Obstetrics and Gynaecology chapters
Anaemia, thalassaemia and coagulation disorders in pregnancy
How pregnancy changes the blood, how anaemia in pregnancy is defined, found and treated, and what the haemoglobinopathies, low platelets and inherited bleeding disorders mean for mother and baby.
- Plasma rises more than red cells, so pregnancy causes haemodilution; true anaemia is Hb below 110 g/L in the first trimester and below 105 g/L later, and the commonest cause is iron deficiency, treated first with oral iron.
- In thalassaemia and sickle cell carriers, screen the partner: two carriers give a 1 in 4 chance of an affected baby.
- A mild late fall in platelets is usually gestational thrombocytopenia; ITP can also lower the baby's platelets, and von Willebrand disease is the commonest inherited bleeding disorder.
On this page
Overview
Blood problems are among the commonest medical issues in pregnancy. Most are mild, but a woman who starts labour anaemic copes poorly with bleeding, and some inherited disorders affect the baby too.
This chapter covers:
- the normal blood changes of pregnancy;
- anaemia: definition, causes, tests and treatment;
- haemoglobinopathies: thalassaemia and sickle cell disease;
- coagulation and platelet disorders: gestational thrombocytopenia, ITP, inherited bleeding disorders and thrombophilia.
Normal blood changes in pregnancy
Haemodilution ("physiological anaemia")
- Maternal blood volume climbs steadily, mostly in the second half, to about 30% above normal near term (Guyton).
- Plasma volume rises proportionally more than red cell mass, so the haemoglobin concentration and haematocrit fall, although the total amount of haemoglobin actually increases.
- This dilution lowers blood viscosity and helps placental flow. It is not a disease.
A falling Hb in mid-pregnancy with a normal MCV and normal ferritin is usually dilution, not iron deficiency. True anaemia is diagnosed only below the trimester cut-offs below.
Coagulation changes
- Pregnancy is a hypercoagulable state, which protects against bleeding at delivery.
- Factors VIII, IX, X and fibrinogen rise; protein S and antithrombin fall.
- Add venous stasis from the uterus pressing on the IVC, and VTE risk is several-fold higher than outside pregnancy, highest after delivery and after emergency caesarean section.
Anaemia in pregnancy
Definition
| Period | Anaemia if Hb is below |
|---|---|
| First trimester | 110 g/L (11 g/dL) |
| Second and third trimesters | 105 g/L (10.5 g/dL) |
| Postpartum | 100 g/L (10 g/dL) |
These are the British Society for Haematology cut-offs quoted by Ten Teachers. WHO uses a single cut-off of 110 g/L throughout pregnancy. A haemoglobin under 70 g/L (7 g/dL) is generally regarded as severe.
Causes
| Type | Causes | MCV |
|---|---|---|
| Iron deficiency | Poor diet, closely spaced pregnancies, twins, previous heavy periods, hookworm in tropical areas | Low |
| Folate deficiency | Poor diet, hyperemesis, twins, anticonvulsants, haemolysis | High |
| Vitamin B12 deficiency | Strict vegetarian diet; very rare in pregnancy | High |
| Haemoglobinopathy | Thalassaemia trait, sickle cell disease | Low (thalassaemia) |
| Haemolysis | Malaria, HELLP syndrome, G6PD deficiency | Normal or high |
| Blood loss and chronic disease | Antepartum bleeding, renal disease, infection | Low or normal |
Iron deficiency is by far the commonest cause of anaemia in pregnancy. Demand peaks in the second half of pregnancy.
Why iron needs rise
Iron is needed for the fetus, the placenta, the bigger maternal red cell mass and the blood lost at birth. Davidson puts the daily need at about 3.5 mg in pregnancy.
Basic daily requirement = 1 mg
Extra for fetus, placenta, red cell mass and delivery = 2.5 mg
Total = 1 + 2.5 = 3.5 mg absorbed iron per day
Effects of anaemia
- Mother: tiredness, breathlessness, poor tolerance of blood loss at delivery, higher chance of needing transfusion, and greater risk of puerperal infection (anaemia is a listed risk factor for sepsis).
- Fetus: iron deficiency in the mother is linked with preterm birth and low birthweight in standard teaching; check local data before quoting figures.
Investigations
- Full blood count at booking and again at 28 weeks.
- MCV sorts the type: low MCV points to iron deficiency or thalassaemia trait; high MCV to folate or B12 deficiency.
- Serum ferritin: the best single test of iron stores.
- B12 and folate if MCV is high.
- Haemoglobin electrophoresis (or HPLC) if MCV is low with normal ferritin, or if the family origin is high risk.
- Look for other causes: stool for ova (hookworm), malaria film in endemic areas, urine and renal function.
Management
Prevention
- Folic acid 400 micrograms daily before conception and through the first trimester for all women.
