Venue: University Hospital, Southampton
Date: 19th January 2016
Summary blog by: Andrew Nash
Mr Bailey -Upper GI Consultant Surgeon
The acute abdomen
Discussion around surgical perspective to the acutely unwell and intensive care patient. NELA outcome data and management of critically ill patients have and are evolving, with an improvement in outcomes from sepsis. Arguably operating on patients with increasing predicted mortality but with no mandatory intensive care intervention.
Approach to ICU patient with an acute abdomen: Ischaemic gut – common and fatal frequently. Suspicion highest in AF (new or old); DM; Peripheral vascular disease/arteriopath. Symptoms often vague.
Failure to absorb feed is not diagnostic and in fact is non-specific and should not be relied upon to help diagnosis. Lactate rising is often a late sign and a normal lactate is frequently falsely reassuring. In order to have best outcomes, surgical intervention should be early!
The most likely cause of an acute (short history) abdomen, in a patient with AF will be ischaemic bowel and this virtually mandates a laparotomy. CT scans are useful in excluding other pathologies, but in these cases theatre is the most appropriate destination.
Examination on ICU is difficult – especially cardiac ICU post theatre. Suspect an ischameic gut if a “well” patients deteriorates suddenly. Differential is embolus vs low flow/hypoperfusion. ALL should be CT scanned (to exclude pancreatitis). Anyone who is increasingly unwell, early on, should have a surgical review and a laparotomy.
Laparotomy vs laparoscopy
The role of these two is in doubt. Laparoscopy is increasingly difficult in ICU patients – complex patients, obesity and cardiovascular instability. Laparotomy is a diagnostic tool as well a curative.
Small Bowel Obstruction
Increasingly common – suspect in a patient with previous surgery, SIRS and peritonism. Requires emergency intervention – however patients should have a CT first to confirm true vs pseudo obstruction. These patients need to be seen immediately.
The role of the surgeon is something the intensivist can influence i.e a discussion regarding the management of a septic patient – damage control operation, removal of dead tissue, abscess drainage, leaving the abdomen open to limit the operative insult and time. Repeated visits. Always remember there may be a radiological intervention in many cases and surgery not always required for sepsis source control.
Frailty and co-morbidity and resource allocation means the decision needs to be right.
Stoma vs anastomosis – choice to the patient? Consideration of futility – conservative option?
CT scan younger patients and think twice in a frail patient.
Take home messages:
1) Be confident in suspecting acute surgical abdomen ischaemia and or pus
2) challenge and contribute to surgical thought process
3) Laparotomy is a diagnostic test
Mr King - Consultant colorectal surgeon
The complex surgical abdomen on ICU
3 common complex disease patterns:
- Short bowel syndromes
- Diseased (IBD)
- Post-operative complications
All of these can be considered as surgical conditions in terms of:
- Plan for surgery
These can develop immediately but the high RISK time is 2-6 weeks (10 days to 6 weeks). During this time the adhesions intensify in number and strength with maximal strength between 2-6 weeks. This is the worrying period for surgeons (often a time of fluctuating illness in a post operative/ICU patient) and the mortality from operative intervention is massive due to adhesion density.
This may explain to us as ICU clinicians, why IR options are always considered around day 10 – and the reluctance to operate.
SIRS & CARS (Compensatory Anti-inflammatory Response Syndrome) discussed
- Complex nutritional and electrolyte issues:
- Require 100cm small bowel and 50 jejunal and colon to maintain health
- Use PN to get some control of electrolytes and disease state
- Try enteral route and monitor water losses and electorlytes carefully
- If PEG in situ and working poorly – slow the rate (increase absorption) using loperamide or PPI (for high lesions); hypersalination.
- The colonic stoma can be used retrograde for water and electrolyte absorption. Water loss (colonic) 1100ml (max. normal range) per day
Nutrition on ICU – The surgical patient perspective
Common dogmas on nutrition:
- mandatory treatment
- Not ICU doctors job but merely a dietitcian and nurse job
- Assessment within ICU is hard and arguably none of them work
- BMI triceps thickness, Mid arm circumference, bio impedance
- Deltatrax – doesn’t work with fio2 above 0.6 (so not in the ICU patient)
• All these inaccurate in oedema
So use the History and food chart (good method)
Laboratory - albumin, pre albumin, micronutrients Mg/PO4/selenium (good method)
Bedside ultrasound - quads thickness (frailty) (research method)
CT abdomen paravertebral lumber muscular thickness (research method)
European and British Guidelines
- Any patient if not established or likely to be on a full diet within 3 days they should receive EN
• Requirement is 20-25kcl/kg/day (schofield) nice guideline
• 1-1.5g/kg protein
• Protein is utilised differently in the critically ill – so anymore than this is a waste
Historical question - Hypocaloric vs close to normal energy requirements
When critically ill - body can't cope with extra calories. It requires energy to metabolise food and thus does worse. Significant risk of AKI. History tells us nutrition not needed in critical illness – i.e when feeling unwell appetite is lost.
Trickle feeding (10-15ml/HR) is feeding gut only. Advantage is hypocaloric and it has immune function role in maintaining IgA function hence these ICU patients do well as proven in….
• Paul marik and Michael hooper intensive care medicine paper
• This looked at medical patients only, single organ dysfunction. No difference in type of feeding. In the multiple organ failure group – trickle feeding was beneficial.
ICU patient considerations
As part of the new process for sepsis management:
Fluid restriction from day 2 onwards
Fluid restriction in terms of fluid balance is difficult to work with TPN in the least volume (centrally 1kcal/ml).
Low no-fibre diet to be instigated post-op from major surgery (causes anastomotic pressure to increase when fibre utilised). Specific formulas and can vary
Enteral is always the preferred route. First choice! In ICU patients (avoids complications of PN)
Calories trial - 2014 sponsored by NICE compared TPN and EN compared functional GI tract
- Aim 20-25kcal/kg/day aim to reach within 2-3days
- Target was NOT reached. Reason not reaching target – parenteral diet was only changed once a day. Whereas enteral changed regularly!
TBL summary of CALORIES
PN is used in malnourished and at risk patients e.g Unsafe or non functioning gut (EPaNIC trial) 2011
- Early PN - within 48 hours , late - day 8
- Late feeding reduced ICU stay, faster recovery, fewer infections and reduced costs
Meeting: FICM RA/Faculty Tutor Day
Date: 11th January 2016
Summary blog by: Steve Mathieu
Slides available here:
GPICS recommendations for ICM teaching programmeA minimum of 30 hours during each year of regional training is required for those in dual, joint and solo ICM training programmes. These training sessions need to be of a high quality, and formal feedback should be collected and acted upon. They should be mapped against the ICM curriculum in order to provide a wide range of clinical, ethical, managerial and other topics. The teaching programmes should be published well in advance, and each department should help facilitate trainee attendance when constructing a rota and when approving study-leave requests.
Download the full GPICS document here
Background - the Wessex story
We commenced a programme in 2008. Run monthly since. Consultant co-ordinator. For the last 5 years a trainee to co-coordinate
- guide written as template for the facilitators to follow model
- template reviewed annually, taking into account curriculum, exam and trainee feedback
- considered pre-FFICM and post-FFICM, but rejected
- started with about 18 joint trainees
- 33 in training presently (5 single, 2 EM, 2 medicine; 13 joint)
Matt Williams has been the consultant lead facilitator for our regional teaching programme since 2008
The guide for the facilitators
Wessex Intensive Care Medicine (ICM) CCT trainees teaching programme
Consultant lead facilitator: Dr Matt Williams
Trainee lead facilitator: Dr Phil McGlone
Guidance for facilitators:
The trainee facilitator should take primary responsibility for the allocated session with support from the Consultant facilitator. The trainee should initiate contact at least 2 months prior to the teaching date (preferably with suggestions of topics and speakers, having reviewed the relevant sections of the ICM curriculum). This will enable external speakers and trainees to prioritise the meetings.
The timetable should be distributed a minimum of 2 weeks prior to the teaching date. This will allow attendees to prepare for the session, including reading any relevant papers circulated.
A summary of the session will be circulated within two weeks of the teaching date by the trainee facilitator. This will be uploaded to the WICS website.
The content of the lectures should follow the ICM syllabus. The trainee should identify the areas of the syllabus covered and reference these in the timetable.
Suggested teaching styles that can be included:
• Review of the recent literature on a topic area
• Case presentations (ideal for case summaries)
• Journal article review
• Expert speaker
It may be pertinent to have part-task or medium fidelity simulation on occasion.
Ideally there should be two or more trainee speakers at each session. External speakers may lend themselves very well to a particular session. Primarily trainees should be taking an active role in presenting and teaching. This responsibility should be shared amongst the group over the course of the programme.
Ideally there should be at least one senior (ST6/7) and one more junior (ST3/4/5) ICM trainee presenting at each session.
To encourage positive responses from the trainee group, it is suggested that the trainee facilitator asking people to present should cc the consultant facilitator into the requesting email.
It is up to the trainee to ensure all the equipment required for the session is in place and working prior to the session.
The ICM Training Programme Director (supported by Specialist Training Committee) has stipulated that ICM CCT trainees must attend the formal training programme throughout their joint/single/dual training.
Any questions or suggestions should be directed to the Lead Facilitators please.
20 minutes presentations
Pre-reading ‘flipping the classroom’
- Combined vs Pre- / Post- FFICM sessions
- Trainee / consultant speakers
- Other specialties; local & external speakers
- Special Skills modules
The challenges of delivering a quality teaching programme
Worth considering why it is difficult to maintain the quality of an ICM (or indeed any specialty) regional teaching programme:
- Curriculum changes
- Shift patterns are evolving
- Different learning needs at different stages of training (pre- vs post- FFICM)
- Trainees may be in non-ICM specialties as part of their training
- May be geographical and service commitment barriers which restrict attendance
- Learning styles are adapting. Generation Y understandably demand us to embrace the digital age
- Voluminous educational material which is not always easily accessible. Reason quality open access resources (FOAMed) are so important
If you do a pubmed search under ‘intensive care’ or ‘critical care’ for 1950 there will be 1 article returned.
Do the same literature search for 2015 and there are 24,000 citations. Let’s say only 1 % are relevant, you would still need to read 50 articles every single week to keep up to date
We therefore need to adapt and take bold steps!
The role of the teaching programme facilitators
Consultants are essential. The programme organiser needs to be aware of the latest curriculum requirements and ensure that content covered is appropriate and achievable. The consultant facilitator is the person that can best assimilate knowledge, appraise it and combine it with their wealth of experience. This is fundamental to the learning process.
A co-facilitator, who is a trainee, is essential so that they can develop non-clinical organisational skills and contribute to maintaining a high quality and relevant session.
Pre-course material (flipping the classroom)
Allows more time for discussion / critical appraisal and tacit knowledge development – skills you just can’t learn from reading e.g. simulation
An example would be from a recent session on expanded case summaries (ECS). The completion of 10 ECS are a UK requirement for all ICM trainees. These are written mini vignettes and focused discussions about core topics in ICM. What are the markers looking for when they review the completed ECS’? I decided to get the trainees to mark 3 examples before the session in order to get a better understanding of this. A useful exercise which was then followed by 6 x 20 minute presentations covering a wide scope of the syllabus (including TTP, refractory hypoxaemia, propranolol overdose and the use of levosimendan)
Promote the teaching session
So you have the content and have organised the date. You now want to make sure everyone attends. A global email will probably suffice but why not use other means of promoting your session. Making the dates easily viewable and getting everyone excited and discussing the content is achievable by using one or more of these applications
G mail + calendar
You have an excellent session organised with some top quality and well rehearsed presentations. Why not keep a record so that it can be viewed by others that were not lucky enough to attend (asynchronous learning)?
1. Summary blog
2. Podcast – this could be recorded in advance (part of the preparation for your talk anyway) or on the day (? Potential to be a distraction; need good quality and portable recording devices)
3. Videocasts e.g. periscope. Again potential to distract. Consideration of sensitive patient info but if planned well a perfect historical record of the session
4. Share & contribute to Free Open Access Medical Education (FOAM)
• Asynchronous learning
• Repository of all sessions wessexics.com
• Promotes you, your department and region
• Why wouldn’t you?
Please do share your examples of challenges & excellence in delivering the perfect teaching programme. Good luck!
Signing up for twitter
Social Media Workshop - ICS State of the Art Meeting 2015
How to get started with twitter
What is FOAMed?
Critical Care Practitioner
Critical Care Reviews
ICM Case Summaries
Intensive Care Medicine Working Knowledge (ICMWK)
Intensive Care Network
Life in the Fast Lane
PulmCrit: Pulmonary Intensivist’s Blog
SMACC (includes podcasts and videocasts of all conferences)
The Bottom Line
EM, Pre-Hospital and Anaesthesia with ICM
Academic Life in Emergency Medicine (ALiEM)
Emergency Medicine Literature of Note
Pre-Hospital And Retrieval Medicine (PHARM)
Skeptics Guide to Emergency Medicine (SGEM)
The Sharp End
A list of all the podcasting sites for critical care can be found here
Critical Care Reviews Meeting 2015
Social Media and Critical Care (SMACC) Video’s
There are many more #FOAMed sites available and the list keeps rapidly growing. You can get more information by doing a search on google FOAM
Venue: Queen Alexandra Hospital, Portsmouth
Date: 17th December 2015
Summary blog by: Duncan Chambler
Is obesity a disease or is it just a lack of will power in lazy individuals!? If it is a disease, then it has a prevalence of 1.9 billion globally. Of this,42 million are children. It has an associated mortality incidence of 2.8 million per year, which is nearly double the mortality from HIV/AIDS and is over 200x the mortality from the most recent Ebola outbreak. This disease affects men and women alike. Here in the UK, five in 10 men suffer from the milder form (overweight) along with four in 10 women. In the USA, prevalence has increased from 10% to 50% in the last 50 years. Although it predominantly affects developed nations, it crosses all borders and communities.
Disease or not, obesity is becoming the greatest threat to humanity’s health. If it is a simple as calories in balanced against calories burnt, then why are we failing to correct our path toward physical, psychological, and economic doom?
What’s relevant to us?
Many aspects of obesity are obvious. So many of our ITU patients are overweight or obese it almost feels normal. So what do we need to learn?
We could have talked about drug dosing, but that’s easily summarised: dose most drugs on “ideal weight + 40% of excess weight” and you won’t go far wrong.
Or, we could have talked about airway management, but usually this isn’t to hard if there is adequate preparation: ramp until their ear, sternum and abdomen are about parallel to the floor!
So instead we had two expert speakers who look at the bigger problems: why do people get fat, and what can we do for them (as members of society, the profession of medicine and the specialty of critical care)?
The history of nutritional advice
As an interlude between the speakers, I presented a brief history of nutritional advice and diets (I confessed my own biases first – I believe sugar is bad and fats may not be so bad).
In 1864, William Banting produced a pamphlet for the public called “A Letter On Corpulence”. Banting had an idea that worked for him, so he wanted to tell the world (these days he would have used Twitter). His high fat and low carbohydrate diet helped him drop weight so effectively it became the popular diet of the time.
In the 1950s and 60s, cardiologists wanted to blame something for coronary disease. Cholesterol and saturated fats became that something after Dr Ancel Keys produced the Seven Countries Study, which strongly associated cholesterol to coronary disease. This evidence, along with a committee in a rush, led to the USDA’s advice and subsequent Food Pyramid, which advises a high carbohydrate and low fat diet. This is still mainstream advice today 50 years later. Take a look at this short YouTube video about the unbelievable McGovern Report
Only now are we beginning to understand that coronary disease is more complicated than just dietary intake, and eggs are back on the menu!
If you fancy a different way of eating, backed up by science, take a look at The Real Meal Revolution by Prof Tim Noakes.
Why people get fatLorraine Albon - Diabetologist at Portsmouth Hospitals NHS Trust with an interest in Obesity Medicine.
• Obesity is a problem for healthcare and health professionals: difficult to examine, investigate, nurse and treat; prone to ulcers, VTE and infection.
• Studies have shown negativity, stereotyping and bias against obese individuals by healthcare professionals.
• Is it a disease? A hands-up polls suggests 50% in the room agree whilst 50% think it is simple calorie maths and will power.
• Problems from obesity can be considered as two disorders:
- a metabolic syndrome associated with multi system disease related to the endocrine and metabolic consequences of excess adipose tissue (e.g. type 2 diabetes, heart disease);
- a physical syndrome of problems related to the excess body mass (e.g. sleep apnoea, lower back pain)
• Individuals can be fit and fat: mortality hazard ratios for aerobically fit but fat individuals are better than unfit thin individuals.
• Edmonton Obesity Staging System is better at discriminating those at risk than classical BMI calculation
• The gut is an extensive neuro-hormonal organ and appetite regulation depends upon many hormones, with particular interest currently in Ghrelin and Leptin
• Monogenic and polygenic polymorphisms have been associated with hormone irregularities and consequential obesity – as many as 5% of severe obesity cases may be due to genetic mutations
• At risk groups for obesity include: those who are vulnerable, have limited opportunities and those with large parents; also ex-athletes (who previous ate well and burnt the calories but now continue to eat well without the exercise!), drivers and night workers
• Energy regulation is tightly controlled – within ±1% margin of error
- One bar of chocolate extra per day = +100 Kcals
- Equates to 35,000 Kcals extra per year
- Which would cause 5 kg weight gain per year if not balanced
• Strong evidence exists demonstrating diets don’t work
• Conversely, strong evidence exists supporting metabolic surgery (new term for obesity surgery – the aim is to correct the metabolic syndrome, as opposed to bariatric surgery that is just cosmetic)
• Obesity surgery is commissioned by NHS England as a specialist service, and NICE quality standards will reward trusts through CQUINS for addressing the issue of obesity through a 4-tier management pathway: essentially common advice, specialist nutritional advice, medical advice / drugs and then finally surgery
• Issues relating to ITU
- Record overweight / obesity as diagnostic text
- Consider malnutrition and treat deficiencies
- Consider further assessment: sleep studies, tier 3 referral
- Warn people about weight loss post ITU
Fat and Malnourished
Denise Thomas is a Dietitian with a doctorate in the study of obesity. She is head of Nutrition and Dietetics at Portsmouth Hospitals NHS Trust.
