Pediatric Drowning Airway Management

Tigger

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During our monthly continuing education from the hospital system, a pediatric drowning scenario was brought forth. Nothing out of the ordinary, 3 year old in a PEA arrest after being removed from a pool.

We don't intubate pediatrics in this system, instead we have iGels down to pediatric sizes.

Without really providing much evidence, the educators say not to use an iGel or SGA as children have strong mammalian dive reflexes and iGel will obstruct their airway while the pressure from using a BVM and OPA will open the airway just fine. This makes absolutely no sense to me. Has anyone else heard anything like this?

I get not intubating kids, but the airway pressures afforded to the patient by ETT (and the ability to suction) would seem to be of benefit in a drowning. Obviously SGAs do not generate significant airway pressures, but it seems that they'd be more effective than a mask ventilation? Or am I just wrong.
 

Carlos Danger

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I don't think you are wrong at all, and I agree that what they told you doesn't seem to make sense.

We all know that laryngospasm is a reflex which occurs when water enters the airway, and even though I wouldn't expect that to be an issue in a patient with PEA, when you do encounter it you need all the help you can get generating sufficient airway pressure to open the glottis without (hopefully) insufflating the stomach any more than a little. An iGel would potentially help with that, and I can't imaging a mechanism by which it would hurt. A properly placed iGel will not cause airway obstruction.

FWIW, I believe that strictly speaking, the mammalian dive reflex concerns vagally mediated bradycardia and vasoconstriction, and that the reflexive glottic closure is another thing entirely.
 

E tank

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I don't think you are wrong at all, and I agree that what they told you doesn't seem to make sense.

We all know that laryngospasm is a reflex which occurs when water enters the airway, and even though I wouldn't expect that to be an issue in a patient with PEA, when you do encounter it you need all the help you can get generating sufficient airway pressure to open the glottis without (hopefully) insufflating the stomach any more than a little. An iGel would potentially help with that, and I can't imaging a mechanism by which it would hurt. A properly placed iGel will not cause airway obstruction.

FWIW, I believe that strictly speaking, the mammalian dive reflex concerns vagally mediated bradycardia and vasoconstriction, and that the reflexive glottic closure is another thing entirely.
well, you beat me to it...the instructors seem to be conflating a well described low threshold for laryngospasm in kids (that are not in full arrest) and the resulting hypoxic bradycardia with some goofy 'dive reflex' explanation.

Even if there were some 'strong mammalian dive reflex' concern in kids, you certainly wouldn't be concerned with it when the brain stem wasn't getting any blood. I'm certainly not when I put them in a coma with medicine and place an SGA.

To the OP, what I would say is that blowing up a small child's stomach with BVM ventilation will absolutely reduce your ability to oxygenate and ventilate because of the significant reduction in lung volumes. That will definitely worsen bradycardia (leading to asystole very quickly).

No ETT? SGA all day everyday....
 
OP
Tigger

Tigger

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Yea, in my head pretty much the first thing we’re doing after compressions is putting an SGA in. The potential for gastric insufflation seems very high with a BVM which is not good news. Not to mention the the challenge to do decent compressions when using mask ventilation.
 

Carlos Danger

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well, you beat me to it...the instructors seem to be conflating a well described low threshold for laryngospasm in kids (that are not in full arrest) and the resulting hypoxic bradycardia with some goofy 'dive reflex' explanation.

Even if there were some 'strong mammalian dive reflex' concern in kids, you certainly wouldn't be concerned with it when the brain stem wasn't getting any blood. I'm certainly not when I put them in a coma with medicine and place an SGA.

To the OP, what I would say is that blowing up a small child's stomach with BVM ventilation will absolutely reduce your ability to oxygenate and ventilate because of the significant reduction in lung volumes. That will definitely worsen bradycardia (leading to asystole very quickly).

No ETT? SGA all day everyday....
Yeah, the one thing that came to mind was the generally low threshold for laryngospasm in kids as well as the perception that SGAs frequently induce airway reactivity in inadequately anesthetized patients, which wouldn't be a concern here.
 

Arctan

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During our monthly continuing education from the hospital system, a pediatric drowning scenario was brought forth. Nothing out of the ordinary, 3 year old in a PEA arrest after being removed from a pool.

We don't intubate pediatrics in this system, instead we have iGels down to pediatric sizes.

Without really providing much evidence, the educators say not to use an iGel or SGA as children have strong mammalian dive reflexes and iGel will obstruct their airway while the pressure from using a BVM and OPA will open the airway just fine. This makes absolutely no sense to me. Has anyone else heard anything like this?

