Maintenance Fluids and Fluid Creep: The Prescription We Write Without Thinking
Dr Neeraj Manikath DNB
Abstract
Intravenous fluid is the most commonly prescribed “drug” in hospital medicine, and probably the least scrutinised. Maintenance fluids are written by reflex, often by the most junior member of the team, and are continued by inertia. Fluid creep is the hidden volume and sodium load that arrives through drug diluents, line flushes, “keep vein open” infusions and nutrition. It never appears on the fluid prescription. This review covers the physiology that matters at the bedside, the trials that have changed practice (PIMS, SMART, BaSICS, CLASSIC, CLOVERS, RELIEF), the diagnostic habits that separate careful prescribers from careless ones, and a practical framework (CREEP) for prescribing, monitoring and stopping fluids.
1. Introduction: Two Patients, One Prescription
Case 1. A 32-year-old woman is admitted for an elective laparoscopic cholecystectomy. The procedure is uneventful. On the ward, the night resident prescribes “maintenance”: 5% dextrose in 0.45% saline at 125 mL/hour, because that is what the order set suggests. She has pain and nausea, so she receives morphine and ondansetron. By 6 a.m. she has a headache and has vomited twice. By 10 a.m. she is drowsy. Serum sodium, which was 139 mmol/L pre-operatively, is now 121 mmol/L. A CT shows diffuse cerebral oedema.
Case 2. A 68-year-old man with septic shock from pneumonia is on day 5 in the ICU. His resuscitation was textbook. Nobody has “given fluids” for two days. Yet he is 9 kg above his admission weight, his albumin is 19 g/L, his abdomen is tense, and he is struggling to wean from the ventilator. The fluid chart shows no boluses. When you add up the antibiotic diluents, the vasopressor carrier, flushes, an arterial line pressure bag, and the “KVO” running at 30 mL/hour, he has received more than 3 litres of fluid and more than 300 mmol of sodium each day in the absence of any prescription labelled “fluids”.
These are the two faces of a single failure. In Case 1 a fluid that is hypotonic relative to the patient’s physiological state causes catastrophic harm within hours. In Case 2 a fluid burden that was never prescribed at all causes slow, cumulative harm over days.
The history explains how we got here. In 1957, Holliday and Segar estimated the water and electrolyte needs of healthy children from the calorie expenditure of a healthy child and the electrolyte content of human milk. Their paper produced the famous 100–50–20 mL/kg/day rule and, almost accidentally, a generation of hypotonic maintenance solutions [1]. Those fluids were designed for healthy, hungry children with no stimulus for antidiuretic hormone (ADH). Sick patients are the opposite: ADH-driven, stressed, and often hypovolaemic or oedematous. By the early 1990s, case series of healthy children and menstruating women dying or suffering permanent brain injury after hypotonic fluids made the point in the most brutal way possible [2].
🎯 Teaching point for the first five minutes: Maintenance fluid is a drug with an indication, a dose, a tonicity, a duration, and adverse effects. If you would not prescribe digoxin without any of these, do not prescribe dextrose-saline without them.
2. Pathophysiology: Only What Changes What You Do
2.1 Why “maintenance” is an unhelpful word
“Maintenance” implies a stable patient with fixed needs. In practice, hospital patients have variable, disease-driven losses and variable, drug-driven water handling. A more honest definition is: the fluid required to replace obligatory daily losses in a patient who cannot meet them orally or enterally.
For an average adult, obligatory needs are approximately:
| Component | Approximate daily requirement |
|---|---|
| Water | 25–30 mL/kg/day |
| Sodium | ~1 mmol/kg/day |
| Potassium | ~1 mmol/kg/day |
| Chloride | ~1 mmol/kg/day |
| Glucose | 50–100 g/day (to limit starvation ketosis) |
These figures are consistent with UK NICE guidance for adults and children in hospital. A 70 kg adult therefore needs roughly 2 litres of water, 70 mmol of sodium, and 70 mmol of potassium per day, which equals about four grams of salt, not eighteen [3].
