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%).
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…
Avoid if QTc is prolonged (risk of Torsade)Risk of dystonic reaction
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”
Pre-alert at 4am: “Status 1 23 yo male, seizures, now GCS 3, BM 6.4, HR 130 BP 90/60 Sats 95% on 15L, NPA insitu. Given 15mg IM midazolam. Seizures have stopped ETA 10 minutes”
On arrival, slightly sheepish paramedic, also says ‘errr he’s in VT but we only found out as we were driving in’
On arrival I do a quick assessment, while the boss takes over the airway.
A, patent, NPA insitu, B equal AE, sats 95% on 15LNRB, good respiratory effort, C BP 80/50 HR 180, monitor looks like broad complex tachy.
1 x 200 J synched shock – Still VT.
I look to the boss “s***” we say together.
Here is the ECG:
What are you going to do?
We got an anaesthetist to manage the airway, and we gave a series of further shocks, and changed the positions of the pads, and we loaded him with Amiodarone.
I pulled up his past medical history, he was involved in a RTC when he was a teenager, had had ORIFs of his right tib and fib, and right femur. No heart conditions.
His girlfriend, who was (understandably) distraught said he was not on any regular medications, and though he had been depressed in the past, wasn’t depressed now. I then asked her if she was on any medication he might have taken. She was taking dothiepin (a TCA).
He’d been in the department now for 30 minutes, still in VT, still not responding to the medications we had. In the end we decided that he was behaving like a TCA overdose, and we had enough evidence to try treating him as such.
The treatment for TCA OD is sodium bicarbonate, as it provides a sodium load for the Na+ channel blocking affect of the TCA (which is why TCAs affect cardiac conduction).
Start with 50ml of 8.4% NaHCO3- over 15 minutes. We used about 6 vials of this stuff, and his ECG turned into this:
After an infusion of HCO3- 4 hours later his ECG looked like this:
About TCA OD:
– TCAs – [STEM]”line” or [STEM]”mine”. Commonest UK ones – Amitriptyline, Nortriptyline.
TCAs [tricyclics – 3 actions] block the reuptake of noradrenaline centrally and peripherally, they have an anticholinergic effect, and also block Na channels in brain and myocardium.
Patients who have taken TCAs get anticholinergic effects: warm, dry, hyperthermia, tachycardic, agitation, blurred vision, hallucinations, urinary retention, ileus. At higher concentrations the symptoms get worse, then affect their consciousness level, then their cardiac conduction.
All ODs need an ECG, look for a long QRS; >100ms increases the risk of fits and coma. Greater than 160ms is associated with ventricular arrhythmias.
Treatment (ABCs as given)
50mmol of 8.4% over 15 minutes, repeated as required, infusions of bicarbonate can be given. If you’ve ventilated the patient you can also hypoventilate them to a pH of 7.45-7.5, which seems to decrease the affinity of the TCA to myocardial Na+ channels.
What happens if the bicarb isn’t working? [thanks to @bedrocteam] for pointing this out:
– Mg2+ is recommended if the bicarbonate isn’t working, though the evidence is getting quite thin at this point. There is also case reports of intralipid being used, when all else has failed .
Emamhadi, Mohammadali, Babak Mostafazadeh, and Marzieh Hassanijirdehi. “Tricyclic antidepressant poisoning treated by magnesium sulfate: a randomized, clinical trial.” Drug and chemical toxicology 35.3 (2012): 300-303.
Engels, Paul T., and Jonathan S. Davidow. “Intravenous fat emulsion to reverse haemodynamic instability from intentional amitriptyline overdose.” Resuscitation81.8 (2010): 1037-1039.
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.
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.
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
% of cases
Down the back
Differential BP >20 mmH in arms or missing pulse
Altered or syncope
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).
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.
As I am sat in Christchurch airports departure lounge, I’m reflecting on my time here. I’ve loved my time away, and there are some things they do here in Christchurch that if I could slip into my carry on and bring to the UK I would.
1. Departmental radiologists
This is our handover room, and in it sits one of 3 full time radiology consultants who do real time reporting and scan protocolling for the ED. I have seen them leave this room, come out to talk to us about a finding, and EVEN examine patients. They are truly awesome, and every Friday they lead us through a greatest hits of our radiology cases from the week.
