Past Teaching Sessions
This was a fantastic presentation from Dr Kiran Veera about how not to ignore the voice of something in your head saying you learnt something once and its telling you to be careful. Also another example of Emergency Medicine being the acute medicine specialists.... Learn about STE in aVR. Do you thrombolyse them (we say no because we understood the pathophysiology). Do you give them clopidogrel? (no...)
Click here for a dive into the DKA cerebral oedema literature and why delayed insulin therapy has been included in guidelines. And what is the good of guidelines anyway?
A couple of other links to articles below.
- Edge JA, Jakes RW, Roy Y, et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia. 2006;49:2002-2009.
- Hom J, Sinert R. Is fluid therapy associated with cerebral edema in children with diabetic ketoacidosis? Annals of Emergency Medicine 2008 52:1 69-75.
- Lawrence SE, Cummings EA, Gaboury I, et al. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005;146:688-692.
- Glaser N, Barnett P, McClaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344:264-269.
- Duck SC, Wyatt DT. Factors associated with brain herniation in the treatment of diabetic ketoacidosis. J Pediatr 1988;113:10-4.
- Rosenbloom A. Intracerebral crises during treatment of diabetic ketoacidosis. Diabetes Care 1990;13:22-33.
- White PC, Dickson BA. Low morbidity and mortality in children with diabetic ketoacidosis treated with isotonic fluids. J Paediatrics 2013 163(3): 761-6
There is a new post over at edcentral.net on breaking bad news in the ED. Click here to read it (it's good, I promise).
Mr Broughton Snell has established his plastic surgery practice in Bendigo and is operating at Bendigo Health as well as SJOG.
Click here for the first post to go straight to our new blog site edcentral.net.
EDCentral has grown and grown over the past few years and so has the level of academic engagement at Bendigo ED. Meanwhile, in the online world, the FOAM community (Free Open Access Meducation in case you missed it) has grown massively too.
We've decided to extend the reach of EDCentral into the FOAM world with the launch of edcentral.net/
This will be the new blog page of EDCentral. What started as a post we could put up the powerpoint slides of the week's teaching for people who missed the session has morphed over time and is gradually becoming more of a medical education blog. If we can keep up the momentum the new blog will be one more voice in the FOAM community.
A new and exciting innovation will be the abilty to comment on the posts. Please be mindful that your comments can be read by the ENTIRE world. If you wouldn't say it in a lift (or a supermarket queue) don't put it on a comment. But please do comment on the posts. It will be the engagement from you guys that will really make it worthwhile.
Keep an eye out on edcentral.net for some new posts coming soon.
Traumatic Cardiac Arrest
- Commotio cordis
- Medical arrest
- Traditionally seen as dismal
- In fact, overall survival is better than medical arrest
- In some series children do significantly better than adults (in contrast to medical arrest)
- Survival can be hard to estimate from the literature and it is important to distinguish between ROSC, survival to hospital discharge and neurologically intact (or at least acceptable) survival.
- Studies also vary greatly in their selection criteria. Patients in arrest on EMS arrival do differently from those who arrest on the way to hospital, on arrival at hospital or in the ED or theatre.
- Optimistic figures are about 50% ROSC and 5% neurologically intact survival. [1-4]
- Predictors of survival are also hard to tease out. Children do better in some series, perhaps because of stronger protoplasm. It is interesting that children do worse in medical cardiac arrests. In the medical cardiac arrest it is usually thought that kids do worse because the arrest is the end result of a long chain of insults rather than a single reversible cause (shock and hypoxia gradually leading to cerebro-circulatory collapse vs single vessel coronary occlusion in adults); probably paediatric survivors of traumatic cardiac arrest have arrested due to a single hyperacute and reversible insult (e.g. tension pneumothorax)
From whom is it reasonable to withhold resuscitation?
Poisition statement from 10 years ago from the American National Association of EMS Physicians and the American College of Surgeons Comittee on Trauma available here.
- Blunt trauma with apnoea, no pulse, no organised ECG on EMS arrival;
- Penetrating trauma with apnoea, no pulse, no “signs of life” (meaning spontaneous movement, organised ECG or pupil reaction) on EMS arrival
- Patients cut in half, with no head or with decomposition in process
- 15 minutes of resus without success or patients more than 15 minutes from hospital
- Special consideration given to situations like lightning strike, electrocution, drowning, hypothermia etc
The problem is that a lot of surviviors of traumatic cardiac arrest (13/14 in Seattle, 3/4 in Victoria, 13/36 in London HEMS) breach these guidelines with the "15 minute rules" the most problematic.[2, 3, 5].
Who can be expected to do “well”?
Mechanism of injury
Traditional teaching is that blunt trauma all do poorly and that penetrating trauma cases do better. In fact, the data can be examined in more detail. Stab wounds do best (especially single stab wounds), blunt trauma comes next, handguns are next and rifles/high velocity weapons do worst.
Medical cardiac arrest occuring during trauma (the coronary artery disease patient who has an AMI and arrest with the stress of trauma) do well
Commotio cordis 15 % survival and 25% if resus intitiated within 3 minutes
Asphyxia (isolated laryngeal injury, conflagration, high spinal injury)
Obstructive (tension pneumothorax or massive haemothorax due to isolated chest injury)
Cardiac tamponade (only if thoractomy performed promptly after arrest)
Who can be expected to do badly?
Isolated head injuries with cardiac arrest all die.
Hypovolameic traumatic cardiac arrests all die except for anectodes and case reports.
Practical approach to traumatic cardiac arrest
Aggressive approach seems justified
- Consider medical cause if trauma seems minimal
- Intubate early
- Doubles the period of tolerated CPR
- Intubate early
- HYPERVENTILATION KILLS
- You only need to oxygenate the patient
- Remember that PPV drops venous return dramatically in the hypovolaemic patient.
- Bilateral thoracostomies are probably highest yield procedures
- HYPERVENTILATION KILLS
- CPR remains the standard of care but has much less to offer than in medical arrest
- Stop bleeding
- Pressure, splint limbs, staple scalp, bind pelvis
- Fluid resuscitation (blood as early as possible) is likely to be valuable
- Remember permissive hypotension if ROSC is acheived
- Clam shell or left anterior thoracotomy
- Some high volume centres use pericardiocentesis however most authorities recommend thoracotmy. Evidence is lacking to settle the argument. In the low volume centre where this is a once or twice a career experience it will come down to the comfort level and skill set of the operator.
- Wondering how to do it? See this poster from the American College of Surgeons
A short (5 minutes) white-board video here outlines the way I like to arrange my team for reception of a peri-arrest trauma patient.
1. Leis, C.C., et al., Traumatic cardiac arrest: should advanced life support be initiated? The Journal Of Trauma And Acute Care Surgery, 2013. 74(2): p. 634-638.
2. Lockey, D., K. Crewdson, and G. Davies, Traumatic cardiac arrest: who are the survivors? Ann Emerg Med, 2006. 48(3): p. 240-4.
3. Pickens, J.J., M.K. Copass, and E.M. Bulger, Trauma patients receiving CPR: predictors of survival. J Trauma, 2005. 58(5): p. 951-8.
4. Jeschke, M.G., D.N. Herndon, and R.E. Barrow, Long-term outcomes of burned children after in-hospital cardiac arrest. Crit Care Med, 2000. 28(2): p. 517-20.
5. Willis, C.D., et al., Cardiopulmonary resuscitation after traumatic cardiac arrest is not always futile. Injury, 2006. 37(5): p. 448-54.
This article from BMJ way back in 1994 is a wonderful illustration of the role of random chance when attempting to demonstrate cause and effect (i.e. trying to prove that a teatment works for example) and the way in which the meta-analysis can amplify rather than diminish error introduced by random chance. Thanks to Brendan Whiting for digging up this one.
Phillip Visser presents Atrial Fibrillation and evidenced based management of this condition in the ED. The push to rationalise management of this condition is through another ECIICN inititive.
Download The talk
Some accompanying articles for the talk
And here (for registered users) is the new Bendigo ED rapid AF pathway.
The Anaesthetic Rotation From ED
Below are some thoughts and experiences that might be helpful to kick you off on Anaesthetic rotation at Bendigo Hospital.
Technically, being a person in involved to provision of anaesthesia you would be required to do equipment checks before each list. Below is the link to the ANZCA website where the equipment checks are described. You would only need to do Level II and III checks. The list looks a bit long, but it is really simple and the whole Level II check takes 3-5min at the most, it is fun and makes you more comfortable with equipment. The anaesthetists or the techs will be able to help you with the orientation around the anaesthesia machine.
Below is a tabled equivalent from the UK society of anaesthetists. It is shorter, but equally covers the main points.
Gas supplies and suction
There are three major shifts during the week:
07:30 – 17:30
13:00 – 23:00
22:30 – 08:00
On weekends the shifts are:
07:30 – 20:00
20:00 – 08:00
The daily stuff
The best way to find out what you are doing on the day is to refer to the roster – find your slot with anaesthetist and which theatre you are assigned to on the day. The theatres usually change after lunch (i.e. if you are doing OBGYN in the morning you will usually do something else after lunch e.g., Trauma). You can then quickly see the list of patients for your session. You can either quickly go on the wards to check whether the patients have been seen and whether anything additional is required before the case starts. The alternative is to check your list for the next day and quickly see your patients the day before. This strategy is unlikely to work if you are on Emergency or Trauma list the next day as the list usually fills up on the day. Also generally it is quite busy and you have very little time to slot in extra things.