2.2 The sodium arithmetic nobody does
One litre of 0.9% saline contains 154 mmol of sodium, which is 9 g of sodium chloride. Two litres therefore supply 308 mmol of sodium, over four times the daily need, and 308 mmol of chloride, nearly three times the chloride in the same volume of plasma-matched fluid. Healthy kidneys can excrete this. Sick kidneys, a failing heart, or a cirrhotic liver cannot.
🪙 Clinical Pearl: Speak in millimoles, not litres.
When someone says “she’s only had two litres,” ask, “How many millimoles of sodium was that?” Patients become oedematous because of the sodium they cannot excrete. The water is carried along behind the sodium.
2.3 Tonicity, ADH, and the Edelman equation
Plasma sodium is determined not by sodium alone but by the ratio of exchangeable sodium plus exchangeable potassium to total body water (the Edelman relationship). A practical consequence: to predict what an infusion will do to the serum sodium, compare the infusion’s (Na⁺ + K⁺) with the patient’s serum sodium. If the infusate’s (Na⁺ + K⁺) is lower than the serum Na⁺, the infusion will tend to lower the serum sodium, as long as the patient is retaining water.
Many hospitalised patients retain water because non-osmotic ADH release is extremely common. Triggers include:
- Pain, nausea, and vomiting
- Opioids, and many other drugs (SSRIs, carbamazepine, cyclophosphamide, vincristine, many others)
- Post-operative state and surgical stress
- Pulmonary disease (pneumonia, asthma exacerbation) and CNS disease (meningitis, SAH, head injury)
- Hypovolaemia and effective arterial volume depletion
- Positive-pressure ventilation
In a patient with raised ADH, a litre of 5% dextrose in 0.45% saline behaves, after the dextrose is metabolised, like half a litre of free water plus half a litre of isotonic saline. The free water is retained. The brain, which has only a few hours to adapt, swells [4].
2.4 Who gets into trouble?
Hospital-acquired hyponatraemia is the commonest electrolyte disorder in inpatients, and the risk of symptomatic cerebral oedema is not uniform. Risk is highest in:
- Children (greater brain-to-skull ratio)
- Pre-menopausal women in the peri-operative period
- Patients with CNS pathology, hypoxia, or raised intracranial pressure
- Patients receiving thiazides, SSRIs, or other ADH-augmenting drugs
2.5 The chloride problem
Large volumes of 0.9% saline carry 154 mmol/L of chloride against plasma’s ~100. Consequences include a hyperchloraemic non-anion-gap metabolic acidosis and, in experimental and some clinical data, renal afferent vasoconstriction, which is the proposed mechanism behind the kidney signal seen in the balanced-crystalloid trials [5].
2.6 What is “fluid creep”?
The phrase first appeared in burn resuscitation to describe over-resuscitation. In general hospital and ICU practice it has a broader meaning, defined by Van Regenmortel and colleagues: all the fluid administered for purposes other than resuscitation or maintenance, i.e., drug diluents, carriers, flushes, and nutritional fluids. In their ICU cohort, maintenance fluid and fluid creep together delivered more sodium, chloride and water than the resuscitation fluids that everyone watches [6].
Sources of creep:
| Source | Typical hidden volume |
|---|---|
| Intermittent IV antibiotics (e.g., piperacillin–tazobactam 4 times daily in 100 mL) | 400+ mL/day |
| Vasopressor, sedative, and insulin carrier infusions | 100–600 mL/day |
| Arterial and central line pressure-bag flushes | ~70–100 mL/day |
| “KVO” infusions at 20–30 mL/hour | 480–720 mL/day |
| Electrolyte replacement (KCl, Mg, phosphate) in 100 mL diluents | variable |
| Parenteral and enteral nutrition, free-water flushes | 500–1500+ mL/day |
| Blood products | variable |
📌 Remember: Fluid creep is a design problem and a prescribing problem. Nobody writes “fluid creep” on a chart; it accumulates one small, individually “harmless” order at a time.
