| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
 
|
|
|
||
|
|
© 2000 International Anesthesia Research Society
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Impaired movement of the cricoarytenoid joint with hoarseness and immobility of the vocal ligament may occur as a consequence of endotracheal intubation. Little is known about the cricoarytenoid joint capsule and its role in intubation. We investigated the joint capsules of 48 cricoarytenoid joints by means of gross anatomy microscopy, histology, and scanning electron microscopy; 30 unfixed cadaver larynges were also subjected to attempts to simulate traumata such as those that may occur during intubation trials. The larynges were intubated with the arytenoid tip entering the lumen of the tracheal tube or extubated with the cuff of the tube only partially deflated. Subsequently, i.e., after dissecting the left and right cricoarytenoid joint from each larynx, the morphologic changes induced experimentally were analyzed by using histologic methods. The cricoarytenoid joint was found to be lined by a wide joint capsule. Unexpectedly large and intensively vascularized synovial folds projected into the joint cavity. After simulation of intubation and extubation, histologic analysis revealed injuries to the synovial folds and joint surface impressions, but no trauma or rupture of the outer joint capsule. We conclude that laxity of the joint capsule and the large synovial folds are predisposing factors for intubation trauma of the cricoarytenoid joint, potentially leading to hemarthros and finally to cricoarytenoid joint dysfunction.
Implications: The present study illustrates by morphological investigations and intubation experiments that laxity of the joint capsule and large synovial folds are predisposing factors for intubation trauma of the cricoarytenoid joint, potentially leading to hemarthrosis and finally to cricoarytenoid joint dysfunction.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Endotracheal intubation, laryngoscopy, bronchoscopy, and other invasive methods are often applied to the respiratory tract, with the result that laryngeal complications are not uncommon. These complications include, for example, submucosal hemorrhage, granuloma formation, and subglottic edema or laryngitis with membrane formation and may be characterized by hoarseness or stridor. Other complications include impaired movement of one or both vocal folds caused by recurrent laryngeal nerve damage, and/or cricoarytenoid joint (CAJ) dysfunction.
The human CAJ can be involved in a number of different pathologic conditions. Trauma as described above, as well as joint diseases such as arthritis (1), osteoarthrosis (2) or rheumatoid arthritis (3) have all been reported to occur in the CAJ. Interestingly, and in contrast to the limb joints, publications elucidating the morphology of the CAJ capsule have, to date, been restricted to some investigations concerning the posterior CAJ ligament.
Anatomically, the CAJ is a diarthrodial joint supported by a wide joint capsule lined with synovia. The capsule is strengthened posteriorly by the cricoarytenoid ligament. The structural arrangement of the joint allows two principal types of motion: a rocking or rotating movement around the axis of the joint, and a linear glide parallel to this axis (4). The function is to control the abduction, adduction, and length of the vocal cords, thereby facilitating respiration, protect the airway, and permit phonation.
The present investigation analyzes the structure of the CAJ capsule and correlates the findings with the histology of the trauma associated with CAJ capsule damage that may occur after endotracheal intubation. We tried to simulate the forces induced by an endotracheal tube lumen extending into the CAJ capsule during intubation or extubation in unfixed human larynges. Results were discussed against the background of the current understanding of CAJ dysfunction subsequent to endotracheal intubation.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Fresh larynges were obtained from 54 donated cadavers (31 men and 23 women, age range 21–92 yr) at the Department of Anatomy (Christian Albrecht University of Kiel, Kiel, Germany) within 48 h of death. Limited information was available on the specimens, which were taken from individuals without recent trauma, infection of the larynx, or diseases that might involve or affect laryngeal function. In some cases, there was limited information on whether any of the donors had been tracheally intubated before death. For ethical reasons, the intubation attempts were not performed with the larynges in situ. Intubation and extubation experiments were performed immediately after dissection of the larynges and without previous fixation.
The CAJs of 12 larynges were dissected for light microscopy. The 24 joints (14 male, 10 female; age 25–88 yr) were fixed in 4% formalin, decalcified in 20% ethylenediaminetetraacetic acid, dehydrated in graded concentrations of ethanol and embedded in paraffin. Sections (7 µm) in three planes were stained with toluidine blue (pH 8.5), azan, resorcine-fuchsine-thiazine-picric acid, and according to the method of Gomori (5). The slides were examined with a Zeiss- Axiophot microscope.
