Consultant Intensivist Transitioning Course

There is a general acknowledgement that medical training programmes focus on the clinical aspects of the job. Insight is important in any illness and there is now a recognition that the non-technical and non-clinical aspects of being a consultant in Intensive Care Medicine are often neglected. We are literally exxpected to lead a multidisciplinary team, interact and negotiate with colleagues from across the hospital and from various specialties in often stressful and challenging situation. Businesses especially the multinationals, invest heavily in developing their team and leaders. The NHS through the organisation such as the Faculty of Medical Leadership and Management are also starting to do the same for healthcare professionals.

In Australia and New Zealand, the Consultant Intensivist Transitioning (CIT) course is a compulsory course for all their registrars. This is the inaugural UK CIT course with national and international experts forming the knowledgeable and passionate faculty. Whilst there are other medical management courses in the UK, this is specifically designed for the Intensive Care Consultant.

The ProgrammeScreen Shot 2016-05-11 at 18.56.07

Aspects and areas covered;

  • Leadership
  • Legal aspects
  • Conflict management
  • Negotiation
  • Managing performances
  • Managing and initiating change

The sessions are interactive with almost no didactic lectures.

Segun provides a more personal account (below) but my take-home message would be:

  1. Decisions are made before the meeting; do your homework and prepare.
  2. Reinforce what you do well to make yourself indispensable.
  3. Legal issues can be very daunting – are your processes robust enough for patient safety?
  4. Work-life balance is a choice.
  5. By knowing yourself, you are better able to manage yourself and understand others.

In conclusion, this course is merely the starting and provides the foundation for a lifetime of learning and development. By better understanding ourselves and what motivates us, we can form better relationship with those around us; colleagues and most importantly, patients. As mentioned above, there are other medical management courses available, but to my knowledge, this is the only on which is specific for ICM.

Dr James Day and Dr Graham Barker should be congratulated for organising this course in the UK and I whole heartedly recommend it. Thanks to @RoodenburgO @cmoMD @DannytheBaker and the rest of the faculty.

Adrian Wong, Consultant ICM/Anaesthetic (ESTJ)

 

Reflections from the CIT

St Anne’s college, Oxford. A rainy Tuesday morning.

I’m sitting with a number of intensive care colleagues, intently concentrating on Dr Owen Roodenburg, Consultant Intensivist. He’s travelled all the way from the Alfred Hospital in Melbourne to speak to us.

His hospital specialises in ECMO, Echo, VADs, and recently ran the CHEER trial looking at Intensivist delivered ECMO for in-hospital arrests.

Yet today, he is talking to us about none of those things. He is talking about…change.

Today is the UK’s first Consultant Intensivist Transition (CIT course). 19 delegates are being taken through a series of exercises, introducing them to the “hidden curriculum” of being a consultant.

It’s a varied and exciting bag. Following this introduction to the mechanics and psychology of change, Jonathan Fielden- an intensivist with a long career in health politics and now working in the department of health- talks to us about his approach to meetings. (Having been BMA Consultant head for many years, he’s been to a few).

We take part in a mock meeting. Role playing different team

Members, each with differing agendas, it’s remarkably realistic- and brings up many discussions about how each of us copes in these environments.

It’s easy to think that we’re going to show up as the new sheriff in town, and change everything. In another session on “initiating change” we are reminded how it’s not always the case. Another mock exercise pitching a new service follows.

We break for lunch and network. Dr Helen Higham from OxSTAR takes us through a fascinating session on managing under stress. Situation awareness and cognitive biases continue to dog us as consultants. Simulation training can help this, thankfully- as can being good to your nursing team. Matt Holdaway from Oxford Adult ICU gave plenty of pointers on keeping nurses happy (don’t touch the ventilator without telling them! And it’s THEIR ventilator!)

Day one ended with a lovely session on work-life balance from Jonathan Goodall, and a session on law talking us through complaints, coroners and all in between.

DAY 2:

“And this above all, to thine own self be true”

We start by learning about our Myers Briggs personality types, and how different traits interact. This leads nicely into sessions on conflict management (not easy!) leadership (not as straightforward as you’d think!) and negotiation (which is not “getting your own way”).

I had to leave after this session, but left fired up and full of idea.

There’s been nothing like this formally taught in ICM training in the UK before. The faculty were engaging, knowledgeable, and genuine.

Most importantly they reminded us of the highest truth.

Intensive care is about people. Patients are people. Staff are people. All of our interactions involve people. And we, the consultants of the present and future, are people.

We need to care about people. Start with ourselves. Do things we love, in and out of work. Rest. Exercise. Eat well. Manage ourselves in stressful situations.

We need to care about our team mates. Listen to them. Be empathic. Train our emotional intelligence. Negotiate with them to achieve the best outcomes for all

Involved, not just to get our own way.

When we do that, the people that we have been trained to care about- the patients- get the best from us, and from everyone else.

Segun Olusanya

ICM

ISICEM 2016 Day 4

The final blog from the our man in Brussels: Adrian Wong. Thanks for all the positive feedback over the last week! JS

Neuromonitoring

What we need to know about cerebral metabolism (Helbok)

Increased metabolism can lead to secondary brain damage

Brain injury as a risk factor for fever upon admission to the icu (ref)

Brain main glucose consumer (50%) – neurons intolerant against changes in energy supply

CBF normally coupled with cerebral metabolic rate – metabolic and neuronal hypothesis for neurovascular coupling

Brain can utilize lactate (Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain)

Cerebral metabolism following traumatic brain injury: new discoveries with implications for treatment – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321351/

Measuring glucose metabolism

  • PET
  • MR Spectroscopy
  • Jugular bulb catheter

Global cerebal oedema in TBI increase brain glucose utilization at time when supply may be limited

Monitoring glucose metabolism is important but monitors are limited by

  • PET – feasibility
  • Microdialysis catheters – invasive
  • Jugular bulb catheter – technical

Integration of cerebral metabolic function (brain tissue glucose, lactate/pyruvate ratio) may guide clinicians to improve management of pts

Impact of axonal damage after TBI (Stocchetti)

Network dysfunction after TBI (ref)

Axons form extensive networks which have retro and anterograde transport systems

Mechanism of damage

  • Direct axotomy
  • Delayed axotomy – ions flux, cytoskeleton disruption, impeded axonal transport

Biomarkers in traumatic brain injury

EEG monitoring – fancy tool or important device (Oddo)

Rationale

  • Seizure detection and treatment
  • Altered GCS in general ICU pts
  • Early outcome prognostication
  • Secondary ischaemic insult
  • Depth of sedation

