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(Chest. 2002;121:1911-1915.)
© 2002 American College of Chest Physicians

Vocal Cord Paralysis After Surgery for Thoracic Aortic Aneurysm*

Shin-ichi Ishimoto, MD; Ken Ito, MD; Masaaki Toyama, MD; Isamu Kawase, MD; Kenji Kondo, MD; Kiyoshi Oshima, MD and Seiji Niimi, MD

* From the Department of Otolaryngology (Drs. Ishimoto, Ito, and Niimi), Faculty of Medicine, University of Tokyo, Tokyo; the Division of Otorhinolaryngology (Dr. Kondo) and the Division of Cardiovascular Surgery (Drs. Toyama and Kawase), Kameda Medical Center, Kamogawa; and the Department of Otolaryngology (Dr. Oshima), Tokyo Teishin Hospital, Tokyo, Japan.

Correspondence to: Ken Ito, MD, Department of Otolaryngology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan; e-mail: itoken-tky{at}umin.ac.jp


    Abstract
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Objective: To determine the incidence, etiology, prognosis, and treatment of vocal cord paralysis (VCP) after surgery for thoracic aortic aneurysm (TAA).

Study design: Retrospective study performed between 1989 and 1995.

Setting: Academic, tertiary care, referral medical center.

Patients: Seventy-one TAA patients underwent surgery at the Kameda Medical Center between 1989 and 1995.

Results: Sixty-two of 71 patients were examined postoperatively for voice quality. Twenty patients (32%) had hoarseness develop caused by VCP, as confirmed by laryngoscopy. The left recurrent laryngeal nerve had been sacrificed in 1 patient during surgery, but it was preserved in the remaining 19 patients. Unilateral left VCP was noted in 19 patients, and bilateral VCP occurred in 1 patient. The incidence of VCP was higher in those patients who underwent surgery for type I aneurysms (9 of 14 patients, 64%). In 16 of the 19 patients (84%) who received follow-up for > 6 months, vocal cord movement did not return to normal. Surgery to improve voice quality, arytenoid adduction in five patients and intracordal injection in two patients, was performed with success.

Conclusions: Our results indicate that surgery for TAA is associated with a relatively high incidence of VCP. VCP occurred despite preservation of the recurrent laryngeal nerve, and the paralysis did not show a spontaneous recovery even 6 months after surgery.

Key Words: cardiovocal syndrome • hoarseness • thoracic aortic aneurysm • vocal cord paralysis


    Introduction
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Thoracic aortic aneurysm (TAA) is relatively uncommon and remains a formidable clinical challenge. The mortality rate in patients undergoing surgery for TAA is high,1 2 3 due to both the high-risk surgical procedure and major complications such as paraplegia, renal failure, and respiratory failure.1 2 3 4 5 We encountered patients who developed hoarseness after TAA surgery, especially in TAA surgery that involved the aortic arch. This complication could be caused by laryngeal edema, arytenoid cartilage dislocation, or vocal cord paralysis (VCP).6 VCP occurred on the left side in some of these patients after TAA dissection or interposition surgeries, despite the preservation of the left recurrent laryngeal nerve during surgery. This nerve crosses the aortic arch, and hence traction of the nerve trunk can occur directly or indirectly from sternal retraction, and surgical procedures on the aorta can lead to various degrees of nerve damage.7 Hoarseness associated with TAA has been reported previously, although the cause and characteristics of vocal cords were not examined by laryngoscopy.1 4 8 The recent advances in chest and open-heart surgeries, which enabled surgery in previously impossible cases, can lead to an increased number of intrathoracic injuries to the recurrent laryngeal nerve.9 However, the recent incidence of postoperative VCP, clinical course of patients, and criteria for treatment of VCP associated with TAA surgery have not been elucidated. The purpose of the present study was to retrospectively determine the incidence, cause of VCP after TAA surgery, and possible treatment for the hoarseness caused by VCP.