Tip: To have the list printed – bring up your theatre list and press F2. This will print out the list.
If you are on the endoscopy list – you will need to see the patients from the list in the day surgery reception (second floor, next door to cafeteria) before the list starts (this can be fun as there are some nine patients that will need to be seen in the space of an hour), plus you will need to set up the theatre for the list i.e. drugs etc. The consultant often will help you – to see the patients, draw drugs etc. This is a fun list - very fast and interesting. Most consultants have their ways of providing sedation for endoscopies (from bare bone Propofol to LMA, to TIVA); you will get the chance to see and feel different drugs at play and perhaps choose your way of providing procedural sedation. You will also hone the skill of monitoring your patients during procedural sedation using ETCO2 and without ETCO2 (i.e., during FGS).
When you are on the emergency list – you will have the phone and every man and his dog will phone you for all sorts of problems – pain management, cannulation requests, epidurals etc. In the case of the request for cannulation – the requirement is that HMO/Intern and Registrar on the requesting unit must try cannulation before they call you. Either of them also must be present at the scene and you must “teach” them how to cannulate (this may involve them inserting the cannula in your presence (this is a bit odd, but this is essentially how Dr Ryley would like the service to be provided as BHCG is a teaching hospital and the anaestheic service is not just there to run around sticking cannulas in willy nilly). You will also have to attend all Code Blues and trauma in ED (Level 1 and 2) when you are on emergency list.
In the case of the request for epidural – ED regs usually are not supposed to insert epidurals, so you will need to speak with an Anaesthetic reg in training (via consultant) and get them to do the job (this usually is not a problem and often the consultant just goes and puts it in – no problems with that – no pucker faces there). It is different with spinal blocks/anaesthesia and the consultants usually will be happy for you to do those. Especially once they see that you know what you are doing.
When you are on the night shift – you are essentially the point of contact for all the troubles in the hospital overnight which may require your service – cannulations, pain issues, Code Blue, trauma and assistance with airways in ED. Generally consultants would like to know of major happenings overnight - airways, trauma level 1 etc. unless they advised you otherwise. In the case of epidural – you still need to phone them. If there is an emergency case that needs to be done there and then – the requesting registrar (surg/ortho/OBGYN) will let the after-hours coordinator know and they will organise the theatre nursing staff call back). Your responsibility is to contact your consultant once it is clear the case is imminent (e.g., CS, trauma etc.).
If you are rostered to work on weekend – you will have to do the pain round and technically see the patients booked for the cases overnight or hang-ups from the day before. This sometimes can be quite daunting, especially if there are a few epidurals on the wards, pain issues, tap catheters and general chaos etc. (That usually does not happen often). If there are tap blocks in ICU (topping up TAP catheters) – their doctors usually can do those, but with the wards – it is your chore.
BITS and BOBS
Do not think: “oh, I will never use this or that in my practice as ED doctor why do I need to do this”. Your attitude is important. Do not be a passenger in this rotation. You want to be at least an equal player to the anaesthetic registrars.
Ensure that, as you prepare induce a patient, provide sedation for FGC, FCS or ANY minor procedure you ALWAYS have ALL monitoring equipment on and attached to the patient (ECG – on and on the patient, sat probe – on and on the patient, BP cuff on and on the patient. ECO2 on and there is trace). ALWAYS. REGARDLESS who you work with. Do not rely on the anaesthetic technicians to have it all set up – they have their hands full. Trust no one, even yourself. Stick to the rules and standards.
For induction it often helps if you ask the anaesthetist what drugs they want prepared for induction and use in the case e.g., Fentanyl, Midazolam, Morphine etc. This helps to smooth the flow.
Think in advance about the case you about to embark on: what mode of anaesthesia you are going to use (e.g., LMA/ETT, GA, spinal, epidural regional etc.), what mode ventilation you are going to use, which gas, what drugs are you going to give to the patient before the case (e.g. antibiotics, antiemetics), when are you going to give the drugs. Entertain a WHAT IF scenario and have plan. Always have at least Plan B. Have plan for can’t intubate situation. When the gig is up – your ability to think critically shrinks. Make sure that you are familiar and comfortable with DAS protocols and guidelines:
Majority of patients get additional drugs during the case for nausea and vomiting post op (Dexamethasone, Ondansetron) as well as simple analgesia (Paracetamol, Parecoxib). Most orthopaedic and surgical patients will have antibiotics IV prior to the case. It is a good habit to ask the surgeons whether they want the antibiotics given or not, they often won’t tell you unless you ask (bizarrely).
For patients who will have PCA, Epidural and TAP catheters post op as well as paravertebral catheters – there is a special form that needs to be filled out along with an “audit form” (for APS follow up the next day). The drugs are usually standard (Naropin, Fentanyl, Morphine). They have standard rates and doses of administration and dilution. You will be fine after a couple of cases. Often the forms are prepared during the case and the recovery nurses set the pumps and have them ready for action. You task is just to prepare the form and pass it to the recovery nurses. There are also a couple of other minor details with regard to paper work for post op pain management – you will get info on that on the job – they are just a technicality.
Know the principles of the anaesthesia machine and are comfortable operating controls. This will save your butt and make your comfortable during cases. Know the volatile gases (BHCG uses Sevoflurane and Desoflurane). Be comfortable with ventilation modes. The modes that are used are:
- Volume Control
- Pressure Control
- Pressure Support
Once you are comfortable with the modes – life is a joy.
One piece of advice during a case: Ensure that all monitoring and adjuncts ALWAYS run underneath the airway tubing. NOTHING sits on top or runs over the airway lines. Make sure you NEVER step over airway lines if you need to get to the other side of the table/patient. Even in emergency. NEVER. It is a taboo. May sound a bit bizarre, but losing airway mid-case is the last thing you want to happen to your patient.
Among the muscle relaxants the most commonly used in the theatre at BHCG are:
Ensure that you are familiar with these drugs, onset, and duration of action, features of metabolism and reversal practices.
At BHCG, for reversal, most anaesthetists will use Neostigmine 2.5mg and Glycopyrrolate 400mcg at the end of the case (but other guidelines include Neo 0.04-0.08mg/kg + GP 0.2mg/1ng AChEI).
There are a number of “emergency” drugs that might be used during a case:
- Ketamine (not really an emergency drug)
- Morphine (ditto Ketamine)
There are useful dilutions below:
This is how most anaesthetists have those drugs prepared.
For a paediatric case – it is best if you have rescue drugs set aside (i.e. Atropine, Metaraminol, Suxamethonium).
For spinal anaesthesia – have Metaraminol at the ready as commonly patients drop the blood pressure within minutes post injection. With chronologically gifted patients be more proactive with the hypotension and careful with how you use Propofol. Anaesthetists would usually give Metaraminol when sBP decreases to 100mmHg in an elderly patient.
Occasionally you will be assigned to Pain Round. Jenny Furness is the APS nurse. You will work with the Pain round consultant and Jenny to do the pain round. Sometimes it will be just you and Jenny, so you will need to make some decisions. If in doubt – phone your consultant for advice. Below is the link on the evidence based management of acute pain brochure on the ANZCA website:
This will get you started on the topic.
Once in a blue moon you will wind up in the Anaesthetic Preadmission Clinic where you will see the patients prior to elective surgeries. Not much fun, but important part of the service, although not necessarily the type of activity you will be involved in as an ED doctor. This is on the ground floor in the outpatients department.
For all trouble in the recovery – once the patient is awake and here are no anaesthesia related complications – the home team registrar should be involved in taking care of the patient. As in if a patient has developed rhythm abnormality and medical consult is required - the home team registrar usually arranges the medical consult.
Be careful with emergency scope cases for GIT bleeding. Every now and then the patients are badly anaemic (the lowest Hb I have seen was 63, this young man would arrest from just looking at Propofol) and there is no blood prepared or cross matched. Beware when asked to arrange anaesthesia for an urgent case. The patient who is septic or hypovolaemic with pH 7.01 and sBP ~90-100 who needs to be resuscitated before induction if you want to see them awake after they are “fixed”. Make sure you check all electrolytes and other biochemistry before you say yes sir. Any problems with resuscitation before surgery – communicate with your consultant, involve ICU and make it someone else’s problem before you undertake full responsibility.
I have been told that the guys in anaesthetics like ED registrars on the whole as we do not bum around – if there is a problem – we go and fix it without requests and reminders, we know how to do things, can do things and are able to function independently.
Overall it is a great rotation, busy, fun and rewarding – a lot to learn and it is your attitude that will shape this rotation for you. Good luck.
We had a big day of fever in the returned traveller today.
Harpreet presented on Malaria and his presentation is attached here. Make sure you watch these fantastic youtube vids on the lifecycle of the parasite in the mosquito and in the human. There is no excuse for people not to know EVERYTHING these days, there is such amazing educational stuff out there.
Tom Brough followed up with Typhoid. His presentation is here.
Finally Alex Archer gave us Dengue, Japanese B encephalitis and Yellow Fever but she hasn't given me the slides to post- Bad Doctor!
There are a few important things to consider when managing a suspected (i.e. clinical suspicion but no Xray evidence) scaphoid fracture.
- Scaphoid fractures can be X-ray negative
- Scaphoid fractures can lead to avascular necrosis and chronic wrist immobility and pain
- X-ray negative scaphoid fractures might be amongst those that have a bad outcome
- Immobilising these in plaster of some sort might make a difference to the rates of those bad outcomes
- Wearing plaster for 10 days is a real pain in the neck, especially if you work with you hands, have both of them in plaster or have others to care for.
