Academic Day Seminars – Sept 16

✔ Delirium:

Take home points:

  • Delirium = “Acute Brain Failure”
    • Acute: onset and fluctuating course of symptoms
      • Impaired: attention, cognition, consciousness
      • Supportive features: hallucinations, illusions, delusions, emotional lability, disturbances of sleep-wake cycle
    • Diagnosis: Confusion Assessment Method (CAM)
  • Types:
    • Hypoactive: confusion, sedation, less often has psychotic features
      • often misdiagnosed as depression, dementia or unrecognized
    • Hyperactive: hallucinations, delusions, agitation, disorientation
      • <5% of ICU delirium are purely hyperactive motoric subtype
    • Mixed
    • >75% of delirium cases are either HYPOactive or mixed!
  • Risks of delirium:
    • Beginning of the down-hill side: Once delirium resolves – in the next year, patients still have a high risk of mortality and residual cognitive deficits which impairs their functioning
    • In hospital: ↑ length of hospital stay and mortality
  • Risk factors:
    • Age > 75 yo
    • Dementia
    • Alcohol misuse
      • Alcohol/drug withdrawal
    • Depression
    • Electrolyte imbalance
    • Relocation
    • Restraints
    • Functional impairment
    • Cognitive impairment
    • History of delirium
    • History of hypertension  (associated with delirium in ICU)
    • Hypotension
    • Hearing/Vision impairment
    • Comorbidity or severity of illness (e.g. high severity of illness at admission)
    • History of TIA/CVA
    • Hypoxia
    • Infection
    • Multiple co-morbidities
    • Surgery/anesthesia
    • BZD use, Narcotics, Cardiac drugs, Anti-psychotics, street drug use
    • Sleep disturbance
    • Coma
    • Receiving 5 or more medications
    • Insufficient data on relationship between propofol use and delirium

From Sue Corrigan’s Slides:

P Pain Assess pain management
Poor Nutrition Dehydration, malnutrition, Assess albumin/protein, lytes, vit def
R Retention Urinary retention, assess fluid in/outs
Restraints Minimize, explore alternatives
I Infection / Injury Consider UTI, pneumonia, wound, diarrhea.   MI, CHF, hypoxemia (COPD).  Recent surgery, trauma, stroke
Immobility Change from premorbid function
M Metabolic Assess acid-base, lytes, renal fx, glucose, albumin
Medications Polypharmacy, anticholinergic meds, BZDs, opioids, antiemetics, glucocorticoids, withdrawal syndromes, toxicity (dig, phenytoin)
E Elimination Constipation / impaction
Environment Unfamiliar place, no exposure to daylight
S Sleep Altered sleep/wake cycle
Skin Assess for skin breakdown/wounds
Sensory Sensory deficits – does pt have hearing aids, glasses, dentures?

Another mnemonic for causes:

  • DIMS – Drugs, Infection, Metabolic, Structural

Summary of evidence:

Prevention:

  • Prevention of delirium: the thought is that incidence of delirium is not necessarily lower, but the severity of delirium is less
  • Haloperidol IV/PO: main evidence is in ICU post-op delirium
    vs. placebo:

    • may prevent post-op delirium in older adults going to ICU post-op
    • no difference in EPS or QT prolongation (as low doses were used)
    • evidence is not generalizable to other hospital pt populations
  • Anti-psychotics:
    • AVOID use prophylctically in older surgical patients to prevent delirium
  • Dexmedetomidine:
    • No evidence to prevent delirium in Adult ICU
    • ?MA showed slightly reduced incidence of delirium in ICU: RR 0.812 (0.68-0.968)
      • a lot of heterogeneity in MA
      • MA exclded cardiac surgery
    • Costs: 17x greater than haloperidol but potentially cost saving by reducing ICU LOS

Treatment:

  • Haloperidol IV/PO/IM:
    vs. other anti-psychotics, BZDs, morphine, ondansetron

