This document outlines goals, definitions, challenges, monitoring, and medication options for sedation and analgesia in the pediatric intensive care unit (PICU). The goals of PICU sedation include patient comfort, pain control, anxiolysis, amnesia, and facilitating procedures. Common drugs utilized are opioids, benzodiazepines, chloral hydrate, barbiturates, ketamine, propofol, and neuroleptics. The document reviews dosing, administration, benefits, side effects and precautions for each class of medication.
3. GOALS
Patient comfort
Control of pain
Anxiolysis
Amnesia
Blunting adverse autonomic and hemodynamic
responses
Facilitate nursing management
Facilitate mechanical ventilation
Avoid self-extubation or self injury
Reduce oxygen consumption
4. SEDATION and ANALGESIA
Inadequate analgesia and postsurgical
stress response is a metabolic, humoral,
and hemodynamic response following
injury or surgery
This neuroendocrine cascade leads to
increased oxygen consumption,
increased carbon dioxide production,
and a generalized catabolic state with a
negative nitrogen balance
5. SEDATION/ANALGESIA
Sedation (seda/shun) [L. sedatio, to calm, allay].
The act of calming, especially by the
administration of a sedative, or the state of being
calm.
Analgesia (an-al-je/zi-ah) [G. insensibility, from an -
privative,negative + algesis, sensation of pain] A
condition in which nocioceptive stimuli are
perceived but are not interpreted as pain; usually
accompanied by sedation without loss of
consciousness.
6. IDEAL PICU
SEDATIVE/ANALGESIA
Rapid onset
Predictable duration
No active metabolites
Rapid recovery
Multiple routes of delivery
Easy to titrate
Minimal cardiopulmonary effects
Not altered by renal or hepatic disease
No drug interactions
Antidote available
Wide therapeutic index
31. OPIOIDS
First line drugs
Provide analgesia and sedation, NOT amnesia
Act similarly as a class
Produce delayed gastric emptying, decreased
intestinal peristalsis, and urinary retention
Narcotic to be used:
Morphine
Fentanyl
Methadone
32. OPIOIDS
ROUTE OF ADMINISTRATION
IV
Oral
Transmucosal
Transdermal
MODE OF ADMINISTRATION
Intermittent/on demand (as necessary)
Fixed interval
Continuous infusion
PCA
33. MORPHINE
Gold standard
Hepatic metabolism
Depresses respiration by altering
chemoreceptor sensitivity to CO2
Depresses rate over tidal volume
Decreases sigh frequency
Can cause hypotension due to histamine
mediated vasodilation
Can block compensatory catecholamine
effect
Prolonged clearance in neonates
35. FENTANYL
Synthetic opiate, 100 x more potent than
morphine
Rapid onset, highly lipophilic, rapidly crosses
BBB, redistributed to fatty tissue
Short distribution t1/2, long elimination t1/2
Minimal hemodynamic effect
Blunts pulmonary vascular responses
May produce “chest wall rigidity”, reversed with
relaxants or naloxone
36. FENTANYL
IV intermittent dosing
1-2 mcg/kg q 1-2 hrs
IV continuous dosing
1-2 mcg/kg/hr
Transdermal delivery system available
Not recommended in children less than 12
yrs
25,50,75,100 mcg/hr
25 mcg/hr is equivalent to 15 mg morphine
in a 24 hr period
37. METHADONE
Equipotent to morphine
Minimal hemodynamic effects
Long half life
Sedation and euphoric properties less
pronounced than morphine
Useful for pain control and abstinence PO dosing
0.1 mg/kg q 4-8 hrs
50 % oral bioavailability
Drug accumulation with repeated doses
caused by extensive protein binding
38. MODE OF ADMINISTRATION
Intravenous bolus administration
Common
PRN - as needed
Half-life of drug determines interval
Disadvantage of pain breakthrough
40. CONTINUOUS INFUSION
Utilized when prolonged analgesia and
sedation needed
Less labor intensive
Better analgesia, initial bolus important
Need for dedicated IV site
42. PCA
Patient controlled analgesia
Allows patient to administer a preset amount of
narcotic at preselected intervals
Improved analgesia with decreased narcotic use
Option to include low basal rate
Nurse controlled analgesia
Eliminates delay
Allows delivery via a closed system
44. OPIATE SIDE EFFECTS
RESPIRATORY DEPRESSION
Reversal - Nalaxone (Narcan)
Full reversal 0.1 mg/kg
Partial reversal - titrate to effect
Half life is less than narcotics
IV,IM,Sub Q, ETT
Abrupt reversal may result in nausea,
vomiting, sweating, tachycardia, increased
BP, and tremors
45. OPIATE SIDE EFFECTS
Pruritis
Individual variability and susceptibility,
alleviated by Benadryl
Tolerance
Need for increase in dose to achieve the
same effect
Generally develops after 2-3 days of
frequent/continuous use
Greater with fentanyl
Treated by increasing the dose as needed
46. OPIATE SIDE EFFECTS
DEPENDENCE
Physiological state leading to abstinence
syndrome on withdrawal of the drug
Generally develops after 7-10 days of
sustained use
Symptoms include: mydriasis, tachycardia,
goose bumps, muscle jerks, vomiting, diarrhea,
seizures, fever, hypertension
Treated with gradual withdrawal of the drug
47. OPIATE SIDE EFFECTS
DEPENDENCE
In general the longer the period of treatment the