For these reasons please:
- Make a proper clinical assessment of the chance of an occult scaphoid fracture
This means the patient having a meaningful mechanism of injury (true FOOSH with wrist extended), tenderness in the snuff box and on the tubercle of the scaphoid at the proximal end of the thenar eminence, pain on axial loading of the scaphoid along the 1st metacarpal, and reduction in grip strength or increased pain when gripping. Also the patient should have some hand function to save.
- Always use a removable thumb spica slab rather than a full cast for the X-ray negative possible scaphoid fracture
They didn't manage to displace the fracture with the injury, why would the displace it now? The slab provides a reminder to be sensible and some comfort. Remember that good advice about avoiding further injury is more important than the slab (stay off the skateboard until fracture is ruled out).
- Consider whether early diagnosis today or tomorrow with CT or MRI is worth the money and resource use.
In a publicly funded health care system the question is always, can we justify the cost of advanced imaging for all these patients. This is compounded by the problem of different departments all trying to shift costs to one another. "Why sould ED pay for that test? Let them go to fracture clinic and they can pay for it" and so on and so on. From a community perspective you might like to consider the cost of the clinic appointment, the cost of having a manual labourer or personal carer in plaster for 10 days unable to do their job, the overloading of your fracture clinic and so on. It may help to put together a guideline for advanced imaging that lays out clinical and other indicators for CT/MRI that prevent every sore wrist being sent for an expensive test. In a private setting the you can ask the patient. A self employed builder will much rather pay for a CT/MR today or tomorrow than be off tools for 10 days.
- If you are opting for traditional management with immobilisation and fracture clinic ensure that follow up X-rays are taken out of plaster.
As to which advanced imaging test to employ, bone scan is pretty hopeless and doesn't differentiate between bone oedema, fracture and ligamenous injury. It just tells you something is going on which you could have told by poking the patient. CT and MR are pretty close. MR shows more detail of the non-fracture injuries which may be useful for the high level sportsperson who is going to have some specially tailored physiotherapy intervention for every ligament sprain. CT is often quicker to get (although an MRI wrist is a pretty quick easy scan). They are close enough together in sensitivity and specificity to justify choosing a test based on availability, time of day and patient factors (MRI for kids and pregnant women for example and CT for the others).
Big thanks to Lev Veniaminov who offered the following comments on this concept when I sent him a copy of George Douros' (Austin Health FACEM) airway checklist card. This post is packed with links for the airway obsessed reader.
The first thing that struck me when I started the anaesthetic rotation was how anaesthetists approach airway, regardless of gender, experience, amount of intestinal fortitude and size of ego.
There always is heightened sense and awareness of disaster lurking around the corner when it comes to airway. EVERY intubation comes with consideration of possible ways, presence of airway adjuncts ready to go. Even in elective cases.
If there is a slightest hint of possible difficult ETT a plan is always discussed should things go out of quilter. Even if it is just "not able to pass the ETT on the first go"... in an uncomplicated AW...
There is interesting podcast on EMCrit.org (EMCrit 49, "amateurs discuss strategy; experts discuss logistics") where Scott talks about approaching various situations... This can be easily applied to AW management.
There also is a very interesting article in BJA in a way echoing this podcast:
It can be accessed through your www.clinicians.vic.gov.au access via OpenAthens
This guy, Tim Cook is like Elvis Presley on the anaesthesia circuit and is heavily involved in NAP works (NAP 4 talks about AW disasters in EM too)...
The Difficult Airway Society (DAS) also offer airway mangagment algorithms that should be a part of the paintwork design of every resus cubicle in ED...
Also of interest is the podcast of Scott with Cliff Reid (he is a retrieval specialist in NSW and with HEMS in UK) on retrievals where Cliff mentions how they approach EVERY intubation. Meticulously planned ETT, stereotypically planned and set up as a result, he mentioned - in the five years of running the protocol they had ZERO failure rate.
Just to add to the importance of having a card like that...
...Oncologist Dr Mark Warren presented on febrile neutropenia and other ocological emergency discussions. Download the presentation here
...Paediatrician Andrew Lovett from Bendigo and Echuca presented on paediatric gastroenteritis. Download the presentation here
Thanks to all these wonderful visitors who have given their time and knowledge to us over the year.
This time we have a believer, Dr Bruce Campbell, consultant neurologist who spoke on stroke and stroke mimics. His powerpoint presentation is here click here.
I missed this talk but the slides look really good. I am going to read it in the next few days and give a potted summary here but in the meantime just download it yourself and have a look!
A talk that I did on childhood stroke needs editing to remove a potenially identifiable case before i post it. Childhood stroke is not terribly common but terribly devestating when it happens.
If there is one thing to take away from the paediatric strokes i have been involved in caring for is to recognise that it occurs so that these poor kids and families don't have the indignity of being told that the symptoms are not real, just because you didn't realise that kids could get strokes. The sad truth is that there is little that can be done for these patients acutely to change their outcome and most of the benefit we can offer them is in the paediatric neurology and rehab ward so good emergency care is about diagnosis, excluding the small number of cases where you can make an acute difference and making sure that these families feel cared for.
Remember that most of what you learn in med school is wrong a few years later but making people feel properly cared for has been right since Hippocarates.
Ben McKenzie went up to Swan Hill to have a discussion about pain relief in the ED. It was an excellent opportunity to talk about acute pain but also have an extended meeting to talk about tid bits arising about more general emergency medicine topics from subarrachnoid haemorrhage to burns dressings.
Click Here to download the presentation
Click here for the NHMRC acute pain manual for emergency departments in Australia - Easy to read, engaging and practical!!! - It is an excellent resource!
A comprehensive approach to the liver disease patient in the ED by Bendigo ED Registrar Dr Alex Archer
A couple of weeks back Dr Hamed Akhlagi, Advanced Trainee in EM, presented a talk on local anaesthetics with a focus on pharmacology and toxicology. Click here for the pdf of the powerpoint presentation.
Risk Stratification in the Real World
Anne-Maree Kelly from Western Health in Melbourne has examined over 700 patients with potentially cardiac chest pain in this paper published in the June issue of Emergency Medicine Australasia. Although the author's main conclusion appears to be that the NHF guidelines are somewhat of a failure in the real world, I think the study goes a long way to clear a lot of the fog around the issue of risk stratifying a chest pain patient.
In case you are unfamiliar with them, the NHF has a well publicised set of criteria for separating patients into high, intermediate and low risk when they present with chest pain. They are available here in a groovy wall poster (just to the right of middle).
High risk patients have one of the following characteristics: a really good story (repetitive or prolonged pain), a suspicious ECG (new T inv, ST depression or non-reperfusable ST elevation), positive Trop or CK-MB, sustained VT, haemodynamic compromise or new MR, syncope, LFEF<40%, PCI in last 6 months or CABG ever, DM with typical ACS symptoms or eGFR <60 with typical ACS symptoms.
Intermediate risk patients have a good story but a late presentation, are over 65, have known IHD, have 2 or more risk factors for IHD, have diabetes or renal impairment with atypical symptoms or are already on aspirin.
Low risk patients are everyone else (i.e. people who ought to have gone to their GP, lost some weight or stopped smoking so much).
The guidelines recommend putting all the high risk patients into CCU, on aggressive anticoagulation (subject to bleeding risk) and on a pathway to angiogram as an inpatient. The intermediates are supposed to get serial enzymes and a negative stress test before discharge and the low risk patients get discharged after a respectable period of observation and have urgent cardiology follow up.
Cough- splutter- choke!
If that is your response to the above then you have probably been working in emergency medicine in Australia for a while. Let's look at some of those recommedations in detail.
First the easy one: low risk patients. These are people who have lost some exercise tolerance on their stable angina or who come and tell you that they had some exertional chest pain 2 weeks ago. Picture these patients. They are actually a pretty broad group (which highlights the limitations of these attempt to break down into dot points the subtle art of medicine). some of these people you are going to want to send urgently to a cardiologist. The 50 year old who says they have had a month of new exertional chest pain that they have managed by curtailing their activity or the person who has been watched for a while with <50% stenoses who has gone from waling up hills to taking it slowly along the flat in the last month and has finally been dragged in by their partner certainly warrant a phone call to the cardiologists rooms to tee up an early review. The rest though, are going back to their GP in my town, so they can coordinate assessment of BP, lipids and lifestyle factors, stress ECG if appropriate and cardiologist referral.
Next, the high risk patients. Now I have no problem with putting people with dynamic ECG changes, positive biomarkers, ventricular tachycardia or cardiogenic shock into CCU or HDU. However, a history of DM or CKD and a good story might get you a telem bed in my hospital and there is every chance that we will monitor you in the ED SSOU for a 6 hour troponin and discharge you for outpatient provocative testing (besides, how dye happy do you want to be with people who have an eGFR<60 or Diabetes?). The fact that you have chronic heart failure or have, at some stage, had the plumbers in, doesn't impress me terribly much in the chest pain workup although it makes me more likely to send them to a cardiologist on discharge rather than back to their GP. Finally, syncope is important with chest pain but it makes me think of PE and dissection more than ACS.
As for the intermediate patients, I have never known what to do with these and most of them get a 6 hour troponin in SSOU and go back to the GP, perhaps with an outpatient provocative study arranged by me before they go.
