Sedation Safety, by Dr. David Fagin in collaboration with the Society for Pediatric Sedation.
Welcome to the Society for Pediatric Sedation's online provider course on sedation safety.
At the end of this lecture, our goal is for you to be able to recognize the most common
adverse events that occur during sedation, understand the key factors that contribute
to safe sedation, and to understand the treatment of sedation-related apnea, airway obstruction,
and hemodynamic instability.
Remember, the events described in this lecture should not result in an unfavorable outcome
if handled properly.
This lecture is divided into three major subsections.
The first describes what we mean by sedation safety and the current state of the sedation
safety literature.
The second will address the management of the most common adverse events, including
obstruction, apnea, excess secretions, excess secretions with aspiration, larygnospasm,
and hypotension.
And finally, we will address specific patient, technique, provider, and systems factors that
contribute to safe sedation.
What is safe sedation?
Not a simple answer.
There are many factors involved, but the goal is for the sedation to be safe, with minimal
risk to the patient while successfully completing the procedure and effectively managing patient
pain and anxiety.
It is often easier to define what isn't safe.
Cote's landmark paper looked at a number of pediatric sedations resulting in a bad outcome,
including death and permanent neurologic disability.
Most occurrences were related to operator error and rule violations.
The adverse outcomes related to events occurring during the procedure were usually respiratory
in nature and related to the depth of sedation.
Adverse events were not associated with any specific drug or route of delivery.
This table displays results from the Pediatric Sedation Research Consortium, a national pediatric
sedation data registry consisting of adverse events drawn from 104,905 patient encounters.
Although the rates are low, they are not 0.
By far, the most common events were complete airway obstruction and the need to administer
bag mask ventilation for impending respiratory issues.
Excessive secretions, hypotension, bradycardia, and laryngospasm are the next most common.
Thus, while adverse events are infrequent, they can potentially happen in any moderate
or deep sedation, and more importantly, can lead to patient harm if not properly managed.
We next move to a consideration of the specific characteristics of the most common serious
adverse events-- airway obstruction, apnea, excessive secretion with aspiration, laryngospasm
and hypotension.
We will discuss their physiology and their management.
Airway obstruction is the most frequent serious adverse event.
It is brought on by muscular relaxation, which decreases pharyngeal tone and causes posterior
displacement of the structures of the upper airway.
Certain patients, such as those with hypotonia, obesity, cranial facial abnormalities, and
sleep disordered breathing are more prone to airway obstruction.
Certain circumstances, such as deep sedation, supine positioning, neck flexion can also
enhance the likelihood of airway obstruction.
To demonstrate, consider this MRI image and drawing representing the anatomy of a normal
airway.
Now consider this airway MRI taken after propofol administration.
Note the airway narrowing that has occurred due to muscular relaxation generated by pharmacologically-induced
sedation and positioning.
Finally, consider these images as an illustration of the effects of positive pressure ventilation
on the collapsed airway.
Note the degree to which the oropharynx is open by this treatment modality.
This brings us to the treatment strategy for airway obstruction.
First, reposition the airway.
This may require the use of a shoulder or neck roll to help align the airway structures.
Suctioning may be tried, though it is important to avoid larangeal stimulation with suctioning,
as this may lead to laryngospasm.
The next phase involves more significant interventions, such as continuous positive airway pressure
or a bag mask ventilation.
Nasopharyngeal airways or oral airways can also be of assistance in this situation and
should be considered.
Finally, if the obstruction persists, the patient may potentially require a laryngeal
mask airway or endrotracheal intubation.
Fortunately, the need for emergent endrotracheal intubation is rare in this situation.
We next consider apnea.
Two broad categories of apnea exist-- central and obstructive.
Obstructive apnea, practically speaking, is the same as airway obstruction, and so here,
we will be considering central apnea.
Central apnea is defined as a lack of respiratory effort for greater than 15 seconds, and can
be potentiated by both patient factors, such as central apnea syndromes and brain stem
abnormalities, as well as sedation technique.
