected - ab cross placenta
* unpredictable which babies effected
* check cord blood and then daily
* may fall for 5 days post preg
* bleeding in 25% of severely affected - need to give IVIG and cranial USS when baby plt count low
* consider MOD - avoid forceps/ventouse

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summarise microangiopathic syndromes in pregnancy

deposition of plts in small blood vessels
thrombocytopenia
plt rich clots sheer the blood cells
fragmentation and destruction of RBC within vasculature
organ damage - kidney, cns, placenta

not effected/cured by delivery

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eg of reasons population getting more prone to VTE

older
IVF
multiple preg
obesity

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summarise the coagulation changes in pregnancy

Factor 8 and vWF increase until term

Protein S (anticoag) falls

PAI-2 is produced by placenta and is fibrinolytic inhibitor

why does pregnancy need to be hypercoaguable

Because 700ml/min is blood flow throigh placenta - need to prevent bleeding at birth

however: uterine contraction, not coag, is one of the main factors that stop bleeding at birth

overall effects of changes in coagulation factors etc in preg

increased thrombin generation
increased fibrin cleavage
reduced fibrinolysis

when is the biggest risk of VTE in pregnancy

Risk goes up through pregnancy - venous stasis due to gravid uterus
Hormonal changes in vessel wall
All 3 of virchows triad

Highest risk is the 6wks post delivery

RF for VTE in preg in women who died of PE

BMI >25
personal/Fhx VTE
air travel
hyperemesis gravidarum -> dehydration
ovarian hyperstimulation syndrome -> upper limb fibrosis
unrelated surgery

how do you assess VTE in pregnancy

Doppler and V/Q scan

RF for thrombosis in pregnancy

prevention of VTE in pregnancy

RFs should get prophylactic LMWH and TED - either: throughout preg, in peri-post-partum period
mobilise early
maintain hydration

Mx of thromboembolic disease in pregnancy

LMWH (enoxaparin) as for non-preg, once or twice daily
doesnt cross placenta
After 1st trimester - measure anti Xa levels because LMWH more unpredictable than when pregnant
*(NOT warfarin - crosses placenta and teratogenic between wk 6-12
NOT DOAC - cross placenta and secrete in breast milk) *

birth plan when on LMWH

stop for labour or planned delivery - esp epidural epidural wait 24 hr after rx dose and 12hr after prophylactic dose

effect of warfarin on fetus

Chondroplasia punctata: abnormal cartilage and bone formation early fusion of epiphyses nasal hypoplasia short stature asplenia deafness seizures

summarise antiphospholipid sundrome

recurrent miscarriage and persistent lupus anticoagulant (LA) (ie 12wks apart) and/or antiphospholipid antibodies 3 or more consecutive miscarriages before 10wks gestation one or more morphologically normal fetal loss >10wks one or more preterm <34wks due to placental disease

rx of antiphospholipid syndrome in pregnancy

aspirin and heparin

definition of postpartum haemorrhage

>500ml blood loss

4Ts of post partum haemorrhage

tone trauma tissue thrombin

mechanisms of postpartum haemorrhage

major: * uterine atony * trauma haematological factors are minor except * dilutional coagulopathy after resus (given red cells, not plasma) * DIC in abruption, amniotic fluid embolism etc

summarise pregnancy and DIC

coagulation changes in pregnancy to predispose to DIC decompensation is precipitated by: * amniotic fluid embolism * placental abruption * retained dead fetus * PET * sepsis ie Exposure of tissue factor to activated factor 7 - these are sources of tissue factor in pregnancy

summarise amniotic fluid embolism

sudden onet shivers, vomiting, shock, DIC high mortality presumed mech - tissue factor in amniotic fluid entering maternal blood stream almost all >25ys usually 3rd trimester

what is the aim of haemoglobinopathy screening

Need to know whether parents are Ao carriers - need to know where in the world this is prevalent

summarise haemoglobinopathy screening in pregnancy

universal screening when background high prevalence in some places - use family origin questionnaire to determine use HLPC - to detect b thal. cant detect a thal like this (needs DNA analysis) HLPC also identifies Hb variants only importnat to detect alpha 0 trait aim to complete screen by 12/40 including of partner

summarise counselling on haemaglobinopathy

important disorders all recessive so if mum heterozygous - partner should be tested combinations as important as homozygous states options: * proceed * prenatal diagnosis (CVS sampling @10-12wks, amniocentesis @15-17wks, fetal blood sampling, cell free fetal DNA) * USS screening for hydrops

differentiate thalassaemia trait from iron deficiency anaemia from blood tets

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Obstetric haematology Flashcards

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