The perks of PERC

The really worrying question sometimes arises (or depending on your luck, most times arises) while you are in an ED, and you see a patient who comes in with ‘some chest pain’ that’s maybe a little pleuritic in nature, but pleuritic chest pain could result from a punch to the chest, or if you cough too hard or too long (I unfortunately speak from experience!) and you don’t know what to do and someone’s already done a D-Dimer on the patient’s initial bloods as they were triaged, before you saw them, if you are lucky enough to work in a department as great as ours (or unlucky, depending on how you view the over-testing of D-Dimers!) – I have been handed the most amazing tool: the PERC score, or the Pulmonary Embolism Rule-out Criteria. For those of you already aware of the existence of such a magic wand – bravissimo and kudos to you, and no need to read on any further. For the ones like me who until very recently hadn’t even heard of it, please proceed further.

Patients who present with clinically low risk for development of a PE can be subjected to the PERC. This is a pre-test probability type situation, whereby you assess a patient based on clinical parameters (which you obviously already do!) but you mentally check them off a list of specific parameters, and if they meet all 8 (yes EIGHT!) criteria, then you can safely say they do not need further assessment RE:pulmonary embolism, D-dimers, CTPA route etc. This creates a warm and fuzzy feeling in me, because almost every patient in the past 3 years of practising emergency medicine in the UK that presents even remotely with pleuritic sounding chest pain, regardless of whether they have a clinical indication or not, automatically had a D-dimer, and, God forbid, should they have an ever-so-slightly-raised D-dimer level, they were referred to the acute medical team faster than you could say enoxaparin. These were then possibly unnecesarily given doses of enoxaparin, until the gold standard rule-out test could be performed, which is the CT PA (CT pulmonary angiography). That’s just the way things worked, because a positive D-dimer can indicated possible pulmonary embolism, but it needs to be taken with the complete clinical picture, and a (very large) grain of salt. D-dimers can, unfortunately or fortunately, be raised in a number of different situations, e.g an underlying active malignancy (which gives the double whammy of raising your chances of getting a PE in the first place), an infection anywhere in the body, certain medications and inflammatory medical conditions.  This lead to over treatment of many patients with anticoagulants till the CTPA was performed to finally confirm the existence or absence of the offending clot. Things may have changed for the better with the PERC, though.

The parameters you base your PERC score on are Age (< 50 years), O2 sats (greater than or equal to 95%), Heart Rate (less than 100 BPM), Absence of Hemoptysis, Absence of Oestrogen usage (Contraceptive pills), Absence of history of surgery/trauma requiring hospitalisation/immobilisation within past 4 weeks, Absence of lower limb swelling (unilateral), and absence of prior personal history of clots/emboli/thrombi.

These parameters and this score are widely used now and available as calculator/apps on most phones.

So the way I understand is, low-risk patients meeting the PERC score criteria need not be further assessed (even if they have had a D-dimer done that’s slightly raised, you can ignore it because the pre-test probability was extremely low). Low-risk patients not meeting the PERC criteria may then go on to be assessed on the D-dimer route, and the high risk patients go directly to CTPA without faffing around with PERCs and WELLS and GENEVAs.

Good luck, and happy PERC-ing!

Transfer Training

Attended a Transfer Training course today. I know what you’re thinking, who needs training to learn how to transfer a patient? What rocket science is involved in the few seconds or minutes to transfer someone from one bed to another? Or how much of preparation and thought needs to go into transferring a patient from one hospital to another? It has to be fairly simple right? Atleast thats what I was thinking when I was applying for the course, I thought it’s going to be like a 30 minute session, Bam Bam, thanK you, Ma’am type situation. Boy was I wrong – this was an 8 hour long proceedings, and I actually learnt quite a bit. Some gems from today’s talks:

Movement effects
Movement of any sort brings with it it’s own demerits. So only move the patient if absolutely necessary. Deceleration causes gastric contents to come up; it also may cause fluid to ‘back up into the lungs’.
Acceleration causes the opposite: hypotension, decreased preload. Both may lead to heart failure

Limit affects of any sort by making sure patient is well hydrated; lift the legs up to counter hypotension(during acceleration)

Head end up (15-30 degrees), NG (during deceleration)

Consider if you need Blue light? Is it time critical? Make sure to limit sudden movements, blue light ambulances are notorious for getting into accidents (large vehicles, moving at high speeds, sometimes against traffic and/or against traffic rules)

