Fluid and electrolyte therapy

• Salt and water handling is organ function, not just a drip rate: every intravenous prescription should have a reason for each litre, a 24-hour plan, and a named review time.
• Resuscitation fluid is a crystalloid containing sodium 130 to 154 mmol/l, given as 500 ml over less than 15 minutes, then reassessed; 30 ml/kg over the first 3 hours is the usual starting point when sepsis is present. ^[1][3]
• Routine maintenance in a fasting adult is about 25 to 30 ml/kg/day of water, roughly 1 mmol/kg/day each of sodium, potassium and chloride, and 50 to 100 g/day of glucose, cut to 20 to 25 ml/kg/day in older, frail or malnourished patients. ^[1]
• A balanced crystalloid is the sensible default for maintenance and replacement, because 0.9% saline carries 154 mmol/l of chloride against plasma 98 to 106 mmol/l, and large volumes produce hyperchloraemic acidosis and interstitial oedema. ^[1][2]
• Volume status is decided at the bedside, not from one test: pulse, blood pressure, capillary refill, jugular venous pressure, oedema, posture, urine output, weight and trends in urea, creatinine and electrolytes, supplemented by dynamic tests when available. ^[1][4]

By the end of this page you should be able to:

1. Assess a patient's salt and water status from history, examination and trends, and write that assessment into an IV fluid management plan.
2. Prescribe a resuscitation bolus and a maintenance regimen using the NICE CG174 quantities and adjustments, and know when to seek expert help.
3. Choose between balanced crystalloid and 0.9% saline from the chloride concentration, tonicity and clinical context.
4. Explain fluid responsiveness, the passive leg raise and basic dynamic indices without laboratory jargon.
5. Outline emergency correction of hyperkalaemia and hyponatraemia and the rate limits that prevent harm.
6. List the main complications of IV fluid therapy and the patient safety habits that prevent them.

Intravenous fluid therapy is a drug-like treatment with its own indications, dose, contraindications and toxicities. ^[1] The two commonest errors are opposites: replacing water and salt that are not missing, which produces peripheral and pulmonary oedema, and withholding them in someone who is genuinely short, which prolongs shock and organ injury. A third error is to prescribe potassium and sodium blindly, without looking at the whole patient.

For a medical student the unifying idea is that fluid therapy has five purposes, the 5 Rs remembered in NICE CG174: Resuscitation, Routine maintenance, Replacement, Redistribution and Reassessment. ^[1] A single patient on a ward often needs two at once, so the prescription must state which purpose each bag serves, in what 24-hour quantity, and when it will be reviewed. ^[1]

This page deals with adults. Children need weight-based maintenance rules and enteral rehydration where possible, which are outside its scope.

Intravenous fluid or electrolyte replacement is indicated when:

• The patient is in shock or has tissue hypoperfusion and the gastrointestinal route is unavailable or unsafe.
• The patient is fasting, vomiting, unconscious, or has an unsafe swallow, so maintenance cannot be given enterally.
• There is a measurable deficit from abnormal losses: vomiting, nasogastric aspirate, high-output stoma, diarrhoea, polyuria, burns or postoperative drainage.
• An electrolyte is outside a safe range and the oral route is insufficient or too slow.
• A drug or procedure requires intravenous access for delivery of fluids or electrolytes.

In every case, if the patient can take and absorb enough orally or enterally, the intravenous route is withdrawn as soon as possible. ^[1]

There is no absolute contraindication to water or salt itself; the contraindications are to the volume, the sodium or the chloride, and to speed. Be cautious, and get senior advice, with:

• Known heart failure, severe valve disease or pulmonary oedema: the same bolus that restores perfusion can precipitate failure.
• Advanced chronic kidney disease or oliguria: potassium, magnesium and phosphate are excreted poorly and accumulate.
• Hepatic failure or cirrhosis with ascites: fluid distribution is unpredictable.
• Acute or recent brain injury and suspected raised intracranial pressure: hypotonic solutions such as Ringer's lactate (about 254 mosmol/kg water) are contraindicated because they can worsen cerebral oedema. ^[2]
• Hyperchloraemia, metabolic acidosis or severe hypernatraemia.
• Patients at risk of refeeding syndrome, in whom energy and electrolytes need a structured plan, not an ad hoc bag.
• Overlap with other fluids already running: total parenteral nutrition, blood products, drug infusions and enteral feeds all count in the daily volume. ^[1]

Potassium must never be added to an IV bag on a ward. It should be prescribed as a standard pharmacy-prepared bag and the prescription rounded to the nearest available bag. ^[1]

Fluid therapy itself needs little equipment beyond reliable access and a clear plan. Have, as a minimum, for the inpatient adult:

• Peripheral cannulae of adequate gauge, or central venous access when concentrated or high-rate replacement is needed, or when the peripheral route is exhausted.
• A fluid balance chart that is filled in and reviewed daily; a chart written but not acted on is, in NICE's words, of no value.
• A scale for weight, repeatable under the same conditions. Small daily changes in weight track total body water better than 24-hour intake/output totals often do.
• A watch or timer for boluses, an infusion pump for potassium, magnesium, phosphate or concentrated solutions, and cardiac monitoring where rates or risks indicate it.
• Laboratory access for urea, creatinine, electrolytes, full blood count and, when needed, venous blood gas or lactate.

In a resuscitation, two large-bore peripheral cannulae usually precede a central line. ^[1][6]

Before prescribing, note that NICE's key priorities say skilled and competent healthcare professionals should prescribe and administer IV fluids, and that hospitals should have an IV fluids lead responsible for training, clinical governance, audit and review of outcomes. ^[1] In practical terms:

• Confirm identity and resuscitation status.
• State the purpose of each fluid, the 24-hour volume and the monitoring plan, in the single visible fluid management plan that every shift can see.
• Tell the patient, when conscious, what is planned and why, and obtain consent for invasive access; in an emergency, treat first and document the reasoning.
• Check allergies: fluid excipients are uncommon, but patients with severe latex or chlorhexidine allergy need product-level checks.
• Review drugs on admission that worsen fluid balance or electrolytes: diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, potassium-sparing diuretics, NSAIDs, lithium, aminoglycosides and digoxin.
• Take baseline weight, urea, creatinine, electrolytes and full blood count. If replacement or redistribution is planned, repeat these more often than once daily. ^[1]

The bedside sequence is deliberately slow and repeats every day, or more often.

Use the assessment in the next section; convert the findings into a 24-hour number. Do not start with the bag and work backwards.

• Resuscitation: for hypovolaemia and shock.
• Routine maintenance: for the patient who cannot eat or drink.
• Replacement: measured deficits and ongoing losses, choosing composition to match the loss.
• Redistribution: fluid sequestered or maldistributed after injury or surgery; this usually warrants expert help. ^[1]

Write the prescription with its purpose, volume, rate and review time. Reassess clinical and laboratory status at least daily initially, twice weekly weights, and more often for replacement or redistribution. ^[1] NICE also asks that clear incidents of fluid mismanagement, such as unnecessarily prolonged dehydration or inadvertent fluid overload, are reported through standard critical incident processes, because fluid errors are a training problem as much as a drug problem. ^[1]

Complex cases include massive redistribution, dialysis-dependent patients, and anyone at risk of refeeding. In these, seek senior, critical care, renal or nutrition input rather than writing a larger bag. ^[1]

The single most common error in fluid prescribing is to treat the chart instead of the patient. Assessment is clinical and cumulative: no one sign is decisive, and the trend is more useful than the absolute value. NICE recommends considering history, examination, medications, monitoring and laboratory tests together. ^[1]

Ask and listen for:

• Thirst, recent intake, and how long the patient has been unable to eat or drink.
• Vomiting, diarrhoea, stoma output, bleeding, fever or polyuria; save and analyse the vomit or aspirate when losses are large or unusual, since the result changes the replacement fluid.
• Reduced urination, dizziness on standing, syncope or palpitations.
• Comorbidities that alter salt and water handling: heart failure, chronic kidney disease, liver disease, adrenal disease, diabetes, cancer, sepsis.
• Medications that hide or worsen the picture: diuretics, vasodilators, beta blockers, ACE inhibitors, ARBs, NSAIDs, steroids, antipsychotics, and oral water intake from culture or IV protocols.
• Malnutrition or recent starvation, because refeeding must be planned alongside fluid. ^[1]

Inspect, palpate and weigh; do not substitute a monitor for this. Useful signs:

• Pulse and rhythm: tachycardia or new atrial arrhythmia point to hypovolaemia; a strong bounding pulse with oedema points to overload.
• Blood pressure: hypotension is a late sign of fluid depletion in adults; postural hypotension (symptoms on standing with a fall in blood pressure) supports volume depletion earlier. ^[1]
• Capillary refill: prolonged refill in the periphery, especially with cold skin or mottling, indicates hypoperfusion.
• Jugular venous pressure: a flat vein at 45 degrees suggests depletion; distension suggests raised central venous pressure, which in the right clinical context points to overload or pump failure.
• Peripheral and pulmonary oedema: ankle, sacral and presacral oedema; new basal crepitations, raised jugular pressure or worsening oxygenation suggest fluid overload.
• Mouth and skin: dry mucous membranes and reduced skin turgor are late, unreliable and age-dependent; they should not be used alone.

NICE lists pulse, blood pressure, capillary refill, jugular venous pressure, pulmonary or peripheral oedema and postural hypotension as the examination markers, while SSC lists skin temperature, mottling and capillary refill time as validated perfusion signs when advanced monitoring is unavailable. ^[1][3]

Both guidelines ask for trend-based rather than point-based interpretation: ^[1]

• NEWS or equivalent early warning score.
• Fluid balance chart, kept accurate and (crucially) reviewed.
• Urine output, watched against the clinical picture, with awareness that drugs, fever and renal dysfunction alter this.
• Weight, measured twice weekly as a minimum in patients on IV fluids, and more often when losing or gaining rapidly. ^[1]
• Urea, creatinine and electrolytes daily at first; full blood count. ^[1]
• Urinary sodium: a value under 30 mmol/l can indicate total body sodium depletion even when the plasma sodium is normal, and it is particularly helpful in high-volume gastrointestinal losses. ^[1] It may be misleading in renal impairment or with diuretic therapy.
• Lactate and capillary refill time in sepsis resuscitation, alongside more direct perfusion markers. ^[3]

Heart rate, blood pressure and central venous pressure by themselves are poor predictors of whether more fluid will help. ^[3] Roughly half of critically ill patients given a fluid challenge do not increase their stroke volume, which is the harm of giving fluid blindly. ^[4]

• Static markers (central venous pressure, simple blood pressure thresholds) are easy to measure and poor at predicting responsiveness. A low value sometimes prompts a fluid trial; a normal value does not exclude benefit; a high value warns against loading.
• Dynamic markers track how the circulation changes with breath or posture. SSC 2021 suggests dynamic measures (passive leg raise or a fluid bolus, using stroke volume, stroke volume variation, pulse pressure variation, or echocardiography) over physical examination or static parameters alone in sepsis. ^[3]
• In a ventilated patient with sinus rhythm, an increase in pulse pressure variation or stroke volume variation with the respiratory cycle suggests preload dependence, but these become unreliable with spontaneous breaths, arrhythmia, low tidal volumes or raised intra-abdominal pressure. ^[4]
• In a spontaneously breathing patient, a passive leg raise (moving from 45 degrees semi-recumbent to 30 to 45 degrees leg elevation for 60 to 90 seconds) acts as a reversible fluid bolus; an increase in stroke volume of more than about 10% indicates preload dependence. A systematic review of 15 studies (649 spontaneously breathing patients) found passive-leg-raise-induced change in stroke volume above 13% and pulse pressure variation during a Valsalva manoeuvre above 52% to have the highest accuracy. ^{[4] [3]}
• Echocardiography is the bedside tool of choice when a line is not present; it can measure inferior vena cava variation, aortic velocity time integral and chamber filling, though it is operator dependent. ^[4]

