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Todd Fraser wrote 05-25-2012 11:42:33 am
Session one

This fascinating session presented cases supporting a tolerance of hypoxaemia, and concluded with the sage wisdom of JLV supporting the middle ground.

Mike Grocott - The Everest experience

Novel intro to the conference with Mike having to Skype in from home after having a new baby!  Mike used the ascent to Everest and it's effects on functioning as an analogy to explore the limits of hypoxia tolerance.  The disabling effects on otherwise superb athletes, even with supplemental oxygen, is astounding.  Grocott's group has used climbers to study the effect of cellular hypoxia in otherwise normal people, giving us some important insights into this problem in critical illness.  They took healthy volunteers from 18-70 and took them trekking to base camp for 12 days, also had investigators and climbers there for prolonged periods.  They used a standard ascent profile.  They set up a physiology lab at the base camp.  Strangely, they found that there was no link between the physiological adaption (such as oxygen carrying capacity) and oxygen consumption, implying that there is some adaptive response at the cellular or microcirculatory level.  This remains to the explained.  Perhaps the better climbers have an ability to adapt at this level in ways we don't understand yet.

There are  changes in mitochondrial numbers, nitric oxide metabolism and capillary density with exposure to hypoxia.  Again, perhaps the difference is explained in how this is expressed in any one ind

Todd Fraser wrote 05-25-2012 01:53:30 pm
Session two

This great session focussed on the delivery of oxygen to the tissues and how to make that happen.  Some fantastic banter between Jamie Cooper, in the RCT corner, and JLV in the  pragmatic corner, will undoubtedly be a highlight of he conference

Jamie Cooper - what about the blood

Of course, oxygen only gets to cells if it's carried on hemoglobin.  Jamie Cooper reviews our current understanding of the place of transfusion in hypoxia.

Limiting transfusion is well evidence based and is largely well accepted and practiced in Australiasian ICU.

Jamie touched on the age issue with blood transfusions, reminding us the changes occur in both the blood and the storage medium with time, with major changes well established in two weeks.  Adverse outcomes are seemingly associated with this "storage lesion".  This has led to the TRANSFUSE trial currently being conducted by the ANZICS-CTG.  This trial will compare the use of the freshest available blood for ICU patients versus standard practice, looking at 90 day mortality.  2 other trials in adults and one in pediatrics are also being conducted.

Provocatively, Jamie pointed out that the number needed to treat to save one life (based on current understanding of the literature) is 97, questioning the real world impact of a change to newer blood.





Benoit Vallet - oxygen delivery needs individual targeting

Furthering this morning's theme, Benoit presented the argument for targeting oxygen delivery to the indivi

Todd Fraser wrote 05-25-2012 02:16:23 pm
Interesting discussion in the question time related to fresh frozen red blood cells. It appears the Dutch are doing it with good cell survivability.

Coming soon to a defense force near you!

Todd Fraser wrote 05-25-2012 03:34:19 pm
Interesting presentation by Jason Pincus on lipid therapy for TCAs, calcium channel blockers and betablockers. It has possible role in increasing myocardial energy stores, and as a absorbative sink for drugs.

Jason reported his findings of some laboratory data where he added lipid to blood samples with known concentrations, then centrifuged and threw out the lipid layer and remeasured.

Impressive reduction for amitryptilline and verapamil, not so much for metoprolol and sotolol. He also compared ClinOleic vrs intralipid - no difference shown.

Todd Fraser wrote 05-25-2012 04:51:29 pm
Some fascinating byplay in the conference today regarding the role of the RCT in clinical practice, with JLV clearly advocating for pragmatism

Todd Fraser wrote 05-25-2012 05:14:05 pm
Session three

The third session focussed on prevention of complications related to oxygenation in ICU.


Gilles Capellier - VALI, is it preventable?

Strolling down memory lane with many in the audience, Gilles remembered the bad old days of high volume, high pressure ventilation for ARDS in the 70s and 80s.  Awareness of the potential for ventilation to contribute to lung injury improved in the 90s and beyond, and today it is thought to be less of a problem.  However, there is probably still some morbidity that can be avoided with careful attention.

