Clinical overview
The full blood count (FBC), urea and electrolytes (U/E), and arterial blood gas (ABG) are the three workhorse investigations of the critically ill obstetric or gynaecological patient. In a resuscitation bay at 02:00, a registrar who can read these three results fluently — and, crucially, read them against the altered physiology of pregnancy — will pick up a concealed abruption, an early HELLP, a developing sepsis, or a deteriorating acidotic shock before the blood pressure collapses. The skill is not defining haematocrit but taking a panel of numbers, recognising the pattern, deciding what is dangerous now, and acting.
The governing principle is that pregnancy shifts every reference range you memorised in medical school. A haemoglobin of 10.5 g/dL, a urea that looks "low-normal", a creatinine of 70 µmol/L, and a PaCO₂ of 4.0 kPa may each be physiological in a healthy term woman — or each may be the footprint of a life-threatening process. Interpreting these tests in the obstetric patient means continuously asking: what should this number be for a pregnant woman, and what does this deviation mean? What follows is the analytic reasoning, not just the values. It complements Shock management, Fluids and electrolytes in O&G and Resuscitation in pregnancy, where these same numbers drive the resuscitation.
Core knowledge
The pregnant baseline — why the ranges move
The physiological adaptations of pregnancy systematically distort the FBC, U/E and ABG, and the direction of each shift matters.
Haematological adaptation. Plasma volume rises by roughly 40–50% from early pregnancy, while red cell mass rises only ~20–30%. The mismatch produces a dilutional anaemia ("physiological anaemia of pregnancy") with a nadir around 28–32 weeks. As a result, the lower limit of normal haemoglobin falls. The WHO and SA practice classically take Hb < 11 g/dL in the first/third trimester (and < 10.5 g/dL mid-trimester) as the threshold for anaemia — values that would be frankly low in a non-pregnant adult are expected here. The white cell count rises physiologically (a neutrophil leucocytosis is normal, often into the teens, and labour/delivery push it higher still), which means a raised WCC alone is a weak marker of infection in pregnancy and the puerperium. Platelets drift down modestly; gestational thrombocytopenia (typically > 100–120 ×10⁹/L, benign) accounts for most mild low counts.
Renal adaptation. Renal plasma flow and glomerular filtration rate rise by 40–50%. Urea and creatinine therefore fall in normal pregnancy. A creatinine that looks reassuringly mid-range for a non-pregnant adult — say 80–90 µmol/L — may represent significant renal impairment in a pregnant woman whose true baseline is ~45–60 µmol/L. Apply pregnancy-adjusted thresholds: a "normal-looking" creatinine can be pathological. Serum sodium drops a few mmol/L (reset osmostat) and a mild respiratory alkalosis lowers bicarbonate as compensation (see below).
Respiratory adaptation. Progesterone drives an increase in tidal volume and minute ventilation. The consequence is a chronic compensated respiratory alkalosis: PaCO₂ falls (typically to ~3.7–4.3 kPa / ~28–32 mmHg), pH sits at the high end of normal, and the kidney compensates by excreting bicarbonate so HCO₃⁻ falls to ~18–22 mmol/L. PaO₂ is well maintained or slightly increased. The practical danger: a "normal" PaCO₂ of 5.3 kPa (40 mmHg) in a breathless pregnant woman is not normal — it signals CO₂ retention and impending respiratory failure, because she should be hypocapnic. The reduced buffering reserve (low baseline bicarbonate) also means a pregnant woman tips into dangerous acidaemia faster when a metabolic acid load is added.
Figure M3.1 — Pregnancy-adjusted FBC, U/E and ABG baselines that make normal adult values misleading in critical O&G.
What each test actually measures
- FBC: haemoglobin and haematocrit (oxygen-carrying capacity and a proxy for volume status/blood loss), MCV (microcytic = iron deficiency, the dominant SA cause; macrocytic = B12/folate, alcohol, some ARVs), WCC and differential, and platelets. In acute haemorrhage the Hb lags behind real loss until dilution occurs, so a normal early Hb never excludes major bleeding.
- U/E: sodium, potassium, urea, creatinine, and usually bicarbonate. Drives recognition of acute kidney injury (AKI), dysnatraemias, hyperkalaemia, and the metabolic component of acid–base disorders. See Fluids and electrolytes in O&G for the electrolyte derangements in detail.
- ABG: pH, PaCO₂, PaO₂, HCO₃⁻ (and base excess), plus lactate and often electrolytes/Hb on modern blood-gas analysers. The ABG is the fastest window onto oxygenation, ventilation, acid–base balance and tissue perfusion (lactate) in the collapsing patient.