    Materials and Methods
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
We conducted a retrospective analysis of 71 TAA dissection or interposition surgeries performed between 1989 and 1995 at the Kameda Medical Center. Generally, the aortic arch surgery was performed via sternotomy, under deep hypothermic circulatory arrest, without topical cooling using ice slush. Surgery for TAA that was limited to the ascending aorta or descending aorta, sparing the aortic arch, was occasionally performed using aortic cross-clamp without total circulatory arrest. Glutaraldehyde-albumin or gelatine-resorcine-formaline biological glues were never used in the repair. Nine patients who underwent TAA surgery were excluded from the analysis because eight patients were unavailable for follow-up (four patients died from TAA within 1 week of surgery, and four patients refused the examination), and one patient had been noted to have VCP-related hoarseness before surgery. As a result, 62 patients entered the study (36 men and 26 women; age range, 39 to 85 years; mean, 65.9 years). Our retrospective analysis included localization of the aortic aneurysm, position of the fixed vocal fold, prognosis of VCP, and treatment for hoarseness. We also included 748 patients who underwent coronary artery bypass grafting (CABG) as the control group: 575 men and 173 women (age range, 29 to 86 years; mean, 65.5 years). The same group of surgeons and anesthesiologists performed the surgery for CABG via sternotomy.

When hoarseness developed and lasted for > 1 week after surgery, the larynx was examined carefully using a fiberoptic laryngoscope. To fully characterize VCP, we also determined the extent of paralysis (unilateral or bilateral), side of paralysis (right or left), association with or without aspiration, and the position of the paralyzed vocal cords (median, paramedian, or intermediate). All patients except one, who died of mediastinitis within 1 month after surgery, were followed up for > 6 months.


    Results
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Among the 62 patients who entered the study, 20 patients (32.3%; 14 men and 6 women; age range, 35 to 79 years; mean, 65.8 years) had hoarseness develop that lasted > 1 week. The left recurrent laryngeal nerve was sacrificed in one patient because the nerve was elongated, thinned, and adhered to the aneurysmal wall. The nerve was preserved in all of the other patients. Fiberoptic laryngoscopy confirmed the presence of unilateral left-sided VCP in 19 patients and bilateral VCP in 1 patient. Although two patients had aspiration develop after TAA surgery, its was not severe enough to lead to aspiration pneumonia. In comparison, 11 of the 748 patients (1.5%) who underwent CABG had VCP develop. The significant difference was found in the incidence of VCP after TAA surgery compared with CABG (p < 0.001, {chi}2 test). This fact suggests that VCP after TAA surgery was not caused by sternotomy.

The incidence of VCP after surgery was determined according to the location of TAA following the classification of de Bakey et al4 (Table 1 ). Type I involves the ascending root and arch, type II involves the ascending segment only, and type III involves the descending thoracic aorta only. The incidence of VCP was most common after repair of type I aneurysms (64%). To statistically elucidate the difference in incidence among the three types, we first confirmed the significant difference in incidence among the three groups using analysis of variance (p = 0.01, multiple comparison), and then we examined the difference between each pair of two groups using the {chi}2 test. Significant difference in incidence was found between type I and type II (p = 0.02) and between type I and type III (p < 0.01).


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Table 1.. Types of TAA in Patients Who Had VCP Develop*

 
Among the 19 patients with unilateral VCP, the position of the paralyzed vocal cord was paramedian in 18 patients and intermediate in 1 patient. A schematic representation of the positions of the vocal cord is shown in Figure 1 . The anatomic association of the nerves to the aortic arch is shown in Figure 2 . The vocal cords in the other patient with bilateral paralysis were fixed in the median position. This patient underwent tracheotomy at the time of extubation but died of mediastinitis within 1 month of surgery.



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Figure 1.. Schematic representation of the larynx showing the position of the vocal cord. a: median; b: paramedian; c: intermediate; d: fully abducted positions.

 


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Figure 2.. Anatomic association of the left recurrent nerve to the aortic arch. a: left recurrent laryngeal nerve; b: left vagus nerve; c: right brachiocephalic artery; d: left common carotid artery; e: left subclavian artery; f: pulmonary artery; g: ligamentum arteriosum.

 
We followed up with the remaining 19 patients with unilateral left VCP for > 6 months using fiberoptic laryngoscope. Three patients (16%) showed improvement of hoarseness associated with normalization of vocal cord movements in approximately 3 months. However, in the other 16 patients (84%), VCP persisted.

Seven patients with persistent VCP (fixed position: paramedian) underwent surgical treatment to alleviate their hoarseness. Arytenoid adduction was performed in five patients, whereas silicone injection into the vocal cord was performed in the other two patients. The maximum phonation time (MPT) is a simple but very practical parameter to evaluate the degree of glottal incompetence. The subject is asked to continue phonation (eg, saying "ahhhh") as long as possible, after deep inspiration, and the duration of his phonation is measured. MPT should be > 20 s for adults and > 15 s for children and the elderly. The MPT in patients who received surgical voice therapy improved from 4 s before treatment to 10 s after treatment, on average.


