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Raj from Australia wrote 12-10-2014 06:55:41 pm
Day 1 ICS:

Session1:

1. Heyland: Iatrogenic under feeding is harmful to high risk critically ill patients


Prof Heyland opened the morning session with a brief overview of the issues surround nutrition within the ICU. He raised the potential issue that by underfeeding critically ill patients, as most of us do, we may in fact be causing harm, as malnutrition is associated with significant physiological derangement. The term ‘optimal’ nutrition was also questioned, with focus on actually delivering the prescribed nutritional requirement (protein/energy) for each patient. A number of studies discussed showed a reduced odds ratio of dying with improved nutrition i.e. patients receive at least 80-85% of their prescribed nutrition.

Prof Heyland emphasised the need for assessing nutritional risk using scores such as the NUTRIC score as high risk patients may indeed benefit with improved outcomes with better nutrition. Protocols such as the PEP-uP protocol may be used to improve volume/feed delivery compliance. More info at: www. criticalnutrition.com

2. Marshall: Is critical illness an iatrogenic disorder?


Within clinical medicine a disease process may be identified often through the clinical signs and history at presentation. In contrast, ICU patients are fundamentally different, as it is in most cases very difficult to identify what disease caused admission to the unit in the first place. Prof Marshall raised an interesting concept that critical illness is in fact an iatrogenic disorder borne out from survivors who without our support would not have survived their initial acute life-threatening disorder. He then raised examples within critical care practice where improvements in patient outcomes have come about by improving or reducing harm associated with our supportive therapies. For example lung protective ventilation in ARDS, conservative fluid strategies within septic shock, reducing the use of vasopressors in bowel surgery patients (as associated increased anastomotic leaks), restrictive blood transfusion policy, iatrogenic hospital acquired infections, reducing oversedation, improving analgesia and early mobilisation. Prof Marshall concluded by stating every intervention within critical care has a COST

3. Bion: Awared Presidents Award: On the 7th day thou shall rest.


Prof Bion discussed recent NHS reconfiguration and the move toward a 7-day service. He discussed the problems of an increasingly complex aging population and the need for a safe and high quality service for all. He discussed the ’weekend effect’ and associated worse outcomes in patients admitted over a weekend. He also presented evidence of an association between higher nursing intensity on shift and potential lower patient mortality.

4. Winter: Awarded the Whittaker Award: Should we close all small critical care units?


Dr Winter raised a controversial topic. He argued the small critical care units should close as:
· High volume units are likely to do better than smaller low volume units. e.g major trauma centre networks have made massive improvements since reconfiguration improving survival by 40% over a two year period.

· Economically easier to specialist staff 24/7 in larger units and to run a more expensive separate oncall list. Easier to buy equipment in bulk through volume purchasing benefits.

He then went on to state that smaller units need to change their focus and that we as a specialty need to drive this process of change and not to have it forced on us by politicians and the government.

J Doyle from United Kingdom wrote 12-10-2014 08:37:33 pm
Day 1 Session 2: Sepsis theme:

5. Marshall: Undesirability of the host response to danger
Professor Marshall discussed bacterial LPS and how susceptibility to the development of sepsis varies between individuals. He showed that genetic mouse studies undertaken in the past showed that with time some mice had the ability to acquire resistance to LPS or lost the ability to respond to it i.e. would not develop a septic response at all. The talk went on to show how the body at a cellular level recognises an infective threat, how the body co-ordinates a response to danger and how through mediator regulation the body tries to resolve the situation. He talked in depth about the Toll-like receptor family. It is no surprise that targeting one receptor or pathway in sepsis treatment often fails, due to the complexity of the body’s response to a bacterial threat. For example LPS presence is thought to alter 3714 genes!

6. Baillie: Why are some people more susceptible to sepsis than others?
Susceptibility to infection is a balance between inherited and environmental factors. This statement is true, but not useful clinically. Profound variation exists in septic susceptibility – the question was raised: why are not all of us resistance to disease, surely this would be a competitive advantage? In reality, patients who have are not susceptible and protected from HIV for example often are more susceptible to other viruses e.g. West Nile virus. Dr Baillie talked further about how pathogens alter our immunity and discussed the concept of positive selection and how infection traits are strongly related to each other within our genome, with host response variation similar to that seen with autoimmune disease. He concluded that in order to treat septic patients with such complexity, individual genes that convey susceptibility to infection could be targeted in future research.

7. Singer: Dissecting the big sepsis papers:
Prof Singer gave a rapid overview of the years sepsis papers. These included a look at the new early goal directed trials: Process and ARISE and compared them to Rivers EGDT trial. No difference was found in mortality between controls and goal-directed therapy. The UK PROMISE trial is due to publish further on EDGT in March 2015.

Further discussion was had on how earlier intervention in sepsis, particularly in the large majority of patients who have less severe sepsis initially on presentation, but who then go on to die from sepsis on the ward needs more focus.

The trial of High vs Lower BP target in septic shock was controversial. Prof Singer explained that the methodology for this study was flawed and that the investigators did not follow their own study rules.

ALBIOS: no difference in septic shock with the use of Albumin. Again, less than half the patients recruited received the targeted Albumin volume causing methodology issues.

Statins – two trials were discussed about statin use in ARDS. Both studies were neutral studies.

Induced hypothermia in severe bacterial meningitis was found to cause harm.

ESMOLOL and the use of Vitamin D3 may offer some benefit in Septic patients, warranting further studies to investigate this further.

Prof Singer concluded: most multi-centre studies have had a neutral effect on our management of sepsis. A great number of trials were unfortunately flawed through poor adherence to trial protocol of the physiological rationale of the study in the first place.

J Doyle from United Kingdom wrote 12-10-2014 08:38:17 pm
Day 1 Ebola session

Dr Bob Winter
Presents on the current situation of the Ebola epidemic. He starts by detailing the response to the aid care workers with possible contamination. With a response banding of 1-3.

Outcome for obstetric and neonates has been dismal. The UK plan to provide level 3 care is only on a case by case basis and is not routine. There have been two cases of patients requiring level 3 care that have survived in Europe.

Of note is that respiratory failure is a very late clinical sign and that diarrhoeal illness always precedes. The likely ICU support would be fluid and potassium management.

The demand to provide ICU care to an Ebola positive patient would be against HSC regulations.

Finally there is the important fever hotline for facilitation to transfer a patient to an infectious disease unit. Transfer in the case of pyrexia only is standard PPE. If diarrhoeal symptoms then a hazardous unit response team would transfer.

Put into context compared to say diphtheria Dr reminds us that this is currently a small contained public health outbreak for West Africa.

J Doyle from United Kingdom wrote 12-10-2014 08:41:08 pm
Day 1 Nutrition. Chair Dr Ella Segaran


Plausible mechanisms that nutrition will reduce attributable mortality is first discussed. As an example the CALORIES study statistical analysis suggested that it would be plausible for a life saved per 16 patients treated, the future need for an ARR of 1% is suggested as a marker for mortality studies.

As a result to prove the importance of nutritional studies perhaps studies of larger magnitude are warranted.

Next Dr Deane goes on to state that caloric intake and mortality is associated. EDEN The open label 2x2 factoral design RCT suggested that tropic feeds where as effective as full feeds. Of interest is that this was a superiority study.however the study did not demonstrate a non-inferiority. Does this suggest that the result of equivalency is an issue with study methodology?

The TARGET study an ANZICS CTG feasibility study for standard and energy dense feed demonstrated a trend to improved survival in patients receiving the energy dense feed. Dr Deane Is cautions to avoid premature conclusions but reinforces the need for large studies suggesting >8000 patients.