• Despite rising obesity rates, food poverty is also increasing
• Recommended eating includes ‘5 portions of fruit & veg per day’, but only 25% of adults achieve this regularly
• High fat and high sugar foods, from take-aways or pre-made meals, are consumed frequently
• A paradox now exists: high energy intake but low nutritional quality
• This is encouraged by agricultural techniques and the low cost of these foods
• Obesity often associated with deficiency of: Vitamins A, E, C and D, selenium, folate, zinc and thiamine
• The best advice is to match the Eatwell Plate! With subtle differences to the USDA’s Food Pyramid in the UK this is the current advice we should give our patients
• If there was one thing society (and government) could do to halt the obesity epidemic, it is to limit and reduce fast-food and take-away outlets
We all felt a little disheartened at the size of the problem, the complexity of the science and the uncertainty of the advice. What should we do for our patients when we meet them for just a short period of time? Nudge them with a suggestion perhaps!
• “Have you thought about how your weight might affect your health?”
• “Do you realise that being overweight might make this problem worse?”
From there, if they’re receptive, they can initiate a referral through the 4-tier pathway via their GP!
We concluded the afternoon with a possibly the most academic Christmas Quiz ever, followed by a pint of beer and fish & chips! I guess we ignored all the learning points.
Venue: Queen Alexandra Hospital, Portsmouth
Date: 19th August 2015
Introduction: Steve Mathieu
Whether you love them or hate them, the Expanded Case Summaries (ECS) remain an integral part of the ICM Curriculum. They are formative assessments and a useful opportunity to focus your learning on some specific topics within the ICM curriculum. They don’t have to be rare cases, in fact more common day material with lessons may be better than once in a lifetime occurrences.
How many do I need to do? 10
Over what period? 2 a year
4 stage in 1 (ST3/4); 4 in stage 2 (ST5/6) and 2 in stage 3 (ST7)
How long should they be? Between 750-1500 words (excluding references)
What are they marked out of?
There are 6 domains (each scoring 1-5). A maximum of 30 points can be awarded. 18 is the minimum score to pass. In addition 4 of the 6 domains must score at least a 3
What do scores of 1-5 represent?
5 - outstanding
4 - Good
3 - Pass
2 - Needs improvement
1 - Poor and needs complete revision
And what else?
- Case summaries should be marked with reference to the marking scheme for ECSs
- It is intended that the ECSs will be reviewed and scored locally by Faculty Tutors. Over the course of a training programme each trainee should have ECSs marked and scored by several tutors
- Feedback on the quality of each ECS should be provided to the trainee by the Faculty tutor marking the report
- The case summaries will be evaluated locally as part of the ARCP programme and it is expected that an assessor from outside the region will be part of this process. In addition, a random number (up to 10%) of these summaries will be assessed centrally
- The purpose of the case summaries is to allow the candidate to demonstrate critical thinking, knowledge of recent literature in the field of Intensive Care Medicine, critical appraisal and a sound approach to evidence-based medicine
- It is envisaged that the standard of these case summaries will reflect the stage of training – please refer to the relevant CCT in Intensive Care Medicine curriculum manual for further discussion on ECS content.
(extract from FICM guidance March 2013)
More information is available in this document and on the FICM website
Are there more examples of ECS?
Yes. We now have a WICS prize awarded each year for the best ECS. Do remember to submit your best one! Previous winners
2016 - Organ Donation - James Keegan
2015 - Neurological Prognostication after cardiac arrest: When and how should it be done? Dr Ben Harris
Are there more?
There is now a repository of ECS at icmcasesummaries.com
The CCT in Intensive Care Medicine (v2.12015) - Part II. Assessment System
Facilitators: Alex Belcher and Pete McQuillan
Venue: QA Hospital, Portsmouth
Edited by: Steve Mathieu
Endocrine Emergencies Quiz
Revisited the UK guidelines on DKA management, discussion around ketone monitoring, speed of fluid resuscitation/reduction of glucose and risk of cerebral oedema. Note the same organisation (Joint British Diabetics Societies) also provides guidelines on HHS (previously HONK) and perioperative management of diabetes: http://www.diabetologists-abcd.org.uk/JBDS/JBDS.htm
Also discussed management of Addisonian crisis and perioperative management of the steroid-dependent patient. Again, specific guidelines found at http://www.addisons.org.uk/topics/2005/10/0021.html
Control of glucose in ICU - Tom Pratt
Review of the major papers including the Leuven papers (Van den Bergh 2001 NEJM 345 1359) that suggested major mortality benefit of tight control, but not replicated since. Criticisms include one small centre, almost all cardiac surgery patients and had high nursing intensity.
Other major trials to note are:
VISEP (NEJM 2008 354 449) halted early as evidence of harm in tight control
Leuven 2 (Van den Bergh NEJM 2006 354 449) no sig difference
Glucontrol (Inten Care Med 2009 35 1738) too many trial violations so halted
NICE SUGAR (NEJM 2009 360 1283) higher mortality with tight control
So, no convincing evidence yet for tight control, and maybe harm with more hypos. ?role of continuous glucose monitors (once calibrated!)
Case summary of hyponatraemia/Mx of hypoadrenalism - Adam Stokes
Overview of presentation/aetiology/diagnosis and management of hypoadrenalism by Adam Stokes
Often vague, long history, but crisis may be profound. Don’t delay treatment for investigations, but dexamethasone may be preferable to not confound the short synacthen test. If primary need both glucocorticoid and mineralocorticoid replacement; secondary/tertiary only the glucocorticoid.
Endocrine changes in ICU
Description of the (patho)physiological changes that occur in the critically unwell, specifically stress hyperglycaemia (critical-illness induced hyperglycaemia), relative adrenal insufficiency and sick euthyroid syndrome.
Discussion around the potential adaptive benefits of these changes versus the maladaptive changes. In general, there does not seem to be any evidence of mortality benefit in treating these changes per se. No need to perform short synacthen tests or TFTs unless evidence of specific disease.
Facilitators: Dr Jamie Plumb & Dr James McNicholas
Summary written by: Dr Jamie Plumb
intrinsic renal failure not to be missed in an ICU presentation with AKI, and diagnostic work up prior to assessment by a renal physician’
Dr Adam Kirk Renal Consultant - Queen Alexandra Hospital Portsmouth
Dr Kirk started of by talking about some of the differences between renal physicians and intensivists. He then touched on when they intervene with their CKD patients. Stating that renal patients will not die from their renal failure any longer but of some other disease, more often than not cardiovascular in origin. He mentioned the classification of AKI which was a common theme for the afternoon. He classified the causes of renal failure- pre, intrinsic and post and then focused on
intrinsic renal failure: discussing their features, causes and treatments.
• Acute Tubular Necrosis (ATN)
• TubuloInterstitial Nephritis (TIN)
• Glomerular Nephritis (GN)
The importance of the rapid treatment of anti- GBM disease was discussed. He then talked about renal transplant patients, either with problems directly related
to the transplant or other problems presenting to the ICU. Important points to know such as the time since the transplant and level of success.
The classic acute rejection triad of Classic triad: Fever, Oliguria, graft tenderness
Prompt Tx essential. Risk factors were discussed. The time course post transplant for when certain infections are likeliest was
reviewed. He ended by pondering when we should call them as intensivists,
- When there is a renal diagnosis requiring renal intervention/advice
- When there may be and further brains/interference may benefit the patient
- Known renal patient esp Transplant
Dr Kirk’s presentation slides are available here with his permission. Please click on slide below to view
The renal ICM quiz
Dr Jamie Plumb - Specialty Registrar in ICM
The slightly controversial quiz contained a mixture of questions; it started off with some of the basics around the modes used within critical care and progressed
towards some rather more debatable single best answer questions (SBAs). For those that are pre the final FRCA and/or the FICM exam then they both contain
SBA questions and they do require a fair amount of technique!
Dr Plumb’s presentation slides (with answers!) are available here with his permission. Please click on slide below to view
‘Dose’, modes and some of the fundamentals, perspective from a proper kidney doctor!
Dr Rosie Kalsi - Specialist Registrar in ICM, Renal & GIM
Rosie’s talk built on themes that arose in the quiz and went over some of the basics with regard to the different modes of RRT used within critical care. Dose-outcome
relationships & IRRT vs. CRRT were discussed along with mechanisms of solute clearance. The basic functions of the kidney were revised, essentially to excrete nitrogenous waste but also some endocrine functions EPO & 1,25 dihydroxycholecalciferol
Classification was revised RIFLE, AKIN, KDIGO
As was the evolving dose story - essentially 25mls/kg/hr exchange is likely better but with the appreciation that ICU patients rarely get the prescribed dosages due to
filter going down & other technical issues.