For scanning electron microscopy (SEM), 24 CAJs (12 male, 12 female; age 21–92 yr) were carefully separated into 48 articular facets by cutting the joint capsule. Afterward, all facets were fixed in 2.5% glutaraldehyde for 1 wk. After careful rinsing of the preparations for 12 h in aqua dest., all of the tissue blocks were impregnated in 2.5% tannic acid for 2 days. Counterfixation in 2% osmium tetraoxide for 4 h was followed by dehydration in ethanol and drying in a critical point dryer. The articular facets were coated with gold and analyzed using a Philips scanning electron microscope.
In 30 larynges (18 male and 12 female; age 25–92 yr), simulation of forceful intubation and extubation was performed with a tracheal tube (Portex, Profile blue line 7.0, SIMS Portex Limited, Kent, UK). During the experiment, the hand held larynges lay on the posterior side. Intubation was tested in 15 larynges (8 times right side and 7 times left side, Table 1). The tube was cautiously introduced into the larynx, then viewed with imaging equipment (Storz endoscope 600 BA with 0° optic, Karl Storz GmbH & Co, Tuttlingen, Germany) until the tip of the left or right arytenoid was inside the lumen. Then the tube was inserted either rapidly (in 10 larynges) or slowly (in 5 larynges) until a distinct resistance was felt. The tube was held in the investigator’s left hand for each intubation procedure. Extubation was tested in 15 larynges (Table 1), whereby the tube was carefully introduced into the larynx under visual control until the cuff had passed the subglottic region. The cuff was then filled with air. In two larynges, the cuff was filled with 10 mL of air, in eight larynges with 8 mL, and in five larynges with 5 mL. After this, the tube was pulled out along with the filled cuff by using a jerky motion. All intubation and extubation trials were performed only once with each larynx (Table 1).
|
No effort was made to control the force exerted with the tube. In any case, the force applied in the trials never exceeded what would be applied by a physician in a living patient. Great care was exercised in performing the simulations.
After dissecting the left and right CAJ of each larynx in which intubation or extubation had been performed, the CAJs were fixed in 4% formalin for 1 wk, decalcified in 20% ethylenediaminetetraacetic acid, dehydrated in graded concentrations of ethanol, and embedded in paraffin. Sections (7 µm) in a horizontal or frontal plane were stained with toluidine blue (pH 8.5), resorcine-fuchsine-thiazine-picric acid according to the methods of Gomori and Goldner (5). The sections were examined under a Zeiss-Axiphot microscope. CAJs that were not in contact with the tube in the intubation simulations served as controls.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Light Microscopy of CAJs Without Preceding Intubation or Extubation
The articulating bodies of the CAJs were surrounded by a wide and lax joint capsule lined with synovium (Fig. 1). Deep reserve folds were visible in the marginal area at the transition from arytenoid to cricoid cartilage (Fig. 1). The thin capsular wall consisted of a network of collagen fibrils with a few scattered elastic fibers. The capsule was strengthened by the cricoarytenoid ligament, which consisted of several layers of collagen fibrils and elastic fibers, in the posterior direction only (Fig. 1). The undersurface of the posterior cricoarytenoid ligament was attached to the upper surface of the cricoid lamina near the midline. Its upper surface was attached to the medial side of the arytenoid cartilage approximatley half way between the vocal process and the back of the muscular process. Large synovial folds, projecting extensively into the joint cavity, were potentially mistaken for a meniscus in a definite histologic section plane (Fig. 2). They were highly vascularized and lined with several layers of synovial cells.
|
|
SEM of CAJs Without Preceding Intubation or Extubation
SEM revealed large synovial folds, which often projected extensively into the joint cavity (Fig. 3). The synovial folds were of different sizes and occurred in different numbers, i.e., a joint could contain one large synovial fold or several smaller ones. In most cases, the synovial folds originated from the ventral and/or dorsal areas of the joint capsule, but origin from the lateral or medial part of the joint capsule was also observed.
|
Intubation and Extubation Trials
The attempts to simulate forceful intubation or extubation with a tracheal tube had no visible effects on the CAJ as detected with imaging equipment. The arytenoid cartilage moved back to its starting position after each manipulation. No dislocation or fixation in an anterior or posterior position was observed.
