Recurrent laryngeal nerve palsy and endotracheal intubation By P. D. M. ELLIS and W. K. PALLISTER (London) Summary VOICE changes developing after endotracheal intubation have been found to be due to a recurrent laryngeal nerve palsy in four patients. In none of these patients was there any obvious cause and this posed the question whether endotracheal intubation itself could result in a paralysis of the nerve. Cadaver dissection has suggested a way in which paralysis could occur and this and other possible aetiologies are discussed. Case histories
Case i. Twenty-four-year-old male. Following a head injury sustained in a road accident this patient required a cuffed endotracheal tube and assisted respiration for five days. After extubation his airway was adequate at rest but he complained of increasing dyspnoea on exercise and eventually required a tracheostomy. Mirror examination showed both cords to be lying in the paramedian position and at direct laryngoscopy the crico-arytenoid joints were found to be normal and mobile. There has been no improvement after 13 months. Case 2. Sixty-year-old male. This patient had a retropubic prostatectomy for beriign prostatic hypotrophy. A Magill No. 9 cuffed endotracheal tube was used and the operation lasted two hours. Ten minutes after extubation his airway became obstructed and he was re-intubated. After i j hours of intermittent positive pressure ventilation he was able to breathe normally and the tube was removed. Post-operatively he complained of hoarseness and mirror examination showed the left cord to be bowed and immobile in the paramedian position. Ten years previously he had had a repair of an hiatus hernia via a left thoracic approach. Following this his wife had noticed that his breathing tended to be noisy at night but there was no definite pre-operative evidence of recurrent laryngeal nerve palsy. Case 3. Forty-one-year-old female. This patient had a repair of an hiatus hernia via a left trans-thoracic approach. A cuffed endotracheal tube was used and the operation lasted two hours ten minutes. Immediately post-operatively she complained of hoarseness and mirror examination showed the left cord to be bowed and immobile in the paramedian position. Nine years later the left cord remains immobile but the right cord has compensated with improvement in her voice. Case 4. Fifty-four-year-old male. This patient underwent minor dental surgery, the procedure lasting 30 minutes. A non-cuffed No. 7 nasotrache a 823
P. D. M. Ellis and W. K. Pallister tube was used. Post-operatively he complained of hoarseness and mirror examination showed the right cord to be bowed and immobile in the paramedian position. There has been no improvement four years later. Cadaver dissection
The recurrent laryngeal nerve was dissected out in cadavers; an endotracheal tube was then passed and the cuff inflated. The nerve runs up in loose areolar tissue in the groove between the trachea in front and the oesophagus behind (Fig. i). It was not possible to exert any pressure on the nerve in this position. The nerve then passes up lateral to the cricoid cartilage which protects it from any pressure from within (Fig. i). Before reaching the superior rim of the cricoid cartilage the nerve divides
FIG. I.
Arrows denote recurrent laryngeal nerve running first in the groove between oesophagus and trachea and then lateral to the cricoid cartilage.
into anterior and posterior branches. The posterior branch passes to the posterior crico-arytenoid and inter-arytenoid muscles and cannot be damaged by the cuff. However, the anterior branch passes medial to the lamina of the thyroid cartilage to supply the lateral crico-arytenoid and thyro-arytenoid muscles. Figure 2 shows how this anterior branch could be compressed between the cuff and the thyroid lamina when the cuff is inflated within the larynx. In our cases the cords were described as being bowed and lying in the paramedian position. This is consistent on 824
Recurrent laryngeal nerve palsy and endotracheal intubation anatomical grounds with a palsy of the anterior branch of the nerve when only the posterior crico-arytenoid, inter-arytenoid and crico-thyroid muscles are left functioning; but it is known that in practice it is difficult to make deductions about the positions adopted by paralysed cords.
Arrow cbnotes P.C.A. I.A. L.C.A. T.A.
FIG. 2. anterior branch of recurrent laryngeal nerve. = posterior ciico-arytenoid muscle. = inter-arytenoid muscle. = lateral crico-arytenoid muscle. = thvro-arytenoid muscle.
