Sedation and Analgesia in Picu
Sedation and Analgesia in Picu
Sedation and Analgesia in Picu
ANALGESIA IN PICU
OBJECTIVE
• Introduction.
• Non Pharmacological interventions.
• Pain and sedation assessment.
• Drugs used in picu.
• Strategies for administering sedation.
INTRODUCTION
• Factors such as: The PICU environment, unfamiliar staff and routines, high intensity
light and noise, fever/environmental temperature, surgical procedures, PICU
procedures and monitoring, positioning and physical movement, and other factors
all contribute to discomfort, pain, anxiety, agitation and fear in our patients.
• Pain and agitation stimulate stress responses and increases metabolic and oxygen
demand. Pain has also been shown to lead to permanent structural and functional
changes in the developing brain.
INTRODUCTION
• Irrespective of the need for sedation, all infants, children and young people have
the right to adequate pain relief.
• Agitated and scared children on PICU are at significant risk of harm due to
unplanned removal of vital monitoring and therapeutic devices.
• Sedation can be helpful in facilitating nursing care and reducing recall of
unpleasant situations. Both under and over sedation present safety risks to the
patient and adversely impacts on PICU length of stay.
NON PHARMACOLOGICAL INTERVENTIONS
• The optimal condition for the non-neuromuscularly blocked patient would be that he is
easily arousable or conscious, comfortable, and breathing in sync with the ventilator, a
state that can be referred to as the Goldilocks Zone (not too deep and not too light).
• The State Behavioral Scale (SBS).
• The COMFORT scale.
• The COMFORT behavior scale (COMFORT-B scale).
• The Richmond Agitation Sedation Scale (RASS).
COMFORT B SCALE
RICHMOND AGITATION SEDATION SCALE
DRUGS USED IN PICU
• Both analgesic and sedative effects (Opiates e.g. morphine, fentanyl,Alpha blockers
e.g. clonidine, dexmedetomidine, Ketamine)
MORPHINE
• Remifentanil is optimal for the patient with renal or hepatic dysfunction, as it avoids the
risk of accumulation of active metabolites.
• Caution: Avoid IV bolus remifentanil in PICU due to risk of severe hypotension.
• ideal for use during short stimulating procedures such as physiotherapy or chest
drain removal.
• May be useful in situations where frequent neurological assessment is needed as it can
be paused/stopped, allowing the child to quickly gain a window of
awareness/consciousnes for assessment.
METHADONE
• Rapid onset (5–10 min and 30–60 min via IV and oral route respectively).
• It has the longest duration of action of all the opioids (4 to 24 h).
• Long duration of action supports its frequent choice to prevent opioid withdrawal for
children who have received continuous morphine or fentanyl for >5 days.
• Caution should be taken when administering methadone to PICU patients with structural
heart disease as it prolong the corrected QT interval that may leads to arrhythmias.
• Dose :- 0.7 mg/kg/day PO/SC/IV/IM divided q6hr PRN; not to exceed 10 mg/dose.
HYDROMORPHONE
• Fastest onset is via the IV route at 1–3 min, followed by IM/IN at 5–10 min and then
PO/PR at 10–30 min.
• IV midazolam has a duration of action of 45 to 60 min.
• Bolus dose :- 50 – 100 micrograms/kg (max 5mg).
• Infusion :- 50 – 120 mcg/kg/hr.
• For refractory status epilepticus, a bolus of up to 0.2 mg/kg with a maintenance infusion
up to 0.4 mg/kg/h is common
• Midazolam is metabolized by hydroxylation to an active metabolite (1-OH midazolam)
and subsequently undergoes glucuronidation to 1-OH-midazolam-glucuronide, also an
active metabolite, which is then renally excreted.
MIDAZOLAM
• Thiopental is short-acting its peak onset is 1–2 min and the duration of action is 30 min.
• Dose :- Infants induction doses of 5–8mg/kg.
Children, teens and adults induction dose of 3–4 mg/kg.
• used more commonly in the operating room for the induction of general anesthesia and
in the pediatric critical care setting for neuro-protective intubations.
• Thiopental is metabolized via hepatic metabolism and it has a long elimination half-life of
up to 12 h.
PHENOBARBITAL
• Pentobarbital is a long-acting barbiturate used for sedation, status epilepticus, and the
treatment of refractory intracranial hypertension after severe traumatic brain injury.
• IV route has an onset of action at 5 min, peaks at 15 min and has a duration of action >6 h.
• Pentobarbital undergoes hepatic metabolism via cytochrome p450-induced hydroxylation and
glucuronidation.
• Pentobarbital has an elimination half-life of 12–24 h.
• Side effects of myocardial depression with resultant hypotension, necessitating pressors, should
be anticipated during treatment.
CLONIDINE
• Clonidine has been used to wean children from prolonged dexmedetomidine and opiate
infusions.
DEXMEDETOMIDINE
• Rapid onset of 30s to 60s when given IV with effective procedural sedation conditions
achieved in 1min and lasting upto 5 to 10min.
• Ketamine is metabolized by the liver to an active metabolite, norketamine; ketamine and
norketamine are then further metabolized by the liver to water soluble compounds that
are then renally excrespir
• It preserves laryngeal reflexes allowing for spontaneous respirations during procedural
sedation.
KETAMINE
• A powerful bronchodilator which makes it the agent of choice in patients with severe
bronchospasm like status asthmaticus.
• Although ketamine is a myocardial depressant with vasodilating properties, its indirect
sympathomimetic activity (stimulating catecholamine release and inhibition of
catecholamine reuptake) preserves cardiac output and leads to increase in blood
pressure and heart rate.
• Side effects :- sialorrhea, psychotogenic reactions such as emergence delirium,
disorientation, hallucinations, and combativeness at higher serum concentrations.
CHLORAL HYDRATE