3. Clinical Pearls 🪙
🪙 Pearl 1: The fluid that makes a patient hyponatraemic is the one that looks “safe”.
Hypotonic dextrose–saline looks gentle and physiological. In a post-operative, nauseated, opioid-treated patient it is a hazard. Hyponatraemic encephalopathy occurs from free water retained, not from “too much saline”.
🪙 Pearl 2: A normal sodium at 6 p.m. does not guarantee a normal sodium at 6 a.m.
Acute hospital-acquired hyponatraemia can develop within hours. If you are running hypotonic fluid in a high-ADH patient, check the sodium at 4–6 hours, not at the next morning round.
🪙 Pearl 3: Positive fluid balance is a vital sign.
Cumulative balance and daily weights deserve the same attention as heart rate. Observational data link a positive balance and fluid overload to worse outcomes in critically ill adults, though association is not causation [7].
🪙 Pearl 4: A falling albumin and haemoglobin in a patient whose creatinine is stable is often dilution, not disease.
Before you chase an occult bleed or a protein-losing state, check the cumulative balance.
🪙 Pearl 5: Stopping fluids is a prescription too.
The most useful sentence in many drug charts is not “start” but “review/stop at 24 hours or when eating and drinking”.
🪙 Pearl 6: The same fluid is a drug and a diluent.
If vancomycin is going in a 250 mL bag of 5% dextrose, you have just given the patient 250 mL of free water and 12.5 g of dextrose. Over several drugs per day, this adds up.
4. Oysters 🦪
🦪 Oyster 1: The “maintenance” order set usually over-delivers even when it is the right fluid.
The default of 125 mL/h (3 L/day) exceeds the 25–30 mL/kg/day target for most adults, particularly smaller or older patients. Starting at 1 mL/kg/h is closer to physiology.
🦪 Oyster 2: Sodium load, not water load, is the main driver of tissue oedema in the “creep” patient.
Many creep fluids are saline-based. Reduce the sodium load by switching diluents to 5% dextrose where compatible (and monitoring sodium), concentrating infusions, and converting IV drugs to oral or enteral when the gut works.
🦪 Oyster 3: “Free water” in tube feeds and flushes is also fluid.
A patient on high-volume enteral nutrition with 200 mL water flushes every 4 hours can quietly accumulate 1.2 L/day of free water on top of IV fluids.
🦪 Oyster 4: Hospital-acquired hypernatraemia has the same root, in the opposite direction.
Febrile, ventilated, or diabetes insipidus patients with high insensible or urinary water loss and inadequate free water replacement become hypernatraemic. Maintenance fluid should be thought of as two questions: how much water, and how much sodium?
🦪 Oyster 5: Oliguric AKI patients do not need “maintenance fluid to make urine”.
In established oliguric AKI, the right “maintenance” is insensible losses (~500 mL/day) plus measured output, not a reflexive litre every eight hours.
🦪 Oyster 6: A patient may be hypovolaemic and fluid-overloaded at the same time.
In sepsis and cirrhosis, intravascular volume can be low (low effective arterial volume) while total body water is high (oedema, ascites). Weight and albumin cannot tell you the intravascular state. That needs the bedside assessment in Section 7.
5. Clinical Hacks & Tips ⚡
⚡ Hack 1: The “Na + K” rule.
Compare the infusate’s (Na⁺ + K⁺) to the serum Na⁺. If infusate (Na⁺ + K⁺) < serum Na⁺ and the patient has ADH drive, you are building a hyponatraemia. Adding 20 mmol/L of potassium to a bag makes it more tonic physiologically (K is effectively osmotically active in the Edelman sense), so check before assuming a “weak” bag is safe.
⚡ Hack 2: The weight check.
1 kg of weight gain ≈ 1 L of retained fluid. A 3 kg gain over three days with a stable diet is not “nutrition”. Weigh daily, on the same scale, at the same time.
⚡ Hack 3: The 60-second creep audit.
