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Ann Thorac Surg 1996;61:1721-1722
© 1996 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Combined Left-Sided Recurrent Laryngeal and Phrenic Nerve Palsy After Coronary Artery Operation

Prabhat Tewari, MD, Surendra Kumar Aggarwal, MCh

Department of Anaesthesiology and Department of Cardiothoracic and Vascular Surgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India

Accepted for publication January 13, 1996.


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Comment
 References
 
Background. Ice/saline slush used along with cold cardioplegia for heart arrest in cardiac operations can cause hypothermic damage to certain structures, an important one being the left phrenic nerve, damage of which results in raised left hemidiaphragm and delayed recovery of the patient. In coronary artery bypass grafting, opening of the pleura and collection of the ice/saline slush in the pleural cavity increases the incidence of injury.

Methods. Three of our nonconsecutive patients underwent coronary artery bypass grafting with cold cardioplegia and open pleura, with collection of ice/saline slush in the pleural cavity for a sufficiently long time.

Results. Simultaneous involvement of left recurrent laryngeal nerve along with left phrenic nerve was found in all patients without any concurrent topical injury around the larynx. The recurrent laryngeal nerve took 8 to 10 months to recover.

Conclusions. The left recurrent nerve as it arches around aorta lies in the thorax very close to the parietal pleura and may be prone to hypothermic injury by ice/slush collecting in the pleural cavity during cardiac operations. Judicious use of ice/saline slush has helped in eliminating the problem to some extent.


    Introduction
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 Abstract
 Introduction
 Patients and Methods
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See also page 1722.

Coronary artery operations may be complicated by left phrenic nerve palsy. Although the exact mechanism of injury is not known, two commonly held views incriminate cold injury during topical myocardial cooling [1] and surgical trauma during internal mammary artery dissection [2]. We have encountered 3 patients in whom both left recurrent laryngeal nerve and left phrenic nerve injury developed after coronary artery bypass grafting.


    Patients and Methods
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 Abstract
 Introduction
 Patients and Methods
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Three of our male patients aged 50 years, 68 years, and 51 years presented with angina class III. On subsequent investigations all of them were found to have severe triple-vessel coronary disease and underwent coronary artery bypass grafting with cold crystalloid cardioplegic heart arrest and topical myocardial cooling with ice/saline slush. The anesthetic induction and maintenance was uneventful and endotracheal intubation was smooth. Three saphenous vein grafts and the left internal mammary artery were used in all patients. The left pleura was opened during left internal mammary artery dissection, and a large amount of iced slush accumulated in the thoracic cavity.

The first and third patients recovered from cardiopulmonary bypass without inotropic support, but the second patient required dopamine infusion (8 to 10 µg • kg-1 • min-1). In the postoperative period chest roentgenograms showed raised left hemidiaphragm in all. The ultrasound and fluoroscopy showed nonmobile to paradoxically moving hemidiaphragm suggesting left phrenic nerve injury. Extubation was done after 14 hours in the first patient and after 10 hours in the other 2. The patients had increased respiratory rates, moderate reduction in static lung functions and peak expiratory flow rates, and hoarse voice. Laryngeal examination revealed nonmobile left vocal cord in all 3 patients suggesting left recurrent laryngeal nerve injury. No evidence of local laryngeal or tracheal injury was present.

The patients underwent rigorous physiotherapy and had recovery after 10 days and went home with advice to regularly come for laryngeal and cardiac follow-up. In the follow-up the vocal cord regained its movement in the first and second patients at 12 and 10 months with a normal voice. In the third patient the voice remained hoarse but the vocal cord was found to show some movement on ear, nose, and throat examination at 8 months, after which we lost trace of him. The hemidiaphragms remained radiologically elevated, indicating residual phrenic nerve injury, but all patients showed marked improvement in their lung functions.


    Comment
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 Patients and Methods
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Various reports have described bilateral vocal cord paralysis after general anesthesia. The procedure of endotracheal intubation has been implicated in some of them. Overextension of the neck during laryngoscopy or an unnatural position of the head and neck during operation can cause traction of the recurrent laryngeal nerve from the mediastinum and thus vocal cord paralysis [3]. The recurrent laryngeal nerve, especially the left, ascends deeply in the tracheoesophageal groove from the thoracic cavity; therefore, it can be compressed by an inappropriate-sized endotracheal tube cuff when the neck is rotated. When the cuff is inflated by mistake in the larynx, the anterior branch of the recurrent laryngeal nerve may be compressed between the cuff and the thyroid lamina. Other rare causes enumerated are downward traction of the esophagus and even faulty insertion of a nasogastric tube [4].

