Category Archives: Clinical

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


Can we electrically cardiovert stable AF in the ED?

True Story:

A 56 year old anaesthetist presents to your department, he states he started having palpitations while cycling up a large hill.  He took his pulse which felt irregular and so he cycled to the ED.  His HR 107, BP 130/75 RR 18 Sats 98% ORA Apyrexial.  His ECG shows AF, with no ST changes.  He ‘demands’ electrical cardioversion.

For the basics the brilliant RCEM learning website, has a great article on ED management of Atrial Fibrillation.   It doesn’t go into much detail about the nuts and bolts of electrical cardioversion in the ED.

Lets try and go into a bit more detail.

Now what does NICE say?  The relevant verse is here:

1.7.2 In people with atrial fibrillation presenting acutely without life-threatening haemodynamic instability, offer rate or rhythm control if the onset of the arrhythmia is less than 48 hours, and start rate control if it is more than 48 hours or is uncertain. [new 2014]  

1.7.3 Consider either pharmacological or electrical cardioversion depending on clinical circumstances and resources in people with new-onset atrial fibrillation who will be treated with a rhythm control strategy. [new 2014]  [page 23]


We can consider EC or PC depending on the clinical circumstances and resources.  The implication here is that EC is more resource heavy.  I would argue that it might be in the ED, but that across the organisation as a whole it is less resource intensive to sort in our department than to clog up an acute ward. This is backed up by studies in Ottawa8, Rochester6 and Pennsylvania which show that length of stay (the biggest determinate of health care cost) is less if we just get on and do it9.

So NICE asks us to consider the clinical circumstances of people with new-onset AF.  So what clinical circumstances do we need to consider?

Cause of AF

AF caused by electrolyte abnormalities, ACS, Sepsis, Structural heart disease, or Thyrotoxicosis is unlikely to resolve with a single shock.  After all you will need to treat the underlying cause first.  It is only really appropriate to offer ED EC to patients with idiopathic AF.  It is also important to note that up to 60% of patients with idiopathic AF revert spontaneously with no treatment at all.

Suitability for Procedural sedationbeaker

This depends on the skills present in your department, as well as the patient’s history.  It is unlikely that it is going to be appropriate to perform EC on a patient who has an ASA grade 3 or more.  Similarly you aren’t going to want to sedate someone whose airway looks like Beaker from the muppets.

Choice of sedation technique and agents depends on your skills and preferences.

Risk of thromboembolic complications (before and after EC)

Most guidance, and most studies seem to have a 48 hr cut off mark.  If the AF has been going for less than that time the received wisdom is that you aren’t going to shoot off a thrombus.  There is some opinion out there that EC might stun the right atrial appendage and a thrombus forms AFTER cardioversion.  This remains to be proven.

If the AF has no definitive time of onset, then the safest thing to do is anticoagulation first (depending on centres this can be clexane + warfarin and a clinic, or an admission and IV heparin), and an elective cardioversion later (usually 4 weeks).

What is the incidence of Thromboembolic events (TE) after EC?  I did find a meta-analysis3 from 1998 (Berger et al) which looked at 32 studies, giving 4621 participants.  92 patients had a thromboembolic episode (2%).  The duration of the AF was less than 2 days in the TE group in only 3 patients (0.06%).

Duration of AF Number of patients with TE episode/4621
<2 days 3 (0.06%)
3 days – 1 month 21 (0.45%)
>1 month 42 (0.9%)
Unknown 26 (0.5%)


The paper doesn’t tell us how many patients were in each group, so the data has little meaning when broken down as above, so we can only really take from this the overall percentage of 2% for thromboembolic events.

Berger et al was more interested in the timing of thromboembolic event after the cardioversion, this peaks in the first few days following the cardioversion no matter the duration of the AF.  I also found a study looking at NOACs (novel oral anticoagulants eg dabigatran) vs warfarin for anticoagulating patients prior to cardioversion but they got a 30 day thromboembolic rate of 0.8% with warfarin10.

A retrospective study from Denmark of 16 274 DC cardioversions7 without and with anticoagulation was published this year.  Unfortunately they didn’t look at the timing of the AF, but conclude quite reasonably that the risk of TE’s is higher in non-anticoagulated people with AF than people who are.

360/16274 Anticoagulation        n=11 190 No Anticoagulation n=5084 NNT
0-30 days0-360 days 32 [0.28%]144 [1.28%] 54  [1%]216 [4.24%] 12934

Weigner et al looked specifically at incidence of thromboembolic events (TE’s) after cardioverting recent onset AF (<48 hours). They conducted a prospective observational study which was published in 19972.  They identified 375 adults with recent onset AF, 66.7% reverted spontaneously, the rest had some form of active management (electrical or pharmacological or both).  Three patients out of the 375 had a TE event, none of them received electrical cardioversion, all were managed with anticoagulation, and various drug combinations.  All 3 of these patients had essentially benign echoes during that admission, suggesting that the ‘safe’ (drugs and anticoagulation) approach isn’t actually that safe.  All 3 patients were elderly people that had multiple co-morbidities that even the most EC fanatical ED doctor would baulk at doing a cardioversion on.

A 2013 Finnish observational study of acute cardioversion5 (EC within 48 hours of AF onset) pegs the rate of thromboembolic events at less than 1%.  There were 38 thromboembolic events within 30 days in a total of 5116 cardioversions, in 2497 patients, this gives us an incidence rate of 1.5% per patient (or 0.7% per cardioversion).  The study goes on to suggest that using either the CHADS2 score or CHA2DS2-VASC score to risk stratify allows us to reduce that risk further if we only attempt to cardiovert low scoring individuals without anticoagulating them first (it remains to be shown if anticoagulating the high risk group actually reduces thromboembolic events).

afdecThey produce this brilliant decision tree, which I think I might use when discussing the options with patients.  The risk of thromboembolism with delayed elective cardioversion and anticoagulation is also about 1% (confirmed by our study into NOACs10 and the big Danish study7).