    • Not compared to placebo arm (Maybe doing nothing would have produced the same results and patients’ delirium would resolve naturally)
    • Haloperidol was genrally safe
    • No strong evidence to support general use of haloperidol or alternatives to treat delirium in hospitalized older adult patients in terms of severity, duration, LOS, mortality
      • No difference in delirium severity, duration, length of stay or mortality
  • Cholinesterase inhibitors:
    • do NOT initiate to prevent or treat delirium without any other indication
  • Anti-psychotics:
    • If severely agitated or distressed and risk of harm to self/others AND other behavioural interventions have failed, may use antipsychotics at LOWEST dose/SHORTEST duration
      • scarcity of quality evidence
      • no difference between different antipsychotic agents
    • Atypical APs may reduce duration of delirium in ICU
      (QTP added to Haldol in 1 study)
  • Benzodiazepines
    • do NOT use 1st line to treat agitated post-op delirium in patients at risk of harm to self/others – may worsen delirium!
    • only role is with BZD-withdrawal
  • Benzodiazepines and antipsychotics have no role ESPECIALLY in patients with hypoactive delirium (exception may be in patients with hallucinations; however, these hallucinations may be comforting to have)
  • Dexmedetomidine (Continuous IV infusion):
    • may be used rather than BZD infusions to treat and reduce duration of delirium in ICU
    • Limited to med/surg ICU (not in cardiac surgery)

For post-op delirium, implement non-drug measures, such as:

  • sleep hygiene, early mobility, adaptations for visual/hearing impairment, nutrition and fluid repletion, pain management, appropriate med usage, adequate oxygention and constipation
  • AVOID medications that induce delirium post-op, such as:
    BZDs, anticholinerigcs, H2RA, sedative-hypnotices, meperidine
  • Optimize pain management with non-opioid pain medications!

Dexmedetomidine:

  • Selective alpha-2 agonist
  • Sedative, analgesic/opioid sparing
  • Anxiolytic and sympatholytic properties (no anticonvulsant properties)
  • Patients are more easily rousable and interactive with minimal respiratory depression
  • Onset of sedation: 15 min, peak: 1 hr, half-life = 3 hr (metabolized)
  • SE: hypotension and bradycaria

Application into practice:

  • Assess my patients’ history: changes in mental status, ROS, review current drugs, review alcohol and sedative use and PAIN!
  • Consider their neurological exam, labs (e.g. ammonia, urinalysis), ECG, CXR, arterial blood gases, EEG
  • If the team and I suspect delirium, to do the following:
    • Treat acute medical issues/underlying causes (e.g. hypoxia, infection, hydration, nutrition, electrolyte, glucose, pain, urinary retention, constipation, alcohol/BZD withdrawal)
      • For constipation, if following bowel protocol – consider what “DAY” of the protocol patient is actually on on admission
    • Reorient patient
    • Maintain safe mobility
    • Normalize sleep-wake cycle
    • REVIEW Medications and assess which ones should be de-prescribed
  • For medications, consider and reassess the following:
    • Any drug withdrawal from prior to admission or recent changes:
      BZDs, opioid, muscle relaxants (strong anti-cholinergic)

      • clean opioids: hydromorphone (less accumulation of active metabolite) and fentanyl (no active metabolite)
        – safer in renal dysfunction
    • Anti-cholinergics – eliminate if possible
    • Evaluate pain regimen (consider efficacy, safety and renal function)
    • Other CNS agents: anticonvulsants or antipsychotics
    • Other drug-related causes:
      OTC use of sleep-aids at home
      Blood glucose control? Electrolytes?
      Appropriate treatment of infection?
      Cardiac meds (e.g. Digoxin)
  • Treating with antipsychotics if appropriate (R/A every 24 hours):
    • Haloperidol 0.5mg po q6h prn
    • Risperidone 0.25-0.5 mg bid prn
    • olanzapine 1.25-2.5 mg bid prn
  • In adult ICU: implement routine monitoring with CAM-ICU and ICDSC

Resources:


✔ BC Case Wide Presentation:

This is a very useful session as my BC Case Wide Presentation is coming up in October.Everything was laid out very clearly and Sally Waignein provided great tips on preparing and executing case presentations!


✔ The Great Translators: Patient Advocacy

Take Home Points:

  • Introduce yourself and your role when doing bed-side rounds, etc.
    • Or go back to patients after rounds to introduce yourself and your role
  • Making time to listen and slowing down
  • Making connections with patients and building rapport, instead of going straight to the medical issues
  • Performing careful discharge counselling
  • Steps:
    Knock, Introduce yourself, Describe what you are there to do, Sit down & Slow down

    • Ask patients if this is a good time for you?
  • Asking:
    [Do you have “some” questions?] is a more positive question than [Do you have “any” questions?]

