Transcript Sedation, Analgesia, and Neuromuscular Blockade in the

Sedation, Analgesia, and Neuromuscular Blockade in the
Adult ICU
Giuditta Angelini, MD
University of Wisconsin
Madison, WI
Gil Fraser, PharmD, FCCM
Maine Medical Center
Portland, ME
Doug Coursin, MD, FCCM
University of Wisconsin
Madison, WI
What We Know About ICU Agitation/Discomfort
Prevalence
• 50% incidence in those with length of stay > 24 hours
Primary causes: unrelieved pain, delirium, anxiety, sleep
deprivation, etc.
Immediate sequelae:
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Patient-ventilator dyssynchrony
Increased oxygen consumption
Self (and health care provider) injury
Family anxiety
Long-term sequelae: chronic anxiety disorders and posttraumatic stress disorder (PTSD)
Recall in the ICU
Some degree of recall occurs in up to 70% of ICU
patients.
• Anxiety, fear, pain, panic, agony, or nightmares reported in 90% of
those who did have recall.
Potentially cruel:
• Up to 36% recalled some aspect of paralysis.
Associated with PTSD in ARDS?
• 41% risk of recall of two or more traumatic experiences.
Associated with PTSD in cardiac surgery
Need for Sedation
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Anxiety
Pain
Acute confusional status
Mechanical ventilation
Treatment or diagnostic procedures
Psychological response to stress
Goals of Sedation in ICU
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Patient comfort and
Control of pain
Anxiolysis and amnesia
Blunting adverse autonomic and hemodynamic
responses
Facilitate nursing management
Facilitate mechanical ventilation
Avoid self-extubation
Reduce oxygen consumption
Characteristics of an ideal sedation agents for the ICU
• Lack of respiratory depression
• Analgesia, especially for surgical patients
• Rapid onset, titratable, with a short elimination
half-time
• Sedation with ease of orientation and
arousability
• Anxiolytic
• Hemodynamic stability
The Challenges of ICU Sedation
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Assessment of sedation
Altered pharmacology
Tolerance
Delayed emergence
Withdrawal
Drug interaction
Sedation
Causes for Agitation
Sedatives
Undersedation
Sedatives
Causes for Agitation
Agitation & anxiety
Pain and discomfort
Catheter displacement
Inadequate ventilation
Hypertension
Tachycardia
Arrhythmias
Myocardial ischemia
Wound disruption
Patient injury
Oversedation
Causes for Agitation
Prolonged sedation
Delayed emergence
Respiratory depression
Hypotension
Bradycardia
Increased protein breakdown
Muscle atrophy
Venous stasis
Pressure injury
Loss of patient-staff interaction
Increased cost
Sedatives
Correctable Causes of Agitation
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Full bladder
Uncomfortable bed position
Inadequate ventilator flow rates
Mental illness
Uremia
Drug side effects
Disorientation
Sleep deprivation
Noise
Inability to communicate
Causes of Agitation Not to be Overlooked
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Hypoxia
Hypercarbia
Hypoglycemia
Endotracheal tube malposition
Pneumothorax
Myocardial ischemia
Abdominal pain
Drug and alcohol withdrawal
Daily Goal is Arousable, Comfortable Sedation
Sedation needs to be protocolized and titrated to goal:
• Lighten sedation to appropriate wakefulness daily.
Effect of this strategy on outcomes:
• One- to seven-day reduction in length of sedation and mechanical
ventilation needs
• 50% reduction in tracheostomies
• Three-fold reduction in the need for diagnostic evaluation of CNS
Protocols and Assessment Tools
SCCM practice guidelines can be used as a template for
institution-specific protocols.
Titration of sedatives and analgesics guided by
assessment tools:
• Validated sedation assessment tools (Ramsay Sedation Scale [RSS],
Sedation-Agitation Scale [SAS], Richmond Sedation-agitation Scale
[RSAS], etc.)
- No evidence that one is preferred over another
• Pain assessment tools - none validated in ICU (numeric rating scale
[NRS], visual analogue scale [VAS], etc.)