Specially important is the need to be careful in head and spinal injury patients
Contrary to popular belief and your gut feeling, the more critical the patient, the slower the transfer needs to be. Not faster. Fast, hasty movements make for bad decisions, wrong or sharp turns (as well as deleterious effects of movements already discussed)

Static effects
Hypothermia is the most common problem
What is the first thing that happens when patients are brought in to ED? Their clothes get taken off. Coupled with cold environment, not a good combo
Children/eldery most vulnerable
Monitor patient during the transfer as well for temperature changes; aim for normothermia
HME filter is one way to counter drop in temperatures – ventilator usually gives cold, not-too-moist air going directly into the lungs, bypassing the moistening and humidifying warmth of the sinus cavities; connecting an HME filter to the ventilator circuit effectively prevents the dry cold air going in, and thereby prevents hypothermia.
Blankets and foil may be used, especially in ambulances
Pre warmed fluids may be considered
Cover open wounds/burns (cling film is best as wound is still visible for any changes, is sterile essentially and can be airtight)

Avoid vibration injury/movememt in ambulance/helicopters
Pad and protect soft tissues to avoid pressure sores, and reduce fractures where possible. Ulnar nerve is most commonly injured during transfer – bean bag padding is ideal for such transfers.
Interference can be caused with electronic monitoring by the unnecessary vibration.movement aberrations from helicopters and ambulances; dislodged/trapped leads may also be a concern.

Motion sickness may develop – stop feeding the potential transfer patient. A couple of hours of NBM won’t kill the patient, but aspirating their own vomit, or vomiting when their neck is immobilised can be quite a significant clinical concern. Consider NG (with free drainage) and sitting upright. Avoid rear-facing seats for transferring teams. Do not read/documentation, as can make things worse. Be prepared. Take antiemetics.

Communication
Sirens/alarms make communication difficult. Make sure you can always hear alarms. And, we all are guilty of doing this, but NEVER ignore alarms.

Immobilisation
Need to ensure patient can undergo immobilisation. Make sure patient can actually physically lie flat for CT scans, etc (e.g. may get short of breath if massively obese or really bad CHF)
Consider sedation (and airway protective measures) if absolutely necessary to scan and lie flat.
Make sure you have everything you need before you leave. And before you need it. Always be prepared for every eventuality, every foreseeable complication.

Lying supine can also have other deletrious effects on even patient who can lie flat – secretions can accumulate, reflux might be an issue, V/Q mismatch occurs, inability to cough when lying flat, strapping someone down for a scan may itself cause restriction of lung movements in an otherwise comfortable-in-lying-flat patient.

NOBODY GETS BETTER DURING A TRANSFER! They may get worse, so only transfer if absolutely imperative.

Special considerations?
Trauma
general information about the Trauma network
ED pitstops – their pitfalls

Head/spinal injuries – RTC, falls, sports, assaults, self harm (gunshots), and non-traumatic
Motor aspect of GCS is more important than anything else in the GCS
Immobilise with correctly fitted collars
Aim for Normal pO2
Normal pCO2 is now the new teaching, as low PCO2 (which was previously the guidelines) causes cerebral vasoconstriction, reducing blood flow, and ischemia is a far worse complication than brain swelling, atleast in the initial phase of the post-injury timeframe.
aim for a MAP of 90 (this is ideal for cerebral perfusion pressures to be optimum)
Normoglycemia
Normothermia
Head up, minimize movements
Urgent Neurosurgical care
Maintain parameters at all times, even if the transfer is for short periods
Monitor pupil size, GCS, Heart rate/rhythm strip, blood pressure, pCO2, resp rate during transfer
Immobilisation and transfer methods were also touched upon, various methods to transfer patients, scoops, trolleys, mattresses, sliding sheets, boards etc
Consider Spinal shock if triad of hypotension+poikilothermia+bradycardia
Avoid fluiding with large volumes if unresponsive to fluids, consider escalating to vasopressors.
Will improve on own if spinal shock
Autonomic dysreflexia – injury above T6 (headache, flushing/sweating above level of injury, urinary retention)

Paeds

Rarely transferred. Only ever in cases of trauma/head injury
CATS
WETFLAG
Broselow tape bag
Vecuronium/pancuronium, fentanyl, ketamine (children) combo in children safe.effective cocktail

Balloon pumps- weigh 70 kg, slows movement, runs off battery

 

My PLAB experience (a VERY long time coming!)