Light Microscopy of CAJs with Preceding Intubation or Extubation
Histologic analysis revealed ragged injuries in the synovial folds of some CAJs as a result of the intubation attempts (Fig. 4). Such synovial damage was seen in 10 CAJs of the intubated larynges (six male, two times on the right side, four times on the left side; and four female, two times on the right side and two times on the left side; Table 1). Impressions on the articular surface were also observed in three CAJs (two female, both on the left side; one male, on the right side, Table 1 ). No synovial damage, cartilage impressions or fractures of the joint body were observed in the extubation group (Fig. 5). Histologic examination of the fibrous capsule and the posterior cricoarytenoid ligament revealed no signs of damage in any of the CAJs.
|
|
Several CAJs showed chondrocyte clusters near the joint surface or a roughening of the entire cartilaginous joint surface. Fissures in the joint surface were also visible in some of these joints. Because these changes were also detected in some of the joints of the control group (Table 1), the changes present previous to the trials were classified as pathologic (Table 1). However, it is also conceivable that the pathologic changes were exacerbated by the simulation experiments.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The increasing literature concerning patients with postintubation CAJ dysfunction suggested the procedure of analyzing the morphology of the CAJ capsule and simulating endotracheal intubation and extubation in unfixed larynges with an endotracheal tube. Experimentation demonstrated that the CAJ capsule consisted, unexpectedly, of large synovial folds, which where often traumatized by careless endotracheal intubation.
Based on results obtained with light and scanning electron microscopy, it is assumed that in vivo injuries to the large synovial folds and outermost layers of the articular cartilage—caused by unphysiologic stress and, in case of incomplete neuromuscular blockade, motor reactions during endotracheal intubation—lead to serosynovitis or joint cavity hemorrhage. After the serosynovitis or hemarthrosis is absorbed, adhesion of articular surfaces or periarticular structures may follow, fixing the arytenoid in an abnormal position. Depending on the localization of crushed synovial folds in the joint cavity, the arytenoid cartilage shifts in an anterior or posterior direction. Muscle contractures conditioned by displacement may then maintain the arytenoid cartilage in a false position. Without treatment, progression may be characterized by fibrosis and consequent vocal fold immobility.
Interest in laryngeal injury from intubation and endotracheal tubes has been steady since the practice of endotracheal anesthesia was instituted. The increasing use of endotracheal tubes in anesthesia prompted an autopsy study of 99 cases by Donnelly (6) demonstrating 44 intralaryngeal lesions after endotracheal intubation. Three of these were characterized by a submucosal lacerating tear, two others showed a "crushing" of the epiglottis, and the remainder had mild to moderate edema. The authors formulated several factors influencing laryngeal damage: 1) proficiency of the anesthesiologist in laryngoscopy; 2) individual anatomical characteristics of the patient affecting ease of intubation; 3) degree of relaxation and urgency of intubation; 4) diameter, shape, and consistency of the endotracheal tube; and 5) duration of intubation. These variables have continued to provide help in understanding the etiology of injury.
Definitive CAJ trauma was first reported at the end of the 1960s and in the 1970s (7–10). Considering the genesis of arytenoid cartilage trauma, restriction of movement can lead to transitory or permanent vocal fold fixation (11). In their analysis of the CAJs of dogs, Stanley and Colman (12) demonstrated that even slight dysfunctions of the joint capsule can result in disturbed joint function.
Remarkably, in terms of anatomical studies and in stark contrast to the limb joints, the human CAJ capsule, with its large synovial folds, has not yet been elucidated, with the exception of investigations of the posterior cricoarytenoid ligament. In a healthy state, the strong posterior cricoarytenoid ligament prevents extensive ventral movement and dislocation of the arytenoid cartilage (13). This was confirmed by our results. Chronic disease states, such as laryngomalacia, renal insufficiency, acromegaly, and chronic glucocorticoid intake, can lead to degeneration of the posterior ligament and have, therefore, been discussed as predisposing factors in intubation trauma (9). Sataloff et al. (14) were unable to confirm this in an analysis of their comprehensive case material. Moreover, diseases such as cricoarytenoid arthritis (1), rheumatoid arthritis (3), or degenerative changes (15) involving the CAJ itself must also be considered as predisposing factors for intubation trauma. A recent study showed that, in persons aged 40 years or older, the incidence of osteoarthrotic changes in the CAJ is approximately 50% (16). Our study confirmed this level of changes.