At every ward round or ICU round, ask the nurse or pharmacist to read out: (a) all infusions and their carrier volumes, (b) all flushes, (c) any KVO, (d) nutrition and free water. Add them. Compare with the prescribed “maintenance”.
⚡ Hack 4: Concentrate, don’t dilute.
Many vasoactive and sedative infusions can be run at higher concentrations through a central line. Ask pharmacy. A 50% reduction in carrier volume is common.
⚡ Hack 5: Convert early.
Ask every day, “Can this IV drug be oral or enteral?” This one question removes both a diluent and a line.
⚡ Hack 6: Name the bag.
Write “Isotonic maintenance, Na 0.9% / KCl 20 mmol/L / dextrose 5%” and a stop date on the chart. Vague orders (“IV fluids, 125/h”) are how prescriptions drift.
⚡ Hack 7: Use your spot urine.
In a hyponatraemic patient on fluids, a urine osmolality > 100 mOsm/kg means ADH is active and free water cannot be excreted. In that case, stop the hypotonic fluid immediately. A urine Na and osmolality take five minutes to send and can change management.
⚡ Hack 8: Teach the nurses.
Nurses will spot the first drowsiness or headache. Empower them to ask, “Did anyone check the sodium?” The best hyponatraemia detection tool in the hospital is a nurse who knows what the bag contains.
6. State-of-the-Art Updates
6.1 Isotonic maintenance fluids in children: the paediatric revolution
Longstanding debate between hypotonic and isotonic maintenance fluids in children was addressed by the PIMS trial (n = 690), in which children randomised to isotonic saline had a markedly lower incidence of hyponatraemia at 24 hours than those receiving hypotonic saline (roughly 5% vs 20%), without more hypernatraemia or other adverse effects of note [4]. The 2018 American Academy of Pediatrics guideline now recommends isotonic solutions with appropriate potassium and dextrose as maintenance fluid for most hospitalised children from 28 days to 18 years of age [5a]. Adult practice has lagged behind, but the physiology is the same.
6.2 Adults: isotonic or balanced solutions
For adults, major guidance (NICE and many national bodies) now supports isotonic maintenance fluids, with sodium 1 mmol/kg/day, potassium 1 mmol/kg/day, and glucose 50–100 g/day to avoid ketosis [3]. A review of maintenance fluids in acutely ill patients argued the same: hypotonic maintenance fluid is not justified in acutely unwell adults [8].
6.3 Balanced crystalloid vs. saline
- SMART (n ≈ 15,800 ICU patients, a pragmatic cluster-randomised crossover trial) found a lower rate of major adverse kidney events within 30 days with balanced crystalloids compared with saline (14.3% vs 15.4%) [9].
- BaSICS (n ≈ 11,000) found no difference in 90-day mortality between a balanced solution and 0.9% saline in ICU patients, although the trial’s results must be interpreted along with its design and population [10].
Take-home: Balanced crystalloids are reasonable first choice, especially in patients needing large volumes or with hyperchloraemia or acidosis. Saline is not “wrong” (it remains appropriate in hypochloraemia, hyponatraemia with vomiting, or traumatic brain injury), but the evidence no longer supports defaulting to it for large-volume resuscitation. The Surviving Sepsis Campaign 2021 guideline suggests balanced crystalloids over saline [11].
6.4 Restrictive vs. liberal strategies
| Trial | Setting | Key finding |
|---|---|---|
| RELIEF (n ≈ 3,000) [12] | Major abdominal surgery | Restrictive regimen did not improve disability-free survival (≈ 82% in both arms) and was associated with more AKI (8.6% vs 5.0%) |
| CLASSIC (n ≈ 1,550) [13] | Septic shock in ICU | Restricting IV fluid after initial resuscitation did not change 90-day mortality (≈ 42% in both arms) |
| CLOVERS (n ≈ 1,560) [14] | Early sepsis-induced hypotension | Restrictive (early vasopressor) vs liberal (fluid-first) strategies: no difference in 90-day mortality (≈ 14–15%) |
How to read these trials: None showed that restricting fluid is clearly better, and RELIEF suggested that overly aggressive restriction may cause harm. The message is “neither flood nor drought.” The goal is individualised, goal-directed fluid use with deliberate attention to when to stop.
