Patient manœuvres if awake:
- ‘Huff and puff’
- 1:100,000 adrenaline (1ml of 1:1000 into 100ml NaCl 0.9%)
- Tranexamic acid (IV + endobronchial)
- Interventional radiology / angiography
Patient manœuvres if awake:
Acute liver failure = syndrome of coagulopathy + jaundice + encephalopathy
Reduced glutathione reserves if poor nutrition, neuromuscular disorders
Raised ALT/AST found in 40% of patients taking ‘normal’ max dose of paracetamol 2 weeks.
NAC paracetamol OD. If in doubt of level, GIVE and continue. Giving ANYTIME after significant paracetamol level is beneficial.
In hyperacute ALF cerebral oedema predomiantes. With positive physchotic features i.e. agitated, delirium. Inter cranial hypertension carries high mortality.
NH3 – measurable and the trend. >200 predicts ICH. <75 is rare
Hypertonic saline. 3-30% NaCl. Aim for Na 145-155. Sedate + ventilate, normal CO2, CPP 60-80.
CVVHDF – removing NH3 affords CVS stability, irrespective of renal failure. High volume ultrafiltration
Steroids. Improve CVS stability, no change in outcome.
AoCLF: Terlipressin, Antibx, lactulose, Hb>7, plt > 50, fib >1
50ml in stomach balloon then pull back +/- CXR
Then approx 350ml in stomach balloon, then CXR. Rarely need oesophageal balloon
TIPPS – risk of encephalopathy for reduced risk of bleeding.
Offer 48-72 hours of ‘trial of therapy’ then reassess. Reasonable to offer full support, including renal replacement therapy (‘all or nothing’ approach), then reassess. Though renal failure is a bad prognostic sign, it should not be a self-fulling prophecy.
Good MDT working
Question is : can we get this patient through ICU to discharge to assessment for liver transplant? What is exit/end-game/long term plan?
NAC in non-paracetamol ALF is ‘routine’ (though not in Acute on Chronic Liver failure)
Refer+/-transfer to liver unit early, preferably prior to needing CVVHDF
Prognosis in ALF – acuteness? Speed of deterioration is important. Age? Burden of MODS
Markers of high severity: encephalopathy, INR>6.5, creatinine > 600
Change in SOFA score at 48 hours probably best predictor
Advanced Care Planning required patient focussed care and goal setting. doi:10.1002/hep.29731
When looking at creatinine and AKI consider underlying muscle mass (which is likely to be low)
Hepatorenal syndrome: urinary Na+ low. Terlipressin + Albumin
ATN: urinary Na+ high
SBP if WCC>250/mm3
Normal liver -> NAFLD –(inflammation/scarring)-> NASH -> cirrhosis
Aim to reduce protein breakdown as it is a catabolic state. Refeeding occurs due to gluocose load rather than protein. Unusual requirement is 25-30kcal/kg/day. In decompensated liver disease it is 35-40kcal/kg/day. Protein 1.2-1.5g/kg/day.
Vitamin C: should we supplement? : Current Opinion in Critical Care
— Read on journals.lww.com/co-criticalcare/Pages/articleviewer.aspx
very interesting, albeit small single centre non-randomised trial. Any takers for a RCT?
Leadership & Management – Merrill & Reid Social behaviour types/personalities. Know who you are and who you are dealing with.
Anaesthesia for PH/protecting RV – Goldilocks. Not overloaded, not undefiled, must be just right.
Pulmonary Hypertension: sPAP>40mmHg, mPAP>25. sPAP = RAP + 4x[TRVmax]^2
ECG: strain pattern. RAD. ST depression V1- V4
On echo: TR Vmax = underestimate.
RHS: TAPSE<15mm, RV thickness >5mm (in diastole)
Tips: Open, not laparoscopic surgery. A-line + CVC. Avoid ketamine/des/N2O (as they increase PVR). fiO2 0.6, PEEP 5-8. PaCo2 4-4.5. Warm everything. Post-op HDU/ICU. Phone a friend – local/own PH unit. Should they be for full MOS? What is disease trajectory? Beware NYHA Class 3-4.