2. Full time departmental Social Workers, alongside physio and OT
These guys activate emergency care packages, inform people of voluntary services, help with child protection, vulnerable adult protection, they are present during major trauma Every morning and afternoon, if someone needs help getting back onto their feet, I can call “the MDT” and get my patients MOVING. If they can’t get people home, they get them into respite care or a residential home (with the social workers help).
“Friends of the Emergency Department” or FEDS, talk to and listen to patients, their families, their children. Grab cups of tea, snack boxes, they make the place so much more civilised, and make the ED more pleasant (and less frightening for the patients).
4. Consistent teams!!
We are rota’d together in teams of 7 doctors. I know each individuals strengths, and interests so if someone has a thing for paediatric emergency medicine, or if someone is a proto-plastic surgeon and likes suturing, when it’s busy we can divvy up the tasks, swap patients and keep the department flowing. As I’m working with these people day in day out, I’ve got the incentive to train them well, and upskill them as much as possible, and they can teach me what they’ve learnt from their other placements. THIS SHOULD BE STANDARD IN EVERY DEPARTMENT.
5. An integrated IT system
The CDHB uses something called concerto which means I can look through old discharge summaries, clinic notes, ECGs, bloods, Xray reports, outpatient pharmacy prescribing (both what’s dispensed and what’s prescribed), and GP diagnoses. I can have a patients old ECG, and cardiology clinic letter printed out and by their bedside to compare to their new ECG before they arrive.
6. This is called a nitrous mixer.
It is great for procedural sedation and analgesia, as people don’t need to coordinate the ‘sucking-in’ from an on-demand valve during the painful bit. It’s useful for kids too.
7. This is called Topicaine Gel. It is awesome for wound analgesia (and haemostasis) for kids and adults.
8. Acute Demand (intergration with outpatient diagnostics and primary care)
Outpatient IVs? Outpatient Biliary USS? Home visits? Home GP Visit? If they can keep you out of an acute inpatient bed. They will move heaven and earth to do so. 24/7, just a phone call away (and present at morning and afternoon handover). This is all funded by the local health authority and saves them millions (patients love it too). Who follows these up? The patients own GP, if they don’t have a GP, Acute Demand’s GPs follow them up.
You’ve heard your consultants tell you that the ARCP isn’t about ‘passing’ or ‘failing’, that they aren’t looking to ‘catch you out’, but there is a lot of stuff to get ready, and it can often feel like the ARCP meeting is a bit of a grilling.
They key to passing the ED ARCP is preparation, from my limited understanding the Anaesthetic ARCP is like a group hug.
Your deanery will have hidden a document which has a list of ‘competencies’ you need to prove you’ve achieved. Get hold of this (it’s normally stuck on the deanery website somewhere). Look at it in the first few weeks of your placement.
You need to register with the college to access the eportfolio. This is expensive (£90 or thereabouts each year), but you can phone up and do it. The people at the college are pretty quick at doing this most of the time.
Now that you’ve got that document and the eportfolio you can capture assessments whenever the opportunity arises. Get assessments filled in as soon as you’ve done whatever it is you’ve been assessed on, the web forms take a few minutes to fill in.
I also annotate the document from the deanery whenever I got a CEX/CBD etc thats relevant, and I upload it to my portfolio as a guide.
It’s also good to keep a list of all of the interesting cases you see while you are just working normally. These cases should be used for CBDs.
Your ARCP assessors have to go through 30-40 of these eportfolios each year, the easier you make it for them, the easier it is for you to get an outcome 1. The other thing to do is to link assessments together, and link them to the curriculum part of the eportfolio. It’s important to do this as you go. If you are struggling to get access to cases that you need to ‘tick off’ then the earlier you can identify them, the earlier you can flag it with your supervisor and they can do something about it (cherry pick, simulate, or CBD it!).
So just to summarize:
Prepare, as soon as possible get eportfolio and ‘how to pass’ document.
Add things to your eportfolio as they happen
Link the heck out of things
Annotate your how to pass document with every piece of evidence you get.
Identify gaps early, and get help to fill them!
On ARCP day:
The dress code is ‘job interview’
Take a paper copy of your ‘how to pass document’, if the assessors have not been able to find things, and you can tell them exactly where your evidence is, you can snatch victory from the jaws of defeat.
Here is the document I made for my CT3 ARCP, – ARCP, make your own.