In all 3 patients in our series the endotracheal intubation was smooth, atraumatic, and without any difficulty. Endotracheal tubes used were of appropriate size and with high-volume and low-pressure cuffs. Cuff pressure was monitored in the operating room, and intermittent deflation was used in the intensive care unit as a routine. Laryngeal examination in the follow-up supported no injury due to pressure of the cuff. The head and neck were slightly extended during intubation; otherwise, the head and neck were kept in a neutral position throughout as a routine. No nasogastric tube was inserted. The noteworthy fact was exclusive involvement of left recurrent laryngeal nerve along with left-sided paresis of the diaphragm, suggesting hypothermic left phrenic nerve injury in all the patients as a large amount of ice cold slush accumulated in the left thoracic cavity.

Diaphragm paralysis, usually unilateral and left-sided, has been recognized after open heart operations, occurring radiologically in 30% to 75% of patients [5]. Phrenic nerve cold injury resulting from the use of ice/saline slush topical hypothermia has been suggested as a common cause, although other mechanisms occasionally have been implicated [5]. This left-sided predominance can be explained by the closer juxtaposition of the left phrenic nerve to ice/slush saline placed in the pericardial sac during aortic cross-clamping. The increased incidence of phrenic nerve dysfunction has been noted with mammary artery grafting, and more so when the pleurotomy has also been done for complete left internal mammary artery dissection. One explanation forwarded for this association is an increased and direct exposure of the phrenic nerve to iced saline slush after left pleurotomy [6].

Similarly, the left recurrent laryngeal nerve as it curves around the arch of the aorta comes very close to the parietal pleura in the upper and posterior part of the thoracic cavity. Once the pleura opens and a large quantity of iced saline slush stays for a long time in the thoracic cavity, it can cause hypothermic tissue damage to vulnerable structures that are adjacent to the parietal pleura and that are bathed in ice-cold slush. The left recurrent laryngeal nerve is one such structure. It is seen in our cases that the recurrent laryngeal nerve injury is recoverable but it takes 8 to 12 months, although in the third patient we cannot ascertain whether recovery was complete as he did not return to follow-up after 8 months. Left internal mammary artery harvesting without opening of the pleura and judicious use of topical ice/saline slush has resulted in a decrease in the incidence of phrenic nerve injury at our center, and routine laryngeal examination has not revealed involvement of the vocal cord in any of our further patients.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Comment
 References
 
Address reprint requests to Dr Tewari, Department of Anaesthesiology and Critical Care, SGPGIMS, Raibarely Rd, Lucknow 226014, India.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Comment
 References
 

  1. Marco JD, Hahn JW, Barner HB. Topical cardiac hypothermia and phrenic nerve injury. Ann Thorac Surg 1977;23:235–7.[Abstract]
  2. Setina M, Cerny S, Grim M, Pirk J. Anatomical interrelation between the phrenic nerve and the internal mammary artery as seen by the surgeon. J Cardiovasc Surg 1993;34:499–502.[Medline]
  3. Faaborg-Anderson K. Recurrent laryngeal paralysis of unknown aetiology. Acta Otolaryngol 1954;118:68–75.
  4. Takae I, Noriomi A, Tanaka Y. Vocal cord paralysis associated with difficult gastric tube insertion. Can J Anaesth 1994;41:431–4.[Medline]
  5. Large SR, Haywood LJ, Flower CD, Cory-Pearce R, Wallwork J, English TAH. Incidence and aetiology of a raised hemidiaphragm after cardiopulmonary bypass. Thorax 1985;40:444–7.[Abstract/Free Full Text]
  6. Hurlbut D, Myers ML, Lefcoe M, Goldbach M. Pleuropulmonary morbidity: internal thoracic artery versus saphenous vein graft. Ann Thorac Surg 1990;50:959–64.[Abstract]

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