The Lactate Conspiracy: Part 1

What is lactate?  A good medical student will tell you something along the lines of

“Lactate is a byproduct of anaerobic respiration that is produced in response to cellular hypoxia secondary to inadequate oxygen delivery.  It is a marker of tissue hypoperfusion and shock”

They might go on to say high lactates are correlated with high mortality.  They might colloquially refer to lactate being ‘badness’.  You’d probably look at them moderately stunned, and say they were correct.

Oh’s Intensive Care Manual states:

 In critically ill patients, lactic acidosis is often due to shock.  In cardiogenic and hypovoloaemic shock hypoperfusion and tissue hypoxia increase lactic acid production while decreased hepatic perfusion decreases lactic acid metabolism.  In septic shock lactic acidosis is multifactorial.  Contributors include global hypoperfusion, microvascular disruption causing regional hypoperfusion and impaired cellular oxygen utiliisation by mitochondria.

The actual truth is far more complex, and though Oh’s not wrong, it’s waaaaay off right.  You’ll hear critical care peeps talking about optimizing lactate clearance4.  Hopefully after reading these two article you’ll understand that the very concept of lactate clearance makes no sense.

Now it’s important to know what lactate is, and how it affects acid-base balance because it’s seen as a marker of disease severity in every specialty.  The more you read, and the more you learn, the likelihood is that like me, you’ll realize that you’ve been taught convenient white lies about lactate to make quick intuitive leaps about people’s clinical condition.  Now short cuts are all very well, but if we don’t know the full picture we make errors based on incomplete data (more on that later).

People assume lactate is the cause of the acidosis, they are wrong.  People assume that lactate is a poison, they are wrong.

So here it is.  Everything we should know about lactate but were never taught. It’s fully referenced, and I encourage you to delve into those references for even more detail.


Lactate was first discovered in the late 18th century in milk.  It was discovered by a Swedish chemist called Carl Wilhelm Scheele in 1780.  He found samples in sour milk.  This led to it being called lactic acid.  It should be called 2-hydroxypropanoic acid.  It’s existence was verified 30 years later in 18101.  Lactic acid can exist in L and D isomeric forms, and it is the L isomer that we use and produce.  Now because lactic acid was originally found in fermenting products, most of the early research into it was done from that perspective.

Lactic acid is used as a preservative, it is used in the beer industry, to make cheese, and even to ferment sauerkraut.  In 1922 Otto Meyerhoff unpicked most of the glycolytic pathway and demonstrated that lactic acid was produced as a side reaction to glycolysis in the absence of oxygen.  Archibald Hill quantified the energy release from glucose conversion to lactic acid and proposed that glucose oxidation in times of limited oxygen availability or demand/supply imbalances can supply a rapid amount of fuel for muscle contraction.  At the time in-vitro studies had shown muscle contracting in the absence of oxygen, and Hills experimental evidence suggested there had to be another fuel capable of providing up to 8 times the amount of energy that oxidative glycolysis could provide. Hill and Meyeroff didn’t know about mitochondria, or the phosphagen system and they also weren’t aware that weak acids pyruvate and lactate are produced as conjugate bases.  They were also held in very high regard, so when they plotted lactate and pyruvate concentrations against pH and showed a linear relationship, they incorrectly assumed that one caused the other, they weren’t questioned in the same way as others might have been.

Correlational evidence is all very well, but what if lactate is an innocent bystander?  Present in higher quantities during times of absolute clinical badness.  What if lactate was there, hands’ bloodied, but trying to help?

We have to talk about the biochemistry now:

First of some basics.  The molecule produced by the lactate dehydrogenase reaction is a base.  Chemistry at it’s simplest tells you that if you add a base to a solution it become more alkaline, not more acidic. Lactate is a conjugate base, it accepts hydrogen ions and can become a weak acid, it’s pKA is 3.86 (that’s the pH at which 50% of lactic acid exists in its ionized form) therefore in humans nearly all of it will exist as a base.  The only way we would “produce” lactic acid, is if our cellular pH was less than 3.86.  I think we can all agree that if our cellular pH is less than 3.86 we probably aren’t respiring at all.

So how can adding a lot of base to a solution make you more acidotic?

Hold that thought.

If you vaguely remember your A-levels or your physiology bits at first year of med school, you’ll know that cells utilize ATP to make stuff happen.  ATP is constantly recycled, and that recycling of ADP to ATP is what cellular respiration is for.  We have 4 ways of making ATP from ADP.