Strategies for Patient Comfort
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Set treatment goal
Quantitate sedation and pain
Choose the right medication
Use combined infusion
Reevaluate need
Treat withdrawal
Overview of SCCM Algorithm
ALGORITHM FOR SEDATION AND ANALGESIA OF M ECHANICALLY VENTILATED PATIENTS
Is the Patient Comf ortable & at Goal?
Yes
No
Reassess goal daily ,
Titrate and taper therapy to maintain goal,
Consider daily wake-up,
Taper if > 1 week high-dose therapy & monitor
f or withdrawal
Rule out and Correct Rev ersible Causes
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2
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Use Non-pharmacologic Treament,
Optimize the Env ironment
*
Use Pain Scale to
Assess f or Pain
Use Sedation Scale**
to Assess f or
Agitation/Anxiety
Hemody namically Unstable
Fentanyl 25 - 100 mcg IVP Q 5-15 min, or
Hydromorphone0.25 - 0.75 mg IVP Q 5 - 15 min
Hemody namically stable
Morphine2 - 5 mg IVP Q 5 - 15 min
Set Goal
f or
Analgesia
(except neuro pt.)
Use Delirium Scale*** to
Assess f or Delirium
Consider continuous
inf usion opiate or
sedativ e
Lorazepam via
infusion?
Use a low rate and IVP
loading doses
Acute Agitation #
Midazolam 2 - 5 mg IVP Q 5 - 15 min until
acute ev ent controlled
Ongoing Sedation #
Lorazepam1 - 4 mg IVP Q 10-20 min until
at goal then Q 2 - 6 hr scheduled prn,
+
or
Propofol start 5 mcg/kg/min, titrate Q 5 min
until at goal
> 3 Day s Propof ol?
4
Yes
Repeat until pain controlled, then scheduled doses
+ prn
Set Goal
f or
Sedation
Yes
IVP Doses
more of ten thanQ
2hr?
Benzodiazepine or Opioid:
Taper Inf usion Rate by
10-25% Per Day
Conv ert to
Lorazepam
Set Goal
f or Control
of Delirium
Haloperidol2 - 10 mg IVP Q 20 - 30 min,
then 25% of loading dose Q 6hr x 2-3 day s,
then taper
Jacobi J, Fraser GL, Coursin D, et al. Crit Care Med. 2002;30:119-141.
Doses
approximate for
70kg adult
Assess Pain Separately
Pain
Visual Pain Scales
0
No pain
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2
3
4
5
6
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8
9
10
Worst possible
pain
Signs of Pain
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Hypertension
Tachycardia
Lacrimation
Sweating
Pupillary dilation
Principles of Pain Management
• Anticipate pain
• Recognize pain
– Ask the patient
– Look for signs
– Find the source
• Quantify pain
• Treat:
– Quantify the patient’s perception of pain
– Correct the cause where possible
– Give appropriate analgesics regularly as required
• Remember, most sedative agents do not provide
analgesia
• Reassess
Nonpharmacologic Interventions
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Proper position of the patient
Stabilization of fractures
Elimination of irritating stimulation
Proper positioning of the ventilator tubing
to avoid traction on endotracheal tube
Address Pain
Is the Patient Comfortable & at Goal?
Reassess goal daily,
Titrate and taper therapy to maintain goal,
Consider daily wake-up,
Taper if > 1 week high-dose therapy & monitor
for withdrawal
Use Pain Scale * to
Assess for Pain
Set Goal
for
Analgesia
Hemodynamically Unstable
Fentanyl 25 - 100 mcg IVP Q 5-15 min, or
Hydromorphone 0.25 - 0.75 mg IVP Q 5 - 15 min
Hemodynamically stable
Morphine 2 - 5 mg IVP Q 5 - 15 min
Repeat until pain controlled, then scheduled doses
+ prn
Opiates
Benefits
• Relieve pain or the sensibility to noxious stimuli
• Sedation trending toward a change in sensorium, especially with more lipid
soluble forms including morphine and hydromorphone.
Risks
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Respiratory depression
NO amnesia
Pruritus
Ileus
Urinary retention
Histamine release causing venodilation predominantly from morphine
Morphine metabolites which accumulate in renal failure can be analgesic
and anti-analgesic.
• Meperidine should be avoided due to neurotoxic metabolites which
accumulate, especially in renal failure, but also produces more sensorium
changes and less analgesia than other opioids.
