3: Obstetric Haematology Flashcards
Anaemia in pregnancy definition (dependant on trimester)
Blood Count Changes in pregnancy
Mild anaemia
- Red cell mass rises (120-130%) Net Dilution
- Plasma volume rises (150%)
Macrocytosis
- Normal
- Folate or B12 deficiency
Neutrophilia
Thrombocytopenia (increased platelet size from increase in turnover of platelets)
Iron and folate requirement during pregnancy
Iron requirement 300mg (foetus); 500mg (maternal RBC mass)
- RDA 30mg
- Increase in daily iron absorption 1-2mg to 6mg
- Iron deficiency → IUGR, prematurity, PPH
Folate requirement increase +200mcg/day
- Growth and cell division
Iron and folate supplements in pregnancy
60mg iron AND 400ug folic acid daily during pregnancy WHO Recommendations
- However, some Cochrane reviews have found iron or folate supplements had no effect on measures of maternal or foetal outcome → maternal Hb higher, Fe reserves higher, foetal ferritin higher
400ug folic acid (and no iron) daily during pregnancy RCOG Guidelines
- Supplement before conception and for more than 12-weeks’ gestation
- High-dose folic acid = 5mg / 5000ug folic acid
Thrombocytopaenia ranges in pregnancy
- Platelet Count Falls in Pregnancy [non-pregnant = 225-249 x 109/L; pregnant = 175-199 x 109/L]
Causes of thrombocytopenia
(1) Physiological (gestational or incidental thrombocytopenia)
(2) Pre-eclampsia (HELLP – Haemolysis, Elevated Liver enzymes, Low Platelets)
(3) Immune thrombocytopenia (ITP) – BM creates lots of platelets but there is peripheral destruction
(4) MAHA syndromes
All other causes – BM failure, hypersplenism, DIC, leukaemia
Gestational thrombocytopenia (a physiological decrease in platelets – affects ~10%)
- >50x109/L enough for delivery (>70 required for epidural)
- Mechanism is poorly defined (dilution and increased consumption potentially)
- Baby is not affected
Platelet count rises 2-5 days post-delivery
Most likely cause…
>70 x 109/L = gestational thrombocytopenia <70 x 109/L = ITP or pre-eclampsia
Pre-eclampsia
- 50% get thrombocytopenia (proportionate to severity)
- Association with increased activation and consumption (incipient DIC (normal PT, APTT))
- Platelet count remits following delivery
Immune thrombocytopenia – ITP
5% of these patients get thrombocytopenia in pregnancy (TP may precede pregnancy; early onset)
Treatment options – for bleeding or delivery:
- IVIG + steroids
- Anti-D (in RhD +ve mothers with spleen) – the anti-D coats the RBCs and is preferentially removed by the reticuloendothelial system in preference to the AB-covered platelets, thus conserving platelet levels
Baby may be affected
- Unpredictable (platelets <20 in 5%)
- Check cord blood and then daily
- May fall for 5 days after delivery
- Bleeding in 25% of severely affected – IVIG if low
- Usually normal delivery
Microangiopathic syndromes [Microangiopathic Haemolytic Anaemia – MAHA]
MAHA syndromes – demonstrates different ways MAHA can present:
- I.E. TTP, HUS, AFLP, SLE, APLS, etc.
- TTP (pentad S/S: MAHA, fever, renal impairment, neurological impairment, thrombocytopenia)
Tx TTP dependant on plts number and current bleeding
- Deposition of platelets in small blood vessels (inc. in the placenta)
-
Cardinal signs = fragmentation (schistocytes) and destruction of RBC within vasculature
- Increased BR
- Thrombocytopenia, schistocytes
- Organ damage – kidney, CNS, placenta
Delivery does not alter course of TTP or HUS
HUS pathophysiology
HUS pathophysiology
Iron cycle andrequirements
VTE during pregnancy
VTE during pregnancy → is more common in women with a high BMI (95% of clots in pregnant women are in the left leg)
PE is the leading direct cause of maternal death in the UK (1.56 per 100,000 maternal mortalities)
Coagulation changes during pregnancy
Coagulation changes during pregnancy
highest risk time for PE, largest predictor of incidence of PE, what can you give
- Deaths from PE (largest maternal killer):
- Highest risk time = post-partum and 1st trimester
- High BMI (>25) is the largest predictor of incidence of PE
- Need to be on heparin from the first trimester
VTE/PE Ix’s during pregnancy
- Doppler and VQ are safe to perform in pregnancy
- D-dimer is elevated in pregnancy (not useful for exclusion of thrombosis [is usually used for exclusion])
Factors increasing risk of thrombosis in pregnancy
Prevention and treatment of thromboembolic disease in pregnancy
Thrombosis → impaired placental circulation → ?
- IUGR (Intra-uterine Growth Restriction) Recurrent miscarriage
- Late foetal loss Placental abruption
- Severe PET (pre-eclampsia)
Thrombophilia → APLS (anti-phospholipid syndrome)
APLS (criteria) and treatment
-
Miscarriages (≥3) + lupus anticoagulant or anticardiolipin antibodies T
- Adverse pregnancy outcomes – 3+ consecutive miscarriages before 10 weeks of gestation
- 1 or more morphologically normal foetal losses after 10w of gestation
- 1 or more preterm birth before 34-weeks of gestation
- Treat with (unfractionated) heparin** and **aspirin → dramatically improved outcomes
PPH causes
PPH (large cause of mortality in high income countries – remained very stable over the years)
- Placenta praevia (placenta attached at vaginal opening)
- Placenta accrete (wall-invading placenta)
- Principal reason for hysterectomy
Post-partum Haemorrhage (PPH) = >500ml blood loss (SVD)
- 5% pregnancies have blood loss more than 1L
- Requiring transfusion post-partum = 1% after vaginal delivery, 1-7% after C-section
PPH – Mechanisms:
- Major factors – uterine atony and trauma (the 4 T’s = tone, tissue, trauma, thrombin)
- Haematological factors minor except:
- Dilutional coagulopathy after resus
- DIC in abruption, amniotic fluid embolism
- Haematological factors minor except:
Decompensation is precipitated by…
Amniotic fluid embolism
Preeclampsia (severe/HELLP)
Abruptio placentae
Sepsis
Retained dead foetus
