Category: Critical care / ICU


Course Review: Advanced Paediatric Life Support (APLS)

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Paediatrics, Uncategorized by Casey Parker — 7 Comments
April 9, 2012

Last week I completed the APLS course over 3 days.  I am an impartial educator and thought I would give my review – so what did I think?

APLS is a well organised and run course.  It covers a lot of material over 3 days.  The level is pitched at the post-graduate trainee – ideally PGY 2 -4 I think.  The days were long – 11 hours of material in a day… this is probably counterproductive.  The course could be streamlined I think without losing too much.

At ~$1900 – it is a reasonably expensive course.  For that money you get a lot of theory, manikin-based scenario training, but no animal / cadaveric models to improve your clinical skills.

The learning is largely based around lectures – not everybody’s preferred format!  I found the lectures a bit long and repetitive, especially if you had done the required pre-course reading of the manual.  The teachers were friendly and well-informed, and an effort to remain entertaining was evident.

The scenarios and skills stations were OK.  As a more experienced participant I found being put on the spot in simulation to be a strong learning tool and allowed me to identify my weaknesses and cognitive errors.  I was aware that some of the more junior participants found the live simulation a bit confronting.

The material presented is largely up-to-date, though there are some areas where there is a lack of evidence base.  For a ‘resus course’ the absence of ultrasound strategy was striking.  The preference for ETT over LMAs in resus seemed odd given recent changes in most major guidelines

The testing and scenarios were OK, but did lack some flexibility to allow more experienced clinicians to make judgement calls rather than blindly follow protocol – ie. there is some ‘lowest common denominator’ effect – I guess this is a function of running such a broad ranging course.  Good for jnior staff, but a bit frustrating if you are 10+ years into your career.

Summary:

APLS is a well run course that covers an ambitious amount of material in 3 days.  The educators are entertaining and well-versed.  I recommend it to junior doctors, and staff who are unfamiliar with Paeds patients and wanting to extend their knowledge from adult care.  For the office GP who wants to brush up their resus skills – it is OK.

If you already do a lot of Paeds, especially in ED or anaesthesia environments than this course might e aiming a bit below your educational needs.

Any one out there got experinces of the APLS to share?    Casey

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C-spine Trauma: in a town with no CT

Filed Under: Critical care / ICU, Emergency, Pearls and Pitfalls, Useful Evidence by Casey Parker — 3 Comments
March 12, 2012

I worked for 4 years in a town with no CT (but plenty of beer) – and it is fair to say that the protocols for managing C-spine trauma were often makeshift.  Logistics rather than clinical acumen often determined who got a CT rather than ‘just’ clinical exam and a set of plain films.  But…. why should my patient get less than gold-standard care – just because of geography?   I realize this is a bit idealistic, but when it comes to life-long disability – do we really want to take that risk?

Now in recent months there has been a lot of posting and banter about C-spine trauma on the popular medical blogs / podcasts.  So I thought I would trawl through the literature and come up with a pragmatic protocol for those of us who work in CT-isolation, or where it is not available 24/7.  Amusingly here is a hot debate about whether you need to MRI patients with pain and a normal CT – Yep, true!  We are not even close to that debate in regional Australia!

The logistics of distance mean that I break (‘scuse the pun) C-spine trauma into 3 main groups:

  1. The minor trauma – these are the patients whom you can clear with clinical history, exam and NO imaging is required.
  2. The fuzzy middle group: they cannot be cleared on clinical grounds for whatever reason, or they have failed the clinical clearance. Yet, they remain asymptomatic, have no high risk features –  your “gestalt” is that they are probably OK.
  3. The major trauma: these patients are high risk – based on the mechanism of injury, associated injuries or the presence of neurology suggestive of a cord injury

I will try and explain how I think each of these should be managed based on my reading of the recent evidence, the reality of rural practice and a measure of common-sense.  If you want to get some great background and refresher in anatomy I have a few suggestions for your valuable time:

OK, without further waffling – lets analyse these 3 groups and try to cook up a rough protocol for each.
In some ways this should be the easiest group – but is also the one that causes the most frequent consternation!
Clearing a C-spine is one of those moments in medicine when you just have to trust your call. This is especially true in the bush – if you decide not to clear them – you are probably committing them to a long transfer strapped to a spinal board: uncomfortable and expensive!
So how do you clear a C-spine clinically? Here is how I do it – I use MDCalc’s Canadian C-spine tool – but be warned – you have to use it properly. These rules are derived and validated by following the protocol to the letter – if you do not follow the protocol as described you cannot achieve the same sensitivity. The Canadian C-spine seems to be better than the NEXUS rule (NEJM, 2003) – but you must have an alert, sober, orientated and cooperative patient – so a lot of our customers are self-excluded! Scot Weingart describes an interesting combination of the 2 rules.
As the receiving doctor in a CT+ town – I really want to know that the patient has had a proper attempt at C-spine rule clearance – otherwise we are squandering valuable flight resources and irradiating unnecessarily.
This group includes the people whom you cannot clear clinically as they are too drunk, disorientated, in pain, etc to qualify for a clear Canadian C-spine rule PLUS those who have failed the rule – ie. they have tenderness, pain on rotation, are too old etc.
So according to the rules they get “imaging”.  Easy: off for a set of plain films, right?  well maybe not such a great idea.
A good number will have sub-adequate views, and then you need to ask – what is the sensitivity OR the negative predictive value of plain films for C-spine injuries…?  Well they are not so great – in fact the term ‘suck’ has been used to describe them!
This series from the Journ. Trauma 2009 showed a sensitivity of plain films c/w CT for serious injury of less than 50% – that is worse than a coin toss!
However, some protocols continue to advocate plain films as a ‘screen’ for fracture in the lower-risk groups.  I guess this means the patient who so nearly passed the clinical clearance test (eg. were just 65 years old only, had transient pain…) But it is a small group – so the role of plain films is vanishing rapidly.
So in summary – there are not many patients we can reliably clear with plain films if you follow the evidence and guidelines as written.
Therefore if you are in a CT-less town, and have one of these patients – you probably should transfer for a CT.  If you think they are low-end risk, and have a good set of films then it is a judgement call on your part.  Traditionally we have cleared patients on this basis – but is it still the standard of care?
This is really the easiest group to decide upon. Sure, the toughest to manage, but the easiest to make a call on C-spine imaging.
If you have a patient with a high-energy mechanism, bony tenderness, neurological signs or major injury (esp head) then you need not bother with plain films. These patients need transfer – not imaging. This is the scenario where you want to get them to a trauma centre ASAP – probably for more than their neck injury. Taking them through the Xray Dept, moving them 3 or 4 times – for a series of images will add little to your management! Assume they have an unstable injury and manage them appropriately. If you are wrong – great, if you are right – then you have done the right thing!
Finally a quick note on C-Spine collars
  • Rigid C-Spine collars are omnipresent in ED trauma patients, they are almost like religious artifacts – there is a lot of belief in their powers, but is there the evidence to back them up??
    • The Journ Emerg Med 2012 published an article by Holla which looked at healthy people and the effect of collars – basically they did not actually immobilize any more than the padded boards / straps and decreased mouth opening.
    • There is no hard evidence to say they actually decrease neurological injury / improve outcomes.
    • We all know they are a pain, ill-fitting and your worst enemy when trying to intubate!
    • So here is my take – immobilisation is good, collars are window dressing.  If you really want to keep the neck still – provide good analgesia and anti-emesis, supervise the patient closely (esp. if they are drunk, head-injured etc), they will need a nurse / doc by the bedside constantly to do this right!
    • If you use a collar  and it is causing problems: pressure, pain, airway obstruction or really making the patient hostile – then take it off and keep a close eye on them.  Prima non nocere.
Twitt
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Post op pain puzzler discussion

Filed Under: Anaesthetics, Clinical Cases, Critical care / ICU, Surgery, Useful Evidence by Jonathan — 2 Comments
March 9, 2012

Hope you guys enjoyed the case. Here is the discussion and hopefully some useful take home concepts.

This case illustrated a number of key acute and chronic pain concepts that all GP anaesthetists should consider when anaesthetising an opioid tolerant chronic pain patient, namely opioid induced hyperalgesia (OIH), central sensitization (wind up) and pre-emptive analgesia.

In this case, our patient did not receive adequate perioperative analgesia or pre-emptive analgesia based on his chronic pain and opioid dependent background. He was left in distress for a period of time in which his pain became unmanageable (wind up) and remained so for 16 hours. It seemingly became non-responsive (OIH) to opioids but rotation to a new opioid, a background infusion of a NMDA antagonist and the use of a regional technique helped immensely.

Opioid induced Hyperalgesia

Opioid induced hyperalgesia is a paradoxical response to opioids in which patient receiving opioids have an enhanced response to painful stimuli resulting in hyperalgesia. This results from the upregulation of pronociceptive pathways in the central and peripheral nervous system.

Acute OIH occurs in various settings, most commonly post operatively in the opioid dependent patient but also in low dose and maintenance dose regimes. OIH is distinct from tolerance in that tolerance is reduced effectiveness of an opioid at a receptor over time.

NMDA receptor activation is important in the development of OIH. Antagonism of this receptor has been shown to reduce progression and improve post operative pain especially in opioid dependent patients (Wu + Macintyre + Huxtable et al).

Using an opioid PCA in opioid tolerant patients allows consumption and background requirements to be monitored. A basal infusion equivalent to the patient’s usual daily opioid use should be considered or given orally as tolerated.