Finally Dr Deane Considers delivery, motility and absorption of caloric feeding. After an interesting video of radioisotope labelled meal presence within the proximal bowel 5 hours after ingestion demonstrates the need for jejunal delivery of nutrients. Data is then presented on the effect of critical illness on glucose transporters.GLUT2 is markedly reduced in critical illness.

J Doyle from United Kingdom wrote 12-10-2014 08:41:33 pm
Day 1: Final Session: Liver

8. Gould: The role of the ICU in the management of chronic liver disease

Notes from talk:
• Cirrhosis admissions to critical care have a higher mortality than chronic renal failure. Depending on the cause of decompensation the prognosis in chronic liver disease is variable.
• Key papers: Clif-sofa score: Moreau gasttoent 2013
• Early tips Garcia nejm2010: benefit of early tips esp in child's Pugh b
• Bajaj 2012 gut: higher sepsis in aclf patients with higher mortality
• Terlipressin: maybe a group of responders (minority) who have a survival benefit, most are non responders
• Probably best to stop blockers in sepsis with aclf
• Meld score well stratified in predicting death on waiting list. However, may lead to poor utility of organs as sickest patients get organs

9. Wendon: Drug induced liver failure
• Almost certainly icu patients have an increased propensity for drug induced acute liver failure.
• Patient with cardiogenic shock very prone to toxicity of drugs with high extraction ratios. As poor liver blood flow. R > 5 more likely hepatocellular r = alt x n/ a phos x n, r< 2 more likely cholestatic
• Women seem to have higher mortality with drug alf ? Oestradiol effect.
• Eosinophilia can be seen in drug alf
• USS to exclude pv thrombus consider liver bx
• Prophylactic antivirals for those with hepbsag receiving immune suppressants eg rituximab
• Initial 60 days of anti tb treatment risk of alf drug induced
• Statins unlikely to cause alf
• Paracetamol increasingly thought to be a co factor, staggered induction likely to have a much higher mortality than acute overdose.

10. Mirza: The management of liver trauma

Mirza delivered an excellent talk giving an overview of liver trauma management – the mainstay of liver trauma management within the UK in both adults and children is non-operative management in the majority of cases.

The liver is prone to injury as it is large: 2% body weight in adults and may be affected by both blunt and penetrating injury. The liver has a huge ability to regenerate enabling non-operative management to be an option.

Clinical approach to liver trauma management:
• Obtain a clear history
• Conduct resuscitation in parallel with imaging. The major trauma centre technique has improved this management.
• CT – good quality contrast is important / repeat scans may be needed 24-36hrs to assess for evolving injury
• If surgery is required – best done in a tertiary centre liver unit / a minimal operative approach is advised / damage limitation surgery

Complications of liver trauma include: delayed sepsis, false aneurysm / haemobilia / bile leak /

MRI is often not helpful in assessing liver complications. Mirza then reviewed Birminghams outcomes both civilian and military liver trauma. The military patients had a higher surgical intervention rate in the field due to less access radiological intervention services.

In children, liver trauma is often conservatively managed, Handle bar injuries are a common cause!

J Doyle from United Kingdom wrote 12-10-2014 08:43:27 pm
Day 1 Novel Therapies

Prof John Simpson. Immunostimulation in the critically ill.
To end the day we have Prof Simpson who starts with data on hospital acquired infection and considers how we may improve treatment on this major issue often with poor outcome.

The modern view of response to sepsis is considered. A cellular review entails with acknowledgment that we have known for some time that Monocytes hla-dr molecule expressed on cells can predict for poor outcome. The question is if they can be down regulated will outcome improve. A rationale for impaired neutrophil phagocytosis is explained in detail.

Ex-Vivo tests demonstrated that the application of gm-csf helps normalise neutrophil phagocytic function

Some interesting data showing that those with normal neutrophil phagocytosis on admission to ICU end up with less nosocomial infection that those without normal neutrophil phagocytosis. Importantly this is independent of how sick a patient was on admission (eg APACHE score)

Human studies for gmcsf. Have started with an RCT currently underway and is seven patients short of completion. More news to come on its important development.

Other candidates include IL-7, thymosin alpha, gamma interferon, cyclin D inhibitors

Prof Simpson finishes by identifying possible treatment strategies for deployment of immunostimulation therapy

J Doyle from United Kingdom wrote 12-10-2014 08:44:06 pm
Day 2. session 1. looking to the future. chair. Dr Andrew Rhodes.

1. First up is urgent care by Prof Jonathan Benger
prof Benger details this 10 step action plan to develop a networked urgent care system. For NHS England. Clearly a large challenge.

Urgent care centre will be the umbrella term for all the out of hospital services such as walk in centres whereas within hospital terminology now reflects specialist emergency centres (those with tertiary care) and general emergency centres. The idea of this is to create a fully networked urgent care system that also enables the sharing of clinical data and sees better flow of patient movement.

An added benefit of this is believed to be the reduction in bed occupancy, this would be preferable to cutting funded beds when it comes to economic savings.
Of interest is the fact that costings for provision of urgent care is fairly static regardless of level of activity. Therefore a more efficient system with reduced bed occupancy will reduce workload.

Prof Benger gives an update on the advances in data sharing between critical care services and other services such as ambulance and pharmacy. Also mentioned is the increased use of the telephone 111 service (a call service for patients requiring advice rather than an obvious emergency) now receiving over 1 million calls a month.

2. Dr Jane Eddleston is next with 'looking to the future'
Dr Eddleston starts with reflections on the past 8 years for example the change in intensive care practice including the increase in service provision for example there are now 1.3million bed days per year.

Looking to current activity there is a change in case mix. For example the increase by (60%) of caring for patients with only 1 or 2 organ support. An interesting statistic is the increases length of stay for those with 0 or 1 organ support which reflects the delayed discharges. This includes up to 3 extra days in ICU with data displayed from 2013. A total cost of 30 million pounds. This is now a major area to tackle going forward with a plan for elimination of delayed discharges by 2015/16

Reference is made to the FICM/ICS standards of care due to be released this will be an important reference tool. Reference is also made to QUIPP a national database populated by ICNARC data.

Future considerations include the emerging evidence that outcome is improved for high volume outcome. Therefore the recomissioning of services will be reviewing collocations. This applies to concentrating both elective and emergency services. Finally the impact of the 7 day working services is mentioned as the heart of these services.

3. Dr Bachelor - Training the future
Starting with where are we now. Over the last 3 years recruitment of trainees I the UK has risen to over 100/yr. Clearly an expansion is required although Dr Bachelor admits that this may be at the expense of training anaesthetists.

Looking next at the bigger picture - Dr Bachelor points out that whilst hospital management could be improved the system does work. Compare this to the community where things are somewhat more 'messy'. As a result national emphasis is more on GP recruitment than intensivists.

Hot topics currently include single versus dual training and the actual role of the intensivist. Particularly the role of the generalist. Also the length of training, Dr Bachelor admits for the single CCT a one year reduction to 6 years is feasible. However for dual the minimum time remains at 8 years.

Reiteration of ICNARC data shows the overall rise of critical care bed days but a decrease in level 3 bed days (by 2% over the last 6 years). Is this due to earlier
patient optimisation? Given this we can't restrict our specialty to only level 3 services but also need to provide robust level 2 care.

The future of training in England may move to the option of single CCT but Dr Bachelor admits that this may take some time.