I can see myself talking patients through this decision tree to help them make an informed choice about their options.

The question about whether we should be offering this cardioverted group anticoagulation is difficult.  On the one hand the Finnish research suggests that CHADS2VASC scores or similar can help us estimate the risk, but the large study from Denmark seems to suggest blanket prescription (but neglected to sub categorise the time of onset of AF).

This may again come down to giving your patient the choice between nothing, something for 4 weeks and something for longer, depending on their CHADS2VASC score.  So the risk of TE’s following ED EC seems to be about 1%, which is similar to the risk of doing an in-hospital EC with anticoagulation.  So if the risk is the same, is one approach better than another?

Is electrical cardioversion more effective than chemical cardioversion for acute onset AF?

Strangely there is not much to go on here.  Most trials use combination therapy if they study EC at all.  I could only find 3 trials that were in any way useful, and only one compared EC to PC directly.

The first trial I found was a single centre randomised controlled trial that compared electricity alone to pharmacological cardioversion from Italy in 20111.  Patients were excluded if their CHADS2 score was >2, if they were unstable, or if it was felt that the AF was secondary to another process (eg Hyperthyroidism, Sepsis, ACS etc).  All patients had an ED transthoracic ECHO, looking for significant valvular disease.  However the authors neglect to say how many patients they excluded because of their ECHO findings.

N= 247 EC 121 PC 126
Success 108 [89.3%] 93 [73.8%] HR 0.34(CI 0.17-0.68 p= 0.02
Adverse Events 1 6 HR 2(0.22-18.29) p=0.29
Recurrence of AF @2/12 26.3% 

31 lost to follow up


52 lost to follow up

HR 0.9 CI 0.45-1.8 p = 0.86]


Patients in the EC arm were more likely to be successfully cardioverted than in the PC arm.  There were more adverse events (flutter, bradycardia and ischeamia) in the PC arm (but this was not significant).  The recurrence rates were broadly similar, but there were a lot more PC patients lost to follow up than EC, so this may have skewed the results in the favour of EC.

The other trial evidence is not as impressive.  Jacoby’s chart review9 compared 30 ED electrical cardioversions with ‘eligible’ controls.  This study also included people with known paroxysmal AF that were managed with a rhythm control strategy (so a few of them got shocked on more than one occasion).  The ED cardioversions were successful 97% of the time.  Follow up was only to 3 weeks, but found no thromboembolic events, however one patient did end up having a mitral valve replacement.  This study was primarily looking at length of stay, and cost per admission.  EC was found to have shorter lengths of stay (23 h vs 56 h), the median cost of admission was also significantly less in the EC group [$1,598 vs $4,274].  This was effectively a small observational study of relatively poor quality, but the conclusions agree with the Italian study.

stiellThis brings me on to my third study – Stiells Ottawa Aggressive protocol for AF6,4.  This was a consecutive cohort study looking at the safety and efficacy of using procainamide and then using electrical cardioversion if cardioversion had not been achieved.

This study included 628 patients with AF. Procainamide successfully cardioverted in 376 (60%) of patients. In the 252 patients where procainamide had failed, EC was attempted in 223 patients of which there was a 92% success rate (203 success, 20 fail). Cardioversion was not attempted in the remainder of the patients (29 patients).

No one was anticoagulated in this study if the onset time was less than 48 hours.  No one in the study had a stroke, no one died, and only 8.6% of patients relapsed, but the follow up was only 7 days.


So in an ED with the right skill set it’s perfectly possible to electrically cardiovert patients with acute onset AF with or without pharmacological cotherapy, in fact electricity might have a better success rate.  The risk of thromboembolic events is also similar to doing a delayed cardioversion with anticoagulation, but recent data suggests it may be worth considering prescribing anticoagulation for a short time afterwards and risk stratifying our patients based on CHADS2VASC score.  If their score is <2 I would offer them EC. If there score is >2 I think I’d try to limit their risk by admitting them for anticoagulation.

Pros and Cons

Pros to ED EC Cons to ED EC
As successful as in-hospital careSame relapse rate

Possibly slightly higher success rate

No side effects from rate control drugs

Risk of thromboembolism 1% same as in hospital care

Can go home faster

Hospital care still an option if ED EC fails

Cheaper for the hospital

Risks of procedural sedationMight not need it (up to 60% revert spontaneously)

Possibly higher risk of thromboembolism after EC if sent home with no anticoagulation

More resource intensive in the ED



  1. Bellone, Andrea, et al. “Cardioversion of acute atrial fibrillation in the emergency department: a prospective randomised trial.”Emergency Medicine Journal (2011): emj-2010.  []
  2. Weigner MJ, Caulfield TA, Danias PG, Silverman DI, Manning WJ. Risk for Clinical Thromboembolism Associated with Conversion to Sinus Rhythm in Patients with Atrial Fibrillation Lasting Less Than 48 Hours. Ann Intern Med. 1997;126:615-620. doi:10.7326/0003-4819-126-8-199704150-00005 []
  3. Berger, Marvin, and Paul Schweitzer. “Timing of thromboembolic events after electical cardioversion of atrial fibrillation or flutter: a retrospective analysis.”The American journal of cardiology12 (1998): 1545-1547.
  4. Safety of Urgent Cardioversion for Patients With Recent-Onset Atrial Fibrillation and Flutter Stiell, Ian G. et al. Canadian Journal of Cardiology , Volume 31 , Issue 3 , 239 – 241 []
  5. Airaksinen, KE Juhani, et al. “Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (Finnish CardioVersion) study.”Journal of the American College of Cardiology 13 (2013): 1187-1192. []
  6. Stiell, Ian G., et al. “Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter.”Cjem 3 (2010): 181-91.  []
  7. Hansen, Morten Lock, et al. “Thromboembolic risk in 16 274 atrial fibrillation patients undergoing direct current cardioversion with and without oral anticoagulant therapy.”Europace 1 (2015): 18-23.
  8. Decker, Wyatt W., et al. “A prospective, randomized trial of an emergency department observation unit for acute onset atrial fibrillation.”Annals of emergency medicine 4 (2008): 322-328.
  9. Jacoby, Jeanne L., et al. “Synchronized emergency department cardioversion of atrial dysrhythmias saves time, money and resources.”The Journal of emergency medicine 1 (2005): 27-30.
  10. Nagarakanti, Rangadham, et al. “Dabigatran Versus Warfarin in Patients With Atrial Fibrillation An Analysis of Patients Undergoing Cardioversion.”Circulation2 (2011): 131-136.

