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a path 3 > HAEM: Obstetric haematology > Flashcards

HAEM: Obstetric haematology Flashcards

1
Q
A

Platelet count falls

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2
Q

What changes in FBC occur in pregnancy?

A

Mild anaemia

  • RBC mass rises (120 -130%)
  • Plasma volume rises (150%)
  • NET DILUTION

Macrocytosis

  • Normal
  • Folate or B12 deficiency

Neutrophilia

Thrombocytopenia

  • Increased platelet size
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3
Q

Why are there increased iron requirements during pregnancy? By how much? What happens to iron absorption?

A

Iron requirement

  • 300mg for fetus required in total
  • 500mg for maternal increased red cell mass

Recommended daily intake - 30mg;

Increase in daily iron absorption:1-2mg to 6mg

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4
Q

Why do folate requirements increase in pregnancy? How much is required?

A

Growth and cell division

Reduces risk of neural tube defects

Approx additional 200mcg/day required - so dose is 400mcg/day

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5
Q

When should folic acid be taken during pregnancy?

A

Before conception to 12 weeks gestation

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6
Q

What are the complications of iron deficiency in pregnacy?

A
  • IUGR,
  • prematurity,
  • PPH
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7
Q

Summarise the iron cycle.

A

RDA - recommended daily amount

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8
Q

How long should you continue iron supplementation post correction of Hb in pregnancy?

A

3 months following correction of Hb

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9
Q

Define anaemia in pregnancy.

A

Hb < 110 g/l = 1st trimester

Hb < 105 g/l = 2nd and 3rd trimester

Hb < 100 g/l = postpartum

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10
Q

What laboratory findings show iron deficiency anaemia?

A

Low Hb

Low MCV

Low MCH

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11
Q

What else should you check in terms of bloods if the patient has a known haemoglobinopathy?

A

Serum ferritin

Treat if ferritin <30mcg/L

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12
Q

What is the pathophysiology of thrombocytopenia in pregnancy?

A

Most plasma expansion happens in the 1st/2nd trimester so platelet count falls here due to haemodilution.

In 3rd trimester the mechanism is increased activation and destruction of platelets so you get giant platelets (on automated counters they may be counted as RBC so much check on blood film)

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13
Q

Apart from physiological, what are the causes of thrombocytopenia in pregnancy?

A
  • Pre-eclampsia
  • Immune thrombocytopenia (ITP)
  • Microangiopathic syndromes
  • All other causes: bone marrow failure, leukaemia, hypersplenism, DIC etc.
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14
Q

Which condition is most likely cause if the platelet count is:

  1. <150 x109/L
  2. <100 x 109/L
  3. <70x109/L
A
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15
Q

What % decrease in plt occurs in gestational thrombocytopenia? What does plt count need to be for delivery/epidural? When do platelets start to rise again?

A

~10% decrease

  • >50x109/l sufficient for delivery
  • >70x109/l for epidural

Count rises at day 2-5 post-delivery

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16
Q

How common is thrombocytopenia in PET? Why does it decrease?

A

Affect 50%

Probably due to increased activation and consumption. Associated with coagulation activation (incipient DIC – normal PT, APTT)

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17
Q

What are the treatments for ITP in pregnancy?

A
  • IV immunoglobulin
  • Steroids etc.
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18
Q

What is a danger of ITP to the baby and why? How is this risk managed?

A

IgG antibodies so cross the placenta and may cause thrombocytopenia in the baby. Although in most cases the baby will be unaffected, it is a possibility

Management: cord blood must be checked and manage delivery if necessary.

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19
Q

Give 3 examples of MAHA syndromes in pregnancy. Which MAHA syndromes are unaffected by delivery of the baby?

A

TTP and HUS i.e. no alteration in course

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20
Q

What is the pathophysiology of MAHA in pregnancy in causing thrombocytopenia?

A

Deposition of platelets in small blood vessels –> thrombocytopenia

Complication: fragmentation and destruction of RBC within vasculature, organ damage (kidney, CNS, placenta)

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21
Q
A
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22
Q

What is the most common cause of mortality during pregnancy?

A

VTE

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23
Q

What coagulation changes occur in pregnancy?

A
  • Factor VIII and vWF ( x3 to x5)
  • Fibrinogen (x2)
  • Factor VII (x1.5
  • (Factor X)

= HYPERCOAGULABILITY

  • Protein S (x0.5)
  • PAI-1 (x5)
  • PAI-2 produced by placenta

=HYPOFIBRINOLYSIS

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25
Q

What net effects cause a procoagulant state in pregnancy?

A
  • Increased thrombin generation
  • Increased fibrin cleavage
  • Reduced fibrinolysis

Interact with other maternal factors

26
Q

When is risk of VTE highest in pregnancy?

A

Postpartum (one third occur postpartum)

27
Q

What are the modifiable risk factors for VTE 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
28
Q

How can you investigate VTE in pregnancy?