Indications for RRT on ICU were then revised
- Oliguria < 200ml/12 hours
- Anuria < 50 ml/12 hours
- Hyperkalaemia > 6.5 mmol/L
- Severe acidaemia pH < 7.0
- Uraemia > 30 mmol/L
- Uraemic complications (pericarditis, nausea, vomiting, poor appetite,
- hemorrhage, lethargy, malaise, somnolence, stupor, coma, delirium, asterixis,
- tremor, seizures)
- Dysnatraemias > 155 or < 120 mmol/L
- Drug overdose with dialysable drug
- Refractory hypertension
Substances with higher degrees of protein binding and is sometimes substances with very long plasma half-lives.
• In general, the size of the molecule and the degree of protein binding determines the degree to which the substance can be removed (smaller, nonprotein
bound substances are easiest to remove).
• Techniques such as sorbent hemoperfusion may also be used.
• These substances include drugs, poisons, contrast agents, and cytokines.
ICU outcomes were then discussed especially the high rates of death when RRT is required for AKI on intensive care. AKI requiring RRT occurs in about 4-5% of ICU
admissions and is associated with worst mortality risk. The evidence for different modes was briefly reviewed:
Key points: no definitive outcome evidence has ever been found for continuous modes to be better than intermittent modes for overall mortality, or renal recovery and need for ongoing dialysis.
Pros and cons of intermittent vs. continuous therapies were discussed
The basics of how the mechanics of the filter work were reviewed which was particularly useful. How the different modes compare to the native kidney with regard to convection and diffusion capabilities was discussed. The concept of replacement fluid and effluent was explained. As was the ratio mix of pre and post blood pump fluid replacement and the reasons for adjusting this ratio. Detailed diagrams explained this nicely (See slides)
Dr Kalsi’s presentation slides are available here with her permission. Please click on slide below to view
Renal ICM Updates - what’s new?
Dr Jamie Plumb - Specialty Registrar in ICM
I have also included a talk on renal updates that there was not time to give but was mostly covered by Rosie’s talk:
‘Dose’ and ‘Dose’ in Sepsis 3 big papers from 2008, 2009 & 2013
• Review of UK ICM Practice is insightful 2013 (Jones)
• Biomarkers- 2014
• Optimal timing - a few papers on this
• Modes (SLED etc.)- Great review from ‘up-to-date’
Take home message from the RENAL 2009 study Link to paper here
“In countries where continuous renal-replacement therapy is now the preferred form of renal-replacement therapy in the ICU, our study has implications for clinical practice. We found that a prescribed treatment intensity that exceeds 25 ml of effluent flow per kilogram per hour adds no significant benefit and exposes patients to the risk of hypophosphatemia.”
Take home message from IVORIE 2013: Link to paper here
“In the IVOIRE trial, there was no evidence that HVHF at 70 mL/kg/h, when compared with contemporary SVHF at 35 mL/kg/h, leads to a reduction of 28-day mortality or contributes to early improvements in haemodynamic profile or organ function. HVHF, as applied in this trial, cannot be recommended for treatment of septic shock complicated by AKI.”
Very good review of UK practice from 2013 - Jones et al: Link to paper here
“Despite its widespread use, there are several controversies about the optimal way that RRT should be delivered, particularly with respect to
modality (convective versus diffusive methods), timing of initiation and discontinuation and prescribed dose.”
Finally some recent data on prolonged (daily) intermittent renal replacement therapy" (PIRRT), very good ‘up-to-date’ article on this
‘Although not yet supported by objective data, our opinion is that PIRRT will become the dominant acute renal replacement therapy over the next 5 to 10 years”
Dr Plumb’s presentation slides are available here with his permission. Please click on slide below to view
Some final thoughts
Dr Jamie Plumb - Specialty Registrar in ICM
The session closed with some quick mentions of contrast induced nephropathy (CIN), NAC, dysequilibrium syndrome and the role of bicarbonate. Slide are available to review here
Finally, some useful resources for further reading were provided. One that is highly recommended is Dr Sara Blakeley’s Renal handbook. This is a superb resource and is available as open access (FOAMcc) (click image to download for free)
Facilitators: Dr Adam Stokes & Dr Dom Richardson
Summary by: Dr Adam Stokes
Diagnosis of Death and Brainstem Death Testing - Dr. Adam Stokes
- Based on “A Code of Practice for the diagnosis and confirmation of death” produced by Academy of Medical Royal Colleges
• Definition of death: “Death entails the irreversible loss of those essential characteristics which are necessary to the existence of a living human person and, thus, the definition of death should be regarded as the irreversible loss of the capacity for consciousness, combined with irreversible loss of the capacity to breathe.”
Conditions necessary to diagnose death:
Known aetiology of irreversible brain damage e.g. intra-cranial event, cardiac arrest, circ insufficiency.
Exclusion of potentially reversible causes of coma.
Circulatory, metabolic & endocrine
No evidence that this state is due to depressant drugs
Length of time between discontinuation & testing depends on total dose, duration, renal/hepatic function & drug level testing.
Use antagonists if possible.
Hypothermia must be excluded
Temp of >34 C recommended.Exclusion of potentially reversible causes of apnoea e.g. relaxants, opiates, sedatives, neuro disorders, c-spine injury.
Diagnosis and confirmation of death following irreversible cessation of brainstem function:
- Absence of brainstem reflexes
◦ Pupils fixed
◦ Absent corneal reflex
◦ Absent oculo-vestibular reflexes – No eye movement following 50ml ice water over 1 min in each ear.
◦ No motor responses within the cranial nerve distribution elicited by adequate stimulation of any somatic area.
◦ No cough reflex to suction catheter placed in trachea to the carina
◦ No gag reflex to posterior pharyngeal stimulation.
◦ No respiratory response to hypercarbia (apnoea test)
◦ Ancillary tests e.g. EEG, angio, may be used when neuro exam difficult.
Diagnosis / confirmation of death following cessation of cardio-resp function:
- Should observe pt for 5 mins to establish irreversible cardio-resp arrest.
◦ Absence of cardiac function confirmed by
- Absence of central pulse
◦ Absence of heart sounds
◦ Can be supplemented with
◦ Asystole on ECG
◦ Absence of flow on arterial line
◦ Absence of contractile activity on Echo
- Any spontaneous return of activity prompts further 5 mins observation
The following then tested
• Pupillary responses
• Corneal reflexes
• Motor response to supra-orbital pressure
The Nuts And Bolts of Organ Donation / Role of SNOD - Dr. Richardson and Bethan Thomas
- Defined clinical trigger factors in patients who have had a catastrophic brain injury
• The absence of one or more cranial nerve reflexes and a GCS of 4 or less that is not explained by sedation
• Unless there is clear reason why the above clinical triggers are not met and/or a decision has been made to perform brainstem death tests, whichever is earlier.
• “The intention to withdraw life sustaining treatment in patients with a life threatening or life limiting condition ”
Management of the Donor
Dr Richardson covered some of the physiological consequences of BSD.
Stabilisation to facilitate neuro exam
Have to balance the harm of inserting lines & giving drugs versus the harm of not fulfilling the patients wish to become a donor.
DBD Donor Optimisation Extended Care Bundle
Gives guidance on target values for CVS, resp, fluids, DVT prevention and lines to be inserted.
- Assess fluid status and correct hypovolaemia
- Perform lung recruitment as at risk of atelectasis
- Identify and treat diabetes insipidus (DI)
- Introduce vasopressin which reduces NA requirement and treats DI
- Give methylprednisolone 15mg/kg to max 1g asap.
- Vasopression – Reduces other vasoactive drugs (Dose 1-4 units/hr)
- Liothyronine (T3) – No clear evidence. May add haemodynamic stability (Dose 3 units/hr).
- Methylprednisolone in all cases (Dose 15mg/kg up to 1g).
The Process and the Role of the SNOD (with timescale)
At 0-4 hours
(1) Signs of BSD
(2) Referral to SNOD
(3) SNOD does initial assessment and checks organ donation register (ODR)
(4) SNOD discusses with Coroner
(5) SNOD goes to ICU to be present when bad news is broken to family.
At 4-8 hours
(6) BSD tests performed
(7) SNOD and ICU staff approach family collaboratively
(8) SNOD consents family and does PMH assessment
(9) SNOD does physical assessment of patient
(10) Bloods are taken for tissue typing and virology
(11) Organ function assessment
(12) Donor management instigated
- Ongoing ICU care, lines, recruitment, bloods, CXR, urinalysis, pregnancy test, echo, ABGs, drug treatment
At 8-14 hours
(13) Potential donor registered with NHSBT duty office via electronic offering system (EOS)
(14) Organs offered to recipient centres
At 11-17 hours
(15) Theatre team mobilised
(16) Ongoing donor management and NOK support
At 14-23 hours
(17) Retrieval can take up to 6 hours
(18) Perfusion of organs
(19) Organs packed for transport
(20) NOK follow-up
Ethical Issues in Organ Donation - Dr. Tom Pratt
- Religious and cultural differences of opinion as to whether brainstem death represents true death
- Organ donation after assisted suicide – in Belgium and Switzerland
- Incentives in Israel have increased donations
- Wales to introduce presumed consent
Facilitators: Dr Tim Martingdale & Dr Kayode Adeniji
Summary written by: Dr Tim Martindale
Journal presentations - James Keegan and Ben Thomas. Historical papers looking at how and why we have developed the weaning strategies that we now have in place.
a) James Keegan - NEJM Esteban et all 1995. A comparison of four methods of weaning patients from mechanical ventilation.
