(not perfect in my opinion, but helpful and informative nonetheless)
(not perfect in my opinion, but helpful and informative nonetheless)
Works as long as:
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)
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
An important question might be along the lines of ‘are there any outcomes for you that would be worse than death?’
Gleaned from our local vascular access expert that I had the pleasure of observing and learning from:
Reference: White et al.
Anaesthesia. 2019 Mar;74(3):357-372. doi: 10.1111/anae.14530. Epub 2019 Jan 11
Take home messages:
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
Useful summary of vascular access devices: