Author: Mark Winstanley / Codes: CC1, CC2, CP1, NepC1, RP7, SLO1, SLO3, VC3 / Published: 01/06/2020
Dr Kirsty Challen
Dr Mark Winstanley @markwinstanley4
1. Gauss T, Ageron FX, Devaud ML, et al. Association of Prehospital Time to In-Hospital Trauma Mortality in a Physician-Staffed Emergency Medicine System. JAMA Surg. 2019;154(12):1117‐1124. doi:10.1001/jamasurg.2019.3475
2. Kassam, F., Cheong, A. R., Evans, D., & Singhal, A. (2019). What attributes define excellence in a trauma team? A qualitative study. Canadian journal of surgery. Journal canadien de chirurgie, 62(6), 450–453. https://doi.org/10.1503/cjs.013418
3a. Beks RB, Peek J, de Jong MB, et al. Fixation of flail chest or multiple rib fractures: current evidence and how to proceed. A systematic review and meta-analysis. Eur J Trauma Emerg Surg. 2019;45(4):631‐644. doi:10.1007/s00068-018-1020-x
3b. Beks RB, Reetz D, de Jong MB, et al. Rib fixation versus non-operative treatment for flail chest and multiple rib fractures after blunt thoracic trauma: a multicenter cohort study. Eur J Trauma Emerg Surg. 2019;45(4):655‐663. doi:10.1007/s00068-018-1037-1
4. Dixon JR, Lecky F, Bouamra O, et al. Age and the distribution of major injury across a national trauma system. Age Ageing. 2020;49(2):218‐226. doi:10.1093/ageing/afz151
5. Probst MA, Gupta M, Hendey GW, et al. Prevalence of Intracranial Injury in Adult Patients With Blunt Head Trauma With and Without Anticoagulant or Antiplatelet Use. Ann Emerg Med. 2020;75(3):354‐364. doi:10.1016/j.annemergmed.2019.10.004
Dr Andy Eynon
Dr Mark Winstanley @markwinstanley4
– can you give pressors peripherally
– Initiation of vasopressor infusions via peripheral versus central access in patients with early septic shock: A retrospective cohort study
– Delaney 2019, EMA
– the swings and roundabouts of fluid resus in sepsis seem to have concluded with the idea that salty water is worse than less salty water and that fluids overall are probably a bit overdone. As a result we should probably be giving more pressors early. This means an ICU bed and a CVC doesn’t it? Well lots of folk have been advocating (without data) that peripheral pressors at least at a short term are a good idea. It’s unclear of how often this is actually being done or how safe it is or how it helps.
– this is a post hoc analysis of the ARISE trial which was one of the big sepsis EGDT studies from a few years back
– it is very simple descriptive data
– they have the bizzarre primary outcome in this paper of 90 day mortality which is not likely to be impacted by peripheral pressor use
– you got into this cohort if you got a peripheral pressor for at least 30 mins and you fulfilled the ARISE inclusion criteria
– 1600 in ARISE, 400 or so who got peripheral pressors
– peripheral pressor patients were much sicker (very unsurprising) and also had higher overall mortality (also very unsurprising)
– mostly norad given peripherally with a smattering of metaraminol and adrenaline
– they don’t have any data on safety but interestingly a small number never went on to get a CVC (probably because they got better)
– all this tells us is that it’s being done quite commonly for septic patients in australasia.
– lots of unanswered questions
1) concentration. usual 3mg/50mls norad is 60mcg/ml. Should it be less
2) which pressor – in Ireland there seems some magical thinking that phenylephrine is safe peripherally and nothing else is
3) what type of bed can you do this in. Seems fine in resus for a few hours but i suspect still needs a critical care admission somewhere
– finally there’s a much larger dutch elective theatre trial that had 14000 norad infusions with 5 extravasation events, none of which required intervention
In the interest in a return to normal business Becky and Chris look at the updated VTE guidance from NICE this month, published in March 2020.
Other great resources are the St Emlyns guidelines review on this and the SGEM 219 on PE!
We’ll look at DVT first.
First and most important is to make sure you are taking a history, examining your patient and considering other causes of leg pain and swelling other than a DVT.
We’d encourage you to use an app, a book or a proforma in your day to day practice to help you remember the different scores and risk stratification systems, there’s loads to remember and outside of an exam it makes no sense to try to.
For DVT you need the two level Wells score if you are considering a diagnosis of DVT.
This will return two options
DVT likely: In which case crack on and get an US doppler organised. This should be done with results available within 4 hours. Also do bloods including a D-Dimer.
DVT unlikely: Do bloods including a D-dimer. If the D-dimer is negative then consider other causes and discharge with safety netting advice. If positive proceed on to ultrasound doppler.
In both groups iof a scan result can;t be achieved within 4 hours then organise interim therapeutic anti-coagulation (we both use LMWH) and organise a scan within 24 hours.