And so for the good news
Well the great news in fact from from Kelly's paper in EMA is that for a start you can more or less forget about the intermediate risk patient. They just don't exist. Out of a total of 768 patients, 1/62 low risk patients went home with a discharge diagnosis of unstable angina and none had an MI or a MACE ("bad outcome" - see below), 1 out of 254 intermediate risk patients got revascularised during the follow-up period and all the rest of the MIs and MACEs were in the high risk patients. That means the high risk criteria were within a hair's breadth of 100% sensitive for the outcomes of interest. On the down side they were only about 50% specific so half the patients you "admit to CCU" have no need to be there (whether the other 50% actually needed to be there either is a whole other question, I think they probably don't for the most part we are not quite there yet). This certainly validates current Australian practice of making good use of SSOU and early outpatient provocative testing and reserving CCU for people who are actually requiring close watching.
What is a MACE?
MACE is a term that you come across a lot in chest pain and ischaemic cardiac disease literature. It stands for Major Adverse Cardiac Event and has become a standard composite end point for cardiology studies. It includes death, cardiac arrest, cardiogenic shock, arrhythmia, revascularisation and MI. It is a term to be very wary of. Remember that MI these days is not what it was 20 years ago. When a patient hears "heart attack" they figure something pretty awful happened to their heart. In fact, MI means a troponin became positive. A troponin of 0.5ng/mL from some inferior ischaemia is not actually in the same ballpark as death or cardiogenic shock. In fact we know that a lot of positive troponins have nothing to do with IHD, especially in a population that includes CKD patients. At most, small troponin leaks mean the patient is a bit more likely to have IHD than we thought and they probably warrant up-triaging toward an angiogram. Revascularisation is worth being a little suspicious of too. If it isn't corrected for insurance status I am not sure what it really means as a statistic. Basically it means a cardiologist thought that some plumbing might be beneficial. Once again, not in the ballpark with death or cardiogenic shock.
It is interesting to note in this study that of the 452 high risk patients, about half went home with a diagnosis of either MI or Unstable Angina, 85 had a troponin leak during the follow-up period, 7 were revscularised and 1 had an arrhythmia.
It is also worth noting that almost all the MACEs occured in the first 7 days after discharged (patients were followed up at 7 and 30 days) so early follow up means early.
What I take from this is that what we do now is about right in terms of safety but it could be a lot more efficient. I am reassured that I can stop feeling uneasy about pretending that the intermediate risk group don't exist as a separate entitiy from the low risk group because for my purposes they pretty much don't (not to say that these factors won't weigh in to the decision making that occurs at follow-up, they just aren't going to make a major impact on ED decision making). I am pleased to see that even high risk only means 50% sensitive and that SSOU pathways are therefore probably valid for selected high risk patients.
This week Chandima Panditharathna gave us a presentation on TCA overdose and touched on Questiapine also. It was a great talk but he was up against stiff competition from LITFL and for the sake of time I am going to just link to this fantastic post from them rather than summarising Chandima's talk. Honestly, if you read this post you neen't bother opening a textbook on the topic.
The only thing I can add is to stress that this is one situation where you should have a very low threshold for taking control of the situation early with sedation and intubation. It is a lot easier to administer Bicarb to a patient who is ironed out and ventilated than one who is fitting on the floor, or worse, one who is fitting below a pile of security guards. Remember that these patients frequently oscillate between periods of deep sedation and periods of agitated delirium in which they are seeing frightening things and are very excitable. This is a really unhelpful thing in someone who is heading towards malignant tachyarrthythmias and metabolic acidosis.
And remember also that like all tox cases, cardiac arrest is bad but can have excellent outcomes despite very prolonged CPR. I am not overly positive about the whole CPR thing in general but in the case of a toxicological cardiac arrest, the heart is otherwise healthy and the insult is completely reversible; this is one of the few situations where I would argue for truly prolonged resuscitation while oxygenation, fluid status and pH are all optimised. When all else fails you might even like to try intralipid.
For Quetiapine, see my entry from a few weeks ago.
Just in case you wondered why you were tired at the end of 10 hours.
A paper by Rongsheng Kee and Johnathon Knott at the Royal Melbourne Hospital in the June issue of Emergency Medicine Australasia (EMA (2012) 24, 294-302) has described the workload of an Australian Emergency Physician. Table 1 is worth showing your partner so they can understand why you are less than talkative when they ring you at work. In case you don't have access, the gist is this.
As a duty consultant (in charge role) in every hour of the shift you will do the following:
Have 13 conversations with other doctors and the same with nurses, make or take 4 phone calls, talk to a patient's family and have around 6 conversations with other staff including police, ambos, clerical staff and students;
Walk 19 times between the different spots that you work in;
Review 5 patients, look at 6 files, use the EDIS system 10 times, use path and xray computer systems a couple of times each, look up some sort of medical reference perhaps once and make 6 medical record entries;
You will also occasionally write a sick note or prescription or discharge letter;
Once every few hours you will snack while working, and you'll have a drink on the floor about once an hour (scotch?); you will go to the bathroom once every 10 hours, go for a meal once in 10 hours and on one other occasion in that time-frame you will sneak away for an "unspecified" purpose (quick dose of ECT from the broken defib machine in the storeroom?);
It is not all bad news though. You will spend 24 seconds an hour on average in "quiet contemplation". I am comforted by that.
Lets get this bit over and done with quicksmart.
TXA is a synthetic derivative of the amino acid lysine.It says so in the CRASH 2 paper. Now plasminogen has lysine binding sites on it that allow it to be activated to plasmin so it can get down to the business of busting up clots and saving stroke patients and making people bleed to death and such. TXA competes for these binding sites preventing activation of plasminogen. So this means it is an antifibrinolytic.
Because the coagulation cascade is an incredibly complex system the precise effect of this on the patient will depend on a whole heap of stuff but in essence it acts to stop clot breakdown.
Oral bioavailability is about 40%, it is distributed in all compartments and filtered at the glomerulus, elimination is via the kidney with a half life of about 4 hours (although effect half life is much longer at about 80 hours) and it is excreted in very small quantities in breast milk (Nillson, J Clin Pathol, 33, Suppl (Roy Coll Path), 14, 41-47).
CRASH 2. What's all the fuss?
What did they do?
20,000 odd patients who were within 8 hours of trauma and whose doctors were considering transfusing got 1g of TXA stat and 1g over 8 hours or placebo. Only a handful of patients needed to be excluded from analysis (either because the withdrew consent after randomisation or it turned out they never met the inclusion criteria in the first place).
Primary outcome was all cause mortality at 4 weeks
They also pre-defined some subgroups that they thought might be meaningful. This offers them more validity than the fishing expedition that is the post hoc subgroup analysis however they are still only subgroups and if anyone can explain to me the difference between these and secondary endpoints I will be very grateful. They divided into death due to bleeding, vascular occlusion (AMI, stroke, PE), multi-organ failure, head injury and other and they divided the patients on the basis of some baseline characteristics (time since injury < 1hr, 1-3hr, 3-8hr; sBP <76, 76-89, >89; GCS 3-8, 9-12 and 12-15; and penetrating vs blunt trauma).There were some actual secondary outcome measures too but these weren't too interesting.
What did they find?
The TXA group had a death rate fo 14.5% and the placebo group, 16%. That means a 9% relative risk reduction, a 1.5% absolute risk reduction and a number needed to treat of 67. Because the trial was huge the result is statistically significant.
The results were best in the people who were sicker (you would struggle to improve mortality in a group of people who were not going to die anyway) and in the people treated in the first hour. in his interview with Scott Weingatt on emcrit.org CRASH 2 investigator, Dr Tim Coats, opined that in the first hours there was the most to gain, that the impact of TXA on the clotting system may be different early vs. late and that early on after trauma people tend to be anticoagulated while later they tend to get more "sticky" (which would fit with clinical experience of smashed up trauma patients being oozy in resus and theatre but getting DVT/PE in the coming days).
What is more, they found that while there was a statistically significant decrease in bleeding deaths there was a trend toward a decrease in vascular occlusion deaths as well.
And the drug costs about $10-$100 per treatment depending on where you are so you can save a life for as little as $670.
What could possibly be wrong with this?
First of all I am bothered by a drug that is great for stopping bleeding but which also probably stops clotting, which has no side effects, and which has the same dose for every patient no matter how big or small or sick or well or complex or simple. To me that sounds like naturopathy and I can't help but be suspicious that the trial has failed to show the full picture. That is not a reason to discount the findings of the trial but I think that when something sounds too good to be true it often is so you had better tread carefully.
Second, I am not totally sure how to relate findings in trauma patients from the countries in which the trial was conducted to patients from Victoria, Australia where we have 5 helicopters covering a quarter of a million square kilometers with 3/4 of the population living in major cities and most of the rest clustered around some major towns, where early access to excellent first aid, rapid transport and decent trauma care is the norm and where that care is likely to involve early access to surgical interventions whenever required. It would be interesting to see which areas got the best results in the trial and whether the bulk of the benefit was not seen in places where people suffer delayed response from a disorganised ambulance service and then there is no organised trauma systerm. Below is a chart I have made demonstrating where the patients were recruited from (the data is sourced from the acknowledgements section of the original paper).
So Who is Excited About It?
The early adopters amongst us certainly are. Scott Weingart is all over it. He is even talking about giving aminocaproic acid (a similar substance whcih is more available in the US) to his SAH patients (although why you don't just get on a clip/coil the damn aneurysm I don't know). Minh Le Cong of RFDS Cairns is looking at pre-hospital use.
So Who Isn't?
