Haematology in Pregnancy Flashcards
1
Q
Physiological Changes in Pregnancy
A
- Haemoglobin declines from 110 to 105 to 100g/l as there is a lower limit during pregnancy. Increase in red blood cells but bigger increase in plasma volume.
- Rise in white blood cells (mainly neutrophils)
- Fall in platelets to lower limit of 80-100x10^9/l - “gestational thrombocytopenia”
- Rise in mean cell volume by 4fl from 84 to 88
- Rise in fibrinogen and factors VIII, IX, X so hypercoagulable state.
2
Q
Anaemia in Pregnancy
A
- Iron deficiency - High level of borderline iron deficiency going into pregnancy and then add on the increased demands if the foetus, results in iron deficiency anaemia. Mean cell volume may be normal, so have to check ferritin levels. It is common to supplement iron in pregnancy but constipation, abdominal pain and nausea are common side effects. IV iron - ferinject is an option.
- B12 defieciency - folic acid 400mcg/day given pre-conception reduce neural tube defects (neural tube formed in 2-4 weeks from conception). Consultation on supplementation in flour. Continued in pregnancy due to increased demands of the foetus. True B12 defieciency us rare but drop in reference range for B12 in pregnancy can cause diagnostic difficulty.
3
Q
Immune Thrombocytopenic Purpura (ITP)
A
- Autoimmune disease of children and adults
- May be triggered by infection, drug or pregnancy
- Auto antibodies to platelets (marrow normal)
- Treated by watch and wait, steroids, immunoglobulins, splenectomy, or drugs to mimic thrombopoetin.
- May need treatment to achieve platelets of 50+ for labour
- Some risk of neonatal thrombocytopenia due to IgG antibodies crossing placenta.
4
Q
Thrombotic Thrombocytopenic Purpura (TTP)
A
- Rare but life-threatening “thrombotic microangiopathy”
- Enzyme (ADAMS13) prevents large Von Willebrands polymers - this becomes deficient and platelets aggregate.
- Presents as fever, neurological and renal disease, low platelets and fragmented red cells. Coagulation screen usually normal.
- Can be associated with auto-immune disease/HIV/pregnancy
- Treated by plasma exchange (to replace enzyme)
5
Q
Thromboembolic Disease
A
- UK maternal death rate is 9/100,000. Pulmonary embolism is the leading direct cause.
- Pregnancy and 6 weeks post-partum is high risk, hypercoaguable state.
- Additional risk factors - age, previous clot, smoking, twins, obesity, thrombophilia e.g. antithrombin deficiency
- In late pregnancy, pelvic veins are compressed (L>R) which leads to leg swelling. Progressive pain, tenderness and unilateral swelling can occur and Deep Vein Thrombosis may occur.
- Investigate using Doppler exam of leg and Chest X-Ray, if abnormal then CT pulmonary angiogram (be aware of higher radiation dose but it is more reliable than ventilation/perfusion scan). D-dimers will be unhelpful as they are raised in pregnancy.
- Treatment of choice is Low Molecular Weight Heparin, increased rate of clearance and volume of distribution requires twice daily dose. Monitoring of anti-Xa levels (3-4 hours post dose) required to show effective dosing. Will need prophylactic anticoagulation in future pregnancies.
6
Q
Pre-Eclamptic Toxaemia (PET)
A
- Results in Hypertension, Fluid Retention, Proteinuria, Headache and High levels of Urate.
- Minority of patients with PET will develop HELLP Syndrome (Haemolysis, Elevated Liver enzymes, Low Platelet count).
- Treatment is prompt delivery of baby and supportive care
7
Q
HELLP Syndrome
A
- H - Haemolysis - anaemia, red cell fragments, raised Lactate Dehydrogenase
- EL - Elevated Liver Enzymes - ALT/AST
- LP - Low Platelet Count
- Serious but rare complication of pregnancy
- Treatment - prompt delivery of baby and supportive care
8
Q
Disseminated Intravascular Coagulation
A
- Acute and serious complication typically following - placental abruption, amniotic fluid embolism, dead foetus.
- Typically haemorrhagic, very unwell, organ failures, depletion of coagulation factors, low platelets, red cell fragments
- Treatment - treating the cause, coagulation factors and platelets
9
Q
Major Haemorrhage
A
- Can be ante- or post- partum
- 2nd most common direct cause of maternal death
- Risk factors - placenta previa (over cervix), placental abruption, retained products of conception, poor uterine contraction after delivery.
- Important to recognise excessive blood loss - treat the cause and replace red cell/platelets/coagulation factors
10
Q
Significant/Transfusiom Dependent Haemoglobinopathies
A
- Sickle cell homozygous
- Sickle cell with Hb C/D/E/beta-thalassaemia
- Beta thalassaemia homozygous
- Alpha thalassaemia 3 gene deletion (Hb H)
11
Q
Detection of Haemoglobinopathies/Thalassaemia Carriers
A
- Ethnic Origin
- Most will be microcytic e.g. mean cell volume <80 and mean cell haemoglobin will be <27
- Blood film - target cells in thalassaemia heterozygous, sickle slide test
- Cellulose acetate or agarose gel Haemoglobbin electrophoresis
- High performance liquid chromotography (HPLC)
- Gene copy number
- Gene sequencing
- Abnormal haemoglobins will show on electrophoresis and/or HPLC
- Beta thalassaemia heterozygous will have low MCV and MCH and Hb A2 >3.5%
- Alpha thalassaemia with one gene deletion - no change. Alpha thalassaemia with 2 gene deletions - low MCV. Gene copy number or sequencing may be needed.
12
Q
Pre-natal Screening in low prevalence areas
A
- FBC at booking at approx 12 weeks - MCH <27pg
- Family origin questionnaire for both partners
- If either “positive” then HPLC to look for thalassaemia or haemoglobinopathy
- May need confirmatory tests
- May need to check partner’s FBC etc (beware non-paternity).
13
Q
Action taken for positive pre-natal tests
A
- Card and letter issued to parent(s) and to GP e.g. carrier
- If foetus is at risk of serious Hb disorders consider: 11-14 week CVS for foetal DNA or 15+ weeks amniocentesis.
- Newborn screening includes for sickle cell disease on heel prick
