I would agree with the OP. I believe its just a matter of the lack data with success that drives the hesitancy.
Drowning physiology relates to two different events: immersion (upper airway above water) and submersion (upper airway under water). Immersion involves integrated cardiorespiratory responses to skin and deep body temperature, including cold shock, physical incapacitation, and hypovolemia, as...
journals.physiology.org
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).
Supraglottic airway devices are routinely used for airway maintenance in elective surgical procedures where aspiration is not a significant risk and also as rescue devices in difficult airway management. Some devices now have features mitigating risk of aspiration, such as drain tubes or...
www.hindawi.com
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].