If your patient is in the DVT likely group and has a first scan that does not show DVT BUT has a raised D-dimer then a repeat scan at 7 days is recommended.
There a great episode of the SGEM worth taking a listen to, with Ken and Jeff Kline talking PE and the PERC score.
In ED if considering a diagnosis of PE and there less than a 15% chance your patient has a PE then use the PERC decision tool. There are a number of strategies for doing this, be it senior clinician gestalt, to applying the Wells score for PE simultaneously. (Use a scores calculator app remember!!)
If your patient scores positive on PERC and is PE likely on Wells then move straight to CTPA. Organise this test immediately. Don’t wait for a D-dimer here.
If PE unlikely then doing a d-dimer is the way to go with a CTPA if positive.
There are a variety of combinations of anticoagulant options recommended in the guideline and we’d recommend taking a look at the guideline and engaging with you local haematology service to ensure you’re doing the right thing in you neck of the woods.
Disappointingly the guideline doesn’t feel like it expands much on our knowledge of thrombolysis for PE but does specify that it should NOT be offered in the context of a stable patient with or without right heart strain, but to consider it in the context of haemodynamic instability. They don’t define what constitute instability so have left it nice and vague. If in doubt, phone a friend, share the decision making!!
We hope the podcast has proved useful. As always we’ve learnt loads in prepping it!
Let us know your thoughts and feedback and we’ll be back next month!
Can patients guide their own IV rehydration requirements?
Title of Paper:
Thirst-guided participant-controlled intravenous fluid rehydration: a single blind, randomised crossover study
Journal and Year:
– Clinical dehydration is a continuum rather than binary state with no internationally recognised definition.
– Clinical signs can be subtle and unreliable
– Thirst is how we manage our body water homeostasis when doctors aren’t around
– Plasma osmolality considered a reliable surrogate objective marker of dehydration
– Increases with uncompensated water loss
– Increase detected by hypothalamic osmoreceptors → ADH from pituitary
– Hypovolaemia also triggers thirst through angiotensin II and baroreceptor mechanisms
– Single-blind, counterbalanced, randomised cross-over trial
– Physically active adult male volunteers
– Excluded if they had: cardiovascular, renal or hepatic disease, heat intolerance, taking medications which might affect thirst or salt / water handling
So most of our patient population then…
What did they do?
– Dehydration of participants with exercise in warm, humid environment followed by participant controlled IV rehydration.
– Dehydration – exercise-heat stress (exercise bike 30 mins on 10 mins off, repeat) until 2-5% reduction in body mass
– Rehydration – 4 hours
– Low versus high volume boluses
– Both had background 4% dext 0.18% saline at 50ml/hour
– VAS measured: not thirst to very thirsty
– Patient controlled pump (like a PCA but with fluids)
– Set to give additional bolus over 10 minutes (allowing 6/hr)
– Low volume – 50ml over 10 mins
– High volume – 200ml over 10 mins
– Timing of each bolus recorded by investigators
– Repeated for opposite condition 7 days later
– Blinding – cold damp towel on arm, couldn’t see pump (just knew it was running or ready for another bolus), earphones so couldn’t hear pump
– After 1 hour drew samples every hour for pOsm and VAS thirst at same time
Summary of Results:
– 10 completed study
– Dehydrated 3.9% in both conditions
– HV thirst scores and push frequency lower at each stage of rehydration assessment
– Push frequency significantly decreased in HV by third hour vs 4th hour in LV
– Total rehydration in the HV group was higher over course of rehydration
– pOsm as reduced from 1h in HV, and not until 3h in LV
– Basically – patients thirst was an indication of hydration / pOsm and this improved with fluid boluses
– Suggests that [healthy] individuals can rely on thirst to manage own parenteral rehydration
– HV had potential to administer excessive fluid
– The timely responsiveness of thirst to IV fluid is particularly important to mitigate risk of fluid overload
– Findings support results of their previous pilot (unblinded) study showing that thirst driven was better than clinician led
Their participants had fluid loss through sweat – extracellular fluid becomes hypertonic vs gastroenteritis where water loss wtih proportionate salt loss so ECF may remain isotonic.
Fit healthy individuals.
– The demand for self-administered IV fluid in response to thirst is related to the degree of dehydration
– The rate of self administration reduces in frequency in proportion to the degree of correction of fluid deficit
– Individuals are able to rely on their thirst to appropriately guide demand for fluid intake, irrespective of fluid delivery rate.
– Future work must focus on whether patient controlled IV fluids could represent a paradigm shift in the management of hydration in the clinical setting.
Clinical Bottom Line:
Clearly not applicable to our patient population but food for thought. How do we think it would pan out in hyperosmolar patients (HHS/DKA) or fluid sensitive patients (CCF)?
Maybe we as clinicians should just stop thinking in 500 and 1000ml volumes.
I’m going to keep asking patients if they are thirsty…