Resuscitation is for hypovolaemia and shock, and the goal is perfusion, not a number on the chart. Give a 500 ml bolus of a crystalloid containing sodium 130 to 154 mmol/l over less than 15 minutes, then reassess clinically; repeat as needed. ^[1] In suspected sepsis or septic shock, give at least 30 ml/kg of IV crystalloid within the first 3 hours, then use dynamic measures rather than the initial volume to guide further fluid. ^[3] For an adult without sepsis, the same small repeated bolus and reassessment approach applies; do not give repeated litres without a defined trigger and end point. ^[1]

Important caveats from current guidance:

• Fluid resuscitation is a bridge. Septic shock also needs vasoactive support to target a mean arterial pressure of 65 mm Hg once volume is restored, and too much fluid too fast causes oedema, prolonged ventilation and renal injury. ^[3]
• Heart rate, blood pressure and central venous pressure alone are poor indicators of fluid status; dynamic testing where feasible reduces unnecessary exposure to fluid. ^[3]
• In resource-limited settings where measurement of stroke volume is unavailable, a passive leg raise producing more than a 15% rise in pulse pressure can suggest responsiveness. ^[3]
• Resuscitation fluids should not be confused with maintenance: a patient who is shocked may need both, but they are prescribed separately and reviewed separately.

Routine maintenance is for the patient who cannot eat or drink, and it covers insensible, urinary and normal salt losses, nothing more. NICE limits the initial prescription to water 25 to 30 ml/kg/day, about 1 mmol/kg/day of sodium, potassium and chloride, and about 50 to 100 g/day of glucose to limit starvation ketosis; glucose at this dose stops ketosis but is not nutrition, so feeding must be organised separately. ^[1] Pragmatic delivery follows the NICE quantity rather than the label on the bag. ^[1]

Adjustments that matter on a ward:

• Older, frail, malnourished, renally impaired or heart-failure patients: 20 to 25 ml/kg/day. ^[1]
• Obesity: prescribe on ideal body weight, because totals rarely need to exceed 3 litres per day. ^{[1] [3]}
• Prescribing more than 2.5 litres per day increases the risk of hyponatraemia, so larger totals need a Replacement or Redistribution justification. ^[1]
• Weight-based potassium prescriptions should be rounded to the nearest commonly available bag, and potassium must never be added to a bag on the ward. ^[1]
• A patient on routine maintenance plus a feed, plus parenteral nutrition, plus drugs must be summed into one 24-hour total and reviewed daily. ^[1]

Replacement covers measured deficits and ongoing abnormal losses, taking both quantity and composition into account. Gastrointestinal losses from vomiting, nasogastric suction, fistulae and high-output stomas are salt-rich, so they need a crystalloid richer in sodium and chloride than maintenance fluid; urine sodium helps distinguish total body sodium depletion from maldistribution, and urinary sodium under 30 mmol/l is a useful clue. ^[1] Water-only or 5% glucose replacement of diarrhoeal or nasogastric losses is a common cause of dilutional hyponatraemia.

Redistribution covers fluid that has moved between compartments after injury, burns or surgery, or fluid excess. NICE asks for expert help for complex redistribution problems, and a daily weight with sodium and weight trends is more useful for judging it than the balance chart alone. ^[1] Fluid that has shifted into the interstitium also re-mobilises over the following days, so a rising weight on day 1 usually warrants reducing maintenance rather than giving diuretics.

The choice of crystalloid is the choice of its strong ions, mainly chloride, and of its tonicity; the name on the bag matters less than the numbers.

