Wessex Intensive Care Society (WICS)

Nigel Chee's Guide to the FFICM exam - what to expect

Author: Dr Nigel Chee
Follow @nigelchee

What can I add to Dr Wong’s guide?

Having navigated the second sitting of the exam (Sept 2013) I can offer some insight into the consistency of the exam and anything I learnt from the Adrian from the first.

Make sure you budget enough time for the exam. Despite being told it’s aimed at ‘intermediate level’ training, that’s not to say it’s a simple exam. Final FRCA was intermediate level too. Don’t take the exam lightly.

Did I follow Adrian’s approach? In parts - I too did not read Oh’s Intensive Care Manual nor the Oxford Desktop Reference. If you have either of them or the time and want to use if for some core knowledge then I think it would be useful- but not necessary. I read the last two years of relevant
BJA CEACCP journals and the JICS articles as well. The ICS website has some guidelines which are ripe for questions.

In addition to the resources already mentioned,
Crit-IQ was quite helpful as they had a bank of MCQ questions marketed at the FFICM audience and reasonably up to date journal club and podcasts, although you have to pay now for access.


Practise, practise, practise…
The Final FRCA RCOA book was helpful, Bennington (the green one) and also the online resources mentioned. Doing them a couple times over seemed to help me. I didn’t notice it being overly anaesthetically orientated, but then they’re both intertwined.


The OSCE consists of 13, seven minute stations with a one minute reading time between stations. All stations must be attempted, there are no ‘killer stations’ and the negative marking is not used. There are 12 ‘live’ stations (marks counting towards the final mark) and one station used for validating new questions (the test station). Neither the examiners nor the candidate will be made aware of the test station, therefore all 13 stations must be approached equally. The examination draws questions from four different areas, Data, Equipment, Professionalism and Resuscitation.

After the first sitting of the OSCE Crit Eye wrote in the Aug 2013 edition,

‘Examiners found that the weakest examination stations were those involving ECG and X-ray interpretation. It would be our intention to continue including such stations in future examinations in an attempt to improve standards in these areas.’

Pay heed to this - in my OSCE about half the stations were ECG or radiology related (including trying to identify the compartments of the calf). The imaging quality has improved and there weren’t any grumbles about poor quality radiology.

My only other advice is to remember the basics - e.g. for a procedure related station -
‘Introduce yourself, get consent from patient/ full monitoring/ staff/ resuscitation equipment available etc..’ they are all ticks on the mark scheme. Also try to keep talking (bullet point answers sometimes required) - once the examiner has moved on, you can’t go back to get marks. Don’t waffle prose in the OSCE, there simply isn’t time for you to mention the latest article or esoteric origins of the disorder/ case.

Structured Oral Exam (i.e. the Viva)
You should all have experience in these exams by this sitting. My advice (which I wish I’d taken) would be to get into small groups and practice viva-ing each other or get a consultant to do this. Skype/ FaceTime vivas work too. The essence of which is to get practised at talking and structuring your answers again. Depending on your department, organising practise session may not be so easy so definitely start early.


I did not attend any MCQ courses for this exam, for the 2nd part I did attend the PINCER course held in Portsmouth - which I found invaluable. Highly recommended.

On the day

So what’s my recollection of the OSCE/Viva?
Well, it began in a hotel room just off Bloomsbury Square. Suited and booted it was a quick walk to the college where I signed in, picked up my candidate number and then fumbled for a £1 coin to use in the locker rooms downstairs. Back in the foyer, now wearing a classy ‘wristwatch locker key’ I nervously acknowledged the presence of the other warriors. There were 8 of us in total; some looking relaxed and chatting whilst others were a little more pallid. Fifteen minutes before the Viva, we were greeted and had the rules of the day read out to us. We were then ushered up to the second floor where we sat with plastic cups of water awaiting further instruction - this is your last time to go to the bathroom before the start.

The exam room has two parallel sets of stations lettered A-D. Starting at your designated station, you have two vivas (7 minutes each) per station before the bell rings and you move on. The stations are partitioned off from one another and pinned to the outside of each station is a sheet of paper with the heading of each viva topic. This may give you some valuable organising time in your head or stress you out even more. Either way forewarned is forearmed. At the bell, you enter the cubicle with a desk and two examiners +/- an observer. After a brief meet and greet you sit down and wait for the fun to begin. Remember to smile.

The examiners are usually quite friendly and will not set out to trip you up. If you have a disaster station you should block it out; I’m not sure how exactly - but like being dumped for the first time, it hurts but move on. You can score a zero for a question scrape a 1 in another and still pass, so don’t give up whatever they throw at you.

Before the OSCE we were again taken to a room where we were briefed and given our starting station number. Each station is numbered and you rotate around. There maybe reading material before you enter, so have a look around. The afternoon was a little tiring and it’s difficult to gauge how you’re doing. In some stations you’ll be pushed to finish whilst others they’ll be time for small talk afterwards. After a gruelling afternoon, you may customarily find yourself at the Square Pig across the road.

For any further information please email me:

Good Luck!


Declaration of interest from webmaster: Steve Mathieu who edits the WICS website is also a co-director for the non-profit PINCER course and is an ICM consultant in Portsmouth (Wessex). He has not contributed to or influenced this guide. There is also (amongst other) courses, the ICS national revision course and details for this can be found on the ICS website

Adrian Wong's Guide to the final FFICM exam - an update

new update copy

Well, Christmas means that 2013 is coming to an end, my relief at passing the FFICM has since been eclipsed by passing EDIC and finally 2014 beckons. Since publication of the initial exam guide, there has been another sitting of the FFICM exam and this forms an update to the original guide.

The detailed analysis of the first sitting has also been published in the
FICM’s Critical Eye magazine . I strongly suggest anyone planning to sit the exam to read it. I’m somewhat bemused that some colleagues have never heard of Critical Eye. Also read the FICM’s guide to the exam

So what does the FICM say? I've quoted the above reference and provide my intepretation on what this means if you are preparing to sit the exam.

As before, please feel free to contact me if you have any further questions, comments or discussions.

Adrian Wong
It’s the Wong way or the wrong way

ST7 Anaesthetics/Intensive Care Medicine
Email –

Follow @avkwong


The MCQ was held on 9th January. 79 candidates sat the exam, of whom 62 passed (78.5%). 55 (88.7%) of these went through to take the OSCE/ SOE part of the examination. The MCQ pass mark was 75.78% which was reached by Angoff referencing, carried out by a dedicated MCQ Angoff group. The Angoff score was adjusted by the use of a Standard Error of Measurement to allow for the borderline candidates.

The exam achieved a Kuder-Richardson (KR-20) score of 0.718, which is considered reasonable and comparable to FRCA Final MCQ exams. The box plot in Figure 1 indicates that candidates scored consistently as a cohort with a standard deviation of 14 marks (3.12%); only two candidates scored low outlying scores (there were no high outliers). The mean score was 77.74% (349.8 out of 450). The average age of candidates at this sitting was 34.2 years; this was slightly lower for those who passed (34) and slightly higher for those who failed (34.9). Figure 2 shows the distribution of candidates’ ages. Figure 3 indicates that the majority of candidates at the exam were of a white ethnic origin (81%); 12% of candidates did not specify their ethnicity.

I am not going to comment on the age and ethnicity issue.

For a medical exam, the pass rate for the first sitting was high (78.5%). If you passed the MCQs, you had a good chance at passing the SOE/VIVA section- hardly surprising. My reading of the narrow box plot of the scores is that is a fair exam. There were few outliers suggesting that the majority of candidates performed to the same standard.

Perhaps most importantly, the report has made reference to the FRCA Final MCQs! As I have previously said, the FRCA exams are a ready pool of tried and tested questions for UK ICM. It would be wise to practise these.