Gilles reviewed the pathology of ARDS and ventilation.  Due to dependent collapse and consolidation, the ventilatable regions of the lung are smaller, leading to the potential for over distension if traditional tidal volumes are used.  This is likely to have both mechanical and inflammatory consequences.  Interestingly, the combination of LPS sepsis and mechanical ventilation has more effect on lung injury than either alone.

So what can we do to protect the lungs from VALI?  Low tidal volumes remain the standard since the original ARDSNET trial, and some interesting dynamic CT scanning studies demonstrate this eloquently.  Less clear is the effect of PEEP - paradoxically, recruiting lung may lead to worsening of hyperinflation rather than improvement.  Perhaps a role for "permissive atelectasis?"

Despite clear recommendations, surveys of practice around the world suggest that significant proportions of patients are

Todd Fraser wrote 05-25-2012 05:22:48 pm
Great comments in question time. Benoit Vallet argues we don't know how to get the balance of vasoconstrictor to fluids right.

Simon also points out that fluid balance is clearly associated with poor outcomes (cause or effect?). He also states that this is one of the most difficult areas in clinical practice.

Todd Fraser wrote 05-25-2012 06:16:46 pm
Neil Orford says :

Felicity Hawker Medal Presentations


Dr Darshana Hewakandamby: A randomized trial comparing the effect of daily interruption of sedation infusion on critically Ill patients on mechanical ventilation.
A prospective RCT of sedation interruption in Hong Kong. Reports sedation interruption did not affect duration of MV, ICU or hospital LOS or mortality.


Dr Asako Ito: Temporal trends in Epidemiology and Antimicrobial Susceptibility
A retrospective study comparing bacteraemia in 2 12-months cohorts (2003-2004, 2009-2010), found 121 bacteraemic patients, an increase in ICU acquired bacteraemia, and in bacteraemia patients a  reduced ICU and hospital mortality, and an increase in gram-negative bacteria in the 2009-2010 cohort.   

Dr Jason Pincus: In-citro comparison of clinoleic and intralipid for select B-blocker, calcium channel blocker, and tricyclics antidepressant toxicity.
Lab based study comparing lipids at reducing fat soluble agents amitryptilline, verapamil, metoprolol, sotalol. Ranged from approx 78% amitryptilline down to approx 1% for sotalol, in keeping with reducing lipid solubility.

The study showed clinoleic is as good as intra-lipid at reducing these drugs.

It also created discussion of issue of lipid rescue ( 1.5 ml/kg bolus then  0.25-0.5 ml/kg/m, total of 500ml) in cardio toxic fat soluble toxidrome.


A Gautam: VAP in tertiary PICU
Prospective VAP  observational study in PICU. 67% pts develop VAP, 7:1000 days. Most develop within 10 d

Todd Fraser wrote 05-25-2012 06:36:34 pm
Session four

This session focussed on organ-specific goals of oxygenation

Stephen Bernard - the brain

Bernard, famous for his work in hypothermia for hypoxia-ischemic brain injury, starts by projecting forward to his view of the future.  A few brave assumptions?

Is brain oxygen monitoring feasible?  Perhaps not yet, but maybe it's not too far off.  Using micro dialysis techniques to enable this, some work has been done on using this endpoint to guide haemodynamic interventions in traumatic brain injury.

The question is how much,  with some evidence that hyperoxia, or even hyperbaric oxygen, may be helpful.  Future trials await...

Strangely though, the reverse seems true in cardiac arrest.  In this group, the potential for oxygen free radicals to cause harm during reperfusion seems to be detrimental, and as such, efforts to limit brain oxygen seems important.  Stephen illustrates this with some interesting lab and clinical papers that support a "normoxic" approach.  Again, we eagerly await further trials.