  1. The mitochondria (aka oxidative phosphorylation)
  2. Lactate Dehydrogenase reaction
  3. Glycolysis
  4. Phophagen system (muscle)

The phosphagen system uses creatinine phosphate as a source of phosphate and creatinine kinase as it’s enzyme.  It eats a proton, makes creatinine and ATP.  It’s super fast, but it’s fuel (the creatinine phosphate) gets used up quickly.  This system only really exists in muscle cells, as they must recycle high volumes of ADP quickly.

Glycolysis is the main respiratory pathway, here we convert either glucose from the blood, or glycogen from our cellular energy stores into 2 pyruvate molecules, 2 or 3 ATPs and produce 1 or two protons, and some water.  We use an enzyme called NAD (nicotinamide adenine dinucleotide), which becomes NADH.  NADH needs to be recycled, and here I think is the clever bit; the lactate dehydrogenase reaction uses the NADH to produce NAD, and converts the glucose or glycogen to pyruvate and onto lactate, and releases 2 or 3 ATPs.  These reactions are linked.  You need to make lactate to help refresh the NADH (though it is recycled in other ways too), the faster you refresh your NADH the more glucose you can convert to pyruvate.  NADH is also needed in the mitochondria for oxidative phosphorylation, so lactate production gives us a bit of energy, and recycles a key enzyme that’s needed in mitochondria, and for basic glycolysis.

Now when you look at the above reactions you can quantify their speed.  The slowest reactions become the rate-limiting step. Look at the maximal rate of mitochondrial respiration compared to the glycolytic pathway1.  If glycolysis goes into overdrive lots of substrate will be provided for the lactate dehydrogenase reaction.  This is rather elegant I think, as it it mitigates the potential acidifying effect of the pyruvate reaction.

So we know that lacate is a base, that it’s production most likely retards cellular acidosis.

The other common belief about lactate is that is is produced in anaerobic conditions.  Now I’m not sure this really matters.  The concept of aerobic and aneorobic conditions is an artificial distinction that was made in the early 1900’s to allow us to more easily understand the complex sea of interconnecting biochemical reactions that allow a cell to function.  Mammallian cells don’t really function that well in the total absence of oxygen, and though I suppose it could be argued that they can survive for very short periods the distinction between one pathway and another, and the idea of a cell switching from one to another is not the case.  I think this is interesting because it probably reflects our understanding at the time.  The pathways were thought of as railway tracks, and we would switch between them based on what was required.  The truth is more complex and harder to pin down.  Mitochondria will continue to work if the oxygen tension is as low at 1 tor (though some studies have shown this critical threshold to be 0.55).  For those of you who don’t know 1 tor = 0.13kpa.

Again I put it to you that if the cytoplasm has an oxygen tension that is as low as 1 tor things stopped going in the right direction some time ago.  As such true anaerobic respiration is unlikely to have a clinical impact, or even really exist, what is a more accurate assessment of events is that as energy demand in the cell exceeds the supply provided by the mitochondria, glycolysis and therefore lactate production becomes upregulated.  Now I think the best analogy here is that the glycolytic pathway is a bit like running your car in first gear.  It will move, but it’s not very efficient and you will quickly run out of fuel (and absolutely knacker your car).

So we now know that lactate is a base, it’s production retards cellular acidosis, and that it isn’t really produced because the cell has switched to an ‘anaerobic pathway’. 

Lactate is produced all the time, (we make 1400mmol/day).  Now considering our normal range for lactate at any point is <2mmol we probably need to know where it is going.  Also if lactate is a poison why we do make so much of it?  Most textbooks say that Lactate is metabolized back into glucose by the liver (this is the Cori cycle).  Why does the Cori cycle switch off when we are acidotic?

Couple of useful things to know.

The lactate dehydrogenase reaction can go forwards and backwards.

There is experimental evidence to show that some cells will use lactate to make pyruvate at times of stress, or just because.  Here is a list of those cells

  • Alveolar Epithelial cells6
  • Cardiac myocytes3
  • Hepatocytes1,2,3
  • Renal Cortex (only uses lactate)8
  • Renal Medulla8
  • Neuron7
  • Astrocyte7

The Cori cycle tends to down regulate or switch off during periods of acidosis.  Adrenaline upregulates the rate of the lactate dehydrogenase reaction.

If lactate is bad – why would these responses evolve in mammalian physiology?

So now we know:

  • Lactate is a base
  • Lactate production retards cellular acidosis
  • Lactate is not produced in anaerobic conditions, and that anaerobic conditions don’t really exist.  Therefore, poor oxygen delivery cannot explain increased lactate production.
  •  Lactate is utilized by cells for energy production, therefore it is a FUEL.

