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Esophageal Insufflation with Normal Fiberoptic Positioning of the ProSeal™ Laryngeal Mask Airway

2002; Lippincott Williams & Wilkins; Volume: 94; Issue: 4 Linguagem: Inglês

10.1097/00000539-200204000-00050

1526-7598

M. Stix, Carl J. Borromeo, Cornelius J. O’Connor,

Tracheal and airway disorders

The drain tube (DT) of the ProSeal™ laryngeal mask airway (PLMA) (Laryngeal Mask Company, Henley-on-Thames, UK) is the separate lumen that exits the leading edge of the mask and contacts the esophageal inlet (1,2). Its functions are to 1) channel regurgitated fluids to the outside, 2) allow easy passage of an orogastric tube, 3) help diagnose PLMA malpositioning, and 4) prevent gastric insufflation with positive pressure ventilation (PPV) (1,2). With regard to this last role, it has been described for theoretical “avoidance of gastric insufflation with positive pressure ventilation”(1). Again, “In theory, gastric insufflation is unlikely because any airway pressure exposed to the upper sphincter should be vented up the drainage tube”(2). Previously, we described esophageal aspiration of air through the DT with spontaneous respiration (aerophagia) (3). Here, we present two cases demonstrating that normal fiberoptic positioning of the PLMA does not eliminate the risk of esophageal insufflation (EI) with PPV. EI can occur simultaneously with venting from the DT during PPV with the PLMA. Case 1 A 63-yr-old woman underwent general anesthesia with a PLMA 4 with PPV for an abdominal hysterectomy. The PLMA was satisfactorily inserted (4) and was inflated to a cuff pressure of 60 cm H2O. Positive pressure applied to the bag of the anesthesia circuit demonstrated no leaks at the PLMA/esophageal seal, as determined by a sensitive “soap bubble DT test”(5). The maximal seal pressure (maximal achievable airway pressure squeezing the circuit bag) was 40 cm H2O and was limited by an oropharyngeal leak, not a DT leak. Maintenance mechanical PPV consisted of a rate of 10 breaths/min, an exhaled tidal volume of 550 mL, an inspiratory/expiratory ratio of 1:1.5, and a peak airway pressure of 23 cm H2O. The patient was positioned in a moderate Trendelenburg position. In the middle of the case, the maximal seal pressure was tested again and, despite full muscle relaxation and adequate anesthesia, was noted to have decreased to 30 cm H2O. There was now a demonstrable leak from the DT, as well. After application of soap solution to the DT port and with sustained inflation, a large bubble was formed. A 5.0-mm-outer-diameter (OD) fiberscope was passed via the airway tube of the PLMA to assess positioning, and it was found to be normal (Fig. 1; bottom, end exhalation). When maximal sustained inflation was applied, the laryngeal relationship to the PLMA changed; the larynx was displaced anteriorly, the cuffs were displaced laterally, and the pyriform fossae were exposed (Fig. 1; top, maximal PPV). A fiberoptic examination was then performed via the DT. Esophageal mucosa was seen to completely occlude the DT tip (Fig. 2; top). During inflation, however, the left aspect of the mucosa peeled away from the DT tip as the esophageal lumen opened with insufflation (Fig. 2; bottom). The esophagus was being insufflated via the left pyriform fossa during the sustained inflation maneuver.Figure 1: Fiberoptic view through the airway tube of the ProSeal™ laryngeal mask airway (PLMA) in Case 1. Top, relationship of larynx to PLMA during maximal positive pressure ventilation (PPV). Arrow points to the left pyriform fossa; bottom, relationship of larynx to PLMA at end exhalation.Figure 2: Fiberoptic images for Cases 1 and 2 obtained through the drain tube (DT). Top images show esophageal mucosa occluding the DT tip at end exhalation. Bottom images show esophageal insufflation beginning from the lateral aspects of the esophagus during the maximal inflation maneuvers.The PLMA was re-taped, adding more longitudinal force to the airway tube and integral bite block. Simply re-taping the PLMA was enough to abolish the leak from the DT. The maximal seal pressure was restored to 40 cm H2O limited by an oropharyngeal leak. Case 2 We were alarmed by the observations of EI in Case 1 and wondered whether it could have been caused by the 5.0-mm-OD fiberscope obstructing the DT and preventing venting. We were also struck by the importance of the relatively simple task of taping and securing the PLMA with proper longitudinal