CCR 15th annual symposium
Non-antibiotic therapies:
liposomes
immunotherapy
utilise other bacteria
bacteriophage
SEPSIS – see NICE guidelines
Fluids:
Watch cumulative fluid balance – if 10% of TBW then likely to be fluid overloaded
Stop when:
Patient stable/improving
no longer responsive to fluids
disadvantages outweigh benefits
Give: titrated volumes + re-evaluate
Targets
SAFE study
Albumin ok. Maybe good in severe sepsis/septic shock
ALBIOS study: 20% HAS given to maintain alb > 30. No difference in outcome. Maybe improved outcome in septic shock
Is tissue oedema an indicator/surrogate marker of lung oedema?
Phylogenetic
Is fever beneficial or harmful? Consider cost/benefit ratio.
In mice fever increases local inflammation, reduces SIRS, reduced colony count. Improved survival in those allowed to mount fever.
Fever appears to be protective, unless too high. ?40C. However, does increase catabolism, O2 consumption, RR, etc
However paracetamol had no difference in 90 day mortality (but slight *improvement* in mortality in first few days)
CLASSIC trial
maternity death in sepsis often due to fluid overload
children die due to excess IV fluid
Fluid resuscitation has little effect on outcome in sepsis (compared to antibx within 1 hour, source control)
radial vs femoral arterial line – may be different traces in severe sepsis due to shutting down of radial artery. Palpate pulses (or insert line). Increasing vasopressor may not be the correct thing to do! ‘Should not die/go onto ECMO prior to insertion of femoral line)
[Dorman]
Litchenstein
CEURF protocol
BLUE protocol
FALLS protocol
AVPLAPS profile
[Imaging in acute respiratory failure]
shock protool
– Is the tamponade?
– Is there cardiogenic shock? is so primary cardiac? or obstructive secondary to PE?
– Is there tension pneumothorax? Stratosphere sign. + asymmetry of chest and AE
– Are there B-lines? cardiogenic shock
– this leaves hypovolaemia
– absolute i.e. hypovolaemic shock
– relative i.e. septic shock S-protocol for site of sepsis
pleural effusion (empyema) or pneumonia, peritonitis (ascites) or pneumoperitoneum, absent abdominal peristalsis of gut, air in portal tract +/- GB. renal tract – kidney ?obsturctive uropathy, ?pyelonephritis – bladder ?sediment/pus
CVP – does not predict fluid responsiveness
ScvO2 is approx SvO2. can target but no impact on outcome
SAP – related to LV afterload
DAP – related to vasomotor tone
PP – approx related to SV
PP variation = good marker of fluid responsiveness (in SV patient?)
[how applicable is PP variation in critical care]
On starling curve, on left the is PP variation, on plateau there is not
EVLW
Source control in sepsis
Perc>open if available
<24, sooner if severe sepsis/shock
[2017 SIS]
Values/targets: aim to optimise, not necessarily normalise
Pressure vs flow parameters
Vasopressor – SSG 2016. NE 1st line. EARLY – help CO (transfers blood from unstressed to stressed volume), contractility, might help to reduce cumulative fluid balance
retrospective r/v showed worse outcome when started late. duration and degree of hypotension is associated with M+M
reduced DAP suggests need for vasopressor
aim for higher MPA in chronic hypertension to give benefit to renal function
If there is increased CVP or increase abdo pressure consider NE
upper dose? 40% of patients with NE >1mcg/kg/min are discharged alive
After NE:
add vasopressin up to 0.03
add adrenaline BUT worse outcome in cardiogenic shock
Outcomes in ICU
Meanings that are important for all stake holders
[Donaghy BMJ quality and safety]
Quality indicators for rehab
Identify complex health and social needs -> refer to appropriate system
give info re: general generic ICU survivor info
provide access to a person if they need more support
point of contact
Discharge summary to GP
VR in ICU
Windtales
VR goggles – google cardboard
Wii rehab – tennis, boxing
p.spronk@gelre.nl or gelne.nl
ABCD of POCUS
Airway: Cricothyroid membrane location
ETT position
NGT placement
Disability: optic nerve. measure 3mm depth then transverse diameter. normal is less than/equal to 5mm
Transcranial doppler
SImulation in ICU. aartisarwal
Wake Forest School of Medicine / ICU
Simulate scenarios, patient flow, emergencies
For new ICU 3 stage process:
1. Info, orientation, checklists
2. simulated single patient
3. simulate multiple patients in parallel. actors are relatives, workflow
In severe ARDS:
cis-atracurium in first 24-28 hours improves outcome
+ protective lung ventilation (+/- super protective lung vent + EtCO2 removal – studies underway)
+ prone for 16 hours
[NIH PEEP TABLE]
Target driving pressure as a therapyeutic tool, individualised PEEP
Transpulmonary pressure = Paw – Ppl => causes VILI
If spot breathing can increase Ppl and therefore Ptranspulmonary
If using NIV – early intubation if no response
more likely to fail if confused, MOF
US diaphragm – excursion, thickening. ideally in right subcostal. can do ant axillary
Protective lung ventilation – NNT = 11 to prevent ARDS, NNT = 23 to prevent death
[child pugh score]
NAVA
useful in COPD + NIV?