Ketamine has been shown to reduce OIH in the post-operative setting (Vadivelu + Huxtable + Macintyre et al). There is evidence that subanaesthetic doses (0.1-0.2mg/kg) of ketamine provides excellent analgesia in opioid dependent patients and prevents opioid induced hyperalgesia in patients consuming high doses of opioid for postoperative relief. (Macintyre et al + Vadivelu et al).

Opioid rotation is the practice switching from one opioid to another to improve analgesia and reduce side effects (OIH in this case). This concept is based on the premise that individual opioids act differently on different opioid receptors and that tolerance between them is likely to be incomplete.

Practically this is preformed by using opioid equivalence charts and commencing with 50% of the equivalent dose and titrating up. (Huxtable)

Methadone together with its mu-receptor agonism has weak antagonistic properties on the NMDA receptor thereby playing a small role in OIH.

Wind up (central sensitization)

Post-operative pain results from peripheral nociception (primary hyperalgesia) from tissue injury and resultant central nociception (secondary hyperalgesia) in the spinal cord.

Any continuous barrage of activity to the spinal chord leads to central sensitization. Perioperatively this is related to periods of inadequate analgesia, extensive surgery or infection (Shipton).

As this central sensitization continues from the noxious stimuli, this maintains secondary hyperalgesia, amplifies post operative pain and contributes to chronic pain.  Central sensitization will manifest clinically as hyperalgesia (increased pain sensitivity) and allodynia (pain in response to a previously non-painful stimulus) (Macintyre et al).

 

NMDA receptor activation plays a key role in central sensitization. Medications such as Gabapentin, Pregabalin and Ketamine have been found to improve post operative pain and thought to reduce the progression to chronic pain.

Using Ketamine at subanaesthetic doses (0.1-0.2mg/kg) antagonizes the NMDA receptor and produces an antihyperalgesic, antiallodynic and anti-tolerance effect. It is useful in pain associated with central sensitization such as severe acute pain and opioid resistant pain.

Pregabalin is a safe and well tolerated and helps to reduce perioperative opioid consumption. It has been shown to decrease the incidence in the progression to chronic pain. Gabapentin similarly has been shown to prevent chronic post surgical pain syndromes (Shipton).

Pre-emptive & Preventative Analgesia

Pre-emptive analgesia is treatment that is initiated before the surgical procedure in order to reduce peripheral and central sensitization. This in effect helps to reduce post operative pain and prevent chronic pain development (Dahl)

Preventive analgesia is simply the well thought out provision of analgesia within the postoperative period and persistence of treatment beyond the expected duration and aims to minimize central sensitisation (Macintyre et al)

Ketamine modulates central sensitization caused by incision and tissue damage and can be used perioperatively to antagonize this (Vadivelu).

Preoperative pregabalin is opioid sparing and improves post operative pain scores. It is a useful adjuvant and anti-hyperalgesic agent used in a multimodal regime.

Prevention of Withdrawal

Inadequate opioid supplementations in the post operative period can lead to withdrawal characterized by excitatory autonomic symptoms. The onset will depend on the individual opioid’s duration of action (Macintyre et al).

Opioid tolerant patients should firstly be identified preoperatively and continue their preadmission opioid regimes with appropriate route substitutions as clinically directed.

Heavily weighted non-opioid regimes should be used with caution as opioid tolerant patient due their risk of withdrawal (e.g.: pure non opioid regime or tramadol as a sole opioid).

If withdrawal is suspected, Clondine can be used orally and intravenously to aid in the symptomatic management.

 

Key Messages

Preoperatively identify opioid tolerant and chronic pain patients and make a peri/post operative analgesia plan

 Always replace a patient’s preoperative opioid use in the post-surgical period

Consider preventative analgesics such as Ketamine, Pregabalin and Gabapentin to prevent central sensitization and subsequently wind up pain.

Consider an opioid rotation in patients who respond poorly to an opioid regime or with escalating requirements

Reverse analgesic ladder on recovery with background opiate titration

 

Hope this helps. Let me know what you think.

Jonathan

 

Baron R (2006) Mechanisms of Disease: neuropathic pain – a clinical perspective. Nature Clinical Practice Neurology 2: 95-106 http://www.nature.com/nrneurol/journal/v2/n2/full/ncpneuro0113.html

Dahl JB, Moinche S (2004) Pre-emptive analgesia. British Medical Bulletin 71(1) 13-27 http://bmb.oxfordjournals.org/content/71/1/13.long

Huxtable CA et al (2011) Acute pain management in opioid-tolerant patients: a growing challenge. Anaesthesia & Intensive Care 39: 804-823 http://www.aaic.net.au/document/?D=20110262