So where does the acid come from?

See Part Two.


  1. Biochemistry of exercise-induced metabolic acidosis Robert A. Robergs, Farzenah Ghiasvand, Daryl Parker American Journal of Physiology – Regulatory, Integrative and Comparative Physiology Sep 2004, 287 (3) R502-R516; DOI:10.1152/ajpregu.00114.2004
  2. Lactate efflux from exercising human skeletal muscle: role of intracellular    Russell S. Richardson, Elizabeth A. Noyszewski, John S. Leigh, Peter D.Wagner Journal of Applied Physiology Aug 1998, 85 (2) 627-634;
  3. Gladden LB. Lactate metabolism: a new paradigm for the third millennium. The Journal of Physiology. 2004;558(Pt 1):5-30. doi:10.1113/jphysiol.2003.058701.
  4. Jones AE. Lactate Clearance for Assessing Response to Resuscitation in Severe Sepsis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2013;20(8):844-847. doi:10.1111/acem.12179.
  5. Lanza IR, Tevald MA, Befroy DE, Kent-Braun JA. Intracellular energetics and critical Po2 in resting ischemic human skeletal muscle in vivo. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. 2010;299(5):R1415-R1422. doi:10.1152/ajpregu.00225.2010.
  6. Lottes RG, Newton DA, Spyropoulos DD, Baatz JE. Lactate as substrate for mitochondrial respiration in alveolar epithelial type II cells. American Journal of Physiology – Lung Cellular and Molecular Physiology. 2015;308(9):L953-L961. doi:10.1152/ajplung.00335.2014.
  7. Schurr, Avital. “Lactate: the ultimate cerebral oxidative energy substrate?.” Journal of Cerebral Blood Flow & Metabolism1 (2006): 142-152.
  8. Bellomo, Rinaldo. “Bench-to-bedside review: lactate and the kidney.” Critical Care4 (2002): 322.

The Lactate Conspiracy: Part 2

So in the last post I established:

  • Lactate is a base.
  • Lactate production retards cellular acidosis.
  • Lactate is produced all the time.
  • Lactate is fuel.

I have suggested that the traditional lactate hypothesis

“Lactate is a byproduct of anaerobic respiration that is produced in response to cellular hypoxia secondary to inadequate oxygen delivery.  It is a marker of tissue hypoperfusion and shock”

 Is not correct.

However we all see, and all know that when people are sick their lactates go up, and when their lactates go up they become acidotic.

Why is this?

There are two reasons.

The first is the simplest.  When people are sick they are generally metabolically very active because they are trying to deal with whatever is making them sick.  At a very basic level that means that each person’s cell is recycling ATP as fast as it can.

The extra protons come from this reaction.

However there are some points to make to this approach of ‘counting’ protons when it comes to cellular chemistry.  The first is that these reactions don’t occur in isolation, they occur in a complex network, and they occur in a solution that is mostly water.  As such this is a slightly reductive way of thinking about cellular respiration.  Water can supply and buffer excess hydrogen to a certain degree (though it’s pKa is 14 so it doesn’t do much of this).  However we upregulate this reaction enough you can see that excess protons can be produced, and they will need to go somewhere.

We can say that the acidosis associated with lactate production is due to an induced hypermetabolic state.  Once the cells own intrinsic attempts at buffering (making more lactate, bicarbonate etc etc) are exhausted those excess protons leak out and make the cell, and the surrounding tissue fluid more acidotic.

The second reason, and this I think is the best reason, is because of the laws of physics.  Essentially when we upregulate the production of lactate, we increase the strong ion difference as lactate is a anion.  Lactate sits alongside, chloride, bicarbonate, and phosphate in the buffer base, and to obey the law of electrochemical neutrality some of the buffer base has to release some free hydrogen into solution to balance things.

If you have no idea what this paragraph or image mean, then you need to read this article.

So the lactate makes you acidotic, in the same way that excess chloride infusion can make you acidotic.  It’s not ‘to blame’ it’s just the last step in a chain reaction that started when cellular metabolism got kicked into first gear and the accelerator got floored.

Now just to summarise (again):

  • Lactate is a base.
  • Lactate production retards cellular acidosis.
  • Lactate is produced all the time.
  • Lactate is fuel.

Lactate is produced as part of normal glycoylsis. An elevated lactate indicates a HYPERMETABOLIC state, IT CAUSES ACIDOSIS by INCREASING the STRONG ION DIFFERENCE.