longer the period of withdrawal needed
A child is at risk for dependence if they have been on
narcotics for a week
Finnegan scoring to monitor adequate weaning dose
Weaning strategies can vary, typically 10% decrease
per day
Do not spread the dosing interval beyond the
normal dosing interval, rather decrease the dose
Can substitute methadone and wean q 48 hrs over
a longer time period
48. BENZODIAZEPINES
First line agents for sedation
Provide hypnosis, anxiolysis, antegrade amnesia,
and anticonvulsant activity
NO ANALGESIA
Can cause abstinence syndrome after prolonged
use
Mechanism in the limbic system via the inhibitory
neurotransmitter, gamma aminobutyric acid
(GABA)
49. DIAZEPAM (VALIUM)
Sedating, variable amnesia, anxiolytic
Irritating to veins, pain in PIV
Multiple active metabolites
Advantage for prolonged sedation
Disadvantage for rapid arousal
Not recommended for continuous infusion
Half-life 12-24 hrs
Hepatic metabolism
50. LORAZEPAM (ATIVAN)
Improved amnesia
No active metabolites
Half life 4-12 hours
Metabolized by glucuronyl transferase
Less influence from other drugs
Better preserved in patients with liver
disease
51. MIDAZOLAM (VERSED)
Rapid onset
Rapid metabolism
Good amnesia
Water soluble, no pain
with injection
Half life 2 -4 hours
Hepatic metabolism with
renal excretion
Active hydroxy-
metabolite may
accumulate
Other routes of
administration
Oral
Nasal
Rectal
Sublingual
Less absorption requiring
increase dosing
52. MIDAZOLAM
Reports of dystonia and choreoathetosis
post infusion, greater risk in neonates
Heparin decreases protein binding,
increases free drug
Disadvantage cost
20 kg patient
80 $/day compared to Ativan = 30 $/day
53. BENZODIAZEPINES
SIDE EFFECTS
RESPIRATORY DEPRESSION
Less than narcotics, but potentiated with
narcotics
Dose related
Reversal
Flumazenil - benzodiazepine receptor antagonist
Contraindicated in patients with chronic benzo use
for seizures, mixed overdose, TCA’s - may result in
seizures
54. BENZODIAZEPINES
SIDE EFFECTS
Choreoathetoid movement disorder
Tolerance
As with narcotics may need to increase dose
following 2-3 days use
Dependence
Withdrawal carefully and slowly if on greater
than 7-10 days
Signs of withdrawal - tremor, tachycardia,
hypertension,
Rapid withdrawal may promote seizures
55. CHLORAL HYDRATE
Sedative hypnotic agent
Metabolized in the liver to its active form,
trichlorethanol
Half life 8-12 hours
Oral or rectal administration
Onset of action delayed
Paradoxical reaction in some older children
Not to exceed 100 mg/kg/day - i.e.: 25mg/kg/q 6 hrs
Caution in children < 3 months or with hepatic
dysfunction
57. BARBITURATES
Useful in patients with increased ICP
Short acting barbiturate useful for
sedation for procedure/imaging in
hemodynamically stable child
Alkaline solution, often incompatible with
TPN or meds.
58. MAJOR TRANQUILIZERS
Phenothiazine
Thorazine
Butyrophenones
Droperidol
Haloperidol
Common in adult ICU, uncommon in PICU
Side effects hypotension due to alpha blockade
and extrapyramidal effects
At times useful in the difficult to sedate child
59. KETAMINE
Dissociative IV anesthetic
Good amnesia and somatic analgesia
Anesthetic state classically described as a functional
and electrophysiological dissociation between the
thalamoneocortical and limbic system
Chemically related to phencyclidine and
cyclohexamine
Water and lipid soluble
Quickly crosses blood-brain barrier, < 30 seconds
60. KETAMINE
Redistribution half-life 4.7 minutes
Elimination half-life 2.2 hours
Clinical effects evident within one minute, resolution within
15 - 20 minutes of dose
Bronchodilation
Sialagogue -“promoting the flow of saliva”
Administer with an anticholinergic
Atropine or Robinol
Minimal net hemodynamic effect
Negative inotrope
Central effect - HR, SVR
Good choice in shock or status asthmaticus
61. KETAMINE
Risk of laryngospasm
Risk of emesis/aspiration
Increases ICP , globe pressure
Seizure inducing
Emergent reactions, hallucinations
Improved with administration of a benzodiazepine
IM: 2 - 4 mg/kg dose q 30 minutes - 1 hour
IV
Intermittent dosing
1 -2 mg/kg dose q 30 minutes to 1 hr
Continuous dosing
1 - 3 mg/kg/hr
62. PROPOFOL
Sedative/hypnotic
Dose dependent - conscious sedation to
general anesthesia
Rapid onset (20-50 seconds)
Quick recovery ( within 30 minutes of d/c)
Lack of active metabolites
Metabolized in liver
Excreted in urine
63. PROPOFOL
Lipid emulsion, reports of anaphylaxis
Soybean oil, egg lecithin, and glycerol
Decreased ICP, may lower CPP
Decreased sympathetic tone
Contraindicated in hemodynamically
unstable
Moderate respiratory depression
Pain with injection/infusion site
Improved with use of 1% lidocaine
0.5 mg/kg
64. PROPOFOL
Neurologic sequela
Opisthotonic posturing
Myoclonic movements
Metabolic acidosis reported with use > 24 hrs
Contraindicated for long term use
Doses
1 - 3 mg/kg induction
20 - 100 mcg/kg/min
Increase infusion rate 5-10 mcg/kg/min increments
of 5 - 10 minutes