The aggressive agitated elderly patient

The alarm has gone off in the CDU toilet.  Inside the toilet was an 87 year old man in only his hospital issue paper y-fronts demanding someone call the police because he is being “held against his will”.  He is refusing to leave the toilet, refusing to let you switch off the godawful crash alarm.  One nurse is hanging for dear life on the other side of the door to keep it open.  2 other patients with dementia in the same bay keep on wandering past, wanting to “help”.

What is your approach to the agitated patient?

There are 2 arms to any case such as this, first off we have to ensure the safety of the patient, other patients in the vicinity, other staff, and ourselves.  The next thing we need to establish is why has this person become agitated?

Medical causes of potential agitation are wide and varied.  Delirium in itself should be thought of as a medical emergency, as it carries a potentially high mortality (though estimates vary hugely 20%-70%).

This mnemonic may help – “SHED WIMP HELPS”

Substances, Hypoxia, Events (vascular), Dehydration, Withdrawl, Infection, Myocardial Infarction, Psychiatric, Head Injury , Endocrine, Low BM,  Pain, Seizures.

The key information here is going to be what you glean from the ambulance record, and whoever normally looks after your patient.  Is their behaviour normal for them?  Is it out of character?  If you are seeing that patient for the first time in the ED you are in the best position to assess them, as very often family members, carers, and other information will be lost prior to the RMO’s clerking them on the medical ward 6 or 7 hour later (on a good day).  If they are more confused than normal this does need investigating.

So say we’ve established that the patient has dementia, that they are in CDU for some form of social care assessment, and that to all intense and purposes there is no medical problem.

The best way to nurse someone with delirium or dementia is to keep them in a brightly lit room, with visual cues as to where they are, and what time it is.  It’s important to have consistent contact with the same individuals, such as carers from a nursing home, or the same nurse.  It’s important that the environment is calm, quiet, and free of interruptions.  Try to make sure that the patient has access to their hearing aids, and glasses, to avoid sensory disturbances.  There should be easy access to food and drink.  If you were going to design an environment to provoke a patient with dementia into confusion and agitation you’d design a place pretty much like an emergency department.

It’s noisy, there is no consistency of staff, patients are moved often, there are often absolutely no visual cues as to what time of day or night it is, if there are clocks they are always wrong.  The trolleys or wheelchairs are not comfortable, there is often no access to food or drink.

If they’ve trapped themselves in the toilet, or a running around the ward trying to escape you might feel under pressure to try some medication.  For elderly patients with dementia most of the literature tends to recommend either haloperidol or midazolam, but there is very little good quality data for elderly patients.  There is a Cochrane review of both antipsychotics and benzodiazepines in depression, they conclude that there is no difference in efficacy between atypical and typical antipsychotics, but no evidence that benzos help with non-alcohol related delirium.  So be cautious with both, haloperidol is thought to be safer because it doesn’t cause as much respiratory depression. IV doses are safer and more predictable if you can get a line in.

IF you can’t get a line in, this is what I’d put in my dart gun, either of…

Haloperidol 1-5mg IM Avoid if QTc is prolonged (risk of Torsade)Risk of dystonic reaction
Midazolam 2.5mg IM Risk of respiratory depression


After some time using de-escalation techniques, offers of food, drink, escape, to downright begging, we tried some IM medication.  I got punched in the face giving our gentleman 2.5mg of IM haloperidol.  About 5 minutes later his daughter arrived.  She took one look at her dad held out her hand, sighed, said “come over here Dad”, her father immediately let himself out of the toilet, and came to his daughter’s outstretched hand.

As she walked him back to his bed I heard him say “Thank god you came, I don’t know why they were keeping my trapped in that loo”

I love my job.


Paediatric Gastroenteritis

vomitWarning.  This is occasionally devolves into a bit of a rant, however it’s a rant with a sound evidence base.

Can we please give kids with gastroenteritis some anti-emetic?  If you happen to be reading this in the US, Canada, New Zealand or Austrailia where standard practice is a little different, I apologise.  Let me give you some background.

In the UK children who get gastroenteritis and come to ED get assessed, usually because parents have been trying and failing to hydrate them.  We tend to give them an oral fluid challenge.  Usually ORS at 5 or 10mls ever 5 or 10 minutes.  They get a full history, examination, their hydration status is documented and usually we wait for them to urinate.  If they don’t vomit, urinate (and the urine dip is okay), we shout hurrah, fist bump (or would but we are British) and send the parent on their way with a prescription or advice to get or make ORS, and to continue with the little and often amount of fluid required.

If they ‘fail’ this challenge by vomiting we are often forced to admit them, and continue with the cycle until they wee.  Paediatric admission units have one or two of these children on the go at any one time, and we just keep ploughing on until the child stops vomiting, or they get dehydrated enough to require NG or IV fluid.