If Lactate is produced in response to badness, and there is experimental evidence that suggests it is metabolised by the heart, lungs, kidney, and brain during times of physiological stress why oh why would we try to ‘clear’ it?

Clearing lactate essentially means doing things to increase oxygen delivery to cells, but we know that it’s not hypoxia that is really driving lactate production it is the energy demand of the cell exceeding the supply available to it, so dumping fluid, and blood into someone’s circulation isn’t necessarily going to improve things (apart from by diluting the lactate when you do your next gas)

This has interesting implications.  If lactate is a fuel.  Can it be a treatment?

Couple of interesting properties of lactate – it can be thought of as a consumable anion, this means you can give a load of cation (ie sodium) without having to give a lot of chloride, or a lot of bicarbonate.  As the cells eat the lactate and turn it into glucose, or break it down completely.

I didn’t find much out there, but I did find 5 studies.  They are recent, small, and of variable quality, but I think they point to a few uses:

In one pilot single blind RCT in Austrailia1.  Patients with pretty horrific heart failure (ICU admissions, needs inotropes, or ventilation) were given 3ml/kg bolus of half-molar sodium lactate and an infusion of 1ml/kg/24hrs versus a hartmanns bolus and infusion.  Their CO was measured by ultransonographers blinded to the treatment arm.  The results show a significant increase in CO at 24 hours.

Intervention Control
CO at baseline 4.05 +/- 1.37  L/min 4.72 +/- 1.3 L/min
CO at 24 hours 5.49 +/- 1.9 L/min 4.96 +/- 1.21 L/min
CO at 48 hours 4.87 +/- 2.38 L/min 4.76 +/- 1.58 L/min

In two studies conducted in the UK on people who has sustained TBI half molar sodium lactate infusion was shown to decrease episodes of raised ICP3, and decrease ICP2 more effectively than mannitol.

In patients with TBI and ICP monitors with the kind of brain injury we can’t do much about other than prevent secondary insult they gave either normal saline or 0.5ml/kg/hr of half molar sodium lactate for 48 hours.  There were 11 episodes of RICP in the SL group and 20 in the control group (p=<0.05).  The other interesting thing was these people’s cumulative fluid balance.  It was much lower. 

They also looked at people’s neurological outcome at 6 months, they showed no significant difference between the two groups: 12 patients (SL group) versus 15 patients (control group) had a poor outcome at 6 months. However, more survivors from the control group had poorer neurological outcome compared to the SL group: nine versus four patients, although this difference did not reach significance (P = 0.14).  Though it is an interesting signal, and were this a paper on stroke thrombolysis probably picked up as hugely significant.

When they compared sodium lactate to mannitol, the effect of the lactate solution on ICP was significantly more pronounced (7 vs. 4 mmHg, P = 0.016), more prolonged (fourth-hour-ICP decrease: −5.9 ± 1 vs. −3.2 ± 0.9 mmHg, P = 0.009) and more frequently successful (90.4 vs. 70.4%, P = 0.053)2.


Another study in Indonesia4 looked at the efficacy of lactate bolus and infusion as a treatment for the horrifically dehydrated patients with dengue shock syndrome.  50 patients aged 2-14 years old received wither 5ml/kg of sodium lactate with a 1ml/kg infusion or ringers lactate 20ml/kg bolus plus standard maintanence therapy.  They looked at the measurement of a endothelial enzyme called SVCAM 1 (they found no difference).  There was no significant difference in outcome between groups (1 death in lactate group, 3 in control group), but the cumulative fluid balance between these groups with similar outcome was vastly different – the control group was 107 ml/kg +ve in 24 hours, whereas the lactate group was 35 ml/kg +ve in 24 hours.

Just a little context for you, the current direction of travel with research into fluid resuscitation is that too much can cause problems with acidosis, acute lung injury, and renal problems so volume sparing fluids that either exert an osmotic effect or do something else (like provide fuel) might be the ‘next’ thing.  Now I’m not saying that this is anything approaching a silver bullet, but if we can resuscitate people with less volume, we probably should.

What about sepsis?  I could only find a study on pigs, it was elegantly done however.  15 pigs were given the same challenge with e-coli endotoxin, and then resucicated over 300 minutes with either 5ml/kg/hr of 11.2% Na lactate, 5ml/kg/hr N saline, or 5ml/kg/hr of 8.4% sodium bicarbonate.  They measured lots of things, but MAP was their primary outcome.  As you can see, there was a significant improvement in MAP in the sodium lactate group.