In order to assist with the standard setting of the SOE exam, Angoff and Ebel standard setting methods were carried out by the SOE Core Group two weeks before the exam using the questions set for the exam. The Linear regression and Hofstee calculations were plotted against exam data post-exam. All statistical analysis was made available and was discussed by the Court of Examiners; the final pass mark of 26 was reached through a combination of statistical analysis and expert judgement after consideration of borderline candidates. This pass mark matched the score obtained from the Hofstee calculation.

Eight candidates failed the SOE, four candidates on each day and therefore failed the examination overall. All fail scores were closely grouped in a range of 22–24; no candidate scored 25. It is also noticeable that all candidates who failed received a low overall global score with the majority receiving scores below the minimally competent.

Figure 4 indicates that there was not a great deal of correlation between scores achieved in the three exam components. This is reassuring insofar as it suggests that the three components are testing different abilities in the candidates.

Therefore 47/55 (85.45%) passed the SOE component. Of the 47 who passed 20 (42.5%) achieved maximum marks of 32, which is an indication of the high calibre of candidate attending this exam.

All OSCE questions were Angoff referenced by the OSCE working party in advance and a cumulative pass mark of 146/240 and 147/240 was reached for the questions sets used on each day of the exam. The Court of Examiners looked at various methods of supportive statistical analysis of the exam data post examination but none of the findings were conclusive. It was therefore agreed that the pass marks reached by the working party were set in good faith using the approved Angoff procedures and therefore should stand.

All 55 candidates (100%) passed the OSCE component, once again a reflection of the high calibre of the candidate cohort. Therefore 47/55 (85.45%) achieved a full pass in
the Fellowship of the Faculty of Intensive Care Medicine examination.

The range of topics covered on both days was considerable. The list below is not fully comprehensive but does give a flavour of the topics covered: Rhabdomyolysis; Diabetic emergencies; Fluid responsiveness; ALI / ARDS; Rehabilitation after ICU; Status epilepticus; Eclampsia; Necrotising fasciitis; Nutrition; Hyponatraemia; Ethylene glycol poisoning; CVC insertion; Anaemia on the ICU; Pancreatitis; Non-invasive ventilation; Endocrine abnormalities on ICU; Ventilator associated pneumonia; Resuscitation; Heparin induced thrombocytopenia; Communication with ICU patient relatives; Plasma exchange; Assessment of delirium; Scoring systems; ECG interpretation; Guillian Barre syndrome; Abnormalities of acid base balance; Tracheostomy; Interpretation of X-rays.As is evidenced by the high pass rate, the questions were handled well overall. However, the Examiners found that the weakest examination stations were those involving ECG and X-ray interpretation. It would be our intention to continue including such stations in future examinations in an attempt to improve standards in these areas.

Firstly, the candidates who failed the exam failed in the SOE component. The passmark was set at 26 out of 32 (81.25%). It is possible to score full marks – over 40% of candidates did. Unfortunately we had 2 colleagues who failed (they have since passed) on the first day. Speaking to them, they maintained that the questions were fair although one of them was particularly agrieved by the discussion on the physiology of the sympathetic nervous system.

The passmark for the OSCE was approximately 60% and all candidates were successful. I thought this was on the low side for medical exams but on the day, I was convinced that if I had failed, it would have been in this section. On several occasions, it was difficult to tell what the examiners were trying to get at but the topic itself was fair.

Note the comment on X-rays and ECGs! This was indeed the case in the second sitting. Due to the nature of an OSCE setting, there is little room for discussion, you either know what the radiograph showed or you didn’t. Remember, you can’t go back to a question you skipped in the OSCE.

Whilst the range of topics examined was considerable, they were hardly surprising – the exam is meant to reflect the day to day work on a General Intensive Care unit.


Again, I must emphasise that this guide is a strategy for passing the exam, and NOT a guide to clinical practice.

IF I were sitting the exam, I would:

  • MCQs – practice from the FRCA database e.g. AnaesthesiaUK, Crit-Iq
  • SOEs/OSCEs – practice, practice, practice. Speak to colleagues who run anaesthesia courses. There are overlaps.
  • I still wouldn’t read Oh’s Textbook or Oxford Desk Reference.
  • FFICM courses are starting to spring up. I can highly recommend PINCER and the Oxford courses.
  • Read FICM’s Critical Eye and the Journal of the Intensive Care Society. They are UK-based resources from the relevant bodies.


Declaration of interest from webmaster: Steve Mathieu who edits the WICS website is also a co-director for the non-profit PINCER course and is an ICM consultant in Portsmouth (Wessex). He has not contributed to or influenced this guide. There is also (amongst other) courses, the ICS national revision course and details for this can be found on the ICS website


State of the Art Meeting, December 2014, Excel

Author: Dr Emma Fitzgerald
Follow @emma_zcharm6

DAY 1 – Opening Session
Ventilation Trials – Prof A Slutsky, Canada

Began with the background of why this is important.....Review this year in NEJM:
Slutsky 2013 ventilator induce lung injury

A change in philosophy has happened in terms of lung protection.

ARDS Patients

  • The graph in Berlin definition paper (ICM journal) provides a rough schematic on how to ventilate patients
  • ARDSnet 2000 - low tidal volume group showed lower mortality
  • JAMA 2010 systematic review and meta-analysis showed a small decrease in mortality using higher PEEP

Neuromuscular Blocking Agents

Papzian - NMB early on will improve outcome - improved survival at 90 days.

The separation in the kapplein-meyer curves occurred quite late considering that the intervention happened early on.

Prof Slutsky editorial described why this may be the case it may be related to over distension due to dyssynchrony. Seems that cytokines are lower in patients that have been given NMB agent

High Frequency Oscilation

  • non-blinded intention-to-treat MCRCT
  • 548 new-onset, moderate-to-severe ARDS patients
  • HFOV vs low TV high PEEP controlled ventilation strategy
  • outcomes:
    -> 47% vs 35% in-hospital mortality (RR 1.33, 95% CI 1.09 to 1.64)
    -> were given more midazolam, more NMBs, more vasopressors
  • Commentary and criticisms:
    — stopped early due to harm from HFOV
    — HFOV strategy had high mean airway pressures – would a lower mean airway pressure strategy make a difference?
    — groups similar at baseline, both had baseline recruitment manoeuvre to improve lung homogeneity
  • Conclusion: Increased mortality in ARDS patients treated with HFOV

  • non-blinded intention-to-treat MC RCT
  • 795 patients
  • HFOV versus usual care control group
  • outcomes:
    -> all cause mortality at 28 days was 41.7% vs  41.1% (P=0.85 chi-square test)
  • Commentary and criticisms:
    — less hemodynamic compromise, lower airway pressures than OSCILLATE and more protocol variation, possibly due to physician judgement limiting the harm from HFOV settings
    — HFOV groups received more sedatives and muscle relaxants
  • Conclusion: no mortality difference at 1 month

Excellent summary of OSCAR & OSCILLATE from LIFTL here
Commentary above extracted from LITFL


PROSEVA Prone positioning would improve mortality and reduce ventilator induced lung injury. 16% absolute decrease in mortality. This is surprising given the good control arm. They only used PF<150. Protocol at least 16 hours. May need a long time and earlier studies didnt do more than eight hours. The study was performed in very experienced centres.

What about patients with normal lungs.?
  • RCT in CCM (Holland). 2010. Fewer patients developed ARDS with lung protective strategy
  • JAMA 2012.3081651 - consistent with the fact that lung injury was less in low TV ventilation
  • NEJM 2013, 369;428 - patients in theatre. Lower LOS, post op ventilation rate and complications all better in the lung protective group.

  • MV is life saving but VILI has bad consequences
  • ARDS - lung protective strategies
  • Normal lungs patients do better with lung protective strategies

Difficult Decision Making in ICU – Prof P Croskerry, Canada

Many factors that make decision making very difficult. Emergency department throughput and pressures etc are added to in the ICU. There is an increased significance of minor errors.