Very recently, I was asked by one of my friends if I could share my experience about the PLAB exams, as guidance for prospective candidates. Having taken the exams quite a while back (2014!) I found it hard to address the issue, so they sent me a questionnaire to make things easier to explain to someone not very familiar with the way forward when contemplating taking the PLAB exams. I am sharing the whole Q&A session here (with a few minor adjustments/deletions with the author’s permission). Thank you @Sadaf Taymor (http://sidtay.blogspot.co.uk) for the opportunity to express myself and to share an important experience with everyone!

The curious case of PLAB (09/10/2017)

What is the PLAB exam and how does it help in initiating a medical career in UK?
There are many routes of entry into the UK for doctors who wish to train here. The easiest and most common one is to take the PLAB  (or Professional and Linguistics Assessment Board) exam and become GMC certified. Let me tell you a bit about this – basically any country that you work in has their own authority that confirms that you are good to practice in that country. For Pakistan, that authority is the Pakistan Medical and Dental Council, for the UK it is the General Medical council. Passing BOTH PLAB 1&2 gets you the license for the GMC to practice. After you get those out of the way and are certified then you are basically allowed to practice in the UK. That’s what people usually do.
The PLAB exams are the basic, entrance-level exams. You could potentially also get GMC certified by taking any of the more advanced membership exams for any of the Royal Colleges (but more about that at a later juncture – let’s keep this simple!)
The bottom line is you can not practice medicine in the UK without being GMC certified, and the easiest and most common route of entry to get that is to take the PLAB exams.
What kind of a format does this exam follow and what time limit does the candidate have for the exam
The PLAB has 2 parts – both are compulsory to pass individually. The first part is theoretical, and is based on the multiple choice questions format (or should I say, the single best answer format). You are given three hours to answer 200 questions. I have often heard people lament that the time is not enough, but I think it is doable. It may be difficult if you are not used to such a format, but in this field, better get used to this format, because later exams are also going to be in the same manner, same time frame (possibly even worse!)
The second part is interactive and consists of multiple stations. It is OSCE-based format, where each candidate rotates in 14 stations, each station assessing a different skill. Examples of such interactive sessions include taking a proper history, examining certain system, counselling a patient about something, and so on.
You can attempt the PLAB 1 as many times as you wish. Once you pass it, you have three years to pass the second part, failing which you will have to take the PLAB 1 again. You have 4 maximum attempts to take the PLAB 2.
Does the test have a certain validity?
Once you pass both parts of the exam and are GMC certified, you do not have to retake it again. You just have to keep up to date your assessments and your competence and you get re-validated automatically every 5 years.
 Any specific tips on cracking the test?
For the first part, I would advise go back to your roots, back to the basics. The whole syllabus is available on the GMC/PLAB websites. Try to practice as many questions as you can, get your tempo going, get used to this format before you take the exam. 2-3 months of prep should be enough.
For the second part, it can only be taken in the UK so make sure you have everything sorted before you travel for the exam. There are course available which guide and prepare and help practice the various stations that may come in the exam. These preparatory courses are much recommended before you take the PLAB 2 (if you have never worked in the UK or similar circumstances before).

Another day, another training…

Attended another training/teaching day sponsored/arranged by the deanery – was a very, VERY useful and informative day – and though it dragged on for hours, it was very interesting and explained quite a few things that I had not known previously – gist of the major salient points of each of the talks are listed below – may expand on 1 or more of these topics in the near future – so inspiring!

There were 4 speakers

PUBLIC HEALTH PROMOTION – how to explore facets of public health while in ED, because most people interact with someone in the ED, and that may be the only point of medical contact they have had up until that point.
smoking cessation, weight loss, exercise, pre-diabetes identification –
screening programs are fixed, inflexible , protocoled care, applied across a particular age group- safeguarding, frailty, VTE, dementia screening, hypertension, alcohol issues, obesity, domestic violence, smoking

case scenario of overweight person presents with orthopaedic problems, upon discharge do you speak to them about their weight? as an ED physician

case scenario of unwell child who has never been vaccinated – what will you do? How do you approach the subject with the parent, or do you even approach it at all?

