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Massive Subcutaneous Emphysema and Bilateral Tension Pneumothoraces After Supplemental Oxygen Delivery via an Airway Exchange Catheter: A Case Report

Hulst, Abraham H. MD; Avis, Hans J. MD, PhD; Hollmann, Markus W. MD, PhD; Stevens, Markus F. MD, PhD

doi: 10.1213/XAA.0000000000000414
Case Reports: Case Report

A patient suffered massive subcutaneous emphysema and bilateral tension pneumothoraces after receiving supplemental oxygen through an airway exchange catheter (AEC). Complications of AEC placement include misplacement, direct injury to the larynx, bronchi or lung, barotrauma related to oxygen supplementation, and a loss of airway. We review these complications and discuss the specific risks of supplementing oxygen using an AEC. We suggest measures to limit pressure from the oxygen source and warn against advancing an AEC too far into the tracheobronchial tree.

From the Department of Anesthesiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Accepted for publication July 11, 2016.

Funding: None.

Conflicts of Interest: See the Disclosure section at the end of the article.

Address correspondence to Markus W. Hollmann, MD, PhD, Academic Medical Centre, Meibergdreef 9H1Z-1321105 AZ Amsterdam, The Netherlands. Address e-mail to

We describe a case of massive subcutaneous emphysema, bilateral tension pneumothoraces, and circulatory arrest after delivering supplemental oxygen via an airway exchange catheter (AEC). AECs often are used to facilitate exchange of an endotracheal tube (ETT) or reintubation in patients with a difficult airway.1 Several guidelines mention temporarily oxygenating a patient through the hollow core of an AEC2,3; however, there are several potential risks associated with the use of an AEC, including misplacement, laryngeal trauma, direct bronchial or lung injury, barotrauma related to oxygen supplementation, and a loss of airway.4,5 In this case report, we discuss these complications and focus on barotrauma and correct placement of an AEC. We obtained written consent for publication of this case report from the patients’ family.

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A 53-year-old man with Klippel-Feil syndrome and obstructive sleep apnea syndrome underwent a revision of a craniocervical posterior spondylodesis under general anesthesia. The anesthesiologist induced anesthesia, mask ventilated the patient, and administered neuromuscular relaxation in preparation for intubation. During direct laryngoscopy, he could not see the epiglottis or vocal cords. Nonetheless, on the first attempt, he successfully placed an ETT (8 mm, Safety Clear Tracheal Tube; Teleflex, Athlone, Ireland) with the aid of an indwelling stylet (Flexi-Slip Stylet; Teleflex). He confirmed correct placement by capnography and bilateral breath sounds at auscultation and fixed the ETT at 22 cm distal to the upper central incisors.

The 5-hour operation, performed with the patient in the prone position, was uneventful. Anesthesia was maintained by the use of sevoflurane, and norepinephrine up to 0.06 μg/kg/min was used intraoperatively for hemodynamic support. Postoperatively, the patient was sedated with propofol and ventilated for 3 hours, with the head of the bed placed in an upright position because of severe facial swelling caused by prolonged prone positioning. Before extubation, the larynx was inspected by videolaryngoscopy, and no significant edema of the larynx was visible. A leak-test (confirmation of audible air movement with a deflated ETT cuff) was not performed because of its limited predictive value for reintubation.6,7

Because of the Cormack Lehane IV score at intubation, an AEC was left in place after extubation to facilitate reintubation, if necessary. An extra firm, soft-tipped Cook 11 Fr AEC (G36401; Cook Medical, Bloomington, IN) was introduced through the ETT without resistance, and with the 40-cm mark of the AEC visible at least one hand width outside the end of the tube. The ETT measured approximately 37 cm, including its connector that was left in place, and the AEC thus did not protrude from the tube at the time of placement. Subsequently, while the patient was awake and breathing spontaneously, the ETT was removed and the AEC was kept in place manually.

Immediately after extubation, a visible rise and fall of the chest and audible breathing were noted. CO2 from the AEC was not measured at this point. Snoring suggested that the airway partially was obstructed, which could be explained by the patient’s obstructive sleep apnea syndrome. During a period of approximately 3 minutes, oxygen saturation gradually declined to 87%. To stabilize oxygenation, 4 L/min of supplemental oxygen was administered via the Luer lock Rapi-Fit adaptor mounted at the proximal end of the AEC via an Ohmeda O2 flowmeter (Ohio Medical, Gurnee, IL). Within seconds, the patient developed subcutaneous emphysema of the lip, face, and neck followed by the thorax, abdomen, and scrotum while his oxygen saturation decreased further to 78%. A size 8 ETT was introduced over the AEC, the AEC was removed, and positive pressure ventilation was started. Unfortunately, no chest movement or expired CO2 was noted. Because of the speed of deterioration, location of the ETT was not confirmed with a fiberoptic bronchoscope, and direct or video laryngoscopy was not considered because of the swelling induced by subcutaneous emphysema. Instead, the ETT was removed and a Melker emergency cricothyroidotomy catheter (Cook Medical) was inserted percutaneously through the cricothyroid membrane into the trachea.

