Carron, Pierre-Nicolas

Pasquier, Mathieu

Reilly, Jennifer

Schoettker, Patrick

Yersin, Bertrand

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EM - MORBIDITY AND MORTALITY REPORTBlaming the balloon: the risk of post-intubation tracheobronchialruptureJennifer Richelle Reilly • Mathieu Pasquier •Bertrand Yersin • Patrick Schoettker •Pierre-Nicolas CarronReceived: 9 July 2013 / Accepted: 21 August 2013 / Published online: 31 August 2013 SIMI 2013Keywords Intubation  Tracheobronchial rupture Airway management  Tracheal injuryCase descriptionThe pre-hospital retrieval service attended the home of an82-year-old, 68 kg woman found unconscious with noevidence of trauma. Her airway was obstructed by vomit,oxygen saturation was 48 % and Glasgow Coma Score wassix. The pupils were small and reactive. A cerebrovascularaccident was presumed. The airway was suctioned, fol-lowed by rapid sequence induction with etomidate andsuccinylcholine. Intubation was performed with a size 7Mallinckrodt endotracheal tube (ETT) (Mallinckrodt Hi-Contour Oral Tracheal Tube Cuffed, Covidien llc, 15Hampshire Street, Mansfield, MA 02048) containing a pre-formed stylet, which was removed once the ETT passedthrough the vocal cords. Post-intubation auscultation wassymmetric, oxygen saturation rose to 95 %, and the ETTposition was confirmed by capnography. No further drugswere administered for transfer while the hemodynamicprofile was uneventful.A CT brain scan was normal, while a cervico-thoracicCT scan revealed mediastinal emphysema predominant inthe left para-tracheal region, subcutaneous emphysema ofthe neck and a sub-glottic ETT cuff measuring 3 cm indiameter. No pneumothorax was present. Lesions of thetrachea or oesophagus were not demonstrated. Changes inthe lung fields were suggestive of bronchoaspiration, andthe patient subsequently developed acute respiratory dis-tress syndrome. The initial chest radiograph is shown inFig. 1.While intubation had been uneventful, the patient wasobserved to cough vigorously on the ETT in the emergencydepartment (ED), but administration of further sedation orneuromuscular blocking agent was withheld to allow sub-sequent neurological assessment. At this time, the Ambubag circuit in use had no expiratory valve.Bronchoscopy showed an ETT tip 4 cm above thecarina, food debris and purulent secretions at the carinaand throughout the tracheobronchial tree. There was a4 cm vertical tear of the posterior wall of the membra-nous trachea between the first and fifth tracheal rings. TheETT cuff was repositioned distal to the lesion. Surgicalrepair was not performed. Spontaneous tracheal healingon day 23 was confirmed by bronchoscopy, but thepatient redeveloped pneumonia with no neurologicalimprovement. An MRI imaging of the brain showed dif-fuse leucoencephalopathy, thought to be from hypoxiasecondary to bronchoaspiration, on a background ofdysphagia. After discussion with the family, treatmentlimits were agreed, and the patient subsequently died onday 40.J. R. ReillyEmergency Department and Anaesthesia Department, LausanneUniversity Hospital, Lausanne, SwitzerlandJ. R. ReillyDepartment of Anaesthesia, John Hunter Hospital, Newcastle,AustraliaM. Pasquier  B. Yersin  P.-N. Carron (&)Emergency Department, Lausanne University Hospital (CHUV),1011 Lausanne, Switzerlande-mail: pierre-nicolas.carron@chuv.chP. SchoettkerAnaesthesia Department, Lausanne University Hospital,Lausanne, Switzerland123Intern Emerg Med (2013) 8:753–756DOI 10.1007/s11739-013-0994-yDiscussionBackground and epidemiologyTracheobronchial rupture (TBR) may present followingtrauma, intubation, tracheal cannulation or positive pressureventilation. Its potentially lethal sequelae include tensionpneumothorax, mediastinitis, tracheal stricture and respi-ratory failure [1]. Iatrogenic rupture occurs more commonlythan traumatic rupture [2], and its major cause is airwayinstrumentation, including intubation, tracheal cannulationor rigid bronchoscopy [3–5]. Airway procedures performedunder emergency conditions pose a particular risk [2, 3, 6–11], and have an associated mortality up to four timesgreater following TBR resulting from elective procedures[11]. A closed claim analysis reveals that one-third ofclaims for tracheal injury are for tracheal rupture, mostlyduring routine intubation, and that delayed presentation oftracheal rupture is common [12]. Situational, mechanicaland anatomical risk factors for post-intubation TBR arelisted in Table 1. An incidence has not been reported forsingle-lumen tubes, but is 0.05–0.37 % for double lumentubes in an elective setting [13, 14]. Mortality relates tounderlying disease rather than tracheal rupture [2].PathophysiologyAcute iatrogenic TBR may result from penetrating mech-anisms such as direct perforation of the tracheal