Signs of problems: High CVP + low BP, low SpO2, reduced end organ perfusion. Consider cautious fluid bolus 150-200ml OR diuretic. Optimise ventilation, Keep in SR (Amiodarone +/- DCCV), avoid b-blocker. Start norad +/- vasopressin. Then adrenaline. Then milrinone. Then iNO, epoprostenol
Think: Is it the culprit or a bystander? Is it treatable? What further investigations (imaging, bloods, bx) will help?
Mortality: encephalopathy > ascites + bleed > other
Citrate RRT seems to be safe. However need to consider low Ca2+:Ca2+ ratio. Monitor for accumulation + toxicity
Use albumin for high volume replacement. Evidence only for paracentesis.
Adrenal dysfunction, so consider steroid (hydrocortisone 50mg qds) if increasing vasoconstrictor.
In GI bleeed -> start NG feed early (despite ‘protein load’ )
BM ventilation usually is biggest challenge. DL usually is ok – though increased difficult predicted in neck circ > 40 cm (especially > 50cm) + MP3. Apples worse than pears.
Proposed induction strategy:
Pre-O2 in ramped position, fiO2 0.8, PEEP 5-10
Early iGel instead of BMV
If predicted difficult DL/VL + can’t access neck think AFOI
Need patient centred (not doctor centred) outcome measures. Ideally standardised.
On fatigue. Samn Perelli scoring system.
In UK all population at risk of Vit D def which increases mortality which can be treated/reversed with treatment. Jury is out on ICU treatment of Vit D, however screening and treatment may be prudent/pragmatic.
VITDAL – ?
Currently in progress VITALISE, VIOLET
Vit D3 better than cholicalciferol.
Should we screen pre-op?
Consider having electronic frailty index (based on Rockwood method). Works with EMIS and SystemOne.
Assessment methods: Gait speed, Clinical Frailty Score, Edmonton Frailty Score
<0.2 unlikely to be bacterial sepsis (though has a lag-time of 2-4 hours from onset)
>0.5 likely to be bacterial sepsis
<0.5 consider stopping antibiotics
Pro-calcitonin guided antibiotic therapy may confer slight survival benefit and reduced lower antibiotic duration i.e. better stewardship
CCR 15th annual symposium
utilise other bacteria
SEPSIS – see NICE guidelines
Watch cumulative fluid balance – if 10% of TBW then likely to be fluid overloaded
no longer responsive to fluids
disadvantages outweigh benefits
Give: titrated volumes + re-evaluate
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?
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)
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)
[Imaging in acute respiratory failure]
– 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
Source control in sepsis
Perc>open if available
<24, sooner if severe sepsis/shock
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
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
VR goggles – google cardboard
Wii rehab – tennis, boxing
email@example.com or gelne.nl
ABCD of POCUS
Airway: Cricothyroid membrane location
Disability: optic nerve. measure 3mm depth then transverse diameter. normal is less than/equal to 5mm
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]
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
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
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
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 readiness criteria
Delirium – quetiapine
Reduced mood – mirtazipine
Above cuff vocalisation – 5L/min. for periods of 10-15min
cuff down 5min x3 then build up duration
[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
has increased M&M in anaesthesia:
BNP > 1400
6 min walk test < 250m
echo: pericardial effusion = strongest predictor of mortality
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
Sleep disorders breathing. OSA is different to OHS
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
HCO2 > 27
headache in mane
CVS greater than OSA
NIV IPAP 26-34
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
[JAMA Adverse effect of antibiotics in hospitalised patients]
consider deescalation/rationalisation at 72 hours
markers – procalcitionin, CRP?
An excellent summary:
Should we still be trying to modify the dysregulated immune response in sepsis? An interesting evolutionary perspective:
Although not improving (or worsening) mortality, if steroids reduce duration of shock and length of ICU stay then they are probably worth a go, given that the absolute possible increase in risk of noteworthy adverse outcomes is very low, although this must be borne in mind. Could still argue it either way though. When we can genotype patients we may be able to identify those specific individuals in whom steroid may do significant benefit or harm. Or maybe not!
Useful online educational resource for ICU covering, amongst other things, ECMO and echo.