4. Dr Nolan - Resuscitation
Dr Nolan deals with trends in outcome and differentiates between out of hospital cardiac arrest (the success story) and in hospital cardiac arrest.

Out of hospital outcome reflects more bystander CPR and use of AEDs (by non-medics). Current strategies In other European centres include text messenging service to registered people within 1km of a OOHCA additionally with details of the nearest AED.. The wonders of smart phone technology. Ideas for the future - mandatory CPR training before eligibility for a driving licence. Mandated school CPR lessons.

The evidence:

Reference is made to the mechanical devices (CERT trial & PARAMEDIC trial) improving quality of CPR, although not a change in outcome.

ROCALPS a study underway for shock refractory VF examines the use of amiodarone versus lignocaine versus placebo

IRWAYS intubation versus igel LMA recruiting 8000 patients

Hyperoxia - reference is made to the interrupted trial (after 18 patients) recently published in Australia. The need for hyperopia versus titration oxygen RCT is clear

Centre regionalisation is considered

The future:
- monitoring the physiological response to CPR with etCO2 with recent studies suggesting aiming for of ET CO2 of 20 during CPR.
- heamodynamic moniting for CPR (in-hospital). Eg use an arterial line to aim diastolic >20mmHg.

Finally the protocolisation of post resuscitation care :
Notable early coronary reperfusion, this is a contentious issue but most probably the future path.
Target temperatures at the minimum to avoid pyrexia. Consensus internationally is not yet obtainable
Rehabilitation, currently no Exeter near that of say stroke rehabilitation

To conclude prognostication a recent systematic review considers this. Next year the 2015 guidelines will be published in October for the first time with graded evidence.

J Doyle from United Kingdom wrote 12-11-2014 07:12:37 am
Day2: ICS meeting: Session 1 (parallel)

Pharmacology
1. Dr Wood: Street drugs: what new drugs are on the streets?
• New drugs on the market in recent times. ‘Legal highs’ – contents of these substances are not often legal and may be extremely harmful. Explosion in market due to the internet.
• 100s of websites often changing on daily basis.
• Drugs often sold as plant food or bath salts or labelled for non-human consumption - to get around legislation. There has been an exponential increase in new substances. Every week often 1-2 new drugs appear. Synthetic cannaboid agonists (K2)have seen a massive increase
• Predominantly a European problem – very large problem in the UK
• Classical drugs: cocaine, MDMA
• Novel: mephedrone (M-cat) has become established now as a classical drug
• About 10% of all ED case 2013-2014 involed novel psychoactive drug use!
• Stimulants: MDMA (ecstasy) / Amphetamines / Cocaine
• Depressants: Heroin / Opium
• Hallucinogenics: LSD / Ketamine
• Potential sources of information on novel drug use: cases series, poisons reports, toxbase
• New drugs overlap many classical symptoms
• Depressants: GHB/GBL
• Stimulants: Peperazines, cathinones
• Hallucinogens – Tryptamines, Methoxetamine

• Cathinones : B-keto derivatives of amphetamine. E.g mephedrone. Common symptoms: tachycardia, restlessness, mydriasis, hypertension, anxiety, dilated pupils. Other seizures, vomiting
• NBOMe Drugs: N-2-methoxybenzyl analogues. Clinical: convulsions, tachycardia, rhabdomyolysis, agitated and confusion. Significant cardiovascular toxicity associated.
• Ketamine Derivatives – methoxetamine. Hallucinogens. Activity at both serotonin and NMDA receptors. Symptoms: dissociative state. Significant hypertension and tachycardia. Cerebellar toxicity can occur with methoxetamine.
• Synthetic Cannabinoids: trade names variable: Spice, K2, K1. Numerous synthetic cannabinoids characterised. Activity at CB1 and CB2 receptors in variable ways. Associated psychiatric presentations / stimulant signs predominantly e.g. SVT, seizures. Acute kidney injury can occur
• MT-45 is a novel opioid. Activity at both opioid and sigma receptors. Present with opioid like symptoms with coma and/or respiratory depression. Bilateral hearing loss can occur.

• Management of novel psychoactive drugs is similar to classical drug overdose – but be aware of cross of symptoms and signs as the drugs may be active over a number of receptors.

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2. Ferner: Adverse drug reactions on the intensive care unit

• Poor submission of the yellow care system amongst the medical profession. Important to report harm. A large number of similar reports highlight quickly a problem with a drug or process.
• Interactions between drugs can be numerous.
• Most patients on ICU are at least on 12 drugs! At least 60 potential interactions and greatly increased risk of toxicity. Many dangerous drugs / many potential interactions. Lots of interactions in the critical care unit go amiss.
• Poor correlation with grading systems of drug interactions currently. Drug interactions within ICU is poorly reported and not widely researched. Literature evidence incomplete.
• The great majority of drug interactions in Sweden: warfarin, potassium sparing diuretics, SSRIs
• Pharmaceutical interactions: iron and tetracycline. Sodium bicarbonate and calcium chloride precipitate! Cocaine metabolised to benxoylecgonine. If take whilst alcohol on board get Cocaethylene, increasing cocaine half life.
• Pharmacokinetics: absorption (increase absorption by increasing motility e.g erythromycin), distribution interactions (p-glycoprotein (ABCB1 – efflux transporter, pumps drugs out of cells / many inhibitors of p-glycoprotein eg, amiodarone or verapamil). Metabolic interactions (Warfarin and azapropazone or fluconazole- > platelet inhibition, Cytochrome p450 inhibitor causing massive rise in Warfarin INR – risk of bleeding +++) / Renal elimination interactions (penicillin and probenicid) / elimination of lithium due to interaction with thiazide diuretics.
• Pharmcodynamic interactions: receptor interactions (endogenous adrenaline and noradrenaline) / opiods (e.g strong opioid morphine and weaker agonist buprenorphine – buprenorphine antagonises morphine effect). Different receptor interactions (vasodilator e.g nitrates will give a tachycardia indirectly)
• Fluvastatin inhibits CYP3A4 (warfarin)
• Daptomycin can cause myopathy. This and statins increase myopathy risk greatly
• Antibiotics Linezolid was initially developed as antidepressant initially– acts on serotonin receptors. Can get serotonin syndrome if patient on SSRIs.
• Clonidine and amitriptyline – can potentiate hypo and hypertension.
• Use pharmacy to help drug decisions on the ICU.
• E-prescribing may reduce the errors that pharmacist count, but may introduce other more subtle errors. Alert fatigue can occur if every potential drug interaction is flagged up! Jury still out whether e-prescribing is safer.



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3. Fischer: Safe prescribing
• This talk covered an overview of adverse prescribing events within critical care -> 2500 events related to medicines 2006-2007 in critical care units in the UK from >12,000 events reports. Noradrenaline commonly involved in adverse events. Morphine, potassium, vancomycin are also involved commonly too.
• 40% of events relate to the prescribing stage.
• Increasing challenges within critical care for safe prescribing -> complexity of patients and constant change in the patients condition can greatly affect the safety of drugs and dosages delivered
• The therapeutic window is the fine line between drug efficacy / therapeutic action and toxicity.
• Acute Kidney injury common – reduced GFR and proximal tubular secretion. Difficult to predict GFR in critical care patients increasing risk of under or overdosing patients.
• Renal replacement therapy through a number of modalities (convection, diffusion or both) affect drug dosing significantly.
• Elderly patients make up a large number of critical care patients -> greater risk of organ failure and delirium development.