Discussion
Laryngologists frequently see patients with a recurrent laryngeal nerve palsy of unknown aetiology. Faaborg-Anderson (1954) analysed 880 cases of recurrent laryngeal nerve palsy seen in Copenhagen over a 20 year period and in ninety cases (10 per cent) no cause could be found. Palsies are regularly encountered after thyroid operations but occur only rarely after surgery unrelated to the head and neck. The four cases reported in this paper illustrate some of the possible aetiologies. 1. Thoracic operations. The intra-thoracic course of the left recurrent laryngeal nerve renders it liable to damage in thoracic operations. Downward traction of the oesophagus during hiatus hernia repair may stretch the nerve causing temporary or permanent palsy. This is the likely aetiology in Case 3. 825
P. D. M. Ellis and W. K. Pallister 2. Previously existing asymptomatic palsy. There is no obvious aetiology in Case 4 where a non-cuffed endotracheal tube was used. Steele Holley and Gildea (1971) suggested that a chemical neuropraxia might be caused by materials used to sterilize the tube, but in Case 4 the tube was sterilized by autoclave. It is possible that there was a pre-existing asymptomatic palsy in this patient. 3. Pressure neuropraxia due to inflation of the cuff within the larynx rather than in the trachea. Hahn el al. (1970) first suggested this aetiology and our dissections in cadavers support it. This may have been of importance in Cases 1 and 2, although in Case 2 a pre-existing palsy due to hiatus hernia repair cannot be ruled out. It is suggested that a pressure neuropraxia of the recurrent laryngeal nerve can be caused by an endotracheal tube. This complication may occur if the cuff is placed at too high a level so that it lies at, or just below, the level of the vocal cords rather than within the trachea. The need to avoid intubation of the right main bronchus or the use of too short a tube may encourage this. Failure to deflate the cuff before extubation could also put the nerve at risk as the inflated cuff is drawn up through the larynx. Endotracheal tubes with 'low pressure, high residual volume' cuffs may be of value in avoiding this complication. It was mentioned earlier that no cause can be found for some recurrent laryngeal nerve palsies. It is suggested that laryngologists consider the possibility of pressure neuropraxia due to a cuffed tube so that further evidence may confirm or refute this hypothesis. We also recommend that those patients with symptoms suggestive of laryngeal pathology should be examined pre-operatively so that anaesthetists may not be held responsible for a pre-existing palsy. Acknowledgements We would like to thank the consultants under whom these patients were treated for permission to report the case histories. We would also also like to thank Miss Carol Johnson of the Department of Medical Photography for her help in the preparation of the plates. Reprints Requests for reprints should be addressed to P. D. M. Ellis, The Farens Institute of Otolaryngology, The Middlesex Hospital Medical School, Cleveland Street, London WiP 5FD. REFERENCES FAABORG-ANDERSON, K. (1954) -Ada Otolaryngologica, HAHN, F. W., MARTIN, J. T., and LILLIE, J. C. (1970)
118, 68. Archives of Otolaryngology,
92, 226. H., and Association, 215, 281.
STEELE HOLLEY,
GILDEA,
J. E. (1971) Journal of the American Medical 826
Case i. Twenty-four-year-old male. Following a head injury sustained in a road accident this patient required a cuffed endotracheal tube and assisted respiration for five days. After extubation his airway was adequate at rest but he complained of increasing dyspnoea on exercise and eventually required a tracheostomy. Mirror examination showed both cords to be lying in the paramedian position and at direct laryngoscopy the crico-arytenoid joints were found to be normal and mobile. There has been no improvement after 13 months. Case 2. Sixty-year-old male. This patient had a retropubic prostatectomy for beriign prostatic hypotrophy. A Magill No. 9 cuffed endotracheal tube was used and the operation lasted two hours. Ten minutes after extubation his airway became obstructed and he was re-intubated. After i j hours of intermittent positive pressure ventilation he was able to breathe normally and the tube was removed. Post-operatively he complained of hoarseness and mirror examination showed the left cord to be bowed and immobile in the paramedian position. Ten years previously he had had a repair of an hiatus hernia via a left thoracic approach. Following this his wife had noticed that his breathing tended to be noisy at night but there was no definite pre-operative evidence of recurrent laryngeal nerve palsy. Case 3. Forty-one-year-old female. This patient had a repair of an hiatus hernia via a left trans-thoracic approach. A cuffed endotracheal tube was used and the operation lasted two hours ten minutes. Immediately post-operatively she complained of hoarseness and mirror examination showed the left cord to be bowed and immobile in the paramedian position. Nine years later the left cord remains immobile but the right cord has compensated with improvement in her voice. Case 4. Fifty-four-year-old male. This patient underwent minor dental surgery, the procedure lasting 30 minutes. A non-cuffed No. 7 nasotrache a 823
P. D. M. Ellis and W. K. Pallister tube was used. Post-operatively he complained of hoarseness and mirror examination showed the right cord to be bowed and immobile in the paramedian position. There has been no improvement four years later. Cadaver dissection
The recurrent laryngeal nerve was dissected out in cadavers; an endotracheal tube was then passed and the cuff inflated. The nerve runs up in loose areolar tissue in the groove between the trachea in front and the oesophagus behind (Fig. i). It was not possible to exert any pressure on the nerve in this position. The nerve then passes up lateral to the cricoid cartilage which protects it from any pressure from within (Fig. i). Before reaching the superior rim of the cricoid cartilage the nerve divides
FIG. I.