Well The Alfred Emergency and Trauma Centre here in Victoria are not using it yet for this indication (although I have heard a rumour that it is going to become part of their massive transfusion protocol). Sceptics like Jerry Hoffman aren't too impressed.
What Am I Going to Do?
Well, I'm sceptical. I suspect there is likely to be little harm if we give the drug early, before hypercoagulability become a problem. It is cheap and generic so it is not a huge burden on the system. It is a huge study of really sick patients which is never likely to be repeated. If I am ever working in the third world I will be looking to see where the TXA is kept. If I get a nasty trauma case in Bendigo where immediate surgical attention is not going to be possible (say a bleeding pelvic fracture that our surgeons are reluctant to mess with) then I'll most likely give it before the patient gets loaded on the helicopter. If my organisation decides that it should be part of our massive transfusion regimen for trauma patients then I won't grumble. But to be honest, I think there are higher priorities in trauma care where I am than this.
I also think you should watch out for the fancy, expensive, 1g minijet version of TXA.
And you should really watch out for it on the ACEM exams in the coming year or so!
The gist of my approach to epistaxis is this:
If the patient is bleeding the first thing to do is to stop it. Get the patient to apply first aid (which means holding their nose firmly as far back on the vestibule as possible- you will need to show them as they will invariably jsut be poking and mopping at their nostril openings with a tissue or spitting noisilly into a bowl). Then get yourself set up for cautery and/or pack (see below).
If the patient is not bleeding but the bleeding nose was enough to bring them to hospital then it will bleed again soon enough. Set up for cautery/pack anyway. This is in adults. Kids get bleeing noses a lot once they learn to get their fingers up there but they don't usually come to hospital for it as someone jsut tells them to keep their finger out for a while and it settles down.
My approach to cautery/packing of the non-bleeding patient is the same as the bleeding one because once you start the bleeding will often start up again too.
Make sure you have a good light source (head lamp is best) and a nasal spec. Have suction, an em-bag and some tissues handy and get a gown for you and put a sheet or bluey over the patient's chest. Warn the patient that you will need to be cruel to be kind and that you will do what needs to be done as quickly and comfortably as you can but that it might be a bit unpleasant. Tell them that you are going to ignore them if they grimace or make unhappy noises but that if they need you to stop they must just say "stop" and you will do so. If your patient knows they have a "safe word" they will tolerate a lot more. Have the patient blow their nose properly once to get the big jellied clots out of the way. Spray the nose, then unroll a cotton wool ball and soak it in cophenylcaine and put it up each nostril while you set up everything else (pack, AgNO3 sticks, lamp, blunt forceps).
Getting a view:
Pull out the cotton wool and suction out clot int he nose. Wrap a little cotton wool around the end of your forceps and soak it in local and then use this to further toilet the nose. This is also useful for applying direct pressure after cautery. Only once the nose is clean can you get access to Little's area for cautery or even confirm a bleeding point.
Roll the end of a AgNO3 stick over Little's area. I once thought you just held it in the middle of the bleeding spot like a spot welder. What this does is digs a nice deep hole that bleeds like mad around the edges. By rolling it over the surface you can cauterise the capillary network that is feeding Little's area.
Wait a moment for the reaction to occur and then apply some direct pressure with your co-phenylcaine soaked cotton wool on the end of your forceps. this will help stop the early bleeing you sometimes get after cautery.
Always apply some vaseline or chlorsig ointment after cautery and have the patient sit quietly for an hour or so. It is quite reasonable to use SSOU for post-procedure observation in case of early re-bleed. If there is no re-bleed the patietn can be discharged with some ointment and a decongestant spray. Re-bleeding means a pack.
If there is a rebleed or if the bleeding is too much and you can't manage to cauterise (although if you take a stepwise approach like I have outlined above this will usually not be the case with anterior bleeds) or if it is a posterior bleed you will need a pack. Be familiar with what you have in your ED but try to make sure it is not Bipp gauze as this is about 20 years out of date. Merocel tampons are ok but pretty nasty. Rapid Rhino is amazing but pricey. Just follow the instructions in the packet. They even make a long one for posterior bleeds. NEVER use plain ribbon gauze- the blood sets like concrete and it may take surgery to remove it.
Adjuncts in difficult cases:
Reverse the warfarin. This is a common culprit and it may need to be switched off for a day or so with some prothrombinex.
Replace platelets. This is usually only an issue in patients with myelodysplastic disorders.
Lower the BP. IV morphine is a great drug in this situation. It eases the pain of what you are doing to the patient, it eases their anxiety and it drops their (often very high) BP so the bleeding can stop.
Inject some local with adrenaline into the greater palatine foramen (just medial to the 3rd molar in the roof of the mouth toward the back of the hard palate). Seriously! You can find it easily enough with a bent 25G needle. Topicalise the roof of the mouth with some cophenylcaine and then raise a bleb of local under the mucosa so you can poke around and find the hole. When you do, avaoid an intraterial injection by aspirating first and then inject. The bloodflow is from nose to mouth so you need to get up into the foramen to have a good effect as you want to contrict the arterioles coming off the artery in the floor of the nose. When they are soaking though the packs and nothing seems to work this has never failed me.
Don't forget the rest of the patient:
Large or recurrent bleeds should prompt a check of the Hb, especially in the elderly or others with compromised bone marrow.
Make liberal use of short stay or admission to hospital for observation for 4-24 hours, especially after a pack.
As for the other ENT infections:
Best just read the powerpoint but some key pearls are:
If the patient can't lie flat, worry about their airway.
If they patient can't look up and down easily think about retropharyngeal infections or tracheitis.
If the patient is toxic it is not croup.
If the patient is too old for croup or it just doesn't seem to fit, think bacterial tracheitis or retropharyngeal abscess.
If you are worried about an upper airway remember :NEVER screw up an upper airway infection all on your own. Share the love with the ENT surgeon, the general surgeon, the anaesthetist, the paediatrician. You can share a taxi to the supreme court that way.
A/Prof Beth Pennington was back to teach on Paediatric Burns. Her talk is attached here.
Gold from Prof Helen Dewey’s TIA and Posterior thecirculation talk at ED teaching February 23rd. Look at her talk here
Thanks to Amanda for the YouTube link for the abnormal head impulse test (the guy in the video has a peripheral vestibular problem). People with cerebellar problems have a normal test. Scott Weingart of EMCrit fame as an iphone approach.
- True TIAs last minutes and are resolved before we see them in ED. They are diagnosed on history.
- Anyone who still has symptoms in ED is a stroke - highly likely to show a stoke on MRI even if they are almost back to normal.
- Strokes and TIA happen suddenly and patients are usually very well at the time.
- Don’t annoy neurologists by not doing a BSL. Think about other causes like dissection (carotid, aorta) or vasculitis.
- Order a CTBrain – tells you if the patient is having multiple bilateral old strokes from paroxysmal AF, tells you the patient is bleeding, has subdural, has tumour, about strokes the patient might not be aware of (non dominatnt).
- Don’t call something a TIA if its really confusion, syncope, patient is unwell, the patient has lost consciousness without focal signs etc etc.
- The greatest risk of stroke after TIA is in 48 hours. The risk drops substantially after this. TIAs are a serious warning for bad things to happen to our patients.
- ABCD2 underestimates risk in Monash study but helps people focus on what needs to be done.
- What needs to be done: Investigations: Carotid Doppler, ECG and fasting bloods as an inpatient in short stay.
10. How hard to you need to chase AF as a cause? If multiple old bilateral infarcts embolism becomes more likely - chase hard or treat with warfarin. Dilated atrium on echo might be enough to suggest it and commence warfarin (in the setting of multiple infarcts, especially if bilateral). If no AF immediately apparent, the echo is not important and can be considered in high risk cases by the physician or neurologist when they see them as an outpatient non urgently.
11. If you diagnose >70% stenosis on carotid Doppler in SSOU then organise transfer same day for endarterectomy that is urgent.
12. If you diagnose AF, commence them on warfarin immediately.
13. You should feel bold and supported starting an ACEI and statin after fasting bloods in SSOU (unless the BP is <130systolic).
14. Always upgrade their antiplatelet therapy – start aspirin or upgrade to assassantin.
Basilar artery Thrombosis
The main event is often preceded by warning signs such as diplopia, bilateral visual disturbance, LOC WITH quadriparesis that resolves, dysarthria with quadriparesis/sensory loss.
Vertigo rarely/never a cause of posterior circulation ischaemia unless associated with hearing loss or other hard focal neurology.
Once established: Quadriparesis and upgoing plantars classic. Lack of dolls eye reflex, pupil changes.
Add CT angiogram to CTB in this situation. Not looking for high tech angio 3D reconstructions like for aneurysms – basilar occlusion easy to see.
Basilar occlusion treatment: IV TPA if less than 4.5 hours (little to lose). Consider time critical transfer for angiographic clot retrieval.
BASICS registry – No benefit of anything after 9 hours in severe cases – palliative.
If delayed presentation and well established significant stroke – beware – further swelling may cause brainstem compression and unconsciousness and require surgical decompression rapidly in the first few days.
Today we had A/Prof Sandy Peake, the lead investigator of the ARISE trial, come and talk about the trial and then Dr Jason Fletcher from ICU. The website for the study is here. Some more details from the session after the jump...
