Why you cannot be oedematous and hypovolaemic at steady state 👇

1/
“Puffy but intravascularly dry?”
A common phrase on the wards – and one of the most persistent myths in IV fluid therapy.

Oedema and hypovolaemia come from opposite pressure states. They cannot coexist once the circulation reaches steady state. 2/
Capillaries filter fluid continuously.
Lymphatics return that filtrate continuously.

Under normal physiology:
• Filtration = several litres/day
• Lymph return = several litres/day
• Net plasma loss ≈ zero

→ No oedema
→ No intravascular depletion

1️⃣
We talk a lot about “capillary leak.”
But the term is often misunderstood.
Fluid doesn’t simply pour out of “leaky” vessels – it follows the same physics every time.
Getting this right changes how we think about fluids 👇 2️⃣ How it really works
In most tissues, fluid always filters out of capillaries at a slow, steady rate.
That filtered fluid is collected by the lymphatics and returned to the bloodstream.
At steady state, capillary filtration and lymph flow are equal – so tissue volume stays constant.

🧵 Why it’s so hard for the body to get rid of IV fluid

1️⃣ Hook:
We talk endlessly about “fluid resuscitation” – but far less about how the body gets rid of excess fluid once we’ve given too much.
Here’s the physiological problem 👇
#MedX #Physiology #Fluids 2️⃣ The sensors aren’t built for it.
Our homeostatic systems evolved for defending volume against loss, not for fine-tuning excess.
Volume sensors in the atria, great veins, and kidneys are coarse – they barely respond until intravascular volume changes by ~10–15%.

1/
“Fluid Accumulation Syndrome (FAS)” is a term used to describe the harms of fluid overload in critical care. It’s a useful shorthand — but the term carries risks. Let’s discuss why language here matters. 🧵
#MedX #FOAMed 2/
Why FAS is attractive:
– Frames a syndrome-like cluster: pulmonary oedema, gut dysfunction, tissue swelling, poor healing, higher mortality
– Makes disparate harms visible under one label
– Draws attention to the seriousness of fluid overload

1/
Why do we keep reaching for IV fluids, even when we have evidence they can cause harm?
It's not based on physiology — it’s cognitive bias.
🧵 2/
For decades, “being unwell” was equated with “needs fluids.”
Shock, low urine output, AKI, high lactate, acidosis — all framed as fluid deficits.
That shortcut skipped diagnostic reasoning and codified bias into medical culture.

1/
💡 IV fluid is the most over-prescribed drug in hospitals.
Why? Because when faced with certain problems, our reflex is always “give fluids”.
Let’s unpack the cognitive biases behind this — and why they harm patients. 2/
⬇️ The reflex problems:
Low BP → fluids
AKI → fluids
Low urine output → fluids
High lactate → fluids
Sepsis → fluids
Pancreatitis → fluids
Different problems, same solution. But mostly the wrong solution.

1/ 💉 Resuscitation fluids – life-saving in true hypovolaemia.

Give them for the wrong reason and you harm patients.

We’ve covered maintenance & replacement fluids — now the trilogy ends with resuscitation. Here’s how to get it right. #MedX 2/ In our hypovolaemia thread we saw:
History of recent fluid loss 🕵️‍♂️ = most reliable clue
Hypotension, tachycardia & poor perfusion = late & non-specific
Non-hypovolaemic shock won’t improve with fluids

https://x.com/Turningthe_Tide/status/1936438468852191425

1/
IV fluids have two main purposes:
💧 To maintain daily needs
🔄 To replace losses

(We’ll come back to whether we should even use the term 'resuscitation' fluid in a future thread).

Let’s talk about maintenance fluids – when they’re needed, and when they’re not.

🧵 #MedX #FluidTherapy 2/
The daily maintenance requirements are easy to remember:
💧 Water: 1 ml/kg/hr (≈ 25 ml/kg/day)
🧂 Sodium: 1 mmol/kg/day
🧂 Chloride: 1 mmol/kg/day
🍌 Potassium: 1 mmol/kg/day

Just remember 1.

🧵 Hypertonic hyponatraemia: when low sodium isn’t a sodium problem

1/
Not all hyponatraemia is created equal.
Most cases are hypotonic – from too much ADH or too little solute (e.g. low protein states).

