Haem: Obstetric Haematology Flashcards

1
Q

What haematological changes are seen on FBC in pregnancy?

A
  • Mild anaemia (DILUTION)
    • Red cell mass rises (120-130%)
    • Plasma volume rises (150%)
  • Macrocytosis
    • Normal
    • Folate or B12 deficiency
  • Neutrophilia
  • Thrombocytopenia
    • Increased platelet size
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2
Q

What are the 3 Hb thresholds for anaemia in pregnancy?

A

<110 in 1st trimester

<105 in 2nd/ 3rd trimester

<100 post partum

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3
Q

What are the increased demands required in pregnancy?

A
  • Iron requirement
    • 300mg for fetus
    • 500mg for maternal increased red cell mass
  • Folate requirements increase
    • Growth and cell division
    • Approx additional 200mcg/day required
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4
Q

How iron deficiency diagnosed?
What is the treatment for iron deficiency in pregnancy?

A

FBC: Low Hb, MCV < 80

200 mg ferrous sulfate daily for 3 months

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5
Q

What does iron deficiency during pregnancy increase risk of?

A

IUGR

Prematurity

Postpartum haemorrhage

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6
Q

What is normal iron absorption per day?

What is iron absorption during pregnancy?

A

Normal absorption 1-2mg a day.

This increases to 6mg during pregnancy.

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7
Q

Why is iron absorption increased during pregnancy?

A

Hepcidin decreases and ferroportin levels increase. This results in increased iron absorption.

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8
Q

What are the RCOG recommendation for daily folate intake?

A

400 mcg daily

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9
Q

What does folate deficiency increase risk of during pregnancy?

A

Neural tube defects

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10
Q

What is the cut off level of platelets required for:

  1. Epidural anaethesia
  2. Delivery
A
  1. > 70 x10^9/L
  2. > 50 x10^9/L

Higher for epidural due to serious risk of spinal haematoma

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11
Q

What are causes of thrombocytopenia in pregnancy?

A
  • Physiological:
    • ‘gestational’ / incidental thrombocytopenia
  • Pre-eclampsia
  • Immune thrombocytopenia (ITP)
  • Microangiopathic syndromes
  • All other causes: bone marrow failure, leukaemia, hypersplenism, DIC etc.
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12
Q

What is the most commone cause of thrombocytopaenia <150x109/L in pregnancy?

A

Gestational thrombocytopenia

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13
Q

What is the most common cause of thrombocytopaenia <100x109/L in pregnancy?

A

ITP and pre-eclampsia

This suggests something pathological is occurring.

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14
Q

What is gestational thrombocytopenia?

A

A physiological decrease in platelet count of about 10% during pregnancy
Does not affect foetus.

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15
Q

What is the underlying mechanism of gestational thrombocytopenia?

A

Mechanism poorly defined.

Possibly due to dilution and increased consumption.

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16
Q

When does platelet count increase following gestational thrombocytopenia?

A

Platelet count rises around 2-5 days after delivery

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17
Q

When does platelet count fall most during pregnancy in gestational thrombocytopenia?

A

Most of the fallen platelet count occurs in 3rd trimester

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18
Q

What percent of women with preeclampsia get thrombocytopenia?

A

50%

Thrombocytopenia is proportionate to severity of preeclampsia.

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19
Q

What causes thrombocytopenia in preeclampsia?

A

Increased activation and consumption of platelets due endothelial injury

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20
Q

What percentage of thrombocytopenia during pregnancy is accounted for by immune thrombocytopenia (ITP)?

A

5% of thrombocytopenia in pregnancy

  • TP may precede pregnancy
  • Early onset
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21
Q

What are the treatment options for ITP in pregnancy?

A
  • IVIG (FIRST LINE)
  • Steroids (not ideal as lots of side effects)
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22
Q

At what point during the pregnancy does platelet count fall most due to ITP?

A

Platelet count tends to fall dramatically early in pregnancy if present

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23
Q

Does ITP affect the baby?

A

Yes / Potentially

Anti-platelet IgG can cross the placenta (5-10%). If foetal platelet count drops can increased risk of intracranial haemorrhage. Check platelet count at birth and give IVIG if below 50.

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24
Q

What is mechanism of microangiopathic haemolytic anaemia?

