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 severe pre-eclampsia 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.
Assessment
Assess volume status and electrolyte status as two linked but separate questions, then ask what is driving each.
Volume status — clinical
- Pulse, blood pressure (and trend), capillary refill, peripheral temperature, mucous membranes, jugular venous pressure, lung bases, peripheral/sacral oedema, and conscious level.
- Urine output is the workhorse: aim to track ≥0.5 mL/kg/h. Oliguria after haemorrhage usually means hypovolaemia; oliguria in severe pre-eclampsia is common, often transient, and must not reflexively be treated with fluid boluses.
- Remember the obstetric distortions: the young pregnant woman compensates for blood loss with tachycardia and vasoconstriction and can maintain a near-normal blood pressure until she has lost a large volume — a "normal" pressure is falsely reassuring. The post-partum uterus and the gravid uterus both hide concealed bleeding.
Electrolyte and biochemical work-up
- Urea and electrolytes (sodium, potassium, urea, creatinine), interpreted against pregnancy-adjusted norms (lower sodium, lower urea/creatinine; a "normal-range" creatinine may signify impaired function in pregnancy).
- Glucose, magnesium, calcium, phosphate where relevant (eclampsia, hyperemesis, refeeding, massive transfusion).
- Full blood count (haemoglobin trend in haemorrhage lags acute loss), coagulation/fibrinogen in haemorrhage and pre-eclampsia, liver enzymes and platelets for HELLP, lactate and arterial/venous blood gas for perfusion and acid–base. See arterial-blood-gas for interpretation.
- Fluid balance chart: meticulous hourly input/output is mandatory in any sick obstetric patient and is the single most useful document for catching creeping overload before it reaches the lung. In severe pre-eclampsia a strict chart is part of the protocol.
- In hyponatraemia, before treating, characterise it: acute vs chronic, symptomatic vs not, and volume status (hypo-, eu-, hypervolaemic) — paired serum and urine osmolality and urine sodium guide this, but in the acute peripartum setting the cause is most often dilutional/iatrogenic and the history (fluids given, oxytocin, oral intake) usually makes it obvious.
Management
Choosing the fluid
- Balanced isotonic crystalloid (e.g. Ringer's lactate / Plasma-Lyte type solutions, or 0.9% sodium chloride) is the default resuscitation and replacement fluid. Large volumes of 0.9% saline cause hyperchloraemic acidosis, so balanced solutions are generally preferred for big-volume resuscitation.
- Avoid hypotonic maintenance fluid as a default in the acutely unwell or peripartum patient — it is the classic route to iatrogenic hyponatraemia.
- 5% dextrose / dextrose-water is free water once the sugar is metabolised: use it deliberately (e.g. as the small-volume vehicle some protocols specify for an oxytocin infusion, or for genuine free-water/hypernatraemia replacement), not as a thoughtless maintenance default, and keep oxytocin-carrier volumes restricted.
- Colloids/starches are not the resuscitation fluid of choice; hydroxyethyl starches in particular are avoided. Albumin has no routine role in pre-eclampsia.
- Blood products are the correct "fluid" in haemorrhagic shock once loss is significant — crystalloid is a bridge, not the destination (see below and postpartum-haemorrhage, antepartum-haemorrhage).
Maintenance and the "give less than you think" principle
For a sick obstetric patient the safe instinct is restraint. Run modest maintenance, replace measured losses, reassess clinically and on the balance chart frequently, and resist the standing order that keeps litres running unwatched overnight. The commonest serious fluid error on an obstetric ward is not under-resuscitation of the well patient — it is silent over-resuscitation of the pre-eclamptic.
Severe pre-eclampsia / eclampsia — run them dry
This is the highest-yield fluid lesson in obstetrics. The pre-eclamptic woman has leaky capillaries, low oncotic pressure, and is exquisitely prone to pulmonary oedema; aggressive fluids to "treat" the oligaria do not improve renal outcome and do cause lung flooding.
- Restrict total fluids (a commonly taught ceiling is in the region of ~80 mL/h / ~1 mL/kg/h, but follow your unit's NDoH-aligned protocol for the exact number).
