#1: HE is a sedated state. If hyperactive, suspect acute withdrawal (impt because Ativan worsens HE but should be used to prevent life-threatening withdrawals); PMID: PMID: 35598629
#2: West Haven Criteria
0: no encephalopathy
1: short attention span, euphoria/depression, sleep-wake disturbance ± asterixis (Ddx: OSA)
2: lethargy/apathy, disorientation, asterixis
3: somnolent but responsive to verbal commands, severe disorientation, no asterixis
4: coma
#3: Diagnosis is clinical; serum ammonia limited role ammonia in cirrhosis-associated HE (may have a role in acute liver failure); brain imaging (e.g., CT, MRI) if diagnosis uncertain or other causes for AMS suspected
UGIB. Hold low dose ASA or not? 1. Primary prev: stop indefinitely 2. Secondary: AGA guidelines rec continuing (conditional, very low certainty). When to restart: AGA rec on day hemostasis endoscopically confirmed (conditional, very low certainty)
🧵 : 1/3
Evidence for continuing (RCT small sample size)
- non significant increased risk of rebleeding in aspirin group
- significantly lower all cause mortality (and mortality 2/2 cardiovasc, cerebrovasc, GI complications) in aspirin group
Meta-analysis looking at timing of resuming ASA post hemostasis (very low certainty) but most thrombotic events ccur about 8d after aspirin stopped, and rebleeding occur within first 5 days in those who resume.
My takeaway, restart ASAP but definitely within 7 days!
Approach to conjugated hyperbilirubinemia taught to us by @dunleavy_katie. 1. Definition: T.bili elevation + >20% conjugated 2. Obtain RUQ US to look for ductal dilation 3. No dilation = intrahepatic cholestasis
- rule out non-ICU vs ICU causes 4. MRCP, ERCP, liver biopsy
Bilirubin thresholds:
- indirect bilirubin usually < 5-6 in massive hemolysis (if > 5-6, something else is going on)
- acute complete CBD obstruction: max bilirubin elevation usually around 15 (with time, hepatocyte dysfunction may cause higher elevations)
AST > ALT seen in 1. Alcohol (> 1.5:1): ALT usually only mildly elevated, AST usually < 300 2. Muscle damage 3. Wilson disease (> 2:1): usually < 2000. ALP:T.bili ratio < 4
Summary of oxygen delivery devices taught to me by Mayo RT
Source of oxygen
- Wall taps by bedside: 0–15L/min
- Home concentrator: 0–10L/min
Oxygen delivered at 100%, put through different devices at different rates to adjust the oxygen concentration that the patient inspires
TLDR
- Low oxygen (<35%): nasal prongs
- Moderate oxygen (35-60%): venturi (high flow but mix with room air)
- High oxygen (>60%): non rebreather or HFNC
- PEEP needed (e.g., ADCHF, OSA): CPAP
- Hypercapnic: BiPAP
- Failure, unable to protect airway: mechanical ventilation
0. Inogen (pulse-dose oxygen therapy); not used in hospital
- Delivers only during inspiration; not expiration
- Up to 4L but intermittent; much less oxygen as unlike continuous oxygen therapy which fills the oral cavity, naso/oropharyngeal with reservoir of oxygen, this does not
ABG vs VBG:
- pH: VBG
- pCO2: VBG (not accurate in shock or hypercapnia); ABG for severe shock or if precise pCO2 needed in hypercapnia
- PO2: ABG (but SpO2 generally good enough)
- CO or methemoglobin: co-ox