Clinical overview
Fluid and electrolyte management is one of the quiet skills that separates a safe registrar from a dangerous one. It rarely arrives as a single dramatic decision; instead it accumulates as a string of small choices — the maintenance bag hung overnight, the bolus given for a low blood pressure, the oxytocin infusion run in a litre of 5% dextrose-water — and the errors accumulate the same way. The pregnant patient is the trap. Pregnancy lowers serum sodium and osmolality, lowers colloid oncotic pressure, raises plasma volume by roughly 40–50%, and re-sets thirst and antidiuretic hormone (ADH) thresholds. A regimen that is unremarkable in a non-pregnant adult — generous crystalloid in pre-eclampsia, hypotonic fluid in a hyponatraemic labouring woman — can precipitate pulmonary oedema or symptomatic hyponatraemia precisely because the maternal physiology is already shifted toward those endpoints.
In the South African setting the stakes are sharpened by the disease mix. Hypertensive disease of pregnancy and obstetric haemorrhage are consistently among the leading direct causes of maternal death in the Saving Mothers (NCCEMD) reports, and both are conditions in which fluid is simultaneously the treatment and the threat — too little in haemorrhagic shock kills, too much in pre-eclampsia with severe features drowns the lung. This chapter builds the reasoning for both the haemorrhaging woman who needs volume and the leaky-capillary pre-eclamptic who must be kept dry, and for the gynaecological surgical patient where fluid overload and dilutional electrolyte derangement (classically transurethral/hysteroscopic fluid absorption) are the recognised hazards.
Core knowledge
Body fluid compartments and tonicity
Total body water is roughly 50–60% of body weight, split about two-thirds intracellular and one-third extracellular; of the extracellular fluid, roughly a quarter is intravascular plasma and three-quarters is interstitial. The clinically load-bearing point is that only the effective osmoles distributed across cell membranes (chiefly sodium and its anions) move water between compartments. Isotonic crystalloid stays extracellular and expands plasma transiently; hypotonic fluid (and the free water generated when 5% dextrose is metabolised) distributes through total body water and will lower serum sodium. This is why a "fluid" decision is always also a "sodium" decision.
How pregnancy changes the baseline
- Plasma volume rises ~40–50% and red-cell mass rises less, producing the physiological dilutional anaemia of pregnancy.
- Serum sodium falls by roughly 3–5 mmol/L and plasma osmolality by ~10 mOsm/kg, because the osmotic thresholds for thirst and ADH release are reset downward. A sodium of 132–135 mmol/L can therefore be normal in pregnancy.
- Colloid oncotic pressure falls (lower albumin), so the gradient holding fluid in the vasculature is weaker and the lung is more easily flooded — markedly so in pre-eclampsia where the capillaries are also leaky.
- Cardiac output and renal plasma flow/GFR rise, increasing the filtered load and the speed at which an inappropriate fluid load distributes.
- Aortocaval compression from ~20 weeks means a supine pregnant woman can be hypotensive from positioning alone — left-lateral tilt or manual uterine displacement before reaching for a bolus.
Figure M2.1 — Tonicity and pregnancy physiology: isotonic fluid stays extracellular, free water lowers sodium, and the pregnancy baseline increases pulmonary-oedema risk.
The principal electrolyte problems
- Hyponatraemia is the commonest dangerous derangement and is usually iatrogenic or dilutional — hypotonic maintenance fluid, oxytocin run in large volumes of dextrose-water (oxytocin has structural similarity to ADH and an antidiuretic effect at high infusion rates/large fluid volumes), or excessive oral free water in labour. Acute symptomatic hyponatraemia (headache, nausea, confusion, seizures) is a cerebral-oedema emergency in both mother and, transplacentally, neonate.
- Hypernatraemia is far less common and usually reflects water deficit (poor intake, hyperemesis, diabetes insipidus — including the transient gestational diabetes insipidus of late pregnancy from placental vasopressinase).
- Potassium: hyperkalaemia in renal failure, massive haemolysis, or rhabdomyolysis is the most immediately lethal (peaked T-waves → widened QRS → arrest); hypokalaemia accompanies vomiting (hyperemesis), diuretics, and large dextrose-insulin shifts.
- Magnesium: relevant mainly because magnesium sulphate is the eclampsia drug; therapeutic infusion intentionally raises magnesium, and toxicity (loss of reflexes → respiratory depression → cardiac arrest) is dose- and renal-clearance-dependent.
- Calcium: ionised hypocalcaemia is a recognised consequence of massive transfusion (citrate chelation) and of magnesium therapy.