Diagnostic errors in ICU were investigated. 6000 autopsies. 28% had at least one diagnostic error and 8% of these could have significantly contributed to death. Example used the cognitive reflection test that distinguishes between analytical and intuitive thinking. Published recently in NEJM.

How we make decisions has two effects on patient care? Making the diagnosis influences the treatment. There is an average diagnostic failure rate of 15%. Different specialties are variable. Some have a diagnostic failure rate of up to 50%.

They developed a schematic model to make these work together. Intuition and analytical reasoning go through a process of calibration before making a diagnosis. You can use executive override to influence the output. There is also irrational behaviour that may also change the process. Pattern recognition and repetition can speed things up. Describes a "system 1" (no work required) and "system 2". The expert spends most of their time in system 1 and the novice in system 2. Need to be able to override and toggle between the two.

So, what decision making needs....
  1. Raise the importance decision making
  2. Know operating characteristics of the DOT model
  3. Educate and train intuition
  4. Promote meta cognition and critical thinking

Strategies for Safety – Ms K Vollman, USA

There are pockets of excellence - but variances. For example, 98% of MI patients in USA got a beta blocker. We need a good framework. E.g. structure, process and outcome.

Isn't just about the people, but it is also about the systems that we create. The goal is to reach the error reaching the patient. Process and people factors are both important.

Human factor engineering aims to solve this.

Concept of "silence kills". 80% spotted an error but 58% didn't speak up. "The Silent treatment" 2011.

Suggests use of checklists, huddles and nurse presentation on ward rounds.
Force function is the strongest way of preventing error, e.g. Can't take keys out of the car until you have handbrake on

Industry Symposium - NAVA
NAVA – Dr S Wimbush, UK

IPPV is not very physiological and it causes harm.
Ventilation has moved to spontaneous, awake and less harmful from mandatory, asleep and harmful in the last few years.

NAVA makes the assumption that the vast amount of triggering comes from the diaphragmatic action because of the innervation from the phrenic nerve. Normally we use flow, volume or pressure triggers which means that that the ventilator is always a step behind the patient. The whole aim is to try to restore neuromuscular coupling.

NAVA uses an NG tube that spans the diaphragm. It has an area that detects the electrical activity generated by the diaphragm. It then tells the ventilator to generate a pressure proportional to the signal from the diaphragm. The electrical signal is called the EDI and is proportional to the effort, it is effected by the physiological reserve of the lungs eg a COPD patient would have a different EDI to someone with normal lungs.

Types of asynchrony:
  • Missed breaths
  • Double triggering
  • Flow asynchrony

Asynchrony leads to increased sedation requirements (and the consequences of this), reduced weaning and increased patient discomfort. In the DGH it seems to be useful to get patients off the ventilator more quickly and reduce ICU LOS.

Evidence for NAVA – Dr P Hopkins, UK
Very heterogeneous population
Very little agreement in the definition or description of weaning failure. Also no gold standard in the best mode of ventilation and the strategy for weaning.

Presentation of Kings College data with their use of NAVA.
3 groups....
  1. NAVA
  2. EaDI monitored
  3. Neither

Crude assessment of outcomes. Reduced ventilator days with NAVA.

Suggested using the EaDI monitoring could be useful after extubation. Can help tailor a ventilator and/or airway wean and assess the impact of physical rehab on neural demand.

Suggestion also in palliative circumstances for assessment of dyspnoea when patients are extubated or given a sedation break. Evidence is a bit sketchy, there are largely observational data with small numbers of patients. Recently, a round table has been published in CCM.

They have just started a PS versus NAVA feasibility study. Intervention group uses EDI and NAVA at night, as you would with a PS wean. I.e. they are testing the potential benefit for the neural trigger and also for the use as a monitoring device to prevent OVER ventilation and OVER sedation.

The Cauldron

Welcome to the uncaring profession – Dr Adrian Wong
Adrian begins with some philosophical reflections about medicine in general. He emphasises the value of a ‘good’ death and the fact that long term outcomes are increasingly used to assign value to ICM. There followed advocacy of guidelines, checklists and protocols.

What is the difference between care and therapy?? Emotions influence care and they cause variability. Being human is a weakness. Thinking isn't for everyone. We need fewer strategists and more doers!

I think, therefore I am - Dr D Garry

The intensive care units of the future are the ICUs of the mind.....
Since the 1950s the ICUs have focused on treatment of PHYSICAL problems.

How do we trust our senses?? Cogito ergo sum....I think therefore I am. Plato - the treatment of the body and the soul should not be separated.

We need to aim to provide the brain with an environment whereby it can think clearly. We need to separate it from the damage caused by a critical illness.

The intensive care units of the future are the ICUs FOR the mind..... If I am not thinking, I am not.

The price of predictive modelling: eliminating bias by eliminating doctors from the decision making process - Dr A Devansen

All humans are prone to cognitive bias. Predictive modelling is a scientific theory to provide accurate and predictive information. Modelling in practise is subject to user bias. Models perform better than people.

"The world of economics is light years ahead of medicine as they use mathematic models and also have no scruples!"

Human fallibility. Machine perfectibility. Is the hospital of the future run by machines?? You would have to have OBJECTIVE inputs to the scoring systems that do not have any objective measurements, e.g. the Wells score would. It work as you have to put a clinical opinion into it that uses someone's clinical judgement about whether a PE is or isn't likely.

The geriatric intensive care unit - Dr Eryl Davies

There are lots of similarities between ICU patients and geriatric patients, e.g. physiological extremes, poly pharmacy issues and end of life discussions.

There may be an influence of the recent publicity of the LCP in the referral of elderly patients to the ICU. Is it appropriate to offer "heroics" in the elderly population? Is age just a number??

Creation of a dedicated geriatric ICU was not a popular option amongst ICM consultants.

Elderly patients are complex and need specialist intervention, knowledge and care.
Closing statement....geriatric ICUs are the future.

Intensive Care's Weapon of Mass Destruction: The Random Misā€Controlled Trial - Dr P Nandhabalan

Started by looking at HFO trials and the other studies that have contract iced each other. begs the question..is it the INTERVENTION or HOW we assess efficacy??

Why are RCTs so dangerous?
  • Heterogeneity in many factor and so the ICU population remains very poorly defined.
  • Design - exclusion and inclusion criteria are often strict, regional differences.
  • Outcome measures are arbitrary
  • Changing disease patterns
  • Statistical lies!!

Looked at steroids, HFO, tight glycaemic control and vasopressin.

The heroes and villains often switch around.
a weapon able to cause widespread devastation and loss of life... This is ONE occasion where further large scale RCTS are not required!!!!

Day 2 - Trauma
Trauma and coagulopathy – Dr K Brohi, UK

Loss of fibrinogen is one of the biggest problems in traumatic bleeding. Cryoprecipitate is the best product to give, but we tend to not give a big enough dose to replace the fibrinogen and restore levels to normal.

Cryostat study - a pilot study
Preliminary results were presented. Early cryoprecipitate seems to reduce mortality, BUT the groups were small and there were significant differences between the groups. They are preparing for a bigger trial.

Fibrinolysis is also a problem. ROTEM doesn't seem to pick it up.

So, trauma patients are in a state of fibrinolysis and also have low fibrinogen levels. If you can modify the production of activated protein C, you can abolish traumatic coagulopathy (in mice). Trauma patients release tPa, which then triggers APC. Therefore tranexamic acid is important even if the ROTEM doesn't suggest it is needed.

Need to focus on the fibrinogen replacement and avoid dilution with crystalloids.

Trauma induced lung injury - Prof S Jaber, France

Many causes of ARDS post trauma...primary and secondary (direct and indirect) causes.
CXR, echo and CT can all be used to identify causes of lung injury.
Recent study used volumetric software to evaluate the degree of lung contusion. ROC curve showed that if you have 21% loss of lung volume, you have an acute lung injury.

Trauma patients are at very high risk of developing a lung injury. They have many risk factors.