For some strange reasons in this group of patients there is a lot of resistance to trying an oral fluid challenge with an anti-emetic.

I have yet to hear a coherent reason as to why this but the commonest one is that it ‘might mask symptoms’.  I can’t understand why this could be the case, as anti-emetics work by blocking receptors in the CTZ.  I’m not sure how this would stop vomiting secondary to some other serious disease process.  If someone has a closed head injury like a subdural they are going to continue to vomit no matter what you do, and will have other signs.  Similarly if a child has a metabolic disorder, their BM is going to be low (or really ‘freakin’ high), or there are going to be other clues in the history.  Also I’m suggesting giving a dose of anti-emetic to kids that we have diagnosed with acute gastroenteritis, which implies that you have assessed the patient, taken a history and examined them.  The anti-emetic the literature seems to favour is ondansetron.

So will we miss something? 

Looking for evidence for this is tricky, as it’s hard to prove a negative, especially when the ‘things we might miss’ are very rare metabolic disorders.  There is some research that backs me up.

Sturm, Jesse J., et al. “Ondansetron use in the pediatric emergency department and effects on hospitalization and return rates: are we masking alternative diagnoses?.” Annals of emergency medicine 55.5 (2010): 415-422.

Sturm conducted a retrospective review of visits to paediatric EDs in Atlanta, USA, between 2005 and 2007.  34 117 charts were reviewed, and ondansetron was used for 19857 patients.  They found that there was no significant change in the diagnosis at discharge between children given ondansetron and those who weren’t, they were also less likely to be admitted.  Children who were given ondansetron were more likely to return, and then be readmitted, but the admission rate globally was less in the ondansetron group than the nothing group.

Okay so it means we probably won’t miss anything but does it actually work?

YES. – NNT is about 5. That’s better than steroids in COPD (NNT 10) and Aspirin in STEMI (NNT 42).

Well the key single RCT was published in the NEJM in 2006, this was a prospective, double blind randomized controlled trial.

P 215 children 6 month – 10 years in the Paeds ED with gastroenteritis AND mild dehydration.
I 1 single dose of orally disintegrating ondansetron
O Primary:Proportion who vomiting while having rehydration


  1. Number of vomits,
  2. Incidence of IV rehydration
  3. Admission rates.
Primary:14% vs 35% RR 0.4 95% CI 0.26-0.61


  1.  0.18 mean vomits Vs 0.65 p<0.0001
  2. 14 % Vs 31% RR 0.46 CI 0.26-0.79 p=0.003
  3. 4% Vs 5% not significant


You can get the study here.

What do these results mean?  Well it looks like the group that were given a single dose of ondansetron we more likely to pass their fluid challenge, less likely to need IV therapy, but were not necessarily more likely to go home.  I like this last result.  I think it means that if a child was still dehydrated, and needed further observation that this was what was happening rather than taking false reassurance from being given a medication.

Children were given 2mg PO ondansetron 8-15kg, 4mg 15-30kg, 8mg if >30kg.

Caveats?  The children participating in the study were assigned a dehydration score by a single rater, which was based on largely clinical, and subjective measures such as skin turgor.  The dehydration score they used is pretty much the same table as exists in paeds textbooks and APLS manuals so seems a reasonable method to use however, it does introduce the potential for bias.  The other concern for me about this study was the number of patients that were excluded prior to randomization, 3067 children were considered but only 243 were asked to enrol, another potential source for bias.

This study on it’s own yields a NNT of 5.  We need to treat 5 children with acute gastroenteritis with ondansetron to stop 1 kid vomiting.

This is all very promising but is there any other data to support it’s use?

I’m glad you asked….

Then a Cochrane review was published in the BMJ in 2012 which looked at the literature from 1980 to 2012.  Ondansetron They found 10 studies and compared ondansetron (oral, and IV) to granestron, dexamethasone, and other antiemetics.  They looked at ondansetron vs placebo for cessation of vomiting, initiation of IV rehydration and hospital admission rates.  Now the review could only find 4 studies looking at the effectiveness of PO Ondansetron vs placebo, but their headline result for cessation of vomiting was RR 1.44 95% CI 1.29-1.61 NNT = 4.  One study was reliable but VERY pro ondansetron and threw the results out a bit, but with that excluded you still got an impress result RR 1.33 9%% CI 1.19- 1.49 NNT =5.  There was no statistically significant difference in hospitalization rates within 72 hours, suggesting that children’s admission might be delayed rather than avoided if you trial them ondansetron.  They did manage to find a reduction in resorting to IV rehydration [RR 0.57 NNT 6].

SO there is good evidence to suggest that it is safe and effective to use oral ondansetron in a vomiting child with gastroenteritis, we will probably decrease length of stay, increase success of oral rehydration, and maybe save some money for the trust.  No one will thank you for it though…

…apart from the kid’s parent, oh and the kid.

Rant ends.



  • Carter, Ben, and Zbys Fedorowicz. “Antiemetic treatment for acute gastroenteritis in children: an updated Cochrane systematic review with meta-analysis and mixed treatment comparison in a Bayesian framework.” BMJ open2.4 (2012).
  • Sturm, Jesse J., et al. “Ondansetron use in the pediatric emergency department and effects on hospitalization and return rates: are we masking alternative diagnoses?.” Annals of emergency medicine 55.5 (2010): 415-422.
  • Freedman, Stephen B., et al. “Oral ondansetron for gastroenteritis in a pediatric emergency department

A tale of 2 dissections…

Thoracic dissection is a diagnostic challenge to say the least.  Coming from a relatively CT-frugal ED background, it’s not normally in many nature to order CTA’s in people who have pain ‘going through to their back’.  Mostly because I’d order about 9 million a day (that may be a slight overestimate).  However I had a ‘remember that lady’ moment a few months ago from a very good friend on the MAU team.  This good friend is a very able colleague (certainly smarter than me), told me about a case he missed, a case I sent him.  His choice of words was interesting because he didn’t imply I had missed it too (though I feel I had).