Some issues need to be overcome though, since controlling inspired fraction of oxygen pre hospital is difficult, and without arterial blood gas sampling, requires confidence in Sats probes at they may not deserve.

What role does near infrared spectroscopy?  What about jugular bulb saturation monitoring?  No role, it seems, based on current evidence.

Finally, where does this leave us with stroke, SAH and other intracerebral catastrophes?  As Stephen says, it

Todd Fraser wrote 05-25-2012 06:51:45 pm
Question time : Rinaldo states the countercurrent mechanism is also present in the gut, protecting it from the relatively large oxygen delivery it has during periods of fasting.

He also reminded us of the disconnect between renal blood flow (which we can't measure clinically anyway), glomerular filtration rate, and even worse, urine output. Basing decisions about controlling haemodynamics on urine output is "delusional" he says! Who knows, do we even want to stress the kidney out by making it work harder if we increase GFR?

Two small studies cast some doubt about higher MAP targets to protect the kidney against hypoperfusion in sepsis, says Rinaldo.

Neil Orford wrote 05-26-2012 09:08:24 am
For me the memorable quotes, and areas of interest on Day 1included..

Altitude: Does the evidence of bleeding or vascular engorgement in optic fundus in climbers, raise the possibility of cerebral injury that may have long term sequelae, like dementia? The Everest project did perform functional MRI on return and saw no damage. Howeverit may be more subtle, or slower, and perhaps there are issues around long-term neuro-cognitive effects of critical illness that could be explored.

Age of blood: The blood story is an interesting one. One unit RBC costs $900 in Australia, and annual national cost of 0.5 billion. 20% of blood is used in ICU. There are Growing concerns regarding transfusion appropriateness in Australia, and there is a lack of evidence regarding use, despite eagerness to apply best practice.

Age of blood may matter. There are studies that show older RBC's may have deleterious effects (infection, oxygen carriage, cerebral injury, mortality), all limited. The Koch trial in NEJM 2008, was a 6000 cardiac surgery retrospective study that reported increased adverse outcomes with older blood. A study from Canada showed increased mortality with older blood through data linkage. A recent meta analysis suggest increase mortality, increased MODS with older blood.

In Australia a large observational "current practice" study, a blood fridge feasibility study, and a pilot RCT of age of blood, have occurred. Overall these suggest association between fresher blood an

Todd Fraser wrote 05-26-2012 11:42:05 am
Session five

Its easy to be distracted by the bight lights of new technology.  Perspective is important, and in this session, 3 highly experienced clinicians look back over the years and give us theirs.

Stephen Streat - does monitoring make a difference?

Day 2 begins with the sage ruminations of Stephen Streat.  He reviews the origins of the right heart catheter, and it's place in the measurement of cardiac output and right heart pressures in the ICU.  Questions about the validity of the widespread introduction to ICU practice began as early as 1985.  The demise of the Swan Ganz Catheter since then has been well documented.  It seems there is little question left, with 6 RCTs in multiple patient groups now showing no benefit, and a number of meta-analyses confirming these results.

But what has filled the void?  Is there still a role for cardiac output monitoring in the ICU?  Streat presents evidence that while PAC sales are falling, the use of cardiac output monitoring is increasing world wide.

Does oesophageal Doppler stack up?  A number of RCTs have been done, some with very positive results, others with dubious outcomes.  There is some evidence to support use in high risk patients, such that the NICE in the UK published guidelines supporting its use.   It appears though that with conflicting results there still remains conjecture over its place in ICU.

And what of pulse oximetry? While it certainly appears to detect hypoxia, there is no evidence it makes any differen

Todd Fraser wrote 05-26-2012 01:46:49 pm
Session five

Jean-Louis Vincent - central venous saturations : useful?

Here he comes again, the muscles from Brussels!

SvO2 represents a global estimate of oxygen extraction.  The lower it goes, the less the cardiac output reserve delivered to the tissues, as this represents a point where oxygen consumption becomes dependent on supply.  It doesn't measure the cardiac output, rather, the adequacy of the CO.  Interestingly this point often coincides with increased lactate production.

