All posts by Matt Rowland

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About Matt Rowland

Clinical Lecturer in ICM and Anaesthetics University of Oxford Oxford University Hospitals NHS Foundation Trust

LIVES 2016: ICU admission in the elderly

elderly

Session on ICU admissions in the elderly. A few RCTs completed but awaiting further data as discussed. Good review below:

Review on the Elderly and ICU

Very old ICU Patients = VIPs

Long term survival important. 1 year mortality >80 is especially bad in AKI patients. Cardiothoracic seem to do much better

Hospital mortality of approx 40% in Dutch octogenarians. But decreasing since 2007

Predicting outcome in >80 difficult – frailty index or simpler frailty scale

Summary here: http://lifeinthefastlane.com/ccc/frailty/

VIP-1 study – looks at all octogenarians after ICU admission. Recruiting now!

Factors impossible to know – Rui Moreno

Dramatic change in number of elderly in general population 1850 – 1990

Need fast decisions but need time to decide whether patient responding to treatment

45% of prognosis already present at time of ICU admission e.g. age, prior disease, genetic background

Acute physiological disturbance only accounts for 35% of prognosis

William Osler: “It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has”

ICE-CUB 2 study – Bertrand Guidet

Planning RCTs investigating admissions of the eldery to ICU – firstly, how to select which patients to admit? ncbi.nlm.nih.gov/pubmed/19866508

ICE-CUB-1 study. No beneficial effect on admission to ICU for patients >80 archinte.jamanetwork.com/article.aspx?a…

2016 ICE-CUB-2 study recruting. Lowered inclusion age to <75. ADL >4, nil active cancer, preserved nutritional status

Primary endpoint for ICE-CUB2 study = 6 month mortality. Right length? Or is that too short term in this group and to show overall benefit

Results embargoed but coming soon!

LIVES 2016: Opening Presentations

Daniel De Backer – President ESICM

What has happened in 2016?

7 key points

  1. Members: 8550 now (continuous increase)
  2. NEXT committee: 115 fellowships since 2014 – trainees and young specialists from across Europe. New Pain/Agitation/Delerium (PAD) and Bayer Fellowships rolling out. ICE-mentoring – 28 mentors/58 mentees
  3. Education: academy and interactive e-learning. EDIC preparation course with mock exam. New courses. New courses e.g. Mechanical ventilation + EDIC 1 and 2 preparation courses. EDEC (Extending knowledge of the diagnosis of cardiac dysfunction and advanced use of echo) – new diploma. 64 intensivists enrolled. Webinars e.g new sepsis definitions, LUNG SAFE study
  4. Research: Increasing investment in research~ €600,000. ESICM Trials Group – 10 studies and 20K patients. JAMA/ICM Journal publications. Protocol Library
  5. Journal: ICM – highest impact factor yet ~ 10.125 currently. Monthly webinars and ICM Pulse related to most relevant publications. ICMx – experimental research
  6.  Communications: Social Media, Blog
  7. Coming soon: EuroAsia 6-8 April 2017. ESICM eBook series on Lessons in ICU. Surviving Sepsis Campaign – revision of SSC Guidelines 2016 coming soon. Paediatrics SSC, Sepsis in resource limited countries.

A new physiology: Caring for the extraterrestrial (Michael Barratt)

Space medicine meets intensive care

  • Three training programs in US for space medicine – board certified
  • On cusp of commercial space flight so ?expanding
  • Informs overall knowledge base of physiology
  • Accelerates avenues of medical and tech development e.g. USS
  • Thriving international community – work closely together

Radiation – by far the biggest limitation of human space travel

International space station the main destination – much roomier than one would imagine!

Basically a functioning laboratory with centrifuge, freezer, gas analyser (VO2 max etc), EEG, animal research etc

Most common issue needing adaptation is WEIGHTLESSNESS

Most changes adaptive and not harmful but can become maladaptive on return to earth

Seconds to minutes to occur:

  • Anthropometry – neutral body posture
  • Fluid shift – headward direction. Expect CVP to increase. PAC inserted in space – decreases!
  • Neurosensory adaptation  – proprioception altered. Tremendous conflict neurovestibular and occular systems. Sensory conflict but adapt in days

Lung: evening out of V/Q distribution (though incomplete)

VT decreases, RR increases —> net decrease of 7% in ventilation overall. DLCO increases

SUBACUTE (first 10 days)

  1. Fluid regulation
  2. Blood volume
  3. Neurosensory adaptation

ACUTE (3 weeks)

20% decrease in MVO2. CO normal/contractility normal

Bone loss – starts immediately but takes while to take effect. Muscle loss too

Neuro issues too: increased ICP (likely but hard to test in space…), ophthalmic disc oedema, choroidal folds —-> USS: x2 increase in optic sheath diameter. But unsure why?