I get not intubating kids, but the airway pressures afforded to the patient by ETT (and the ability to suction) would seem to be of benefit in a drowning. Obviously SGAs do not generate significant airway pressures, but it seems that they'd be more effective than a mask ventilation? Or am I just wrong.
How about a BVM?
 
OP
Tigger

Tigger

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DesertMedic66

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You're new, but come on man. It really helps to read the whole thread before asking a question or commenting.
Not to mention BVM was mentioned in the first post…
 

ffemt8978

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Sorry, I have ADHD, And I don't read things thoroughly.
Take this as a lesson then...take the time ti read and understand the threads first. It will help you down the road in many things in life, such as reading patient charts.
 

HardKnocks

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I would agree with the OP. I believe its just a matter of the lack data with success that drives the hesitancy.​

Emesis​

Detailed data on the occurrence of emesis in drowning are also lacking. One study, reported 25–60% of drowning victims vomited (151). Another study revealed that emesis occurred in 86% of drowning victims who required cardiopulmonary resuscitation and in 50% of those who required no intervention (154). Autopsy series have disclosed aspiration of gastric contents in 24% of drowning victims (80). In a large series on out-of-hospital cardiac arrest (CA) with a cardiac and non-cardiac etiology, emesis occurred in 30–35% of all patients (247). The trigger can be the condition underlying the arrest, CA itself, gastric distension caused by artificial ventilation, or improper chest compression that increases intra-abdominal pressure.
The main vagal sensory afferents responsible for emesis originate from mechano-, osmo-, and chemoreceptors activated by gastric distension or mucosal irritation (14, 21). Mucosal chemoreceptors in the stomach can be stimulated by hydrochlorides or hypertonic saline (13). These afferents relay information to the nucleus tractus solitarium and then to the medulla oblongata, where a neural network (central pattern generator) coordinates the efferent response (21, 110). This integration area receives afferents also from the cerebral cortex, the vestibular region, and a chemoreceptor trigger zone located between the medulla and the floor of the fourth ventricle. The chemoreceptor trigger zone detects, within the blood, emetic stimulants, including hypoxia and ketoacidosis. The efferent motor pathways innervate the upper gastrointestinal tract via cranial nerves V, VII, IX, X, and XII, the diaphragm and abdominal muscles via spinal nerves (21, 26, 110).
Emesis includes retroperistaltic activity from the small intestine, relaxation of the pyloric sphincter, downward contraction of the diaphragm with decreased intrathoracic pressure, increase in intra-abdominal pressure, contraction of the abdominal wall muscles, squeezing and contraction of the stomach with elevation of intragastric pressure and closure of the pylorus, relaxation of the esophageal sphincter, and expulsion of gastric contents (130, 172). The extent to which these classical reflex mechanisms explain emesis in drowning is undefined.
During drowning, gastric contents can be aspirated into the airways, resulting in pulmonary infection and chemical irritation (68, 274). Emesis can also interfere with pulmonary resuscitation. In drowning, both vomiting and cardiopulmonary resuscitation may cause gastric mucosal tears, the frequency of which varies widely among studies but has been detected in as many as 21% of patients (15, 33, 55, 145).


The i-gel differs from the devices described above in that it has a cuff that does not require inflation. The i-gel also possesses a separate gastric channel. Despite, and in some cases because of, these features there have been cases described in the literature of both regurgitation and aspiration of gastric contents: Gibbison et al. described a case series of three patients who regurgitated under anesthesia [41]. In two of these cases, the authors stated that the i-gel protected the patients from aspiration. The third case did aspirate, but with no complications, and was discharged the same day. The authors state that the drain tube allowed recognition of regurgitation, which they suggest may have gone undiscovered with the use of a first-generation device. They conclude that the incidence of regurgitation and aspiration for the device is low and noted that—at the time—no patients appeared to have come to harm from such episodes. This phenomenon of “recognition of regurgitation” is also described in a case by Liew et al. [42].

The i-gel has been found to have a lower esophageal seal than both the cLMA and PLMA, but together with the PLMA it was found to drain away regurgitated fluid effectively [43]. The lower esophageal seal is likely due to the fact that the tip of the i-gel is narrower—which was a deliberate design intended to decrease dysphagia associated with SGAs [3].

The SLIPA, LTS-II, and its disposable version LTS-D have no published reports referring to either regurgitation or aspiration.

There is still a lack of high-quality evidence associated with those SGAs with an incorporated gastric channel with regard to their ability to deal with the risk of regurgitation and aspiration and large, well-conducted trials are needed in this area. Despite this lack of evidence, the authors of NAP4 made recommendations regarding the use of 2nd-generation SGAs, including the following: “If tracheal intubation is not considered to be indicated but there is some (small) increased concern about regurgitation risk a second generation supraglottic airway is a more logical choice than a first generation one.” Similar recommendation has been also published in a recent editorial [44].
 