Convulsive status is a clinical diagnosis

Guidelines for the evaluation and management of status epilepticus – https://www.neurocriticalcare.org/sites/default/files/pdfs/SE%20Guidelines%20NCS%200412.pdf

EEG monitor allows us to titrate therapy

  • Clinical termination of SE
  • EEG termination of SE
  • Burst suppression pattern in EEG

EEG is crux of diagnosing of non-convulsive status

Recommendations on the use of EEG monitoring in critically ill patients: consensus statement from the neurointensive care section of the ESICM – http://icmjournal.esicm.org/journals/abstract.html?v=39&j=134&i=8&a=2938_10.1007_s00134-013-2938-4&doi=

Pic of prognostication flowchart

G2015_Prognostication

When to monitor ICP? (Maas)

Guidelines

  • Level 2: all pts with GCS <8 and abnormal CT
  • Level 3: GCS <8 and normal CT if at least 2 of the following; age < 40, SBP < 90mmHg, abnormal extension 

A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury BEST:TRIP

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565432/

BUT

  • Both groups received ICP targeted treatment. More aggressive therapy in control group.
  • Power calculation should NOT be based on the total number of patients but on the expected number with raised ICP i.e. IT WAS UNDERPOWERED

Conclusion

  • ICP monitoring should not be abandoned
  • Think in terms of strategy
  • Better characterization aiming for more personalized approaches. Aim for multimodal approach

Goal-directory therapy (pic)

Cd08euKWEAIF73V.jpg-large

ACS TQIP Best practices in the management of TBI – https://www.facs.org/~/media/files/quality%20programs/trauma/tqip/traumatic%20brain%20injury%20guidelines.ashx

Optic nerve sheath diameter (Stocchetti)

Optic nerve sheath diameter is ideal as it is non-invasive

Watanabe – effect of intracranial pressure on the diameter of optic nerve sheath – http://www.ncbi.nlm.nih.gov/pubmed/18671637

Use of T2-weighted magnetic resonance imaging of the optic nerve sheath to detect raised intracranial pressure – http://ccforum.biomedcentral.com/articles/10.1186/cc7006

Review – http://www.criticalcarehorizons.com/optic-nerve-sheath-diameter-icp/

OND sheath is technically challenging; could use colour Doppler to identify artery 1st 

Non-invasive monitoring (Taccone)

TCD – http://www.ncbi.nlm.nih.gov/pubmed/17325830

Cerebral oxygenation monitoring – http://www.medscape.com/viewarticle/749603_5

Conclusion (pic * 2)

Subarachnoid Haemorrhage

When to measure ICP in SAH? (Citerio)

Pathophysiology of high ICP post SAH

Cd0pNe8UAAAj9gwCdYXoK6W4AArUpd

300mls/min of CSF turnover in and out of skull

Pt not following commond or WFNS >3 and acute hydrocephalus à EVD set at 10-15cmH2O

Contrast-enhanced echography to detect vasospasm (Duranteau)


  
 Experimental technique

Compared to traditional TCD better at detecting vessel and velocity. Clinical significance of this is still uncertain.

SAH: Medical management (Oddo)

Target SBP < 160mmHg with IV agent eg nircardipine or labetolol

Optimise CPP

Management of hyponatremia and volume contraction. – http://www.ncbi.nlm.nih.gov/pubmed/21748503

Other drugs – Statins, Magnesium, ET-1 Receptor blocker and Intrathecal thrombolysis ALL DO NOT WORK

Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference –

http://www.wvww.neurocriticalcare.org/sites/default/files/pdfs/Critical%20Care%20Management%20of%20Patients%20Following%20Aneurysmal.pdf

Delayed neurological deterioration after subarachnoid haemorrhage – http://www.ncbi.nlm.nih.gov/pubmed/24323051

Summary pic

Heart-Brain Injury (Mayer)

Priorities

  • Minimise early brain injury and ICP
  • Prevent rebleeding
  • Minimise delayed ischaemia and vasospasm

Trop > 2ng/ml is associated with poor outcome in SAH

Left ventricular dysfunction and cerebral infarction from vasospasm after subarachnoid hemorrhage. – http://www.ncbi.nlm.nih.gov/pubmed/20945116

Diastolic dysfunction is common after SAH (70%)

Cardiac injury after SAH exacerbates early brain injury and increase risk of vasospasm

Neurogenic stunned myocardium – takasubo on echo

QTc prolonged and inverted T waves – ECG changes following SAH

Rx

  • Fluids are not beneficial if not hypovolaemia
  • Pressor choice – guided by PiCCO. Usually start with NorAd and can consider milrinone

When do you need a neurosurgeon? (Le Roux)

ALWAYS

UIATS – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560059/

International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial – http://www.thelancet.com/journals/lancet/article/PIIS0140673602113146/abstract

Predictors of Rehemorrhage After Treatment of Ruptured Intracranial Aneurysms

The Cerebral Aneurysm Rerupture After Treatment (CARAT) Study – http://stroke.ahajournals.org/content/39/1/120.abstract?ijkey=171bfa46eb0f0b1c7cb2ffb2628ec9802abffdff&keytype2=tf_ipsecsha

Combined approach of surgical and endovascular for some SAH

Blood pressure management (Reuter)

MAP – CVP = SVR * CO

MAP – CVP = SVR * SV * HR

MAP does not equal perfusion or flow

BUT need to consider right and left heart; Normally COleft = COright

Hemodynamic variables related to outcome in septic shock – http://icmjournal.esicm.org/journals/abstract.html?v=31&j=134&i=8&a=2688_10.1007_s00134-005-2688-z&doi=

MAP < 65mmHg BAD

For effective filtration to occur in the kidney, renal perfusion pressure of 50mmHg is required

Classically, sepsis was thought to be distributive shock. This is clearly not solely the case. Cardiac dysfunction is very common.