ESICM Society Medal – Rui Moreno

Extremely well deserved – huge contribution to ICM – both clinically and through research

Terror victims in the ICU (Serge Jennes)

Description of the ICU and burns management of the Brussels terror attacks this year

Hospital built as disaster hospital – entrance corridor has drop down panels with O2 and suction

Incredible response – hard hearing about paediatric admissions with severe burns. And families who lost parents – just tragic

1/3 of patients from outside of Belgium – families needing to be reunited in hospital so transfers arranged

18 admissions overall – 6 years to 49 years

9 surgical procedures

120 radiological investigations

20 dressing changes a day for 15 days

Key message: computers are not fast enough. Use paper. Whiteboard for movement of pts

Additional workload: VIP visits (King and Queen of Belgium), insurance company, arrange transfers

Plus – dont forget hospital becomes target itself. Security issues

Take home messages:

  1. Be prepared: know your enemies and treat first what kills first
  2. Rebuild: practice drills, training, improve protocols
  3. Apply and practice protocols learned from recent conflicts in the prehospital and ICU settings

Acute Kidney Injury: Diagnosis, Management and Controversies

Probably the area I feel least comfortable with on the AICU so looking forward to an update – especially with regard to RRT. Brexit jokes only allowed for first hour according to the chair….

Excellent overview from basic pathophysiology to RRT. 3 excellent reviews worth mentioning that were highlighted:

Acute kidney injury and sepsis:

http://www.nejm.org/doi/full/10.1056/NEJMra032401

Pathophysiology of acute ischaemic kidney injury:

https://www.ncbi.nlm.nih.gov/pubmed/21364518

Fluid management in AKI:

 https://www.ncbi.nlm.nih.gov/pubmed/24217464

Acute Kidney Injury

Is all AKI the same? (Lui Forni)

NO! AKI is a syndrome –  IMPORTANTLY does not include the cause…

Includes:

  1. Specific kidney diseases e.g. glomerulonephritis
  2. Non specific e.g. ischaemia
  3. Extra renal e.g. obstruction

Beware the hidden tiger in the AKI without obvious cause

Transjugular renal biopsy by interventional radiologists potential option in coagulopathic patient

Pathogenesis of AKI (John Prowle)

Again – reinforcing AKI is a heterogenous clinical syndrome – multifactorial

ATN first described in 1941 in Blitz survivors. Crush injuries with secondary mortality from renal failure: https://www.ncbi.nlm.nih.gov/pubmed/20783577

Key points:

  1. Baseline risks e.g hypertension
  2. Acute pathology e.g. sepsis
  3. Nephrotoxicity e.g. drugs

Like playing the fruit machines in UK – if all three come up, highly likely to develop AKI

Treatment of the above:

  1. Recognise risks
  2. Treat and mitigate pathology
  3. Avoid unnecessary nephrotoxin exposure

Conventional belief that AKI is driven by global organ ischaemia – theory that has now been challenged

Commonest association with AKI is sepsis BUT unlikely due to purely global hypoperfusion

More important = balance between kidney ischaemia and inflammation injury

Endothelial cell activation, injury and reduced microvascular flow play major role – may not be dependent on global macrovascular flow –

Noradrenaline may increase glomerular pressure without compromising renal perfusion and restore GFR

BUT if tubular injury due to inflammation – cant be manipulated by systemic haemodynamics as reduction in renal blood flow in AKI – mediated by tubular dysfunction

Take home messages:

  1. Initially in septic shock – increasing BP may increase UO.
  2. In establised AKI – nil benefit. (except potentially in HT patients – renal hypertension challenge to assess improvement in UO)

Epidemiology of AKI – Ville Pettila

Incidence of AKI in ICU around 40-60%

RRT in AKI 300-600 per million population

Top 5 causes: Hypovolaemia/diuretics/hypotension/colloids/severe sepsis

Even stage 1 AKI associated with increased mortality

Interesting question about lack of routine followup for patients with AKI? e.g. compared to acute MI

Need to engage local nephrology services early in arranging followup review

Prevention of AKI – Miet Schetz

Reinforcing above: Patients at risk of AKI

  1. Baseline risks
  2. Acute conditions
  3. Nephrotoxicity

Interplay between risk factors v insults

Radiocontrast, aminoglycosides, ACE-I

Limited evidence in witholding ACE-I  – cardiac cath: https://www.ncbi.nlm.nih.gov/pubmed/26093871

Seem to be functional but not structural changes to kidney – ?lack of evidence of harm

Fluid overload bad for the kidney. Two excellent papers on fluid management:

https://www.ncbi.nlm.nih.gov/pubmed/25204700

https://www.ncbi.nlm.nih.gov/pubmed/26507493

Choice of fluid also important:

General message – starches = bad

6S trial NEJM  – https://www.ncbi.nlm.nih.gov/pubmed/22738085

Myburgh 2012 NEJM – https://www.ncbi.nlm.nih.gov/pubmed/23075127

So then, saline or buffered crystalloid solution?

https://www.ncbi.nlm.nih.gov/pubmed/23073953 – choride restrictive regime associated with reduced incidence of AKI and RRT

https://www.ncbi.nlm.nih.gov/pubmed/26444692 – SPLIT trial – nil difference in renal outcomes with buffered crystalloid v saline (but ?low risk pts and low volumes crystalloids)

Take home messages:

  1. Starches nephrotoxic in sepsis and ICU
  2. Hyperchloraemia may induce renal vasoconstriction
  3. Hypotension duration/severity related to AKI
  4. Earlier use of vasopressor may be advantage
  5. No adverse effect of vasopressor on renal function in patients with vasoplegic hypotension
  6. Targets should be individualised

 

Renal replacement therapy

Case study? Need for RRT? (Eric Hoste)

Majority of people would not start RRT in AKI stage 1 in patient with abdominal sepsis and laparostomised abdomen

By AKI – stage 3, still a third of audience wouldnt start RRT

Such a disparity. Compared to cardiac/respiratory support – potentially clearer decisions on e.g. intubation etc

When to start RRT? (Michael Darmon)

Current practices

Survey of practice in nephrologists: https://www.ncbi.nlm.nih.gov/pubmed/22207332

Median Ur 20/ Cr 322 for initiation of RRT

Should we start earlier in patients with haematological instability?

https://www.ncbi.nlm.nih.gov/pubmed/19237881  –  Small RCT – deleterious effect of haemofiltration during early phase sepsis

Risks/Benefits of early RRT pre-classical indications?

Risks of early RRT?

  1. Unrequired RRT in pt with spontaneous recovery
  2. Risk of catheter insertion and extracorporeal circuit
  3. Depletion of drugs, nutrients, electrolytes
  4. Resource consumption

Benefits of early RRT?

  1. Prevention of electrolye disturbance
  2. Homeostasis – better fluid balance

Should we start premptive RRT then? Before classical indications?

https://www.ncbi.nlm.nih.gov/pubmed/21352532 – suggestion of beneficial effect on survival but heterogeneous studies ++

AKIKI study – RCT in NEJM 2016:  https://www.ncbi.nlm.nih.gov/pubmed/27181456

  • KDIGO stage 3
  • Within 6h or discouraged until usual criteria or >12h
  • No difference in mortality. Decrease in RRT requirement by 50%

ELAIN study may provide more data – https://www.ncbi.nlm.nih.gov/pubmed/26993261

Issues:

  • Definition of delayed RRT differs across studies
  • Most of studies are at high risk of bias
  • Factors leading to RRT initiation are not taken into account
  • A single study was randomised
  • Patients with severe AKI who did not require RRT are usually excluded from observational studies

Take home messages:

  1. Optimal timing remains unknown
  2. Most interventionalists would start RRT within 24 hours in KDIGO stage 3 patients (without waiting for conventional indications)
  3. Data resulting from RCTs remains conflicting and hard to interpret 
  4. Late strategy may help avoiding RRT in up to 50% patients
  5. What is the role of uraemia (beyond fluid overload) in systemic organ failure

What modality to choose? (Heleen Oudemans-van Straaten)

Key points from the talk:

  1. Timeframe (intermittent/continuous)
  2. Mechanism (HD/HF)
  3. Type of buffer (lactate v bicarbonate)
  4. Type of A/C (heparin v citrate v nothing)

Boils down to short term benefits, long term benefits and local expertise/facilites

Intermittent HD could provoke hypotension in unstable patient

Dialysis disequilibrium syndrome. Early from cirulation, late from brain —> cerebral oedema. Due to reversed osmotic shift

Cochrane review in 2007 – no difference in mortality/renal recovery and haemodynamic stability

BUT: Higher MAP and lower need for vasopressor dose escalation

KDIGO recommendation: Use IHD and CHD as complementary techniques in ICU patients

HD v HF v HDF – need to choose dependent on patient and timing

Take home messages:

  1. Initial RRT modality? Consider
    • Haem instability
    • Fluid overload
    • ICP
    • Renal recovery
    • LIKELY CRRT AS PRIMARY THERAPY FOR PT ACUTELY ON ICU
    • IHD in patients with stable clinical picture and improving
  2. No robust clinical difference between HD and HF
  3. Cautious with lactate buffering in shock/liver dysfunction

Citrate v Heparin coming later!

 

Which membrane for RRT? (Thomas Rimmele)

Which polymer?

Molecule removal = function of size and plasma concentration.

But uraemic toxins and essential proteins – comparable mol weights

Plasma concentration – like looking for needle in a haystack? Might want to be more specific in which molecules to focus on