I’ve subsequently found a similar study in sheep6, that suggests that sodium lactate infusion is harmful, so I’m not raising hypertonic sodium lactate as a panacea by any means, but the research into it’s volume sparing effects, and ability to decrease ICP needs to continue.

In Summary

The general textbook understanding of lactate physiology makes a number of basic errors which lead to inaccurate assumptions by medical staff, which can lead to inappropriate or inadvisable treatment strategies which are perpetrated throughout the world by the most junior doctor to the most senior critical care physician.

That is the lactate conspiracy.

Lactate is a fuel of last resort, and it may have therapeutic uses as a volume sparing resuscitation fluid.


  1. Nalos, Marek, et al. “Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial.” Critical Care2 (2014): R48.
  2. Ichai C, Armando G, Orban JC, Berthier F, Rami L, Samat-Long C, Grimaud D, Leverve X: Sodium-lactate vs mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients. Intensive Care Med. 2009, 35: 471-479. 10.1007/s00134-008-1283-5.
  3. Ichai C, Armando G, Orban JC, Berthier F, Rami L, Samat-Long C, Grimaud D, Leverve X: Sodium-lactate vs mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients. Intensive Care Med. 2009, 35: 471-479. 10.1007/s00134-008-1283-5.
  4. Somasetia et al. Critical Care 2014, 18:466
  5. Duburcq, Thibault, et al. “Hypertonic sodium lactate improves fluid balance and hemodynamics in porcine endotoxic shock.” Critical Care 18.4 (2014): 467.
  6. Su, Fuhong, et al. “The harmful effects of hypertonic sodium lactate administration in hyperdynamic septic shock.” Shock: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches6 (2016): 663-671.



Delirium: the forgotten medical emergency.

We have all seen a little old lady crumpled onto a hospital trolley. Referred in eye-rollingly from their family who visited the nursing home and meekly say ‘she is more confused than normal’.  Talking to her you think she’s good value, she thinks she’s on a cruise ship, that you’re a terribly nice young man and that you’d make an excellent match for her daughter.

You smile, send off a random panel of blood tests and refer her to care of the elderly. Instruct an exasperated nurse to collect a urine sample (how?!?), maybe you catheterise and cannulate her. No one screams and shouts at you.  The family have got what they want (an admission) and bugger off home.   The poor CofE SHO is used to taking veterinary histories like this and expects nothing better.

This patient has delirium.

Delirium is a medical emergency.

We are emergency physicians.  Patients with delirium stay in hospital longer, are twice as likely to die, and less likely to leave hospital independent than age-matched patients who are with it.  We need to be better at this.

In the last RCEM audit (2014-2015) only 11% of patients were being screened for delirium or dementia, so we have no idea what the ED incidence is.  The incidence of delirium in the community is relatively low, as it will generally lead to someone being admitted quickly.  The incidence in hospital is pretty high.  10-20% on average with a further 10-30% developing delirium during their stay.  Different wards have different incidences; 15-53% of post-op patients get it, and 70-87% of ICU patients.

Now replace ‘delirium’ with ‘sepsis’, or ‘AKI’ and there’d be national outrage that we are not checking people for a condition that increases their risk of death at the front door.  Delirium is a sign of end organ dysfunction, if a patients’ urine output drops to less than 30mls/hr all manner of screaming and shouting occurs, but we don’t do this when people’s brains have stopped working properly.

Delirium is an acute, fluctuating, disturbance in attention, arousal and other aspects of mental status.

If you have delirium you slide up and down a scale with hyperactive symptoms at one end and hypoactive symptoms at the other.  Hyperactive delirium is when people are convinced the nurses are going to kill them, or are restless and agitated.  Hypoactive delirium is more common, and patients with it are withdrawn, quiet and drowsy (we like patients like this, they are no trouble).

The key point is the fluctuations and changes in mental state.  Over time you might initially talk to someone and they seem to make sense, and go back and they might not remember you, or remember why they are here. Hypoactive delirium has a higher mortality and is more common than hyperactive delirium. 


Delirium is an acute illness (it comes on over a period of hours to days), but it has a variable and potentially long course. Recovery time is variable, sometimes as long as weeks and months. It can also lead to long term cognitive impairment.

Patients also recall events while they were delirious and can get flashbacks and PTSD like symptoms.  This can be quite upsetting and affect their feelings about subsequent medical treatment and hospitalisation.