4. Felton: Improving dosing of B-lactam antibiotics in critically ill patients:
• B-lactams in UK in hospital inpatients used greatly- > 6 of the top 10 are B-lactams
• Majority of patients improve on B-lactam therapies. Often a lot of our patients are underdosed!
• A number of patients who have HAP/VAP have resistant organisms to B-lactams. Increasing trend in resistance.
• Outcomes from ABX therapy: efficacy (survival, clinical or microbiological cure, biological markers) / increasing resistance. Scoring systems now more frequently used. Attempt to avoid toxicity of B-lactams.
• Predictors of ABX failure: treatment delay, disease severity, shock presence, the organism (pseudomonas/acinetobacter) involved and whether resistance exists, drug exposure.
• Exposure – importance of protein binding. Free drug is the active part of the drug. Adjust exposures due to organism susceptibility. Look at MIC/AUC and other measures of exposure.
• Probability of response increases with exposure at a cost of increased toxicity. Low drug exposure can amplify pathogen resistance mechanisms.
• Similar dosing in the ICU results in a range of drug exposure within our populations. Increased doses cause better treatment success but more toxicity, underdosing results in more treatment failure and emergence of resistance.
• Resistance suppression – minimum trough piperacillin concentration:MIC ratio. Felton 2013.
• B-lactam toxicity: hypersensitivity reactions, C.diff diarrhoea, agranulocytosis, nausea and vomiting, transaminitis, cholestasis
• Penicillins / Cephalosporins / Carbapenems. Pre-clinical trials predict clinical outcome well when investigating exposure-response relationship. Each agent must be considered individually due to MIC differences.
• Large pharmacokinetic variability in plasma with B-lactams trough concentrations.
• Effect of this variability may affect efficacy. The DALI study found that 20% of patients would predict to failure as drug exposure too low (fT>MIC).
• Variability: volume of distribution changes and dilution effects of drugs /
• Clearance related to organ function. B-lactam clearance can increase massively with the inflammatory response and associated increased renal perfusion particularly in young patients. Burns patients may have augmented renal clearance due to their response to injury.
• Renal replacement therapy – pump speed affects B-lactam clearance
• Effect of protein binding -> ceftriaxone, flucloxacillin and ertapenem are highly protein bound and can be influenced by albumin
• Obesity has a small effect on volume of distribution.
• Continuous or extended infusions of B-lactams increase the time of drug concentration above the MIC. Dulhunty 2013 CID. Found increase in cure rates. However, further meta-analysis done – only 1 out of 4 meta-analysis showed benefit of continuous infusions over bolus dosing. Jury still out!
• BLING II awaited to assess the benefits of continuous infusions
• Combination chemotherapy: B-lactams and aminoglycoside or quinolone. Synergistic effects and reduced resistance. Useful against difficult organisms (pseudomonas / acinetobacter). Evidence currently NOT there for combination chemotherapy.

J Doyle from United Kingdom wrote 12-11-2014 07:13:38 am
Day 2 session 2. Chair Prof Barbara Phillips

1. Life After the Liverpool Care Pathway - Prof Patrick Stone

Liverpool care pathway an overview
Section 1 - explanation of plan of care to patient -
Section 2 - assessment. 4 hourly assessment of pain / agitation etc
Section 3 - post death cares

Noted initial negative review of the Liverpool care pathway in the media. Concern that the LCP became a self fulfilling prophecy. Especially noting the financial incentive for pathway. Finally the poor prognostication ability of doctors.

In response to the Neuberger report an end of life pathway was replaced and decision to use this made by the senior responsible clinician who also is to write in the notes.

A document entitled 'one chance to get it right' produced by organisations in response to the 44 recommendations of the Neuberger report. The main findings of this report; 5 general advice recommendations
1. recognise patient is dying
2. speak to patient and family
3. involve family in decision making
4. explore wishes of the dying patient
5. provide expert symptom control and holistic care


2. Resuscitation: Why do we bother? Prof Peter Brindley
The reality 80% of all comers to ICU get to leave better... But not if they arrest! So why bother.

Well first can we define what is resuscitation I.e. Is it CPR only or is it fluid and abx. For the purposes here we talk only of adult CPR.

The question really should be who gets resuscitated not how to resuscitate. This is the difference between saving good outcome and prolonging death.

Data is displayed for in hospital mortality in Canada - less than 1 in 2 obtained ROSC. Less than 1 in 5 to ICU discharge. 45% of hospital arrests were unwitnessed.

The greatest impact on survival is arrest time and whether the arrest is witnessed or not. In fact not a single unwitnessed cardiac arrest was discharged from their hospital. Again the majority of in hospital arrests are PEA and asystole.

A brief discussion on ECMO and it's benefit on the patient with an acute reversible event

Prof Brindley finishes with a discussion on communication and DNR's with an acknowledgement of doctors discomfort in discussing end of life. The next step is surely patient focused care (an example is the new form '3Rs, 2Ms, 2Cs').

In summary resuscitation of the sick works but following in hospital cardiac arrest it doesn't!


3. Advanced Kidney Disease: Intensive Care or Not? Prof Edwina Brown
Prof Brown starts with a case study of a 75yr male with ESRF with multiple comorbidities recently started on PD. However an inguinal hernia resulted in pooling of fluid in the scrotum. Communication with the patient revealed his desire was for improved mobility. Haemodialysis was not indicated. However 3 weeks later patient dies in ICU of a CAP. So where did it all go wrong? Who should have communicated to the patient that RRT was not a fix all for his significant comorbidities.

There is recognition that prognostication is difficult. possible assessment tools: the more ADL assistance the higher the mortality. The higher the level of frailty the higher the mortality. Survival studies of conservative management versus dialysis for the elderly with impaired GFR does not show a survival difference.

A brief mention of the 'cause for concern' registers. Exists in many renal units and identifies the at risk patient. Advance care planning - an annual review is necessary. Of interest is that more HD patients wanted suppportive care only if they are aware of their prognosis (one year survival rate). In fact with a 1 yr survival rate of 75% a resulting 90% of patients chose supportive care only (compared to life prolonging measures). This demonstrates the importance of regular communication and advance care planning.

Prof Brown concludes with a second case of an elderly gentlemen also of reduced mobility on HD and multiple comorbidities. This was a patient that had been reviewed annually and on recent advanced care planning had decided to opt for supportive care only. As a result on recent admission ICU support was declined HD stopped and patient discharged for palliation at home.

J Doyle from United Kingdom wrote 12-11-2014 07:14:40 am
Day 2: Session 2: (parallel session)

1. Watkinson: Detecting early patient deterioration
• Discussion surrounding Early warning score use
• 40,290 patients admitted to ICU following 2 or more days on general wads. 1620 arrest first! 34% died before the left hospital. Massive problem. 4-10% of all ICU discharges die before leaving problem
• “The ward is still a dangerous place to be”
• How can patients who may benefit from ICU be identified early and admitted to the ICU at the right time?
• Why is it that we are not identifying these patients early?
o Track and trigger charts -> limitation of scores. Clinically we look at the overall trend rather than a narrow data set
• Analysed 64,000 hours of data -> looked at normal patient distributions of observations to aid the building of a track-trigger score. Helps identify the 12.5% of patients whose observations are abnormal and that could be acted upon. Small changes in physiological parameters could herald major deterioration. Use of data modelling may improve warning scores (either could die soon or need ICU).
• Personalised monitoring / ambulatory monitoring may help both in identifying patients who need ICU and those who at considerable risk of stepping down out of the ICU. Patients on ICU discharge often do not have normal physiological parameters.
• Statistical modelling with large ICU data sets can assist in determining limits of normality in and post ICU.