Like a lot of people, when I read this article in the BMJ that claimed a 100% sensitivity of CT for SAH within 6 hours of onset of headache, I was pretty excited. Finally we don’t have to do the LP anymore! I posted the paper on this blog here, without much comment, hoping smarter people than me would start to talk about it. Well they did, and a lot of people are excited about it. But good old Jerry Hoffman has taken the paper apart on the January 2012 Emergency Medicine Abstracts tape. His expert analysis is well worth a listen if you are a subscriber (if you are not you should be or you should make friends with someone who is). Below is a summary of all the reasons this paper doesn’t tell us that we don’t need to do LPs anymore (with thanks to Rick Bukata and Jerry Hoffman).
But first, why don’t we want to do the LP?
"The patient won’t like it. It will hurt, they’ll be frightened of it, I’ll need to take time convincing them to have it and then if they hate it and I’ve told them that it won’t be so bad they won’t trust me anymore."
"What if I get a traumatic tap? Or can’t get it at all? Do I just tell the patient that I’ve changed my mind and we don’t need the test after all? Do I get an alternative test? What alternative is there? If there’s an alternative why don’t we just do that instead of the LP?"
"It will take forever. I’ll need to get all sterile and position the patient. I’ll need to find a nurse to help or the patient is going to roll around and move. Just when I get sorted the AO phone will ring or there’ll be a trauma or the patient will decide they need to go to the toilet. Worse still, the resident will want to be supervised doing it and it will take three times as long, be even more likely to be traumatic and the patient will look at me with those eyes that say “You want to stick a needle where?! And you want to let that guy do it!? And he has never done one before? How come you don’t do it if you’ve done heaps of them?!” The patient might need some sedation while we do it because they are totally freaked by the whole thing so there goes another doctor for the duration of the procedure."
"The CT scanner is really good. It’s brand new and we had to put up with a week of jackhammers and workmen just through the wall from resus when they installed it. It can CT a whole body in 10 seconds and it has 2000 detectors and it has really nice pictures and I can look at them on my beautiful giant screen in the staff base magnified so big it could be the head of a wooly mammoth. It must work. It should work. Why doesn’t our technology work!???"
So, why doesn’t CT work for SAH?
No matter how good the scanners get, why can’t we get beyond about 95% sensitive?
Well it is not about the scanner. It is about the blood and the CSF and the difference between them. Take 1mL of blood and dilute it in 100mL of CSF and you have something that looks on CT pretty much like CSF. Take 5mL of blood and dilute it in 10mL of CSF and you have something that looks quite different. The smaller the bleed and the longer it has had to diffuse away from the site of haemorrhage the less the “haematocrit” of the CSF and the harder it is to detect on CT. Don’t forget it is small bleeds that we want to find. That is, the GCS 15 patient with a warning leak who we can save from the big one; the guy who comes in with stertorous breathing, GCS 5 and a dense hemiplegia has a big bleed we are rarely going to miss on CT and his prognosis is not great anyway.
So, to the paper.
The gist is this. 3000 odd people with essentially a thunderclap headache were looked at prospectively in a bunch of EDs in Canada. The patients and the settings were very similar to ours in Australia and the inclusion criteria were realistic so it was certainly going to be generalisable to our setting. Overall there was about a 7.7% incidence of SAH which is about what we would expect with this presentation. And overall the sensitivity of CT was 93% which is again what we would expect. It is a bit lower than what is usually quoted but it included people with some delayed presentations and we know that sensitivity of CT after 24 hours is hopeless (~80% by day 3 and 50% at a week). The CTs done within 6 hours however (953 with 121 cases of SAH) had 100% sensitivity. With such big numbers the confidence intervals were good. Done deal.
Wait a second. Here are the problems.
Only 40% of the people with a negative CT actually got the gold standard test of an LP. In the rest they trusted to phone follow-up to catch any missed bleeds. So the first problem is the assumption that phone follow up (and a search of the coroner’s records for the province) is equal to LP as a diagnostic strategy for SAH.
Only 78% of people who needed follow up (negative CT, no LP) got the 6 month telephone follow up. 50 patients (about 2.5%) were lost to all follow-up, 157 got a call at 1 month but not later, 200 (10%) were still having entries in their medical records at 6 months so were therefore alive, and 8 were “dead of other causes” (see below).
Anyone who has ever filled in a death certificate knows that what killed the patient and what is listed as COD are linked only by the tenuous thread of an intern’s brain. Also, we don’t know if they died of something else while waiting for the big SAH that was just around the corner. One death was “presumed cardiac” on the basis that it was a sudden death 32 days after his headache and 4 days after a presentation with chest pain; no autopsy was done.
Final read of the CT
The CT was called positive if the final radiology report said it was positive. 3 patients got a false negative read at the time and were called back the next day after the radiology report, fortunately before a re-bleed. What we don’t know is in how many cases the ED doc read the scan as negative, did the LP, found blood or xanthachromia, and then went back to the CT and said “oh! There it is. I wondered about that bit.”
CT had 100% specificity in all comers in this study. Fantastic! But a true positive was defined as blood on CT or blood /xanthachromia on LP. So it had to be 100% specific because it was its own gold standard for a positive result.
So, what we have is a big study that comfirms some things we knew already about SAH.
- About 8% of thunderclap headaches have a SAH.
- CT can pick up more than 90% of them in the first 24 hours.
- CT probably gets better the closer to the onset of the symptoms you do it.
- But, “CT is 100% sensitive for SAH if done within the first 6 hours of the symptoms”? No, I’m afraid we are not there yet.
So what to do about LP avoidance.
Do more LPs. The more you do the easier it gets. It is one of the best tests we have in medicine. Does my patient have meningitis? The LP tells me yes or no. Does my patient have SAH? The LP tells me yes or know.
When you find a bit of blood in the CSF wait a few minutes and let it wash out of the needle before you start collecting. Look closely and you’ll see the blood has settled to the bottom of the hub and clean CSF is flowing over the top of it. Now take a syringe and blunt 18G needle and aspirate that bloody CSF from the bottom of the hub (never suck on the spinal needle with a syringe unless you want to suck out a piece of nerve root!). Clean CSF can now flow out without picking up cells from your traumatic blood.
Have a plan for what to do with a failed or traumatic tap. If you work in a place where the radiology department is guarded by registrars who feel it is their job not to do tests, get your plan agreed on at an interdepartmental level. I would suggest CT, followed by LP if negative. If the LP fails or is indetirminate follwo up with a CT angiogram (or in a pregnant patient an MRI/MRA). Remember that theset ests don't look for a bleed, they look for an aneurysm and abuot 1/50 ro 1/200 people have one, the great majority of which will never bleed. But if you save these tests for where CT/LP fails you, at least you won't be creating too much disease where there is none.
Stop doing CT’s for headaches that never needed one in the first place. One of the reasons people feel like the LP after CT is pointless is that they have such a low yield but this is because they are sending a whole lot of people down that pathway who never had a thunderclap headache, “just in case”. Take a good history. You need a CT for a headache in ED if it is thunderclap in onset, if it is associated with trauma, if the patient has a coagulation problem or immunosuppresion (especially HIV) or cancer, or if it is a chronic headache that might be a tumour.
Remember that although it feels like CT is the nice test and LP is the nasty one, no one ever got cancer from a lumbar puncture. If the headache was bad enough to justify irradiating a young person’s brain it was bad enough to justify LP.
What's with the title of the post?
You need to watch more old movies.
Essentially, for those who don't know, ARISE is attempting to enrol 1600 patients to look at whether a bundle of care called Early Goal Directed Therapy is better than standard care in sepsis.
EGDT is an algorithmic approach to sepsis managment where we ensure the following:
SpO2>93% (acheived with oxygen +/- ventilatory support)
CVP>8 (or 12 if ventilated) (achieved with fluid loading)
MAP 65-90 (achieved with noradrenaline)
Antibiotics given early (appropriate ABs, after cultures taken)
Then we add some bells and whistles. Note though that up to this point there is really not much there that is not happening in standard care (except perhaps that we are getting onto things more aggressively because the patient is part of a study) so effectively randomisation kicks in at this point. Standard care patients will have a normal central line and just be managed as usual. EGDT patients will have a special CVC that allows continuous monitoring of ScvO2 (central venous oxygen saturation). If this is < 70% dobutamine is started to increase oxygen delivery and if that doesn't work the patient is transfused up to Hb>100g/L and if that doesn't work the patient is paralysed and cooled to decrease oxygen consumption.
I suspect that we will find that there is no difference and what we will really take away from the study is that we need to do those basic things well. Recognise the septic patient and get in early with fluids, vasopressors, oxygen and antibiotics.
Which brings me to which patients to include. If your patient has a suspected infection and has any physiological derangement they are a potential ARISE subject. Strictly speaking they need suspected infection and two SIRS criteria:
- Core temperature < 36.0°C or > 38.0°C
- Heart rate > 90 beats/minute
- Respiratory rate > 20 breaths/minute or PaCO2 < 32 mmHg or the requirement for mechanical ventilation for an acute process
- White blood cell count > 12.0 or < 4.0 x109/L or > 10% immature band forms
Then they need to have some evidence of shock defined as sBP<90 despite 1L fluid bolus OR lactate >4.
There are various exclusion criteria but if your patient is worth giving IV antibiotics to, consider whether they meet any of the SIRS criteria and call ICU and let them sort it out.
Here is a link to the powerpoint of the talk we gave at the regional teaching day at St Vincent's Hospital on 14th Dec 2011.
I like to think of chest trauma in terms of damage to great vessels and heart (bleeding), damage to the chest wall and pleural spaces (ventilation), damage to the lung (oxygenation) and something else- i.e. damage to other parts of the body that might mimic thoracic trauma (e.g. ugly CXR but the real reason for the hypotension is the belly full of blood or the real reason for the poor ventilation is the messy head).