Macintyre PE et al (2010) Acute Pain Management: Scientific Evidence 3rd Edition. Australian & New Zealand College of Anaesthetists & Faculty of Pain Medicine http://www.anzca.edu.au/resources/college-publications/Acute%20Pain%20Management/books-and-publications/acutepain.pdf

Mitra S et al (2004) Perioperative Management of Acute in the Opioid dependent Patient. Anesthesiology 101: 212-27 http://journals.lww.com/anesthesiology/Fulltext/2004/07000/Perioperative_Management_of_Acute_Pain_in_the.32.aspx

Patanwala A et al (2007) Opioid Conversion in Acute Care. Annals of Pharmacotherapy 41: 255-67 http://www.theannals.com/content/41/2/255

Shipton E.A (2011) The transition from acute to chronic post surgical pain. Anaesthesia & Intensive Care 39: 824-836 http://www.aaic.net.au/document/?D=20110056

Vadivelu N et al (2010) Recent Advances in Postoperative Pain Management. Yale Journal of Biology and Medicine 83: 11-25 http://www.ncbi.nlm.nih.gov/pubmed/20351978

Wu CL et al (2011) Treatment of acute postoperative pain. Lancet 377: 2215-25 http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60245-6/abstract

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Clinical Case 043: Post-op pain puzzle

Filed Under: Anaesthetics, Clinical Cases, Critical care / ICU, Surgery by Casey Parker — 4 Comments
March 4, 2012

This case comes from Dr Jonathan Ramachenderan.

59 yo man presents with a small bowel obstruction likely secondary to adhesions. He has a background history of 4 previous laparotomies for recurrent bowel obstructions and Chronic Back pain with a spinal fusion 10 years previously.

He appears chronological older than his age and currently takes 100mg BD of Morphine Sulfate, Tramadol SR 150mg BD, Paracetamol SR 775mg TDS and Duloxetine 30mg. His renal and liver function is normal and he is intolerant of NSAID due to gastric irritation.

The procedure is long due to difficult division of adhesions and takes 5hours. He requires 30mg of Morphine intraoperatively and receives 100mg of Tramadol and 1gram of Paracetamol. Ketamine is considered but not given.

Possible alternatives: TAP blocks, Continued Ketamine boluses and or infusion

2 hours later he is in extreme pain, moaning, uncomfortable and unmanageable on the ward. You are called to assess and manage him.

Ketamine infusion is started (0.1-0.2mg/kg/hr) [80kg = 8-16mls/hr of Ketamine 200mg in 200mls] PCA bolus is increased to 2mg with a background of 3mls (3mg) an hour

There are multiple calls through the night as the patient’s analgesia isn’t adequate. He is uncomfortable and obviously distressed when you see him the next morning. He isn’t able to move in the bed and simply lifting his gown to examine him is painful. He has used 200mg of morphine in 16hours.

TAP block is preformed for the patient’s acute pain (Tranversus Abdominis Plane identified under ultrasound and 20mls of 0.25% bupivacaine is infiltrated bilaterally). TAP Blocks are described here at the NYSORA site,  evidence for their efficacy is here from Anaesthesia-Analgesia  2007, McConnell Et al.

His opioid is rotated (morphine to fentanyl) and opioid requirement is revisited and an equivalency is calculated (200mg oral morphine = 1200mcg fentanyl/ 24hours). He is then given a background of 50mcg/hour with a 20mcg bolus.

Methadone is also started intravenously 10mg BD.

Ketamine is continued at 0.1mg/kg/hr.

His pain relief is instant following the TAP block on the ward. The opioid rotation helps to alleviate his pain and as his oral intake begins, he is re-started unto a lower oxycontin dose (75mg BD) with breakthrough oxycodone. His ketamine is first to come down as his pain remits and his fentanyl PCA is soon to follow. He is also commenced unto his regular tramadol with pregabalin 50mg TDS.

On discharge the “Reverse analgesic ladder” is described and handed over. The patient’s preoperative opioids are given together with his oral “as required” opioids titrated down over 1-2 weeks. This is on a baseline of multimodal analgesia. Importance of multimodal analgesia is that multiple analgesic agents are additive and synergistic in their action and opioid sparing.

Great Case JR!  We will run a second post discussing the theory and practicality of managing post op pain in chronic pain patients soon.  Love to hear your feedback and pearls around this scenario.  Thanks – Casey.

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Dr Tim’s other cookbook

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls by Casey Parker — 6 Comments
January 5, 2012

Dr Tim Leeuwenberg, from sunny Kangaroo Island, South Australia – author of the KI Docs blog has just finished his year in Anaesthesia training and has created a great resource for all to share.

Tim has spent many long hours collating a series of checklists, emergency reference cards and resources to cover pretty much anything that can go wrong in a small hospital ED or theatre.  And being the generous guy that he is – it is all free as a gift to you from Dr Tim, via Broome Docs – nice!