But high glucose causes hypertonic hyponatraemia – a water shift, not water overload.

Different mechanism. Different treatment. 2/
📊 Glucose is an effective osmole.
It stays outside cells and pulls water out – diluting sodium.

So plasma Na⁺ drops, but there’s no sodium loss.
This is translocational hyponatraemia, not water excess.

💧Fluid creep accounts for more fluid than resuscitation in ICU.
But nobody prescribes it — and most don’t even notice it.
The truth?
🧨 Most ICU patients don’t need routine maintenance fluids.

Here’s what’s really going on 👇🧵 2/
A study of 14,654 patients over 100,000 ICU days found:
– Resuscitation fluids = just 6.5% of daily volume
– Fluid creep = a massive 32.6%
– Median creep = 645 mL/day
– Sodium burden often exceeded recommendations【Van Regenmortel et al, ICM 2018】

🧵Why does low protein intake cause hyponatraemia?

Most people find this confusing.

But the underlying physiology is beautifully simple.

Let’s walk through it 👇

#Hyponatraemia #FluidBalance #MedTwitter #FOAMed 2. Your kidneys have an impressive range — but they need the tools.

A healthy kidney can:

🧪 Concentrate urine to ~1200 mosmol/kg (in dehydration)
🧪 Dilute urine to ~50 mosmol/kg (in water overload)
But even perfect kidneys can’t excrete water without solutes.

🧵 Lymphangions: The Hidden Pump Protecting You From Oedema
1️⃣ What if I told you that you have hundreds of tiny hearts quietly pumping litres of fluid every day?
They’re called lymphangions—segments of your lymphatic system that actively contract to return interstitial fluid to the blood.
Let’s dive in. 💧🫀 2️⃣ ~8–12 L/day of fluid filters out of your capillaries.
❌ It doesn’t get reabsorbed by venules.
✅ It’s returned by the lymphatic system.
That’s how you avoid swelling up every day.

1/
Fluids can harm.
But fluids also save lives.
Let’s talk about the life-saving side of fluid therapy — from IV resuscitation in cholera to global oral rehydration campaigns. 💧🧵
#MedTwitter #FOAMed #CriticalCare 2/
The first recorded use of IV fluids came in the 1832 cholera outbreak in Britain.
Patients were dying of hypovolaemic shock from catastrophic fluid loss.

Dr Thomas Latta infused saline directly into the veins. Patients revived within minutes.

🧵1/
Hypovolaemia is the most overdiagnosed concept in medicine.
We say it reflexively — especially in sepsis.
But here’s the uncomfortable truth:
We can’t measure blood volume.
We infer it.
Often wrongly.
Let’s unpack why that matters. 👇
#MedTwitter #FOAMed 2/
There’s no practical way to measure blood volume at the bedside.
Tracer methods?
🔹 Radioactive albumin
🔹 Evan’s blue dye
🔹 Indocyanine green
They’re slow, assume no fluid shifts, and need intact capillaries.
💧 In sepsis or shock, those assumptions collapse.
Leakage, redistribution, and time lag make the results meaningless.
We don’t use them clinically — and we shouldn’t pretend we can.

🫁 What happened to ARDS?

20 years ago ARDS was everywhere.

Now we rarely see it.

We didn't cure it.
We just stopped causing it.
Here’s how IV fluids quietly created (and solved) an epidemic of iatrogenic lung injury 🧵 The lungs are uniquely fragile:

✅ Massive capillary surface
✅ Thin barrier for gas exchange
✅ Minimal tissue volume
Excellent for oxygen.
Disastrous when overloaded.
This makes them highly sensitive to both pressure & permeability injury.

1/
You might think:
"Why give NaCl to someone overloaded with salt and water? Shouldn’t we be pulling sodium out, not putting it in?"
🧂💧
It feels wrong — but correcting chloride can unlock natriuresis.
Let’s break the paradox. 🧵 2/
🧠The problem:
In volume overload, we use loop diuretics to promote natriuresis.

But hypochloremia is common.
Hypochloremia:
Stimulates RAAS activation.
Worsens sodium & water reabsorption.
Reduces diuretic responsiveness.
Chloride isn't passive — it's regulatory.