2. Wolff: Biochemical track and trigger
• Over the years able to search a number of datasets
• Electronic data capture on ICU very useful
• Able to use such data to look at track and trigger systems and ICU performance
• Computerised data tracking able to integrate between different tests and give warning or potential diagnoses.
• Laboratory results can be used to generate lists electronically for Outreach teams who can assess trends and review patients
• Some trigger systems can email interested parties of potential deterioration or results or flash up on a dash board.
• Admission and Discharge results can be compared easily and assess ICU performance: ratio number of patients who ICU of benefit versus those who’ biochemistry is worse following discharge.
• Sodium abnormalities -> what doctors worry about include: when to repeat the test. Admission sodium and in-hospital mortality looked at. If Na+ 137-140 mortality in hospital 5%. Low sodium <135 around 12% mortality. Na+141 still have a high mortality (7%). Massive increase in mortality from Na+145 upward (9-10%). A rise of plasma Na+ 3mmol (equivalent to deprivation of water 1litre) can have a significant effect on 30-day mortality. Electronic monitoring able to assess this and capture data. If patient admitted from a nursing home and Na+>145 mortality about 12%, compared to 1.2% if admitted from home reflecting increasing age. Care home residents have a 5x increased risk of admission with hypernatraemia. Steady rise in risk of hypernatraemia with duration in hospital.
• 30-day emergency readmissions to hospital can also be tracked.
• The future: electronic patient record, electronic observations and e-prescribing. This technology is very powerful if the data is integrated which could provide intelligent support for us and make a massive difference to patients!
• Information governance -> we should be concerned at a failure to analyse data and not the reverse. We should not require perfection before data can be used to inform our management. IT departments need to work closely with critical care to ensure these systems are robust and become a success. Courses to train clinicians in the use of this technology would help the applicability and accessibility of this technology in clinical practice.

3. McCallum: Pooling multicentre data in real time
• NIHR HIC focuses on five themes: ACS, critical care etc
• Collaboration for critical care research between data held throughout the UK in NHS hospitals / NHS sites and cohort databases.
• Key to building infrastructure to undertake research
• Focus on longterm outcomes of patients who survive critical care

J Doyle from United Kingdom wrote 12-11-2014 07:15:39 am
Day 2 session 3. Chair Dr Chris Danbury

This session included:

NELA national emergency laparotomy audit - update Dr Mike Grocott
The driving factors for NELA: 1998-2012 high incidence of adverse outcome / poor supervision / low critical care usage / high cost.

The emergency laparotomy network outcomes demonstrated a 10 fold difference in mortality existed in different centres, this was not explained by differing case mix. As a result the ELN were successful in commencing NELA.

The first year of data collection has been completed. Note a clinical reference group of 30 types of professionals. Preliminary data shows a lack of documented risk assessment, however those that were documented were accurate. Presence of consultant anaesthetist and surgeon still only 88% with patients with a documented mortality of >10%. Finally critical care admission was low despite high documented risk.

NELA next step is quality improvement by using national data for local improvement.

Reference is made to the EPOCH study. Detailing an enhanced recovery integrated care pathway, currently underway. With a wedge cluster RCT and a primary outcome of 90 day mortality.

Improving patient safety - Dr Ganesh Sunthralingam
dr Ganesh mentions reviews of patient safety incidents with 6 prospective audits. Several longitudinal studies. Clearly a persistent issue.

The impact of this is a significant increase in ICU and hospital length of stay, although not mortality.

The possible solutions - reduction in variability (eg VAP care bundles) and the minimisation of errors (eg structure and staffing)

Consider also structure (unit layout / staffing), cognitive tools (check lists), physical tools (pre-filled syringes / barcode medication entry) and technology (theatre managements system)

Finally the use of process information: disclosure of errors and adverse events, what to disclose and how to go about it. The issue of increasing accountability.

J Doyle from United Kingdom wrote 12-11-2014 07:16:31 am
Day 2: Session 3: (parallel session)

Maternity and Critical Care
1. Quinn: New date from ICNARC
• Ecoli and Group B strep greatest cause of septic shock in maternal population
• <50% high risk women looked after in specific maternal HDUs. High proportion nursed by midwives with no critical care training
• Using ICNARC dataset to look at obstetric critical patients and aim for high quality care for all mothers
• Owe to mothers who have died to improve critical care services in maternity.
• More information 2011 document to provide equity for maternity critical care.

2. Elton: Key issues and solutions
• Up to 5% of parturients require level 2 care
• Haemorrhage / preeclampsia / sepsis / sinus venous thrombosis most common reasons for admission
• What about baby? Can the baby come with mum onto the unit? If not, why not? How is the baby going to feed? Is the baby dead?
• “equity” to satisfy ICS standards – either alter ICU units to look after mother and baby or adjust ward round to ensure appropriate intensivist cover.
• EMBRACE-UK 2009-2012 report: looked at death due to sepsis. Death rate in pregnancy falling. Sepsis highest cause of death. Thrombosis is also a major cause of death, as is haemorrhage. Indirect deaths -> cardiac deaths commonest killer.
• “Think Sepsis” – early recognition and treatment key
• Haemorrhage: iron supplementation, avoiding uterine hyperstimulation. A single Hb result should not delay treatment / surgical intervention. Uterine atony and genital tract trauma are causes of significant haemorrhage.
• Atonic uterus; blood stops uterine contracting, worsening bleeding and consumption of clotting factors. Fibrinogen concentration falls first in severe haemorrhage. Fibrinogen normally increased in pregnant patients as it needs to be.
• ROTEM can be used to assess fibrinogen status in women. Possible research area. Blood components given reduced overall if ROTEM used to guided blood product replacement.
• Tranxamic acid may increase thrombosis in pregnant women who are bleeding
• Amniotic fluid embolus -> perimortem section should be delivered within 5minutes and trigger major obstetric haemorrhage protocol. Mortality remains high about 20%. Pathophysiology of this condition now thought to be an immune cascade producing an anphylactoid syndrome. Massive coagulopathy associated. Massive fall in fibrinogen seen / fibronlysis. Fibrinogen needed to replace. Use of critical care TTE has helped assess maternal situation. See a biphasic response in AFE. RV failure initially and then LV failure / pulmonary oedema.
• There a lot of ill pregnant women out there -> some of them need ICU. Most of them should stay on the delivery suite, but need ICU input to manage safely.

3. Gauntlett: Pregnancy and critically ill: when to deliver?
• Is most situations keep the mother well the fetus should be well
• In critical care this is not always coincident.
• In genital tract sepsis –in severe maternal ecoli septicaemia. A key causal factor in delaying the evacuation of the uterus and source control of sepsis may contribute to death.
• Maternal cardiac arrest: resuscitation guidelines to undertake a perimortem C-section within 5 minutes in all cases. Return of spontaneous maternal circulation often happens at time of c-section (relief of aorto-caval compression / improved mech vent)
• Large trials in sepsis often exclude pregnant women. Evidence vacuum. Case reports can sometimes be worse than no literature at all.
• Pregnancy physiological changes - > poor evidence or studies looking into normal values in such women. Future projects may help provide normal values and trends. Almost absent data sets to help analysis when to deliver in critically ill mothers.
• ICNARC dataset in obstetric critical care is groundbreaking!
• Critical care mortality of mothers is very low and so it is difficult to design studies to assess any differences.
• What about fetal outcome in maternal critical illness? 27 burns in Egypt: fetal loss about 60% in 15-20% maternal burns.
• Mayo clinic: Mothers developed ARDS whilst pregnant. 9/10 mothers delivered within 4 days of ARDS development. Very poor fetal outcome associated.
• Adverse fetal outcome rate of 41% in the USA study.
• Is H1N1 a special case? 88% live birth rate in mothers within H1N1. Over 60% born preterm. 20% had severe fetal morbidity.
• Human factors in reaching a decision to undertake delivery in critically ill mothers play a huge part. In many cases this may cause failure of the pregnancy. Massive decision and irreversible. Fetal outcomes worse in the 22-27wks group. Clinical experience may not be the best teacher in this situation. Practice may reinforce prejudice.
• Emotionally / psychologically critical illness in pregnancy is a very difficult time for mothers.