Pharmacology of Selected Analgesics
Agent
Dose
(iv)
Half-life
Metabolic
pathway
Active
metabolites
Fentanyl
200 g
1.5-6 hr
Oxidation
None
Hydromorphone
1.5 mg
2-3 hr
Glucuronidation
None
Morphine
10 mg
3-7 hr
Glucuronidation
Yes
(Sedation in
RF)
Meperidine
75-100
mg
3-4 hr
Demethylation & Yes
hydroxylation
(neuroexcitati
on in RF)
Codeine
120 mg
3 hr
Demethylation & Yes (
Glucuronidation analgesia,
sedation)
Remifentanil
3-10 min
Plasma
esterase
None
Keterolac
2.4-8.6
hr
Renal
None
Opioids
Morphine
Hydromorphone
Fentanyl
Lipid
Solubility
Histamine
Release
Potency
+/-
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1
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5
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50
Opioids
Onset
Peaks
Duration
Morphine
2 min
20 min
2-7 hr
Fentanyl
30 sec
5-15 min 30-60 min
Opiate Analgesic Options: Fentanyl, Morphine, Hydromorphone
Fentanyl
Rapid onset
X
Rapid offset
X*
Hydromorphone
Avoid in renal disease
Morphine
X**
Preload reduction
X
Avoid in hemodynamic
instability
X
Equivalent doses
100 mcg
* Offset prolonged after long-term use
** Active metabolite accumulation causes excessive narcosis
1.5 mg
10 mg
Sample Analgesia Protocol
Numeric Rating Scale
Sedation Scoring Scales
• Ramsay Sedation Scale (RSS)
• Sedation-agitation Scale (SAS)
• Observers Assessment of Alertness/Sedation Scale
(OAASS)
• Motor Activity Assessment Scale (MAAS)
BMJ 1974;2:656-659
Crit Care Med 1999;27:1325-1329
J Clin Psychopharmacol 1990;10:244-251
Crit Care Med 1999;27:1271-1275
The Ramsay Scale
Scale
Description
1
Anxious and agitated or restless, or both
2
Cooperative, oriented, and tranquil
3
Response to commands only
4
Brisk response to light glabellar tap or loud
auditory stimulus
5
Sluggish response to light glabellar tap or
loud auditory stimulus
6
No response to light glabellar tap or loud
auditory stimulus
The Riker Sedation-Agitation Scale
Score Description
Definition
7
Dangerous
agitation
Pulling at endotracheal tube, trying to
strike at staff, thrashing side to side
6
Very agitated
Does not calm despite frequent verbal
commands, biting ETT
5
Agitated
Anxious or mildly agitated, attempting to sit
4
Calm and
cooperative
Calm, awakens easily, follows commands
3
Sedated
Difficult to arouse, awakens to verbal
stimuli, follows simple commands
2
Very sedated
Arouse to physical stimuli, but does not
communicate spontaneously
1
Unarousable
Minimal or no response to noxious stimuli
The Motor Activity Assessment Scale
Score
Description
Definition
6
Dangerous
agitation
Pulling at endotracheal tube, trying to strike at
staff, thrashing side to side
5
Agitated
Does not calm despite frequent verbal
commands, biting ETT
4
Restless and
cooperative
Anxious or mildly agitated, attempting to sit
3
Calm and
cooperative
Calm, awakens easily, follows commands
2
Responsive to
touch or name
Opens eyes or raises eyebrows or turns head
when touched or name is loudly spoken
1
Responsive only to Opens eyes or raises eyebrows or turns head
noxious stimuli
with noxious stimuli
0
Unresponsive
Does not move with noxious stimuli
What Sedation Scales Do
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Provide a semiquantitative “score”
Standardize treatment endpoints
Allow review of efficacy of sedation
Facilitate sedation studies
Help to avoid oversedation
What Sedation Scales Don’t Do
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Assess anxiety
Assess pain
Assess sedation in paralyzed patients
Predict outcome
Agree with each other
BIS Monitoring
BIS Monitoring
BIS Range Guidelines
BIS
100
80
60
40
20
0
Awake
Responds to normal voice
Axiolysis
Responds to loud commands
or mild prodding/shaking
Moderate
sedation
Low probability to explicit recalls
Unresponsive to verbal stimuli
Burst suppression
Flat line EEG
Deep Sedation
Address Sedation
Is the Patient Comfortable & at Goal?