wall, orblunt mechanisms such as a sudden increase in trans-tra-cheal pressure resulting in separation of the membranoustrachea. The majority of post-intubation tears are longitu-dinal, occur in the lower third of the trachea, and mayextend into the main bronchi [5, 9], while tracheostomy-associated tears are often in the middle third of the trachea[5]. Post-intubation tears usually occur in the midline or onthe right side of the membranous posterior wall of thethoracic trachea [9, 15]. In traumatic TBR, tears from blunttrauma occur in the thoracic trachea, while tears frompenetrating trauma occur commonly in the anterior extra-thoracic trachea [4].Intrathoracic tracheal rupture displaces air into themediastinum, which redistributes at very low mediastinalpressures by dissection along fascial planes. It is thusuncommon in non-traumatic TBR to raise mediastinalpressure to the near 20 mmHg pressure required to rupturethe mediastinal pleura and cause a pneumothorax [16].When a pneumothorax does occur, it is universally pre-ceded by subcutaneous or mediastinal emphysema [4, 14].Differential diagnoses of pneumomediastinum includerupture of other air-containing structures, such as theoesophagus or alveoli, by blunt chest trauma or positivepressure ventilation [14].DiagnosisThe first signs of TBR may be clinical (Table 2) orradiological (Table 3). Diagnosis is confirmed by com-puted tomography or fibre-optic bronchoscopy [5]. The CTscan sensitivity for tracheal injury is 85 % [4]. Bronchos-copy reveals the site and extent of tear, which in turndetermine conservative or surgical management. Radio-graphic signs of TBR relate to overinflation of the ETTcuff, and thus increased cuff diameter, presence of air inthe mediastinum, and possible abnormal ETT position(Table 3).ETT cuff overinflation may occur when the presence ofan existing rupture requires an increased amount of air inthe cuff to seal the trachea. This occurs commonly intraumatic TBR [4]. The presence of cuff overinflation givesno indication as to mechanism or timing of TBR.The average diameter of the human trachea is 2 cm inwomen, and 2.4 cm in men; a horizontal cuff diametergreater than 2.8 cm, measured at the widest point, indicateslikely rupture of the healthy trachea [14, 17]. To estimatevertical cuff expansion, the distance between the inferiorborder of the cuff and the distal ETT tip is measured; it isnormally more than 2.5 cm [14]. A reduction in this dis-tance may indicate cuff overinflation with or without TBR,or cuff anchoring following ETT repositioning with inad-equate cuff deflation [14]. One case series of post-intuba-tion TBR reports cuff diameters of 2.8–4.3 cm and cuff-to-Fig. 1 Initial chest radiograph demonstrating endotracheal tube cuffoverinflation and bronchoaspiration754 Intern Emerg Med (2013) 8:753–756123tip distances of 0–1.2 cm [14]. Cuff inflation to 6.5 cmdiameter has been reported [6]. Differential diagnoses of anoverinflated ETT cuff on imaging include TBR, oesopha-geal ETT placement, simple cuff overinflation, or diseasecausing tracheal enlargement or dilatation [14].Mechanisms of endotracheal tube cuff-related TBREarly reports of post-intubation TBR relate to the firstgeneration of cuffed ETTs. These cuffs were poorly com-pliant (low volume–high pressure), required inflationpressures of over 180 mmHg, created a seal by deformingthe trachea, and inflated asymmetrically, directing the ETTtip against the tracheal wall [18]. As cuff design evolved,these were followed by the first high volume–low pressurecuffs, but both types could easily be filled with 60 ml air,producing a cuff distended greater than 4 cm [14].Numerous reports were made of post-intubation TBR likelyresulting from cuff overinflation [3, 19, 20].Modern high volume–low pressure ETT cuffs are highlycompliant, and conform to the shape of the trachea ratherthan deform it. Their symmetric inflation directs the ETTtip to the central trachea rather than its wall, and a seal isachieved with inflation pressures of\30 cmH2O [17]. Oneproposed mechanism of post-intubation TBR commenceswith accidental initial right main bronchus intubation,requiring large air volumes to seal a cuff inadvertentlylocated at the carina, detection of the error by auscultation,Table 1 Risk factors for post-intubation tracheal rupture from single-lumen tubes [3, 5, 6, 10, 11, 21, 22]Situational Mechanical AnatomicalPre-hospital or emergency setting Multiple vigorous intubation attempts FemaleOperator inexperience Stylet protruding from ETT Short statureUnsuccessful intubation attempts Malposition of ETT tip Congenital tracheal abnormalities(e.g. tracheomalacia)Inadequate tube size Weakness of membranous trachea (e.g. chronicsteroid use, chronic obstructive pulmonary disease)Rapid cuff inflation Inflammatory lesions of