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. This is a HOTS (higher-order thinking) objective: the FCOG(SA) examiner is not testing whether you can define haematocrit, but whether you can take a panel of numbers, recognise the pattern, decide what is dangerous now, and act.
The single most important framing 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? This chapter teaches the analytic reasoning, not just the values. It complements shock-management, fluids-electrolytes-og 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. You must hold the direction of each shift in your head.
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-electrolytes-og 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.
Assessment
Reading the FBC analytically
Start with haemoglobin in context. Is the patient bleeding? In obstetric haemorrhage the initial Hb may be deceptively preserved; trend it, and resuscitate to the clinical picture, not the number. A falling Hb with a falling platelet count and a rising LDH and bilirubin suggests haemolysis — think HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets) in a hypertensive woman, or microangiopathic processes. Look at the MCV: a microcytic anaemia in an antenatal South African woman is iron deficiency until proven otherwise; a normocytic anaemia with reticulocytosis points to blood loss or haemolysis.
Platelets carry disproportionate weight in obstetrics. A drop is the canary for pre-eclampsia with severe features/HELLP, for disseminated intravascular coagulation (DIC) in abruption or sepsis, and occasionally for primary thrombocytopenic disorders. A platelet count < 100 ×10⁹/L in a hypertensive woman should prompt the full HELLP/severe-features work-up and is one of the laboratory criteria for pre-eclampsia-and-hellp. A rapidly falling count with prolonged clotting times and a low fibrinogen is DIC until proven otherwise.
The white cell count is the least reliable single marker in pregnancy because of the physiological leucocytosis. Weight the differential and trend: a left shift, a rising count over hours, a markedly raised or paradoxically low count with clinical signs, all matter more than an isolated mildly high WCC. Combine with lactate and clinical signs for sepsis recognition.
Reading the U/E analytically
Anchor on pregnancy-adjusted renal thresholds. Because creatinine should be low, treat the upper-normal lab value with suspicion. Calculate the picture: oliguria (< 0.5 mL/kg/hr), rising urea and creatinine, and hyperkalaemia define evolving AKI — common after major obstetric haemorrhage, in severe pre-eclampsia, and in sepsis. Distinguish a urea raised out of proportion to creatinine (suggests hypovolaemia/pre-renal state or a GI bleed) from a proportionate rise (intrinsic renal injury).
For sodium, hyponatraemia in O&G is frequently iatrogenic or oxytocin-related: oxytocin has antidiuretic activity, and prolonged infusion with hypotonic fluid can cause dilutional hyponatraemia and, if severe and rapid, seizures — a genuine hazard during induction/augmentation and in hyperemesis. Hypernatraemia usually reflects water deficit. For potassium, hyperkalaemia (with AKI, acidosis, or massive transfusion) is the one that kills first — it demands an immediate ECG and the standard emergency drill below. The bicarbonate on the U/E previews the metabolic acid–base state and should be cross-read with the ABG.
Reading the ABG analytically — a disciplined sequence
Do not eyeball an ABG. Use the same stepwise method every time so you never miss a mixed disorder.
- Oxygenation first. Look at PaO₂ and SaO₂ against the FiO₂. Hypoxaemia (PaO₂ low for the inspired oxygen) flags ARDS, pulmonary oedema (pre-eclampsia, tocolysis-related, cardiac), pulmonary embolism, aspiration, or severe pneumonia.
- pH — acidaemia or alkalaemia? < 7.35 acidaemic, > 7.45 alkalaemic. Remember the pregnant baseline pH sits high-normal.
- Identify the primary disturbance. Respiratory (PaCO₂ moves opposite to expected for the pH) or metabolic (HCO₃⁻/base excess moves with the pH)? A low PaCO₂ in pregnancy is expected; a normal-to-high PaCO₂ in a sick, breathless pregnant woman signals ventilatory failure.
- Assess compensation and decide whether it is appropriate or whether a second (mixed) disorder is present. Compensation never fully normalises the pH.
- Calculate the anion gap for any metabolic acidosis: a high anion gap points to lactate (shock/sepsis — the commonest in our setting), ketones (DKA, which can occur at near-normal glucose in pregnancy), toxins, or renal failure; a normal-gap acidosis suggests bicarbonate loss (diarrhoea) or renal tubular causes/large-volume saline.
- Read the lactate. A rising lactate is one of the earliest, most actionable markers of tissue hypoperfusion in haemorrhagic or septic shock — frequently abnormal before blood pressure falls. Trend it; clearance with resuscitation is a good sign.