- Folic acid 5 mg daily for higher-risk women (for example sickle cell disease, previous neural tube defect, epilepsy on anticonvulsants, inflammatory bowel disease).
- Routine iron supplements are often advised in multiple pregnancy because of higher demand.
Treatment
- Oral iron is first line. A rise in Hb within 2 weeks confirms that the cause is iron deficiency and that treatment is working.
- Advise taking it on an empty stomach where tolerated; warn about constipation and dark stools.
- Parenteral (intravenous) iron: for women who cannot tolerate or absorb oral iron, do not respond, or are near term with significant anaemia.
- Blood transfusion: reserved for severe or symptomatic anaemia, active bleeding or very late presentation. After delivery, women with Hb below 70 g/L or marked symptoms should be offered transfusion; mild to moderate postpartum anaemia (above 70 g/L) is treated with iron tablets.
Do not give iron blindly to a woman with a known haemoglobinopathy. Check ferritin first; give iron only if ferritin is below 30 micrograms/L. Iron overload is a risk in thalassaemia.
"Low MCV, check the iron store": low ferritin means iron deficiency; normal ferritin means think thalassaemia trait.
Haemoglobinopathies
Thalassaemia
- Inherited autosomal recessive disorders with reduced production of normal globin chains.
- Carrier rates are high in people of South Asian, Southeast Asian, Mediterranean, Middle Eastern and North African origin, so this matters greatly in Pakistan.
| Type | Genes affected | Picture |
|---|---|---|
| Alpha: one gene | 1 of 4 (chromosome 16) | No symptoms |
| Alpha-thalassaemia trait | 2 of 4 | Mild anaemia |
| Haemoglobin H disease | 3 of 4 | Chronic anaemia, may need regular transfusion |
| Alpha-thalassaemia major | All 4 | Hydrops fetalis and intrauterine death |
| Beta-thalassaemia minor (trait) | 1 of 2 (chromosome 11) | Mild microcytic anaemia; no antenatal problem |
| Beta-thalassaemia intermedia | Both, milder mutations | Not transfusion dependent |
| Beta-thalassaemia major | Both | Lifelong transfusion from infancy |
Antenatal approach
- Screen every woman at booking (FBC indices, family origin, electrophoresis).
- If she is a carrier, test her partner.
- If both are carriers, offer referral to fetal medicine for prenatal diagnosis (CVS or amniocentesis).
- Beta-thalassaemia trait: give iron and folate if needed, after checking ferritin.
Each parent passes on either the normal gene or the trait gene (1 in 2 each)
Affected (two trait genes) = 1/2 × 1/2 = 1/4
Carrier = 2 × (1/2 × 1/2) = 1/2
Unaffected non-carrier = 1/4
Two carriers = 1 in 4 risk of an affected baby in each pregnancy (beta-thalassaemia major, alpha-thalassaemia major or sickle cell disease).
Sickle cell disease
- HbS has a substituted beta chain that polymerises when deoxygenated, so cells sickle and block small vessels.
- Variants: sickle cell trait (HbAS), HbSS (most severe), HbSC (milder anaemia but severe crises in pregnancy, easily underestimated), sickle beta-thalassaemia.
- Pregnancy risks: more crises, acute chest syndrome, VTE, infection, pre-eclampsia, FGR, miscarriage and preterm labour.
- Crisis triggers: hypoxia, dehydration, cold, infection, stress and bleeding.
- Prepregnancy and antenatal care: folic acid 5 mg daily and low-dose aspirin 75 mg daily from early pregnancy; review medicines; screen partner.
- Managing a crisis: prompt analgesia, fluids, oxygen, screen for infection and give antibiotics, thromboprophylaxis with heparin, transfusion or exchange transfusion when indicated, and fetal monitoring.
- Sickle cell trait: usually well; more prone to urinary infection.
Platelet disorders
Causes of low platelets (below 150 × 10⁹/L)
- Gestational thrombocytopenia (commonest, 7-8% of pregnancies)
- Immune thrombocytopenia (ITP)
- Pre-eclampsia and HELLP syndrome
- DIC (abruption, amniotic fluid embolism, sepsis, retained dead fetus)
- Antiphospholipid syndrome, TTP, hypersplenism
- Reduced production: sepsis, HIV, marrow infiltration
Gestational thrombocytopenia vs ITP
| Feature | Gestational thrombocytopenia | ITP |
|---|---|---|
| Timing | Late pregnancy (usually after 28 weeks) | Any time, often known before pregnancy |
| Platelet count | Usually 100-150 × 10⁹/L | Can fall below 50 × 10⁹/L |
| Cause | Diagnosis of exclusion | Antiplatelet autoantibodies |
| Baby | No fetal thrombocytopenia | 5-10% chance of fetal platelets below 50 |
| Treatment | Monitoring only | Steroids or IV immunoglobulin if count is low near term |
| After birth | Resolves | Persists |
ITP points
- Incidence about 1 in 5,000 pregnancies.
