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.
Useful summary of vascular access devices:
<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
Useful infographic from BMJ
For procedures up to (max) 2 hours duration.
Quicker recovery than bupivicaine making it suitable for day-case
3.5ml of 2% hyperbaric prilocaine +/- 20mcg fentanyl
Saddle block: 0.5 – 1.0 ml
> T10 block: 3+ ml
< T10 block: 2-3 ml
Perspective from The New England Journal of Medicine — What Is Value in Health Care?