During pregnancy, physiological processes change to facilitate the developing fetus. Some of these changes can be reflected in the haematological and biochemical blood results.
Full blood count
To cope with the increased demands of the gravid uterus, maternal blood volume increases.
Plasma volume increases by 50 per cent at 32-34 weeks whereas the concomitant rise in red blood cells is not as dramatic, creating a relative drop in haemoglobin concentration and haematocrit in pregnancy.
As the haemoglobin remains unaltered, the mean cell volume (MCV) remains unchanged. This relative dilution means anaemia in pregnancy is only diagnosed when the haemoglobin falls below 10.5g/dl.
There is also a decrease in platelet concentration. This is due to an increase in platelet consumption due to the normal inflammatory response in the placental bed. Around 8 per cent of pregnant women will have a platelet count of 100-150x109/l without any significant pathology, and thrombocytopenia is not diagnosed until levels of <100x109/l are reached.
Pregnancy is a hypercoagulable state. Despite this increased clotting tendency, the standard laboratory tests of coagulation:prothrombin time (PT), activated partial thromboplastin time (APTT) and INR, remain within non-pregnant levels.
Anticoagulation proteins, such as protein C and protein S are decreased and clotting factors (except XI and XII) are increased. In addition, there is an increase in fibrinogen breakdown and fibrinogen degradation product (FDP).
Clinically, in suspected venous thromboembolism (VTE), FDP serum levels have a poor predictive value. Diagnosis of VTE should be made on clinical judgment and be supported by imaging (venous Doppler or CT pulmonary angiography).
There is an increase in kidney size and perfusion in pregnancy with an associated increase in glomerular filtration. There is an increase in creatinine clearance by approximately 50 per cent.
As excretion of creatinine and urea is increased, serum levels drop. Electrolyte concentration remains similar to the pre-pregnancy state.
During pregnancy, metabolism by the liver increases, with an associated increase in hepatic blood flow. Plasma volume expansion causes a dramatic dilutional effect on albumin concentration and a marginal decrease in alanine amino-transferase (ALT) and aspartate aminotransferase (AST).
Bilirubin concentration is similar to the non-pregnant state. In contrast, bile acid production is marginally increased in pregnancy due to high levels of circulating estrogens, which increases breakdown in bile.
In addition, alkaline phosphatase (ALP) levels rise dramatically as a consequence of placental production.
The thyroid gland slightly increases in size during pregnancy. There is also an increase in hepatic production of thyroid binding globulin (TBG), due to elevated serum estrogen concentration. These effects result in an increase in total T3 and T4 secretion. Free levels remain relatively stable as there is an increase in urinary secretion of T3 and T4.
Human chorionic gonadotrophin (hCG) shares a common alpha sub-unit with TSH causing it to have a mild stimulating effect on the thyroid. In the first trimester, TSH levels decrease and T4 levels increase slightly due to the negative feedback of copious hCG.
This fall in TSH is transient, and by the third trimester there is marked increase in TSH, as hCG levels fall.
Conditions related to high hCG levels (hyperemesis, molar pregnancy, etc) can cause biochemical hyperthyroidaemia without clinical manifestations of thyrotoxicosis.
Therefore, the assessment of thyroid function in pregnancy should be done by TSH, free T4 (fT4) and clinical examination rather than assessing TSH in isolation.
Pre-eclampsia (PET) is a pregnancy-specific multi-organ condition. The spectrum of the disorder ranges from mild pre-eclampsia to HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome and eclampsia.
Investigation of suspected pre-eclampsia includes BP, urinalysis and blood tests.
Hyperemesis gravidarum (HG) is excessive vomiting in early pregnancy, and can result in dehydration. Excessive levels of hCG stimulate vomit receptors in the brain.
Urinalysis and ultrasound should form the basis of initial investigations, identifying possible causes of HG, such as UTI, multiple or molar pregnancy.
When ketonuria exceeds 3+ on dipstick, admission for IV rehydration is advisable.
Obstetric cholestasis is a condition characterised by pruritus and abnormal liver function.
Excessive circulating estrogens lead to diminished clearance of bile acids resulting in raised bile acids.
The increased bile acids have an inflammatory effect on the liver. It is a diagnosis of exclusion; hepatitis serology and immunology are normal.
- Dr Breslin is clinical lecturer in obstetrics and gynaecology at the University of Warwick, Warwickshire and Dr Houghton is a GP in Ibstock, Leicestershire
- Girling J C, Dow E, Smith J H. Liver function tests in pre-eclampsia: importance of comparison with a reference range derived for normal pregnancy. Br J Obstet Gynaecol 1997; 104: 246-50.
- Girling J, Cotzias C. Thyroid and other endocrine disorders in pregnancy. Obstet Gynaecol Reprod Med 2007; 12: 349-55.