• 0.9% saline contains 154 mmol/l chloride against plasma 98 to 106 mmol/l, and its strong ion difference is zero against a plasma strong ion difference of about 40 mEq/l, so large volumes cause a hyperchloraemic metabolic acidosis. ^[2]
• Excess chloride causes renal vasoconstriction and reduces renal cortical perfusion, and 0.9% saline expands the extracellular (interstitial) fluid more than an equivalent balanced solution, so it is more likely to cause fluid overload and interstitial oedema. ^[2]
• Ringer's lactate and Hartmann's solution are hypotonic, with in vivo osmolality around 254 mosmol/kg water, and perioperative administration is a significant free-water load that may not be excreted while antidiuretic hormone is high, producing weight gain and oedema; they are contraindicated in patients with or at risk of cerebral oedema. ^[2]
• Balanced solutions also differ from one another: Hartmann's solution contains 2 mmol/l calcium and is contraindicated with blood products and with ceftriaxone because of precipitation. ^[2]
• No fluid is physiologically perfect and none is "normal". ^[2]

The practical default, supported by NICE's restriction of resuscitation crystalloids to 130 to 154 mmol/l sodium and its requirement to monitor chloride daily when chloride-rich fluids are used, is a balanced or chloride-restricted crystalloid for maintenance and replacement, with 0.9% saline reserved for resuscitation in which hyperchloraemia is unlikely to persist, for chloride depletion or hypochloraemic states, and for conditions such as diabetic ketoacidosis where its composition is useful. ^[1][2] The randomised and observational evidence is consistent in showing that saline lowers pH and raises chloride, but has not shown consistent differences in short-term renal outcomes; the SPLIT trial in 2262 ICU patients found no difference in acute kidney injury or day-90 survival, and a surgical study of 1100 patients found only a transient postoperative hyperchloraemic metabolic acidosis. ^[2]

• Always seek and treat the cause: the same low sodium may be due to loss, dilution, redistribution or drugs, and replacement without a cause recurs.
• Replace electrolytes at a rate the body can accommodate, and recheck levels on a defined schedule.
• Correct magnesium and phosphate abnormalities alongside potassium, because potassium replacement is often ineffective until magnesium is replaced.
• Electrolyte deficits in renal or cardiac impairment accumulate and should be supervised.
• Express doses per kg where the guideline provides them, and round to available bags.

Serum potassium under 3.5 mmol/l is hypokalaemia: mild 3.0 to 3.4, moderate 2.5 to 2.9, severe under 2.5 mmol/l. ^[10] Biochemical severity does not always match clinical severity, which depends on symptoms and the ECG. ^[10]

Replace potassium rather than chasing a number, because most hypokalaemia reflects depleted total body stores. ^[7] Oral replacement is preferred when tolerated; RCHT suggests Sando-K two tablets three times daily (72 mmol/day) for mild disease. ^[7] Intravenous replacement is reserved for severe (under 2.5 mmol/l) or symptomatic hypokalaemia, or when the oral route is unavailable. ^[7] A 2025 trust guideline suggests 20 to 40 mmol potassium chloride in 1 litre of 0.9% saline over at least 8 hours when the level is 2.5 to 3.4 mmol/l, and 40 mmol over 6 hours when it is under 2.5 mmol/l or the patient is symptomatic, with the rate not exceeding 10 mmol/hour. ^[7] Glucose-containing solutions should not be used for initial potassium replacement, because glucose drives potassium into cells and may worsen the deficit. ^[7] Continuous ECG monitoring is advised when rates exceed 20 mmol/hour, with cardiac disease or with digoxin therapy. ^[7] Always correct magnesium and phosphate alongside potassium. ^{[7][8] [6]}

Hyperkalaemia is classified mild 5.5 to 5.9, moderate 6.0 to 6.4, severe 6.5 mmol/l or greater; treatment escalates with level and ECG changes. ^{[1] [6]} The UK Kidney Association 2026 hospital pathway uses a 5-step approach: protect the myocardium, shift potassium into cells, remove it from the body, monitor, and prevent recurrence. ^[6]

