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HAEM - Abbie > 16. Obstetric haematology > Flashcards

16. Obstetric haematology Flashcards

1
Q

What does FBC show in pregnancy?

A
  1. Mild anaemia: red cell mass rises (120-130%); plasma volume rises (150%); net dilution. 2. Macrocytosis: could be normal, due to folate or B12 deficiency. 3. Neutrophilia. 4. Thrombocytopaenia - increased platelet size.
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2
Q

What are demands of pregnancy in terms of vitamins and minerals?

A

Iron and folate requirement increased

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3
Q

What is the iron requirement in pregnancy?**

A

300 mg for foetus; 500 mg for maternal increased red cell mass. Recommended daily intake: 30 mg. Increase in daily iron absorption from 1-2 mg to 6 mg.

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4
Q

What is the folate requirement increase?

A

Needed for growth and cell division. Additional 200 mcg/day required

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5
Q

What is the effect of iron deficiency on pregnancy?

A

May cause IUGR, prematurity or post-partum haemorrhage

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6
Q

What supplements does the WHO recommend daily in pregnant women?

A

60 mg iron; 400 mcg folic acid

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7
Q

What supplements does RCOG recommend daily?

A

400 mcg/day folic acid. Supplementation should be started before conception and for > 12 week gestation.
Folic acid supplementation reduces the risk of neural tube defects. NO routine iron supplementation in the UK. However, it may be supplemented on an individual basis

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8
Q

What is the physiological drop in platelet count in pregnancy?

A

There is a physiological drop in platelet count of around 10%.

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9
Q

What platelet count is concerning?

A

You may be concerned if the platelet count is 70-80 x 109/L because it can increase risk of spinal haematoma following epidural anaesthesia

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10
Q

What happens to the size of platelets in pregnancy?

A

Increase in platelet size

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11
Q

Why might the FBC give an underestimation of platelet count? What can we do about this?

A

Sometimes the large platelets in pregnancy may be counted as small red cells by the FBC machine which gives an underestimation of the platelet count. Therefore, it is worth doing a blood film as well.

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12
Q

What are causes of thrombocytopaenia in pregnancy?

A

Physiological (aka gestational or incidental thrombocytopaenia); pre-eclampsia; ITP; microangiopathic syndromes; all other (non-pregnant) causes: bone marrow failure, leukaemia, hypersplenism, DIC etc.

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13
Q

When are pregnant women considered to have gestational thrombocytopaenia?

A

The vast majority of pregnant women with platelet counts < 150 x 109/L have gestational thrombocytopaenia

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14
Q

How does the cause of thrombocytopaenia change as the platelet count drops?

A

The vast majority of pregnant women with platelet counts < 150 x 109/L have gestational thrombocytopaenia. Some cases are caused by pre-eclampsia and very few due to ITP. As the platelet count drops further (< 100), there is more of an even split of cases being caused by gestational thrombocytopaenia and ITP. The lower the platelet count, the more likely it is to be a pathological cause.

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15
Q

What is gestational thrombocytopenia?

A

Physiological decrease in platelet count of about 10%. The baby is NOT affected.

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16
Q

What platelet count is sufficient for delivery in gestational thrombocytopaenia?

A

Platelet count >50 x 109/L is sufficient for delivery

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17
Q

What platelet count is sufficient for epidural in gestational thrombocytopaenia?

A

Platelet count >70 x 109/L is sufficient for epidural

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18
Q

What is the mechanism of gestational thrombocytopaenia?

A

Likely to be a combination of dilution and increased consumption.

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19
Q

What happens to platelet count after delivery?

A

Platelet count rises around day 2-5 after delivery

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20
Q

What percentage of pre-eclampsia patients will get thrombocytopaenia?

A

50%. Proportionate to severity.

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21
Q

What is thrombocytopaenia in pre-eclampsia due to and associated with?

A

Probably due to increased activation and consumption. Association with coagulation activation. Incipient DIC - normal PT/APTT. NOTE: despite the platelet count being low, you have a paradoxically pro-thrombotic phenotype because the platelets are more aggregable

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22
Q

What happens to thrombocytopaenia in pre eclampsia patients after delivery?

A

Usually remits following delivery

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23
Q

What percentage of thrombocytopaenia in pregnancy is caused by ITP?

A

5% of thrombocytopaenia in pregnancy

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24
Q

When does ITP in pregnancy present?

A

May precede pregnancy. Early-onset

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25
Q

What is the treatment of ITP (for bleeding or delivery)?

A

IVIG; steroids; anti-D (where RhD +ve)

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26
Q

What is the effect of ITP on the baby?

A

Baby MAY be affected. Unpredictable; check cord blood. May fall for 5 days after delivery. Bleeding in 25% of severely affected. Usually normal delivery (avoid ventouse, forceps etc.)

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27
Q

What happens in microangiopathic syndromes (MAHA) and what are the effects?

A

Deposition of platelet-rich thrombi in small blood vessels. Leads to shearing of red cells –> haemolytic anaemia; thrombocytopaenia and organ damage (kidney, CNS, placenta)

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28
Q

In what conditions does delivery not affect its course?

A

Delivery does NOT affect the course of TTP or HUS. TTP requires plasma exchange. The other conditions are likely to subside after delivery

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29
Q

What is a leading cause of maternal mortality?

A

Coagulation changes in pregnancy result in a leading cause of maternal mortality (VTE). The coagulation changes are there to try and reduce the risk of bleeding

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30
Q

What coagulation changes in factor VIII and vWF occur in pregnancy?

A

Increases 3-5 fold

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31
Q

What coagulation changes in fibrinogen occur in pregnancy?

A

Increases 2 fold

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32
Q

What coagulation changes in factor VII occur in pregnancy?

A

Increases 0.5 fold

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33
Q

What coagulation changes in factor X occur in pregnancy?

A

Hypercoagulable

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34
Q

What coagulation changes in protein S occur in pregnancy?

A

Falls to half basal

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35
Q

What coagulation changes in PAI-1 occur in pregnancy?

A

Increases 5 fold

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36
Q

What coagulation changes in PAI-2 produced by placenta occur in pregnancy?

A

Hypofibrinolytic

37
Q

Why do coagulation changes occur in pregnancy?

A

These changes occur to rapidly control bleeding from the placental site at the time of delivery. The net effect of these changes is a procoagulant state

38
Q

What are the changes in pregnancy which have led to a net effect of a procoagulant state?

A

Increased thrombin generation; increased fibrin cleavage; reduced fibrinolysis; interact with other maternal factors; this leads to an increased rate of THROMBOSIS

39
Q

What happens to the procoagulant state after delivery?

A

These changes should return to normal in the weeks/months after delivery

40
Q

When do deaths from PE occur in pregnancy?

A

Deaths from pulmonary embolism tend to occur around week 40-46 gestation. However, a reasonable proportion also occur in the first trimester

41
Q

What is a major compounding risk factor of thrombosis/VTE/PE?

A

Obesity

42
Q

What is the relative risk of thromboembolic disease in pregnancy?

A

10 fold in pregnancy

43
Q

What proportion of cases are post-partum?

A

1/3 of cases are post-partum (within 6 weeks post-partum)

44
Q

What are investigations for VTE?

A

Doppler and VQ scans are SAFE to perform in pregnancy. D-dimer is often elevated in pregnancy; so, it is NOT useful for exclusion of thrombosis.

45
Q

What are factors increasing risk of thrombosis in pregnancy?

A

Changes in blood coagulation, reduced venous return, vessel wall.

46
Q

What variable factors increase the risk of thrombosis in pregnancy?

A

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

47
Q

What happens to the risk of thrombosis with age?

A

The risk increases dramatically over the age of 35 years. (Inherited thrombophilias further increase the risk of thrombosis in pregnancy)

48
Q

What can be given if patients are at risk of thrombosis in pregnancy?

A

Thromboprophylaxis

49
Q

How can we prevent thromboembolic disease in pregnancy?

A

Women with risk factors should receive prophylactic heparin + TED stockings. Either throughout pregnancy or in peri- or post-partum period. Highest risk will get adjusted dose LMWH. Mobilise early, maintain hydration. RCOG Green-top Guideline is used to determine the risk.

50
Q

How is thromboembolic disease in pregnancy treated?

A

LMWH (as is used in non-pregnant people) - does NOT cross the placenta. RCOG recommend once or twice daily. After 1st trimester, monitor anti-Xa.
STOP anticoagulation when labour begins or planned delivery, especially if using an epidural. If giving an epidural, wait: 24 hours after treatment dose of heparin, 12 hours after prophylactic dose of heparin

51
Q

Why should warfarin not be given for thromboembolic disease in pregnancy?

A

Do NOT change to warfarin because it crosses the placenta. Teratogenic between 6-12 weeks

52
Q

What is the hypothesis for increased thrombosis in pregnancy?

A

It is hypothesised that increased tendency for thrombosis in pregnancy is associated with impaired placental circulation

53
Q

What would impaired placental circulation result in?

A

IUGR; recurrent miscarriage; late foetal loss; abruptio placentae; severe pre-eclampsia toxaemia. (This is biological plausible but NOT proven)

54
Q

What are the main features of antiphospholipid syndrome?

A

Recurrent miscarriage; persistent lupus anticoagulant or anticardiolipin antibodies.

55
Q

What are indications for testing for antiphospholipid syndrome?

A
  1. Adverse pregnancy outcome: three or more consecutive miscarriages before 10 weeks of gestation. 2. One or more morphologically normal fetal losses after the 10th week gestation. 3. One or more preterm births before the 34th week of gestation owing placental disease.
56
Q

What could potentially increase the chances of having a live birth in patients with antiphospholipid syndrome?

A

There was evidence to suggest that giving aspirin + heparin to patients with antiphospholipid syndrome will increase their chances of having a live birth. However, aside from antiphospholipid syndrome, there is insufficient evidence to support the use of thrombophilia testing or aspirin + heparin use in patients with > 2 miscarriages.