The impact of it - increase in mortality if a trauma patient develops a lung injury (OR 1.6)

Prevention is an important way to improve the outcome...
  • Limit fluid overload
  • Limit transfusion
  • Use NIV where possible
  • Lung protective ventilation

Article in American journal of respiratory and critical care medicine.... implementation of evidence-based extubation readiness bundle in 499 brain injured patients.

Acute Kidney Injury – Anything New?
Urine output and Urinalysis – Dr R Beale, UK

Urine output depends on the scenario.... Solute load and concentrating ability

Kidneys filter about 1.5kg of salt per day. Maximum concentrating ability is 1400mosmol. Solute load is 700mosmol.

The pre-AKI is possibly the intervention phase, once AKI is established it is probably too late to improve things.

Physiological oliguria.... RAAS, ADH, sympathetic nervous system. Oliguria may imply a physiological or a pathological response.

In terms of differential diagnosis, oliguria adds very little. It can be of a prognostic use...AKI with oliguria may correlate with a poorer outcome.

Anuria - probably the most important finding. Is obstruction or lack of peer fusion until proven otherwise.

Modified urine output.... Using frusemide.
  • No evidence that diuretics can alter outcome, but there is a signal that if people are passing urine then they have a better outcome compared to those who are not.
  • CCM paper this year...frusemide stress test to predict severity of AKI. IV frusemide was given. Patients that responded to frusemide had a higher rate of recovery. Probably tells us that the tubules are still working (the frusemide needs to be transported across the tubules).

Urinary electrolytes
  • Fractional excretion of sodium test. Is supposed to differentiate between pre-renal failure and ATN. Many exceptions may it pretty useless in the ICU e.g. timing. CCM paper (Darmon) dismisses it.
  • Fractional excretion of urea is similarly useless...

Can sometimes be useful, e.g. GN (casts), porphyria, rhabdomyolysis

  1. Urinalysis isn't that helpful
  2. Volume balance is important

Biomarkers for AKI – Dr J Prowle, UK

We are unable to risk stratify patients as we can't recognise AKI early and the treatment or intervention we need to do needs to be done early for it to be effective. Therefore, we need to develop better predictive markers of AKI.

Ideal marker would
  • Enable risk stratification for the likelihood of AKI but is biochemical AKI the right measurement?
  • Prognosticate
  • Provide the earliest possible diagnosis
  • Reliably distinguish tubular and pre renal causes
  • Identify sub-clinical injury if it exists

Creatinine is a poor marker of renal impairment. We need better biomarkers. Some are in the blood, some in the urine. Some are established e.g. Cystatin 3 and beta2microglobulin. Other novel ones such as NGAL

  • Seems to be significantly upregulated in the kidney in ischaemic conditions.
  • Source of NGAL - produced in the distal nephron.
  • The AUC was good in Paeds cardiac patients (0.98) but is only 0.7 in ICU patients. Is not very useful in chronic kidney disease.
  • Urinary NGAL may be useful as a triage tool in ED.
  • What about high NGAL and normal creatinine? May have sub clinical AKI. Not really sure what the significance of this is.

Procalitonin levels have been shown to be related to development of AKI.

Kashani, in critical care 2013 17-R25 identifies 2 biomarkers that could predict the development of AKI, even multiplied them together to improve the detection. AUC was above 0.8. Choice if threshold is difficult. Likely to be marketed with the choice of two thresholds. These biomarkers are associated with G1cell cycle arrest and appear therefore to be linked to the development of cellular injury.

What do we do with biomarkers results?? We probably need to gather more evidence. the "treatment" is largely supportive care and preventing secondary injury, but we do this anyway... Maybe better to use them to triage or de-escalate care.

How best to prolong extra-corporeal circuit lifespan – Dr M Ostermann, UK

Why does the filter clot?
  1. Haemoconcentration
  2. Thrombogenic clot surface
  3. Exposure of blood to air (ie in drip chamber)
  4. Risk factors (e.g. SIRS, filter size, hypercoagulable patient, lipid infusions - some are modifiable)

We could manipulate the following...
Pre-dilution associated with a longer circuit life, at expense of reduced clearance
Membranes: No good RCTs comparing different membranes with regards to circuit life
Choice of modality: Suggestion that CVVHF is associated with more clotting, but poor evidence
Heparin: LMWH vs heparin - no evidence
- Weak anticoagulant
- Limited number of studies. Alone, it is inferior to it being combined with heparin, but is an alternative to people who can't have heparin
Others (eg argatroban, anti thrombin, fondaparinux): No real evidence
Regional anti coagulation - Citrate, heparin/protamine

Citrate: More popular than heparin/protamine for regional anticoagulation
- Binds calcium, thereby inhibiting the clotting cascade at multiple steps. Calcium needs to be added back to the blood as it goes back to the patient. Citrate is eliminated as the blood flows through the filter. About 50% of the citrate goes back into patient
s systemic circulation, slots into Krebs cycle and gets metabolised to bicarbonate, can be quite useful in patients with renal failure
- Does it work to keep the membranes patent? Six RCTs have been done
. Largest one = crit care medicine. 2009(37):545, Helene et al. No change in filter lifespan. Equally efficacious, but citrate was safer.
Two meta-analyses have been done
- Wu et al Am J Kid disease 2012;59. Some RCTs show increased circuit survival... Suggested a trend in the direction of citrate, but undoubtedly, citrate was safer in terms of bleeding risk.
- Different analysis by Zhang et al 2012 ICM. They differed in final conclusion about lifespan but agreed citrate was safer.

What should we do in real life?
2012 kidney international (KFIGO) 2;1-14. Felt there was enough evidence that in patients receiving CONTINUOUS RRT, citrate should be first line, heparin reserved for those intolerant of citrate.

The RCT results don't always reflect the real clinical goings on. Data from the first year of using citrate at guys and Tommy's was presented. (Towey et al nephron clin practice 2013: 124.119-123):
  • Citrate performed better than heparin and prostacyclin
  • Rate of premature clotting was reduced by 76.5% with citrate
  • No difference between heparin and prostacyclin

  1. Anticoagulation is not a substitute for poor access
  2. Choice should be influenced by local expertise and patient characteristics
  3. KDIGO suggest citrate as first line anticoagulant
  4. Citrate offers regional anticoagulation with less bleed don't and potentially better circuit latency
  5. Protocol and attention to detail are essential (independent of type of anticoagulation)

Trainee Research Session
Preparing and writing for publication

Understanding the publishing process
Write first for:
  1. Editors
  2. Reviewers
  3. Your audience

What drives editors?
Which papers get cited most (long term)?
  1. Methodological papers
  2. Discussion papers and concept analysis
  3. Review papers
  4. Original research i.e. the further down the list, the more it has to shine

Which papers get cited most (short term)
  1. Review
  2. Methodological
  3. Discussion papers including concept analysis
  4. Original research

Process of writing - 4 rules of writing
  1. Read the guidelines
  2. Set realistic targets and count words
  3. Seek criticism, don't write in isolation.
  4. Treat a rejection as the start of the next submission

Journal guidelines
  • Look at the guidelines and write to them with ideas and find out how they want it to be written
  • Length... Gives an idea about dividing the contents
  • Layout... Font and spacing, wide margins.
  • Organisation of the paper... Takes you form the broad idea, to discussion to conclusion. Use the headings that they suggest. Think about writing the paper before you have done the experiments. Don't start at the intro, start with the method and work backwards as you don't know what you are introducing yet
  • Other conventions
- Spelling (esp North America)
Presenting stats
- Number (words, numerals etc)

Setting Targets: All good writers do this. Try to write a specific number of words per day or every time you sit down to write. When you have reached your target and STOP....!!