Step 1, membrane stabilisation: if ECG changes are present, give an equivalent dose of 6.8 mmol of IV calcium: 30 ml of 10% calcium gluconate over 10 minutes, or 10 ml of 10% calcium chloride over 5 minutes, with calcium chloride preferred in resuscitation or peri-arrest. ^[6]

Step 2, shift into cells: in severe hyperkalaemia (K+ 6.5 mmol/l or more) give insulin-glucose 10 units of soluble insulin in 25 g of glucose by intravenous infusion; for moderate disease (6.0 to 6.4 mmol/l) the same dose is used as a suggestion. Add nebulised salbutamol 10 to 20 mg as adjuvant; glucose infusion at 50 ml/hour of 10% for 5 hours should follow insulin-glucose if pre-treatment glucose is under 7.0 mmol/l. ^[6] Sodium bicarbonate is not used routinely. ^[6]

Step 3, remove potassium: sodium zirconium cyclosilicate in emergency severe hyperkalaemia, with patiromer as an option; calcium resonium is no longer routine. Dialysis is urgent for severe or refractory hyperkalaemia, especially in haemodialysis patients. ^[6]

Monitoring follows a fixed schedule: K+ at least 1, 2, 4, 6 and 24 hours, and glucose at 0, 30, 60, 90, 120, 180, 240, 300 and 360 minutes after insulin-glucose. ^[6] All patients with K+ 6.5 or higher need a 12-lead ECG and continuous 3-lead cardiac monitoring. ^[6]

A useful trap is that glucose infusions can be harmful in hyperkalaemia management if they create rebound hypoglycaemia; the UKKA pathway deliberately prescribes calcium, insulin-glucose and binders as distinct steps rather than a combined "hyperkalaemia bag". ^[6]

Hyponatraemia is usually a disorder of water handling, and the crucial first distinction is between acute and chronic onset and between symptomatic and asymptomatic patients. Severity categories from guidelines: mild 130 to 135 mmol/l, moderate 125 to 129 mmol/l, severe under 125 mmol/l. ^[5]

Correction rules that matter for safety (US expert panel and European guidelines): ^[5]

• Urgent correction in acute symptomatic hyponatraemia aims for a 4 to 6 mmol/l rise in the US and 5 mmol/l in European guidance, delivered in the first hour; moderate symptoms use continuous 3% saline at 0.5 to 2 ml/kg/h (US) or a single 150 ml bolus of 3% saline over 20 minutes (European). ^[5]
• For chronic symptomatic disease, hypertonic saline is given at about 4 to 8 mmol/l per day in the US if low risk of osmotic demyelination syndrome, and 4 to 6 mmol/l per day if high risk, with the first day's rise achievable within the first 6 hours in severe cases; European guidance sets a limit of no more than 10 mmol/l in the first 24 hours and no more than 8 mmol/l in every 24 hours thereafter. ^[5]
• In asymptomatic chronic hyponatraemia the limits are tighter: 10 to 12 mmol/l per day but no more than 18 mmol in 48 hours if low risk, and 8 mmol/l per day if high risk (US); no more than 10 mmol/l in the first 24 hours and 8 mmol/l thereafter (European). ^[5]

Overcorrection in chronic hyponatraemia carries a risk of osmotic demyelination syndrome; risk factors include malnutrition, hypokalaemia, alcohol misuse, liver disease and central nervous system disease. ^[5] Where overcorrection begins, stop or slow correction, use desmopressin and free water as directed by local protocol, and aim to avoid overshoot to hypernatraemia. ^[5]

Hypomagnesaemia is serum magnesium under 0.7 mmol/l; mild 0.5 to 0.7, severe under 0.5 mmol/l. ^[8] Untreated low magnesium can cause arrhythmia and tetany, and it frequently coexists with hypokalaemia and hypocalcaemia. ^[8]