A worked obstetric example: a collapsed woman after a concealed abruption shows pH 7.18, PaCO₂ 3.0 kPa, HCO₃⁻ 10 mmol/L, lactate 7 mmol/L. That is a high-anion-gap metabolic (lactic) acidosis with appropriate respiratory compensation — the hyperventilation (low CO₂) is the body trying to defend the pH. The message is: she is in shock and hypoperfused; resuscitate aggressively, find and stop the bleeding (postpartum-haemorrhage, antepartum-haemorrhage).
Figure M3.2 — A disciplined ABG sequence for oxygenation, pH, primary disturbance, compensation, anion gap and lactate, with the pregnancy PaCO₂ trap.
Management
Interpreting the numbers is only useful if it changes what you do. Tie each abnormal pattern to an action, and remember the resuscitation priorities always run alongside the diagnostics — airway, breathing, circulation first (resuscitation-in-pregnancy).
Acting on the FBC
- Anaemia / falling Hb with bleeding: activate the haemorrhage drill — large-bore IV access, crossmatch, and early transfusion guided by clinical loss and trend, not a single Hb. In major obstetric haemorrhage give tranexamic acid 1 g IV early, within 3 hours of onset (WOMAN trial). Use a massive transfusion protocol with balanced product ratios and correct coagulopathy.
- Thrombocytopenia in a hypertensive woman: complete the severe-features/HELLP work-up, control blood pressure, give magnesium sulphate for seizure prophylaxis where indicated, and plan delivery. Transfuse platelets per local threshold mainly when actively bleeding or before operative intervention.
- Suspected DIC (low platelets, low fibrinogen, prolonged PT/aPTT, with abruption/sepsis): treat the cause and replace product (fresh frozen plasma, cryoprecipitate/fibrinogen, platelets) guided by results — see fluids-in-og.
Acting on the U/E
- AKI: treat the cause (restore circulating volume in pre-renal/haemorrhagic states, treat sepsis, deliver in severe pre-eclampsia), monitor urine output hourly, review nephrotoxic drugs, and involve a physician/nephrologist early; dialysis for refractory hyperkalaemia, acidosis, fluid overload or uraemia.
- Hyponatraemia: if oxytocin-associated, stop/reduce the infusion and the hypotonic fluid; manage symptomatic/seizing patients cautiously, correcting at a controlled rate to avoid osmotic demyelination. Detailed electrolyte correction is covered in fluids-electrolytes-og.
EMERGENCY DRILL — HYPERKALAEMIA. A potassium that is high with ECG changes (peaked T waves, widened QRS, loss of P waves) or any K⁺ ≳ 6.5 mmol/L is a cardiac arrest waiting to happen. Act immediately and in this order, while calling for senior/ICU help:
- Protect the myocardium — IV calcium (calcium gluconate) to stabilise the membrane; repeat if ECG changes persist.
- Shift potassium into cells — insulin with dextrose (and salbutamol nebuliser as an adjunct).
- Remove potassium from the body — treat the cause, consider dialysis if refractory; stop all potassium-containing fluids and nephrotoxins. Use SA EML / local protocol doses; recheck the ECG and K⁺ after each step.
Acting on the ABG
The ABG tells you how sick and how fast. A worsening metabolic acidosis with a climbing lactate despite fluids means the source is not controlled — escalate to definitive haemorrhage control or source control of sepsis, and call ICU. A rising PaCO₂ in a tiring, breathless woman means she needs ventilatory support now — do not wait for the pH to fall further; secure the airway/support ventilation and call for anaesthetic/critical-care help. Hypoxaemia refractory to oxygen (think pulmonary oedema in severe pre-eclampsia, ARDS, PE) needs the underlying cause treated and respiratory support escalated.
EMERGENCY DRILL — SEVERE METABOLIC ACIDOSIS IN SHOCK. pH < 7.2 with a high lactate in a collapsed obstetric patient = under-resuscitated shock until proven otherwise. (1) Restore circulation — control the bleeding/treat the source; (2) replace volume and blood product; (3) ensure adequate ventilation so respiratory compensation is not lost; (4) trend lactate and gas every 30–60 minutes; (5) ICU referral. Routine bicarbonate infusion does not fix the underlying problem and is generally reserved for specific, senior-led indications.
Figure M3.3 — High-risk FBC, U/E and ABG patterns that should trigger haemorrhage, HELLP, DIC, AKI, hyperkalaemia, ventilatory and shock escalation.