A

Deposition of platelets and fibrin in microvasculature leading to thrombocytopenia. The deposits can also shear RBCs leading to intravascular haemolysis. Organ damage can also occur due to vessel occlusion

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25
Q

What would you expect to see on the blood film of microangiopathic syndromes?

A

Schistocytes

Nucleated red cells consistent with increased red cell turnover

26
Q

What are the causes of MAHA in pregnancy?

A
  • Preeclampsia
  • HELLP
  • TTP (Thrombotic thrombocytopenic purpura)
  • HUS (Haemolytic uraemic syndrome)
  • AFLP (Acute fatty liver of pregnancy)
  • SLE (Systemic lupus erythema)
  • APLS (Antiphospholipid syndrome)
27
Q

What is HELLP?

A

Haemolysis
Elevated liver enzymes
Low platelets

28
Q

What is a leading cause of maternal mortality?

A

Coagulation changes in pregnancy - VTE

29
Q

What change in pro- and anti-coagulative factors are seen in pregnancy?

A

Hypercoagulability

  • Factor VIII and vWF - increases x3-5
  • Fibrinogen - increases x2
  • Factor VII -increases x0.5

Hypofibrinolytic

  • Protein S - falls to half basal level
  • PAI-1 - increases x5 fold
  • PAI-2 produced by the placenta
30
Q

What is the reason for coagulation changes seen in pregnancy?

A

Rapid control of bleeding from the placental site (700ml/min) at time of delivery. Coagulation changes control this bleeding.

31
Q

What are the net effects of coagulation changes seen in pregnancy?

A
  • Increased thrombin generation
  • Increased fibrin generation
  • Reduced fibrinolysis
  • Interact with other maternal factors

This leads to an increased rate of THROMBOSIS

32
Q

When do coagulation changes in pregnancy return back to normal?

A

Weeks/months after delivery

33
Q

When are VTEs most likely to occur?

A

1-6 weeks post partum

34
Q

When are deaths due to pulmonary embolism during pregnancy most likely to occur?

A

A third of cases are post-partum (within 6 weeks post-partum). However, a reasonable proportion also occur in the first trimester.

35
Q

What investigations for VTE may be done during pregnancy?

A

Doppler and VQ scans are SAFE to perform in pregnancy CTPA in some cases although increases maternal breast cancer risk

(D-dimer is often elevated in pregnancy so is NOT useful for exclusion of thrombosis)

36
Q

What are three main factors that increase risk of VTE?

A

Virchow’s Triad

  • Changes in blood coagulation (hypercoaguability)
  • Reduced venous return (stasis)
  • Vessel wall changes
37
Q

What are variable factors during pregnancy that increase risk of thrombosis?

A
  • Hyperemesis/dehydration
  • Bed rest/immobility
  • Obesity
  • Preeclampsia
  • Operative delivery (C-sections)
  • Previous thrombosis/thrombophilia
  • Age >35 significant
  • Parity - after 4th child, risk increases massively
  • Multiple pregnancy
  • Other medical problems: HbSS, nephrotic syndrome
  • IVF: ovarian hyperstimulation
38
Q

How may thrombosis be prevented in pregnant women?

A

Identify women with risk factors at booking

  • Thromboprophylaxis - LMWH
  • Mobilise early
  • Maintain hydration
39
Q

Describe antenatal and postnatal thromboprophylaxis management in:
1. High risk women
2. Intermediate risk women
3. Low risk women

A
  1. High risk: antenatal LMWH continued until 6 weeks postpartum
  2. Intermediate risk: consider antenatal LMWH either starting in first trimester (4 risk factors) or from 28 weeks (3 risk factors) until 10 days postpartum
  3. Low risk: mobilisation and avoidance of dehydration throughout
40
Q

What is the treatment of thromboembolic disease in pregnancy?

A

LMWH

  • Safe as does not cross placenta
  • RCOG recommend once or twice daily injections
  • After 1st trimester monitor anti-Xa
  • Stop LMWH for labour or planned delivery, esp. for epidural

Epidural: wait 24 hours after treatment dose, 12 hours after prophylactic dose

41
Q

What anticoagulant drugs must you avoid in pregnancy?

A

Warfarin and DOACs

  • Both cross the placenta and are teratogenic
  • Especially in 1st trimester
42
Q

What complications of pregnancy are associated with thrombophilia?

A

It is hypothesised that an increased tendency to thrombosis is associated with impaired placental circulation.