Seek Criticism - Find a "critical" friend

Understand the peer review process: Not a scientific process or black and white, about judgement
Follow international guidelines:
    Creating, Presenting, designing and promoting a poster
    No point in doing research unless you deliver your message.
    Design courses are very useful. They are very personal too though.
    Poster design
    • Content
    • Anatomy and circulation
    • Rules

    Communicates visually

    Attracts and holds attention
    Concise and organised
    Stands alone when you are not there

    Needs to be readable from 6 feet away.
    Needs to deliver the message in ten seconds
    What do you want to add to this field of research.
    What are your conclusions?
    What are your messages?

    40-50% text
    >30-40% graphics
    <20% white space

    Title... Think really big. Convey the theme, needs to be catchy max 1-2 lines.
    Contact details
    Intro - should place your work into context.
    Aim - 1-2. Lines. What am I adding?
    Methods - important, but limit. How am I adding knowledge? Bare essentials, not to the details of the manuscript. Flow-charts and diagrams are useful. Adding links may be useful.
    Results - always the largest section.. What did I find? Graphs are good. Figures better than tables
    Conclusion - give your interpretation of the data.
    Take home message

    Don't fight reader gravity. Down and then across.

    Clarity: Attract, Inform, Engage, Conclude
    Title with a message
    Make findings obvious
    Link images with the text

    Use graphs well
    Take home message and killer bundles

    PowerPoint most popular.
    Adobe illustrator is more difficult to learn, bit good design software.

    Use sans serif fonts. Calibri or arial
    Keep to 1/2 front types
    Avoid excessive text and out breathing space around your words
    Font size - should be able to read the smallest font from 6 feet. Ascribe level of importance through font size
    . Tittle 85pt / Authors 60 / Subheadings 36-54 / Body 32

    Colour and contrast
    Light background with dark font is the easiest to read. No more than two or three colours. Not blue on red, or yellow on white or red on blue

    Communicate concepts quickly.
    Not too many
    Ideally should see from six feet
    Avoid 3D and hashed ones
    Get rid if grid lines and backgrounds so that you can convey tour message
    Resolution at least 150dpi, ideally 300dpi but no higher

    Other things to consider
    Add-ons: QR codes to link supplemental materials, contact emails, the poster, your website
    Screen versus print. Bear in mind the back lit monitor as you would with photos

    Design and layout summary
    Justify to left
    White space and balance.
    Font sizes and colours

    Types of poster sessions
    Thematic poster - related abstracts under a few main themes, discussion with moderator
    Poster discussion/corner/e-co. Session/ViPER - computer session. Ecomm max 3 slides & 5 mins
    Imagine your stage and prepare.Who is my audience?
    • Body language is important
    • Check and show your poster
    • Prepare a 3-5 min presentation.. Focus on discussion
    • When you are there....attract, engage, inform, conclude. Sound excited, even if you are the only one!!! Get the message across, know your limitations and conclude. Ask for their contact details. Give a summary sheet or have a QR code.

    The future... Video links, screens not paper etc.

    Organ Donation
    Task force says that we have to consider that organ donation should be a part of EOL care and that if we put donation leads into our hospitals and we get the infrastructure we need, we should get more people having donation as part of mire people's end of life care.

    GMC 2010 said doctors have a duty to offer donation, NICE reminded us of when donors should be referred.

    Government accepted all of the recommendations from the taskforce. Baseline was 2007. Have seen an increase in donation. 49.7% increase in donation. Increased DCD. More transplants done than ever before. The waiting list has also gone down.

    Progress continues. This year, until dec 8th compared to previous year, the numbers have gone up by a further 13%. The transplant rate has also gone up from 2000 to 2500.

    The new target is to match the performance of world class donation and transplant programmes.

    The problem with hitting a target, is being given a new target. By doing more brainstem testing by making it more a part of EOL care, will we refer more patients as there have been many who met the criteria for BSD testing, that were not tested.

    Retrieval and transplantation need to have the same level of implementation as critical care. W must maximise the gift of donation. Is regional reperfusion or explant and recondition the organs. Is me it about variability of decision making?? One unit turned down 80% of kidneys offered too them, despite them seemingly being "ok".

    However, we will never have a fully functioning system whilst 43% of the families are saying no.

    Society still views donation as the exception, not the norm. Defaulting to "no" seems to be the best option as people feel more comfortable not donating organs in someone who would have wanted to, rather than donating organs from someone who wouldn't have wanted to. Maybe we need more hardcore advertising programmes... I.e. "By donating you are saving Jill, by not you are killing jack" idea.

    Discussion around the concept of introducing organ donation consent when having a procedure or operation. Controversial as patients may think that it will influence their subsequent care maybe though it should be discussed even more in other situations.

    Discussion about the concept of donating kidneys in the patient before the patient dies. They won't die from renal failure and it would reduce the warm ischaemic time. Not taken well by the panel...thoughts were to "sort out society" first and mend/establish a good system for dead donors before tackling this and the problems it may/will cause.

    Reference...BJA 2008 June editorial.

    Pot Pourri of Infections
    Optimising antibiotic therapy and the DALI study

    Focus of antibiotic therapy is largely still all about timing.
    The dose - one size, does it really fit all?? We are told to give an "appropriate" dose...

    Antibiotic dosing is related to
    • The microorganism - SENSITIVITY
    • High MIC, but still susceptible bug, have a high chance of failing treatment, eg pseudomonas and MRSA. Don't always get the MIC data from the lab, there is quite some susceptibility of the microorganism to the antibiotics you are giving.
    • Volume of distribution and pharmacokinetics change when patients are critically unwell as compared to healthy fit and well patients. Most of the drugs - there is an increased VD to 2 or 3 fold. Most of the time we are only concerned when the clearance is low, however the opposite is more often actually a problem. Hyper filtration causes increased removal if the drug than you would probably want. Calculated cr clearance is the best way to detect this problem. The other drugs and fluids we give will increase the clearance
    • Incidence of ARC (augmented renal clearance) was high in 52% of patients, 18% permanently (Ghent data). Was related to drug (antibiotic) failure...High risk patients include low sofa score, burns patients.
    • The drug and it's PHARMACODYNAMICS.
    • Giving a dose results in a concentration. How this concentration results in a clinical effect is the pharmacodynamics. Some drugs are time dependent (eg b lactam) need a prolonged exposure, amino glycosides need a high peak as they are concentration dependent. We can use this to our advantage by adjusting the dose to ensure the efficacy with minimal toxicity.

    Potential consequences of under dosing
    • treatment failure
    • need for multiple antibiotic courses
    • antibiotic resistance

    DALI study - Primary aim was to describe the ok of the beta lactam antibiotics point prevalence. International study. Blood samples taken. Slightly different timing for different antibiotics and those on continuous infusions. Used the EUCAST MIC values. They investigated whether the patients actually reached the required antibiotic level. The sample population was relatively representative of a typical ICU. Overall mortality 24%.

    1. clearance for the drug was lower
    2. VD - lots of variation, but generally higher
    3. Enormous variability in antibiotic concentration.
    4. Confirms that that the concept of "one size fits all" does not ring true.
    5. Minimum target - only 80% reached the minimal beta lactam target...20% not getting an effective dose

    Drug exposure and outcome....the time above the MIC was correlating well with the success of treatment. Ie probability of cure is related to the drug level.

    Factors associated with reaching the PKPD targets...only 2 were associated with reaching target
    • creatinine clearance was negatively correlated with reaching the target, ie augmented clearance was bad.
    • Use of continuous infusions - 4x increase in chance of achieving the PKPD target

    How to solve this?
    1. Everybody gets double The dose, but you may cause toxicity
    2. Front-loading - extended and continuous infusion with a loading dose, or a double first dose if dosing intermittently.
    3. The use of continuous infusion...if you increase the infusion time, you increase the PKPD, i.e give the same dose over a longer period of time, rather than having a peak and a rapid decline.
    4. Continuous infusion of meropenem gave better outcomes in a feasibility study and a better clinical outcomes as well as a better PKPD

    "We can and should do better. We should use the antibiotics we have in a better way"

    There is no single patient characteristic that improvement things, but augmented clearance seems to be important..