It was busy, I was the boss on overnight.  I was trying to make some room in my department, so I was trying to ‘improve flow’ now I don’t care how perfect a doctor you are; we all do this.  In about 30 minutes I’d sent a non-toxic OD’s to the mental health team, and someone with flu home.  Then I went to see this delightful, charming 89 year old lady, who had some chest pain, unfortunately about 3 minutes into the consultation I was grabbed to go and calm down a drunk fat girl with a personality disorder and a cut foot, who had been ‘disrespected’ by the security staff.  I sewed up her ankle while she simulated oral sex on the handle of bay operating light.

After finishing that I went back to my 89 year old.  She had developed chest pain whilst walking up some stairs, the pain had lasted maybe a minute, she told me she nearly blacked out.  The family called her an ambulance.  I noticed from ambulance sheet, her initial BP was 60/40, but it had rapidly improved to a ‘normal figure’ 145/80 while she was with us.  She’d had vasovagals before she told me, and apart from treatment for hypertension, and IHD.  ECG –  flattened lateral T’s, nothing exciting.  The CXR, showed a widened mediastinum, which I noticed, I then looked back at her old CXRs, and I saw one from a month ago that ‘looked the same’ (she had a widened ectatic, unfolded aorta).  So off she went to medicine for a 12 hour troponin, and someone to stop her bendroflumethiazide.  My friend clerked her in, and did the same.  All the way through this she was pain free, and her obs were totally unremarkable.


A CXR with a widened ectatic thoracic aorta.
A CXR with a widened ectatic thoracic aorta. (this is not her CXR, but is close enough for the purposes of this case)

The CXR was reported that morning as showing a widened mediastinum, the medical team arranged urgent CTA and a large type B dissection was noted on the scan.  She went for interventional radiology EVAR, her aorta was perforated, and she died in ICU later that day.

Now I find out about this through my friend, on the grapevine.  The patient was the subject of an M+M meeting which I didn’t attend (as in my current institution we keep the ED M+M and Medicine M+M separate).  I felt awful about this, I’d missed the diagnosis, my colleague had missed the diagnosis, and had we managed to pick it up would she have survived?  It’s difficult to say.  There is evidence that suggests for every hour a diagnosis of AAD is missed the mortality goes up by 1%, however the mainstay of treatment in this group is aggressive BP control, and her BP was normal to low.  Her history was not pathognomonic for AAD, straining at stool (like King George II), chest pain radiating through to back, but I had the CXR which was also abnormal, but not normally abnormal.

On reflection, I made at least 2 cognitive errors; Attribution bias (I saw her old CXR, which showed an ectatic aorta, and I felt her current CXR showed a continuation of that process); and confirmation bias – I felt that the St John low BP finding confirmed my thought that she had had a vasovagal or angina from exertion, neglecting to fit this in with the pain that she very well described to me.

The second case occurred on a busy Saturday evening a few weeks later.  I had picked up a card for a 29 year old gentleman in our monitored bay that said “Leg pain”.  I started looking through his old clinic letters, and scans (a wonderful byproduct of where I work’s beautifully integrated IT system), and I found that he was being treated for idiopathic hypertension.  This letter from a renal physician commented on a normal MRI of renal arteries, drilling down to that report referenced an MRI of his heart which showed a dilated aortic root.  I clicked through a few DNA’s on the computer system, and as I was pondering if his hypertension could be related to his leg pain.  I got grabbed by one of my colleagues who had noticed this guy was being a bit odd.

The guy worked as a woodsman, and had been brought in by his friend.  His friend said he’d come home, complained of pain in his leg, got sweaty and confused, so he’d brought him here.  Now we were all thinking ‘toxins’ at this point but he pointed to his chest, and his belly and said ‘hurts’ then kept trying to sit up, move around and generally make himself more comfortable.  He looked awful.  That was the most history I got from him, after that he had a profound expressive and receptive dysphasia.  The patient’s flatmate, in one of those wonderful moments of honesty, told me he was the only one in the flat that didn’t take synthetic cannabinoids.

This man’s BP was 220/160 he had all of his pulses, no delays, a normal ECG, he got a portable CXR which showed a normal mediastinum, to my eye (and the radiologist the next morning).  His left leg was a little cooler perhaps than his right.


An example of a normal CXR
An example of a normal CXR, (this is not his CXR, but it is close enough for the purposes of this case)

I was pretty worried about this gentleman, and asked for my first ever CTA, then I grabbed one of the ED consultants to have a look at him with me.   She also suggested we start banging in labetalol at this point so we did (it didn’t really work).  I took him up to scan, and after a few attempts to get him to lie flat and stay still we got our diagnostic images (with very very small doses of midazolam).  They showed a type A dissection.

He came back down to ED, and went to theatre about 25 minutes later.  He survived his repair without having to have a valve replacement, but did have some embolic events post op (and probably pre-op), but he’s alive, and independent.

Now I had these cases within about 3 weeks of each other, I’m not sure, but I wonder if my failures with the first, primed me to pick up the second.  I certainly did a fair amount of reading on dissection after I found out about my error.  What has struck me about that is how difficult and nebulous the symptoms can be, but it seems any combination of acute onset pain, and neurology could be a dissection’s only symptoms (and you may not even get that).