- A cohort of mechanically ventilated patients, inclusion criteria was ventilated for over 24 hours. Randomised to PS/IMV/SBT (Spontaneous breathing trial) with weaning.
• Difference noted at day 4 with SBT groups with increased probability of weaning. Large proportion of extubations with SBT.
• This paper effectively put to be the use of IMV as a weaning technique.
b) Ben Thomas - Am J Respir Crit Care Med 1994. Brochard et al. Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mechanical ventilation.
- 3 modes of weaning from ventilator – T piece, SIMV, PSV. Less time apent ventilated than Esteban (>24 hours). Successful weaning defined as no ventilation for over48 hours. Failure conversely was reintubated within 48 hours post or struggling at 21 days.
• 456 met inclusion, 109 failed SBT
• Results: 23% failed at PSV at 21 days (p=0.05), decreased length of stay PSV had significantly fewer failures at 21 days.
The physiology perspective on weaning patients – Susan Calvert (Senior critical care physiotherapist, QA hospital)
a) Group discussion on reasons for failing weaning focussing on
i. Load eg Pleural effusions, extra pleural, fat, rib fractures, fibrosis
ii. Capacity eg Cardiovascular reserve, neuromuscular fitness
iii. Patient drive eg Cognitive engagement, reserve
b) Strategies aimed at optimising all components, eg cough assist, re-expansion manoeuvres etc
c) Rehabilitation improved by strength exercise. Avoidance of NMB and steroids.
d) Motivators, sedation level prompts by PT to nursing staff and doctors, increase mood by excursions etc.
Journal presentation - Balas et al, Effectiveness and Safety of the Awakening and Breathing Coordination, Delirium Monitoring/Management, and Early Exercise/Mobility Bundle. Crit Care Med
a) Multi centre trial attempting to create a multi-bundle package to firstly identify practicalities of implementation
b) Primary endpoint – number of ventilator free days (VFD) in cohort
c) Secondary endpoints
Prevalance, duration of ICU days of delirium and coma.
Mobilised from bed during ICU stay?
28 day ICU and total hospital mortality
d) 3 day reduction in VFDs, slight reduction in delirium, no difference in mortality
e) BUT very small numbers for 18 month trial, difficulty recruiting due to complexity, poor bundle adherence.
Bronchoscopy indications and practicalities - Dr Lesley Bishop
a) Indications for performing - lobar collapse, haemoptysis, diagnosis, biopsies
i. Lobar collapse - 4 case series and one case report (n=47). Good immediate outcomes.
ii. Hameoptysis – control of bleeding. But consider rigid bronch or IR as 1st line. One study showed increase rate of diagnosis from bronch (89%) vs CT (80%)
iii. Infection – BAL/Brush. Systemic review 2008, no difference in mortality, los. Bronchoscopy not superior to less invasive strategies as a diagnostic strategy. Used only if unable to identify an organism.
iv. Transbronchial Biopsies – Single case series, established diagnosis in 46%. Significant complications (31%) 2 pneumothoraces, 1 Haemorrhage, 1 Arrhythmia. n=13
v. Needle biopsies. 1 series (n=8) Sens 83&, Spec 100%, 63% led to change in management.
b) Discussion around procedures and equipment.
Weaning from mechanical venitation – Dr Kay Adeniji
a) Weaning from mechanical ventilation Statement of the 6th international consensus conference on ICM – seminal paper
i. Simple weaning
ii. Difficult weaning – 3 SBT or over 7d post initial SBT
iii. Prolonged weaning
c) Rapid shallow breathing index >100 = failure, Insp pressure >20 = failure (both very good NPV)
d) Emphasis of daily assessment of SBT 20-120 minutes (he uses 30 mins)
e) You must determine cause of failure of SBT
f) A cochrane analysis of use of a weaning protocol in the management strongly favours protocol (I2 97%) but no effect on mortality or los
g) Failure to ventilate generally occurs at 5 days. Use of bundles in ICU increases ventilator free days in a single centre study.
h) Prolonged weaners are those with ARDS, CHF/CAD, COPD
i) Summary of key points from respiratory weaning centres:
i. Ventilate adequately
ii. Get diagnosis right eg sepsis (persistent CRP), resp fluid overload, arryththmia, motivitaion
iii. Normalise bulbar function
iv. Wean to the appropriate level of support
Venue: University Hospital Southampton
Summary: Dr Phil McGlone
Trevor Smith Cons Gastro UHS.
- Gastric residual volume less than 200mls not evidenced based
- Only one study suggests that less than 500m is safe
- All PN vs EN trails are of high versus low volume feeding.
- The meta analysis from the early 2000’s are based on old, outdated trials and probably have little if any relevance to care in the ITU today.
Practical aspects of prescribing nutrition Mark Tomlin Cons Pharmacist
Malnutrition Universal Screening Tool (MUST)
1 - Score for low BMI (20, 18.5-20, <18.5)
2 - Score for recent weight loss (5%, 5-10%, >10%)
3 - Score for poor nutrition for last 5 days, or likely to be poor for over 5 days.
1+2+3 Score > 2 Identifies high risk patients
40% of hospital patients are malnourished and this is linked to slow recovery and poor wound healing. ICU patients may loose 10% of their muscle mass each week.
Is it evolutionary that we don’t eat when acutely unwell?
MUST score quantifies detection of malnourished patients for dietetic support (>2 implies refer)
Patients who are not eating oral foods normally get referred to dieticians
If still not eating orally, consider enteral tube feeding (NG, NJ, PEG).
Document length of enteral tube at nostril
Note position check. pH <5 aspirates (H2A,PPI) and X-ray
Use of a size 8fr will aid aspiration. Use a fine bore tube unless continuously high gastric aspirates and patient is at risk of aspiration
30 degree elevation to avoid reflux and aide diaphragm movement
Macronutrients - Normal
- 25-35kcal/kg/day total energy ave. 70kg = 1750-2450
- 1kcal per kg/hr (actual body weight)
- 6.2G protein = 1G Nitrogen
- (0.13-0.24G nitrogen) per Kg/dayave. 70kg = 9.1-16.8G N/day
- 30-35ml/kg/day fluid ave 70kg = 2.1-2.5L/day =>85-100ml/hr
- Fibre as appropriate
Macronutrients – Acutely unwell
- Energy total – 1500-2000 kcal/day, ideally 1:1 CHO to fat ratio
- Protein – 7-12 G N/day
- Fluid – 1-2.5L/ day, 40-100ml/hr
- However always first bag over 48hrs
- Not on same day of operation due to SIRS
- What can a sick or under-perfused liver utilise, before jaundice or ALP rise
- Bariatric patients still need feeding. Stress of ITU is not the time to diet. ABW for 1kcal/Kg/hr? (Obese IBW +25%)
- Increase rate of enteral feed in increments of 30ml/hr if gastric residuals remain <250ml at 4hrly aspirates
- Continuous feeding or physiological breaks?
- Achieving targets
- Phenytoin, doxy, cipro. Other IV/oral conversions
- TPN vs PN/EN do you believe in a trickle?
- Start at 30ml/hr standard feed
- Aspirate after 4 hours, if less than 200ml replace and increase by 30ml/hr until full rate (70-90ml/hr).
- If more than 200ml aspirate replace 200ml, discard remainder and decrease rate by 30ml/hr to minimum 10ml/hr
- At 10ml/hr, continue for 24 hours then add metoclopramide
- If still not absorbing after 48 hours, reduce opioid if possible to Morphine < 5mg/hr or Fentanyl < 2ml/hr
- add Erythromycin 500mg BD IV/NG
- After 48 hours (OR day 5) consider TPN
- Last resort, not an emergency
- Unstable mixtures, incompatible with other drugs, dedicated line
- Risk of line insertion
- Audit of line placement and X-ray check
- Plan for more than 5 days, or persevere with Enteral
- EN 10ml/hr to avoid gut atrophy and translocation
- Phased introduction of PN over 48 hours
- Phased re-introduction of enteral
- Reliable EN for 24 hours before stop PN
- Poor nutrition previous week –obvious and oesophagectomy, post op. actual calories
- Previous nutrition status (BMI<18.5kg/m2)
- Recent wt loss > 10% in 6 months
- Alcoholics, drug abuse, IDDM, laxatives, antacids, diuretics, cytotoxics
- Start with 10kcal/kg/day (70kg=700kcal)
- Slow increases
- Thiamine 200-300 (Pabrinex 250) per day
Vitamins & Minerals
Vitamin B compound Strong (2TDS RFS)
Vitamin C 500-1000mg/day (Pabrinex 500)
Selenium ACE 1 daily
Solvazinc 1 TDS
Sanatogen A-Z 1 daily
Folic Acid 5-10mg
Vitamin B12 – Hydroxocobalamin 1mg IM/IV
Don’t fiddle with the food to manage the fluid
Central preferred – but PICC, or peripheral
Maintenance - High flow
Minimal interruption – discuss
Not usually haemofiltration Lines
Expected other drugs, compatibility reshuffle
New Line – last option due to risks of insertion
Monitoring central lines
Parenteral nutrition is not a preferred option, it is undertaken when enteral is not possible.