J Doyle from United Kingdom wrote 12-11-2014 07:17:46 am
Day 2: Session 4:
1. Gupta: Subarachnoid haemorrhage
• SAH associated with significant morbidity and mortality
• CPP = MAP-CSF pressure
• At moment of bleed: rate of bleed = MAP-CSF pressure /R
• CPP= rate of bleed x R
• Amount of blood at time of bleeding correlates with outcome and presentation
• Raised ICP: Cushing reflex seen and massive catecholamines release. Cardiomyopathy / Takaysubo cardiomyopathy seen. Catecholamine toxicity and development of neurogenic pulmonary oedema
• Main determinant outcome is global cerebral ischaemia. Delayed cerebral ischaemia causes patchy hypoperfusion on angiograms. Assessment and focus of not just macrovascular vasospasm but also on a microvascular level
• SAH -> ischaemic neurological damage / stress cardiomyopathy / acute hydrocephalus / rebleed / prevention of delayed ischaemic deficits key. Significant complications associated including venticulitis, venous thromboembolism etc.
• Diagnsosis: typical presentation worse headache ever. Longer the delay in CT scanning reduces the sensitivity in picking up SAH. LP is more sensitive up to 2wks plus for SAH post 24hrs.
• Misdiagnosis of 12% due to delayed presentation
• Investigation -> CTA.
• How monitor vasospasm or cerebral ischaemia. Use of CTA and transcranial Doppler for assessing large vessels (screening tool only)
• CTP (CT perfusion) is an excellent new modality for assessing cerebral CBF. CTP gives us a great degree of information including mean transit time, CBF, CBV etc
• Prevention of vasospasm: Triple H -> only hypertension good.
• Cases and management discussed.
• Hypertension mx sometimes not appropriate particularly if stress cardiomyopathy. Hypertonic saline may improve CBF and brain oxygen through improvement of microcirculation.
• Sedation and cooling can reduce cerebral O2 uptake and metabolism and may improve recovery
• MAP augmentation – ideal target not clear. Stratify patients depending on cardiovascular risk (young/old). Young MAP 50-150, old map 70-110. CTP used to stratify neurological risk with established infarcts or areas at risk of infarct. This may then influence the MAP chosen. Individualisation of MAP targets important in clinical management.
• Alternative measures: Hypertonic saline, CSF drainage, reduce cerebral metabolic rate of O2
• Thromboembolic prophylaxis is paramount in these patients.
• Acute hydrocephalus should be treated before prognosis
• Nimodipine (60mg 6x daily for 3wks):key in prevention of vasospasm and reduces mortality and improves outcome. Nimodipine is proven. It should not be stopped even if MAP targets are not met.
• Magnesium has no evidence in SAH and high (supranormal) levels may even worsen outcome.

2. Hutchinson: Rescuing the injured brain:
• Decompressive craniectomy around many years and in-out of vogue. May reduce pressure within the brain in traumatic brain injury. About 30 or so different approaches for this operation described.
• TBI management: Sedation / 10-15’ head up / control ICP <25mmHg, L/P<25, brain O2 >10mmHg. PaCO2 4.5-5. SaO2>97%, PaO2 11kPa. Temp <37’C. Further stages with introduction inotropes/mannitol/hypothermia. Final stage surgery vs thiopental coma
• Poor literature for early decompressive craniectomy. In Afganistan very early decompressive craniectomy undertaken.
• Problems- brain contusions, hygromas, midline shift, hydrocephalus incidence higher in decompressive craniectomy (shunt vs cranioplasty for these patient. Cranioplasty not a benign operation! (associated seizures, infection)
• Unilateral craniectomy causes a greater shift in the brain compared to bifrontal
• Decompressive craniectomy does reduce ICP, but may increase number of patients in a vegetative state or may have been unnecessary. No evidence currently for DC use. Operation should not be used indiscriminately.
• DECRA trial – secondary DC. 155 patients in 2011. Raised ICP >20mmHg for 15mins. Study showed mortality similar in two arms between medical management and DC. Poorer neurological outcome in the DC group.
• RESCUE ICP – 400 patients. >25mmHg >60mins. Last tier of therapy in the UK. Results to be published in 2015-2016.
• RESCUE ASDH trial in Primary DC ongoing - > primary removal of ASDH and then decide on whether leave bone flap off or not. Raised ICP following ASDH drainage causes poor outcome. Study underway.







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3. Zandi: NMDA and Autoimmune encephalitis
• Encephalitis commonly caused by infective causes e.g. HSV.
• Encephalitis can be non-infectious associated with cancer: paraneoplastic syndromes generate antibodies to cell surface antigens in the brain.
• Encephalitis not associated with cancer -> Autoimmune antibodies to the NMDA receptors.
• NMDA receptor antibody encephalitis discovered in 2007. Rhythmic movement disorder seen. Characteristic psychotic episode first prior to deterioration: central apnoea, seizures, intubated, prolonged duration on ICU. Brain MRI in these cases often normal. Disorder of two phases: presentation to neurologist or psychiatrist. Movement disorder in second phase presenting to ICU. Seizures / movement disorder. Sometimes see slow EEG at presentation. Delta brush frontal slowing on EEG (EEG picture can also be caused by benzodiazepines also)
• Associated ovarian teratoma with NMDA encephalitis.
• Aggressive therapy for NMDA encephalitis (high dose steroids, IVIG and /or plasma exchange) likely to have better outcomes. Second line chemotherapy agents (cyclophosphamide sometimes used).
• Occurs in children
• Two assays to test for antibodies. Live cell based assay versus commercial fixed antigen.
• Prior to 2007 was thought to be encephalitis lethargica
• NMDA receptor antibody associated with psychosis and schizophrenia . Ketamine therapy used and immunomodulatory agents.

• Brief dystonic contractures of the face, arm and leg associated with cognitive decline. Potassium channel antibodies (LG-I antibodies) associated. Problem with proteins associated with the potassium channel itself. Patient started on Rituximab / plasma exchange and steroids.

• Progressive encephalitis, rigidity and myoclonus (PERM) – antibodies to glycine receptor. Startle and rigidity seen.
• Autoimmune encephalitis – unclear how common this problem in. In the very young may be more common than HSV encephalitis.
• Presence of prodromal psychosis, movement disorder and dysautonomia more likely caused by Autoimmune encephalitis.
• No evidence base for treatment at present. Treat for both infective encephalitis and Autoimmune encephalitis. Japanese encephalitis and listeria can present in a similar way to autoimmune encephalitis. Treatment: IVIg, plasma exchange, steroids. Refractory cases Rituximab or cyclophosphamide.
• In severe cases in the ICU need to look for tumours (particularly ovarian teratomas).