It takes less of an insult to cause delirium in a frail brain.  You or I with our giant young brains require severe sepsis, hypoxia, or lots of beer to make us delirious.  Older people might only need to be slightly dehydrated, or a little constipated. Common causes:-

  1. Drugs (this is a big one, and i’ll try and cover it in more detail later).
  2. Infection
  3. Metabolic
  4. Pain
  5. Infarction
  6. Sleep disturbance
  7. Constipation

(This can be abbreviated to the mnemonic DIMPISS if that’s how you roll).

You are often going to find a story that is like this: An older lady who has been started on a new medication, which has made her less mobile, so she’s become dehydrated, which has led to constipation, and urinary retention and overflow.

In a complete departure from most of your previous medical training, I encourage you to find more than one cause (Occam’s razor be damned), and try and sort out as many simple things as possible.  Don’t be frightened of not knowing the ultimate cause, and having a myriad of options to choose from.  It’s likely to be multifactorial.

What should I do in the ED?

  1. If you think someone might have delirium, ask them to tell you the months of the year backwards, and what day of the week it is. This has a sensitivity of 93% (CI 91-99%) and a specificity of 64% (56-70%).
  2. If they can’t do that try and do an AMT. If they have a lower than normal score, and you’ve got evidence of things fluctuating.  You’ve diagnosed delirium.
  3. Write : Delirium ?Cause in the notes then go onto your differential (You should be able to find 2 or 3 possibilities to fit into DIMPISS).
  4. Investigate and check for each one. That means most patients are going to need a PR, bladder scan, a panel of blood tests, and an ECG.

Please note I have not suggested you do a urine dip.  This is not an omission.  Please come back soon for reasons why…


The biggest problem in the ED is we don’t screen for delirium.  If we start trying to ascertain how big the problem is, we might be able to do something about it.  Now I don’t think that it’s something the nurses need to do at triage, but every time we see an elderly person in majors we need to consider it.

In the ED there is a tendency to stop the diagnostic train once we’ve decided people can’t go home and let other specialities pick up the slack.  Admitting delirious patients to hospital is a bad option.  Often it’s the only one we have, but it’s going to make their delirium last longer, and likely speed their functional decline.  So families need to be aware of this.  It’s important to note that sometimes these delirious patients have been gently starved, and waited many many hours for the paramedics to bring them to you.  People you pick up first thing in the morning will be sleep deprived, dehydrated and hungry.

We also like to find a ‘cause’ for the confusion in the ED.  This probably leads to us diagnosing UTI way more than it actually happens.  This is bad for our patients because it leads admitting specialities to an anchoring bias from our own sloppy work.  Leaving the diagnosis open, encourages further original thought.


What would be ideal for these patients?

Patients with delirium need to be nursed in a quiet calm environment, with consistent staff, and consistent cues for orientation they need to have the bare minimum of procedures done on them (catheters, cannulas etc).  They should not be restrained, and should be allowed to gently wander.  Therefore the ED is almost designed to be a bad place to have delirium.  It is noisy, busy, lacks continuity, and patients are moved around a lot. We need to build ED’s or use processes to limit the bad things, or move patients with delirium out to wards quickly, possibly with investigations en route.


So remember:

Screen all your elderly patients for delirium.  TWO questions.

  1. What day is it?
  2. Months of the year backwards.

Admitting your delirious patients to hospital may cause more harm than good.

Delirium usually has more than one cause and it is better to leave the diagnosis open, rather than prematurely close it.


List of terms used in medical documentation that should make you think of delirium

  • Pleasantly confused
  • Aggressive
  • Muddled
  • Sleepy
  • Drowsy
  • Restless
  • Withdrawn
  • Guarded
  • More confused than normal
  • Not his/her normal self
  • Knocked off
  • Off legs
  • Not quite right
  • Flat
  • Not eating/drinking


Siddiqi, Najma, Allan O. House, and John D. Holmes. “Occurrence and outcome of delirium in medical in-patients: a systematic literature review.” Age and ageing 35.4 (2006): 350-364.

RCEM Clinical Audits.  Assessing for Cognitivie Impairment in Older People. 2014-2015.

Beales L, Mercuri M BET 1: Screening for delirium within the emergency department Emerg Med J 2016;33:741-743.

Fick, D. M., Inouye, S. K., Guess, J., Ngo, L. H., Jones, R. N., Saczynski, J. S. and Marcantonio, E. R. (2015), Preliminary development of an ultrabrief two-item bedside test for delirium. J. Hosp. Med., 10: 645–650. doi:10.1002/jhm.2418