High versus Low Blood-Pressure Target in Patients with Septic Shock –  http://www.nejm.org/doi/full/10.1056/NEJMoa1312173

CPR

Managing the airway during cardiac arrest (J Nolan)

Objectives

  • Improve ROSC and improve survival
  • Improve oxygenation and ventilation
  • Protect airway

ETT regarded as gold standard BUT skill of operator

Intubation learning curve – http://www.resuscitationjournal.com/article/S0300-9572(15)00877-1/abstract

  • Need at least 50
  • Skill maintenance is also an issue

Waveform capnography is recommended to confirm and continuously monitor the position of a ETT. ERC Guidelines – MUST have capnography

Endotracheal intubation versus supraglottic airway placement in out-of-hospital cardiac arrest: A meta-analysis – http://www.resuscitationjournal.com/article/S0300-9572(15)00209-9/abstract

Randomised comparison of the effectiveness of the laryngeal mask airway supreme, i-gel and current practice in the initial airway management of out of hospital cardiac arrest: a feasibility studyhttp://bja.oxfordjournals.org/content/116/2/262.abstract

Revisiting ventilation during CPR (Richard)

Ventilation during CPR interrupts chest compression and causes a drop in perfusion pressure

Too much ventilation i.e. above FRC is bad for circulation

Quality metric of CPR (Morrison)

Ensure high quality chest compression

  • 100-120bpm
  • 40-55mm depth

Keep pre-shock pause short – http://circ.ahajournals.org/content/124/1/58.long

EtCO2 can be used a marker of quality of CPR; increased in ETCO2 favours ROSC

Hemodynamic Directed CPR Improves Short-term Survival from Ventricular Fibrillation Cardiac Arresthttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812371/

Still a place for epinephrine? (Nolan)

Adrenaline used to increase coronary perfusion pressure

Trial suggest that it does but most recent studies suggest that EtCO2 and cerebral oximetry doesn’t improve

Hagihara JAMA 2012 307 1161-1168 – propensity matched; adrenaline = better ROSC but much worse survival outcome – http://jama.jamanetwork.com/article.aspx?articleid=1105081

Intravenous Drug Administration During Out-of-Hospital Cardiac Arrest – http://jama.jamanetwork.com/article.aspx?articleid=184947

Data suggest that there might be harm in the long run – large placebo-controlled trial essential.

PARAMEDIC2 trial ongoing – http://www2.warwick.ac.uk/fac/med/research/hscience/ctu/trials/critical/paramedic2/

Do we need any drugs at all? (Sunde)

ALS guidelines – adrenaline every 3-5min, amiodarone after 3rd shock

Vasopressin also showed no difference in favourable outcomes compared to adrenaline

Vasopressin, Steroids, and Epinephrine and Neurologically Favorable Survival After In-Hospital Cardiac Arrest – http://jama.jamanetwork.com/article.aspx?articleid=1713589

New Strategies (Fries)

ISICEM 2016 Day 3

The 3rd instalment in the quadrumvirate of oxicm blogs by Dr Wong from Brussels. JS

Principles of triage of ICU admission (Gomersall)

Principles

  • Only when necessary
  • Fair
  • Transparent

Balancing supply and demand

Maximising supply

  • Cut staff ratio
  • Temporary increase in beds; but can increase in adjusted odds ratio as needs to be staffed e.g. temporary staff; quality vs quantity

Decreased demand

Ethics – mainly beneficence and distributive justice. No role for autonomy in triage?

Triage – Egalitarian (first come first serve vs utilitarian (benefit most)

Benefit = probability of survival in ICU – without ICU. Effects of ICU may be overestimated.

ELDICUS study – http://www.ncbi.nlm.nih.gov/pubmed/21926598

Risk factors for death – >60, refereral location, dependent on ADLs, cirrhosis, AKI

BUT equation needs to also factor in Life expectancy (quality adjusted) – old ppl have a lower life expectancy!

 

Improving the ICU Environment (Curley)

Hospitals are dangerous places

http://icudelirium.org/

Post-hospital syndrome – http://www.nejm.org/doi/full/10.1056/NEJMp1212324

What can we do?

Change paradigm

Restore resilience (R2)

IMG_7560

Circadian rhythm assessment

Align family with care plan – decision making and care

Noise contamination and thus containment is good for patients and staff

Protocolized Sedation vs Usual Care in Pediatric Patients Mechanically Ventilated for Acute Respiratory Failure

 

ICU diaries Crit care 2010 14 r168 – http://ccforum.biomedcentral.com/articles/10.1186/cc9260

Nurses and pts/families knowing each other – synergy and continuity

 

Optimal Alarms (JD Chiche)

Alarms in the ICU – why do much noise?

Nurse Crit Care 2007 12 188 Noise levels in a general intensive care unit – http://onlinelibrary.wiley.com/doi/10.1111/j.1478-5153.2007.00229.x/abstract

 

Crit Care Med 2016 44 147 Noise levels in Surgical ICU are consistently above recommended standards – http://journals.lww.com/ccmjournal/Abstract/2016/01000/Noise_Levels_in_Surgical_ICUs_Are_Consistently.17.aspx

Alarms are the main cause of noise

We are not very good at identifying them – http://inc.sagepub.com/content/13/2/122.refs

Bad alarm – desensitisation, disruption of workflow, sleep disruption

72-99% of alarm false or non-clinically significant

Alarm fatigue – http://www.ncbi.nlm.nih.gov/pubmed/26539788

Smarter alarm algorithm – adaptive time-delays e.g. derangement needs to be sustained to trigger alarm – http://www.ncbi.nlm.nih.gov/pubmed/26621389

 

False Alarm Identification and Reduction (FAIR Study)

IMG_7562

IMG_7571

Evaluating the risk state of the ICU (Talmor)

Traditional approach to safety – checklist e.g. CLABSI, VAP

Openness and transparency

Root-cause-analysis for all preventable harm

Safety in Healthcare – traditional vs systems (pic)

IMG_7573

Reengineering the ICU (Brown)

Problems

  • Medical errors
  • Communication poor
  • Respect and dignity threatened
  • Fragmentation of information

Developing a comprehensive model of intensive care unit processes – http://www.ncbi.nlm.nih.gov/pubmed/25909826

Technology – Accelerometers to document pt mobility or agitation?

Observations of respect and dignity in the intensive care unit. – http://www.ncbi.nlm.nih.gov/pubmed/25772729

Emotional harm from disrespect: the neglected preventable harm – http://qualitysafety.bmj.com/content/early/2015/06/17/bmjqs-2015-004034.full

ISICEM 2016 Day 2

Adrian strikes again with a neat summary of his second day in Brussels JS

How we decide

Protocols and guidelines: misaligned and misdistributed (Kavanagh)

Do protocols work in CCM?

Sevransky Crit Care Med 2015: Protocols and hospital mortality in critically ill pts

They don’t help – no difference in outcomes BUT not related to protocol compliance

Hypothesis:

Protocols surely do some good in some settings but overall the net impact is nil… therefore protocols must do harm in some settings!!

 

WHY DON’T THEY WORK

  1. Protocols misattribution

Hayes et al NEJM 2009 Surgical Safety Checklist to Reduce Mortality and Morbidity – 1/3 less complications which was attributed to implementation of key ‘processes’

BUT did increase implementation cause improved outcome?

NO concordance, almost perfect discordance – no ‘cause and effect’

DO NOT RELY ON CHECKLIST!

