Sedation and Analgesia in Picu

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SEDATION AND

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

• Sympathetic care from staff and family.

• Reducing environmental noise and light.


• Promotion of sleep and day–night orientation.
• Relaxation / Distraction therapy.
• Play and Music therapy (inc. bubble tubes and fibre-optic lights) • Parental involvement in care.

• Comforting touch/ massage or rocking.

• Consider swaddling and non-nutritive sucking in infants.

• Addressing feeding and hydration needs wherever possible.


PAIN ASSESSMENT

• Physiological markers like tachycardia,Tachypnoea, rise in blood


pressure,sweating,pupillary dilatation,increase in muscle tone etc
• Numerical or visual analogue scale.
• Facial pain scale.
• FLACC Scale (faces,legs,activity, cry,consolability).
• Grimace score.
FLACC SCALE
SEDATION ASSESSMENT

• 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

• Analgesia only (Paracetamol, Non-steroidal anti-inflammatory drugs e.g. Ibuprofen)

• Sedation only (Benzodiazepines e.g. midazolam, lorazepam,Propofol,Chloral hydrate


Antihistamines).

• Both analgesic and sedative effects (Opiates e.g. morphine, fentanyl,Alpha blockers
e.g. clonidine, dexmedetomidine, Ketamine)
MORPHINE

• Dose :- Bolus :- 0.1- 0.2 mg/kg/dose, Max(1mg).


Infusion :- 0.025-2.6 mg/kg/hr. Avg dose is :- 0.06 mg/kg/hr.
• Under Sedation: Comfort score > 26 or greater than target comfort score
Give a morphine bolus 50-100 micrograms/kg IV (max 5 mg) and review comfort
score in15 minutes.
Repeat morphine bolus if Comfort score still not in range twice more
reviewing Comfort score every15 min.
Increase morphine infusion rate by 20% if Comfort score still not in target
range after 3 morphine boluses.
MORPHINE

• Peak effect in 10 to 20 min and has a duration of action of approximately 2–4 h


• Metabolised in liver by glucuronidation and excreted by kidney.
• Have an active metabolite morphine-6-glucuronide (10%).
• Vasodilation, hypotension, bronchospasm, and pruritus are the common side effects
however they are not usually clinically significant.
• Avoid in acute asthma/bronchospasm due to histamine release associated with
morphine.
• Effect prolonged in severe renal failure or hepatic failure.
FENTANYL

• Fentanyl is an opioid analgesic 100 times more potent than morphine.


• Fentanyl has a rapid onset of action (1 – 2 minutes) and brief duration of action
(approx. 30 minutes).
• Dose :- 1– 5 micrograms/kg IV bolus to be administered over at least 30 seconds,
max(50 mcg).
1– 6 micrograms/kg/hr IV infusion.
• Fentanyl should be avoided in children on extracorporeal membrane oxygenation
(ECMO) due to high drug loss within the ECMO circuit.
• Unlike morphine, fentanyl has an inactive metabolite, norfentanyl, that does not cause
histamine release.
FENTANYL

• Prolonged infusion (> 48 hours) of Fentanyl should be avoided due to dramatic


increase in half life and reduction in clearance. This causes significant withdrawal
problems if used long term.
• Caution:
- Chest wall rigidity with rapid large dose (>5mcg/kg) injection, may necessite
intubation or naloxone.
- Effect prolonged in severe renal failure or hepatic failure.
- Fentanyl depresses the heart rate response, it can have a negative effect on children
who are heart rate dependent and rely on increased heart rate for augmentation of
cardiac output.
REMIFENTANIL

• Equipotent to fentanyl and has an ultrashort half-life of about 3 to 4 min.


• Metabolized by plasma esterases.
• Dose :-
Neonate 0.4 –1 microgram/kg/min IV infusion.
Child one month – 12 years 0.05 – 1.3 microgram/kg/min IV infusion.
Child 12 - 18 years 0.05 – 2 microgram/kg/min IV infusion.
• Similar to other opioids, remifentanil does have respiratory and myocardial depressant
effects.
REMIFENTANIL

• 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

• Hydromorphone is hydrophilic and has 7 to 10 times the potency of morphine.


• Hydromorphone has an onset of 5 to 10 min and a duration of action of 3 to 4 h.
• Dose :- 0.024mg/kg/hr – 0.05mg/kg/hr.
• Metabolized by hepatic glucuronidation to hydromorphone-3-glucuronide.
• Excreted in the urine.
• Hydromorphone is associated with less sedation, nausea, and pruritus than morphine.
MIDAZOLAM

• 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

• Midazolam is particularly associated with problematic withdrawal symptoms and a


significant number of children will get more agitated with increased dosing. It is
therefore recommended to not use more than 200 micrograms/kg/h rinstead consider
adding or changing agents
• Side effect :- respiratory and cardiac depression, hypotension, paradoxical
agitation,tolerance,dependence,withdrawal.
• Patients with renal insufficiency or failure require dose adjustment.
DIAZEPAM

• Used for its anxiolytic, muscle relaxant, and antiepileptic properties.