This is such a great resource I have decided to put it up in the permanent “Clinical Resources” section at the bottom end of the site.  Or you can be lazy and just click this link!

I am sure Tim is keen to get your feedback and I know he is gearing up to run a survey looking at the management of Airways in small hospitals – he is truly a man on a misison.  So hit us with your comments on this site – or direct to Tim via KI Docs.

Oh, in case you were wondering – Tim’s first cookbook was “Roadkill Recipes”  which you can check out at Wrong Side of the Road.

Enjoy and learn from Tim’s hard labour

Casey

 

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Clinical case 039: Ectopic ectopic – a Gedankenexperiment

Filed Under: Anaesthetics, Clinical Cases, Critical care / ICU, Emergency, Obstetrics, Pearls and Pitfalls, Specialist Tips by Casey Parker — 12 Comments
December 29, 2011

This case starts with a bad gas.  This patient arrived ‘in extremis’.  Suspected ectopic transferred in by plane with the following data:

  • Urinary HCG positive
  • Abdominal pain for a few days
  • No urine output for the last 24 hours
  • Hb in the remote clinic was 130 g/l yesterday
  • A 14 second US in ED showed a lot of free fluid, black with swirling clots in it….

She got an arterial line at the door and here is her opening ABG:

pH = 6.90

pCO2 = 58

 pO2 = 255 (on rebreather 10L)

 HCO3 = 10

BE = – 15

 Na = 140

K = 8.9

Ca = 0.76

Glucose = 21  (~ 380 in the US)

Lactate = 10.5

Hb = 58 g/l (was 130 a few hours ago, and she has had 4 units PRBCs in transit)

The Obstetrician and Surgeon are there, keen to get in and control the bleeding ASAP.  But I am a bit nervous about “whizzing her off to sleep” without a little more resus and think time. 

So here are a few random questions about this case that I would like to hear your answers to.

  1. What drugs / agents would you want to give this patient before induction / intubation?
  2. What is you plan A for induction and intubation, including ventilator settings?
  3. What blood products / factors do you want to give in the next 30 minutes or so…?

Ok, those are the questions to ponder.  Tough case.  And that is all the info that was available at the time.  Clearly not one where we can wait too long before jumping in and getting control.  So what are you going to do?

Casey

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Clinical Case 036: Silent, sitting sepsis

Filed Under: Clinical Cases, Critical care / ICU, Emergency, Tropical disease by Casey Parker — 8 Comments
December 15, 2011

This case is part of my “Sepsis week” at Broome Docs.  Lets say this case happpens in January, just after the first big rain for the wet season.

58 yo Aboriginal man, presents to triage at ED complaining of “cold sick” [flu] symptoms. Has been feeling hot, sweating and had a non-productive cough intermittently for a week.  No good localising symptoms.

Obs:  P= 110,   temp = 38.9,    RR = 20,   BP 110/50,   SpO2 = 97% RA   BGL = 17.7 mmol

PMHx:  type 2 DM, untreated.   Hypertension,  gout and  recently investigated for PR bleeding = diverticulosis, old rheumatic heart disease – mild MR on ECHO.  “Drinks a bit”

Meds = perindopril / hydrocholothiazide,  allopurinol, aspirin.

Examination:  Sitting up, smiling.  ENT – normal, chest clear, systolic murmur c/w MR, abdomen soft, though mildly tender in the RUQ.  No loin tenderness.  No skin lesions. Alert and quiet, happy to sit…  Urinalysis = gluc 3+, protein 2+, blood +

This man gets a triage score of 3 – which means he should be seen within 30 minutes.  So after waiting his allotted 30 minutes he collapses in the ED waiting room and gets carried into the Resus bay….

Obs: pulse = 150 thready, BP = 70/30,  RR = 35 shallow,  Spo2 unrecordable, GCS = 8ish.  Groaning, localising to pain.   A bedside BSL = 20.3 mmol.

A portable CXR is done, and an ABG is drawn on 15L via NRB

pH = 7.19

PaO2 = 84

PaCO2 = 29

HCO3 = 12

Lactate = 6.3

BE  - 14

Here are the questions?  I will give it a day or two for answers to come in from the readers…

Q1:  What is your next move?

Q2:  What bugs do you need to cover to ensure you give adequate early empirical antibiotics?

Q3:  If you chose to intubate this man – what ventilator settings would you go for?

 

 

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Sepsis: Can we pick who’s sick?

Filed Under: Critical care / ICU, Emergency, Internal Medicine, Uncategorized, Useful Evidence by Casey Parker — 3 Comments
December 12, 2011

I have been going on about sepsis for a while now around the hallways.  So – what is all this talk about?  I think we need to have a robust system in place that allows a small hospital to detect early (occult) sepsis, intervene early and manage it in a way that is evidence-based and inline with the ‘best practice’ out there.  

If you are like me you find new information hard to process – so I think the best analogous process we have to “map” this onto is the “Chest Pain Pathway“.  The principle is the same:

  • Acute coronary syndromes and sepsis are both severe life-threatening problems
  • They can be subtle / difficult to diagnose, especially in the early stages, or in patients with atypical presentations
  • They both benefit greatly from early aggressive intervention (thrombolysis vs.resus & IV ABs)
  • We need to cast the net wide to ensure we “catch” all the badness – this means we will find nothing in 99 out of 100 people we screen – but that is OK, if we catch the sick one (eg. we do ECG and troponin on anyone with pain between their head and bum “just in case” – it is a low-cost, low-risk test to do)
  • The protocol is “nurse-based” – it kicks off at triage, therefore gets done early and is not dependent on the whim of the doctor or the busy-ness of the department – it just happens.

So how do I think it should work?  well, similar to the Chest Pain pathway.  Here goes:

IDENTIFY Patients at risk

This is where we cast the net wide.  Essentially this is the same as using the current MET criteria or COMPASS tool that has been rolled out in the last year or so.  

I have hijacked a simple set of criteria out of the Greater NY Hospital Sepsis Collaborative – with a few modifications which I think are a reasonable screening tool for triage nurses to use in identifying patients who should be in the 100 we look at to find the 1 sick one.  Here are my proposed Sepsis Screening criteria -

STEP  1  Does the patient have any 3 of the following?

  • Suspected infection
  • Temp > 38 deg  or under  35.5 deg,  or history of rigors
  • Heart rate > 90  (or over age adjusted max.)
  • RR > 20  (or over age adjusted max.)
  • Any altered mental state
  • SpO2 < 90
  • Systolic BP < 90 mmHg (or under age adjusted minimum)
  • Prolonged > 2 sec central capillary refill
  • Any child under 3 months of age
  • Any indwelling invasive devices (PICC, IDC, Hickman etc)
  • Dialysis patient (Haemo or peritoneal)

So if your patient meets these criteria, then you go to step 2 – activate the screening tool:

STEP 2 

If 3 criteria met => Activate the Sepsis screening panel

  1. Notify senior Doctor
  2. IV access and take blood set:
  • FBP, UECr, CRP, VBG / lactate, blood cultures, coags – URGENT to lab / ED gas analyser
  • Catch urine culture

     3.   Commence frequent obs in monitored bay.

So now – if you screen include 100 patients at Step 1, you can hopefully narrow it down to 10 using Step 2.  The bloods will either be OK, or not OK.  Your best indicator of early sepsis if you had to pick 1 is the lactate.   Lactate can be < 2: normal;  2 – 4: grey zone,  > 4:  bad – needs resus

Lactate is difficult to understand for the uninitiated – so here is a nice summary (Click) (Emcrit)

STEP 3

So now we have narrowed it down to a handful of patients whom might have sepsis from the general ED population.  Armed with a bit more info we can now treat them and  split them into 2 groups -

  1. Fluid responders:  those who get a bolus of fluids and they get better – BP comes up, pulse down, maybe their lactate clears to normal – you are winning.  These patients are good to go to the ward with “normal care”.  They need monitoring for subsequent deterioration on the charts but are not looking likely to “go south”.
  2. Non-responders:  these patients still ahve dodgy looking Obs and unwell after a generous fluid resuscitation over 30 – 60 minutes.  This is the 1 out of 100 whom is going to need the full treatment – and probably invasive monitoring

SAFETY NET

Of course no system is perfect so there are a few Safety net concepts I would like to introduce.  We can also catch patients at the backdoor of the ED.  Those who did not get identified at triage, got the usual workup then came to a point where they need admission or further investigation for PUO, or other infection.  So I think we should runa VBG (lactate) on any body who meets any of the following:

  • Doctor takes blood cultures for any reason – if you do a BC, then do a lactate at the same time.
  • Admission diagnosis = pyelonephritis, pneumonia, severe skin infection, PUO, diabetic foot etc… anyone with a possible severe infection that might go systemic
  • Any infant (< 6 months) sick enough to need admission for infectious cause

Lactate is not the “golden-bullet” for sepsis, but it is better than nothing, and cheap as chips.  The idea is to identify patients who were off to the ward for “usual care” who might benefit rfom a more aggressive strategy and closer monitoring.

Let me know what you think. More sepsis stuff this week
Check out the post on Shock: beyond the BP if you are interested
Casey

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Massive Transfusion Protocol

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls, Pharmacology, Useful Evidence by Casey Parker — 1 Comment
November 24, 2011

Hi – Apologies for recent sluggish activity- I have been a busy Doc lately and working on what I hope are some good posts / resources for you all.