The places you can make the biggest difference in the resus phase, especially as an occasional trauma practitioner, are to the chest wall and pleural space and to the something else section. Provision of a secure airway, control of ventilation and decompression of tension pneumothorax/haemothorax are going to do most of what you need to do for these patients in the resus room of the non-trauma hospital.
The exception is in the stab wound to the chest with a pericardial tamponade in which case you need to be prepared to decompress the pericardium, either by needle of knife (lots of controversy here, I lean toward knife but you need to have a plan well rehearsed in your head one way or another). The other big vascular injuries need to be recognised and urgently moved to a MTS but if the reason your patient is going down the tubes is an aortic rupture or hilar tear there is not much you are going to do in resus other than pick up the phone that is going to help.
Oxygenation problems usually become a problem late on day 1 or into day 2 in ICU when the pulmonary contusion starts to consolidate or the aspiration starts to get inflammed.
Which intervention first? There is a risk with ETT then ICC of creating or worsening a tension pneumothorax but there are significant practical problems with trying to knife the chest of a semi-consious, frightened, intoxicated, hypoxic trauma patient with a busted clavicle and scapula. My approach depends on how many people I have and how urgent the chest wall and airway are. If there is an obstructed airway and an OPA isn't tolerated or doesn't work you just need to do the ETT first and move on to the chest second. If there is a frank tension pneumothorax and the patient is in extremis you might just need to decompress it (this is one of the few cases where I would still use needle decompression- see Scott Weingart's post on this (link below) for some more discussion around this). Most patients however are somewhat less clear cut (decreased GCS, restless, SpO2 80ish, HR 130, BP 90, airway compromised but open seems to be a pretty standard format for the patients who arrive in ED from major blunt thoracic trauma in Victoria, possibly because the more extreme cases get their major life-saving interventions from the MICA paramedics at the roadside).
When I am the only one who can do these procedures in the place I announce to everyone that we are going to intubate and then do an ICC on such and such a side. I have one nurse set up the ICC tray and another preoxygenate while I get a gown and two pairs of sterile gloves on. After the ETT is in, pull off the outer gloves and move to the axilla and make a finger thoracostomy (remember that in a ventilated patient you don't make a sucking chest wound because the chest is under positive pressure so once the chest is open the problem is solved for now). Then I move on to other tasks and come back to place the chest tube with better aseptic precautions when the rest is stable.
When there is another person present who can help one should be all set to go with the ICC while the other passes the ETT. Once the airway is secure the ICC can go in quickly.
The tension danger come when you pass the ETT, put in an orogastric, get a CXR to check position and get distracted getting more IC access before you deal with the pleura.
And don't forget, if there is no IV access within 30 seconds, grab the IO gun.
Remember that ribs start high at the back and end low at the front and that while the nipple line is the 4th ICS at the front it is also the top of the diaphragm (liver, sleen, juicy stuff) and not where you want to go with your ICC. In the MAL the 4th ICS is the end of the armpit hair. Everyone has some sign of where armpit hair was no matter what wonderful hair removal techniques have been used. Don't count ribs.
We didn't get a chance to look at the slides on tension pneumothorax. What I was going to say was that the traditional clinical signs of tension pneumothorax are hopeless and are based on patients from early last century who got observed dying of the disease rather than getting treated. If your patient is allowed to get cyanotic from their tension pneumothoax you might as well go and become a psychiatrist. And tracheal deviation is rarely present and when it is present people get the side of the pneumothorax right about 50% of the time! As team leader, stand at the end of the bed with your head down near the level of the patient and get a skyline view of the chest movement. If it looks ineffective or assymetrical there is a big problem. If not there might still be. I was also going to say that getting a CXR first is a very different thing in 2011 with a trauma call getting you a radiographer with a mobile machine or gantry within a minute or two and pictures available on a screen in resus a minute or two later than it was in 1960 when a patient had to go to the next building on a trolley for a CXR and wait their turn behind all the twisted ankles. CXR first will save significant morbidity from uneccesary procedures if the patient is stable enough to get one. Reasons not to are on the slide.
Scott Weingart at emcrit.org has done two blogposts/podcasts on needle vs knife in trauma resuscitation. Episode 1 looks at needle vs knife for cricotyroidotomy and Episode 2 looks at needle vs knife for Thoracostomy, There are a bunch of good articles related to the topic listed on his posts that are worth checking out too if this topic piques your interest. I haven't listened to this one yet but it looks like being a good discussion of traumatic cardiac arrest. Remember, you can download any of Scott's podcasts for free at itunes or you can listen straight from the web. Read the comments section too. The respondents list is a who's who of critical-care critical-thinking and elearning.
Quetiapine (Seroquel TM)
Quetiapine is a relatively new "atypical" antipsychotic agent. By "atypical" it is meant that it does not act predominantly as a dopamine antagonist and therefore can be expected to be free of extra-pyramidal side effects.
Due to fairly intense marketing it is being used for a wide range of off license indications, particularly as a calmative agent for impulsive or ill-tempered patients with personality disorders, as a mood stabiliser for bipolar affective disorder, and as a sleeping tablet for patients in whom it is judged best not to use an addictive agent. The evidence for its use in these situations is parlous at best.
Primary Exam Stuff
Quetiapine acts at serotonin, alpha adrenergic, histamine and dopamine receptors but its potency at dopamine receptors is a lot less than that of other agents. The mechanism of its activity is opaque.
Effects include sedation and decrease in psychosis.
Side effects include weight gain and hypertriglyceridemia, increased risk of type 2 diabetes and lowering of arrhythmia threshold.
Oral bioavailability is high. Protein binding his high.
Metabolism is largely hepatic and excretion of metabolites is mostly renal.
Half life is 7 hours (and 12 for the active metabolite) so once daily dosing is effective.
In small overdoses quetiapine is a fairly safe agent causing only a low grade tachycardia without QT or QRS prolongation and sedation.
Neurotoxic effects occur in large doses with the familiar pattern of agitation/sedation, seizures and coma occurring at doses over 3g in an adult.
Likewise, cardiotoxicity is dose dependant but is much less of an issue than with antidepressants. Most people will get some tachycardia. In doses of over 3g hypotension can be expected. In massive doses arrhythmias have been reported in a handful of patients only (and co-ingestants might have had a role to play).
Delirium may respond well to physostigmine but this may be at the risk of seizures and arrhythmias.
Both sedation and cardiotoxicity may be significantly potentiated by co-ingestants especially antidepressants but also benzodiazepines and alcohol.
This blog post from The Poison Review looks at an article reporting a case series of massive overdoses.
According to Dr Shaun Greene, Emergency Physician and Toxicologist, quetiapine overdose is fast becoming one of the most common overdoses in Australia so you better get used to it.
Vital signs are vital, and respiratory rate more than any other. Abnormal vital signs and particularly RESPIRATORY RATE predict who is going to have an arrest! Link to MJA article.
O2 Saturation is not a replacement for respiratory rate! Learn to count the respiratory rate properly and when someone presents a case to you make sure they give you a respiratory rate.
And while we are on the topic, this article in The Lancet provides quality data on the normal ranges of vital signs in chldren of different ages and calls into question the established numbers taught in APLS. It is taken from a metanalysis of a large amount observational data of normal children of different ages. Click here for the centile charts generated from that review.
This article (NEJM- read full text for free from within Victorian public hospitals via clinicians health channel) is a major paper in critical care medicine in the last 12 months. thanks to everyone who took part in our journal club look at it. What do we conclude? Why should it not change our managment? Why can we not write it off altogether? All this after the jump...
How is the study quality?
Well it is a great study. It set out to prove something that the authors thought was true (fluid boluses in septic African kids will save lives) so that they would have the ammunition they need to get this fairly basic and presumably life-saving intervention happening in hospitals that lack any coherent emergency medicine or triage or critical care system. Then, low and behold, it proved the opposite. Fluid boluses were actually killing these patients.
Now you have to love a paper that proves the opposite of what it set out to prove. Why? Because the fact that it hasbeen published means that it was a powerful enough result to overcome the prejudices and assumptions of the investigators and because it is a result that brings truly new knowledge.
As far as internal validity goes this paper was pretty good. The numbers were huge (how long would it take do you think to find that many truly septic children in a first world setting?), the randomisation was robust, the groups well matched, the intervention focussed on a single thing, protocol breaches minimal, analysis on intention to treat and differences between the two groups both statistically convincing and clinically meaningful. Inclusion and exclusion criteria were defined in the body of the article. There was only one primary end-point. No huge claims were made on the basis of secondary end-points or post-hoc sub-group analysis.
When I read an article like this there are a few things that jump out at me as potential weak spots (but which were not in this case):
- Three groups (albumin, saline and no bolus)- multiple groups should always make you wary. There are two potential errors that crop up in RCTs using multiple groups. First you can declare that there is no difference because you ended up splitting up your population into too small groups (underpowered study). That was not a problem in this case: the numbers were huge and power was adequate and they did find a difference anyway. Secondly, multiple comparisons are a great way to find a random difference (compare new drug, new drug on alternate days, new drug with salt tablets, new drug on Wednesdays and placebo- WOW! new drug on Wednesdays is better than placebo! Get the press release out.) That was also not a problem in this case as both bolus groups were essentially the same compared to placebo and whether looked at separately or together the result was consistent.