force. Case 2 addressed these concerns by making observations with a 4.0-mm-OD fiberscope in a very brief situation, deliberately attempting to mimic loose taping of a PLMA. A 45-yr-old woman underwent general anesthesia with a PLMA 4 with PPV for an abdominal hysterectomy. The PLMA was satisfactorily inserted (4) and had no leaks at the PLMA/esophageal seal, as determined by the bubble test (5). The maximal seal pressure was 38 cm H2O and was limited by an oropharyngeal leak. A 4.0-mm-OD fiberscope was passed via the airway tube and verified normal PLMA positioning. Soap solution was then applied to the DT port. While maximal inflation was administered, traction was applied to the airway tube and integral bite block, which remained taped to the maxilla. Fiberoptically, the traction on the airway tube did not change the PLMA position behind the cricoid cartilage. However, at a certain point the DT abruptly developed a leak, which promptly burst the soap membrane. A fiberoptic examination was then performed via the DT. Esophageal mucosa was seen to completely occlude the DT tip (Fig. 2; top). Maximal inflation was applied and identical traction slowly applied to the taped airway tube and integral bite block. Figure 2 demonstrates how, at a certain moment, the right lateral esophageal mucosa moves away from the DT tip, exposing the esophageal lumen. Sustained EI was fiberoptically observed during the remainder of the maximal inflation maneuver. During the subsequent exhalation, the esophageal lumen initially remained open but then gradually collapsed. Discussion We have presented two cases suggesting that normal fiberoptic positioning of the PLMA does not eliminate the risk of EI. These cases indicate the likelihood that EI can occur simultaneously with venting from the DT when there is a breach of the PLMA/esophageal seal during PPV. Below, we discuss several of the mechanisms involved in EI as well as the use of the DT for diagnosing this potentially dangerous clinical entity. It is worthwhile to reexamine Figure 1 to understand some of the mechanisms involved in EI. The photographs show how PPV dynamically changes the anatomic relationships of the larynx and PLMA. During maximal PPV, the larynx seems displaced anteriorly, away from the tip of the mask, and the undersides of the arytenoid and cricoid cartilages are exposed. The cuffs of the PLMA are displaced laterally by the PPV within the bowl. The net result is that the pyriform fossae are broadly exposed, allowing an easy route for gas to reach the lateral aspects of the esophageal inlet. It is interesting that the human upper esophageal sphincter (UES) is asymmetric and is weaker laterally compared with anteroposteriorly (6,7). Exposure of the pyriform fossae and UES asymmetry may explain why EI occurred from the sides in both Cases 1 and 2. The junction of the PLMA with the esophagus occurs in the UES. This entity is a well defined anatomic structure compared with the lower esophageal sphincter and consists of two parts. The first component is the striated cricopharyngeus muscle that attaches anteriorly to the cricoid cartilage. This circular band of muscle has a craniocaudad extent of approximately 1–2 cm (8). The second component is a variable 1- to 3-cm extent of smooth muscle within the esophageal tube itself (6–8). The manometrically defined “high-pressure zone” of the UES is usually identified with the cricopharyngeus muscle (6–8). The tip of the PLMA lies behind the cricoid cartilage, and it is reasonable to assume that the component of the esophagus that squeezes the cuff at the tip is the cricopharyngeus muscle. The cricopharyngeus muscle forms a PLMA/esophageal or PLMA/UES seal. For EI to occur, PPV must breach this PLMA/UES seal on the way to the esophageal lumen. Beyond the PLMA/UES seal lies an additional length of the functional UES that may include a segment of cricopharyngeus muscle as well as the smooth muscle component. EI involves overcoming both the PLMA/UES seal as well as this residual sphincter component residing distal to the cuff tip. As maximal PPV from the bowl forces its way through the PLMA/UES seal, it ultimately follows the path of least resistance. The excess PPV can either enter the esophageal lumen or exit via the tip of the DT. The photographs in Figure 2 make an important point concerning the venting route via the DT; before EI takes place, the DT tip is actually occluded by mucosa. Therefore, during the initial conditions