    Discussion
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Repair of arch aneurysms remains a formidable surgical undertaking, but improvement in surgical techniques, anesthesia, and postoperative care allows such repair to be conducted in appropriate patients with acceptable morbidity and mortality.1 2 3 4 5 Major problems remain to be solved, particularly with respect to the major complications such as paraplegia, renal failure, and respiratory failure.1 2 3 4 5 Hoarseness is one of the minor complications in TAA surgery. This complication could be caused by laryngeal edema, arytenoid cartilage dislocation, or VCP.6 It was recommended that patients with hoarseness lasting > 5 days should undergo direct laryngoscopy to rule out recurrent laryngeal nerve paralysis after CABG.6 In our study, the patients with hoarseness after TAA surgery had VCP. We believe that when hoarseness continues for > 1 week after extubation in TAA surgery, it is important to examine vocal cord movement with a laryngoscope.

Left VCP associated with TAA surgery probably depends on the anatomic relationship of the left recurrent laryngeal nerve to the aortic arch and ligamentum arteriosum (Fig 2) , rendering the nerve vulnerable to compression and trauma by TAA surgery and repair.7 Although the left recurrent nerve was preserved for all patients but one, VCP was observed in 32% of patients. VCP after TAA surgery might be caused by the median sternotomy retraction, which produces a lateral and anterior stretching of the subclavian arteries.10 However, the most common cause of VCP is considered to be nerve damage caused by the surgical procedure used for aortic arch replacement. Nerve traction can occur directly or indirectly from sternal retraction, and can lead to various degrees of nerve damage, which could not always be technically avoided.7 One patient who developed bilateral VCP required long-term (> 2 weeks) endotracheal intubation after surgery, suggesting that this prolonged intubation might have been the cause of bilateral vocal cord paralysis. Both vocal cords in this patient were fixed in the median position, requiring a tracheostomy. This patient died of mediastinitis within 1 month of surgery.

We encountered one patient who had hoarseness as a symptom of left recurrent laryngeal nerve paralysis before surgery for TAA. de Bakey et al4 reported that 8.6% of their patients complained of hoarseness caused by paralysis of the vocal cords caused by stretching or compression of the left recurrent laryngeal nerve. Teixido and Leonetti7 reported that 8 of 168 patients with TAA (4.8%) manifested hoarseness, and all had type I (de Bakey’s classification) aneurysms. In 1897, Ortner11 described this symptom as cardiovocal syndrome. He was the first to describe left recurrent laryngeal nerve paralysis in patients with mitral stenosis. Other conditions associated with unilateral recurrent laryngeal nerve paralysis included atrial septal defect, patent ductus arteriosus, primary hypertension, Eisenmenger syndrome, and aortic aneurysm.12 In this regard, only 1 of 62 patients (1.6%) in the present study already had hoarseness caused by VCP before TAA surgery. However, because the median fixation of the vocal cord does not always cause hoarseness, the incidence of VCP in patients with TAA might be higher.

Abnormal phonation has been reported after surgery for TAA.4 7 Teixido and Leonetti7 reported postoperative voice changes in 11 of 92 patients (12%) after TAA surgery, and they were equally divided between type I and type III aneurysms according to the classification of de Bakey et al.4 From our experience, type I TAA has significantly higher risk of VCP than the other types (Table 1) .

In the present study, paralyzed vocal cords were most commonly seen in the paramedian position. In such cases, the other normally functioning cord can compensate for the deficiency on the contralateral side. It swings past the midline to make contact with its counterpart, and this produces a normal or nearly normal voice.13 When mobility of the cord fails to return spontaneously in patients with unilateral VCP, surgical intervention can be considered. The indications for surgery include the patient’s needs for phonation and desire for improvement of occupational and social functions. Furthermore, other symptoms such as aspiration may prompt more immediate intervention.14 Seven of 16 patients with persistent VCP underwent phonosurgical treatment to alleviate hoarseness. The other patients did not desire such intervention because they believed that the hoarseness was a minor complication. Generally, treatment of unilateral VCP is performed either by laryngoplasty, intracordal injection (silicone injection), or arytenoid adduction. The arytenoid adduction and laryngoplasty are surgical procedures, performed via skin incision, which physically shift the position of the vocal cord. However, intracordal injection simply inflates the tissue beneath the vocal cord, with relatively uncertain and occasionally transient effects. Selection of silicone injection or arytenoid adduction should be based on the position of the paralyzed vocal cord, age, MPT, and patient’s desire. Usually, an elderly patient with an immobile vocal cord caused by a terminal pulmonary neoplasm or other severe medical problems may benefit from the relative simplicity and quickness of injection therapy.14 We used arytenoid adduction as permanent surgical therapy for those who were relatively young with a strong desire for normal phonation, while we recommended injection medialization for elderly patients. Adduction surgery was chosen, instead of laryngoplasty, because we were more experienced with it. As the material of choice for injection in cases of medialization, silicone has recently been replaced by collagen, in response to the reports of connective-tissue diseases occurring after silicone breast implants.15 16 17 Woodson and Miller18 reported that recovery of VCP should occur within 6 months after surgery, but laryngeal muscle atrophy, cricoarytenoid fixation, and synkinesis were postulated as reasons for the lack of late functional recovery. Therefore, in our series, phonosurgical intervention was not considered before 6 months after TAA surgery.