The point at which this occurs is higher in patients with sepsis, reflecting an inability to extract or consume oxygen, possibly due to mitochondrial failure.

Increased extraction occurs in anaemic and hypoxia also, important confounders of SvO2.  It also occurs when metabolic demand is increased.  

JLV argues that this is a far more meaningful endpoint to titration therapy to compared with estimates of cardiac output.  He outlines a decision tree based on high or low cardiac output, with lower branches of high and low SvO2.  These 4 outcome branches are useful for guiding diagnosis and treatment.

He says the rate of complications post surgery can be reduced by avoiding low SvO2.  He also uses it to guide other therapy such as when to reintroduce beta blockade post op in high risk cardiac patients.

What about ScvO2?  The advantages of course are it is significantly less invasive.  Unfortunately, there is a relatively poor correlation between the two, demonstrated in multiple studies.  But d

Todd Fraser wrote 05-26-2012 01:49:26 pm
Neil Orford says :

8 take home messages from Bobs trip down memory lane
For those of you know Bob, the opportunity to hear him reflect on 50 years of practice is an opportunity not to be missed. The brief history he provided is unique. He performed 100 post-mortems as a med reg in the 1960's, and in 1971became Director of SVH Sydney ICU, 20 beds, one of the first ICUs in the countries. They treated tetanus, GBS, chest trauma, and "therapeutic drowning". In the early days they didnt know what they were doing, and learnt by trial and error, talking to each other. This led to  CBM "common sense based medicine", where  basic sciences came from anaesthesia, medical guidance from physicians and surgeons, and advice from nurses. He described 1st case of ECMO in 1970's. They did 6, 1 survived, and they stopped because the impact on hospital pathology, blood bank, cardiac surgery was unsustainable.  They now do 40 per year, with 1 nurse looking after them. All due to change in technology.


Th messages of CBM included;
1. ICU nurses are the secret to good ICU
2.  we need to be skeptics. "as any financial advisors will tell you, doctors are real dopes, we can be sold anything"
3. Dont inappropriately use mask NIV in decreased LOC, sputum load, upper GI surgery
4. Anaemia: favorite topic, argued why we are wrong to have permissive anaemia. Took a big swipe at TRICC ( only enrolled 1/3 of patients, underpowered ). The argued it is hard to make up for bad su

Todd Fraser wrote 05-26-2012 05:02:19 pm
Session seven

Non invasive ventilation is a huge and growing component of what we do in modern ICU

To review the role, this session features masters of the ventilator nobs, John Fraser and Dave Tuxen

John Fraser - use it for everyone

Fraser begins by outlining the history of NIV.  Interestingly, NIV was where mechanical ventilation began, albeit fairly unsuccessfully.  He argues that though time has made IPPV better tolerated, improvements in NIV will still mean some patients are better managed non invasively.

Curiously, he notes, no positive pressure mode had every been shown to change outcomes.

Increasing data over the past decade seems to support its use in multiple groups such as immunosuppressed, in acute pulmonary oedema, and patients with COPD.  However, evidence was increasing that it should be at least offered in other groups also.  Worldwide data suggests a widespread adoption of NIV for all conditions, with as many as 25% of ARDS and pneumonia patients treated this way, conditions traditionally thought to be inappropriate. On the former, data remains preliminary, but there is increasing evidence that there are groups of patients who do well with NIV for ARDS.

Interestingly, patients who do well in NIV have better outcomes than if they are tubed straight away.  Is this just selecting out the winners?  Possibly.  Clearly though, the longer the time from starting NIV to intubation, the hier the mortality, suggesting that failure to tolerate NIV should be recogn

James Doyle wrote 05-26-2012 06:34:00 pm
Session Eight

Prof Benoit Vallet talks on the Grey Zone assessing the pulse pressure variations and response to fluid variations. This educational talk highlights the principles behind these concepts.