Reassess goal daily,
Titrate and taper therapy to maintain goal,
Consider daily wake-up,
Taper if > 1 week high-dose therapy & monitor
for withdrawal
IVP Doses
more often than Q
2hr?
Consider continuous
infusion opiate or
sedative
Use Sedation Scale **
to Assess for
Agitation/Anxiety
Set Goal
for
Sedation
Ongoing Sedation #
Lorazepam 1 - 4 mg IVP Q 10-20 min until
at goal then Q 2 - 6 hr scheduled + prn, or
Propofol start 5 mcg/kg/min, titrate Q 5 min
until at goal
> 3 Days Propofol?
(except neuro pt.)
Yes
Acute Agitation #
Midazolam 2 - 5 mg IVP Q 5 - 15 min until
acute event controlled
Convert to
Lorazepam
Lorazepam via
infusion?
Use a low rate and IVP
loading doses
Benzodiazepine or Opioid:
Taper Infusion Rate by
10-25% Per Day
Choose the Right Drug
• Benzodiazepines
• Propofol
• -2 agonists
Sedation Options: Benzodiazepines (Midazolam and Lorazepam)
Pharmacokinetics/dynamics
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Lorazepam: onset 5 - 10 minutes, half-life 10 hours, glucuronidated
Midazolam: onset 1 - 2 minutes, half-life 3 hours, metabolized by cytochrome
P450, active metabolite (1-OH) accumulates in renal disease
Benefits
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Anxiolytic
Amnestic
Sedating
Risks
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Delirium
NO analgesia
Excessive sedation: especially after long-term sustained use
Propylene glycol toxicity (parenteral lorazepam): significance uncertain
- Evaluate when a patient has unexplained acidosis
- Particularly problematic in alcoholics (due to doses used) and renal failure
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Respiratory failure (especially with concurrent opiate use)
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Withdrawal
Sedation Options: Propofol
Pharmacology: GABA agonist
Pharmacokinetics/dynamics: onset 1 - 2 minutes, terminal halflife 6 hours, duration 10 minutes, hepatic metabolism
Benefits
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Rapid onset and offset and easily titrated
Hypnotic and antiemetic
Can be used for intractable seizures and elevated intracranial pressure
Risks
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Not reliably amnestic, especially at low doses
NO analgesia!
Hypotension
Hypertriglyceridemia; lipid source (1.1 kcal/ml)
Respiratory depression
Propofol Infusion Syndrome
- Cardiac failure, rhabdomyolysis, severe metabolic acidosis, and renal failure
- Caution should be exercised at doses > 80 mcg/kg/min for more than 48 hours
- Particularly problematic when used simultaneously in patient receiving
catecholamines and/or steroids
Sample Sedation Protocol
Sedation-agitation Scale
Riker RR et al. Crit Care Med. 1999;27:1325.
Sedation Options: Dexmedetomidine
Alpha-2-adrenergic agonist like clonidine but with much less
imidazole activity
Has been shown to decrease the need for other sedation in
postoperative ICU patients
Potentially useful while decreasing other sedatives to prevent
withdrawal
Benefits
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Does not cause respiratory depression
Short-acting
Produces sympatholysis which may be advantageous in certain patients such as
postop cardiac surgery
Risks
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No amnesia
Small number of patients reported distress upon recollection of ICU period despite
good sedation scores due to excessive awareness
Bradycardia and hypotension can be excessive, necessitating drug cessation and
other intervention
Benzodiazepines
Onset
Peaks
Duration
Diazepam
2-5 min
5-30 min
>20 hr
Midazolam
2-3 min
5-10 min
30-120
min
Lorazepam
5-20 min
30 min
10-20 hr
Propofol
Propofol
Onset
Peaks
Duration
30-60
sec
2-5 min
short
Propofol Dosing
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3-5 g/kg/min antiemetic
5-20 g/kg/min anxiolytic
20-50 g/kg/min sedative hypnotic
>100 g/kg/min anesthetic
Problems with Current Sedative Agents
Midazolam
Propofol
Opioids
Prolonged weaning
X
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X
Respiratory depression
X
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X
Severe hypotension
X
X
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Tolerance
X
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X
Hyperlipidemia
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X
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Increased infection
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X
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Constipation
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X
Lack of orientation and
cooperation
X
X
X
Use Continuous and Combined Infusion
Load
Maintenance
Plasma
Level
Repeated Bolus
Plasma
levels
Choose the Right Drug
Sedation
Amnesia
Analgesia
Hypnosis
Anxiolysis
Propofol
Benzodiazepines
Patient Comfort
-2 agonists
Opioids
Altered Pharmacology
T 1/2 hours
Midazolam and Age
5
4.5
4
3.5
3
2.5
2
1.5
1
0.5
0
10
20
30
40
50
Age (y)
Harper et al. Br J Anesth, 1985;57:866-871
60
70
80
Delayed Emergence
• Overdose (prolonged infusion)
– pK derived from healthy patients
– Drug interaction
– Individual variation
• Delayed elimination
– Liver (Cp450)
– Kidney dysfunction
– Active metabolites
Opiate and Benzodiazepine Withdrawal
Frequency related to dose and duration
• 32% if receiving high doses for longer than a week
Onset depends on the half-lives of the parent drug and its active
metabolites
Clinical signs and symptoms are common among agents
• CNS activation: seizures, hallucinations,
• GI disturbances: nausea, vomiting, diarrhea
• Sympathetic hyperactivity: tachycardia, hypertension, tachypnea, sweating,
fever
No prospectively evaluated weaning protocols available
• 10 - 20% daily decrease in dose
• 20 - 40% initial decrease in dose with additional daily reductions of 10 - 20%
Consider conversion to longer acting agent or transdermal
delivery form
Significance of ICU Delirium
Seen in > 50% of ICU patients
Three times higher risk of death by six months
Five fewer ventilator free days (days alive and off vent.),
adjusted P = 0.03
Four times greater frequency of medical device removal
Nine times higher incidence of cognitive impairment at
hospital discharge
Delirium
1. Acute onset of mental status changes or
a fluctuating course
&
2. Inattention
&
3. Disorganized
Thinking
or
Courtesy of W Ely, MD
4. Altered level of
consciousness
Risk Factors for Delirium
Primary CNS Dx
Infection
Metabolic derangement
Pain
Sleep deprivation
Age
Substances including tobacco (withdrawal as well as
direct effect)
Diagnostic Tools: ICU
Routine monitoring
recommended by
SCCM
• Only 6% of ICUs use
Confusion Assessment
Method (CAM-ICU) or
Delirium Screening
Checklist (DSC)
Requires Patient
Participation
• Cognitive Test for Delirium
• Abbreviated Cognitive Test
for Delirium
• CAM-ICU
Ely. JAMA. 2001;286: 2703-2710.
Delirium Screening Checklist
No Patient Participation
• Delirium Screening Checklist
Bergeron. Intensive Care Med. 2001;27:859.
Treatment of Delirium
Correct inciting factor, but as for pain…relief need not be
delayed while identifying causative factor
Control symptoms?
• No evidence that treatment reduces duration and severity of
symptoms
• Typical and atypical antipsychotic agents
• Sedatives?
- Particularly in combination with antipsychotic and for drug/alcohol withdrawal
delirium
No treatment FDA approved
Haloperidol
No prospective randomized controlled trials in ICU
delirium
> 700 published reports involving > 2,000 patients
The good:
• Hemodynamic neutrality
• No effect on respiratory drive
The bad:
• QTc prolongation and torsades de pointes
• Neuoroleptic malignant syndrome - only three cases with IV
haloperidol
• Extrapyramidal side effects - less common with IV than oral
haloperidol
Atypical Antipsychotics: Quetiapine, Olanzapine, Risperidone, Ziprasidone
Mechanism of action unknown
Less movement disorders than haloperidol
Enhanced effects on both positive (agitation) and negative
(quiet) symptoms
Efficacy = haloperidol?