Most investigations of the healthy CAJ have focused on joint biomechanics and motion analysis (17,18). The types of injuries the CAJ can sustain are presumably similar to those associated with other synovial joints (18), including ligamentous joint capsule strain, ligamentous joint capsule tear, hemarthros, joint subluxation, and joint dislocation. The number of patients with postintubation cricoarytenoid dislocation or subluxation reported in the literature has increased steadily. Before 1988, case reports involving adults and infants were published only sporadically. Since 1988, patients with cricoarytenoid dislocation or subluxation have been reported in greater numbers, with the largest contribution coming from a single large series (14,19). The most common cause of cricoarytenoid dislocation or subluxation is still endotracheal intubation. Notably, a study (20) analyzed the recent literature on arytenoid cartilage subluxation and reported that, in general, endotracheal intubation was performed for a brief time only and was managed without difficulty. In many cases, symptoms of arytenoid cartilage subluxation were not noticed immediately, but rather within one to seven days of extubation. Moreover, it was concluded that laryngeal trauma from endotracheal intubation does not result in subluxation of arytenoid cartilage, per se, but rather that the formation of a hemarthros leads to fixation of the joint surface. Our simulations confirm these findings.
Injury to the CAJ typically occurs after intubation. It has been proposed that the left CAJ is more frequently injured because the laryngoscope is typically held in the left hand with the endotracheal tube being inserted from the right side (9). Consultation of the literature does not confirm this theory, although our experiments show a slight left-side dominance. The velocity of intubation also seems to have an effect on damage to the CAJ capsule; rapid intubation resulted in significant frequency in synovial fold damage, i.e., more often than gradual intubation (Table 1). Extubation was not seen to influence capsule damage.
Early symptoms and findings of CAJ dysfunction include throat discomfort, odynophagia, decreased vocal ligament mobility, and swelling of the arytenoid. Later, when the edema and discomfort have been resolved, the symptoms and findings of hoarseness, malpositioned arytenoid, and abnormal or no movement of the arytenoid make it difficult to distinguish CAJ dysfunction from vocal fold paresis or paralysis (18). The symptomatology of CAJ dysfunction is of course highly specific (hoarseness, vocal ligament immobility) but not highly sensitive, which is the reason why diagnosis and therapy of cricoarytenoid injury is routinely delayed.
We conclude that CAJ dysfunction should be considered whenever any of the symptoms mentioned occurs after endolaryngeal manipulation (21). Patients showing no improvement of the laryngeal dysfunction, even on accompanying medication [we recommend nonsteroidal antirheumatics based on the finding that the CAJ is comparable to synovial joints at the limbs, despite its extracellular matrix composition and involvement in joint disease (22); at the limbs, nonsteroidal antirheumatics are a common drug in the therapy of synovial disorders and have shown good therapeutical results], should present to an otorhinolaryngology specialist. The specialist should test arytenoid mobility and, as soon as possible after recognition of arytenoid displacement and as allowed by patient status, achieve arytenoid cartilage mobilization. In these cases, detachment of joint fixation by using a spatula under light pressure or endoscopic mobilization will be successful in many cases (9,10,23–25).
In summary, the present investigation demonstrates that the CAJ often contains extraordinarily large, highly vascularized synovial folds, and that laryngeal trauma caused by endotracheal intubation can lead to damage of these folds. Therefore the synovial folds must be considered a predisposing factor for intubation trauma, and each physician working in the area of the larynx should be aware when inserting a tube or other instruments to avoid such synovial damage. After a trauma, serosynovitis or formation of hemarthros may occur, with subsequent fixation of the arytenoid in an abnormal position.
|
Acknowledgments |
|---|
Support was provided by a grant from the German Society of Otorhinolaryngology, Head and Neck Surgery.
We would like to thank Mrs. K. Stengel and Mrs. R. Worm for their expert technical assistance as well as Mrs. H. Waluk and Mrs. H. Siebke for the photographic work.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
- Miller FR, Wanamaker JR, Hicks DM, Tucker HM. Cricoarytenoid arthritis and ankylosing spondylitis. Head Neck Surg 1994;120:214–6.
- Paulsen FP, Tillmann BN. Osteoarthritis in cricoarytenoid joint. Osteoarthritis Cart. 1999. In press.
- Lofgren RH, Montgomery WW. Incidence of laryngeal involvement in rheumatoid arthritis. Med 1962;267:193–5.
- Lenden vH, Moore P. The mechanics of the cricoarytenoid joint. Arch Otolaryngol 1961;73:541–50.
- Romeis B. Färben der Schnitte. In: Böck P, ed. Mikroskopische Technik. 17th ed. Baltimore:Urban & Schwarzenberg, 1989:179–249.