The first Big project I am wanting your feedback on is my “Massive Transfusion Protocol” which you can click here – or I have added as a permanent resource in the “Clinical Resources” section at the bottom of the blog.

Why have I decided to spend hours on this? 

I have always found the current published Massive Bleeding Protocols to be either too simplistic or not descriptive enough.  There are a few crucial decision points – such as” when to activate” – which are glossed over frequently.

Most protocols deal only with trauma – and in my world, the big bleeding happens on the labour ward, in theatre… etc NOT just in the ED resus bay.

So I have written a protocol for me – one which I can with a click on a page access and remind myself of the steps and “recipes” for resuscitaing in major trauma / bleeding.  I have downgraded the role of platelets – because – we do not use them in smaller hospitals and the evidence is not great for empirical use.

I have tried to include some evidence in a ‘hidden’ way to keep it simple in a crisis – or you can read at your leisure later.

Be aware: this protocol relies heavily on your hospital having in place a system-wide approach to this emergency. Your lab have to have a predefined system, your surgeon should be aware of the protocol and the concepts associated with “damage control” operations. This is not the time to get into a territorial dispute, you need to have your chickens all lined up before it happens!

So please read it- this is my draft, I hope to make it more useful with your feedback.

Let me know what you think.  Casey

Twitt
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Shock: Back to basics, beyond the BP

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls, Specialist Tips, Useful Evidence by Casey Parker — Leave a comment
November 6, 2011

Apologies to the smart ones reading this – but I have been trying to explain this concept to my students for a while – so I thought I would share.

Shock: this is defined by hypoperfusion of the tissues resulting in insufficient substrates (oxygen, sugar etc) for aerobic cellular respiration.

The good news is that evolution has supplied us with a back up plan in the event of “inadequate substrate for aerobic respiration” – namely anaerobic respiration – neat eh!  But there is a limit to this – you eventually need to get back to Aerobic metabolism, clear the toxic byproducts of anaerobic respiration and repay the oxygen debt.

Ok that is the technical bit done.  Now onto the clinical application of this science.

In order to maintain tissue perfusion (and fuel / oxygen supply) you need to have blood passing through those little terminal arterioles / capillaries at a rate fast enough to keep up with the demands of the tissue – this can vary also.

Here we meet the problem – we (clinicians) have got no good direct way of measuring the flow or demand in those little vessels.  At the bedside we can just guess as to what is going on.  Unfortunately our instincts for this “guess work” are a bit skewed and that is the point of this post – we need to develop better instincts here.  So this is how I do it.

The blood pressure is an important piece of information – very important – but it is not the only player when it comes to working out the perfusion of the important organs.

Problem is – we all cut our teeth on relatively stable, healthy patients who have good physiological reserve and are operating towards the centre of the comfort zone of perfusion.  In these patients the BP is probably a good proxy for “perfusion”.  BUT – in the patient who is sick (ie. the one where you really want to know what is going on ) the physics are not ‘normal’ – you need more info and here the instinct needs to be developed.

Ok, some boring mathematics now :-

Cardiac output (CO) =   HR   x   stroke volume (SV)                  and              BP   =   CO  x   systemic vascular resistance (SVR)  or  CO  = BP  / SVR

So therefore:     HR  x  SV    =     BP  /  SVR.    Yep, I just tried to reduce CV physiology to 4 numbers. Not always so simple – but its a start.

You can read HR and BP off of the monitor, or even do it manually!

The SV  - hard to measure clinically – you can palp the radial pulse and guess its ‘volume’, you can ask the patient if they have some chronic cardiac disease / cardiomyopathy / IHD.  Or you can pick up an ECHO probe and eyeball it, or ask an ECHO tech to give you a number (LVEF).  Knowing that the preload is good certainly helps – so look at the IVC – is it collapsing?

So that just leaves the SVR – and this is tough.  In a sick patient – you cannot interpret the BP or guess the cardiac output without having some idea about the SVR.  So how can we measure this?  Look at the patient – are they red, flushed or pale and white.  Feel the hands and radial pulse – are they cool and thready or bounding and warm?  Urine output – if this is low – there is a good chance the normotensive patient has a high SVR.  Or you can get a fancy monitor which gives you a number – SVV (stroke volume variation) or Oesophageal Doppler etc.  None of these are perfect.

So once you have guessed the patient’s SVR you are in a position to interpret the BP and make an estimate of the perfusing  cardiac output / cardiac index  (NB: the cardiac index sounds impressive, but it is just the CO divided by the patient’s body surface area.  ie. big people need more CO to perfuse their body than little people)

Confused yet?  Lets look at a few common clinical scenarios to illustrate these points.  Also to look at the uses and abuses of inotropic meds in the hypotensive patient.

If you give a decent slug of propofol to anybody over about 60 – they will probably crash their BP. Is this a bad thing? well yes, but not as bad as you might think.