6.5 The four phases and four D’s of fluid therapy
Malbrain and colleagues have proposed the ROSE model for the phases of fluid therapy: Resuscitation, Optimisation, Stabilisation, Evacuation. They pair it with the “four D’s” of fluid prescribing: Drug, Dose, Duration, De-escalation [15]. This reframes fluids as drugs with a life cycle.
6.6 Sodium correction: a safer approach
When hyponatraemia does occur, hypertonic saline correction rates matter. The SALSA trial compared rapid intermittent bolus with slow continuous infusion of 3% saline for symptomatic hyponatraemia and found that the intermittent bolus approach reduced the risk of overcorrection [16]. Current guidance (US and European) supports limiting correction to approximately 8–10 mmol/L in the first 24 hours, with a lower limit (about 8 mmol/L) in patients at high risk of osmotic demyelination (alcoholism, malnutrition, hypokalaemia, advanced liver disease, Na < 105 mmol/L) [17].
7. Diagnostic Nuances: Separating Good from Great
7.1 History
- Ask what the patient has been drinking, not just what they have been given. Habitual large oral water intake is a classic precipitant of hyponatraemia on top of IV fluids.
- List every drug that causes ADH release or potentiation (SSRIs, carbamazepine, opioids, cyclophosphamide, vincristine, thiazides, proton pump inhibitors rarely).
- Document the diet. Low-solute diets (“tea and toast”) and beer potomania reduce free-water excretory capacity.
- Pre-operative sodium and renal function are the baseline you need.
7.2 Examination
Volume status is one of the hardest bedside assessments, and no single sign is reliable. Combine:
- Weight trend (best single tool)
- JVP and its response to abdominojugular pressure
- Peripheral and sacral oedema (sacral in bed-bound patients)
- Lung examination for crackles, orthostatic BP and heart rate response
- Capillary refill, skin turgor (poor in elderly), mucous membranes
- Point-of-care ultrasound (B-lines in lung for pulmonary congestion; IVC collapsibility; consider VExUS in advanced assessment)
🪙 Pearl: No single sign is sufficient. Use the pattern. A patient with orthostatic hypotension, flat neck veins and low urine sodium is volume-depleted. A patient with raised JVP, B-lines, positive balance and peripheral oedema is overloaded, regardless of what the blood pressure says.
7.3 Investigations
| Investigation | What it adds |
|---|---|
| Serum Na⁺, K⁺, Cl⁻, HCO₃⁻, urea, creatinine | Baseline and trend; chloride load; AKI |
| Serum and urine osmolality, urine Na⁺ | Is ADH active? Is the kidney avid for sodium (low urine Na suggests hypovolaemia; high suggests SIADH, diuretics, salt wasting)? |
| Glucose | Hyperglycaemia causes translocational hyponatraemia (adjust for ~2 mmol/L fall in Na per 5.5 mmol/L of glucose rise, with some variation) |
| Albumin, Hb trend | Dilution (see Pearl 4) |
| Lactate, blood gas | Perfusion; hyperchloraemic acidosis |
| Daily weights and cumulative balance chart | The non-negotiables |
| Intra-abdominal pressure (if abdomen is tense) | Over-resuscitation is a cause of intra-abdominal hypertension |
⚠️ Caution: Fluid balance charts under-record both input and output. Treat them as an estimate; weights are the check.
8. Management Intricacies
8.1 Do you need maintenance fluid at all?
Question 1: Can the patient safely use the gut? If yes, use it: oral, or enteral by tube. IV maintenance is only for patients who cannot meet needs enterally. This is the most effective way to eliminate both maintenance and creep.