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4. Smith: Outcomes of brain injury: data from the RAIN study
• Risk adjustment in Neurocritical care
• Some evidence that improved survival of managing brain injured patients in a neuroICU compared to general ICUs.
• 1996-2003. Management of TBI practice reviewed. 35% severe TBI not treated in a neuroscience unit. Mortality in these units 65% compared to 35% in neurocentre. Subsequent study 2003-2009. Now <20% treated in a neurounit. 12% reduction in mortality also.
• Patients with a non-neurosurgical TBI. Outcomes : some evidence of improved outcomes who are treated in specialist units. Results currently inconclusive.
• RAIN study aimed to investigate: is there a difference in outcomes in those managed in a neuro icu vs combined neuro/general ICU? What was outcome in early transfer <18hrs compared to no or late (after 24h) transfer?
• Major cause of TBI is falls followed by RTCs and assaults. Predominance of young men. Extracranial injury presence in 41%. GCS at presentation 3-8 present in 50% of admissions. Fewer than 10% had unreactive pupils. Mortality of cohort about 26% at 6months (falls 32%)
• Functional outcome: more than 60% unfavourable GOS at 6months, only 26% had good recovery. 35-70% of survivors reported problems with functional ability. Self-rated health was 70 overall.
• RAIN study produced 3 risk models. The IMPACT lab model best discriminated for mortality but poor for overall functional outcomes.
• From dataset: Majority of deaths occur in first 30day overall on both types of ICU. No real difference between those managed on neuro icu vs combined tertiary units.
• No or late transfers had a higher proportion of those with a high mortality rate and poorer outcomes. Early transfer more cost effective in those with severe TBI and associated with lower mortality and high associated quality of life. No data statistically significant after adjustment.

J Doyle from United Kingdom wrote 12-11-2014 07:18:40 am
Day 2 session 4.
(A brief note from the parallel session)

Chair Dr Stefanie Brummer-Smith & Dr Claire Colebourne

1 Prof Antoine Vieillard-Baron
With some excellent case examples of ECHO loops. With regards to ARDS and RV function specifically the effect of therapeutic manoeuvres such as recruitment and prone positions are visualised with improved ECHO.

Www.ECHO-rea.uvsq.fr


2 Prof Monnet. Discusses septic cardiomyopathy starting with a case study of respiratory focused sepsis requiring admission to ICU and commencement of level 3 support. With this case Prof Monnet highlights that basic haemodynamic asessment is easy. As a result ECHO assessment can be performed by any intensivist (with basic ECHO training) and that early ECHO assessment allows elimination of large PE or RA thrombus / major LV dysfunction / AR / tamponade. This directly enables one to trailer therapy to fluid / inotropy or chronotropy.

Prof Monnet acknowledges the limitation of EChO (including the low tv and high resp rate in spontaneous breathing patient) impacting the ability to assess fluid responsiveness

J Doyle from United Kingdom wrote 12-11-2014 07:20:32 am
Day 3: Session 1: Update
1. Davies: Cardiology in Critical Care
• Cardiology important in critical care

• Chronic Heart Failure: enormous burden. Accelerating decline in natural history once started (e.g. following an MI). The bodies response of salt and water retention worsen heart failure. ACEI, B-blockers and Aldosterone antagonists used in management.
• BNP -> cause diuresis and excretion of sodium / vasodilatation. Neprilysin (enzyme that degrades BNF). Inhibitors of neprilysin ‘Sacubitril’. This also blocks neprilysin and angiotensin inhibitor (valsartan): LCZ696 an angiotensin-receptor-Neprilysin inhibitor (ARNIs) works significantly in reducing death and hospitalisation in heart failure. The trial PARADIGM-HF Study assessed LCZ696
• CONFIRM trial: replacing iron by intravenous infusion may be beneficial in chronic heart failure. Powered to assess exercise tolerance. Compared to placebo heart failure patients treated with ferric carboxymaltose exhibited a significantly improved exercise tolerance and reduced hospitalisation rates compared to placebo.

• Acute Heart Failure: Mechanical circulatory support (IABP, tandem heart, impellor (can be used in severe AR and whatever the rhythm. Can cause haemolysis), ventricular assist devices.
• Advantages of IABP are ease and familiarity. Impellor device very useful. Haemolysis limits use.
• Move to VA-ECMO as an outreach in the Emergency department (survivors of OHCA) and then bring back to cardiology ICU.
• Echocardiography role has increased. Very useful for assessing heart function. 3D TOE very good at assessing valve lesions. Focused Echo through small hand-held devices are very useful and enable ICU staff and even paramedics to answer simple and specific questions e.g the 4H’s and 4T’s in arrest situations. Some training required for focused echo and does require accreditation. FICE and FEEL courses very good.

• Valvular heart disease: Transcatheter interventions. TAVI in aortic stenosis.
• Mitral stenosis / mitral regurgitation can be treated using catheter interventions, but the mitral technologies at present are far behind the aortic therapies. The Mitral valve clip technique trades off severe MR for some mitral stenosis. The transcatheter mitral valve implants are now starting to be used.

• CAD: CULPRIT. PCI beter than thrombolysis in acute MI. Not clear what to do about diseased coronary arteries that are not the culprit lesions. Should we stent all lesions found. CULPRIT lesion only had worse outcomes to patients who had all lesions stented.
• CvLPRIT – swing towards aggressive PCI for everything

• Antiplatelets – ADP receptor antagonists form mainstay of treatment. Clopidogrel was for many years the gold standard. Problem with clopidogrel was that it is a prodrug and slower acting. Ticagrelor now used much more often, faster onset and offset of action. In elderly compliance with ticagrelor not as good as BD medication.
• GpIIb/IIIa antagonists (reopro) – work immediately in the cath lab (whilst waiting for ticagrelor to work)

2. Perner: Which fluid for critical care?
• Perner author of TRISS
• Fluids in critically ill? Crystalloids or colloids? Balanced solutions?
• Colloids: data from 4 blinds trials (SAFE, CHEST, 6S, Crystmas) – no difference in potency between colloids and crystalloids for fluid expansion
• Perner 2014 Scandinavian Journal: GRADE guideline published recently. Compared crystalloid to HES, albumin and Gelatins. Systematic reviews undertaken. Cochrane review recently favours crystalloid. HES associated with increased need for RRT. Recommended crystalloids used instead of starches. HES should no longer be used in critically ill patients. Weak recommendation that crystalloids used instead of albumin. Albumin is a limited and expensive resource. No evidence for benefit or harm. Recommendation based on economy. Weak recommendation crystalloids used instead of gelatins. Low quality of evidence in this area.
• Patients with sepsis: albumin. Patel BMJ 2014. No benefit with albumin use vs crystalloid. HES not to be used in sepsis. Gelatin use also not recommended (weak) in sepsis (low quality of evidence).
• Trauma patients: albumin increased mortality in trauma compared to crystalloids. HES or gelatin no difference in mortality. Crystalloids recommended in trauma over colloids.
• Burn patients: systematic review and meta-analysis. Poor data / papers. Potential indications of harm with colloids when compared to crystalloids. Clear recommendations not able to be made, but recommend that colloids should be used in a research setting only.
• Resuscitation: Perner recommends use of crystalloids over colloids.
• Which crystalloid? Non of the available crystalloids match plasma. Poor data set at present. Saline vs balanced solutions? NaCl risk of hyperchloraemic acidosis (not sure if this is harmful or not), Ringer risk of hyponatraemia and lactataemia. Others contain acetate, gluconate, malate? Further studies in the future will enable better recommendations in the future.
• Hepatologists in HRS still use Albumin. Perner meta-analysis included Albios study. No benefit of Albumin in sepsis.
• Queries: Anders.perner@regionh.dk
• More trials and protocolised care needed in this area