Many of the problems of PN are due to gut atrophy, i.e. a lack of EN. Thus wherever possible give 10ml/hr EN to maintain gut integrity. PN for feeding the patient, EN for feeding the gut thus TPN is no longer appropriate
PN increases the infection risk but not mortality
PN is a planned event when EN has failed for 5 days. It is an inherently unstable mixture, takes 3 hours to make and costs about £100/day
Indirect Calirometry, Glutamine, & Selenium - Richard Lowe ST4 ICM
TEE - total energy expenditure
BEE – Basal energy expenditure
REE – Resting energy expenditure
DIT – Diet induced thermogenesis
AEE – Activity energy expenditure
TEE = (BEE + DIT + AEE)
RQ – respiratory quotient
CO2 produced (VCO2) / O2 used (VO2)
Normal range 0.7 – 1.2
Dependent on fuel source
Carbohydrate - 1
Protein - 0.8
Fat - 0.7
Production of chemical energy proportional to gas exchange
Weir equation used to calculate energy expenditure
Energy expenditure = (3.9VO2 – 1.1VCO2) – 2.17(urinary N2)
Abbreviated weir equation used
REE = (3.94 x VO2) + (1.1 x VCO2)
BEE may be significantly altered in critical illness
Obligatory feeding – PN
PN often results in overfeeding
Liver function abnormalities
EN often associated with feeding intolerance
BMR increased up to 40% in critical illness
Burns and trauma patients known to be heavily catabolic
Indirect calirometry (metabolic cart)
Substitute for calirometry (cumbersome / expensive)
Measures inspired & expired gas flows / volumes and concentrations (CO2 /O2)
Non invasive and accurate
Intensive Care Medicine Feb 2011
Randomized but unblinded
Mechanically ventilated for at least 3 days
Patients over 18
Expected to be ventilated > 3 days
Enteral nutrition with an energy target determined by INDIRECT CALIROMETRY
25 kcal/kg/day of enteral nutrition
PN used to supplement EN when needed
Primary outcome – 30 day survival
Length of mechanical ventilation
New pressure sores
Unplanned surgery / surgical complications
Assigned within 48 hours
REE calculated by IC
Deltatrac 2 monitor used
Fed enterally as per protocol
PN used to make up shortfall
Weight from patient / relative
IC measurements taken also
PN to make up shortfall from EN
Study group received more calories than measured to need
Control received less calories than calculated to need
Mean calorie intake significantly higher in study group
Study group patients had higher mean energy and protein intake
Significantly more in study group had PN in days 1 – 3
Trend towards lower mortality in study group with “intention to treat” p = 0.058
Significantly lower mortality for study group when “per protocol”
Hospital (28.5% v 48.2% p = 0.023)
60 day (57.9 +/- 9.9% v 48.1 +/- 7.6% p = 0.023
Similar ICU mortality
Increased length of ICU stay
Increased ventilation days
More total infections
Trend towards higher VAP
Dietician led care
Relatively small numbers
Could it be related to type of feeding
Was it just that they were fed more
Calculated energy requirements looked quite good
Feed (EN or PN) enriched with pharmaconutrients to
IMPROVE IMMUNE RESPONSE
MODULATE INFLAMATORY RESPONSE
Critical illness response
Oxidative stress and SIRS – free radicals, inflamatory cascade
Mitochondrial damage – contributing to MODS
Vitamins and trace elements taken into organs for protein and immune cell production
Relative deficiency of antioxidants
Non essential amino acid
Participates in many metabolic processes
Increased utilisation in critical illness
Plasma levels decrease
Low glutamine shown to have worse outcomes in some studies
Oudemans-Van Straaten 2001 Int Care Med (n = 25)
Favourable outcomes in burns patients – reduced bacteraemia, mortalilty and LOS
Garrel 2003 Crit Care Med
Canadian clinical practice guidelines suggest enteral glutamine should be considered in trauma and burns patients
When Parenteral nutrition prescribed to critical care patients glutamine supplementation “should be considered”
AVOID in patients with SHOCK and MOF - REDOXS
NEJM – April 2013
1223 patients – ventilated with 2+ organ failure
40 ICU’s: US, Canada and Europe
4 way randomisation
Glutamine give IV and oral
Dipeptiven 0.35 g/kg / day IV
42.5 g alanyl-glutamine / glycine-glutamine dipeptides enteral
IV selenium 500mcg
Selenium 300mcg enterally
Zinc - 20mg
Beta Carotene - 10mg
Vitamin E - 500mg
Vitamin C -1500mg
Trend towards increased mortality at 28 days in patients receiving glutamine
32.4% v 27.2% (p = 0.05)
No significant difference attributed to antioxidants
30.8% v 28.8% (p = 0.48)
In hospital mortality
6 month mortality
Median time to discharge alive
ALL SIGNIFICANTLY HIGHER WITH GLUTAMINE
No significant effect on secondary outcomes with antioxidants
Big study population
Relevant to our practice
High dose of glutamine
Low glutamine levels not consistently found in their patients
Funding – Fresenius / Biosyn
P = 0.044
Many patients excluded
Not all prescribed supplements given
Cocktail of antioxidants
Canadian clinical practice guidelines (2013) - Arginine
4 level 1 studies, 22 level 2 studies
No clear evidence of benefit (Mortality / infection)
3 studies showing possible harm (Bower / Ross / Bertolini)
NOT RECOMMENDED FOR CRITICAL CARE PATIENTS
Important precursor to glutathione peroxidase
Important plasma antioxidant
RDA 40 – 80 mcg/day
Selenium levels inversely proportional to APACHE 2
Angstwerm 1999 – replacing selenium increases glutathione
Number of studies
Cocktail of antioxidants – never alone
SIGNET study probably best study
502 ICU / HDU patients with GI failure needing PN
No clear evidence of benefit
Significant reduction in infections in selenium group who received PN for > 5 days
Recent Trials in nutrition Phil Mcglone ST5 ICM/Anesthetics
What does the recent literature tell us about how much and when to start nutrition in critical care?
Initial trophic versus Full enteral feeding 6 days
Trophic feeding – increase VFD
<48hrs of ALI onset
6hrs to extubation, death or 6 days
Protocol 25ml/hr to target 25-30Kcal/kg/day
90% achieved this
Protocol 10mls/hr (20kcal/hr)
VFDs to 28 days
Secondary end points
60 day mortality
Daily % of goal feeding
Organ failure free days
No significance difference
14.9 VFDs vs 15
Except GI intolerance
Regurg .4 vs .7 %
Vomiting 1.7 vs 2.2%
Elevated GRVs 2.2% vs 4.9% (>400mls
Modest differences in calorie provision for well-nourished patients during the first week of ALI/ARDS does not appear to affect patient outcome in the ICU.
Reduced-calorie feedings may reduce perceived GI intolerance and decrease administration of prokinetic and anti-diarrheal medications.
What doesn’t it tell us
BMI 30, these patients were well nurished
AGE 50 these pts were young
Severe malnutrition were excluded
½ extubated within 6/7 so quite early!
GI difference no clinical ramifications in the study….
Enteral nutrition fewer complications
Miss Targets however
? Combining Parenteral and Enteral
Liver dysfunction, infection and death
controversy regarding PN
underfeeding with EN alone for up to 7-10 days (American guidelines)21
supplemental PN (European) within 24-48 hours in patients who are expected to be intolerant to EN within 72 hours of admission.
Canadians conclude there are insufficient therefore maximize the benefits of EN (small bowel feeding tubes and motility agents) are used prior to starting PN.
Proponents of the use of early supplemental PN have focused on data demonstrating that the cumulative energy deficit or caloric debt is associated with adverse clinical outcomes in critically ill patients.24
Opponents cite the literature demonstrating increased adverse events in patients who receive PN during their ICU stay.
Data from existing randomized trials are inconclusive
PN to prevent caloric deficit
Supplement EN early in disease
Lead to reduced complications
Withholding PN for 1/52
MC 7 ICU’s
2328 patients delayed PN until day 8
2312 patients received PN within 48hrs
Admission to a participating ICU, a nutritional risk screening (NRS) score of 3 or more (on a scale of 1 to 7, with a score ≥3 indicating that the patient was nutritionally at risk) and did not meet any of the exclusion criteria.
The primary end points
ICU days (for survivors and nonsurvivors)
time to discharge from the ICU.
new infections, infection site, duration of antibiotic therapy, inflammation (C-reactive protein), time to vent wean, need for tracheostomy, acute kidney injury, need for and duration of pharmacologic or mechanical hemodynamic support, liver dysfunction, duration of the hospital stay and time to discharge from the hospital, functional status according to the distance walked in 6 minutes and the proportion of patients who were independent in all activities of daily living, and the total incremental health care costs from randomization to hospital discharge!!!!!
The early PN group
D20 at 45 mL/hr on the day of admission
day 2 the difference between calculated goals and the amount of EN was provided as PN.
When EN provided at least 80% of nutrition needs PN was held.