case scenario of alcoholic patient with head injury – would you address the alcohol issue? (unit is 8 gm or 10 ml) 25 in whiskey, 10 in wine and 40 in spirigel
alcohol problems discussion
(having withdrawal symptoms when not drinking is being dependant on alcohol)
who should you be screening for problem drinking – selected presentations
how do you ask for alcohol intake?- use PAT scale – CAGE questions are useful in establish alcohol related problems.
important because intervention is helpful

PUBLIC HEALTH AND EMERGENCY MEDICINE
as doctors/physicians it is our ethical duty to reduce injury and illness, wherever we interact with patients.
we tend to have more interaction with the general public
you are more likely to see violence/injuries than the police – some studies show more than 3 times!
how can you help as doctors? injury survielance, mandatory reporting, better design, improve treatment, collate data and improve conditions – location of assault, date/time of assault, weapon, age
is anonymous,
crime rates went down because of data collected due to targeted policing
what are barriers to implementation? – police expectations, IT issues, governance, receptionist, leads
pitfalls – mission creep, fatigue, silos
conclusion? violent injury surveillance and control is effective in reducing violence. implementation can be challenging

QI (Quality Improvement)
audits are important but rarely work
why do they fail? – tick box exercise, temporary staff, lack of feedback, career advancement a priority rather than care advancement, lack of collective responsibility (if your rotation ends, the audit ends with you, no continuity)
has now become quality assurance rather than improvement. “maintaining/meeting set standards” rather than “improving the standards”
RCEM guide to QI is the QI bible.
do less, do it better
choose a standard to improve:is it important?, is it fundamental?, is it fixable?
talk to the stakeholders (nursing staff, frontline staff, triage, juniors, etc), ask them why this is not happening – how to improve conditions?
measure the standard
intervene to implement a change, and then re-measure after a suitable timeframe.
establish or convey a sense of crisis – reiterate how important/imperative this measurement is.
rapid cycle

CARDIOLOGY – ACS
definition of ACS
reiteration of importance of history – onset and character
repeat ecg, compare with previous
do not delay treatment waiting for biomarkers in “cardiac-sounding” chest pain.
consider bedside imaging if hemodynamic instability
escalate appropriately, consider involvement of tertiary care
dissection a differential? CT aorta stat (discussion about d dimer as useful in this scenario – some people say a negative d dimer rules out a dissection – research shows that is not the case)
management – analgesia+dual antiplatelet therapy, GP2B3AI, antihypertensives (b blockers) ACEI. statin, REGARDLESS OFWHETHER AN INTERVENTION TAKES PLACE LATER ON OR NOT, GIVE THE MEDICAL TREATMENT. if already on aspirin, 300 or 225 of aspirin either way doesn’t matter, 600 of clopidogrel and 80 of tigacrelor (not to use if warfarinized – MAKE SURE INR IS THERAPEUTIC)
immediate management – angio +/- PCI (for STEMI within window, ongoing symptoms, cariogenic shock, for NSTEMI – hemodynamic instability, ongoing schema or shock, IF REFRACTORY TO INITIAL MEDICAL THERAPY)
high risk/labile/recurrent schema – urgent angio
all others get routine angio
12 hours stemi – def PPCI, greater than 12 hours – if symptoms, PPCI, greater than 48 hours – no PPCI.
<30 mins door in door out in non pic centers. <60 mins door to wire crossing in PCI centre. and LBBB/RBBB considered equally. no o2 if >90 sats on RA.
consider CPAP, IF DISTRESS. iv amiodarone for AF, Look for hyperglycaemic states, MRA if CF.

if unable to decide if LBBB is new or old, compare to previous but if none available to compare, look at the patient. vast majority are not acute, unless they’re in cariogenic shock.

 

DIARRHOEA
definition
types
causes
symptoms
may be a symptom of sepsis – does not mean primary focus is gastrointestinal- particularly in the elderly
rotavirus most common in children – vaccine now available, rotarix at 8 and 12 weeks, seasonal
COD – dehydration/acidosis
use dioralyte instead of pure water for replacement. diluted juice.
norovirus and c.difficile has to be reported.
electrolyte disturbances – hypo/hypernatremia, acidosis, acidosis, hypoklemia (3-3.5: oral replacement or 20/1000 ml saline over 2-3 hours; 2.5-3: 40/litre over 4-6 hours; <2.5 or with ecg changes at any low level such as prolonged QTC, flat t waves at risk of arrhythmia; <1.5 will be paralysed, muscular weakness, apneoic. ECG-CARDIAC MONITOR-CONSIDER RESUS
discussion about hyponatremia and its management

 

PALPITATIONS
multiple cases discussed and shown, along with rhythm strips, interactive 1 hour session with responses from the audience tailoring the talk. VERY interesting.