✔ Liver Function Tests:

Frank was the first of the residents to present on an Academic Day Seminar, and he did a great job on guiding us through liver function tests!

Take Home Points:

  • ↑ aminotransferases/ALP/GGT: markers of liver injury (not dysfunction)
  • Albumin, bilirubin, INR can be affected by extrahepatic factors (e.g. abs, nutrition, hemolysis)
  • When looking at changes in LFTs, identify:
    • MAGNTIUDE of enzyme alteration :
      • Mild
      • Moderate 5-10 times
      • Marked >10 times
    • Rate of change over time
    • Nature of course (trend)
  • Two predominant patterns:
    • Hepatocellular
    • Cholestatic

View LFTs in Pairs:

  • Hepatocellular damage/inflammation: AST, ALT
    • AST/ALT ratio
      >1: alcoholic liver disease (often >2), drug-induced injury, malignancy, cirrhosis, non-liver disease

      • AST and ALT require vitamin B6 as co-factor
        ALT is more dependent on B6 for its synthesis
    • >3x ULN – correlate with history/clinical picture or consider further investigations if asymptomatic
  • Chloestatic: ALP, GGT
    • causes: gall stone, abdominal masses, pregnancy, primary biliary cirrhosis, systemic sepsis, medications
    • General pattern:
      • ALP (>4x normal) and bilirubin are elevated
      • Sometimes, ALP is raised in isolation with a normal bilirubin
      • If GGT is also elevated, liver is the most likely source
      • If GGT is normal, source is likely non-hepatic
    • GGT: high sensitivity but non-specific
      • limited usefulness in isolation – raised in ANY liver disease (hepatocellular or cholestatic)
  • Useful indicators of hepatic function: albumin and INR
    • Albumin: has a long half life so many not be reduced in aucte liver injury

Drug causes of hepatocyte injury:

drug-causes-of-hepatocyte-injury

Overview of some conditions associated with LFT abnormalities:

Fatty Liver (steatohepatitis):

  • Non-alcoholic fatty liver disease:
    • suspected with risk factors (associated with metabolic syndrome, insulin resistance, diabetes and hyperlipidemia)
    • Hepatocellular predominant pattern
    • U/S shows echogenicity
    • AST/ALT
    • Mild to moderate increase in aminotransferases

Acute viral hepatitis:

  • Hep A, B, C, D, E, CMV, EBC
  • AST/ALT peak before jaundice, more gradual decrease after
  • Greater increase in serum bilirubin levels
  • Jaundice: Hep A (70%), Hep B (33-50%), Hep C (20-33%)
  • Always check history and exposure
  • If suspect acute viral hepatitis, check: Hep A IgM, Hep B IgM, Hep BsAg, HCV antibodies + HCV RNA test if negative for other tests

Chronic hepatitis:

  • may present with LFTs within normal range
  • pattern: AST/ALT ~100’s, decreased albumin
  • Chronic Hep B: Usually transmitted via sexual contact of IV drug use
    • <5% develop chronic infection after acute infection
    • Significant risk of developing liver damage (i.e. cirrhosis, liver failure, liver cancer)
  • Chronic Hep C:
    • usually transmitted by blood transfer (e.g. IVDU, sharing of needles)
    • >80% develop chronic hepatitis after acute infection
    • Carriers ta risk of developing liver damage

Ischemic/Hypoxic Acute Liver Damage:

  • Very high aminotrasferase levels (often >50-75x ULN)
  • Peaks and decreases rapidly
  • LDH raised 80% (ALT/LDH <1)
  • Rarely jaundiced
  • *Closely monitor bili and INR for risk of hepatic failure!*

Clinical Pearls:

  • Normal LFTs do not exclude liver disease
  • Degree of abnormalities in LFTs not always indicative of disease severity (not prognostic)
    • E.g. improve LFTs does not necessarily indicate that condition is getting better and hepatic damage is not there
  • Drugs may confound or modify LFT patterns – consider discontinuation of hepatotoxic agents
  • Always interpret with consideration of clinical context and underlying etiology
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