- Donnelly WH. Histopathology of endotracheal intubation. Arch Pathol 1969;88:511–20.[Web of Science][Medline]
- Gosepath J. Morphologische veränderungen nach luxationen des menschlichen krikoarytaenoidgelenkes. Z Laryngol Rhinol 1967;5:346–57.
- Schulz-Coulon HJ. Luxation of the arytenoid cartilage caused by endotracheal intubation. HNO 1974;22:242–5.[Web of Science][Medline]
-
Quick CA, Merwin GE. Arytenoid dislocation. Arch Otolaryngol 1978;104:267–70.
[Abstract/Free Full Text] - Komorn RM, Smith CP, Erwin JR. Acute laryngeal injury with short-term endotracheal anesthesia. Laryngoscope 1973;83:683–90.[Web of Science][Medline]
- Whited RE. A study of post-intubation laryngeal dysfunction. Laryngoscope 1985;95:727–9.[Web of Science][Medline]
- Stanley RB, Colman MF. Unilateral degloving injuries of the arytenoid cartilage. Otolaryngol Head Neck Surg 1986;112:516–8.
-
Maue WM, Dickson DR. Cartilages and ligaments of the adult human larynx. Arch Otolaryngol 1971;94:432–9.
[Abstract/Free Full Text] - Sataloff RT, Bough ID, Spiegel JR. Arytenoid dislocation: diagnosis and treatment. Laryngoscope 1994;104:1353–61.[Web of Science][Medline]
- Segre R. Senescence of the voice. Eye Ear Nose Throat Month 1971;50:62–8.
- Paulsen F, Tillmann B. Degenerative changes in the human cricoarytenoid joint. Otolaryngol Head Neck Surg 1998;124:903–6.
- Wang RC. Three-dimensional analysis of cricoarytenoid joint motion. Laryngoscope 1998;108 (Suppl):1–17.[Web of Science][Medline]
- Kasperbauer JL. A biomechanical study of the human cricoarytenoid joint. Laryngoscope 1998;108:1704–11.[Web of Science][Medline]
- Sataloff RT, Feldman M, Darby KS, et al. Arytenoid dislocation. J Voice 1988;1:368–77.
- Paulsen FP, Rudert HH, Tillmann BN. New insights into the pathomechanism of postintubation arytenoid subluxation. Anesthesiology 1999;91:659–66.[Web of Science][Medline]
- Tolley NS, Cheesman TD, Morgan D, Brookes GB. Dislocated arytenoid: an intubation induced injury. Ann Roy Coll Surg Engl 1990;72:353–6.[Web of Science][Medline]
- Paulsen F, Tillmann B. Composition of the extracellular matrix in human cricoarytenoid joint articular cartilage. Arch Histol Cytol 1999;62:149–63.[Web of Science][Medline]
-
Dudley JP, Manculo AA, Fonkalsrud EW. Arytenoid dislocation and computed tomography. Arch Otolaryngol 1984;110:483–4.
[Abstract/Free Full Text] - Frink EJ, Pattison BD. Posterior arytenoid dislocation following uneventful endotracheal intubation and anesthesia. Anesthesiology 1989;70:358–60.[Web of Science][Medline]
- Pröschel U, Eysholdt U. Short-term changes of larynx and voice after intubation. Rhino Otol 1993;72:93–7.
This article has been cited by other articles:
|
|
 |
|
  S. Vijayasekaran, R. Sances, R. Cotton, and R. G. Elluru Changes in the Cricoarytenoid Joint Induced by Intubation in Neonates Arch Otolaryngol Head Neck Surg, December 1, 2006; 132(12): 1342 - 1345. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. D. Mentzelopoulos, M. Tzoufi, K. Rellos, A. S. Michalopoulos, E. Stamataki, C. Roussos, and S. G. Zakynthinos An Evaluation of McCoy Balloon Laryngoscopy in Patients With Moderate-to-Major Endotracheal Intubation Difficulty Anesth. Analg., October 1, 2005; 101(4): 1233 - 1237. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. D. Mentzelopoulos, C. N. Romana, D. S. Corolanoglou, M. J. Tzoufi, and E. A. Karamichali Balloon Versus Conventional Laryngoscopy: A Comparison of Laryngoscopic Findings and Intubation Difficulty Anesth. Analg., December 1, 2000; 91(6): 1513 - 1519. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