2) Protocols misalignment

Variation in hospitals settings e.g. basics vs advanced, primary vs tertiary

  1. Could sophisticated setting work in rudimentary setting? NO e.g. FEAST trial.
  2. Could rudimentary protocol work in sophisticated setting i.e. dumbdown? NO

Standardized Intensive Care. Protocol Misalignment and Impact Misattribution
http://www.atsjournals.org/doi/abs/10.1164/rccm.201502-0314CP#.Vulm8hIrKRs

IMG_7489

Situation where good

  • non-Tacit knowledge: difficult to put into words, demands talent, requires practice e.g. playing flute
  • Issue is simple and explicit
  • Reduce variability e.g. ECMO (caveat no variability = no health care research)
  • Research

In research, protocols need to be followed exactly. BUT expert clinicians nee to be more flexible.

IMG_7492

Conclusion

  • Avoid misattribution
  • Avoid misalignments
  • Understand limitations of protocols
  • Assess protocols as drug
  • Understand need for protocol in research
  • Understand why you need protocol IF you need protocol because of lack of staffing or expertise, address this first!

 

Why don’t all ICUs use SDD? (A Gordon)

WHO Report on burden of healthcare infections

Selective decontamination of the digestive tract: the mechanism of action is control of gut overgrowth

Effect of selective decontamination on antimicrobial resistance in intensive care units: a systematic review and meta-analysis

Use of SDDT in UK ICU Bastin and Ryanna – 192 UK ICUs only 10 did

Decontamination of the digestive tract and oropharynx in ICU patients.

 

SDD does require consensus amongst my colleagues – you need a champion

New evidence R-GNOSIS RCT in 12 European ICUs – http://cordis.europa.eu/result/rcn/163125_en.html

 

How personal biases influence decisions (Funk)

Illustrated by case of misdiagnsosis

Cognitive biases

Two modes of thinking (Kahnemann)

  • Fast – automatic and effortless, associations and heuristic
  • Slow – active reasoning and effort, calculations and probability

Dunning Kruger effect – unskilled doctors overestimating their ability; very skilled doctors underestimating their ability

Status quo bias – slow to change. Ignore new evidence in favour of current practice e.g. sedation, SDD

Sunk cost fallacy – when you’ve invested so much, you keep going

Omission bias – someone starts unnecessary drug (in case), and another who fails to stop it

Omission bias and decision making in pulmonary and critical care medicine CHEST 2005 128 1497

Bias blind spot – we think are not bias

De-biasing is possible

Protocols promote familiarity and hence development the clinicians’ “gut-feeling”

 

The influence of human factors: Looking into the mirror (Brett)

Humans are variables

Thought outside the box: ICU freakonomics and decision making in ICU (reference)

Rationale economics doesn’t make sense – if we have an emotional attachment or bias, we make foolish decisions

A lot of what we do is pattern recognition

IMG_7499

Different ppl in teams may not see/hear the same thing – FEEDBACK/READ BACK AT END OF ROUND IS IMPORTANT

 

The therapeutic conflict: When each of your decisions may cause harm (Perel)

Therapeutic conflicts are common especially in pts with MOF. E.g. septic pts with ARDS, how do you manage fluids. 30mls/kg advocated by SSC

Marik and Bellomo: A rational approach to fluid therapy BJA 2015 – most septic pts are not fluid responders

 

How to approach?

  1. Recognise there is a conflict – ask if the pt can afford the mistake your decision might result in?
  2. Gain more information – Acting in the Face of Uncertainty: Annals Int Med 2014. Combine and integrate parameters
  3. Identify the most critical problem
  4. Choose the least potentially harmful option
  5. Make decision and closely follow its results
  6. Repeat steps from the top

 

Changing strategies at the right time (Hall)

IMG_7504

 

 

How to implement changes (Stelfox)

Research should inform changes to clinical practice (discover new rx, replace current rx or reverse current rx)

BUT there is a 17 year journey from bench to clinical practice

  • Limited knowledge on implement science
  • Inefficient dissemination method
  • Inadequate assessment of cost and societal values
  • Science and clinical communities operating in isolation

The story of tight BM control on ICU; LEUVEN 1 (good) à NICE-SUGAR (bad)

Predictors of adoption – teaching vs non-teaching hospital, medical vs surgical admission

 

LOOKING AFTER THE ICU TEAM

ICU Nurses: A physician’s perspective

So important and respected (especially by patients)

The nurses role 4Cs – convening, checking, caring and continuing

Developing a model of interprofessional shared clinical decision making in the ICU Crit Care Med 2016 – http://journals.lww.com/ccmjournal/Abstract/2016/04000/Development_of_a_Model_of_Interprofessional_Shared.5.aspx

 

The forgotten family: caregivers (Herridge)

Informal caregivers are given very little support

Caring for Caregivers of the Chronically Critically Ill – http://ajcc.aacnjournals.org/content/20/1/24.full

Post-ICU Syndrome – http://www.myicucare.org/Adult-Support/Pages/Post-intensive-Care-Syndrome.aspx

Mortality after the Hospitalization of a Spouse – http://www.nejm.org/doi/full/10.1056/NEJMsa050196

RECOVER Programme

IMG_7529

 

Burnout and Moral Distress

Increasing problem

Definitions

Burnout Syndrome in Critical Care Nursing Staff – http://www.atsjournals.org/doi/full/10.1164/rccm.200606-806OC#.VukunxIrKRs

High Level of Burnout in Intensivists: Prevalence and Associated Factors –  http://www.atsjournals.org/doi/full/10.1164/rccm.200608-1184OC#.Vuku3hIrK34

Causes of moral distress theme : EoLC, communication, complex pts, bed capacity strain

Intervention (pic)

IMG_7526IMG_7527
Summary (pic)

 

 

Vasoactive drugs in septic shock

Noradrenaline (JL Teboul)

Early NA increases cardiac preload and CO – crit care 2010 14 R

Due to redistributive effect from unstressed to stressed volume

OK as unstressed volume is abnormally increased during sepsis and further overfilled by volume

5 reasons to start NA

Cdq-TT0XIAA0U6j.jpg-large

Start it when diastolic BP is low

 

High high should we go? (Martin)

NE: not too much, too long – http://www.ncbi.nlm.nih.gov/pubmed/26125087

HIGH-DOSE NOREPINEPHRINE TREATMENT: DETERMINANTS OF MORTALITY AND FUTILITY IN CRITICALLY ILL PATIENTS http://ajcc.aacnjournals.org/content/22/1/22.full.pdf

Non-Adrenergic Vasopressors in Patients with or at Risk for Vasodilatory Shock. A Systematic Review and Meta-Analysis of Randomized Trials

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4641698/

 