57
Q

What is placenta accreta?

A

(75-78% of abnormal attachment of placenta) where the placenta goes through the endometrial lining

58
Q

What is placenta increta?

A

(17% of abnormal attachment of placenta) where the placenta goes into the uterine wall

59
Q

What is placenta praevia?

A

(5% of abnormal attachment of placenta) where the placenta goes through the uterine wall and can stick to other organs)

60
Q

What can increase the likelihood of having issues with the site of placental implantation?

A

C-sections

61
Q

What is the key reason for a hysterectomy?

A

Abnormal placental implantation

62
Q

What protocols are used to help in fatal bleeding in pregnancy?

A

Use of major obstetric haemorrhage protocols

63
Q

What is considered a post-partum haemorrhage?

A

Post-partum haemorrhage (PPH): > 500 mL blood loss

64
Q

What percentage of women have blood loss > 1 litre at delivery?

A

5%

65
Q

What percentage require blood transfusion after delivery?

A

1% after vaginal, 1-7% after c-section

66
Q

What are the mechanisms of non-fatal bleeding?

A

Uterine atony (uterus does not contract sufficiently); trauma; haematological factors (usually quite minor) such as dilutional coagulopathy after resuscitation and DIC in abruption, amniotic fluid embolism etc.

67
Q

What are the 4T’s of PPH?

A

Tone, trauma, tissue, thrombin

68
Q

Why do pregnant women get DIC?

A

Coagulation changes in pregnancy predispose to DIC

69
Q

What is decompensation (in DIC) precipitated by?

A

Amniotic fluid, abruptio placentae, retained dead foetus, pre-eclampsia (severe), sepsis

70
Q

What is the presentation of amniotic fluid embolism?

A

Sudden-onset shivers, vomiting, shock, DIC

71
Q

What is the mortality rate of amniotic fluid embolisms?

A

86% mortality (used to be 100%)

72
Q

What is amniotic fluid embolism due to?

A

Thought to be due to DIC triggered by tissue factor within the amniotic fluid

73
Q

When does amniotic fluid embolism occur?

A

Usually in the 3rd trimester

74
Q

What does haemoglobinopathy screening aim to do?

A

Aims to avoid birth of children with alpha-0 thalassemia, beta-0 thalassemia, HbSS, other compound HbS syndrome (HbSC)

75
Q

Why screen for alpha-0 thalassemia?

A

Death in utero, hydrops fetalis

76
Q

Why screen for beta-0 thalassemia?

A

Transfusion-dependent condition - patients require frequent and long-term transfusion support to sustain their life

77
Q

Why screen for HbSS?

A

Sickle cell disease, life expectancy = 43 years

78
Q

How did the screening programme start?

A

In 2009, the NHS Sickle Cell and Thalassemia Screening Programme was launched (in areas of high prevalence).
If selected individuals are screened, it is based on the results of a Family Origin Questionnaire.

79
Q

What FBC result can be used for screening of haemoglobinopathy?

A

FBC is done to look at the MCH - microcytosis indicates the possibility of thalassemia

80
Q

What does HPLC (high performance liquid chromatography) identify and quantify?

A

HPLC can identify haemoglobin variants (EXCEPT it cannot identify alpha thalassemia). HPLC can quantify HbA2 (>3.5% = beta thalassemia)

81
Q

What is used to diagnose alpha thalassemia?

A

Alpha thalassemia requires molecular diagnosis

82
Q

When should haemoglobinopathy screening be done by?

A

Aim to complete by 12 weeks (including partner testing)

83
Q

What does counselling about haemoglobinopathy entail?

A

Important disorders are ALL recessive. So, if the mother is heterozygous, the partner should be tested. Options: proceed, prenatal diagnosis, CVS sampling (10-12 weeks), amniocentesis (15-17 weeks), foetal blood sampling. Ultrasound screening for hydrops.

84
Q

Vaso-occlusive crises becomes more frequent in which condition?

A

SCD

85
Q

What are complications of SCD in pregnancy?

A

Foetal growth restriction; miscarriage; preterm labour; pre-eclampsia; venous thrombosis. Furthermore, vaso-occlusive crises become more frequent
and anaemia and existing chronic diseases can become exaggerated.

86
Q

What is the management of SCD in pregnancy?

A

Red cell transfusion (top up or exchange); prophylactic transfusion; alloimmunisation (make sure blood is matched)

87
Q

Summarise investigation results of iron deficiency in pregnancy

A

Hb: normal or low; MCH: low in proportion to Hb; MCHC: low; RDW: increased; RBC: low or normal; Hb electrophoresis: normal

88
Q

Summarise investigation results of thalassaemia trait in pregnancy

A

Hb: normal (rarely low); MCH: lower for same Hb; MCHC: relatively preserved; RDW: normal; RBC: increased; Hb electrophoresis: HbA2 increased in B-thal trait and normal in A-thal trait.

89
Q

What are other important diseases in pregnancy?

A

Haemolytic disease of the newborn and neonatal alloimmune thrombocytopaenia

HAEM - Abbie (16 decks)

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