    Conclusion
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Twenty of the 62 patients (32%) followed up after TAA surgery developed hoarseness caused by VCP. Most of them (n = 19) had left-sided VCP, whereas one patient developed bilateral paralysis. The incidence of VCP was most common after repair of type I aneurysms (64%). In 16 of the 19 patients (84%) followed up for > 6 months, vocal cord movement did not return normal. Surgery to improve voice quality was performed in seven patients with success: arytenoid adduction in five patients and intracordal injection in two patients. Surgery for TAA was associated with a relatively high incidence of VCP, despite preservation of the recurrent laryngeal nerve. If the paralysis persists 6 months after surgery, appropriate phonosurgical intervention can be considered according to the patient’s needs.


    Footnotes
 
Abbreviations: CABG = coronary artery bypass grafting; MPT = maximum phonation time; TAA = thoracic aortic aneurysm; VCP = vocal cord paralysis

Received for publication July 16, 2001. Accepted for publication January 7, 2002.


    References
 TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

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  4. de Bakey, ME, McCollum, CH, Graham, JM (1978) Surgical treatment of aneurysms of the descending thoracic aorta: long-term results in 500 patients. J Cardiovasc Surg (Torino) 19,571-576[Medline]
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  6. Casthely, PA, Labagnara, J (1992) Hoarseness and vocal cord paralysis following coronary artery bypass surgery. J Cardiothorac Vasc Anesth 6,263-264[CrossRef][Medline]
  7. Teixido, MT, Leonetti, JP (1990) Recurrent laryngeal nerve paralysis associated with thoracic aortic aneurysm. Otolaryngol Head Neck Surg 102,140-144[Medline]
  8. Finkelmeier, BA, Mentzer, RM, Jr, Kaiser, DL, et al (1982) Chronic traumatic thoracic aneurysm: influence of operative treatment on natural history: an analysis of reported cases, 1950–1980. J Thorac Cardiovasc Surg 84,257-266[Abstract]
  9. Hirose, H (1978) Clinical observations on 600 cases of recurrent laryngeal nerve paralysis. Auris Nasus Larynx 5,39-48[Medline]
  10. Horn, KL, Abouav, J (1979) Right vocal-cord paralysis after open-heart operation. Ann Thorac Surg 27,344-346[Medline]
  11. Ortner, N (1897) Recurrenslahmung bei mitral stenose. Wien Klin Wochenschr 10,753-755
  12. Thirlwall, AS (1997) Ortner’s syndrome: a centenary review of unilateral recurrent laryngeal nerve palsy secondary to cardiothoracic disease. J Laryngol Otol 111,869-871[Medline]
  13. Hahn, FW, Jr, Martin, JT, Lillie, JC (1970) Vocal-cord paralysis with endotracheal intubation. Arch Otolaryngol 92,226-229[Medline]
  14. Benninger, MS, Crumley, RL, Ford, CN, et al (1994) Evaluation and treatment of the unilateral paralyzed vocal fold. Otolaryngol Head Neck Surg 111,497-508[Medline]
  15. Weinzweig, J, Schnur, PL, McConnell, JP, et al (1998) Silicon analysis of breast and capsular tissue from patients with saline or silicone gel breast implants: II. Correlation with connective-tissue disease. Plast Reconstr Surg 101,1836-1841[Medline]
  16. Giltay, EJ, Bernelot Moens, HJ, Riley, AH, et al (1994) Silicone breast prostheses and rheumatic symptoms: a retrospective follow up study. Ann Rheum Dis 53,194-196[Abstract/Free Full Text]
  17. Righi, PD, Wilson, KM, Gluckman, JL (1995) Thyroplasty using a silicone elastomer implant. Otolaryngol Clin North Am 28,309-316[Medline]
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