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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 6  |  Issue : 1  |  Page : 17-19

Postintubation vocal cord palsy: possible role of pre-existing laryngeal deformity?


1 Department of Anaesthesiology and Critical Care, Army Hospital (Research & Referral), New Delhi, India
2 Department of Otorhinolaryngology, Army Hospital (Research & Referral), New Delhi, India

Date of Submission22-Sep-2017
Date of Acceptance15-Jul-2018
Date of Web Publication27-Feb-2019

Correspondence Address:
Mridul Dhar
Department of Anaesthesiology and Critical Care, Army Hospital (Research & Referral), New Delhi, 110010
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/roaic.roaic_80_17

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  Abstract 

Background Unilateral or bilateral vocal cord (VC) paralysis following atraumatic intubation is extremely rare and has been reported even in the absence of any predisposing factors. Occurrence of such a complication is disconcerting to the clinician as well as the patient alike.
Case A 42-year-old man suffering from cryptogenic cirrhosis of the liver, who underwent a deceased donor liver transplant, developed left-sided VC palsy postoperatively. No apparent cause was found and his symptoms recovered after conservative management. It was concluded that the patient possibly had recurrent laryngeal nerve neuropraxia due to compression by the endotracheal tube cuff.
Conclusion We would like to briefly describe the case, possible mechanisms for VC palsy following intubation, its benign course and the possible role of pre-existing laryngeal deformity, with the aim of enhancing the awareness among anaesthesiologists about this rare complication. Although not unique to liver transplant surgeries, the relatively longer perioperative period of ventilation in such surgeries may accentuate any pressure effects.

Keywords: endotracheal intubation, recurrent laryngeal nerve, vocal cord palsy


How to cite this article:
Dhar M, Sreevastava DK, Nair S. Postintubation vocal cord palsy: possible role of pre-existing laryngeal deformity?. Res Opin Anesth Intensive Care 2019;6:17-9

How to cite this URL:
Dhar M, Sreevastava DK, Nair S. Postintubation vocal cord palsy: possible role of pre-existing laryngeal deformity?. Res Opin Anesth Intensive Care [serial online] 2019 [cited 2019 May 23];6:17-9. Available from: http://www.roaic.eg.net/text.asp?2019/6/1/17/253125


  Introduction Top


Short-term endotracheal (ET) intubation during general anesthesia is a safe procedure. However unilateral or bilateral vocal cord (VC) paralysis following intubation has been reported even in the absence of any predisposing factors [1],[2],[3],[4]. Occurrence of such a complication is disconcerting to the clinician and also has medico-legal implications.

A case report of left-sided VC palsy detected after a relatively long period of intubation is presented. The aim of the report is to enhance the awareness among anaesthesiologists about this rare complication and to highlight its otherwise benign course. A possible role of the pre-existing external laryngeal deformity is also discussed.


  Case report Top


A 42-year-old man suffering from cryptogenic cirrhosis of the liver was scheduled for a deceased donor liver transplant. Preoperative evaluation revealed hepatosplenomegaly, ascites, and other features of chronic liver disease. Airway anatomy was normal with airway assessment revealing Mallampati class II with adequate mouth opening with a minimal deviation of the larynx towards the right ([Figure 1]).
Figure 1 External laryngeal deviation.

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The patient was administered general anesthesia using propofol, fentanyl, and atracurium. The trachea was intubated atraumatically, after complete relaxation of the VCs and making sure that the cuff was distal to them, guided by the markings on the ET tube. An 8.5 mm cuffed polyvinyl chloride ET tube was fixed at 24 cm at the teeth. The cuff pressure was monitored regularly and maintained at 25 cmH2O. Anesthesia was maintained with isoflurane admixed with air and oxygen. The intraoperative period was marked with haemodynamic and metabolic instability as anticipated during liver transplant surgeries. Appropriate management was undertaken according to standardized protocols. The position of the head and ET tube remained fixed during the surgery. At the end of surgery, the patient was shifted to the ICU for elective mechanical ventilation and was extubated the next day. The total duration of mechanical ventilation including the operative time and postoperative ventilation was about 30 h.

A change in voice was noticed following extubation which was initially attributed to the poor general health of the patient. Three days later, after improvement in his general condition, he complained of a persistent hoarseness of voice and irritation in the throat. Hopkin’s telescopy performed by the otorhinolaryngologist revealed left VC palsy which lay in the paramedian position at rest ([Figure 2]a) and showed no movement on vocalization ([Figure 2]b). The rest of the laryngeal framework appeared normal. A presumptive diagnosis of VC palsy possibly caused by tracheal intubation was made. The patient did not have difficulty in breathing or symptoms suggestive of aspiration. No further intervention was planned as hoarseness started to improve gradually. At the end of 3 months, his voice was near normal and Hopkin’s telescopy showed completely normal movement of both VCs ([Figure 3]a and b).
Figure 2 (a) Vocal cords (VCs) at rest (1 week after surgery). (b) Vocal cords on vocalizing (1 week after surgery).

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Figure 3 (a) Vocal cords (VCs) at rest (3 months after surgery). (b) Vocal cords on vocalizing (3 months after surgery).