- Do not bolus-chase oliguria in an otherwise stable severe pre-eclamptic; transient oliguria is expected and usually self-resolves. Treat persistent/true renal failure on its merits.
- Magnesium sulphate for seizure prophylaxis and treatment (evidence from the MAGPIE trial; regimen and monitoring per pre-eclampsia-and-hellp and hypertension-in-pregnancy): monitor reflexes, respiratory rate and urine output, and reduce/withhold in oliguria or renal impairment because magnesium is renally cleared. Keep calcium gluconate at the bedside as the antidote for magnesium toxicity.
- Control blood pressure with labetalol/nifedipine/methyldopa rather than with fluid.
Obstetric haemorrhage — the volume emergency
Here the fluid imperative is reversed: restoring circulating volume and oxygen-carrying capacity is life-saving. Manage in parallel, not in sequence.
EMERGENCY DRILL — major obstetric haemorrhage
- Call for help — senior obstetrician, anaesthetist, theatre, blood bank, extra hands; declare a major haemorrhage.
- Airway, breathing, high-flow oxygen; left-lateral tilt/manual uterine displacement if undelivered.
- Two large-bore IV cannulae (14–16G). Send: cross-match, FBC, coagulation/fibrinogen, U&E, point-of-care Hb/lactate.
- Resuscitate with warmed balanced crystalloid as the bridge, then move early to blood — packed cells, and in massive/ongoing loss activate the massive transfusion protocol with FFP, platelets and cryoprecipitate/fibrinogen per protocol. Do not over-fill with clear fluids before blood: dilutional coagulopathy and hypothermia worsen bleeding.
- Tranexamic acid 1 g IV, given early — within 3 hours of onset (WOMAN trial). May repeat per protocol.
- Stop the bleeding in parallel: uterotonics (oxytocin first-line in SA), bimanual compression/massage, examine for tears/retained products, escalate to balloon tamponade, sutures, interventional or surgical control.
- Keep warm, monitor electrolytes/ionised calcium (citrate from stored blood chelates calcium — replace ionised hypocalcaemia), watch potassium, correct acidosis by restoring perfusion.
The E-MOTIVE bundle (early detection + Massage, Oxytocic, TXA, IV fluids, Examine/escalate) operationalises this; full detail in postpartum-haemorrhage and transfusion practice per RCOG GTG 47. See also shock-management and resuscitation-in-pregnancy.
Figure M2.2 — The two opposite O&G fluid reflexes: restrict and monitor in severe pre-eclampsia, but resuscitate early with blood and bleeding control in haemorrhage.
Correcting hyponatraemia safely
- Symptomatic acute hyponatraemia (seizure, marked confusion, depressed consciousness) is an emergency: small carefully-monitored aliquots of hypertonic (3%) saline to raise sodium just enough to abort symptoms, with senior/critical-care involvement.
- Asymptomatic/chronic hyponatraemia: correct slowly and treat the cause. Over-rapid correction risks osmotic demyelination — the standard caution is to keep the rise within conservative limits over 24 hours; use unit/critical-care protocol thresholds rather than improvising.
- Most peripartum hyponatraemia is dilutional: stop the hypotonic fluid, restrict free water, restrict oxytocin-carrier volume — removing the cause is often most of the treatment.
Potassium and the gynae surgical patient
- Hyperkalaemia with ECG changes: calcium gluconate to stabilise the myocardium, insulin–dextrose (and salbutamol) to shift potassium intracellularly, then remove potassium (correct the cause, consider dialysis in renal failure). This is shift-then-remove; the calcium buys time, it does not lower potassium.
- Hypokalaemia: replace with caution and rate limits, ideally with cardiac monitoring for larger deficits; correct coexisting hypomagnesaemia or potassium will not stay corrected.
- Hysteroscopic/operative fluid absorption: prolonged hysteroscopic surgery with hypotonic distension media can cause dangerous dilutional hyponatraemia and fluid overload (the "TUR-type" syndrome). The defence is a strict fluid-deficit limit and continuous deficit monitoring with predefined stop thresholds (AAGL guidance; see operative-hysteroscopy and perioperative-fluids). ERAS principles (see eras-principles) favour euvolaemia and goal-directed rather than liberal fluids in gynae-oncology surgery.