• Oral: 10 to 24 mmol of magnesium per day in divided doses; for patients who cannot take oral replacement, give 1 to 5 g (4 to 20 mmol) intravenously depending on severity. ^[8]
• Severe or symptomatic: initial 5 g (20 mmol) IV magnesium; up to 40 g (160 mmol) over 5 days may be needed. ^[8]
• IV rate usually 1 to 2 g/hour (4 to 8 mmol/hour), not exceeding 9 g/hour (36 mmol/hour); concentrations must not exceed 20% through a central line or 5 to 10% peripherally. ^[8]
• Continue for 1 to 2 days after levels normalise, reduce the dose by 25 to 50% in mild to moderate renal impairment, and seek specialist advice in severe renal impairment. ^[8]
• Oral magnesium is poorly absorbed and causes diarrhoea in large doses; take it with meals and in divided doses. ^[8]

Hypocalcaemia is common in critical illness and usually presents with neuromuscular irritability and QT prolongation; acute symptomatic hypocalcaemia is treated with intravenous calcium under close monitoring and with correction of magnesium and potassium. ^[9] Asymptomatic chronic deficiency or mild depletion is replaced orally with calcium and vitamin D as appropriate. ^[9]

Severe hypercalcaemia requires urgent treatment before the cause is fully established: correct dehydration first with 0.9% saline, stop thiazides and vitamin D compounds, restrict dietary calcium, and use bisphosphonates, calcitonin or corticosteroids as the clinical picture requires; bisphosphonates such as pamidronate are the most effective, while calcitonin (salmon) is used in malignancy-associated disease. ^[9] Intravenous calcium salts must be given slowly because rapid administration can cause arrhythmia. ^[9]

Phosphate is usually corrected alongside potassium and magnesium; most replacement is intravenous and requires senior guidance because rates, formulations and availability vary, and it is given with concurrent magnesium and potassium correction and with renal function in mind. ^[7]

• Pregnancy and the postpartum period: increases in plasma volume and glomerular filtration alter sodium and water handling; resuscitation and electrolyte correction follow the same physiological rules, but imaging and access decisions need obstetric, anaesthetic and medical review.
• Older adults: lower total body water, impaired thirst, reduced renal concentrating ability and diuretic use make them prone to both dehydration and hyponatraemia; default to the 20 to 25 ml/kg/day maintenance range and reassess drug causes before adding salt. ^[1]
• Chronic kidney disease: potassium, magnesium and phosphate handling are impaired, so replacement is cautious and supervised; hyperkalaemia pathways are essential, and fluid overload is a constant risk.
• Malnutrition and refeeding: introduce energy and electrolytes deliberately, not through a full maintenance bag; deficits and shifts need a plan.
• Adrenal disease, SIADH, diabetes insipidus: sodium disorders are driven by the underlying condition; fluid choice follows the diagnosis, and free water or salt replacement must be directed at the cause rather than the trend.
• Heart failure and cirrhosis: treat the mechanism, and use lower starting volumes.

• The cheapest monitoring tools are a daily weight, a reviewed fluid balance chart, and an examination each shift. ^[1]
• In settings without balanced crystalloids, 0.9% saline can be used, but the volume should be limited, chloride monitored, and hyponatraemia and oedema watched for; 0.9% saline plus glucose mixtures can still be appropriate when chloride repletion is needed.
• Enteral rehydration and feeding are available almost everywhere, including through nasogastric tubes, and should replace IV routes as soon as possible.
• Sepsis resuscitation with 30 ml/kg of crystalloid may not be safe without monitoring; guidelines from high-resource settings may need adapting to staff, beds and oxygen availability, and a raised jugular venous pressure, respiratory distress or oxygen desaturation should stop further loading. ^[3]
• Neonates and children need different, weight-based rules and should not be treated by this adult framework.