8.2 Prescribing maintenance fluid in an adult who truly needs it
A sensible starting prescription (adapt to weight, comorbidity, and local protocol):
- Volume: 25–30 mL/kg/day (≈ 1 mL/kg/h)
- Sodium, potassium, chloride: ~1 mmol/kg/day each
- Glucose: 50–100 g/day
- Tonicity: isotonic base (e.g., 0.9% saline or a balanced solution with 5% dextrose and potassium as indicated), rather than a hypotonic base [3, 8]
- Stop/review time: 24 hours or sooner
Lower the volume (and watch closely) in: elderly or frail patients, heart failure, cirrhosis with ascites, advanced CKD, malnutrition and refeeding risk, and those at risk of overload. NICE suggests starting at around 20–25 mL/kg/day in such patients [3].
Add potassium (usually 20–40 mmol per litre) only once there is urine output and potassium is not high. Pre-mixed bags reduce dangerous mixing errors.
8.3 Which fluid base?
| Fluid | Na (mmol/L) | Cl (mmol/L) | Notes |
|---|---|---|---|
| 0.9% saline | 154 | 154 | Hyperchloraemia with large volumes; useful in hypochloraemic alkalosis, TBI |
| Ringer’s lactate / Hartmann’s | ~130 | ~109 | Contains K and Ca; slightly hypotonic relative to plasma; avoid in TBI with raised ICP |
| Plasma-Lyte 148 | 140 | 98 | Balanced; contains Mg, acetate, gluconate |
| 5% dextrose | 0 | 0 | Free water. Not a volume expander. Use only to treat hypernatraemia/free-water deficit or as a diluent |
| 0.45% saline | 77 | 77 | Rarely justified in acutely ill patients |
8.4 Special situations
- Heart failure/cirrhosis: Minimise sodium load. Count creep carefully; use 5% dextrose diluents where drugs are compatible, and monitor Na.
- Neurosurgical/TBI patients: Avoid hypotonic fluids. Aim for isonatraemia or a slightly higher sodium, as per neurocritical care guidance.
- Diabetic ketoacidosis and HHS: Fluid replacement here is treatment, not maintenance. Follow local DKA protocol and then switch to maintenance once resolved.
- Post-operative patients: Reintroduce oral intake early. Avoid routine “maintenance” after minor surgery. Individualise and use goal-directed fluid therapy in major surgery.
- Sepsis: Resuscitate initially (the Surviving Sepsis Campaign suggests at least 30 mL/kg of crystalloid within 3 hours for hypoperfusion, though this is a weak recommendation based on low-quality evidence [11]), then apply the ROSE framework and move early to optimisation and de-escalation.
8.5 Treating fluid-induced hyponatraemia
🚨 Emergency: Symptomatic hyponatraemia (seizure, coma, vomiting, severe headache, respiratory distress)
- Stop the offending hypotonic fluid.
- Give 3% hypertonic saline: typically a 100–150 mL bolus over 10–20 minutes, repeatable up to two or three times, aiming for an initial rise of 4–6 mmol/L (enough to reverse the cerebral oedema).
- Check sodium frequently (every 1–2 hours initially).
- Do not exceed ~8–10 mmol/L in 24 hours (and ~8 mmol/L if high-risk for ODS).
- If the patient is overcorrecting (e.g., brisk water diuresis once ADH drive switches off), re-lower the sodium with DDAVP and/or 5% dextrose per local protocol and expert advice [17].
A rough working rule: 1 mL/kg of 3% saline raises serum sodium by about 1 mmol/L. Use it only as a guide and always re-measure.
8.6 De-resuscitation: removing fluid is also management
Once the patient is stable and overloaded (the “E” of ROSE):
- Stop all non-essential fluids (the creep audit).
- Diuretics (loop diuretics ± thiazide-like) in patients with adequate renal function and clear overload.
- Renal replacement with net ultrafiltration in refractory cases.
- Reassess daily with weights and ultrasound [15].
8.7 Common pitfalls
- Continuing maintenance fluids “until further notice” while the patient is eating.