Figure M2.3 — Electrolyte danger board: symptomatic hyponatraemia, potassium emergencies, magnesium/calcium hazards, and hysteroscopy fluid absorption traps.
Red flags / pitfalls
- Bolus-chasing oliguria in severe pre-eclampsia. The single most dangerous reflex on the obstetric ward — it floods the lung without helping the kidney. Restrict, monitor, do not chase.
- Hypotonic maintenance fluid by default. The classic cause of iatrogenic, occasionally fatal, hyponatraemia — especially compounded by oxytocin in large dextrose volumes. Use isotonic fluid and restrict oxytocin-carrier volume.
- Trusting a normal blood pressure in a bleeding young woman. She compensates until late; watch pulse, perfusion, lactate and the actual blood loss, not just the cuff.
- Crystalloid instead of blood in significant haemorrhage. Over-filling with clear fluid dilutes clotting factors, drops the temperature, and worsens bleeding. Move to blood and the massive transfusion protocol early; give TXA within 3 hours.
- Forgetting ionised calcium in massive transfusion (citrate chelation) and forgetting that magnesium is renally cleared — magnesium toxicity in the oliguric pre-eclamptic. Keep calcium gluconate ready.
- Over-rapid correction of chronic hyponatraemia → osmotic demyelination. Slow and protocol-bound for chronic; hypertonic saline only for the acutely symptomatic, with seniors.
- Ignoring the fluid-deficit limit in hysteroscopy. Set the threshold and the stop-rule before you start, and have someone watching the deficit, not the screen.
- No fluid balance chart, or a chart nobody adds up. Creeping positive balance is invisible until the patient desaturates. Total it hourly.
- Treating a pregnancy-adjusted "abnormal" value as a crisis (sodium 133, low-normal creatinine) — know the shifted reference ranges before you act.
Evidence anchors
- National Integrated Maternal and Perinatal Care Guideline, South Africa (NDoH, 2024) (NDoH) — the SA obstetric source of truth, including fluid restriction in severe pre-eclampsia and obstetric haemorrhage management.
- Saving Mothers / NCCEMD reports (South Africa) — hypertensive disease and obstetric haemorrhage as leading direct causes of maternal death; fluid mismanagement (over-resuscitation in pre-eclampsia, under-resuscitation in haemorrhage) as avoidable factors.
- NICE NG133 — Hypertension in Pregnancy (2019) — fluid restriction, magnesium sulphate (MAGPIE) for severe pre-eclampsia/eclampsia, blood-pressure control with labetalol/nifedipine/methyldopa.
- RCOG GTG 52 — Prevention and Management of Postpartum Haemorrhage and the WOMAN trial (Lancet 2017) — early tranexamic acid (1 g IV within 3 hours); E-MOTIVE bundle (NEJM 2023); SA: oxytocin first-line uterotonic.
- RCOG GTG 47 — Blood Transfusions in Obstetrics — transfusion and massive-transfusion principles in obstetric haemorrhage.
- RCOG GTG 56 — Maternal Collapse in Pregnancy and the Puerperium — resuscitation, including left-lateral displacement and perimortem caesarean timing.
- South African EML — Hospital Level (Adults) — crystalloid choice, magnesium sulphate, calcium gluconate, tranexamic acid, uterotonics, potassium replacement.
- AAGL hysteroscopy fluid-management guidance — fluid-deficit limits and monitoring for operative hysteroscopy with hypotonic distension media.
- ERAS Society gynaecologic/oncology guidelines — euvolaemia and goal-directed rather than liberal perioperative fluids.
Author's note on uncertainty: specific maintenance-rate ceilings in severe pre-eclampsia and exact hyponatraemia-correction rate limits are stated cautiously here and must be read against the current NDoH/critical-care unit protocol — the numbers vary by source and the chapter deliberately defers exact thresholds to the local protocol rather than asserting a single figure.