better synchrony, maintain pressures
but does it improve outcome?
weaning failure secondary to pulmonary oedema/cardiac failure when doing SBT
High risk if COPD, cardiomyopathy, obesity
Dx: ?echo – LVEDP, increase E/A E’/A
raised BNP
haemoconcentration (when failed) – increase in plasma protein by 6%
lung US – if increase in B-line by at least 6 in total of 4 quadrants when comparing after to before
Therapeutic options:
nitrates
ACEi
B-blocker – for HR/cardiac stress/anti-adreneric
fluid removal – furosemide or RRT – **until PLR +ve**
[Weaning from mechanical went. Bronchurst? Int Care Med 2016]
secretions: anticholinergics – atropine drops (1% eye drops) 1-2 drops ads, or hyoscine patch, 7% NaCL nebs, carbocysteine
[WIND study]
SBT – should be using T-tube
Protocolised weaning. Daily SBT.
RF’s to failure: secretions, cough, LVEF <30%
In literature weaning failure rates are 10-20%
Weaning protocol
Sedation protocol
Weaning readiness criteria
Delirium – quetiapine
Reduced mood – mirtazipine
Manchester weaning:
Above cuff vocalisation – 5L/min. for periods of 10-15min
cuff down 5min x3 then build up duration
SALT
[Haven Crit Care]
In prolonged wean:
maintain good Vt (8ml/kg) to prevent atelectasis
control hypercapnia with adequate rest ventilation
sprints: deceased pressure support, decreased TC, cuff down – leading to SBT
then full rest
aim to increase duration of sprints
azetozolamide to centrally reset if high CO2
initially – mobilise + rehab during rest period
open adbo – usually with vac dressing
what can we do?
negative fluid balance/reduce oedema
early enteral nutrition
there will be excess fluid and protein loss – supplement, esp protein
sedation hold/no need to keep sedated
Pul HTN
has increased M&M in anaesthesia:
BNP > 1400
6 min walk test < 250m
echo: pericardial effusion = strongest predictor of mortality
Cardiac MR
If mild pul HTN – treat as normal
If mod – severe (may have NYHA FS III/IV) – regional / PNB if possible
NEVER stop prostacyclins
Prevent RVF – by preventing hyper/hypo everything i.e. maintain normality. Low PEEP, Pplat < 30, VT 4-6ml/kg
In subcostal view SETAK is approx same as TAPSE
look for mid systolic notch on continuous dopple across TV in TR
Obesity
Sleep disorders breathing. OSA is different to OHS
OSA
ODI = oxygen desaturation index – when SpO2 drops by 4%. if >15/hr is highly sensitive for OSA
Treatment: reduce weight, CVS risk management, CPAP (not optiflow) – with mask. PEEP 10-15 possiblly
OHS
obesity
PaCO2>6
HCO2 > 27
headache in mane
CVS greater than OSA
NIV IPAP 26-34
EPAP 6-10
General
Base Vt on Ideal body weight. 6ml/kg
sit at 45 degrees
PEEP 10-15. extuabte to CPAP/NIV
VTE. May need 0.5mg/kg enoxaparin of TOTAL BW
RV is sensitive to volume, pressure
systolic PAP>50
Peak TR>
[JAMA Adverse effect of antibiotics in hospitalised patients]
consider deescalation/rationalisation at 72 hours
markers – procalcitionin, CRP?