After cricothyroidotomy, the lungs could be ventilated with high driving pressures (>40 cm H2O) and CO2 was detected in the expired air; however, oxygen saturation had continued to fall, and the patient developed asystole. CPR was started, but chest compressions were nearly impossible because of the stiffness of the chest. Needle thoracentesis was attempted, but the pleurae were not reached because of subcutaneous swelling. Bilateral chest tubes were inserted with audible release of air, and subsequently effective chest compressions were delivered. Return of spontaneous circulation was achieved after 12 minutes, with a 24-minute duration of oxygen saturation below 80%. A chest X-ray, ordered after chest tube insertion, showed extensive mediastinal and subcutaneous emphysema (Figure). Surgical tracheotomy was performed with the femoral vessels cannulated and extracorporeal circulation facilities in stand-by.



Ventilation pressures had returned to normal, and the patient was admitted to the intensive care unit for postresuscitation support. Unfortunately, the patient had developed a persistent postanoxic coma. Bronchoscopy (via the mouth and through the tracheotomy) and a computed tomography scan did not reveal bronchial or tracheal lacerations. At discharge to a neurological care facility on postoperative day 27, the patient remained ventilated via tracheostomy, had a Glasgow Coma Scale score of 8, could open his eyes spontaneously, withdrew from painful stimuli, and had a tracheostomy tube in situ.

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This patient developed massive subcutaneous emphysema, bilateral tension pneumothoraces, and circulatory arrest associated with oxygen supplementation via an AEC. The literature suggests several potential risks associated with the use of AECs, including misplacement, laryngeal trauma, direct bronchial or lung trauma, barotrauma, and a loss of airway.4,5 In our case, because the AEC was introduced through the ETT, the larynx was bypassed, and laryngeal trauma was unlikely. One possible mechanism for the subcutaneous emphysema we observed was submucosal positioning of the AEC tip, eg, under an already preformed mucosal membrane injury, possibly induced during intubation. Alternatively, despite the soft-tip, the AEC itself may have caused a mucosal tear. Another potential mechanism of injury is closure or narrowing of the airway, preventing exhalation and causing barotrauma. Complete obstruction did not occur because expiratory snoring was present, but the escape of supplemental oxygen may still have been limited with resulting auto positive end-expiratory pressure. Both of the aforementioned possibilities (subcutaneous emphysema or auto positive end-expiratory pressure) can explain the high airway pressures we observed when ventilating through the emergency cricothyroidotomy. Because bronchoscopy and computed tomography did not display a definite injury of the airway, the precise mechanism causing this patient’s devastating injury remains obscure.

Many current guidelines on difficult airway management recommend the use of an AEC as a guidewire for reintubation during extubation of the difficult airway.2,3 They mention the option of temporarily oxygenating and ventilating a patient via the hollow core of an AEC but do not emphasize complications specific to its use. Nonetheless, in the instruction manual delivered with every AEC, Cook Medical identifies barotrauma as a potential complication of use. Although oxygenating a patient via an AEC buys time, reintubation is a more definitive strategy and arguably safer when an extubation trial is considered unsuccessful.

We found one case report8 in which low pressure oxygen insufflation of 5 L/min via an AEC resulted in a pressure pneumothorax and death. That report cites one other case9 of pulmonary barotrauma after oxygen supplementation through an AEC by manual ventilation. In their review of the literature, the authors note that jet ventilation was used in all other published cases of barotrauma after oxygen administration. The authors concluded that over a wide range of driving pressures and clinical conditions, jet ventilation through an AEC may be associated with a clinically significant risk of barotrauma. In contrast, oxygen insufflation through an AEC was associated with a lower risk.