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  Discussion Top


VC palsy has been observed after multiple intubation attempts or traumatic intubation. It can also be a manifestation of neoplastic, inflammatory, cerebrovascular, and degenerative disorders of the neck, head, and the thorax [5],[6]. However, etiology of VC paralysis after short-term as well as long-term tracheal intubation in isolation and in absence of any direct injury or pathology has not been ascertained with clarity [5].

Ellis and Pallister [7] brought out that the anterior branch of recurrent laryngeal nerve (RLN) which supplies most of the adductor muscles can be indirectly compressed by the cuff of the ET tube between the arytenoid and cricoid cartilages leading to VC palsy. This nerve can also be damaged by an overinflated cuff which slips out to rest against the VCs [2]. Cavo too showed that the anterior branch of the nerve is vulnerable to compression between the expanded cuff and the overlying thyroid cartilage on the superoanterior border of the posterior cricoarytenoid muscle in the subglottic region located about 6–10 mm below the posterior third of true VC. He recommended inserting the tracheal tube to a depth which allows the upper edge of cuff to lie below this region [8]. Increased cuff pressure may cause degeneration and paralysis of the RLN due to compromised microcirculation leading to ischemic neuronal degeneration [6]. Curvature of the racheal tube or unequal cuff pressure can conceivably occur in the presence of a distorted larynx and cause VC palsy. Occasionally, concurrent paralysis of RLN and hypoglossal nerves, known as Tapia syndrome, is seen in surgeries of the head and neck where a throat pack has been used leading to pressure neuropraxia of both nerves [9]. Left VC is affected more commonly compared with the right possibly because of the more tortuous course taken by the left vagus nerve [4].

Unilateral paralysis of the anterior branch of the RLN results in hoarseness of voice, with no symptoms of aspiration, stridor, or any respiratory distress unlike bilateral VC paralysis as seen in the present case. While investigating such cases, fibreoptic laryngoscopy should be done to assess the exact disposition of VCs. Risk of VC paralysis due to intubation increases threefold in patients aged 50 years or older and increases twofold in patients with chronic diseases like hypertension and diabetes [10]. Nearly all cases of unilateral VC paralysis or immobility show good recovery with conservative management and voice therapy.

In the present case, no obvious pathology could be identified. As mentioned previously, unevenly distributed cuff pressure may have a role in unilateral nerve stretching or injury. Anatomical variations in the structure of the larynx have not been studied much in the existing literature. In the present patient, there was a visible external deviation of the larynx to the right ([Figure 1]). It is thus hypothesized that this could have led to unequal pressure on the left side causing unilateral VC palsy. External appearance of the larynx should thus be able to give a clue to the clinician regarding the etiology of the paralysis.

In conclusion, the patient possibly suffered RLN neuropraxia due to compression by ET cuff, which was possibly aggravated by a deviated larynx causing unequal cuff pressure distribution. While it is important to be aware of such rare complications of ET intubation, it is reassuring to know that this condition usually recovers with conservative management.

Financial support and sponsorship

Nil.

Conflicts of Interest

There are no conflicts of interest.

 
  References Top

1.
Fauzdar S, Kraus J, Papageorge M. Vocal cord paralysis following orthognathic surgery intubation. Ann Maxillofac Surg 2011; 1:166–168.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Lu YH, Hsieh MW, Tong YH. Unilateral vocal cord paralysis following endotracheal intubation: a case report. Acta Anaesthesiol Sin 1999; 37:221–224.  Back to cited text no. 2
    
3.
Shin YH, An DA, Choi WJ, Kim YH. Unilateral vocal cord paralysis following a short period of endotracheal intubation anesthesia. Korean J Anesthesiol 2013; 65:357–358.  Back to cited text no. 3
    
4.
Marie JP, Keghian J, Mendel I, Gueit I, Dehesdin D, Andrieu-Guitrancourt J. Post intubation vocal cord paralysis: the viral hypothesis. A case report. Eur Arch Otorhinolaryngol 2001; 258:285–286.  Back to cited text no. 4
    
5.
Seyed Toutounchi SJ, Eydi M, Golzari SE, Ghaffari MR, Parvizian N. Vocal cord paralysis and its etiologies: a prospective study. J Cardiovasc Thorac Res 2014; 6:47–50.  Back to cited text no. 5
    
6.
Vyshnavi S, Kotekar N. Aphonia following tracheal intubation: an unanticipated post‑operative complication. Indian J Anaesth 2013; 57:306–308.  Back to cited text no. 6
[PUBMED]  [Full text]  
7.
Ellis PD, Pallister WK. Recurrent laryngeal nerve palsy and endotracheal intubation. J Laryngol Otol 1975; 89:823–826.  Back to cited text no. 7
    
8.
Cavo JW Jr. True vocal cord paralysis following intubation. Laryngoscope 1985; 95:1352–1359.  Back to cited text no. 8
    
9.
Gevorgyan A, Nedzelski JM. A late recognition of tapia syndrome: a case report and literature review. Laryngoscope 2013; 123:2423–2427.  Back to cited text no. 9
    
10.
Kikura M, Suzuki K, Itagaki T, Takada T, Sato S. Age and comorbidity as risk factors for vocal cord paralysis associated with tracheal intubation. Br J Anaesth 2007; 98:524–530.  Back to cited text no. 10
    


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  [Figure 1], [Figure 2], [Figure 3]



 

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