• One prospective randomized study showing equal efficacy of
olanzapine to haldol with less EPS
Issues
• Lack of available IV formulation
• Troublesome reports of CVAs, hyperglycemia, NMS
• Titratability hampered
- QTc prolongation with ziprasidone IM
- Hypotension with olanzapine IM
Neuromuscular Blockade (NMB) (Paralytics) in the Adult ICU
Used most often acutely (single dose) to facilitate
intubation or selected procedures
Issues
• NO ANALGESIC or SEDATIVE properties
• Concurrent sedation with amnestic effect is paramount analgesic as
needed
• Never use without the ability to establish and/or maintain a definitive
airway with ventilation
• If administering for prolonged period (> 6 - 12 hours), use an objective
monitor to assess degree of paralysis.
Neuromuscular Blockade in the ICU
Current use in ICU limited because of risk of prolonged
weakness and other complications
• Maximize sedative/analgesic infusions as much as possible prior to
adding neuromuscular blockade
Indications
• Facilitate mechanical ventilation, especially with abdominal
compartment syndrome, high airway pressures, and dyssynchrony
• Assist in control of elevated intracranial pressures
• Reduce oxygen consumption
• Prevent muscle spasm in neuroleptic malignant syndrome, tetanus, etc.
• Protect surgical wounds or medical device placement
Neuromuscular Blocking Agents
Two classes of NMBS:
• Depolarizers
- Succhinylcholine is the only drug in this class
- Prolonged binding to acetylcholine receptor to produce depolarization
(fasciculations) and subsequent desensitization so that the motor endplate
cannot respond to further stimulation right away
• Nondepolarizers
- Blocks acetylcholine from postsynaptic receptor competitively
- Benzylisoquinoliniums
• Curare, atracurium, cisatracurium, mivacurium, doxacuronium
- Aminosteroids
• Pancuronium, vecuronium, rococuronium
Quick Onset Muscle Relaxants for Intubation
Patients with aspiration risk need rapid onset paralysis
for intubation.
Not usually used for continuous maintenance infusions
Rocuronium
• Nondepolarizer with about an hour duration and 10% renal elimination
• Dose is 1.2 mg/kg to have intubating conditions in 45 seconds
Succinylcholine
• Depolarizer with a usual duration of 10 minutes
• All or none train of four after administration due to desensitization (can
be prolonged in patients with abnormal plasma cholinesterase)
• Dose is 1 - 2 mg/kg to have intubating conditions in 30 seconds
Potential Contraindications of Succinylcholine
Increases serum potassium by 0.5 to 1 meq/liter in all
patients
Can cause bradycardia, anaphylaxis, and muscle pain
Potentially increases intragastric, intraocular, and
intracranial pressure
Severely elevates potassium due to proliferation of
extrajunctional receptors in patients with denervation
injury, stroke, trauma, or burns of more than 24 hours
Neuromuscular Blocking Agents
Nondepolarizing muscle relaxants
• Pancuronium, vecuronium, cisatracurium
• All rapid onset (2 - 3 minutes)
• Differ in duration (pancuronium 1 - 2 hours, vecuronium 0.5 hours,
cisatracurium 0.5 hours)
• Differ in route of elimination (pancuronium = renal/liver, vecuronium =
renal/bile, cisatracurium = Hoffman degradation)
Neuromuscular Blocking Agents
Infusion doses
• Pancuronium 0.05 - 0.1 mg/kg/h
• Vecuronium 0.05 - 0.1 mg/kg/h
• Cisatracurium 0.03 - 0.6 mg/kg/h
Other distinguishing features
• Pancuronium causes tachycardia
• Vecuronium has neutral effects on hemodynamics but has several
renally excreted active metabolites
• Elimination of cisatracurium is not affected by organ dysfunction, but it is
expensive
Monitoring NMBAs
Goal - To prevent prolonged weakness associated with
excessive NMBA administration
Methods:
• Perform NMBA dose reduction or cessation once daily if possible
• Clinical evaluation: Assess skeletal muscle movement and respiratory
effort
• Peripheral nerve stimulation
- Train of four response consists of four stimulae of 2 Hz, 0.2 msec in
duration, and 500 msec apart.
- Comparison of T4 (4th twitch) and T1 with a fade in strength means that 75%
of receptors are blocked.
- Only T1 or T1 and 2 is used for goal in ICU and indicates up to 90% of
receptors are blocked.