This results in:

  • Fetal growth restriction (IUGR)
  • Recurrent miscarriage
  • Late fetal loss
  • Placental abruption
  • Severe preeclampsia
43
Q

What is the diagnostic criteria of antiphospholipid syndrome?

A

At least 1 clinical and 1 biochemical criteria

Clinical criteria:

  • Vascular thrombosis
  • Pregnancy morbidity

Biochemical criteria
(all must be on 2 occasions >12 weeks apart)

  • Lupus anticoagulant
  • High anticardiolipin antibodies
  • Anti-b2-glycoprotein 1 antibodies
44
Q

What are the diagnositic criteria of pregnancy morbidity in anti-phospholipid syndrome?

A
  • Adverse pregnancy outcome: three or more consecutive miscarriages before 10 weeks of gestation (where anatomical, hormonal, and chromosomal causes have been excluded)
  • One or more morphologically normal fetal losses after the 10th week of gestation
  • One or more preeterm births before the 34th week of gestation owing to placental disease
45
Q

What treatment may be given to improve outcome in women who have had recurrent miscarriages?

A

Aspirin

OR

Aspirin + Heparin

46
Q

What is placenta praevia?

A

When the placenta covers the cervical os

47
Q

What is placenta accreta?

A

When the placenta is attached to the surface of the myometrium

48
Q

What are placenta increta and percreta?

A

Placenta increta: the placenta penetrates into the myometrium

Placenta percreta: the placenta penetrates through the myometrium to the uterine serosa

49
Q

What do C-sections increase the risk of in future pregnancies?

A
  • Placenta praevia
  • Placenta accreta

C-sections increase the likelihood of having issues with the site of placental implantation

50
Q

What is the definition of post-partum haemorrhage?

A

> 500 ml blood loss

51
Q

What are the main causes of postpartum haemorrhage?

A

4 T’s:
Tone: uterine atony (main cause)
Trauma: perineal tears
Tissue: placenta accreta
Thrombin: hypocoagulative state (DIC in aminotic fluid embolism)

52
Q

Name some obstetric causes of DIC

A
  • Amniotic fluid embolism
  • Placental abruption
  • Retained products of conception
  • Severe preeclampsia
  • Sepsis
53
Q

What is amniotic fluid embolism?

A

AFE is a rare childbirth (obstetric) emergency in which amniotic fluid enters the bloodstream of the mother to trigger a serious reaction.

Very catastrophic with high mortality rate (86%)

54
Q

What are the symptoms of AFE?

A
  • ARDS - SoB, hypoxia
  • Shock
  • Neurological - confusion, coma, seizures
  • DIC

Manifests during labour or immediately after but can occur up to 48 hours postpartum

55
Q

Which haemoglobinopathies are screened for?

A
  • Sickle cell disease
  • Alpha thalasaemia
  • Beta thalasaemia
56
Q

How are individuals selected for the haemoglobinopathy screening program

A
  • If from high prevalance area
  • Family Origin Questionnaire
57
Q

What diagnostic technique is used in the haemoglobinopathy screening program?
What can this techique not diagnose?

A

High performance liquid chromatography

HPLC can identify haemoglobin variants (EXCEPT it cannot identify alpha thalassaemia)

  • Alpha thalassaemia requires DNA diagnosis.
  • HPLC can quantify HbA2 (>3.5% = beta thalassemia)
58
Q

What antenatal tests may be done to diagnose potential foetal haemoglobinopathies?

A
  • CVS (10-12 weeks)
  • Amniocentesis (15-17 weeks)
  • Fetal blood sampling
  • Ultrasound screening for hydrops
59
Q

What are the key features of haemoglobinopathy counselling?

A

Important disorders are all recessive
Therefore if mother is heterozygous partner should be tested
Combinations as important as homozygous states
Prenatal diagnosis by 12 weeks: allows for termination of pregnancy in severe cases

60
Q

What are the differences in FBC and Hb electrophoresis of iron deficiency anaemia vs. thalassaemia trait?

A
Hb, MCV, MCH, Red cell count thalassaemia smaller cells so MCHC same Red cell count always increased in thalassaemia trait (normal in IDA)
61
Q

Name 2 other important immune disorders in pregnancy that affect the neonate.

A
  • Haemolytic disease of the newborn (HDN)
  • Neonatal alloimmune thrombocytopenia (NAITP)

Maternal immune responses against fetal antigens requiring monitoring and intervention during pregnancy.