- Spontaneous bleeding is unlikely above 20 × 10⁹/L; delivery bleeding unlikely above 50 × 10⁹/L.
- Treat if the count falls below 50 × 10⁹/L approaching 37 weeks: prednisolone (works in 2-3 weeks) or IV immunoglobulin (faster; preferred close to term).
- Avoid regional anaesthesia if platelets are below 80 × 10⁹/L.
- Aim for vaginal birth; avoid fetal blood sampling and ventouse.
- Take cord blood for platelets; the baby's lowest count comes 2-5 days after birth.
Maternal platelet count and antibody levels do not predict the baby's platelet count in ITP.
Inherited bleeding disorders
- Von Willebrand disease, haemophilia A and B carriers and factor XI deficiency make up over 90% of inherited bleeding disorders in women.
- Von Willebrand disease: the commonest inherited bleeding disorder (about 1%), usually autosomal dominant.
- Haemophilia A (factor VIII) and B (factor IX): X-linked; carriers have about 50% of normal factor levels. Factor VIII rises in pregnancy; factor IX rises very little.
- Factor XI deficiency: bleeding risk does not match the factor level.
Management
- Counsel before pregnancy; check factor levels at booking and in the third trimester.
- In haemophilia carriers, find out fetal sex (ultrasound, or testing fetal DNA that circulates in maternal blood).
- Plan delivery with a haematologist: factor concentrate, tranexamic acid or desmopressin (DDAVP). DDAVP is most useful for type 1 von Willebrand disease and for women who carry haemophilia A.
- If the baby may be affected, avoid fetal scalp electrodes, fetal blood sampling, ventouse and rotational forceps; send cord blood for clotting.
- Risk of primary and secondary PPH is high.
"No suction, no scalp": in any mother whose baby may bleed (ITP, haemophilia carrier), avoid ventouse and scalp procedures.
Thrombophilia
- Inherited: factor V Leiden, prothrombin G20210A mutation, deficiencies of protein C, protein S and antithrombin.
- Acquired: antiphospholipid syndrome (lupus anticoagulant and/or anticardiolipin antibodies with recurrent miscarriage or thrombosis).
- Linked with VTE and adverse outcomes such as recurrent pregnancy loss.
- Women with a past VTE should be screened; those with thrombophilia plus a past clot usually need heparin prophylaxis in pregnancy.
Expect: the trimester-specific haemoglobin cut-offs and the WHO cut-off of 11 g/dL; plasma volume rising more than red cell mass; iron deficiency as the commonest cause and oral iron as first-line treatment with a response by 2 weeks; ferritin before iron in haemoglobinopathies; folic acid 400 micrograms versus 5 mg; partner screening and the 1 in 4 risk; alpha-thalassaemia major causing hydrops; sickle crisis triggers and the role of aspirin and folate; gestational thrombocytopenia versus ITP; avoiding ventouse and scalp sampling; von Willebrand disease as the commonest inherited bleeding disorder and DDAVP; the clotting factor changes that make pregnancy hypercoagulable.
Quick revision
- Anaemia: Hb below 110 (T1), 105 (T2, T3), 100 g/L (postpartum); WHO 110 g/L throughout.
- Commonest cause: iron deficiency; first line oral iron; IV iron if intolerant, unresponsive or late; transfuse if severe.
- Folic acid 400 micrograms for all; 5 mg for high-risk women.
- Low MCV with normal ferritin: electrophoresis for thalassaemia; screen partner; 1 in 4 if both carriers.
- Sickle cell disease: folate 5 mg, aspirin 75 mg, avoid hypoxia, dehydration and infection.
- Gestational thrombocytopenia: late, mild, harmless; ITP: may affect the baby.
- No regional block below 80 × 10⁹/L platelets in ITP.
- von Willebrand disease is the commonest inherited bleeding disorder; DDAVP helps type 1.
Written by The House Job from standard references (Obstetrics by Ten Teachers; Guyton and Hall Textbook of Medical Physiology; Davidson's Principles and Practice of Medicine).
FAQ
Is a haemoglobin of 105 g/L at 30 weeks anaemia?
Not by the British cut-off, which is below 105 g/L after the first trimester, though it is anaemia by the WHO cut-off of 110 g/L; check the MCV and ferritin either way.
Why is ferritin checked before giving iron to a thalassaemia carrier?
Carriers already have a low MCV without being iron deficient, and unnecessary iron can build up; iron is given only if ferritin is low.
Does gestational thrombocytopenia harm the baby?
No. It is not linked with low platelets in the baby and settles after delivery, but it is diagnosed only after ITP, pre-eclampsia and other causes are excluded.
Why is pregnancy called a hypercoagulable state?
Several clotting factors and fibrinogen rise while natural anticoagulants such as protein S and antithrombin fall, which limits bleeding at birth but raises the risk of venous thrombosis.