The late PN group
D5 to meet whatever hydration was not provided by EN
only received PN if enteral feedings were not providing at least 80% of calculated needs by day 8.
corrected ideal body weight
with 24 kcals/kg for females > 60 years
30 kcals/kg for females < 60 years
30 kcals/kg for males > 60 years
36 kcals/kg for males < 60 years.
The primary outcome
median stay in the ICU was 1 day shorter in the late-initiation group than in the early-initiation group.
There was a statistically significant increase in the likelihood of earlier discharge alive from the ICU (hazard ratio, 1.06; 95% confidence interval [CI], 1.00 to 1.13; P=0.04).
There were no significant differences in ICU, hospital or 90-day mortality between the groups.
The median duration of hospitalization was 2 days shorter in the late-initiation group
There were significantly fewer patients that developed new infections in the late-initiation initiation group,
Duration of mechanical ventilation and the course of renal-replacement therapy were significantly shorter in the late-initiation group.
“Early initiation of PN to supplement insufficient EN during the first week after ICU admission in severely ill patients at risk for malnutrition appears to be inferior to the strategy of withholding PN until day 8 while providing vitamins, trace elements, and minerals. Late parenteral PN was associated with fewer infections, enhanced recovery, and lower health care costs.”
How Do These Results Apply?
Can these result be generalized to all Critical care
early PN group received a large parenteral glucose load (1200 kcal) over the first 48 hours
Van den Berghe study.10 This concept of tight glucose control has subsequently been shown to be ineffective and potentially harmful.
How Do These Results Apply?
ninety percent surgery patients (mostly cardiac),
(58.5%) appeared to be admitted electively.
70% of subjects averaging only a 3-4 day length of stay.
Only moderately severely ill, with an 8% ICU mortality (and 11% hospital mortality).
Almost 75% of study patients had a normal or slightly high BMI between 20 and 30.
Most practitioners would not consider there to be a role for early PN in low mortality risk patients with short ICU stays and a normal BMI
Finally, it is hard to attribute the adverse events seen in this study to early PN, when the majority of study patients received very little exposure to early PN.
(58%) of the patients in the early PN group were exposed only to 1 to 2 days of PN.
Only 25 % late PN patients ever received PN.
It is plausible that the increase in adverse events seen in this study in the early PN group were due to the delivery of a large glucose load in the first 48 hours in the ICU. This may be related to increased insulin resistance in the early phase of acute illness.
While early PN in low risk patients is clearly harmful, it is not clear whether supplemental PN added to insufficient EN early in the course of high risk patients would also be harmful
EPaNIC results targeted wide spectrum of patients
Systematic reviews show benefits PN when EN Contraindicated mortality and infection however these were based on Small Trials
Uncertainty surrounding infection implications
This is reflected in the guidelines Reflected in guidelines within 24-48hrs (European) vs 7-10days (US)
RCT, single blinded
Assess effects of PN within 24hrs of ICU admission
With short term relative contraindications to enteral nutrition.
Within 24hrs admission
Expected to stay remain on ITU calendar day after enrolment
Considered to be ineligible for EN as decided by attending
Were not expected to get EN day of or after enrolment
Not expected to survive 24hours
Known long term contraindication to EN
Height < 140cm
Malnutrition as primary reason for admission
Received PN on day 1 and reached goal calories by day 3
Reevaluated day 3 for EN
60 day mortality
Quality of life and physical function measures
Tertiary end points
Fat loss, muscle loss etc
No difference in 60 day mortality
Statistically difference in quality outcome measures but not enough to meet the pre established definition that would be clinically meaningful
No difference infection rate
1.07 days fewer ventilation early PN
0.43 fewer coagulation failure days early PN
Less Fat and muscle wasting early PN
Early PN reduced mechanical ventilation days
Did not shorten hospital stay of ICU stay
No harm in early PN
Subjective opinion that patient could not have EN
Bias as investigators knew which group ? Earlier extubation
25% PN <48hrs in >1/3 standard care got PN
? Too similar to detect difference in infection rate
?? Measures of Fat and Muscle loss, skin fold and upper arm measures shown to be poor
I would have liked to have seen europe vs US debate answered.
Allowing larger tx differences
More likely to see outcome differences
Indeed subgroup analysis of 40% standard grp whom remained unfed maybe useful
EN – GI intolerance
PN – Infectious problems ? Reducing
Formulations and central access improvements
The primary objectives:
To estimate the effect of early (defined as within 36 hrs of the time/date of original admission to the ICU) PN compared with early EN on mortality at 30 days.
To estimate the incremental cost effectiveness of early PN compared with early EN at one year
Secondary objectives: to compare the following:
Duration of specific & overall organ support in the ICU between PN & EN
Infectious & non-infectious complications in the ICU between PN & EN
Duration of ICU & acute hospital length of stay between PN & EN
Mortality at discharge from the ICU & from hospital between PN & EN
Mortality at 90 days & at one year between PN & EN
Nutritional & health-related quality of life at 90 days & at one year between EN & PN
Resource use & costs at 90 days & at one year between PN & EN
Estimated lifetime incremental cost-effectiveness between PN & EN
Patients who either on, or soon after admission within 36 hours that are:
Adult (18 years or over)
An unplanned admission (including planned admissions becoming unplanned e.g. unexpected postoperative complications)
Expected to receive artificial nutrition for two or more days in the ICU
Not planned to be discharged within three days from the ICU
Results to follow !!!
1. Microbiology Quiz (and answers!) - download here
2. Clinical Implications of antibiotic pharmacokinetic principles in the critically ill (NEJM 2013) - critique by Dr Emma Fitzgerald - download here
3. Summary of lectures
Author: Dr Ben Harris
Fungal infections in the ICU – Dr Chesterfield
- Very few places have a specific fungal infection (ITU) policy – national survey, Chalmers et al, 2011.
- A few units screen for candida on admission
- 10% colonised on admission to hospital
- 80% are colonised by the end of their ITU stay
- Of that 80% in ITU, 5-30% develop invasive candida – blood/peritoneum etc.
- Colonisation is a risk factor for invasive disease so in PHT they try and identify & type & find out sensitivities for all candida positive cultures so if it becomes a problem later on they are ahead of the game.
- Diagnosing invasive candida is not easy
- Blood cultures only have a 50% chance of being positive in a known case of candidaemia.
- Slow growing 2-3 days
- There are some other PCR and beta D glutan tests but they have to go off to a reference lab and therefore this limits their clinical use
Clinical predictors of invasive candida infection are
Increasing numbers of positive cultures over time in an increasing number of sites (e.g. NBL, then wound swab, then urine)
Candida present in more than 2 sites
Colonisation index: Number of distant sites colonised:total number of body sites cultured. If >0.5 suggests high risk of invasive candida
Other risk factors for invasive candida:
- Multifocal colonisation o TPN
- Severe sepsis
- ITU stay >7 days
Empirical antifungal therapy
- Very variable the approach to this. Depends a lot on the individual microbiologist.
- Virtually all agree candida on an NBL or BAL or ET aspirate is not significant. Candida pneumonia is very rare.
- Threshold for empirical antifungals falls with multiple sites of colonisation, still spiking temperatures, or if they have liver cirrhosis (higher risk).
- Who benefits most from empirical antifungal treatment?
- Those who have risk factors (liver cirrhosis, GI perforation), have multiple colonisation sites, who are immunosuppressed, who continue to spike fevers despite antibiotics etc.
What is the empirical antifungal of choice in the ICU?
caspofungin and then change to fluconazole when sensitivities come back. Remember that lots of people are on prophylactic fluconazole in the community so no point giving them the same agent as treatment.
Up to 40% mortality with invasive candida, worse if a non-albicans species.
Infectious disease society of America is the ‘gold standard’ guidelines for invasive candida.
Use caspofungin for invasive candidia and switch to fluconazole if sensitivities allow.
Need a two week course (clock starts from time of last negative culture). Things to look out for in invasive candidia infections
Need to do retinal examinations to rule out endophthalmitis (15% risk of this, treated with surgery or intrathecal amphotericin)
Echo to exclude seeding to the heart.
Lines are often the focus of candida, remove for 48 hours after a positive culture if possible.
Ideally try to be ‘plastic free’ or ‘plastic minimal’ for a period of time after diagnosis of invasive candida.
Remember many antifungals can be given orally so might not need a line (less likely in ITU)
Common ITU scenarios
Candida on NBL/BAL/ET aspirate has a VERY poor predictive value for candida pneumonia.
This is different if you have candida in NBL, urine and elsewhere. This represents an increasing risk of invasive disease as described above.
Candida in the urine
Don’t treat unless high risk of dissemination such as neutropenia, sepsis, undergoing urological intervention.
If treating you should get urological imaging to exclude fungal balls in ureters. o Antifungals in those groups not at risk of disseminated infection make little difference, 75% clear candida on their own with no treatment. Don’t forget to remove the catheter!
Single positive culture + cirrhosis + not getting better
- Start treatment with antifungals.
- Stop if subsequent cultures negative? No as only 50% ever are positive.
- Better to continue for 14 days and then review.