The propofol causes a loss of SVR by relaxing all the peripheral vessels.  So both the BP and SVR have fallen – the CO is proabably not crashing as much as the BP would suggest.  Of course if the propofool renders the heart bradycardic and negative inotropy reduces the ability of the heart to compensate – this is not great.  But any Anaesthetic doc will tell you – if you give them a whiff od metaraminol / phenylepherine  – the BP comes up quick.  And as soon as the surgeon inflicts pain – they settle quickly.  So here is an example of ‘relative’ hypotension – sure it is low – but so is the SVR – so it isn’t so bad.

This is usually a vasoplegic state – all those inflammatory cytokines cause a decrease in SVR,  the vascular bed expands – making the patient “relatively hypovolemic”.  There is a fall in CO due to poor venous return – so the BP drops as does the perfusing pressure – and shock occurs.  In some (maybe 15%) they get myocardial depression form the toxins of sepsis and also therfore suffer from “pump failure as well as the other mechanisms of shock at play.

So – for sepsis the rule of thumb is :-  give a heap of fluids – more than you think.  Give 2 litres and ask questions later.  If they remain hypotensive / acidotic / high lactate then you might need to give inotropes.  BUT you have to “prime the pump first” – check the IVC / SVV (or CVP if you believe in it) to ensure they are fluid loaded adequately.  So which fluid?   The SAFE trial - no difference between saline and albumin, though there was a trend towards benefit in giving albumin in the septic subgroup.  To me, in a small place Hartman’s (Ringer’s) seems to make sense – it is chaep, easy and doesn’t screw with your acidosis too much?

Then, and only then give inotropes…which one?    I think the answer is noradrenaline – it is widely used for sepsis and makes sense as it has good alpha agonism – so combats the low SVR.  You could also use phenylepherine if you cannot get a CVC.  If htere is evidence of myocardial depression – then you might need to get smarter and use adrenaline or call a friend for help! Having said that Myburgh et al (Aussie ICU crew) showed no difference between norad and epi – so it is a bit theoretical.

This is not the same as the septic patient.  In my mind this is the opposite of sepsis in a way.  Consider a 30 yo. motorcyclist with crush chest and pelvic fracture.  The BP is lowish, you guess he is bleeding into his chest, pelvis, ?abdo… and his endogenous adrenaline is surging – so he has a massive SVR.  So here – a lowish BP equals a crappy CO and his perfusion of the terminal vessels is terrible.  This is not a place to use vasopressors – you will make his SVR go higher and kill the perfusion further.

The patient with hypovolemic shock needs volume +++ – see recent post on Massive transfusion in trauma.  Blood, clotting factors, keep them warm and manage acidosis.  And acidosis is the result of the anaerobic metabolism in the O2-starved tissues – muscles, livers etc.

So here what you want to do is open up the vascular bed, get the perfusion happening ASAP – you actually want to drop the SVR – the catch phrase is “sympatholytic resuscitation”.  You do this by filling them up with volume, then giving fentanyl (or your favourite alternative) to reduce the endogenous sympathetic drive and allow the red cells you are pumping in to get to the areas that need the oxygen.

Remember – target MAP is 65 initially – so if your patient has a comfy MAP of 85, yet you know they have bleed a lot – your BP is giving you a seriously false sense of goodness. The best guide here is the pH, or lactate or base deficit or the temp of the hands – these are the markers of poor perfusion – not the BP so much!

This is pretty uncommon… unless you are an Obstetric Anaesthetic doc – then you come across it everytime you do a C-section. So I will use this as an example.

When you do a spinal – the first nerves to go ofline are those little sympathetic fibres – so you lose your peripheral vascular tone and the SVR drops quick – and your patient vomits, looks very grey and sweaty.  If the spinal goes higher, you lose the sympathetic fibres to the cardiac plexus – and your patient gets bradycardic, maybe some aorto-caval compression = a problem (CO = HR x SV), a double whammy – SVR crash, then CO crash – not good at all. {pray there isn’t a big bleed mid-op!}

So how to manage this – well it depends on the level of the cord lesion / block.  Lower levels, without bradycardia – maybe just a phenylepherine infusion.  Higher blocks with slow heart – you might need some chronotropy to help – good old adrenaline is my choice (ephedrine is an option – though a bit weak)  The high-spinal is the one emergency that goes C, B, A  - not A, B, C in real time!

So that is my super-simple and pragmatic approach to SHOCK.  In my experience – the big problem with SHOCK is recognizing it.  Once you have made the diagnosis he management is easier – but just remember – the BP is just part of the story.

If you don’t think about the other players – CO, SVR etc then it is a bit like walking into a movie theatre half way through a good “who-dun-it” murder mystery.  You might never guess who the killer was!

Twitt
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