The South African context
In the SA public system you will often work where point-of-care testing is limited and results are delayed. Several practical realities follow. First, the National Integrated Maternal and Perinatal Care Guidelines (NDoH, 2024) structure where care happens: district, regional and tertiary levels differ in their access to blood-gas analysers, NHLS turnaround, blood-bank stock and ICU beds. A registrar at district level must interpret a venous gas/lactate on a point-of-care device, make a resuscitation decision, and refer early rather than wait for a perfect dataset. Second, the SA disease burden colours every result: iron-deficiency anaemia is highly prevalent, so a low MCV antenatally is expected and treatable; the high HIV prevalence means cytopenias may be disease- or ARV-related, and infection (a leading non-pregnancy-related cause of maternal death in the Saving Mothers/NCCEMD reports) must always be on the differential for an abnormal WCC or lactate. Third, obstetric haemorrhage and hypertension remain leading direct causes of maternal death in SA — exactly the conditions these three tests are designed to catch early. Use the EML for emergency drug doses, and treat blood as a scarce resource: transfuse on sound triggers and use tranexamic acid early.
Red flags / pitfalls
- Applying non-pregnant reference ranges. The single commonest analytic error. A "normal" creatinine, a "normal" PaCO₂, or a "reassuring" Hb may each be pathological in pregnancy. Always re-baseline mentally for the gravid state.
- Trusting a single early Hb in haemorrhage. Haemoglobin lags acute loss. A normal Hb never excludes major bleeding; resuscitate to the clinical picture and the trend.
- Dismissing a raised WCC as "just pregnancy" — or panicking over it. The physiological leucocytosis cuts both ways: it neither confirms nor excludes sepsis. Anchor on the differential, the trend, the lactate, and the clinical picture.
- Missing the falling platelet count. A drifting-down platelet count in a hypertensive woman is an early HELLP/severe-features signal; do not wait for it to reach a textbook threshold before acting.
- Misreading a "normal" PaCO₂ as reassuring in a breathless pregnant woman — it signals impending ventilatory failure because she should be hypocapnic.
- Ignoring lactate. Lactate rises before the blood pressure falls in shock; a normal BP with a high lactate is occult hypoperfusion. Treat it as a resuscitation trigger.
- Forgetting the anion gap. Skipping the gap calculation hides the cause of a metabolic acidosis (lactate vs ketones vs renal vs bicarbonate loss) and misdirects treatment. DKA can present at near-normal glucose in pregnancy.
- Iatrogenic dysnatraemia. Oxytocin plus hypotonic fluid causing dilutional hyponatraemia and seizures is preventable — watch the fluid balance during prolonged induction.
- Hyperkalaemia complacency. Any high potassium with ECG changes is a periarrest emergency; act before the rhythm deteriorates.
- Treating numbers, not the patient. These tests support — never replace — clinical assessment and the resuscitation sequence.
Evidence anchors
- National Integrated Maternal and Perinatal Care Guidelines for South Africa (NDoH, 2024), NDoH — the SA obstetric source of truth for levels of care, anaemia management, and referral pathways.
- Saving Mothers / NCCEMD (latest triennial report) — obstetric haemorrhage, hypertension and non-pregnancy-related infection (HIV) as leading SA maternal-death causes, contextualising the abnormal FBC/U/E/ABG patterns above.
- South African EML — Hospital Level (Adults), current edition — emergency drug doses for hyperkalaemia and resuscitation.
- NICE NG133 — Hypertension in pregnancy (2019) — laboratory criteria (platelets, renal, liver) and management thresholds for pre-eclampsia with severe features/HELLP; see pre-eclampsia-and-hellp.
- RCOG Green-top Guideline No. 52 — Prevention and Management of Postpartum Haemorrhage, with the WOMAN trial (Lancet 2017) supporting tranexamic acid 1 g IV given early (within 3 hours) — the haemorrhage drill behind the falling-Hb pattern.
- RCOG Green-top Guideline No. 56 — Maternal Collapse in Pregnancy and the Puerperium — the resuscitation framework within which these investigations are interpreted; see resuscitation-in-pregnancy.
- South African National HIV/ART Consolidated Guidelines (2023; TLD first-line) — context for cytopenias and infection in the high-HIV-prevalence SA population.
- Acid–base and pregnancy-physiology reference ranges quoted here are standard physiological teaching; exact local cut-offs should be confirmed against your laboratory's pregnancy-adjusted reference values.