Beyond 1mcg/kg/min do not switch to other catecholamine

 

Vasopressin (Gordon)

Cochrane review: http://www.cochrane.org/CD003709/ANAESTH_vasopressors-hypotensive-shock

The cardiopulmonary effects of vasopressin compared with norepinephrine in septic shock.

http://www.ncbi.nlm.nih.gov/pubmed/22518026

VASST Trial – http://www.nejm.org/doi/full/10.1056/NEJMoa067373

Anthony Gordon presenting the VANISH Trial @ICSmeetings #icssoa2016 soa.ics.ac.uk/2015/12/16/van…

Vasopressin not superior to Norad

Alternative inotropes

  • Levosimendan: calcium channel sensitiser, K-ATP activator
  • LEOPARDS trial

 

Vasopressin analogues in septic shock (Russell)

Norad doses vary widely between RCTs

Selepressin Evaluation Programme for Sepsis-Induced Shock – Adaptive Clinical Trial (SEPSIS-ACT) – https://www.clinicaltrials.gov/ct2/show/NCT02508649

Kanji et al J Crit Care 2014 Echocardiography guided care – http://www.sciencedirect.com/science/article/pii/S0883944114001464

Selepressin in septic shock – http://journals.lww.com/ccmjournal/Citation/2016/01000/Selepressin_in_Septic_Shock___A_Step_Toward.29.aspx

Summary

  • NE doses vary widely between RCTs
  • Excessive NE associated with organ dysfunction and mortality
  • Vasopressin and selepressin decrease NE requirement
  • Selepressin also moderates permeability injury more than vasopressin

Angiotensin 2 (Chawla)

Intravenous angiotensin II for the treatment of high-output shock (ATHOS trial): a pilot study – http://ccforum.biomedcentral.com/articles/10.1186/s13054-014-0534-9

IMG_7539

 

Vasodilators (Bakker)

Vasodilators are counterintuitive in hypotensive pts

Effects of thoracic epidural anesthesia on survival and microcirculation in severe acute pancreatitis: a randomized experimental trial – http://ccforum.biomedcentral.com/articles/10.1186/cc13142

Nitroglycerin reverts clinical manifestations of poor peripheral perfusion in patients with circulatory shock – http://ccforum.biomedcentral.com/articles/10.1186/cc13932

Testing a conceptual model on early opening of the microcirculation in severe sepsis and septic shock: a randomised controlled pilot study – http://www.ncbi.nlm.nih.gov/pubmed/25032942

Conclusion

  • Vasodilation optimizes venous pressure in pts with hypotension.
  • Nitroglycerin infusion improves microcirculation and lowers CVP

 

Nitric Oxide (De Bakker)

NO has a role in regulating microvasculature

NO synthase enzyme has several forms – constitutive and inducible

Non-selective NO inhibitors in pts with septic shock and are unlikely to be of value

 

IMG_7542

Beta-blockers in sepsis (Singer)

Some sympathetic activation is necessary and good. BUT too much of a good thing, or if it persists for too long, is bad.

Neurohumoral Features of Myocardial Stunning Due to Sudden Emotional Stress – http://www.nejm.org/doi/full/10.1056/NEJMoa043046

Catecholamine treatment for shock–equally good or bad? – http://www.ncbi.nlm.nih.gov/pubmed/17719998

Nonselective beta-blockade enhances pressor responsiveness to epinephrine, norepinephrine, and angiotensin II in normal man. –

http://www.ncbi.nlm.nih.gov/pubmed/6705443

Effect of Heart Rate Control With Esmolol on Hemodynamic and Clinical Outcomes in Patients With Septic Shock – http://jama.jamanetwork.com/article.aspx?articleid=1752246

IMG_7544

 

 

 

ISICEM 2016 Day 1

Adrian Wong is at The International Symposium on Intensive Care and Emergency Medicine, which is often affectionately known as “Brussels”.  He has written a mega blog covering the talks he attended today – if you are there he would love you to come up to him, say hello and tell him what you think of his blog! JS

Opening plenary

Personalised Intensive Care Medicine (JL Vincent)

3Ps pyramid – population-based/broad definitions –> personalised. We need to move from population-based to precision medicine.

Failure of large RCTs in ICM can be in part be explained by the sheer heterogeneity of population being studied.

Medicine has always been personalised (Osler)

Genomics – does survival rely solely on the individual’s genetic makeup?

                        e.g. response to vasopressin is different in population

The host response to inflammation is variable

Biomarkers

            ARTISAN study which looks at THROMBOMODULIN

Wong et al – Developing a clinically feasible personalized medicine approach to pediatric septic shock.

“SIRS is a hiccup in history”

Report of round table meeting re: recovery after critical illness (Azoulay/Herridge)

3rd round table meeting – 2002 and 2009

2002 – Angus: Surviving Intensive Care

2009 – Griffiths and Hall: Exploring ICU-acquired weakness

Broached the idea of extending rehabilitation outside ICU but also focussed on the long-term effects on patients beyond ICU

Opportunities to improve care

  • Critical care is a disease continuum
  • Patient and family centred and engagement
  • Sound biological plausibility
  • Pts are heterogeneous
  • Role of rehabilitation in changing outcome

Long term cognitive impairment after critical illness (BRAIN-ICU study)

Depressive symptoms in patients and spouses are common

The Impact of High Versus Low Sedation Dosing Strategy on Cognitive Dysfunction in Survivors of Intensive Care Units: A Systematic Review and Meta-Analysis.

Early intensive care sedation predicts long-term mortality in ventilated critically ill patients.

The longer MV, the greater the weakness

NICE guidelines on rehabilitation after critical illness (2009)

Patient-centred outcomes/spiritual care – independent life, cognitive function, ability to work, absence of chronic pain, etc

            These may not be the same as what the doctor is aiming for

Intensive care may need to integrate with palliative care

  • Relieve distress
  • Support person
  • Manage uncertainties
  • Elicit values
  • Help caregivers

10 recommendations:

  • Look outside the ICU and embrace continuum including pre-ICU trajectory/recovery/adaptation
  • Patient and family engagement and personalised care
  • Heterogeneity risk stratification
  • Open the ICU doors
  • Addressing pain
  • Understand role, timing, indication and duration of rehabilitation
  • Comprehensive understand of neuroendocrine derangements
  • Role of long germ follow up
  • Adoption of proven strategies from other clinical settings
  • Development a comprehensive education agenda for all stakeholders

ICU-acquired infections (van der Poll)

Incidence, Risk Factors, and Attributable Mortality of Secondary Infections in the Intensive Care Unit After Admission for Sepsis

Host-response to sepsis: balance of pro- and anti-inflammatory response

Strategies = anti-inflammatory agents and immune stimulatory agents

Primary end-point – ICU-acquired infection (>48hrs after admission)

Patients who developed secondary infection where sicker (SOFA, APACHE2)

13.1% of patients admitted to ICU with sepsis will develop an ICU-AI (with attributable mortality of 10.9% by day 60)

15.1% of patients admitted to ICU with non-sepsis diagnosis will develop ICU-AI

Age isn’t a risk factor (with attributable mortality of 21.1% by day 60)

LOS with ICU-AI is significantly increased

 

DahLIA trial: Dexmedetomidine to lessen ICU agitation (Reade)

Effect of Dexmedetomidine Added to Standard Care on Ventilator-Free Time in Patients With Agitated Delirium

We don’t know how to treat delirium

Efficacy and safety of quetiapine in critically ill patients with delirium: a prospective, multicenter, randomized, double-blind, placebo-controlled pilot study.

Mechanism of dexmedetomodine – sedative a2-agonist (substantially less hypotentive than clonidine)

Inclusion – pts who remain intubated only because of their degree of agitation require such a high dose of sedative medication

Intervention dex 0.5ug/kg/hr (0-1.5) or placebo

Primary end-point: ventilator-free hours after extubation

74 patients randomised (96 target)

Fewer pts in dex group required additional sedative drugs

Dex group had significantly more ventilator-free hours: 144.8 vs 127.5

Nurses thought patient was ready for extubation quicker

Time to extubation faster

Dex patients had less time CAM-ICU positive

Adding dex to standard care is likely to be a cost-effective intervention

 

Early vs late parenteral nutrition in critically ill children (PEPaNIC) Van der Berghe

Early versus Late Parenteral Nutrition in Critically Ill Children

Critically ill patients unable to be fed by mouth

Cochrane collaborative (2009) Nutritional support in critically ill children

Nutritional practice in PICUs varies

  • 70% start EN within 24-48hrs
  • 50% start PN within 24-48hrs
  • Adult trials question the benefit of early PN

This trial looked at early PN to supplement EN compared to EN alone

PN initiated within 24hrs after PICU admission

Both groups had early EN

End point – new infections and duration of PICU stay

1440 randomised

No difference in mortality (hint that early PN might be harmful)

Early PN associated with more infection

Duration of ICU stay increased by PN

Early PN increased MV days

Withholding PN for 1 week superior to early PN

 

Hypoxaemia following major surgery – NIVAS study (Jabir)

Effect of Noninvasive Ventilation on Tracheal Reintubation Among Patients With Hypoxemic Respiratory Failure Following Abdominal Surgery

Development and validation of a score or prediction of postop respiratory complications Brueckmann et al

A Trial of Intraoperative Low-Tidal-Volume Ventilation in Abdominal Surgery

 

Treatment of Acute Hypoxemic Nonhypercapnic Respiratory Insufficiency With Continuous Positive Airway Pressure Delivered by a Face Mask

This trial – primary outcome number of re-intubation within 7 days. Inclusion resp failure within 7 days of surgical procedure

300 pts randomised

NO HIGH-FLOW NASAL CANNULA. Only traditional NIV mask used

Re-intubation 46 (control) vs 33% (NIV)

NIV group had less lung infections within 30 days

NIV increased ventilator-free days

 

Post-extubation high-flow nasal cannula vs conventional oxygen therapy in low-risk pts

Effect of Postextubation High-Flow Nasal Cannula vs Conventional Oxygen Therapy on Reintubation in Low-Risk Patients

Would HFNO prevent reintubation in low risk pts within 72 hours

Low risk – <65, APACHE2<12, BMI<30, adequate secretion management, absence of heart failure, <1 co-morbidity, absence of airway patency problems

10347 screened; 527 randomised. Majority excluded as deemed high risk for intubation

HFNO had lower reintubation rate (4.9% vs 12.2%) – also less laryngeal oedema and stridor

 

Individualised management of ARDS (L Brochard)

Max Harry Weil Memorial Lecture

ARDS initially described in Lancet 1967

LUNG-SAFE study

4499 pts with hypoxemic respiratory failure

3022 with ARDS

We don’t ventilate them very well – too much TV, PEEP variable etc.

 

ARDS – is not a single entity.

Comparisons of Berlin definition for ARDS with autopsy (Thille AW et al AJRCCM 2013)

Subphenotypes of ARDS (Calfee CS et al Lancet Resp Med 2014)

2 phenotypes identified – Phenotype 1 has better survival characteristics

Higher vs lower PEEP in ALI/ARDS Systematic Review (JAMA 2010)

PEEP induced lung volumes to predict alveolar recruitability (Dellamonica ICM)

Oxygenation response to PEEP predicts mortality in ARDS (Goligher EC et al)

 

ARDS management

The concept of the baby lung. Small lung does not mean stiff lung

Stress (pressure) and Strain (deformation)

Strain – increase in lung vol/FRC

Lung stress and strain during mechanical ventilation: any safe threshold?

 

Compliance = tidal volume/driving pressure

Driving Pressure and Survival in the Acute Respiratory Distress Syndrome

 

 

Conclusion

Reducing VILI is still the most important possibility to improve survival post ARDS. Individualised ventilation should be based on

  • Recognising ARDS
  • Assessing severity
  • Individually titrating Vt (strain) and PEEP

 

 

SOSD Phases of fluid resuscitation

Circulatory Shock – JLV and De Backer

Four phases of intravenous fluid therapy: a conceptual model

Salvage (Shapiro)

  • Fluid management in sepsis has changed considerably despite it being a time critical diagnosis
  • Obtain a minimal acceptable BP

Perform lifesaving measures

(pic)

During salvage, LIBERAL FLUID RESUSCITATION – 30mls/kg??

ARISE, PROMISE, PROCESS

The Bottom Line – Fluid review section

Conclusion

  • Approximately 4-5l
  • IDENTIFY EARLY
  • Antibiotics
  • Ensure critical interventions
  1. Qns which fluid – anything you can swim in
  2. Qns diastolic dysfunction – becoming more important. BUT not in the salvage phase
  3. Qns what are your markers for success – multiple e.g. BP, HR, biochemistry. When you have a BP you can leave the bedside for a minute

 

Optimisation (De Backer)

  • Provide adequate oxygen availability
  • Optimise CO, SvO2, lactate

Why give fluids? Expect an increase in tissue perfusion

Delayed fluid is associated with greater activation of inflammation CCM 2012 40 2841

Improvement in microcirculation associated with improved organ function

Fluids and CO (Muller Anaesthesiology 2011) – not all improve CO

Why restrict fluids? Oedema deleterious – lung oedema and tissue oedema

A positive fluid balance is associated with a worse outcome in patients with acute renal failure

Sepsis in European intensive care units: results of the SOAP study.