About Acute Aortic Dissection

Clinical Features % of cases
Severe/worst ever 90%
‘abrupt’ 84-90%
Sharp 64%
Tearing 50%
Migrating 16%
Down the back 46%
Differential BP >20 mmH in arms or missing pulse 15-30%
Altered or syncope 13%
Hemiplegia 5%
Focal neurology 17%
Abdo pain 43% (descending0 22% (ascending)



CXR: Widened mediastinum in 56-63% of patients.  Abnormal aortic contour 48-71%.

Transthoracic echo 75% diagnostic type A, 40% type B

CT sensitivity is 83-98% (but probably better than this now due to high res scanners).

I think the clinical features make more sense if you imagine the process going on in your patient.  The pain is from the initial tear, the pulse differential, or BP differential is due to the involvement of the arch vessels, and depends entirely on the physical shape of the tear.  It’s the same with neurological symptoms, you might get hemispheric signs if a major vessel is blocked, or you might get random neurology that doesn’t make sense because of embolic phenomena (which is by it’s nature random).  As the tear elongates it will affect lower branches, giving appropriate syndromes (renal failure/infarction, mesenteric ischaemia).


There is some discussion in the literature of using d-dimers has a ‘rule-out’ test for dissection.  As you are forming clot inside the false lumen, in theory the d-dimer should be pretty high.  Certainly a negative d-dimer might rule out a dissection, but I don’t think there are any prospective trials out there to say for definite that this is a safe strategy.   I did find a recent meta-analysis (of observational studies) with approximately 500 participants which suggests it might be sensitive enough to use as a rule out test, (this is quite an interesting topic, and I think I’ll revisit it later).


Type A Vs Type B



Type A dissections need go to theatre, patients need to have either an AVR, and graft, or just a graft to pin the false lumen back.  Other options the cardiothoracic surgeon has is to fenestrate the false lumen (basically cut through it) which allows blood to flow through both lumens.  Type B dissections (which start after the arch) used to be controlled with BP control only, sometimes some centres are using large stents, to push the false lumen closed.  The theory behind controlling the BP is to decrease the pressure flowing through the false lumen and stop the dissection tearing any further.

Management in the ED is mostly around identifying the problem and making the diagnosis, it’s an often missed or delayed diagnosis because the features are so nebulous and changeable, for us you should ask yourself “Could this be a dissection?” for every one of your chest pains.  If you do suspect it, talk to a boss, and consider more investigation.

Once you’ve found one, start lowing the BP, labetalol as a bolus and infusion is recommended in most centres, GTN infusions can also be used (or used together).  Nitroprusside is also still in the textbooks, I’ve never seen this used, but I’m sure other people have.  Aim for a target of <140/90.  Slipping in an arterial line would also be a good idea while the cardiothoracic people are getting ready for theatre.  It will aid your BP management, and make the anaesthetist moderately grateful (as it will make their RSI safer).

Further information

–          Excellent SMACC podcast on dissection from Rob Rogers

–          LIFTL review – here



Useful literature and references

Shimony, Avi, et al. “Meta-analysis of usefulness of d-dimer to diagnose acute aortic dissection.” The American journal of cardiology 107.8 (2011): 1227-1234.

Harris, Kevin M., et al. “Correlates of Delayed Recognition and Treatment of Acute Type A Aortic Dissection The International Registry of Acute Aortic Dissection (IRAD).” Circulation 124.18 (2011): 1911-1918.

Howard, Dominic PJ, et al. “Population-based study of incidence and outcome of acute aortic dissection and pre-morbid risk-factor control: 10-year results from the Oxford vascular study.” Circulation (2013): CIRCULATIONAHA-112.

Howard, Dominic PJ, et al. “Incidence, risk factors, outcome and projected future burden of acute aortic dissection.” Annals of Cardiothoracic Surgery 3.3 (2014): 278-284.

Coyle, Siobhan, et al. “Diagnostic Testing in Acute Aortic Dissection.” Current Emergency and Hospital Medicine Reports 2.2 (2014): 97-103.


I had a patient gifted to me from the nigh/day handover.  Don’t we just love ‘em?  

“Wait for the bloods and then talk to the surgeons”

I just had to wait for the bloods on a pleasant chap in his mid 50’s who had woken at 5am with severe central abdominal pain.  The pain had been adequately treated by the paramedics with 5mg of IV morphine, he had no fever, no Ds or Vs.  He might, if pushed, concede to some mild nausea.  Examination as reported to me was – slightly tender in the RIF, not peritonitic.

Bloods came back, totally in the black.  Except his troponin – 168ng/ml, [our house negative level is less than 32].   WTF – why had we done a troponin??

I went to re-examine the patient, and re-visit the history.  I took a slightly more cardiovascular bent.  No chest, back, neck, or tooth pain.  This gentleman could have been anaesthetist he cycled so much; 30km daily (no unhealthy obsession with apple products though).  I asked about changes in exercise tolerance, nada.

My examination echoed that of the overnight doctor who saw him at 5:30; tender RIF.

I did a bit of bedside USS, aorta looked normal calibre, heart was contracting slowly,  but well.   His resting HR was around 34,  Sinus bradycardia with ?high take off in the anterioseptal leads, I wondered about an inferior MI .  Posterior leads didn’t help.   CXR looked normal.  We repeated the TNI and did a VBG (VBG was normal).

Risk Factors?  Well after Prof Carley’s talk I’m less interested in these, but he had none.

I explained the result of the blood test, in the context of him not having chest pain (which he confirmed patiently to me for the nth time), was confusing.