Many commonly-used sedation drugs can cause apnea.
It may be especially common with propofol.
The onset of central apnea, when it occurs during sedation, is abrupt, but is usually
very brief.
Typically, lack of ventilation precedes the development of hypoxia, which makes detection
of this hypoventilation critical to avoid desaturation.
Use of capnography is crucial to the early detection of apnea, as it will detect apnea
before there is a change in pulse oximetry.
This allows for the earlier treatment of apnea and a reduction in hypoxemia.
Treatment of central apnea that has prolonged always involves bag mask hyperventilation.
It is important to remember that for true apnea, blow by oxygen is not sufficient.
Given its brevity, it is rare that the sedation needs to be stopped.
But if necessary, this can be done.
If applicable, a reversal agent might also be given.
The next adverse event to be considered is excessive secretions and aspiration.
Although excessive secretions occur commonly as a sedation event, fortunately, true aspiration
is very rare.
Although a full stomach can be the cause of aspiration events, in most circumstances,
it is due to the drug-related loss of the protective airway reflexes used to handle
secretions.
Certain patients, such as those with cerebral palsy or neuromuscular disease, may normally
have problems handling oropharyngeal or nasal secretions.
Certain sedation drugs, most notably ketamine, can cause an increase in secretions.
Early recognition and management of excessive secretions is key for successful treatment,
and clinical outcome will vary based on the amount and type of secretions, illness severity,
depth of sedation, and timeliness of intervention.
An important consideration in the management of excessive secretions is prevention of secretion
aspiration into the larynx, which may result in coughing and laryngospasm, a much more
severe condition which will be discussed in the next slide.
Treatment of problem secretions involves airway positioning and suctioning followed by bag
mask ventilation if needed.
Glycopyrrolate or Atropine may be helpful in patients who have trouble with their own
secretions.
We now move to laryngospasm, perhaps one of the most frightening sedation events.
Laryngospasm occurs due to an uncontrolled, involuntary closure of the vocal cords from
a spasm of the glottic musculature.
Most typically, this happens during induction or emergence from sedation, and may be either
partial or complete.
Certain patient factors predispose to laryngospasm, such as upper respiratory tract infection,
gastroesophageal reflux disease, age under one year, and higher ASA level.
It is also more common with certain procedures, particularly with those involving airway manipulation,
such as endoscopy or bronchoscopy.
Laryngospasm is also more commonly associated with ketamine than other sedation drugs, although
it can happen with any drug or drug combination.
Sedation clinicians must consider this a possibility in any deep sedation and are prepared for
it, as immediate recognition and treatment are critical for successful management.
Know the signs-- stridor or no air movement, respiratory distress, and hypoxia.
Management is stepwise, beginning with airway repositioning with chin lift and jaw thrust
and followed by suctioning.
If this does not work, consider pressure in the laryngospasm notch.
This will be demonstrated in the simulation aspect of the course.
The most important aspect of treatment is applying pressure to the airway, either via
PEEP or bag mask ventilation.
Deepening the sedation may also treat the laryngospasm and allow effective bag mask
ventilation.
Finally, neuromuscular blockade followed by endotracheal intubation can be employed, although
fortunately, this is rare.
Finally, we consider hypotension.
Often, a combination of factors leads to hypotension during sedation.
Many of our patients are febrile, dehydrated, and fasted.
Many invasive procedures for which we are sedating the patient can lead to fluid or
blood loss.
Finally, many of the sedative drugs, such as propofol, or drug combinations, such as
fentanyl and midazolam, can result in hypotension, secondary to vasodilatation, and/or bradycardia.
Treatment of hypotension, again, hinges on preparedness, and in many cases, hypotension
can be prevented.
For most sedatives, unwanted cardiovascular effects are dose-dependent.
And conversely, some agents, such as ketamine and etomidate, have a favorable cardiac profile.
Proper agent choice and titration of smaller doses can be used to avoid hypotension in
at-risk patients.
If hypotension does occur, it can typically be resolved with volume expansion, using 10-20
CCs per kilo of isotonic saline and by decreasing the set of doses and/or infusion rates.
To conclude the lecture, we will look at the different factors that can contribute to a
safe sedation.
These factors will be considered under the following outline-- know who to sedate, know
the potential effects of your medications, know your own capabilities, and know the rules.
First, know who to sedate.
Here's a list of key factors when considering adverse event risk in an individual patient.
The first and second considerations are age and ASA class.
Younger and sicker patients are more likely to experience adverse events.
Third, an airway assessment is important, as patients with anatomic airway issues, such
Pierre Robin, Down syndrome, or Treacher Collins are at higher risk.
A fourth factor is obesity, as patients with elevated body mass index are at higher risk
of obstructive apnea.
It is also important to check allergies to drugs or food, as some items may cross-react
with common sedatives.
Clinicians should also review previous sedations or surgical history to determine if an adverse
event has occurred in the past, and if so, what regimen was used.
Finally, cardiorespiratory history should be elicited, as patients with a significant
cardiac or chronic respiratory issue are potentially very problematic.
Patients with a cyanotic heart disease may benefit from consultation with a specialized
cardiac anesthetist.
By way of illustration, this graph demonstrates the effect of patient age on sedation risk.
Here, it can be seen that young infants have a higher complication rate during sedation.
Many sedation and anesthesia services advise postponing sedating patients for elective
procedures and tests when below a certain age, often 4-6 months of post-term birth age.
This graph demonstrates the effect of higher ASA class on complication risk, with ASA class
3 or 4 having a significantly higher complication risk than ASA class 1 or 2.
It is important to be familiar with the ASA classification scale and evaluate patients
before sedation using its principles.
We next consider the potential effects of medications-- sedative drug factors.
This following list includes a number of common sedation drugs and the most common adverse
effects associated with them.
Compared to other regimens, propofol most often results in hypotension, apnea, and upper
airway obstruction.
Ketamine has been more closely associated with laryngospasm and emergence reactions.
Dexmedetomidine can cause bradycardia and hypertension.
Etomidate can cause emesis, and in multiple doses, can result in significant adrenal suppression.
Fentanyl, in addition to causing apnea and coughing, can cause chest wall rigidity if
infused too quickly.
One important way to avoid these effects is by the use of specific drug combinations,
such as ketamine and propofol, which can reduce the vasodilating effects of propofol.
By using these drugs in combinations, individual doses can be lowered and complications avoided.
Next, we consider provider and clinician factors.
Crucial here is the consideration that pediatric sedation is performed by a multitude of provider
types with different qualifications and capabilities.
This list is provided to give a sense of what these different provider types are.
Providers must know what they are capable of, and perhaps more importantly, where their
scope of practice does not extend.
Doing this will enable good decisions to be made regarding the appropriateness of individual
cases.
Providers also need to consider differences in the environment of care, specifically the
skills and capabilities of the other clinicians involved in the care of the patient.
Differences in backup and rescue services available also must be considered.
A single provider may make very different management decisions for the same patient
located in two different clinical settings.
Finally, system factors must be considered.
Many sedation services are under pressure to complete procedures quickly, but it is
imperative that all patients undergo the same process every time in a deliberate and well-thought-out
manner.
In this course, we emphasize a team approach as the best means to assure patient safety.
Every sedated patient should undergo the same sedation process every time they are sedated.
This should also include a sedation timeout.
The timeout process should be an active process, used by the team as a prompt to verify important
facts, such as whether this is the correct patient, what procedure will be performed,
what site the procedure will occur at, the positioning required for the procedure, and
whether the needed equipment is present.
In this, the sedation clinician must take a central role.
In summary, serious adverse sedation events in children are relatively uncommon, yet may
cause significant morbidity and even death.
Pharyngeal obstruction, laryngospasm, apnea, and hypotension are among the most common
serious adverse events, and practitioners should be prepared to manage them.
Appropriate training, knowledge of medications, understanding of personal limitations, and
adherence to sedation policies and procedures will reduce adverse events and improve outcomes.
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