In 3 case series that reported the use of an AEC for oxygen supplementation between 1 and 8 L/min via an AEC in 96 children and adults, no barotrauma was reported.4,10,11 All authors mentioned that humidified oxygen was used and the AEC was placed at the same depth as the ETT to avoid carinal irritation. The Luer lock Rapi-Fit connector was described in one case series.4 In our patient, we used an AEC with a smaller diameter (11 Fr) and a much softer tip, which we hoped would decrease the likelihood of tissue trauma. We cannot definitively rule out tissue trauma, and a 2015 preclinical study noted that tracheal tears are still possible via a soft-tipped AEC.12

In a single-center retrospective observational study13 of 527 AEC uses for tube exchange and 650 for facilitating difficult intubation (type of AEC and soft or hard tip were not specified), the authors reported an airway injury rate of 7.8% (41/527; 95% confidence interval, 5.7%–10.4%) and a radiographically verified pneumothorax rate of 1.5% (8/527; 95% confidence interval, 0.7%–3.0%). Taken together, current literature suggests that the newer soft-tipped catheters may have a lower risk of complications14; however, this assumption has not yet been verified by (pre)clinical studies.12,15

Barotrauma after oxygen delivery via an AEC was another potential mechanism of injury in our patient. In a pig model of oxygen administration that used AECs (32 cases), no barotrauma occurred when the catheter tip was placed above the carina, but in all cases where the tip of the AEC was placed below the carina, macroscopic barotrauma occurred.12 Furthermore, no difference between stiff versus soft-tipped catheters was noted. Of note, isolated and collapsed pig lungs were used in this model, which limits the translation of these findings to clinical practice.

Many recommendations have been made for the safe use of oxygen delivery over an AEC. These include confirmed mid-tracheal placement, assessing airway patency around the AEC, eg, by confirming sufficient expiration, and administration of oxygen at a low driving pressure. Other authors, however, have noted that airway patency and guarantee of expiration is difficult to assess in clinical practice.8 In the literature, driving pressure is seldom mentioned when oxygen insufflation is reported. However, we measured a pressure of 4.7 bar (68 psi or 4800 cm H2O) developing within seconds, in a system of an O2-tube and a distally occluded AEC with an oxygen flowmeter set at only 1 L/min, using the same AEC and flowmeter as mentioned in our case report. Although pressures as low as 40 cm H2O and less can induce pneumothorax and air emphysema, it is possible that the rapid development of tension pneumothorax and subcutaneous emphysema in this case may be due to development of high pressure in an occluded system.

Without knowing the specific cause of the subcutaneous air in our case, one strategy to reduce the damage associated with buildup of high pressure is to pressure-limit oxygen sources. For example, with the use of a pressure limiting valve or pop-up valve as usually are now included in bag valve mask system. Such a safeguard might have reduced the severity of injury in the case we describe and limit adverse events known to be associated with high-pressure supplemental oxygen.16–18

In addition, malpositioning of the AEC, causing trauma to the smaller airways or “wedged” deep enough in the airway to prevent ready exhalation, is another possible cause of the complication we encountered. Although at placement the tip of the AEC will have been inside the tube, with the 40-cm mark on the AEC clearly visible several centimeters outside the 37-cm long tube, it may have been displaced during removal of the tube despite our efforts to maintain its position.

Positioning of the AEC below the carina is contraindicated as described in the user manual by Cook Medical, and may cause parenchymal injury with as little as 2 L/min O2 flow over an AEC in the porcine airway.12

Some also have argued that the length of 100 cm of the 11 Fr. Cook AEC far exceeds the length necessary for safe ETT exchange and may lead to overly deep AEC placement.19 They advocate reducing the length of these catheters to reduce the incidence of complications. Although we carefully measured the depth of insertion of our AEC, it is possible that the catheter may have moved or the excess length may have made the catheter more difficult to manipulate.

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Although an AEC is certainly a valuable tool, there are potential risks associated with its use, which might lead to devastating outcomes. Supplementation of oxygen through an AEC may lead to severe barotrauma, even if great care is taken to position the device properly, when the pressure of the oxygen source is not limited to a safe level by a pressure-limiting valve. Users should pay close attention to the depth of insertion of an AEC and confirm sufficient expiration of air, especially when considering administration of oxygen.

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Name: Abraham H. Hulst, MD.

Contribution: This author helped prepare the manuscript.

Conflicts of Interest: None.

Name: Hans J. Avis, MD, PhD.

Contribution: This author helped prepare the manuscript.

Conflicts of Interest: None.

Name: Markus W. Hollmann, MD, PhD.

Contribution: This author helped prepare the manuscript.

Conflicts of Interest: Markus W. Hollmann is the Section Editor of Preclinical Pharmacology in Anesthesia & Analgesia, and Section Editor NTvA.

Name: Markus F. Stevens, MD, PhD.

Contribution: This author helped prepare the manuscript.

Conflicts of Interest: None.

This manuscript was handled by: Avery Tung, MD, FCCM.

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