The Intestinal Obstruction That Wasn’t

84 year old male – known to have chronic constipation, and on warfarin for atrial fibrillation – referred in by his GP for ‘inability to open bowels for 2 weeks’ – yes you read that right folks, T-W-O W-E-E-K-S! – ‘increasing abdominal distension and abdominal pain, along with decreased appetite and a possible mass in the pelvis/abdomen going above the umbilical area’.
The nurse triaging him came to me, asking for some pain relief for the patient ‘and an enema because that’s what he usually has for his constipation’ – I decided to go see the patient myself. I stepped into the cubicle and the gentleman seemed to be in some discomfort, but he kept saying that he was in an uncomfortable position/posture rather than anything else causing him discomfort. I introduced myself and asked him what had brought him to ED – he replied by telling me he had not opened his bowels for 2 weeks now, and though was still passing wind and had passed some today, he was drinking very little and felt nauseous and omitted a few times in the past 3 days. I asked him if he had been passing urine normally, and he reported that yes he was peeing fine, but that he was drinking so less due to the nausea that only small amounts were trickling when he needed to go. I took that statement at face value and moved on. He was lying in a trolley, awake but lethargic and completely oriented. His observations were all within normal limits except for a systolic BP of 89, and his GP notes reported a background of chronically low blood pressure. I examine him, of particular note is his visibly very distended tummy – which assort but distended, feels like gaseous distention from the percussion notes, and with tinkling infrequent bowel sounds – and is quite sore particularly in the lower half of the abdomen, and I can also palpate a mass in the lower part of the abdomen – the patient reports that’s been going on for atleast 3-5 days, possibly when the vomitting began as well. This seemed very much to me to be a classic case of intestinal obstruction – and the management plan is – do baseline bloods (already very kindly done by the triage nurse), get venous access (also done), start some fluids, abdominal X-rays, nasogastric tube and surgical referral, and also catheterise patient, to monitor intake and output.
I speak to my registrar who agrees with said plan of action and while I request the X-rays and take the patient down for it, the lab apparently calls back and my registrar takes the call – the patient’s urea is 44, and the creatinine is 469, last creatinine 3 weeks ago was 141 – so he is going into renal failure, if not there already. While I seemingly faff around with the surgical consult, my registrar gets an ultrasound machine, and I assume it is to rule out a AAA, so I walk into the cubicle with him. And he explains to me a great pearl of wisdom that clearly comes with experience but is such a simple thing that I am left berating myself for not thinking about it earlier. He told me that if someone comes in with such significant renal function decline so acutely, always think of and rule out an obstructive cause for this presentation before moving on to other more sinister things. He was doing an ultrasound to look for hydronephrosis or hydroureter, which is basically the dilated urine collection channels in the kidney downwards and the reason they are dilated is due to an obstruction further down the channel. And that is exactly what he found. The left kidney was moderately enlarged but the right kidney was massive and its ureter was like a fire hydrant pipe rather than the small thin tube – and the mass in the lower part of the abdomen, going from pelvis and extending up from the umbilical area? His urinary bladder!!! I was in shock – as my registrar then gave me the second pearl of wisdom: never believe anything you are told, do not take it for granted until you have objective evidence. The patient felt he was peeing less and less because he wasn’t drinking enough. Yet he was peeing less because the channels beyond his bladder were so narrowed and obstructed that they did not allow emptying of the bladder and it just kept filling up till it was a massive huge thing floating in his belly. I at once made arrangement to catheterise the patient, whereby 2000 ml (that’s 2 litres!!!) of dark brownish urine poured forth out of him.

He had been in urinary retention for the better part of 3-4 days, possibly due to an enlarged prostate that had just gotten worse, and his constipation (though being chronic) was either a factor of his massive bladder pressing on his rectum/colon and not allowing the contents to move ahead; or (a bit like the chicken and egg thing, of which came first?) he was constipated, which gave him some abdominal pain (expected) and that pain had the added effect of causing urinary retention – anyways, after passing the catheter and draining all that urine the patient felt quite comfortable, and the surgeons took him away to do their wonderful things.