- 2 strata (severely hypotensive kids who all got a bolus and the rest who got albumin, saline or placebo). This means you are essentially running two experiments. You have to be careful to ensure that the results from one are not muddled up with the question being asked by the other. (e.g. you give a drug or placebo to two groups of people with, oh, let's say stroke and in one group you are looking at 24 hour mortality and in the other you are looking at 4 month function and mortality and you find no difference in 24 hour mortality in the first group but when you have a post-hoc look at 24 hour mortality in the second group you find a difference and report that). In this case the two strata issue was not much of a one as the severly hypotensive group was trivially small compared to the huge size of the main group.
- Early cessation. Always beware early cessation. Was it really becasue of safety? Was it because the pendulum happended to have oscillated over to the result we were looking for? Not a problem here I think.
So why should it not change our managment?
Well the big question you must ask yourself is how similar is my population of sick kids to this one?
Remember that these are sub-saharan African kids. And they were really sick. They defined "prostration" as inability to sit up (or breast feed in pre-sitting kids). They defined severe malnutrition as kwashiorkor or visible wasting. The mean baseline Hb was 71 with 75% of kids having a Hb <10 and 30% an Hb <5. Half of the kids had malaria and 4% had HIV.
What will a 20-40mL/kg fluid bolus do to a baseline Hb of 4g/dL? There was a transfusion protocol for these kids but they got their transfusion relatively slowly (the protocol was 10mL/kg over 4 hours and looking a the fluid volumes delivered I am not certain how many of these kids would have actually got that blood in that time).
And what disease did these kids have? Half had malaria. The other causes are not reported and were probably hard to define given the resource limitations of the setting but one would suspect that meningitis and pneumonia featured highly. Both of these are associated with SIADH meaning that a fluid bolus might have significant negative implications.
Remember also that these kids had no access to ICU. Most pneumonias do not die of septic shock but of respiratory failure and ventilatory support was not available to these kids.
So why should we not write it off completely?
Interestingly, the kids with HIV fared no differently than those without it. APO and raised ICP were not found to be more common in the kids who died (although how they were detecting raised ICP in this setting is not clear). In fact it is not clear what killed the kids in the bolus group. Until more research is done we are going to have to keep this study in mind when taking care of even fat healthy first world kids.
What this study really brings home for me is that in really sick kids we need to think past the simple APLS scenarios where a fluid bolus and a dose of ceftriaxone fixes everything and reach for vasopresor and intrope support early. Treating an adult with temperature of 40, HR 130 and BP 60/- we would not expect to give 20-40mL/kg of fluid and a shot of antibiotics and save the day. We would be reaching for the norad before the first litre was though. The fact that most of us rarely see a very sick child makes us hesitant managing them in the same way. This study reminds me that we need to overcome that.
This week we talked about GI bleeding.
Dr Lev Veniamanov gave a talk on proton pump inhibitors in acute upper GI bleeding (the gist is you can expect a decrease in rebleed rates but not in mortality, the risk from the drugs is low so even the modest benefit probably justifies their use however they are not a high priority when resuscitating a sick upper GI bleed patient).
Dr Hatem Elkady gave a talk on beta-blocker use in chronic liver disease (gist is they give a significant reduction in rates of variceal bleed with a number needed to treat of only around 10 however they have no role in acute bleeds).
Dr Saif Abdulrahman gave a talk on Vasopressin and related drugs. Vasopressin or Terlipressin have a role in acute variceal bleeding when octreotide (which has a better safety profile) and urgent endoscopy are not available. Vasopressin, Terlipressin and Desmopressin also have uses in salt/water management (Vasopressin is ADH) and in haemophillia and vWBD (by uncertain mechanism).
My clinical presentation is here. See if you can work out where the three cases are bleeding from.
The normal ventricular septum is made of the infundibular septum that grows down from between the aortic and pulmonary valves and the rest of it that seems to reach up from the apex (but because of the twisted nature of the heart also extends around to be continuous with the interatrial septum). In TOF the infundibular septum is pushed forward (toward the right heart) encroaching on the pulmonary outflow tract so it fails to meet up with the rest of the septum. The result is that you have a big VSD with an opening that points straight up the aortic outflow tract and a variably narrowed pulmonary outflow tract. The pulmonary valve can be normal, small, bicuspid or non-existant and there may or may not be a pulmonary artery.
TOF is a form of cyanotic heart disease because it results in blue blood from the right side being sent to the left side.
Severity depends upon the degree of RV outflow obstruction.
The mild cases start off with a bit of a murmur from the tight pulmonary outflow tract and VSD and a predominantly left to right shunt because the left heart is stronger than the right. The kids are pink and present late with heart failure because of the shunt. Later they develop RV hypertrophy and a Right to Left shunt and start to get cyanotic.
The nastier cases have a right to left shunt from the start and so are blue to begin with.
Really severe RV outflow tract obstruction leaves the neonate dependant on either a PDA (ductus-dependant heart disease) to get blood to the lungs or on unusually large collateral supply to the lungs (remember the bronchial arteries that come off the aorta and supply the bronchial walls with red blood in normal people? They are the reason that big proximal PE's don't cause pulmonary infarcts in normal people. These arteries don't reach the distal alveolar bits of the lung which get by on blue blood which is why the small peripheral PE's cause the infarcts. I digress...). These kids are usually in trouble in the first hours of life and go to NICU for prostaglandin to keep the ductus open and then either get definitive repair early (the new approach) or a Blalock-Taussig shunt (the old approach) which is a Gortex shunt from the left subclavian artery to the left pulmonary artery which replaces the function of the ductus and keeps them going until they are big enough to tolerate definitive surgery.
Milder cases may present to ED pre-operatively with Tet spells or cyanotic spells.
From time to time these kids get themselves into a pickle with increasing right to left shunt and increasing cyanosis. They get distressed and cry which puts up intrathoracic pressure and probably makes it harder to get blood through the already difficult pulmonary circulation. They get tachycardic which is not good (just like in AS where tachycardia significantly compromises the emptying of the LV across a tight aortic valve, the RV in these kids can't cope with tachycardia and just dumps it's blood across the VSD to the left side). They get hypoxic which causes more pulmonary vasoconstriction and worsens things further).
Left alone one of two things happens. Option A is they get exhausted and go to sleep or become unconscious, either way breaking the cycle of distress, right-to-left shunt and hypoxia, and they improve dramatically to fight another day. Option B is they get a metabolic (lactic) acidosis, worsening cardiac function and spiral into cardiogenic shock and die.
Management of cyanotic spells.
The aim is to calm the kid down, increase the systemic vascular resistance (SVR) but decrease the Pulmonary vascular resistance and oxygenate as much as possible.
1. Nurse on parent's lap and keep the IV away for the time being.
2. Put the kid onto their belly with knees drawn up to the chest. This increases SVR. Toddlers and big kids with uncorrected TOF will apparently squat down instinctively when these spells occur.
3. Give lots of O2. Because there is shunt this won't change the oxygen saturation much directly but it may decrease the pulmonary vasoconstriction that results from hypoxia and improve things indirectly.
4. Give morphine Subcutaneously 0.2mg/kg. This calms the kid down and may break the cycle. It also means that later IV insertion will cause less distress. But won't morphine drop the SVR? I suspect that morphine's role in this is similar to it's role in APO and that it is only the fact that paeds moves a lot slower than adult medicine that it hasn't been replaced with something more glamorous and modern but what the hell, that is what they recommend, who am I to argue? It seems to me that IN fentanyl might be a better option as it does not involve a needle and would not drop the SVR as much as morphine but it probably hasn't been trialled yet. So give the damn morphine and stop trying to be a clever pants.
5. Ensure there is no precipitating factor that is uncorrected. Panadol for pain or fever, warm if cold, check and fix glucose.
6. If all this doesn't help get an IV in and check for acidosis. If acidosis is present the kid is potentially in trouble and is likely to go to Melbourne. If not then they can probable push on here.
6. If you are still getting nowhere (and by now the paediatritian should be holding your hand and PETS should be on the phone) then the next steps tend to be:
6.a. 10mL/kg fluid bolus,
6.b. Correction of acidosis is the usual next step with bicarb 2-3mmol/kg
6.c. Propanolol IV 0.1mg/kg slowly, once or twice to correct tachycardia
6.d. Phenylepherine to increase the SVR and push blood left to right again.
Once definitively corrected they are pretty much right and able to live a normal life although I suspect that the kids with no pulmonary artery at all probably struggle a bit. Obviously they need to watch out for endocarditis.
The one case I have seen, an 8 month old boy having his second ever cyanotic spell and due for surgery in a few months, I tried the knees to chest thing hesitantly and the boy dropped from SPO2 of 75 to 70% and I got nervous and stopped. I did not have him prone, I just pulled his knees up to his chest sitting. This might have been the problem. Alternatively this step is just folk lore and doesn't help. My one anecdotal experience is not a reason not to try it however and next time I would be more proactive with positioning the kid properly. We then gave him the morphine which helped dramatically, raising his sat from mid 70s on oxygen to 95% but the effect only lasted about 20 minutes. The paediatrician came in and put on 100% O2 for a while (luckily the boy was robust enough to draw O2 through the air-Viva without being actively bagged, a smaller kid would have needed a black bag circuit to get 100% O2) and this helped a lot. After about 20 minutes on 100% O2 his sats were in the 90s again and he went off to sleep and they stayed there. We put in an IV (causing a temporary drop to the 70s again) and he wasn't acidotic so he stayed on paeds ward.