- Remember swabs are hard to interpret due to colonisation so if feasible try to send tissue samples
Resistance patterns: Dr Wyllie
- Main ITU infections are pneumonia, urine and surgical wound infections
- Catheter related bloodstream infections are getting really rare!
- Ecoli and pseudomonas most common in ITU
- It is increasingly common for community acquired pathogens to be resistant to common antibiotics, a relatively new phenomenon in the last few years.
- ‘Replacement pathogens’ common in the ITU such as candida.
- It is more critical than ever to get specimens because of all the multi-resistant bugs in the
- 100% of NBL’s in 2012 from ITU grew something.
- Co-amoxiclav resistance rates in coliforms, most common NBL isolate, now 30-40%
- The big worry is the EXPLOSION of Tazocin use for HAP.
- Use of Tazocin has gone up 200% in the last 4 years in PHT
- Use of meropenem has gone up 100% in the last 4 years at PHT
- Ciprofloxacin resistance is very low but very good to give you CDIFF and MRSA!
- Tazocin usually has good pseudomonal cover
- Rotation of antibiotics over time throughout the region is a good idea to reduce resistance
but there are not enough antibiotics out there to do this!
- Gentamicin resistance is low in PHT so far but a big problem in some London hospitals.
Most wound swabs will grow something but is it important?
A new beta lactaminase has been found that can inactivate Tazocin.
MRSA is now very rare in PHT, not in USA though.
- Meropenem resistant pseudomonas is increasing in prevalence, especially in southern Europe.
- In Europe, southern Europe is really bad for multi-drug resistant bugs. Italy seems to be especially bad.
- Need to remember that any exposure to healthcare systems in Southern Europe is a really big risk factor for the patient having a multi-drug resistant bug. Remember it’s not just holidays but also medical tourism – for cosmetic and other surgery.
The problems are not just due to antibiotic overuse. It is the whole package
- Hand washing
- Use of antibiotics in animals
- Seeing as MRSA has plummeted after a focus on hand washing etc. practice before must have been terrible!
- With these nasty bugs the aim is to Identify & Isolate ASAP
- Faecal transplantation: Five done in Portsmouth due to CDiff diarrhoea. Close family members screened or there is a pool of screened lab staff who can donate. NJ tube. Well tolerated. 80% success rate for difficult to eradicate CDIFF in PHT. Some patients are so fed up of diarrhoea they have asked for faecal transplantation.
Q&A session: Dr Wyllie & Dr Adeniji
What can ITU do better? Nothing really, no inappropriate antibiotic prescriptions in PHT ITU.
Next pandemic of flu, are we ready? Yes, after SARS the communication and surveillance mechanisms are much better now. There is the technology and communication now for a quick response and quick vaccine production so yes, we probably are ready.
CSF specimens: Ideally get CSF in meningitis BUT not always straight away if worried about ICP. PCR can be done 48 hours after antibiotics. CT scan ok but ?raised ICP? This is a difficult one because without fundoscopy (which unless you are doing it regularly) is not that helpful, and papilloedema is a late sign) then you only really have the CT and clinical examination to go on. Beware the time lag between the CT report and the LP – raised ICP might have developed. You have to balance the risk of finding out what the bug is vs doing the LP and coning. Balance of risk. Now that we have molecular tests you don’t have to rush in to get a CSF sample necessarily.
Do aprons make a difference? As part of the whole package (hand washing etc.) yes they do.
Line sepsis: PICC lines have less incidence of infection for several reasons. They are further from the mouth and all its associated bugs, they are often put into ‘less sick’ patients. They are often less exposed to bacteria as they commonly are used in patients at home rather than in hospital. Always wait for the chlorhex in alcohol to dry when putting in any line.
Suspected line sepsis – issues.
No evidence to remove lines at 7 days BUT there are severe financial penalties attached for infections.
Arterial lines – have a much higher threshold to remove as they are difficult to put in, are painful to put in and are associated with blood coming out rather than stuff going in i.e.cvc’s.
Although MRSA bacteraemias are rare, MSSA, bacteraemias are still occurring. This is a really significant infection with significant morbidity attached.
- Remove the line if worried and try to get paired line and peripheral cultures.
- Selective gut de-contamination in the ITU
- We already do this a bit, chlorhexidine mouthwash!
- The trend of all the evidence is that it probably helps but the worries about resistance will only really be answered with trials going on for 10 years or when its use becomes
- The antibiotic to use will depend on the local flora and patterns of resistance.
- Abdominal sepsis
- Remember gentamicin and metronidazole is for SURGICAL PROPHYLAXIS only
- If they have abdominal sepsis you should use;
- Amoxicillin + gentamicin (single dose) + metronidazole o Or tazocin + gentamicin
- If using Tazocin you don’t need metronidazole.
Should be 5mg/kg, maybe even 7mg/kg as that’s what the original nomogram was based on.
Date: 22nd October 2013
Venue: Queen Alexandra Hospital, Portsmouth
Facilitators: Dr Emma Fitzgerald & Dr Sara Blakeley
Author of summary: Dr Emma Fitzgerald
1. Introduction - Emma Fitzgerald
- Summary of the reasons why we use scoring systems in ICU. They are largely most useful in the context of research and to a limited point in audit.
- Explanation of the way in which the scoring systems are constructed (i.e validation and discrimination)
- Overview of the classification and common ones
- Discussion about the limits of the different scoring systems
2. SOFA Score - Ben Harris
Summary and demonstration of the score – a sequential scoring system
Simple measurements of organ dysfunction
Ability to regular scoring to monitor and plot a trajectory
Able to be used by anyone
Easy to do
Not so good as predicting mortality as APACHE II
Which values to use in the score input data at which time is tricky.
3. APACHE II Score - Ruth Thomas
Worlds most widely used severity of illness score.
Summary of score – Acute physiology Score + Age points + Chronic Health points
APACHE III -1991 & 1997
Added in haematological malignancies
Stats package under strict licensing and so not widely used
Could be used for prediction of length of stay in ICU.
APACHE IV – 2002/3
Can be used to look at ICU length of stay and efficiency of units – best predictive accuracy
APACHE systems slightly superior to SAPS and SOFA for prediction of mortality
COMBINING SOFA and APACHE II best when combined – i.e. complement rather than compete with each other
Cons – needs to be continually updated.
CONCLUSION – Not that useful! Combination is better than 1 alone
4. TARN - James Keegan
Overview of the TRISS score and how to calculate it. Used up until 2004
- Out of date
- Lots of variables not recorded and so couldn’t be calculated
- Transferred patients and intubated patients were excluded – v skewed
More complicated score validated from more recent data.
Removed physiological variables from the equation
Compared the estimated probability to actual survival to give individual hospital data
It is the best we have got
Acts as a driver for improvement – people are starting to measure themselves against it
Open to public interpretation
Key performance indicators – no evidence base for these
Consultant trauma team leader
Time to CT
Airway management GCS<9
Useful measures of performance and can help drive improvements in
Also, it is useful to use the scores to measure trends over time.
The interpretation of the data from Southampton e.g time to intubation has been improved since starting to collect the data
The time constraints enforced – can be detrimental and also difficult to make a clinical decision with regards to response to treatment in a short space of time
5. Quality Measures - Neil Richardson
Defining quality – Quality and safety are inextricably linked in healthcare
Quality indicators are different to minimum standards
They can be categorized into STRUCTURE, PROCESS, OUTCOME
Deciding on which ones to use
They need to be 1) Relevant & 2) Important to clinician 3)Measurable 4) Evidence based
Who decides which ones to use In the UK?
Critical care networks, ICS,
ICS Indicators - 2009 (through a questionnaire)
Low response rate. Used Likert 5-point scale
They used these:
1. Availability or presence of ICU doctor 24/7
2. Nurse: patient ratio
3. Number on non clinical transfers
4. Hand hygiene compliance
5. Regular review of unit morbidity and mortality
6. Unitacquired bacteraemias
7. Unitacquired MRSA infection
8. Catheter related blood stream infections,
9. Unit acquired c. difficile or MRSA
10. End of life care pathway
11. Standardised Mortality Ratio (SMR)
12. Patient with infections appropriatelyisolated
13. Instigation of early appropriate enteral nutrition
14. Days of 100% occupation of the unit
15. Operational Daily Rounds Sheet
16. MDT ward rounds take place
17. Structured handover in place
18. Readmissions within 48 hours
19. Proportion of discharges between 2201 and 0659
20. Quality improvement programme in place.
Additional ones from ESICM – expert discussion panel:
1. ICU fulfils national requirements to provide Intensive Care.
2. 24h availability of a consultant level Intensivist
3. Adverse event reporting system
4. Presence of routine multidisciplinary clinical ward rounds
5. Standardised Handover procedure for discharging patients
6. Reporting and analysis of SMR
7. ICU readmission rate within 48h of ICU discharge.
8. The rate of central venous catheter related blood stream infection.
9. The rate of unplanned endotracheal extubations.
Debate about the usefulness of the indicators on the list and whether it is the right way to measure quality or not.
Some may be political (e.g. nurse : patient ratio)
Some can be turned into standards (e.g MRSA)
Also have to consider what you do with the data once you have collected it.
.....Why do you want it ???.....Who is going to use it???