    Why aren't we doing selective decontamination?

    Hospital acquired infections seem to come from the organisms that are colonising the patient. Enteric gram negatives and yeasts. Doesn't target anaerobes

    Topical and enteral treatment. Short course of IV antibiotics.

    Does it work? Cochrane review
    • Reduction in rates of pneumonia and improve survival with topical and IV
    • Reduction in pneumonia but not mortality with just topical
    • Cluster RCT was excluded. De Smet 2009 NEJM
    - Crude mortality not different
    - Had to adjust for the differences caused by the cluster randomisation

    Not used in the UK - not enough evidence and there is concern about antibiotic resistance. NICE specialist advisors commented that there were concerns about C. difficile.

    Cuthbertson CCM 2013 - Clinical stakeholders' opinions of SDD
    Broke it down into their knowledge, professional role and their beliefs
    Most people were not strongly opposed, but were uncertain
    Skew towards a belief it causes antibiotic resistance
    People thought that it hadn't been adequately addressed....so they did a SR (lancet this year) for all the point estimate favours SDD, except for MRSA which is above 1

    De smet paper ended up giving less days of broad spectrum antibiotics in the SDD group overall

    Is it generalisable?? It does seem to be a concern.... Lots of evidence comes from the Netherlands. But there is some evidence from the UK and USA.

    UK evidence
    • B Winter. Small RCT 20 years ago with historical controls. Only 90 patients. Concluded it could be safely used in the ICU.
    • Cheating cross experience 2007 - SDD introduced in 2007. Reduced rates of MRAB. MRSA certainly hasn't increased, VRE not really gone up.
    • Email survey (unpublished) 13 units said they use SDD. ICNARC looked at the outcomes from these units. Antibiotic resistance does not seem to be increased. Mortality is adjusted for units and there doesn't appear to be much difference. Caution comparing the different units. In those that used the IV component had a reduction in blood stream infections
    • SuDDICU
    - people equivocal about c diff. No data to say it does increase it
    lots of uncertainty about the benefits.

    SDD - all of the consultants need to be involved. Can't just have some people doing this. Intensivists seemed to be less opposed than the microbiologists

    Direct quotes HPA report
    • Data from Netherlands doesn't count
    • We just never discussed it
    • Haven't gotten rd to it yet
    • Still worried about resistance, but I know the evidence doesn't Support this
    • Need an SDD champion

    1. very few strongly opposed
    2. lots of equipoise
    3. 85% were keen to be involved in a big international RCT with a hard endpoint and monitoring of antibiotic resistance during and for a prolonged period afterwards
    4. new large cluster trial is being designed. Resistance monitored for a year afterwards no cross over as they want to see the ecology
    5. Need 24000 patients

    Experience of a novel (beta) corona virus infection
    June 2012 HCoV-EMC. Closely linked to bat virus. First human case that made it to the ICU NEJM case report
    Case report of a patient cannulated for vv ECMO for refractory hypoxaemia

    Day 3

    Review of the Ely study from the 1990s.
    Study was repeated and published in the blue journal in 1994 - showed no difference

    Protocols may be useful, but probably not in the difficult prolonged weaning phase patients.

    Presented the data from their unpublished study.

    6% of patients in icus in Scotland require a prolonged period of mechanical Ventialtion. 5-10% seems to be the figure that represents the number of patients facing a prolonged weaning period.

    45% of the weaning failures manage to get off the ventilator. 20% get to NIV. Neuromuscular disease patients have the lowest mortality, COPD patients have a shorter wean but the highest mortality.

    We need to reverse the reversible.

    Description of the MDT approach to the management of the weaning patient. Described...therapy, physiology, exercise etc...

    Concluded that we need bespoke weaning and rehab plans for these patients. We also need to ventilate them properly at night.


    Has become a fast moving speciality in the last few years, after the creation of stroke units and hyper-acute services - hyper acute stroke units....

    Stroke units have reduced mortality. Thrombolysis has improved functional outcomes. If you bleed though, there is a 70% mortality at one year.

    The data for strokes is quite old and probably doesn't represent the current improved practice in the UK.

    Overall mortality in the uk in Icu is about 39%.
    OOHCA 50%
    Oscillate mortality around 30%
    BMT 69%.

    Ischaemic cva patients...if they survived to discharge... 66% chance of favourable outcome, 33% gain independence.

    Description of the development of the surviving sepsis campaign and the guidelines.

    Controversies and changing evidence led to the reviewing of the guidelines. There has been a guide to the guidelines written by JL Vincent and J Marshall after the publication of the 2008 guidelines. There were then a series of papers published to look at the impact of and adherence to the recommended guidelines. It had improved but was not good enough.

    The latest guidelines change the bundles. The management one was dropped and the resuscitation one was split into two phases. We are in the "reinvigoration phase" of the surviving sepsis campaign. There has been a suggestion that they should be mandatory which clearly has big issues.

    There has no been a moved to completely avoid the involvement of industry in the creation and implementation of the SSC. More involvement from professional bodies, but strong feeling that industry involvement is bad.

    For better or for worse, it seems that the bundles that we create are increasingly being used as a marker of performance.

    The positive effect of bundles was more marked in severe sepsis rather than in septic shock, suggesting that there is perhaps more opportunity to intervene in these patients. Most of the things that make a difference are PROCESS things.

    The new guidelines dropped a lot of controversial, harmful and out of date things. A lot of these actually are things that are too late, ie the horse has already bolted. The bundle approach has been successful in achieving a reduction in mortality, whether it is because it is an operational lever or due to the individual components is unclear... But does it really matter???!

    Charles sprung lecture...does one size fit all?

    Should the CVP target be changed in patients with heart failure?
    Should a MAP target of 65 be higher in those patients with hypertension?
    A BP target should be titrated to your patient. 

    Is the urine target the right one in patients with renal failure?

    Should you change your targets in those patients being fed? Or in patients with diabetes?
    Swings in glucose are probably bad

    Typically using 6ml/kg. 
    There is some data to suggest patients with normal compliance with low TV had higher mortality

    Most people agree that an Hb trigger of 7g/dl is what we should use

    Hard to define adequate fluid resuscitation and vasopressor limit to trigger steroid administration 

    The slide presentations for the data giving the guidelines by each author are almost all completed now and are published in Critical care med 2013 (41) and ICM 2013 (39). 

    Mervyn Singer Lecture
    One size cannot fit all. The simple rigid protocol may be applicable in a small closed community, but we should be using generic guidelines instead that we can adjust to our specific patients.

    Initial empirical antibiotic therapy... Challenges the benefits of early antibiotics. Critical care med 2011.
    Other papers also suggest that maybe taking cultures and waiting to give antibiotics. There was a lower mortality in the less aggressive group. Lancet infection. University of Virginia.

    Antibiotics may not be the panacea that we think they are.

    ICM journal last week... De-escalation of empirical therapy is associated with lower mortality in patients with septic shock.

    New York have started using them as protocols NOT guidelines, meaning that patients are being given MINIMUM amount of 30ml/kg I fluid. Looks like the sepsis bundle will be a standard of care across America. Massive implications.

    "Benchmarking the incidence of severe sepsis in the US"...
    Coding is becoming important. How are we diagnosing it?? However, promos and Process have really struggled with recruitment.

    1. Principle is great
    2. Need to be cautious and embrace the guidelines but we need to combine it with individualised expertise

    Resuscitation End-points
    • Remember the balance between production and clearance. Sometimes is very difficult to distinguish between some of the conditions
    • Can you use lactate to guide resuscitation? The lactate pyruvate ratio may be important. The interventions should focus on he early stages when tissue hypoxia is occurring
    • More rapid decreases in lactate are related with better outcomes, but is it the manipulation of the lactate that is responsible?
    • Changes in lactate seem to be important in identifying the patient that may benefit from your haemodynamic interventions.
    • Not much data to suggest whether targeting lactate levels is beneficial. Target to 10% is likely not enough

    Lactate guided therapy study in the blue journal.