- Using the same bag for “maintenance” and then adding drug diluents without recounting.
- Adding potassium to anuric patients.
- Over-reliance on charts.
- Mixing up “resuscitation” and “maintenance”. A hypotensive patient needs a resuscitation assessment, not a faster maintenance rate.
9. When to Escalate, When to Watch
| Situation | Action | Reasoning |
|---|---|---|
| Na < 135 and falling on hypotonic fluids, no symptoms | Stop hypotonic fluid; switch to isotonic; review in 4–6 h | The ADH-driven trajectory will continue unless the cause is removed |
| Na < 125 or any neurological symptoms (headache, nausea/vomiting, confusion, seizures) | Escalate urgently (senior/ICU/nephrology); consider hypertonic saline | Symptoms suggest cerebral oedema; time matters |
| Na rising > 8–10 mmol/L in 24 h during hyponatraemia correction | Stop active therapy; consider re-lowering | ODS risk |
| Cumulative balance > +5 L (or > ~5–10% body weight) with organ dysfunction | Stop non-essential fluids; consider de-resuscitation | Overload is associated with worse outcomes [7] |
| Tense abdomen, rising airway pressures, falling urine output | Measure intra-abdominal pressure; escalate | Abdominal compartment syndrome is a recognised consequence of over-resuscitation |
| Persistent hypotension despite fluids | Don’t just give more. Reassess, consider vasopressors, look for the cause | CLOVERS supports early vasopressors as an acceptable strategy [14] |
| Stable, eating, drinking, no losses | Stop IV maintenance | The best fluid is no fluid |
👀 When it is safe to watch: a well, normonatraemic patient on a short, isotonic, appropriately dosed maintenance prescription with a stop time, daily weights, and no creep. Check electrolytes at least daily, and sooner if clinical status changes.
10. Memorable Summary: The CREEP Framework
C — Count every millilitre
Include diluents, flushes, KVO, feeds, free water. Check daily weight and cumulative balance.
R — Reassess daily
Indication, volume, sodium, weight, and whether the patient still needs it.
E — Enteral first
If the gut works, use it. Convert IV drugs to oral wherever possible.
E — Eutonic (isotonic) fluid, electrolytes tailored
Ensure infusate (Na⁺ + K⁺) is not far below serum Na⁺ in high-ADH patients. Consider balanced solutions.
P — Prescribe like a drug
Name the fluid, the dose, the rate, the potassium, and the stop date.
Quick reference table
| Question | Answer |
|---|---|
| Daily adult maintenance (typical) | 25–30 mL/kg water; ~1 mmol/kg each of Na, K, Cl; 50–100 g glucose |
| Safest default tonicity in acutely ill patients | Isotonic |
| Biggest hidden source of fluid | KVO, drug diluents, flushes, nutrition |
| 1 L of 0.9% saline contains | 154 mmol Na⁺ (≈ 9 g NaCl) |
| Hyponatraemia correction limit | ~8–10 mmol/L per 24 h (8 in high-risk) |
| Best single bedside tool for fluid status | Daily weight (plus the pattern of signs) |
| Best fluid stewardship habit | Stop it when you can |
11. Conclusion
Maintenance fluids and fluid creep illustrate a recurring theme in internal medicine: common interventions cause large harm when they are prescribed without thought. The central insight is simple but demanding. Intravenous fluid is a drug whose dose, tonicity and duration must be chosen, whose adverse effects (hyponatraemia, hyperchloraemia, oedema, organ dysfunction) must be anticipated, and whose hidden sources must be counted. The trials of the last decade (SMART, BaSICS, RELIEF, CLASSIC, CLOVERS) tell us that extremes in either direction are unhelpful and that the quality of fluid decisions matters more than the volume dogma. Prescribe deliberately, count honestly, reassess daily, and stop early.
💎 Final master-clinician tip: Before you sign any fluid chart, ask three questions: “Why does this patient need this? What is in it, in millimoles? When will I stop it?” If you cannot answer all three, you are not yet ready to prescribe.
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