15th Annual Critical Care Symposium – notes

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?

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