    Maybe lactate clearance is important. Need to reduce production. If you bind and remove the lactate and try to remove it, you worsen hypoxia especially in the heart. Need to stop the fire.

    Can echo be used to titrate therapy during resuscitation?

    Echo can help to establish a diagnosis and avoid unnecessary interventions.

    • IVC diameter. Above 2cm the pt is unlikely to respond to a fluid challenge
    • Changes in diameter during spontaneous respiration. Complete collapse seems to be related to fluid depletion. In positive pressure ventilation you can use the distensibility index
    • Measurement of contractility. "Eyeballing"
    • LVEDArea. Gives you information quickly. You can use the fractional area change
    • Remember to consider the whole picture

    Not much evidence out there but is being used a lot more. There is a BJA article about the impact of echo.

    Inter-observer variability
    Discontinuous measurement
    Measurements are affected by angulation
    Poor views affect results.

    Closing Session
    Management of therapeutic hypothermia (TH) after cardiac arrest. Prof Kjetil Sunde, Norway

    After successful CPR, normally the temperature increases within the first 48hours. This is worse in those who have the worst outcomes. The post cardiac arrest syndroms have 7 stages. It is a severe repercussion syndrome associated with haemodynamic instability.

    TH inhibits several aspects of the reperfusion. TH reduces cerebral blood flow and so there is a 10% reduction in oxygen consumption per degree in temp drop.

    Initially non randomised trials and then 3 RCTs showed a benefit from TH. Led to the ILCOR statement suggesting cooling post cardiac arrest to counterculture the reperfusion syndrome which appears to be unrelated to the rhythm causing the problem.

    Most studies since have shown improvement in outcomes and certainly no harm was detected.

    The whole point seems to be the reperfusion syndrome.

    BUT we don't know the therapeutic window, the ideal temperature nor the duration.

    NEJM TTM trial was discussed
    • Led from Lund in Sweden. 950 patients 10 countries in Europe and Australia. 36 hospitals
    • Prognostication was blinded and outcome was blinded
    • Followed for 6months after discharge
    • No major differences between groups. High bystander CPR time to ROSc was about 25mins

    No major differences in survival at any point in he trial
    Excellent follow up
    CPC score - no differences

    Adverse events (in the supplement)
    No major differences but more low k in cooled group and tendency for bleeding.

    Targeting 33 - no benefit.
    Excellent study
    .Strict criteria and prognostication and excellent control.

    Discussion points
    1. Only one minute to starting CPR. Therefore very low anoxia time. Although it was pointed out later that the time to ROSC was still quite long. Suggestion from other papers (resuscitation journal) that cooling IS beneficial if the downtime was more than 3 minutes, thereby making TTM trial difficult to interpret and compare cooling benefits
    2. The 33 degree group should have been prognosticators later due to the effect of cooling on sedation. They might have lost survivors in the cooled group. Suggestion that there are a good number of late wakers after cooling. These could have been CPC 1 survivors. We measure good outcomes with CPC1-2. For the relatives the difference between these is actually very important. We should aim for good CPC 1s.
    3. The period from discharge to 6m. Significantly more cooled patients got up to CPC 1 from2 than in the other group. What about the following 6m/12m etc? May again be missing people.
    4. In animal studies, there is a suggestion that time to target temp doesn't matter. Some clinical trials suggest it maybe matters. JAMA this month - 2l saline to cool pre-hospital didn't improve outcome

    Problems with cooling
    • Shivering - need a sedation protocol
    • BM disturbance - insulin resistance. Need insulin infusion
    • Hyperventilation and low co2 can be a problem.
    • Haemodynamic instability can also be a problem. Need to maintain vital organ blood flow. Can have issues with bradycardia, patients with a lower HR seem to have a better outcome at any point in the cooling process. Don't treat it if the Bp and lactate are ok

    Use targeted temp management
    Avoid fever
    Suggestion that we need more data and we shouldn't withdraw care too early
    Advised to await ILCOR and probably continue cooling for now

    ILCOR have since released an interim advisory statement

    Acute pancreatitis. Professor Jan De Waele, Belgium

    New scoring systems

    Updated Atlanta classification
    Modified Marshall score

    nfection and organ dysfunction are the two drivers for a bad outcome. Essentially need a CT for Modified Marshall score as you need to identify necrosis. Not needed for Atlanta score
    Previously used biochemical, physiological and radiological scores. These scores seem equivalent. Concluded that you don't need radiology to confirm diagnosis nor to prognosticate
    BUN may be useful. Lots of variation though
    Fluid over-resuscitation is likely to affect the micro-circulation and this can not only affect organs, but worsen the pancreatic necrosis. Not giving enough fluid equally is not good! Trial in Chinese medical journal - more restrictive arm did better on many counts
    Intra abdo hypertension is linked to organ dysfunction. Percutaneous drainage seemed to help and improve outcomes. Decompression may be needed but not much evidence. Usually last resort.

    Some other useful resources from the meeting

    Blog from the ICS

    References from many of the presentations available

    Storify feed from ICS meeting available

    Summary of presentations attended by Dr J McNicholas (consultant at QA Hospital, Portsmouth)


    Southampton Trans-Thoracic Echocardiography for Emergency Medicine and Intensive Care (STEMI)

    Author: Adrian Wong
    Follow @avkwong


    Aimed at consultants and trainees with little experience in trans-thoracic echocardiography. Faculty consisted of a mixture of anaesthetists, cardiologists and sonographers. Included in the pre-course material is a copy of “Pocket Guide to Perioperative and Critical Care Echocardiography”.

    Untitled copy

    The one day course is divided into a morning of lectures and an afternoon of practical sessions. Participants were limited to 10 in total.

    The lectures covered

    • Course introduction and FATE Scanning
    • Sono-anatomy and the cardiac views in detail
    • Optimising image quality
    • LV Function and filling
    • Colour-flow Doppler and valvular pathology
    • Visualising the pleura and pericardium and identifying pneumothoraces
    • Quality control, reporting and FICE accreditation.

    Well delivered from enthusiastic speakers. “Real world” images that illustrated the lectures were a welcome difference to the beautiful text-book images that the novice can only dream about. Rather appropriately, the last lecture of the morning on quality control and accreditation was a useful poke in the right direction for beginners trying to navigate the minefield of making the transition from keen amateurs to full FICE or even BSE accreditation. It also introduces the challenges and issues when it comes to setting up an echocardiography service in the non-cardiology setting.

    Like most of these courses, the practical session of the afternoon was the highlight of the day. There were two circuits of 5 stations with participants rotating in pairs. Each of the circuits gave participants an opportunity to practice obtaining one of the standard views of FATE echocardiography including a station on lung scanning. Unlike other courses, the “models” were real life patients rather than fit-healthy and perhaps more importantly, slim individuals. The second circuit had patients with actual pathology. I am not going to reveal what the abnormalities were and spoil it for future participants.

    Overall, the course was a good introduction to critical care and peri-operative echocardiography. Personally I would have preferred more practical time but equally, FICE accreditations requires some theoretical knowledge and underlying principals, hence the relevance of the lectures. However, make no mistake, the key to learning echocardiography is actual bedside experience with a mentor and expert. The course will arm you with the knowledge and basic skills to build echocardiography competence.

    DOI: Candidate on 8th November 2013 course

    Please email
    if you would like more details about this course and future dates


    Microbiology for Intensivists

    Author: Dr Neil Richardson
    Follow @NellyRicardoson

    One day of lectures and case presentations at The RCoA on current themes in ICU (23rd October 2013). Attended by trainees and consultants from the Wessex region, it was informative, with some excellent speakers and good clinical advice. Only thing notable by its absence was selective oral/digestive tract decontamination.
    Here are a few notes and take home messages from the day.