Aftercare is daily reassessment rather than a single decision. Review clinical status, daily (at first) urea, creatinine and electrolytes, the fluid balance chart, and weight at least twice weekly; replacement and redistribution need more frequent review. ^[1]

Complications worth anticipating:

• Fluid overload and oedema: interstitial oedema, pulmonary oedema, delayed wound healing and prolonged ileus, particularly with saline excess. ^[2]
• Hyponatraemia and water intoxication from excess hypotonic fluid; higher total daily volumes and postoperative vasopressin both raise the risk. ^[1][2]
• Hyperchloraemic metabolic acidosis from large volumes of 0.9% saline. ^[2]
• Electrolyte excess: hyperkalaemia from unmonitored potassium, calcium accumulation, phosphate overload in renal impairment.
• Cardiac, respiratory and neurological sequelae of both overload and of rapid correction, including osmotic demyelination after hyponatraemia correction. ^[5]
• Infection and thrombophlebitis from prolonged cannulae and repeated access.
• Refeeding and iatrogenic under-nutrition when patients stay on maintenance fluid for days.

Safety habits that prevent these: one visible 24-hour plan, daily weight, daily biochemistry initially, no potassium added to bags on the ward, no patient on more than 2.5 litres a day without a documented Replacement or Redistribution reason, and reporting of fluid incidents. ^[1]

• Fluid therapy should always be given for a named purpose: Resuscitation, Routine maintenance, Replacement, Redistribution, with daily Reassessment.
• Resuscitation uses 500 ml boluses of crystalloid (sodium 130 to 154 mmol/l) over less than 15 minutes, reassessed; sepsis resuscitation starts at least 30 ml/kg over 3 hours. ^[1][3]
• Routine maintenance is water 25 to 30 ml/kg/day, about 1 mmol/kg/day each of Na/K/Cl, 50 to 100 g/day glucose; 20 to 25 ml/kg/day in older, frail or malnourished patients. ^[1]
• Balanced crystalloids are the default; 0.9% saline is reserved for specific needs, and chloride is monitored daily when chloride-rich fluids are used. ^[1][2]
• Serum chloride 154 mmol/l in 0.9% saline versus 98 to 106 mmol/l in plasma is the key mechanistic difference. ^[2]
• Ringer's lactate and Hartmann's solution are hypotonic and contraindicated in patients with or at risk of cerebral oedema. ^[2]
• Volume status is clinical: pulse, blood pressure, capillary refill, JVP, oedema, posture, weight, output and trends in urea, creatinine and electrolytes. ^[1]
• Static pressures are poor at predicting responsiveness; dynamic tests (passive leg raise, pulse pressure variation, echocardiography) do better when conditions allow. ^[3][4]
• Roughly half of fluid challenges do not increase stroke volume. ^[4]
• Hyperkalaemia is treated as protect-shift-remove with 6.8 mmol calcium for ECG changes, insulin-glucose 10 units in 25 g, and monitoring to a defined schedule. ^[6]
• Hyponatraemia correction has strict limits to prevent osmotic demyelination: under (or no more than) 10 mmol/l in the first 24 hours. ^[5]
• Hypomagnesaemia is replaced orally at 10 to 24 mmol/day, or IV as 5 g (20 mmol) initially, at 4 to 8 mmol/h. ^[8]
• Potassium must never be added to bags on the ward, and rates in deficiency are usually capped at 10 mmol/h. ^[1][7]
• Report fluid mismanagement as a critical incident and get senior help for redistribution. ^[1]

Acid-base disorders (physiology/acid-base-disorders); dehydration and paediatric fluids (paediatrics/dehydration-and-paediatric-fluids); hyperkalaemia and hypokalaemia (renal/potassium-disorders); hyponatraemia and hypernatraemia (renal/sodium-disorders); acute kidney injury (renal/acute-kidney-injury); heart failure (cardiology/heart-failure); sepsis management (critical-care/sepsis); perioperative fluids (surgery/surgical-fluids-and-nutrition); nutrition support (surgery/nutrition-support).