when the PLMA/UES seal is being breached, the effective area of opening at the tip of the DT is zero. Venting via the DT requires that the abutting esophageal mucosa be pushed away. Therefore, as the PLMA/UES seal is being bypassed, the route to the esophagus may already be chosen in many cases. Figure 2 shows that in Cases 1 and 2, DT venting occurred after the esophageal lumen itself opened and the mucosa at the tip of the DT peeled away. The determination of the increase in pressure within the DT during EI is important and requires further investigation. The increase in DT pressure ultimately determines how sensitive a DT test must be for diagnosing this clinical entity. There are several reasons why the pressure increases within the DT may not be dramatic in all cases. The cuff at the tip of the PLMA probably wedges open a significant proportion of the functional UES. The maximal PPV within the bowl of the PLMA will therefore undergo a resistive pressure decrease across this PLMA/UES seal. Also, because the jet of inspired gases entering the esophageal lumen takes place lateral to the DT, the pressure within the DT orifice may be reduced by a Venturi effect. Finally, the venting route back into the DT tip may be variably narrowed by esophageal mucosa. The exact proportion of EI versus DT venting, when PPV overcomes the PLMA/UES seal, remains unknown and may vary from patient to patient. In some patients, the entirety of excess PPV may exit the DT, whereas in other patients the DT venting could be slight. In our clinical practices we regularly check the DT port with bubble solution intraoperatively to rule out DT leaks (9). This is an extremely sensitive test of DT pressure change and gas flow, and we believe that most, if not all, cases of EI could be diagnosed by this method. We consider any leak from the DT to be abnormal. We were concerned in Case 1 that our observation may have been artifactual because of the 5.0-mm-OD fiberscope effectively obstructing the DT. Observations in Case 2 were obtained with a 4.0-mm-OD fiberscope and convinced us that EI is not artifactual. Case 2 also illustrates the importance of the rather mundane process of securing and taping the PLMA with sufficient longitudinal force. Merely fiberoptically observing that the PLMA lies behind the cricoid cartilage does not guarantee satisfactory behavior of the PLMA/UES seal. This seal is like a compression fitting whose quality depends on the contact force at the applied surfaces. Both Cases 1 and 2 emphasize that the PLMA should be secured with moderate (not excessive) longitudinal force. Finally, EI is different from gastric insufflation. All of the gas insufflated into the esophagus may not ultimately be forced into the stomach. EI occurs during the inspiratory phase of the ventilator cycle, and one must consider what happens during exhalation—during exhalation, the DT might be able to decompress the esophagus to atmospheric pressure. This is an advantage of the PLMA compared with the Classic LMA design. We imagine that the normally positioned Classic LMA functions much like a ball valve at the upper esophagus, permitting EI during PPV inspiration but preventing esophageal decompression during exhalation. The PLMA may promote esophageal decompression during exhalation if esophageal mucosa does not occlude the DT tip during the expiratory phase. In summary, anesthesiologists should not be lulled into a false sense of security that the DT, even if properly situated, will vent all PPV away from the esophagus. The proportion of PPV breaching the PLMA/UES barrier that enters the esophageal lumen versus the DT remains unknown and may vary from patient to patient. The determination of the pressure increase within the DT under these circumstances is also unknown and will dictate the required sensitivity for DT tests used to diagnose EI. EI can occur simultaneously with venting from the DT during PPV with the PLMA. In our clinical practice we use an extremely sensitive soap bubble technique for measuring any change in DT pressure and flow (5). Without proof, we believe it is possible to use PPV without ever insufflating the stomach as long as the PLMA is adequately positioned (4) and has zero venting from the DT as determined by frequent intraoperative DT checks with the bubble method (9). Finally, one of the DT’s roles in preventing gastric insufflation could be to decompress the esophagus during the expiratory phase of the ventilator cycle.