A

Doppler and VQ are safe to perform in pregnancy. Venograms and CTPA can also be done.

NB: D-dimer often elevated in pregnancy so not useful for exclusion of thrombosis

30
Q

How do you prevent VTE in pregnancy?

A

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

32
Q

What is the management of VTE in pregnancy? What about if an epidural is required?

A

Management - LMWH

  • Does not cross placenta, RCOG recommend OD or BD
  • Do not convert to warfarin (crosses placenta + teratogenic in early pregnancy)
  • 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

33
Q

What are the complications of warfarin in pregnancy?

A

Chondrodysplasia Punctata

  • Abnormal cartilage and bone formation
  • Early fusion of epiphyses
  • Nasal hypoplasia
  • Short stature
  • Asplenia
  • Deafness
  • Seizures

Teratogenic in 1st trimester

34
Q

Define antiphospholipid syndrome in pregnancy.

A

Recurrent miscarriage

Persistent lupus anticoagulant (LA)

+/- Antiphospholipid antibodies

35
Q

What are the complications of antiphospholipid syndrome in pregnancy?

A

_>_3 consecutive miscarriages before 10 weeks of gestation

_>_1 morphologically normal fetal losses after the 10th week of gestation

_>_1 preterm births before the 34th week of gestation owing to placental disease.

36
Q

What management can significantly increase fetal survival in women with recurrent misacrriage and antiphospholipid syndrome?

A

Aspirin and heparin

37
Q

Name 2 causes of fatal bleeding in pregnancy which are the principal reasons for hysterectomy.

A
  1. Placenta praevia
  2. Placenta accreta
38
Q

Define PPH.

A

> 500 mL blood loss

39
Q

How common is blood loss of >1L at delivery?

A

5%

Requiring transfusion post partum

  • 1% after vaginal delivery
  • 1-7% after C-Section
40
Q

What are the main 2 mechanisms of PPH in delivery?

A
  • Uterine atony
  • Trauma

Others:

  • Dilutional coagulopathy after resuscitation
  • DIC in abruption/amniotic fluid embolism
42
Q

What are the causes of DIC in pregnancy?

A
  • Amniotic fluid embolism
  • Abruptio placentae
  • Retained dead fetus
  • Preeclampsia (severe)
  • Sepsis
43
Q

What is one of the most catastrophic complications in obstetrics?

A

Amniotic fluid embolism - but rare affecting 1 in 30,000

44
Q

What are some clinical features of amniotic fluid embolism?

A
  • sudden onset shivers,
  • vomiting
  • shock
  • DIC
45
Q

What is the pathophysiology of amniotic fluid embolism? What is a potential risk factors?

A

Presumed due to Tissue Factor in amniotic fluid entering maternal bloodstream

Usually occurs in 3rd trimester - drugs used to induce labour e.g. misoprostol increase risk

46
Q

Which severe haemoglobinopathies does screening aim to avoid in children?

A

a° thalassaemia (Hb Bart’s, g4)

b° thalassemia

HbSS (sickle cell disease) = life expectancy 43 yrs

Other compound HbS syndromes = symptomatic, stroke etc.

Some compound thalassaemias = transfusion dependent, iron overload

47
Q

What are the complications of the two severe thalassaemias?

A

a° thalassaemia (Hb Bart’s, g4) = death in utero, hydrops fetalis

b° thalassemia = transfusion dependent

48
Q

What is the usual blood loss during C/S?

49
Q

Describe the investigations which are part of the NHS sickle cell a

A

Testing depends on prevalence in the area i.e. if _>_1.5/10,000 it is universal and if <1.5/10,000 is selected screening only.

  1. Family origin questionnaire (FOQ)
  2. FBC - check MCH
  3. HPLC - identifies variants
  4. Aim to complete by 12/40, including partner testing where required
50
Q

When can MCH indicate thalassaemia in the screening programme?

A

MCH <27 possible thalassaemia trait

MCH <25 possible α thal trait - NB: Alpha thal requires DNA analysis to detect alpha zero trait

51
Q

What is the aim of HPLC in the screening programme? When does it suggest beta-thalassaemia?

A
  1. Identifies Hb variants eg: S, C, E
  2. Quantifies Hb A2 (>3.5% → β thal)
52
Q

When should you offer partner screening for haemoglobinopathies?

A

If the mother is heterozygous

53
Q

If screening suggests haemoglobinopathy, what prenatal tests can be done for diagnosis?

A

CVS sampling at 10-12 weeks

Amniocentesis at 15-17 weeks, fetal blood sampling

US screening for hydrops

54
Q

What are the differences in laboratory FBC findings in Fe deficiency vs thalassaemia trait?

55
Q

Name two other immune mediated disorders in pregnancy.

A

HDN - haemolytic disease of the newborn

NAIT - neonatal alloimmune thrombocytopenia

58
Q
A

HELLP - red cell fragments

59
Q
A

Iron deficiency

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