Obstruction of a non-resterilized reinforced endotracheal tube during craniotomy under general anesthesia

Abstract

Many cases of reinforced endotracheal tube (ETT) obstruction were reported in the literature. In most of these cases, the obstruction was related to the use of a resterilized tube with or without the use of nitrous oxide (N₂O). Resterilization and autoclaving of the tube may result in dissection or formation of a bleb between the two layers of the tube that may expand after the use of N₂O. We describe a case of acute non-resterilized reinforced ETT obstruction, by bleb formation, during occipital craniotomy under general anesthesia.

INTRODUCTION

Occipital craniotomy surgeries are usually done with the patient in the prone position. The anesthesiologists frequently use a reinforced endotracheal tube (ETT) In order to avoid tube kinking in the prone position and while manipulating the head and the neck during patient positioning. Despite that using a reinforced tube may be associated with several problems, including external kinking of the tube and internal collapse of the inner lumen causing partial or total occlusion of the tube. The majority of the intraoperative ETT obstruction cases reported in the literature were due to a bleb or an air bubble included during re-sterilization and expanded after nitrous oxide (N₂O) exposure. We described a similar case of a reinforced ETT internal obstruction during an occipital craniotomy. However, in this case, a non-resterilized tube was used.

CASE REPORT

An 18-year-old female patient, American Society of Anesthesiologists II, known to have mild asthma controlled on bronchodilators scheduled for occipital craniotomy.

The patient was premedicated with midazolam 2 mg intravenously. Standard monitors including train of four (TOF) were applied, and general anesthesia was induced intravenously with fentanyl 150 mcg, thiopental 250 mg, and cisatracurium 8 mg. Using a video laryngoscope, a 7.5 mm I.D. reinforced non-sterilized ETT (Safety Flex, Mallinckrodt, Covidien, Ireland) was introduced smoothly over a new shapeable stylet with aluminum core and a soft touch outer casing (VBM Medizintechnik, GmbH, Germany). Cormack Lehane grade 1 was noted, and the tube was fixed to 20 cm at the level of the lips.

After intubation, another intravenous peripheral line, an arterial line and an ultrasound-guided internal jugular central line were inserted.

After putting the patient in the prone position, the ETT was rechecked and showed a bilateral equal air entry on auscultation with no change in the tube position.

Anesthesia was maintained with sevoflurane in a mixture of 40% N₂O and 60% oxygen (O₂), supplemented intravenously with boluses of fentanyl and a continuous infusion of cisatracurium.

The ventilator was set on volume controlled ventilation at 8 ml/kg, 12 breaths/min, without positive end-expiratory pressure. These settings maintained adequate oxygenation and ventilation with peak airway pressures (PAP) <20 cm H₂O. 3 h later, while the surgery was in progress, airway pressures started to rise from 20 to 55 cm H₂O progressively associated with a decrease in O₂ saturation down to 88% even after fraction of inspired O₂ was increased to 100%. Blood pressure and heart rate remained within normal range.

Auscultation of both lungs revealed very poor air entry with very high pressures encountered during manual bag ventilation. Few ventolin puffs were administered through the ETT but did not improve the obstruction. Patient was fully relaxed (TOF = 0) and was not biting on the tube. An 18 French suction catheter was advanced through the ETT failed to pass beyond 11 cm, and suctioning did not reveal any mucus plug.

A chest X-ray was done in the operating theater with patient in the prone position, it ruled out the possibility of a pneumothorax.

After turning the patient into the supine position, the ETT was removed and exchanged with another 7 mm I.D. reinforced ETT using video laryngoscopy. Ventilation became easy, and all parameters including the airway pressures returned back to normal baseline values.

Repositioning the patient into the prone position was done, and surgery was completed uneventfully. The patient was extubated at the end of the procedure without any respiratory complication or sequelae.

The external inspection of the removed ETT showed a longitudinal internal halo between 18 and 22 cm depth markings [Figure 1]. The internal inspection with a 3.3 mm fiberoptic bronchoscope confirmed the presence of a bleb inside the tube with partial occlusion and failed to bypass the obstruction [Figure 2].

Figure 1.

External inspection of the reinforced endotracheal tube showing the longitudinal halo between 18 and 22 cm depth marking

Figure 2.

Fiberoptic inspection showing the bleb inside the tube

The damaged tube was sent to the manufacturing company, they replied the following: “Visual examination shows that there is an occlusion at the 19 cm depth marking to the 23 cm marking restricting the internal diameter of the tubing. The inner layer is restricting the main stem of the tubing. An attempt made to place the returned unit on the patency check mandrel failed” [Figure 3].

Figure 3.

Image from manufacturing company showing the failed mandrel patency test

DISCUSSION

We presented a case of reinforced ETT obstruction by expansion of an internal bleb.

Many similar cases of reinforced ETT obstruction were reported in the literature. In most of these cases, the obstruction was related to the use of a resterilized tube with or without the use of N₂O.[1,2,3,4] Resterilization and autoclaving of the tube may result in dissection or formation of a bubble or bleb between the two layers of the tube that may expand after the use of N₂O. However; in our case, the tube was not resterilized. The hypothesis of a bleb or an air bubble formation during manufacturing of the tube, which expanded after N₂O exposure, is most probably. The stylet aggression hypothesis is unlikely to be responsible of the ETT damage since we did not face any difficulty neither while introducing the stylet into the tube nor while threading the ETT over it. In addition, the manufacturer did not report any scratches or flaps in the inner wall of the tube.

The PAP took 3 h after induction of general anesthesia to rise; this is probably due to an increase in size of the bleb resulting from the use of N₂O. We did not have enough time to see any improvement in the obstruction after turning off the N₂O because of the severity of the obstruction that required an immediate exchange of the ETT.

A rise in airway pressures in patients undergoing general anesthesia may be due to many causes including: Kinking of the tube by oral biting, internal obstruction of the tube by secretions, mucus plugs or blood clots, severe bronchospasm, pneumothorax, and ETT obstruction due to mechanical causes described earlier in this report.

Upon suspecting an ETT obstruction, the following actions might be done immediately: Turn off N₂O, put the patient on 100% O₂, introduce a suction catheter through the tube and perform a fiberoptic examination. These maneuvers were done in our case except the fiberoptic examination because of the prone position and the severity of the obstruction that required an immediate exchange of the ETT.

A reinforced ETT is recommended for single use only and cannot be resterilized or autoclaved as per manufacturer's recommendations.

Although rare, obstruction of a non-resterilized ETT can occur and can be life-threatening. A meticulous inspection, checking of the ETT and its cuff before usage need to be done. If a rigid stylet is required, it should be introduced gently into the ETT and removed gently while advancing the ETT during intubation.