Arrows denote recurrent laryngeal nerve running first in the groove between oesophagus and trachea and then lateral to the cricoid cartilage.
into anterior and posterior branches. The posterior branch passes to the posterior crico-arytenoid and inter-arytenoid muscles and cannot be damaged by the cuff. However, the anterior branch passes medial to the lamina of the thyroid cartilage to supply the lateral crico-arytenoid and thyro-arytenoid muscles. Figure 2 shows how this anterior branch could be compressed between the cuff and the thyroid lamina when the cuff is inflated within the larynx. In our cases the cords were described as being bowed and lying in the paramedian position. This is consistent on 824
Recurrent laryngeal nerve palsy and endotracheal intubation anatomical grounds with a palsy of the anterior branch of the nerve when only the posterior crico-arytenoid, inter-arytenoid and crico-thyroid muscles are left functioning; but it is known that in practice it is difficult to make deductions about the positions adopted by paralysed cords.
Arrow cbnotes P.C.A. I.A. L.C.A. T.A.
FIG. 2. anterior branch of recurrent laryngeal nerve. = posterior ciico-arytenoid muscle. = inter-arytenoid muscle. = lateral crico-arytenoid muscle. = thvro-arytenoid muscle.
Discussion
Laryngologists frequently see patients with a recurrent laryngeal nerve palsy of unknown aetiology. Faaborg-Anderson (1954) analysed 880 cases of recurrent laryngeal nerve palsy seen in Copenhagen over a 20 year period and in ninety cases (10 per cent) no cause could be found. Palsies are regularly encountered after thyroid operations but occur only rarely after surgery unrelated to the head and neck. The four cases reported in this paper illustrate some of the possible aetiologies. 1. Thoracic operations. The intra-thoracic course of the left recurrent laryngeal nerve renders it liable to damage in thoracic operations. Downward traction of the oesophagus during hiatus hernia repair may stretch the nerve causing temporary or permanent palsy. This is the likely aetiology in Case 3. 825
P. D. M. Ellis and W. K. Pallister 2. Previously existing asymptomatic palsy. There is no obvious aetiology in Case 4 where a non-cuffed endotracheal tube was used. Steele Holley and Gildea (1971) suggested that a chemical neuropraxia might be caused by materials used to sterilize the tube, but in Case 4 the tube was sterilized by autoclave. It is possible that there was a pre-existing asymptomatic palsy in this patient. 3. Pressure neuropraxia due to inflation of the cuff within the larynx rather than in the trachea. Hahn el al. (1970) first suggested this aetiology and our dissections in cadavers support it. This may have been of importance in Cases 1 and 2, although in Case 2 a pre-existing palsy due to hiatus hernia repair cannot be ruled out. It is suggested that a pressure neuropraxia of the recurrent laryngeal nerve can be caused by an endotracheal tube. This complication may occur if the cuff is placed at too high a level so that it lies at, or just below, the level of the vocal cords rather than within the trachea. The need to avoid intubation of the right main bronchus or the use of too short a tube may encourage this. Failure to deflate the cuff before extubation could also put the nerve at risk as the inflated cuff is drawn up through the larynx. Endotracheal tubes with 'low pressure, high residual volume' cuffs may be of value in avoiding this complication. It was mentioned earlier that no cause can be found for some recurrent laryngeal nerve palsies. It is suggested that laryngologists consider the possibility of pressure neuropraxia due to a cuffed tube so that further evidence may confirm or refute this hypothesis. We also recommend that those patients with symptoms suggestive of laryngeal pathology should be examined pre-operatively so that anaesthetists may not be held responsible for a pre-existing palsy. Acknowledgements We would like to thank the consultants under whom these patients were treated for permission to report the case histories. We would also also like to thank Miss Carol Johnson of the Department of Medical Photography for her help in the preparation of the plates. Reprints Requests for reprints should be addressed to P. D. M. Ellis, The Farens Institute of Otolaryngology, The Middlesex Hospital Medical School, Cleveland Street, London WiP 5FD. REFERENCES FAABORG-ANDERSON, K. (1954) -Ada Otolaryngologica, HAHN, F. W., MARTIN, J. T., and LILLIE, J. C. (1970)
118, 68. Archives of Otolaryngology,
92, 226. H., and Association, 215, 281.
STEELE HOLLEY,
GILDEA,
J. E. (1971) Journal of the American Medical 826
