All posts by Stephen Shepherd

Effect of Systematic Intensive Care Unit Triage on Long-term Mortality Among Critically Ill Elderly Patients in France

Hot Topics Session

It is well recognised that critically ill elderly patient have a higher mortality and therefore the beneficial effect of intensive care unit (ICU) admission variable ICU use among this population have let to significant difference in uptake.

Guidet and colleagues performed a cluster, randomised trial of admission versus standard care in 3036 elderly patients aged 75 years and above. In their multicentre randomised trail, suitable patients were allocated to routine or non-routine admission as per the following:


Outcome Measures

  • Primarily 6 months
  • Secondarily ICU admission rate, in-hospital death, functional status and quality of life.





  • Disappointingly there was no difference seen in any of the outcome measures, even after adjustment for differences in illness severity and patients admitted to ICU had an INCREASED risk of death at six months despite an increase ICU admission rates.
  • Functional status and physical quality of life at six months did not differ significantly.


What does this mean?

  • As our ICU population changes it may be that a systematic approach which admits all elderly patients has no effect upon outcome.
  • Further international trials are needed before we know whether this is applicable to other populations.

Multi-System Vasculitis on ICU #LIVES2017

Marlies Ostermann from Guys & St. Thomas’ NHS Trust in London gave an excellent overview of this uncommon but difficult condition.

Firstly, vasculitis is rare and non-specific in its presentation. Unless you work in a specialist centre you might not come across a diagnosis of it (although you might find may more cases you don’t know about…).

Vasculitis involves inflammation of any vessel, arterial or venous and clinical presentation so variable as it depends what organs those vessels are supplying as to what organ dysfunction you get. Classification is completely arbitrary and has changed in recent years as we’ve moved away from Nominals for syndromes.


Distribution of vessel size and Vasculitis


ALL vasculidities are triggered by something which produces antibody mediated reaction with inflammatory vessel wall and vessel occlusion/necrosis. Type of damage differs with different mediator and particularly important for small vessel diseases, i.e.


  • If the antibody is raised and directed the blood vessel wall itself, this is Anti-Glomerular Basement Membrane disease, previously called Goodpasture’s Syndrome.
  • If the antibody is raised by B-cells against systemic cellular components which then cause secondary wall attach, these are usually Anti-Neutrophil Cytoplastic Antibody (ANCA) associated vasculidities.
    • There are different patterns of staining and hence classifications of ANCA depending upon what the antibody is attacking
    • Perinuclear (pANCA) is raised against the antigen myeloperoxidase (MPO) and this causes staining around the nucleus (!)
    • Cytoplasmic (cANCA) is raised against the cytoplasmic (!) antigen PR3. You can see the difference below:

ANCA Staining Patterns

    • pANCA isn’t just raised against MPO though, it can also be raised against lactoferrin or ‘bactericidal permeability inducing protein’ which why pANCA can be positive in sepsis, although it’s usually at a low titre.
      • GPA (Wegner’s) mainly cANCA
      • MPA mainly pANCA
      • Eosinophillic GPA (Churg-Strauss) mainly pANCA
  • You can also form antibodies against drugs like hydrazine, propothyrouracil, D-penicillamine which are similarly deposited in vessel walls and hence can cause a lupus like presentation.
  • If you have some other kind of immune-complex-antigen reaction and those form big complexes, they can occlude the really small blood vessels rather than directly causing wall issues – this is cryoglobulinaemiaIgA vasculitis (Henoch-Schonlein) etc.


The chance of it being vasculitis go up with age. Important to remember as well our tests are getting better – the current classification is pretty ANCA heavy, yet as the assays get better it is possible that what we thought of as ‘ANCA-negative’ might not be. Watch this space. The test can also be falsely positive in a number of conditions, particularly autoimmune thyroid disease but also inflammatory bowel disease and viral hepatitis.

We don’t know why some people get lung involvement, others kidney, others rash, etc. However, most do get renal dysfunction hence nephrology’s intimate involvement. Rashes classically petechial and no-blanching, limited to lower limbs


Organ Involvement


Typical Vasculitis Rash


Most people end up on ICU because of their respiratory presentations – this might be respiratory failure which can mimic pulmonary oedema or airway bleeding. HOWEVER, one third of patients with airway bleeding don’t have haemoptysis but you can see blood if CT chest/bronch. Don’t miss important differentials – sepsis (particularly meningococcal), syphyllis and TTP/HUS.

What tests? Most important thing is a degree of suspicion. Do urine dip for blood (non-CSU) and casts, autoab screen, CT chest for bleeding/fibrosis & look for tissue you can get (skin/kidney). Do an echo if is a low pANCA titre and you’re wondering about endocarditis.

Aims of treatment two fold:

  • Remove existing antibodies – plasma exchange
  • Stop making new ones – steroids and chemotherapy

The clear indications for plasma exchange are severe CNS involvement and severe pulmonary haemorrhage. Borderline evidence for indications other than this but that doesn’t mean it might not work.

Classical chemotherapeutic agent was cyclophosphamide – however in recent years there has been a switch towards Rituximab. They both do the same thing, i.e. stop B cell activity but recent trials have shown Rituximab to be non inferior with a better long-term safety profile (marrow/infertility/cancer) hence popularity. No-one is ever going to do a trial of cyclophosphamide or rituximab in critically ill patients so we have to extrapolate. Should be an MDT consensus – they all have major side effects so depends on how bad they are as to how much you want to poison them.

Largest ICU series to date from France – 82 patients from 20 French ICUs over 20 years (!). However, other populations the incidence is much higher so it’s probably that we do not look for it. ICU mortality was only 16% – 70% died of disease and 30% from sepsis underlining why we need to have open mind – they respond to treatment if you do it.

