Category Archives: critical care

Notes from 6th East Mids Critical Care and Peri-op medicine conference

Fit for surgery school

Works as long as:

  •  1. patients attend
  • 2. in good time to make a change


Check BM and pregnancy status (to r/o eclampsia)

Status epileptics definition:

Status epilepticus is when a seizure lasts longer than 5 minutes or when seizures occur close together and the person doesn’t recover between seizures. Status epilepticus can be convulsive and non-convulsive.

1st line: lorazepam

2nd line 30mg/kg of valoprate or (if CI e.g. pregnant) then levetiracetem then 1g bd. Conveniently they have the same dose

3rd: consider phenytoin, thiopentone

NB thiopentone infusion – causes intravascular movement of K+, so risk of rebound hyperkalaemia. Also WCC and temperature regulation affected so unreliable to use to monitor for infection. May need serial cultures.

CT +/- LP

Check drugs levels, toxicology

Rx of limbic encephalitis: IVIG, plasmaphoresis, corticosteroids


Normal: 35.6 – 38.2 – diurnal variation. lowest in morning. increases in evening. mean 36.5

cultures it T>= 38.3 (SCCM & IOSA)

Opioid light acute peri-operative pain management

Pre-op counselling, ascertain and manage expectations.

If going to use gabapentin prob need 900-1200mg. Useful for chronic pain/complex patient? Could make very drowsy.

It is possible to do major surgery without opioids.

Dexamethasone – need >= 0.1mg/kg for effect

If using MR oxycodone or morphine then STOP before discharge

An option is clonidine 150mcg made up to 10ml and give 15mcg increments akin to morphine. NB will cause hypotension, so be patient and wait for long enough before giving next dose.

Ketamine. 0.2-0.4mg/kg (10-40mg) at induction, after midazolam, then bolus as needed


Peri-op shared decision making

An important question might be along the lines of ‘are there any outcomes for you that would be worse than death?’

Liver study day @ ICS

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.


Viral screen

Autoimmune screen

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

Sengstaken Tube:

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.

Principles of some liver units:

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

‘Early trache’



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

Validation of CLIF-C ACLF score to define a threshold for futility of intensive care support for patients with acute-on-chronic liver failure

Advanced Care Planning required patient focussed care and goal setting. doi:10.1002/hep.29731

Other thoughts

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.

ESPEN guidelines:

Some stuff on Procalcitonin


<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



15th Annual Critical Care Symposium – notes

CCR 15th annual symposium

Non-antibiotic therapies:



utilise other bacteria


SEPSIS – see NICE guidelines


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


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?


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)



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


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 goggles – google cardboard

Wii rehab – tennis, boxing or


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


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

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:



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


[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

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


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

EPAP 6-10


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?

ADRENAL trial – to steroid or not to steroid in septic shock

The original:

An excellent summary:

Should we still be trying to modify the dysregulated immune response in sepsis? An interesting evolutionary perspective:

My verdict:

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!