J Doyle from United Kingdom wrote 12-11-2014 07:21:11 am
Day3: Session 2. New Aspects:

1. Brindley: Resuscitation…. Not as easy as ABC
• Safety data in Canada not widely shared. Tough to develop curriculum. Unsure once curriculum done that if teaching works.
• Train, educate or simulate?
• What competence is most important in patient safety? Human factors (80%) / Communication (70%). Brindley 2014 BJA
• Meaning -> Understanding. Content sometimes lost due to many factors self /relationship /appeal / stress etc. Part of skill in communication is about reframe / reinterpret
• Human factors issues and dangers with communication. Use of tools to improve: e.g. SBAR tool
• Our most important skill is verbal dexterity.
• Individual -> Team -> culture factors
• Error of planning, not execution. “Never venture where your brain didn’t already go”. E.g. plan A, B and C.
• Cognitive preparation -> plan the route before you do this. ‘Elevator thoughts’ can improve patient outcome. E.g. planning a difficult airway management. This may be superior to practical teaching, supplements training and simulation.
• Procedures: ‘a team of experts is not an expert team’. Science of managing complexity -> e,g, pit stop racing car team performance. See Gawande, Pronovost papers
• About 180 steps per patient per day. Use of checklists
• If an anaesthetists lead the team (De Vita et al) errors 2-3x higher. Team leader led may be better.
• Elaine Bromiley case. See youtube for case. Too early vs Too late. Cognitive dissociation and bad culture.
• System A (focus) vs System B (vigilance) -> teams need both to work well.
• Resuscitate by VOICE. Blindfolded Simulation (J Crit Care 2008, Brindley). Stressful situation communication may get worse and quieter (helmet head!). Blindfolding simulation improved performance of the individual and the team
• 5 dimensions of culture
• Where does education start? ER 2 seasons – 41 intubation attempts. Zero correctly positioned! Brindley 2009.
• Airway positioning key skill. ‘Win with the chin’. BJA 2010 Brindley. Significantly better than sniffing the position.
• Educators can make people worse!
• Simulation is very efficient for learners. It is a patient safety lab. It’s deliberate and emotional. Addresses human factors (personality, teams, cultures).

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2. HPA axis during critical illness: novel insights. Van de Berghe
• HPA axis and stress: CRH hypothalamic release ACTH from pituitary to adrenal gland releasing cortisol. Negative feedback loop
• Relative adrenal insufficiency – theory that adrenal cortex is maximally stimulated but not enough. Cortisol <9mic/dL on synacthen test (250 ug ACTH)
• Stress of critical illness -> cortisol up? down?
• Low ACTH during critical illness tricky to do on ICU. ACTH only high transiently then falls below healthy controls in critical illness. Cortisol often remains high during this time.
• Speculation why ACTH falls? Or reduced cortisol breakdown? If stress increases the need for cortisol – broken down in kidney and liver. Bile acids are powerful suppresses of cortisol enzyme breakdown. Critical illness increases 10x total bile acids. This may explain why cortisol not broken down and why ACTH so low (-ve feedback)
• Investigated this further:
o Boonen 2013 NEJM 368:1477-1488: looked at reduced cortisol production in critical care. 158 patients and 64 matched controls. Elevated cortisol and depressed ACTH in first 7 days from admission. Using tracer technology able to measure cortisol production and clearance. This found that D4-cortisol higher in patients than healthy controls. Cortisol production 83% higher in the morning in patients than controls (not in patients with SIRS). Cortisol clearance reduced to 47% of controls. 100mg hydrocortisone given to patients: patients clearance longer than controls
o Which enzymes responsible for this? Looked at A-ring reductase and 11B-HSD activity. Both reduced in patients.
o Bile acids very high in patients
o Proposal that bile acids / bilirubin levels which are raised are part of the stress response and
o Conclusions: cortisol production is less than doubled, non-ACTH driven and in patients with SIRS not elevated at all.
• ACTH and Cortisol plasma secretion investigated. Boonen 2014 Am J Physiol E&M online first.
• Overnight pulsatile secretion of cortisol is lower than controls. Also lower secretion of ACTH production overnight in patients.
• Adrenal gland -> lower ACTH for long periods of time, causes the adrenal gland to atrophy and fail.
• The liver in ICU stress plays a key role in the stress response by reducing cortisol breakdown.
• Overall no increase in cortisol production during critical illness
• Relative adrenal insufficiency: the concept of maximally activated adrenal cortex not really hold true.
• Van De Berghe View: a reduced cortisol response to ACTH bolus does not necessarily indicative of adrenal failure requiring treatment. Treating acute patients with hydrocortisone for suspicion of relative adrenal failure not often indicated.
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3. Perner: Transfusion requirements in septic shock (the TRISS trial)
• Chair of Scandinavian Clinical Trials Group: Author of TRISS trial
• 2007: odds ratio for blood use was high in resuscitating critically ill patients. 50% of patients in septic shock received blood in 2012.
• Balance of risk of anaemia vs risk of transfusion harm
• Transfusions triggers: lots of modalities for triggers. Often Hb value.
• Rosland 2014: trigger 7, 8 , 9g/dL
• TRISS trial undertaken to investigate further: NEJM 2014
o Septic shock with anaemia randomised
o RBC transfusion <7 or 9
o Primary outcome 90day all cause mortality
o Secondary outcome: patient event measures
o Power study done based on TRICC trial NEJM 1999
o 32 Scandinavian ICUS.
o 1005 randomised. 503 to lower hb-threshold. 497 to higher threshold.
o Well balanced baseline / some exclusions
o 4633 units RBCs during the trial given. Lower 1545 (median 1), 3088 in higher threshold group (median 4 units)
o Sustained anaemia throughout the ICU stay in lower threshold group
o Primary outcome: 43 vs 45% lower vs higher threshold. No difference in 90 day mortality or subgroup analysis or life support.
o Few adverse events - only 1 patient of acute hemolysis. No TACO or TRALI. No difference in any ischaemic events or mean days alive
o Conclusion. 99.8% follow-up. No differences in death at 90 days or ischaemic events when using lower hb-threshold (7g/dL) in patients with septic shock when compared to higher hb threshold values (9g/dL).

J Doyle from United Kingdom wrote 12-11-2014 07:23:26 am
Thats all from Crit-IQ folks… did you get to a parallel session that we missed? What were the key points? What were your top 5 take home messages from the state of the art conference? Comments below please….

Segun from UK wrote 12-11-2014 09:51:40 pm
There was a large session on burnout chaired by Dr Jonathan Goodall which raised numerous pertinent issues for the future of the ICM workforce.

Scores for burnout are high amongst ICM staff with several studies proving this. This may become worse with the single CCT...

The UK also takes a major step forward in critical care ultrasound training by offering a general ultrasound accreditation called CUSIC http://www.ics.ac.uk/ics-homepage/accreditation-modules/cusic-accreditation/

My top 5 messages?
1. Burnout is real, related to the environment we train/work in, and is not inevitable
2. There are still more questions than answers around ICU nutrition
3. The patient is probably the biggest determinant of ICU outcome
4. A team of experts is not necessarily an expert team
5. Ultrasound is useful and awesome!!!

Alfalah12345 from United Arab Emirates wrote 12-19-2015 07:27:01 pm
There was a large session on burnout chaired by Dr Jonathan Goodall which raised numerous pertinent issues for the future of the ICM workforce.
http://www.afu.ac.ae/en/Admission-&-Registration/goals-and-objectives/