The Adult Respiratory Distress Syndrome Cognitive Outcomes Study Long-Term Neuropsychological Function in Survivors of Acute Lung Injury

Fluid challenges in intensive care: the FENICE study A global inception cohort study

What DBD would do (pic)

 

Qns what markers? Lactate. Arterial Veno CO2 gradient

 

 

Stabilisation (Slama)

  • Provide organ support
  • Minimise complications

Aim for zero or negative balance during this phase

FINNAKI study – http://www.ncbi.nlm.nih.gov/pubmed/23075459

A positive fluid balance is an independent prognostic factor in patients with sepsis

Chloride – Association between intravenous chloride load during resuscitation and in-hospital mortality among patients with SIRS.

Meta-analysis of chloride – Meta-analysis of high- versus low-chloride content in perioperative and critical care fluid resuscitation.

RRT and diuretics to transition to de-escalation phase

 

De-escalation (Marshall)

  • Wean for vasoactive drugs
  • Achieve a negative fluid balance

Prefers the term de-resuscitation

How? Spontaneous, diuretics, RRT

Strategies – fluid restrict, initial resuscitation then restrict, active de-resuscitation

Who? >72 hrs in ICU and net fluid balance > 6l

IMG_7435

 

 

Early resuscitation in sepsis

Arterial BP targets (JL Teboul)

Why do we use vasopressor?

When to initiate?

  • Early. May not have completely be fluid resuscitate yet.
  • Look at diastolic BP

Which MAP target in septic shock?

 

INDIVIDUALISED ASSESSMENT

 

Lots of oxygen (P Rademacher)

Altered oxygen extraction in illness and sepsis

Understanding the benefits and harms of oxygen therapy

Hyperoxia in experimental sepsis CCM 2009 37 2465

  • In animals studies, hyperoxia is anti-inflammatory and improves hemodynamics/metabolism
  • And does not cause ALI

Eur J Emerg Med 2014 31 233 Stojmeijer et al.

Hyper2S – hyperoxia and hypertonic saline (2*2 trial)

BUT trials stopped early due to worse outcome in both intervention groups

Results

  • Hyperoxia group had better PaO2 (obviously)
  • Hyperoxia group had better SOFA by D7
  • BUT adverse events noted. Hyperoxia had more weakness, atelectasis
  • Higher mortality in hyperoxia group at D28 and D90

Hyperoxia CANNOT be recommended in pts with septic shock

 

Should EGDT be abandoned (De Backer)

Varpula et al ICM 2005 31 1066

Rationale for EGDT – prevent development of tissue hypoperfusion achieving targets for  MAP, SvO2 and CVP

Rivers – more fluids, RBC, Dobutamine and vasodilatory agents, sedation and mechanical ventilation. BUT criticism – single centre, potential confounders, few pts made the difference….

PROCESS, ARISE, PROMISE all didn’t show a difference

EGDT: do we have a definitive answer – De Backer and JLV 

 

Difference with Rivers

High ScVO2 can mean anything!

 

How useful are changes in lactate levels? (Fries)

EGDT what do we do now? Levy

Serum lactate as predictor of mortality in patients with infections (ICM 2007)

Serial blood lactate levels can predict the development of MOF following septic shcok (Bakker 1996 Am J Surg) – time with high lactate probably more important than the initial lactate

Lactate clearance

EMShockNet investigators – lactate clearance vs non-lactate clearance groups

Early lactate-guided therapy in intensive care unit patients: a multicenter, open-label, randomized controlled trial.

Lactate Clearance vs Central Venous Oxygen Saturation as Goals of Early Sepsis Therapy: A Randomized Clinical Trial

German Lactate in Severe Sepsis trial

IMG_7452

 

HAEMODYNAMICS

How to interpret veno-arterial pCO2 (JLT)

Simplified Fick equation

High PCO2 difference is due to blood stagnation caused by low cardiac output state

6mmHg is the magic number

 

EtCO2 as a cardiac output monitor (Monnet)

Revision of physiology of etCO2

3 determinants of etCO2

  • Alveolar ventilation
  • Pulmonary blood flow
  • CO2 production

Provided production of CO2 is constant, etCO2 can be used to reflect CO

End-tidal CO2 pressure determinants during hemorrhagic shock – http://www.ncbi.nlm.nih.gov/pubmed/11193267

Relationship between etCO2 and CO is not linear

Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study – http://ccforum.biomedcentral.com/articles/10.1186/cc7009

etCO2 can be used with fluid balances

IMG_7466

 

Haemodynamic monitoring

Why (Perel)

Haemodynamic instability in sepsis – http://www.ncbi.nlm.nih.gov/pubmed/14644922

Haemodynamic status of a critically ill patients is very complex

Clinical review: Update on hemodynamic monitoring – a consensus of 16 – http://ccforum.biomedcentral.com/articles/10.1186/cc10291

Getting the Full Diagnostic Picture in Intensive Care Medicine: A Plea for “Physiological Examination”
–  http://www.atsjournals.org/doi/abs/10.1513/AnnalsATS.201509-571LE#.Vugk5BIrKRs

No evidence that any form of monitor improves outcome on the ICU

Perioperative cardiovascular monitoring of high-risk patients: a consensus of 12

http://ccforum.biomedcentral.com/articles/10.1186/s13054-015-0932-7

 

How (Biais)

  • PAC
  • Transpulmonary thermodilution
  • Pulse pressure analysis
  • Arterial line – calibrated vs non-calibrated
  • Oesophageal Doppler
  • Bio-reactance/bio-impedence

Conclusion

  • Many device available
  • Perfect device doesn’t exists
  • Know limitations
  • Will not improve outcome by itself

 

Who (Monnet)

Database of Abstracts of Reviews of Effects (DARE): Quality-assessed Reviews [Internet].

A systematic review and meta-analysis on the use of preemptive hemodynamic intervention to improve postoperative outcomes in moderate and high-risk surgical patients

Choice of monitor in theatre depends on whether vascular resistance is going to be stable

IMG_7471

Also see Robs trial summary:

Critical Care Reviews meeting 2016 blog – Session 1

Critical care reviews is a one day meeting in Belfast by Rob Mac Sweeney and the Northern Ireland Intensive Care Society.  Adrian Wong and Jamie Strachan attended and have put together these notes for oxicm. Rob is going to put all the talks online over the next few weeks.

The Great Debate: RCTs are Killing Critical Care

Jean-Louis Vincent (@jlvincen): Damn Right!

We should abandon randomized controlled trials in the intensive care unit.

