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It was reported in a journal article that a (b)(6) patient 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, the surgeon could not see the epiglottis or vocal cords.Nonetheless, on the first attempt, an endotracheal tube (ett) was successfully placed with the aid of an indwelling stylet.The surgeon 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 ug/ 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.Because of the cormack lehane iv score at intubation, an airway exchange catheter (aec) was left in place after extubation to facilitate reintubation, if necessary.A double lumen extra firm soft tipped airway exchange catheter 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 a flowmeter.Within seconds, the patient developed subcutaneous emphysema of the lip, face, and neck followed by the thorax, abdomen, and scrotum while their 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 an emergency cricothyroidotomy catheter 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 their eyes spontaneously, withdrew from painful stimuli, and had a tracheostomy tube in situ.
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Investigation ¿ evaluation: a review of the complaint history, documentation, drawing, instructions for use (ifu), manufacturing instructions, and quality control of the device was conducted during the investigation.No issues were found related to the reported complaint.Complaint sample evaluation was not performed since no product or imaging was returned to assist with this investigation.The lot number for this complaint device is unknown.Consequently, the work order record or its related non-conformances could not be evaluated.Additionally, it could not be determined if additional complaints from the same lot have been reported.The potential adverse events listed in the ifu include "barotrauma" and "perforation of the bronchi or lung parenchyma." one possible mechanism for the subcutaneous emphysema observed is that the aec may have caused a mucosal tear.Another potential mechanism of injury is closure or narrowing of the airway, preventing exhalation of the supplemental oxygen delivered and causing barotrauma.The inability for excess oxygen to escape would cause a build-up of pressure and it is possible that the rapid development of tension pneumothorax and subcutaneous emphysema in this case may be due to this development of high pressure in an occluded system.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 complications encountered.Although original placement was verified, it may have become displaced during removal of the endotracheal tube.Based on the information provided it is feasible to suggest the cause of this event was user technique and/or medical procedure related.The paper indicated that an oxygen source flowing at 4 l/min was connected to the proximal end of the exchange catheter.Per the ifu, if a high-pressure oxygen source is used for insufflation (e.G., jet ventilator), begin at lower pressure and work up gradually.There is no indication that the flow was started lower and slowly increased to 4 l/min.A high flow of oxygen or oxygen jet ventilation delivered via the lumen of the catheter or the bronchoscope may result in barotrauma and catastrophic tension pneumothorax.Per the ifu, ¿attention should be paid to insertion depth of catheter into patient¿s airway and correct tracheal position of replacement endotracheal tube.Catheter and endotracheal tube should not be advanced beyond the carina.To avoid barotrauma, ensure that the tip of the cae catheter is always above the carina, preferable 2 ¿ 3 cm.¿ per the article, the tube may have been displaced during removal from the tube.Several risk controls are in place to mitigate the reported hazard.Per the quality engineering risk assessment, no further action is required.The appropriate personnel will be notified and we will continue to monitor for similar complaints.
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