E tank

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I would agree with the OP. I believe its just a matter of the lack data with success that drives the hesitancy.​

Emesis​

Detailed data on the occurrence of emesis in drowning are also lacking. One study, reported 25–60% of drowning victims vomited (151). Another study revealed that emesis occurred in 86% of drowning victims who required cardiopulmonary resuscitation and in 50% of those who required no intervention (154). Autopsy series have disclosed aspiration of gastric contents in 24% of drowning victims (80). In a large series on out-of-hospital cardiac arrest (CA) with a cardiac and non-cardiac etiology, emesis occurred in 30–35% of all patients (247). The trigger can be the condition underlying the arrest, CA itself, gastric distension caused by artificial ventilation, or improper chest compression that increases intra-abdominal pressure.
The main vagal sensory afferents responsible for emesis originate from mechano-, osmo-, and chemoreceptors activated by gastric distension or mucosal irritation (14, 21). Mucosal chemoreceptors in the stomach can be stimulated by hydrochlorides or hypertonic saline (13). These afferents relay information to the nucleus tractus solitarium and then to the medulla oblongata, where a neural network (central pattern generator) coordinates the efferent response (21, 110). This integration area receives afferents also from the cerebral cortex, the vestibular region, and a chemoreceptor trigger zone located between the medulla and the floor of the fourth ventricle. The chemoreceptor trigger zone detects, within the blood, emetic stimulants, including hypoxia and ketoacidosis. The efferent motor pathways innervate the upper gastrointestinal tract via cranial nerves V, VII, IX, X, and XII, the diaphragm and abdominal muscles via spinal nerves (21, 26, 110).
Emesis includes retroperistaltic activity from the small intestine, relaxation of the pyloric sphincter, downward contraction of the diaphragm with decreased intrathoracic pressure, increase in intra-abdominal pressure, contraction of the abdominal wall muscles, squeezing and contraction of the stomach with elevation of intragastric pressure and closure of the pylorus, relaxation of the esophageal sphincter, and expulsion of gastric contents (130, 172). The extent to which these classical reflex mechanisms explain emesis in drowning is undefined.
During drowning, gastric contents can be aspirated into the airways, resulting in pulmonary infection and chemical irritation (68, 274). Emesis can also interfere with pulmonary resuscitation. In drowning, both vomiting and cardiopulmonary resuscitation may cause gastric mucosal tears, the frequency of which varies widely among studies but has been detected in as many as 21% of patients (15, 33, 55, 145).


The i-gel differs from the devices described above in that it has a cuff that does not require inflation. The i-gel also possesses a separate gastric channel. Despite, and in some cases because of, these features there have been cases described in the literature of both regurgitation and aspiration of gastric contents: Gibbison et al. described a case series of three patients who regurgitated under anesthesia [41]. In two of these cases, the authors stated that the i-gel protected the patients from aspiration. The third case did aspirate, but with no complications, and was discharged the same day. The authors state that the drain tube allowed recognition of regurgitation, which they suggest may have gone undiscovered with the use of a first-generation device. They conclude that the incidence of regurgitation and aspiration for the device is low and noted that—at the time—no patients appeared to have come to harm from such episodes. This phenomenon of “recognition of regurgitation” is also described in a case by Liew et al. [42].

The i-gel has been found to have a lower esophageal seal than both the cLMA and PLMA, but together with the PLMA it was found to drain away regurgitated fluid effectively [43]. The lower esophageal seal is likely due to the fact that the tip of the i-gel is narrower—which was a deliberate design intended to decrease dysphagia associated with SGAs [3].

The SLIPA, LTS-II, and its disposable version LTS-D have no published reports referring to either regurgitation or aspiration.

There is still a lack of high-quality evidence associated with those SGAs with an incorporated gastric channel with regard to their ability to deal with the risk of regurgitation and aspiration and large, well-conducted trials are needed in this area. Despite this lack of evidence, the authors of NAP4 made recommendations regarding the use of 2nd-generation SGAs, including the following: “If tracheal intubation is not considered to be indicated but there is some (small) increased concern about regurgitation risk a second generation supraglottic airway is a more logical choice than a first generation one.” Similar recommendation has been also published in a recent editorial [44].
Guess I'm missing something. Is aspiration a concern here? Especially because the OP was about using a BVM v. SGA?
 

RocketMedic

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CPR, ETI, PALS it. Relying on the tiny little gastric port on an iGel is silly.
 
OP
Tigger

Tigger

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CPR, ETI, PALS it. Relying on the tiny little gastric port on an iGel is silly.
Well we don't intubate children as was in the original post sooo...
 

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