First a reminder that pulse pressure variation analysis is to be performed in the positive pressure ventilated, sedated patient. Parameters include the stroke volume variation (stroke volume max to min), pulse pressure variation (pulse pressure max to min). The principle behind these parameters relates to the volume responsiveness as per the Frank-Starling relationship. On the occasion where there is a large PPV or SVV this represents the step portion of the curve and hence a greater degree of fluid responsiveness if given.

Note that PPV and SVV cannot be assessed in case of arrhythmia, spontaneous breathing, Vt <7ml.kg, HR/RR <3.5, open chest

Benoit suggests that in the presence of a PPV or SVV > 12% then you have the green light for a fluid challenge as there will be a response. Conversely if less than 9% do not proceed. The question is what to do between these points  or the grey zone.

Zimmermann et al in Eur J Anaesthesiology 2010 showed that flotrac SVV and Mximo PVI (pulse variation index) quoted the best threshold values to predict fluid responsiveness where 11.1% with PVI, 9.5% with SVV. Two other single center trials recommended values between 8 and 12%.

With these smaller studies in mind Benoit and his team looked at the grey zone approach as t

Neil Orford wrote 05-27-2012 01:26:27 pm
Session 12: Manipulating the microcirculation

Bala Venklatesh: Tissue oxygenation - Quo Vadis

Firstly Bala has credibility in the area, with thesis, research, and ongoing interest. In 1896 Haldane proposed lungs secrete oxygen, then 1920 Barcroft disproved this. During this process provided classification of anoxia. The tissue hypoxia definition of dysoxia was developed.

Before the 80's lactate was used as the marker of dysoxia. In the 80's (Shoemaker, Bihari) developed oxygen debt theory, and limitations of arterial lactate as measure of dysoxia. In the 90's organ beds were investigated. The GI tract as the "canary" (splanchnic ischemia ) using GI tonometry, which was shown to be inaccurate after initial enthusiasm. The nail in the coffin being the Gomersall RCT in CCM. The brain was looked at with LICOX, a multi parameter was trialled, other organs probed included urinary bladder, skeletal muscle, subcutaneous tissue, renal, oesophageal, sublingual, and liver. All promising, but a lot of variability and have not progressed beyond experimental. This is due to heterogeneity of tissue beds, with differing oxygen and carbon dioxide responses to endotoxaemia. Finally tissue oxygenation affected by many factors, some of which we can effect (Hb, CO2, arterial PO2, flow etc), making the results difficult to determine. Other techniques include near infra-red spectroscopy, thenar and knee oxygenation, high energy phosphates.Trials looking at tissue oxygenation improvem

Todd Fraser wrote 05-27-2012 10:10:56 pm
Final Session :

David Tuxen: Permissive hypercapnea in ARDS
Could hypercapnoea be protective to the lung?

Tux started the case with evidence for lung protective evidence from animal data, then moved onto evidence showing sustained hypercapnic acidosis leads to antiinflammatory effects in humans. The balance of course is the benefit of antiinflammatory effect reducing lung injury vs the detrimental effect due to susceptibility to infection. He presented an argument regarding time of hypercapnic acidosis and antibiotics to balance these conflicts in lung injury,mie antibiotics can attenuate the rants inflammatory risk

Is it the acidosis or the CO2?
Animal model evidence that if buffer the CO2 aspect of acidosis with HCO3 benefit lost, ie suggest the acidosis effect benefit.

Human data?
Reanalysis of ARDS net data by pH and CO2 strata showed difference in outcome in high Vt group,ie hypercapnea associated better outcome in this group. There was no effect in low Vt group.

Concludes that hypercapnea is usually present in protective ventilation, good animal model of injury reduction, the increase sepsis risk can be offset by antibiotics, benefit mediated by academia and negated by buffering, and their is some (re-analysis) evidence of benefit in humans.

Benoit Vallet: Additional goals for goal directed therapy: central venous to arterial CO2 difference.

ScVO2 literature suggests hypoxia, hyperoxia is associated with increased mortality, while normoxia better. The difficulty