Back to the history.  Sudden onset abdominal pain, started in the middle of his stomach, now beginning to hurt in the RIF.  No fever, mild nausea.  No constipation, no diarrhoea.  WCC and CRP normal.  I googled the list of non ACS causes of troponin rise:

System Causes of Troponin Elevation
Cardiovascular Acute aortic dissection
Medical ICU patients
Heart failure
Apical ballooning syndrome
Cardiac inflammation
• Endocarditis, myocarditis, pericarditis
Infiltrative disease
• Amyloidosis, sarcoidosis, hemochromatosis, scleroderm
Left ventricular hypertrophy
Myocardial Injury Blunt chest trauma
Cardiac surgeries
Cardiac procedures
• Ablation, cardioversion, percutaneous intervention
Hypersensitivity drug reactions
Respiratory Acute PE
Infectious/Immune Sepsis/SIRS
Viral illness
Thrombotic thrombocytopenic purpura
Gastrointestinal Severe GI bleeding
Nervous system Acute stroke
• Ischemic stroke
• Hemorrhagic stroke
Head trauma
Renal Chronic kidney disease
Endocrine Diabetes
Musculoskeletal Rhabdomyolysis
Integumentary Extensive skin burns
Inherited Neurofibromatosis
Duchenne muscular dystrophy
Klippel-feil syndrome
Others Endurance exercise
Environmental exposure
• Carbon monoxide, hydrogen sulfide


Now appendicitis wasn’t on that list.  SIRS was.  I went back to something I heard over and over again at medical school.  The history gives you the answer 90% of the time.  This man was complaining of abdominal pain which started in his umbilicus and was migrating to the RIF.  If I ignored his bloods or didn’t have his bloods what would I do?

A kind cardiologist came to review him for me, and agreed that ACS was not the cause of this gentleman’s elevated TNI.

I asked the surgeons to take a look, which they dutifully did.  I told them about the trop rise (which was falling again now 128ng/ml at 2 hours).  They took him for observation, with the diagnosis “?biliary”.

He had an USS the next day which demonstrated a thickened appendix, and had a laparoscopic appendectomy that evening.

Why had we done a troponin?  Someone who was just coming off their night shift had ticked the box by accident.

I’m wondering whether this was a true false positive because this chap was fit enough to have the generally elevated TNI that some endurance athletes have been shown to have1, or if his small pocket of intra-abdominal sepsis was enough to cause some mild myocyte damage.  Hell could it be mix of the 2?

Should I have just disregarded the first result and ignored?  This chap was adamant he had no chest pain, and had no risk factors for silent-MI.  On reflection the elevated TNI meant I felt that there was ‘something’ to find, and I went digging.  If I had had no blood tests at all, I’d have probably sent him to the surgeons, just like the tired overnight doctor who handed him over to me was going to.

  1. Shave, Rob, et al. “Exercise-Induced Cardiac Troponin ElevationEvidence, Mechanisms, and Implications.” Journal of the American College of Cardiology56.3 (2010): 169-176.

Ankle Injuries

 Ankle injuries account for a massive amount of ED work.  Many patients present following accidents at home or while playing sport.  Often all the patient actually wants is some reassurance; this is often easier to give if you know a little about the ankle.

Ankle Sprain accounts for up 5% of ED visits in the UK, which is approximately 5600 attendances a day.  Once someone has sprained their ankle once, they often go onto have residual symptoms of instability and ‘resprain’.  We often think of it as a relatively benign injury, but it’s common, it often necessitates a period of rest to recover, and this has a wider economic impact.  The US army estimated in 1994 that it lost $1 billion in lost duty time due to ankle sprain alone.


ankle3The ankle is a hinge synovial joint.  The tibia and fibula articlulate with the talus.  The end of the tibia and fibula along with the posterior tibifibular ligament form a mortise, that the top of the talus (trochlea) fits into.

The talus articulates on the sides, and on it’s superior surface.

The talus is widest at its anterior edge.  This means that when your foot is down flat the widest part of the talus is inside the mortis, pushing against the fibula and tibia.  This is inherently very stable.  When you are plantar flexed the narrowest part of the talus is inside the mortis, the fibula and the tibia cannot grip both sides of the talus which means it is more likely to move suddenly and cause injury.  The majority of ankle sprains occur as a result of unexpected inversion of a plantarflexed foot.



Lateral ligaments (the weaker set, outer aspect of ankle)

ankle1Anterior Talofibular ligament – (weak) anteriomedial band from lateral malleolus to neck of the talus.  This one is the weakest, and is the ligament that tears most often in ankle sprains.

TEST – anterior draw test: grab the heel, stabilise the calf, and see if you can pull the foot toward you.  You should feel an end point, if there is some give (or lots of pain, the ATFL is probably gone).

Posterior Talofibular ligament – (strong) horizontal band malleolar fossa to lateral tubercle of talus

Calcaneofibular ligament – posterioinferiorly from the tip of the lateral malleolus to the lateral surface of the calcaneus

TEST – stabilise the lower limb and invert the foot under stress.  There should be an end point, if there isn’t the ligament is probably broken.  This is painful! Most of the time patients stop us doing this test, so its utility is marginial.

From our point of view these three ligaments are the most common to tear or break.  The distinction to a certain degree is academic in the context of an acute injury.


Medial Ligaments (the stronger) AKA Deltoid ligament.

This is a fan (or triangular) ligament that begins at the medial malleolus and attach to the talus, calcaneus and navicular, forming

  • Tibionavicular ligament
  • Anterior and Posterior tibiotalar ligament
  • Tibiocalcaneal ligament.

The deltoid ligament is pretty strong.  A tears much less readily than the lateral ligamentous complex.


Example Case

“Jake” a 36 year old Sunday league footballer presents with left ankle pain and swelling following a “bad tackle”.

History is as important in minor injuries as it is in medical problems, when taking a history from someone with an injury it is important to try and visualise exactly what their limb was doing at the time of the injury.  The direction of force, impact site, and immediate symptoms all give useful clues.