tracheobronchial treeCuff overinflation Large mediastinal collections, lymph nodes orneoplasms distorting tracheaRepositioning ETT with inadequate cuff deflationVigorous coughing on ETTAbrupt head/neck movement while intubatedMoving patient while cuff inflatedN2O diffusion into cuffPositive pressure ventilation or oxygen flush againstclosed expiratory valveDirect connection of pilot balloon to pressurisedoxygenTable 2 Clinical signs of tracheal rupture [3, 5, 15]Respiratory distressDifficult ventilationPersistent air leak around ETT despite adequate cuff inflationCyanosisHaemoptysisMediastinal emphysemaSubcutaneous emphysemaPneumothoraxTable 3 Radiological signs of tracheal rupture [15]1. Overdistended endotracheal tube cuff, with tube tip oriented torightCuff diameter [2.8 cmCuff to distal ETT tip distance \2.5 cmIncreasing intratracheal diameter compared with previousimaging2. Air in surrounding structuresDeep cervical emphysema, paratracheal air, subcutaneousemphysemaPneumomediastinum, pneumothoraxPneumoperitoneum, pneumoretroperitoneum3. Tracheal wall abnormality or extratracheal ETT locationTracheal wall deformity, defect, discontinuity extending aboveor below carinaExtratracheal location of ETT tip or herniated cuffIntern Emerg Med (2013) 8:753–756 755123followed by ETT withdrawal into the narrower lower tra-chea with incomplete or absent cuff deflation, whichoverstretches the membranosa [5]. Patients of short statureare at particular risk of right main bronchus intubation [5].In cadaver studies with modern Mallinckrodt single-lumen ETTs, cuff pressure required to rupture the intubatedhealthy trachea is extremely high ([120 cmH2O), and rup-ture is difficult to achieve, requiring a corresponding cuffvolume of 75 ml [4]. There is a marked increase in resistanceto further inflation of the cuff after injection of 50 ml air,highlighting the physical difficulty of achieving a cuffpressure or volume sufficient to cause tracheal rupture [4].The tissue properties of cadaver trachea differ from livingtrachea, and these studies have not been replicated in theliving trachea. Although cuff overinflation continues to bereported as a cause of post-intubation TBR in the literature[5, 8], cadaver studies suggest that this may be unlikely withmodern single-lumen ETTs in the healthy trachea, within thelimits of simple accidental overinflation by hand [4].Our female patient was intubated under emergent con-ditions in the pre-hospital setting with the aid of a stylet, byan experienced pre-hospital emergency doctor. She wasventilated by positive pressure, coughed vigorously on theETT, and was transferred between different beds on mul-tiple occasions intubated with the cuff inflated. She did nothave any other risk factors described for TBR. There isinsufficient evidence to determine whether overinflation ofthe ETT cuff caused tracheal rupture; it is possible thatcoughing on the ETT with no expiratory valve in the circuitwhilst awaiting neurological assessment was the cause.Alternative causes may include direct trauma from the ETTtip or stylet at intubation or during transfer of a critically illpatient.ConclusionThis Mortality and Morbidity case highlights severalimportant points and demonstrates many of the risk factorsfor intubation-related tracheal rupture. Coughing on anendotracheal tube may put the trachea at risk of rupture,and should be treated by sedation or paralysis. Mechanicalforces associated with intubation remain a likely cause ofintubation-related tracheal rupture. There is insufficientevidence in the literature to conclude that simple accidentalcuff overinflation, as might occur in routine clinical prac-tice, causes rupture of the healthy trachea with modernhigh volume–low pressure cuffed single-lumen tubes.Conflict of interest None.References1. Smith B, Hopkinson R (1984) Tracheal rupture during anaes-thesia. Anaesthesia 39:894–8982. Hofmann HS, Rettig G, Radke J, Neef H, Silber RE (2002) Iat-rogenic ruptures of the tracheobronchial tree. Eur J CardiothoracSurg 21:649–6523. Orta DA, Cousar J, Yergin B, Olsen GN (1979) Tracheal lacer-ation with massive subcutaneous emphysema: a rare complicationof endotracheal intubation. Thorax 34:665–6694. Chen J, Shanmuganathan K, Mirvis S, Killeen K, Dutton R(2001) Using CT to diagnose tracheal rupture. AJR176:1273–12805. Massard G, Rouge´ C, Dabbagh A, Kessler R, Hents JG, RoeslinN et al (1996) Tracheobronchial lacerations after intubation andtracheostomy. Ann Thorac Surg 61:1483–14876. 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Blaming the balloon: the risk of post-intubation tracheobronchial rupture

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Blaming the balloon: the risk of post-intubation tracheobronchial rupture

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