Short answer – not all MIs are atherosclerotic. Not all confusion is ‘delirium.’ Not all AKI is sepsis. We need to get to diagnoses not syndromes.




ECMO Course

Session 1 – Antonio Pesenti, Refractory Hypoxaemia Therapuetic Strategies

Before deciding on support, first need to know what targets. One might be PaO2? If you climb up a mountain it’s low? Is this important – not according to Grocott in NEJM 2009 where low levels were compensated for by higher Hb.

Rx hypoxia broadly divided as follows

  1. Treat cause – antibiotics, thrombolysis, etc, etc
  2. Increase FiO2
  3. Reduced atelectasis – PEEP
  4. Increase pulmonary blood flow
  5. Reduce venous admixture – ECMO

Reabsorption atelectasis complicates high FiO2 administration.

PEEP prevents collapse = recruitment manoeuvres are needed to open collapsed lung. Indeed main difference between traditional IPPV & HFOV/APRV is high airway pressure – theory being more recruitment AND retention.

Don’t forget effects of heart + shunt upon O2 but iNO doesn’t work.

The benefits of proning extend beyond its effects on PaO2 – failure to improve this variable does not mean you should stop doing it.

Longer term, hypoxemia is a risk factor for long-term neuropsychological impairment but HYPEROXIA IS BAD.


Session 2 – Jan Bakker, Haemodynamic effects upon ECMO

Very variable! Limited prospective scores – ENCOURAGE might be useful for VA, or clearing fluid balance on day three but in essence little evidence.

When considering you need to ask:

  • What other support have you got?
  • What configuration are you using?

Peripheral VA-ECMO can significantly increase after load – first consider dilators, then increase forward flow whilst remember to treat acidodsis/anaemia. If that doesn’t work, add an IABP.

With VV-ECMO, RV afterload will fall with PVR effect because of beneficial effects upon CO2/PAO2.


Session 3 – Weaning from ECMO Giacomo Grasselli

No science to this – lack of definite criteria, indications from guidelines and local protocol and personal experience

Four scenarios

  1. wean ECMO, then vent
  2. Emergency discontinuation, e.g. bleed
  3. First wean vent, then ECMO
  4. Withdraw

Weaning from VV is weaning gas flow – you don/t need to reduce flow

Weaning GF increases muscle effort and needs vent support 

ELSO guidelines

You need haemodynamic stability as well as respiratory improvement. Measure oxygen delivery – the target is tissue oxygenation NOT PaO2.

How long do you keep the gas off? – Karolinska say 4 hours

Some authors propose leaving cannulae in place for put to 48 hours flushed with heparinised solution – practice VARIABLE

How to decannulate VV?

  • Stop/reduce heparin
  • Put purse string around insertion cannula
  • Clamp lines
  • Stop pump
  • Remove pipe allowing small amount of leakage to red air embolism
  • Manual compression 20 min for venous and 30 min for arterial.
  • Close monitoring distal perfusion for arterial and consider  vascular ultrasound in both as high incidence of clot or injury


Keynote – Michael QUINTEL, 50 years of ECMO

ECLS first developed by John Gibbon and Mali in 1936 in response to sudden death young patient with PE and first used in ORD for ASD repair May 1953

First trials negative – but badly done – so perhaps can be better interpreted as even if you do ECMO badly, you don’t kill everyone…

CESAR trial

First oxygenators bubble before developed hollow fibre oxygenator

The development of heparin-coated circuits allowing limiting APTT was one the major steps in reducing morbidity and mortality

Single centres such as Michigan have led the way – now more adult/paed, less neonates

Then H1N1 prompted exploration

H1N1 make worldwide excessive use of the technology but there is no new real data.

Reasonable data about risk/benefit ratio does not exist. Cerebral micro emboli are universal. 85% get DVT.

Is informed consent even possible?


Pro: Is ECMO always an Option? Steffen Weber-Carstens

UK evidence summarised by @CochraneUK in 2015

Similar International Consensus Position Paper by Coombes and colleagues on what defines an ECMO centre

Triage essentially as duration IPPV significant risk factor of deaths.

Con: Giacomo Bellani 

In one series, 87% of referrals had at least one relative contraindication

25% of patients in CESAR didn’t get it

EOLIA trial has not reported and is ongoing – we are in the infancy of what we know

16% rates of head bleed

20% nosocomial infection

Why use more resources when you can achieve the same thing with less? LungSafe shows we still don’t get optimium PEEP, NMBA, fluid balance and supportive care in ARDS.



Basic Bundle

  • Hand hygeine
  • Surgical asepsis insertion conditions
  • Avoid aqueous iodine
  • Subclavian and radial preferred
  • Remove useless catheters
  • Immediate change of soiled dressings

What about alcohol-iodine versus chlorhexidine-alcohol? Scrubbing or no-scrubbing of line areas?

2×2 factorial design

Muticentre RCT, primary outcome CRBSI

2349 enrolled with 5159 catheters!

Patients generally matched, mainly medical patients with 70% mechanically ventilated

Most patients had radial catheters (68%)

Chlorhexidine was significantly better than alcohol-PVI in reducing CRBSI. Addition of scrubbing of area added no real benefit. Chlorhexidine group had more skin reactions but they were slight.

Conclusion: 2% chlorhexidine is superior to iodine in reducing the risk of CRBSI

Skin antisepsis with chlorhexidine–alcohol versus povidone iodine–alcohol, with and without skin scrubbing, for prevention of intravascular-catheter-related infection (CLEAN): an open-label, multicentre, randomised, controlled, two-by-two factorial trial