Jakes say he was about to shoot, when a defender came in with a slide tackle from his left hand side and struck his left ankle.  He was trying to kick the ball with his right foot.  Jake hit the floor immediately, “he knew he had done something” but managed to take the penalty that was awarded to him (me missed).

Examination of ankle injuries should be from the knee down.  Look for tenderness over

  • Proximal fibula
  • Lateral Malleolus and ligaments – with anterior draw test, and forced inversion test
  • Medial Malleolus and ligaments
  • Navicular
  • Calcaneum
  • Achilles Tendon
  • Base of 5th Metatarsal

When to Xray?

Ankle rules diagram from (looks a lot like the BMJ one).  Borrowed.
Ankle rules diagram from (looks a lot like the BMJ one). Borrowed.

Use the ottowa ankle and foot rules:  derived to increase the specificity of ankle xray.

It is important to examine the ankle fully, as well as assessing if they are “ottowa positive or negative”.  You should have a lower threshold for Xray in the following patient groups

  • Young children <6
  • Pregnant women (ligamentous laxity)
  • Intoxicated individuals
  • Elderly patients

So in Jake’s case, our decision to Xray will depend on our examination findings, however the likelihood of him having a serious fracture is unlikely as he took the penalty he was awarded.

So we Xray Jake’s ankle, and there is no fracture.  So if Jake has a ‘simple ankle sprain’ what advice can we give in terms of rehab?


Acute phase 1st week

RICE, No sport, Gentle mobilisation, script for analgesia, If in a manual (non-sitting job) sign off for 5 days.  I don’t routinely give crutches.

I also always suggest physiotherapy after the first week especially if they are a in any way serious about sport.

Rehab phase 2nd week to 5th week.

Start returning to sport.  Phased return.  Use of ankle brace/tubigrip when exercising to decrease risk of re-injury.

Prevention phase – week 6 plus

I suggest wobble boards (improve proprioception), and during exercise using tape or a brace (depending on their personal preference).


If you get yourself into the situation with a patient when you are convinced it’s a sprain but they won’t walk you can try the following strategies

  • Double and triple check the film.  Are you missing a small avulsion or a mid foot fracture?
  • Have you given them enough analgesia?  Load ‘em up!
  • Try them with crutches
  • LAST RESORT – back slab and OOPD follow up + crutches.  Sometimes if the sprain is severe this is all that you can do in the acute setting.

pH 7.51…lactate of 20??

Blood Gas!

This 74 year old gentleman attended the ED after phoning a friend because he ‘though he was having a stroke in both hands’.  Paramedics had to gain entry to the house, which was in a state of disrepair, cold, and unclean.  The patient was found on the floor, surrounded by vomit.  I tend to do a VBG in situations like this because I get an acid/base status and other useful information back faster than formal bloods.

His observations were essentially normal, apart from his 3 lead which was a veritable soup of short lived atrial arrhythmias, and PVCs.  He was also a bit cold 34 degrees C.  What is your interpretation of this gas?

pH 7.51
pCO2 60
pO2 28
BE 22
Na 145
K 2.2
AG 55.4
Cl 44
iCa 0.74
Gluc 9.8
Lac 20.0
HCO3- 40.8


My interpretation:

So starting from the top the patient is Alkalotic, with an elevated CO2.  This means they have to have a metabolic alkalosis with respiratory compensation.  Lets looks more closely at the metabolic component, the BE is 22, which means we have ‘22’ more bases than normal, we can also see that his bicarbonate is 40.8. (thats where they are coming from).

There are clues here.  We know that bicarbonate takes time to respond to problems.  This man must have a chronic problem causing his bicarbonate to go up.  We can infer this is a chronic metabolic alkalosis with a degree of respiratory compensation which is probably new.

Lets examine the AG – the gap is 55.4! Which is the highest gap I have EVER seen.  Remember that AG is calculated by adding the Na and K, and taking the chloride from bicarbonate.  Where is the source of the gap.  It’s predominantly from the Chloride.  Look it’s 44!  That’s less than HALF what it should be, I suspect that it’s not the only cause of the Gap here,  as we’ve got a lactate of 20 , pushing in the other direction and perversely helping to correct the alkalosis.

If you fancy you can calculate his SID which is 96!  High SID alkalosis is usually caused by gastric outlet obstruction, vomiting, excessive NG suctioning, diuretic mistakes,  primary hypoaldosteronism, or volume depletion.

This man has pyloric stenosis from untreated chronic H pylori, and acute renal failure secondary to volume depletion.  I think his gas shows a chronic metabolic alkalosis with respiratory compensation and a hyperlactaemia.   I have never seen this pattern in an adult before!


Na 147
K 2.1
Cl 51
Urea 33.8
Creat 542
Ca2+corr 2.1
Mg2+ 2.0
CRP <3





So a couple of weeks ago we got a lovely gentleman through our doors who had a medical problem.  He was mid 60s and had a pneumonia, but was tolerating it pretty well.  He had HTN, and CLL.

 What irked our collective team noodle was his K+ of 8.9, his ECG was normal, and he wasn’t in renal failure.

No tenting, sineing, PR prolongation, or P wave abnormality, or weird block.

“No, the sample isn’t haemolysed” the lab told us.

The repeat came back 8.7. – not haemolysed (this time written in block capitals).

The VBG we did, and ran to ICU to analyse gave us a value of 8.2.

So we turned to google, pubmed, and litfl, and all learnt about pseudohyperkalaemia:

The commonest cause is sloppy venepuncture, but it can also occur in patients with thrombocytosis, or leucocytosis.  Effectively it is a measurement error that occurs if you have tonne of cells in the sample all gently, slowly lysing.

Our gentleman’s WCC was 200

Pseudohypokalaemia has also been reported with leucocytosis as well.  As always I suppose we should always interpret lab results in light of what the patient looks like in front of us.