• It can be given PO or IV.
• IV Diazepam has anonset of action of 4–5min and a duration of action of 60 to 120 min.
• Diazepam is metabolized in the liver to active metabolites which accumulate in renal
failure, and lead to a half-life of diazepam which can range from 20 to 120 h.
• IV Diazepam is highly water insoluble and is dissolved in propylene glycol.
• May cause phlebitis with prolonged infusion.
LARAZEPAM

• Used in the PICU for its antiepileptic and anxiolytic properties.


• Lorazepam can be administered PO, IM, and IV at the same dose of 0.5
mg/kg (maximum of 2 mg per dose).
• IV lorazepam is dissolved in propylene glycol which at high levels can
produce metabolic acidosis and renal dysfunction. Therefore, IV lorazepam
is not used as an infusion.
• Oral lorazepam plays an important role for converting and weaning
patients from long term midazolam infusions to an oral regimen.
SODIUM THIOPENTAL

• 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 can be delivered PO, IV, transdermally, or epidurally.


• Typical clonidine dose is 4 to 5 mcg/kg.

• Clonidine IV bolus dose is 1 to 2 mcg/kg .

• 1 mcg/kg/hour as an infusion rate.


• The dose for neuraxial Clonidine is 1–2 mcg/kg.
• The transdermal patch delivers 0.1 mg per 24 h and is changed weekly.
• The elimination half-life of enteral clonidine is 12 to 16 h; the CSF elimination half-life is 1.3 h

• Clonidine has been used to wean children from prolonged dexmedetomidine and opiate
infusions.
DEXMEDETOMIDINE

• 8 times more selective for alpha-2 receptor than clonidine.


• Dose :- 0.7 – 1.4 micrograms/kg/hr IV infusion (for 48 – 72 hrs only).
• It reduces sympathetic activity and agitation and induces sedation via activation of
alpha-2 receptors at the locus coeruleus of the brainstem.
• Approved for administration only by the IV route but is effective also by the IM, IN.
• It is metabolized by the liver via glucuronidation and oxidation and it has no active
metabolites; the half-life of dexmedetomidine is 2 h.
• Dexmedetomidine’s sedative effect closely mimics natural sleep, with EEG activity in children
resembling Stage 2 sleep.
DEXMEDETOMIDINE

• A patient sedated with Dexmedetomidine can be easily roused with minimal


stimulation and experiences minimal respiratory depression
• Dexmedetomidine also has analgesic effects through modulation of pain impulses
mediated by noradrenergic bulbar/spinal pathways. It can therefore reduce the
need for opioid analgesics.
• Side effects: bradycardia and hypotension; nausea; dry mouth; initial transient
hypertension with reflex bradycardia; discontinuation syndrome.
PROPOFOL

• Propofol is a GABA agonist.


• Advantageous in the critical care setting due to its rapid onset (1–2 min), high potency,
and short duration of action (2–8 min), and antiemetic and euphoric properties that lead
to more positive patient experience.
• Dose :- Bolus 0.5 to 1 mg/kg
Infusion rate of 1 to 3 mg/kg/h.
• In general, the half-life of propofol after an infusion is 30 to 60 min, longer with prolonged
infusions as it is highly lipophilic, redistributed from fat stores.
PROPOFOL

• Propofol is metabolized by hepatic glucuronidation and hydroxylation.


• Adverse effect :- pain on injection, vasodilation or negative inotropy leading to
hypotension,bradycardia, respiratory depression, apnea, hypertriglyceridemia, and
pancreatitis.
• With prolonged infusion rates of >4 to 5 mg/kg/h and use of long-term propofol infusion
in pediatric patients, there is a risk of propofol infusion syndrome (PRIS).
• PRIS :- lactic acidemia, rhabdomyolysis, dysrhythmias, cardiac arrest, and a high mortality
rate (52% in children).
KETAMINE

• Ketamine is a phencyclidine derivative and an NMDA antagonist.


• Used as an adjunctive sedative agent or as part of a multimodal analgesic regimen.
• At Low doses (0.5 – 1 mg/kg) it provides sedation and analgesia of the skin, muscle and bone, while
preserving airway reflexes, whereas higher doses (1 – 2 mg/kg) produce general anaesthesia.
• Dose :- Neonate :- Bolus :- 0.5 – 2 mg/kg IV.
Infusion :- 8 micrograms/kg/min (max. 30 micrograms/kg/min)
Child :- Bolus :- 0.5 – 2 mg/kg IV.
Infusion :- 600 – 2700 micrograms/kg/hr.
KETAMINE

• 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

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