Monitoring Sedation During Paralysis
Bispectral index is based on cumulative observation of a large
number of clinical cases correlating clinical signs with EEG
signals.
While used to titrate appropriate sedation (and amnesia) in
anesthetized patients to the least amount required, not proven to
achieve this goal.
Increased potential for baseline neurologic deficit and EEG
interference in ICU patients
No randomized controlled studies to support reliable use in ICU.
Other neuromonitoring (awareness) modalities are likely to be
developed.
Cessation of NMB as soon as safe in conjunction with other
patient parameters should be a daily consideration.
Complications of Neuromuscular Blocking Agents
Associated with inactivity:
• Muscle wasting, deconditioning, decubitus ulcers, corneal drying
Associated with inability to assess patient:
• Recall, unrelieved pain, acute neurologic event, anxiety
Associated with loss of respiratory function:
• Asphyxiation from ventilator malfunction or accidental extubation,
atelectasis, pneumonia
Other:
• Prolonged paralysis or acute NMBA related myopathy
- Related to decreased membrane excitability or even muscle necrosis
- Risk can be compounded by concurrent use of steroids.
Sample NMBA Protocol
References
Jacobi J, et al. Crit Care Med. 2002;30:119-141.
Jones, et al. Crit Care Med. 2001;29:573-580.
Cammarano, et al. Crit Care Med. 1998;26:676.
Ely, et al. JAMA. 2004;292:168.
Case Scenario #1
22-year-old male with isolated closed head injury who was
intubated for GCS of 7
He received 5 mg of morphine, 40 mg of etomidate, and 100
mg of succinylcholine for his intubation.
He is covered in blood spurting from an arterial catheter that
was just removed, and he appears to be reaching for his
endotracheal tube.
What sedative would you use and why?
What are the particular advantages in this situation?
How could you avoid the disadvantages of this drug?
Case Scenario #1 - Answer
Propofol will rapidly calm a patient who is displaying
dangerous behavior without need for paralysis.
Titratable and can be weaned quickly to allow for neurologic
exam
Can treat seizures and elevated ICP which may be present in
a head trauma with GCS of eight or less
Minimizing dose and duration will avoid side effects.
Case Scenario #2
54-year-old alcoholic who has been admitted for Staph sepsis
Intubated in the ICU for seven days and is currently on
midazolam at 10 mg/hour
His nurse was told in report that he was a “madman” on the
evening shift.
Currently, he opens his eyes occasionally to voice but does
not follow commands nor does he move his extremities to
deep painful stimulation.
Is this appropriate sedation?
What would you like to do?
How would you institute your plan of action?
Case Scenario #2 - Answer
This patient is oversedated. Not only can a neurologic exam
not be performed, but it would be unlikely to be able to
perform a wakeup test within one 24-hour period.
Given the need to examine the patient, midazolam should be
stopped immediately.
Rescue sedatives including midazolam should be available if
agitation develops.
Flumazenil should be avoided.
Case Scenario #3
62-year-old, 65-kg woman with ARDS from aspiration pneumonia
Her ventilator settings are PRVC 400, RR 18, PEEP 8, and FIO2
100%. She is dyssynchronous with the ventilator and her
plateau pressure is 37 mm Hg.
She is on propofol at 50 mcg/kg/min, which has been ongoing
since admit four days ago.
She is also on norepinephrine 0.1 mcg/kg/min and she was just
started on steroids.
What do you want to do next?
Do you want to continue the propofol?
Why or why not?
What two iatrogenic problems is she likely at risk for?
Case Scenario #3 - Answer
This patient needs optimization of her sedatives, and
potentially chemical paralysis to avoid complications of
ventilator dyssynchrony and high airway pressures.
If you continue to use propofol, higher doses are required and
the patient is already on norepinephrine. In addition, if
paralysis is used, you do not have reliable amnesia.
She is at risk for propofol infusion syndrome and critical
illness polyneuropathy.
Withdrawal
• Withdrawal from preoperative drugs
• Sudden cessation of sedation
– Return of underlying agitation
• Hyperadrenergic syndrome
– Hypertension, tachycardia,sweating
• Opioid withdrawal
– Salivation, yawning, diarrhea