-Fluid, BP, Hb, feeding all have been RCTed to show no benefit.

-Chest compression has never been RCTed and yet we still use and continue to investigate around its “fringes” e.g. LUCAS, continuous vs interrupted.

-Its the process of care NOT the actual RCTs that have advanced ICM.

-In conclusion, JLV advocates personalized and precision treatment plans

Luciano Gattinoni (@gattinon): You’re Having a Laugh?

The logic of RCTs and scientific reasoning

1

– It is not the RCTs but the interpretation and implementation of their findings that is the problem.

– Are we (all) too quick to throw away treatments after RCT? ECMO was discarded for 30 years after 1970 says @gattinon

– Problems with RCTs – premise and external validity. Not asking the right question – Wrong study=wrong result

2.png

Discussion

JLV and Gattinoni both say – we are asking the WRONG questions.

Interesting articles

Paul Young (@DogICUma): Saline or Plasmalyte? Is SPLiT the Solution?

Great discussion on this trial – well covered online in other places:

Original paper | Editorial to manuscript |@WICSBottomLine Review | @stemlyns Review

6.png

New data from Young was presented at this meeting however:

 

But this a non-significant result and was from a post hoc analysis of a non predefined subgroup, as Simon Carley pointed out from the twittersphere:

What it did do is help Dr Young and his colleagues with their next project- the PLUS trial: PlasmaLyte versus Saline trial – 40 sites, 8800 pos ? the definitive trial comparing plasmalyte and saline.

John Holcomb: How to Resuscitate PROPPRly

Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1 vs a 1:1:2 Ratio and Mortality in Patients With Severe Trauma The PROPPR Randomized Clinical Trial

Again well covered elsewhere but a great run through today from John:

@WICSBottomLine Review | @stemlyns Review | @theSGEM Review

Other points:

– plasma is a drug with thousands of proteins in it

– Holcomb explains survival bias: Did they live because they got the whole blood or did they live long enough to get the whole blood?

– PROMMTT data: “transfusion was random across centres”

– KM Curves in PROPPR already started separating within 3 hours

– Median time to haemorrhagic death in trauma 2.5hrs. It is products we give before this time that hold importance

– No point of care coagulation test is fast enough to keep up in active bleeding.

Tim Walsh (@Ed_TimWalsh): Is Old the new Young? The ABLE Trial

Age of Transfused Blood in Critically Ill Adults | @WICSBottomLine Review

7

The conclusion?  – Fresh red cells do not appear to be superior to standard issue red cells in critically ill adult patients.

Tim Walsh made the great point that so-called negative randomised control trials can reassure us we are doing no harm.

 

Critical Care Reviews meeting 2016 blog – Session 2

Critical care reviews is a one day meeting in Belfast by Rob Mac Sweeney and the Northern Ireland Intensive Care Society.  Adrian Wong and Jamie Strachan attended and have put together these notes for oxicm. Rob is going to put all the talks online over the next few weeks.

Session 2 was “How i manage…”

Luciano Gattinoni (@gattinon): Hypoxaemic Respiratory Failure

Know the baseline sats and RR (without O2) – response to oxygen tells you about the shunt

Knowing the PaCO2 tells you how much tired the patient is

If sats don’t improve with O2, shunt fraction is close to 30%

Gattinoni would intubate moderate/severe ARDS immediately

Know the diagnosis and the treatment! Don’t just manage ARDS

Test the oxygenation at PEEP 5

When increasing PEEP, measure central venous oxygenation and check scvO2. If scvo2 & paO2 both go up good. If 1 goes down serious harm instability

Friday night ventilation: a safety starting tool kit for mechanically ventilated patients

Jean-Louis Vincent (@jlvincen): Septic Shock

Give antibiotics – early and the correct ones

8.png(@Doctor_J_)

Trial of Short-Course Antimicrobial Therapy for Intraabdominal Infection

Source control needs to be rapid.

9.png(@david_menzies)

Microorganism is ultimately discovered in 77% of @jlvincen septic patients

So de-escalate antibiotics – quickly if you can

10.pngVIP – ventilate, infuse and pump

Individualise the fluid strategy

The phases of fluid strategy – SOSD – salvage, optimize, stabilization, de-escalation

Four phases of intravenous fluid therapy: a conceptual model

Don’t touch pt during fluid challenge!

Passive leg raise – but it’s too complicated. Just give fluid challenge and watch cardiac output

JLV – start noradrenaline early and he would start dobutamine

Concept of SEPSIS Team

Paul Young (@DogICUma): Pyrexia in ICU

Acetaminophen for Fever in Critically Ill Patients with Suspected Infection

@WICSBottomLine Review

Paul had 6 take home messages:

  1. “Converting peripheral temp to core by adding 0.5 is a bit dodgy”
  2. “The temperature that is not on the chart is not as accurate as you think”
  3. “If temperature >39 intermittently, consider continuous monitoring”
  4. “If temperature control is important, I typically administer paracetamol regularly”
  5. In morbidly obese, external cooling may worsen things initially because of vasoconstriction
  6. 48hrs of ibuprofen appears to be safe and well tolerated in sick ICU pts

Young: Keep the pts alive for long enough so that they will get better themselves

John Holcomb: Traumatic Haemorrhage

Think about 2am medicine when planning strategies/guidelines

Most trauma deaths occur within 1 hr

Moving thawed plasma from lab to ED, reduced time of administration by 40 minutes

No blood test is fast enough to manage the initial phase – No point in lab tests whilst pt actively bleeding. Goal directed transfusion starts when bleeding stops

“Giving blood does not stop bleeding”

How I treat patients with massive hemorrhage

Tim Walsh (@Ed_TimWalsh): Anaemia in ICU

Anaemia is common

Causes of anaemia on ICU

  • Haemodilution
  • Blood letting
  • Blood loss
  • Marrow suppression
  • Iron met supprssn
  • Chronic disease
  • Reduced RBC life

11.png

10 good practice points:

  1. Transfuse blood when it obviously saves lives
  2. What does Hb mean – concentrated etc
  3. Avoid excessive blood letting
  4. Don’t routinely administer iron – IRONMAN trial awaited
  5. Don’t administer erythropoietin
  6. Use single unit RBC transfusion in non-bleeding pts
  7. Early sepsis might be different BUT only when there is a clear evidence of tissue hypoxaemia
  8. Make individual judgements for the pt with cardiovascular disease
  9. Don’t ask for fresh blood
  10. Don’t transfuse unless Hb<7 in young, healthy pt

Restrictive versus liberal transfusion strategy for red blood cell transfusion: systematic review of randomised trials with meta-analysis and trial sequential analysis