    Severe Community Acquired Pneumonia - what should we be treating? How should we care for the patient?
    Dr Matt Wise
    Nothing ground breaking but good to cover this common problem on ICU.
    • 10% of ICU admissions between 2005-2011 (52,000). Mortality currently running at 28%. Better outcome if admitted to ICU earlier.
    • ICNARC case mix - 128% increase in CAP over time period? This seemed remarkably high. Only 24% increase in ICU capacity over the same period.
    • H. Influenza still main culprit. Strep. pneumoniae also important - resistance patterns (from Spanish data) suggest resistance to clarithromycin increased by 30% in the last 20 years.
    • Some data was presented from early part of 20th century (pre antibiotics)  in regards to survival from S. pneumoniae CAP. 20% mortality in the small case series. Not advocating that abx should not be given but is evidence that there is an immune system which can be effective. Further to that, severe pneumococcal infection rates of survival and length of hospital stay improved if abx were given within 4 hours of diagnosis.
    • Severe CAP - CRB65 score. Not useful for Intensivists. Is a good predictor of mortality though.
    • What antibiotics to give? BTS guidelines state Beta lactam or 3rd gen cephalosporin plus macrolide. Better outcomes seen if stick to abx guidelines. Thought macrolides confer a survival benefit as quorum sensing inhibited therefore biofilm less effective. Biofilm seemed to be the topic of the day with many microbiologists stating biofilm makes bacteria very difficult to kill.  
    Fungal Infections in Intensive Care
    Prof. Rosemary Barnes
    A good lecture from an authority on fungal infection
    • Over-riding theme of lecture was that invasive fungal infection is rare and we are probably over treating. Prof Barnes refers to a small study looking at fungal infection in gut perforation where she beliefs most of justification to start antifungals empirically comes from. She disputes the weight we should place on this study (apologies did not get the name - have been looking). I was left slightly confused as most of the lecture was spent saying invasive fungal infection is rare, but, at the end, data was presented showing that if there is delay in treating, mortality increases. Not sure where the balance is.
    • Invasive fungal infection is rare - est <1% (Fungal Infection Risk Evaluation [FIRE])
    • £112 spent on antifungals in a year
    • Invasive candidosis is the most common invasive fungal infection
    • Much of isolates represent colonisation
    • Fluconazole is still appropriate to use in the UK as resistance levels are low
    • Removal of central venous catheters is essential if candidaemia diagnosed
    • Risk tools e.g. Leon (Crit Care Med. 2006 Mar;34(3):730-7) and MSG not validated in UK population.
    • ICNARC data and cost effectiveness for fungal prophylaxis initially not in favour of fluconazole - price was reduced 90% - became cost-effective!! However, rate still very low so Prof Barnes argues should we be using it prophylactically anyway.
    • Testing for candida - PCR well validated but positive test could mean just colonised. Might be used to rule out infection. Other tests such as beta - D glucan, germ tube etc also might start to be used to help diagnosis in the future. However, currently diagnosis is still made based on risk e.g. immunocompromised, tests, cultures and clinical picture.
    • Brief mention on aspergillosis - risk factors for include COPD, immunocompromised. Treatment is long term Ambisome as very difficult and/or impossible to eradicate.

    Viral Scenarios in ICU
    Dr Jaisi Sinha
    This session comprised of short clinical vignettes with take home messages
    Briefly here they are:
    • At risk - pregnant, immunocompromised. Dx by skin sample - PCR/viral immunofluorescence.
    • Sepsis from this e.g. encephalitis - high dose IV aciclovir. Steroids - contentious - no strong evidence in favour of its use.

    • H1N1 - nothing new presented - re-iterated what we already know about population being 15-44yr olds.
    • Avian H5N1 - high mortality rate (248/393 to date). No confirmed human-human spread. H7N9 in March 2013 - 44/135 dead.
    • Asked us to refer to the HPA website for details of how to treat!
    • Looked at a case of toxoplasmosis. IgG/M for todo was negative. Need PCR on CSF to confirm diagnosis as patient unable to mount a immune response.

    MERS (Middle East Respiratory Syndrome)
    • Coronavirus
    • 139 cases confirmed. 60 deaths. All had connections from Middle East
    • Spread from close human contact
    • Case in London
    • Presents as pneumonia +/- renal failure

    Cases for discussion with the experts
    Dr Jack Parry-Jones
    • Some interesting cases. I took a few things away from this session including
    • Infective endocarditis - large vegetations should rouse the suspicion of fungal infection as staph. would erode the valve before they get very big.
    • CNS (Coag. neg Staph.) infective endocarditis - male:female 9:1 usually in 60’s. Thought shaving of the face might be a causative factor.
    • Necrotising fasciitis - clindamycin is drug of choice 1.2G QDS as it decreases toxin production.

    Pseudomonas in your patients and in your ICUDr Vanya Grant
    Very interesting but scary lecture. Pseudomonas is the thing of Intensivists nightmares. Pseudomonas is a big problem and it will get worse. Due to its large genome it has a larger genetic variability and there is an emerging strain that is carbopenem resistant. It has an affinity for warm wet conditions, can colonise places like taps (as in the case of the Neonatal ICU in Wales) and is very difficult to eradicate. It also causes damage in industry including pipes, ships etc.
    • Reason for the difficulty in treating pseudomonas is its ability to form a biofilm. Quorum sensing by pseudomonas helps to sense when population density is maximal, changing gene expression and triggering biofilm production. Although bacteria not dividing, impenetrable layer formed to antibiotics and immune response. Can still damage respiratory endothelium and is pro inflammatory.
    • Longer tubes present in patients e.g. ETT, increased likelihood that it will be colonised.
    • Pseudomonas pneumonia is rare but difficult to treat and can cause pulmonary vessel infarction. Gentamicin and aminoglycosides do not penetrate lung well.
    • Treatment of pseudomonas infection is becoming increasingly difficult due to antibiotic resistance. Tazocin 10%, Cipro 10% (and mutagenic therefore can actually cause resistance) Gen. 4%, Carbopenem resistance emerging from Middle East. This poses a huge threat in the future.
    • 1 agent is just as good as 2 (Cochrane review)
    • Conclusion - if pseudomonas isolated need to ask; Is it colonisation? Do I need to treat it? If need to treat impossible to eradicate if plastic is in-situ.

    Resistance patterns in ICU - the importance of knowing local resistance patterns in your clinical management
    Dr Jack Parry-Jones
    A really useful conclusion to the day. Because the speaker is from South Wales, much of the resistance patterns probably applicable to Wessex as well. Take home message was however have a good relationship with your microbiologist and learn local resistance patterns. If site/source in doubt, give Tazocin and Gentamicin - covers 98% gram negatives and 95% staph. aureus (in Wales).
    Severe sepsis in numbers
    • Incidence 1 in 1000/yr
    • 2% hospital admissions
    • 10% critical care admissions
    • 37,000 deaths/yr - more than lung, bowel breast cancer deaths combined
    • Men>Women (mortality also worse in men)
    • Mortality approx. 20%. For every organ failure, mortality increases by approx 20%
    • 30% of severe sepsis - organism not identified
    • Gram negative sepsis - 35% co-amoxiclav resistant
    • Staph. aureus - flucloxicillin resistance decreasing

    3 prong attack is required:
    1. Diagnosis - key aim of surviving sepsis campaign. History is the absolute key to establishing cause. 40-70% respiratory, 10% genitourinary, 10% abdominal, 10-20% bacteraemia - of which most common bacteraemia culprits are e.coli, staph, enterobacter, klebsiella, CNS in that order.
    2. Treatment - source control and antibiotics - goes without saying. Give the right antibiotic - mortality increases 5-fold if wrong abx administered. Also - dont forget viruses, 50% of CAP is either due to or co-infected with viruses.
    3. Supportive - we are good at this. Less good at 1 and 2.