The severity and clinical outcomes of VCP are shown in Table 2. VCP occurred in 32 (4.7%) patients, which included 12 mild (1.7%), 10 moderate (1.5%) and 10 severe (1.5%) cases. All 12 patients with mild VCP recovered fully within 6 months and the median recovery time was 9 weeks [interquartile range (IQR) 2.5 to 13.0]. Two patients in the moderate VCP group had full recovery after 36 and 50 weeks. The overall full recovery rate was 43.8% and the overall median recovery time for these patients was 9 weeks (IQR 3.5 to 20.8).
The types of surgery that were related to persistent VCP included VAD implantation (four cases), ascending aortic surgery with BCA reconstruction (two cases) and valve replacement surgery with coronary artery bypass grafting (one case). Of the 10 cases with severe VCP, reintubation was required in all of the patients because of upper airway obstruction after extubation, and seven of these patients later required tracheostomy. The length of ICU stay was significantly longer for patients with severe VCP [12.5 days (IQR 5.5 to 25.5)] than it was for patients without VCP [3 days(IQR 2 to 5), P = 0.0002]. Bilateral VCP was observed mainly in patients with severe VCP in whom airway obstruction was present. Unilateral VCP occurred on the right and left sides of the vocal cords throughout the groups (Table 2). The rates of pulmonary complications associated with VCP were aspiration 40.6% (13/32) and pneumonia 25% (8/32). The area under curve for intubation periods was 0.66 (P < 0.01).
After adjusting for potential confounding factors in our multivariable analysis, type 2 diabetes mellitus [odds ratio (OR) 1.853, P = 0.009), intubation period (OR per 24 h 1.136, P = 0.014), ascending aortic arch surgery with BCA reconstruction (OR 8.708, P < 0.001) and VAD implantation surgery (OR 3.460, P = 0.005) remained independent predictors for the severity of VCP (Table 3).
In our single-centre retrospective study, we evaluated the frequency and severity of VCP in patients who underwent thoracic cardiovascular surgery to identify any potential risk factors. We found that VAD surgery, ascending aortic arch surgery with BCA reconstruction, prolonged intubation periods and the presence of type 2 diabetes mellitus were independent risk factors for VCP. Other well established risk factors were not significant in our study.
In the present study, 4.7% of patients who underwent cardiovascular surgery experienced VCP to some degree, which is concerning for several reasons. In severe cases, VCP may cause life-threatening complications such as aspiration, stridor and airway obstruction. Each of these situations may require reintubation, resulting in longer ICU stays and morbidity.4–6 Glottic incompetence secondary to VCP impairs swallowing, which can delay oral feeding and bowel movement recovery.7–9 Although not life-threatening, iatrogenic dysphonia greatly affects the patient's quality of life and is susceptible to litigation where the anaesthesiologist is often named as the defendant.10
Moreover, the true incidence of VCP after cardiovascular surgery is difficult to establish, as laryngeal examinations are not routinely performed. Thus, the incidence varies, with reported values ranging from 0.67 to 23% for all types of thoracic cardiovascularprocedures1,2,11,12 and from 7.3 to 32.3% for aortic arch surgery;3,13 our incidences of 3.9 and 9.9%, respectively, are within these previously reported ranges.
The recovery of patients from VCP after thoracic cardiovascular surgery has not been fully examined in the adult population. Joo et al.2 reported that the time required for functional recovery was less than 6 months in 10 of the 13 adult patients they studied and that the estimated rate of persistent VCP was 3.5 to 5.3% after a mean follow-up time of 14.8 months. A systematic review of hoarseness after thoracic cardiovascular surgery, which included newborn and paediatric patients, suggested that the rate of persistent hoarseness was 33%.14 In our study, the overall rates of partial recovery and persistent VCP were 34.4 and 21.8%, respectively. Overall, only 43.8% of the patients had full recovery after follow-up at 1 year. The median time to recovery in these patients was 9 weeks (IQR 3.5 to 20.8). The low rate of full recovery in our cohort may be related to the inclusion of high-risk patients and shorter follow-up periods. We also found a significantly longer ICU stay in patients with severe VCP compared with patients without VCP. The delayed recovery in patients with severe VCP highlights the importance of evaluating laryngeal function before extubation in high-risk patients.5,15,16 Although there were eight cases of mortality in our cohort, they were not directly related to VCP and we did not include these cases in our analysis.
A unique finding of our study is that even after adjusting for confounders such as ejection fraction, New York Heart Association status and intubation period, VAD implantation surgery remained a significant independent risk factor for VCP, which to our knowledge has not been reported previously. Furthermore, when VCP occurred, it often caused severe disabilities requiring tracheostomy. Particularly, four of the seven patients with persistent VCP underwent VAD implantation. The pathological mechanisms for VCP in patients who underwent VAD implantation are unclear but may be the result of several factors related to RLN and laryngeal injuries. Patients who require VAD implantation suffer from low cardiac output with enlarged left atrium and elevated pulmonary artery pressures secondary to high end-diastolic ventricular pressures. Left RLN injury may occur because of compression by such enlarged cardiovascular structures (Ortner's syndrome).17,18 Direct manipulation and retraction of the heart during VAD insertion may also cause RLN injuries.1 Cardiovascular instability during the perioperative period may cause low perfusion and ischaemia in the laryngeal membrane, which can produce oedema and inflammation. The laryngeal membrane may be further aggravated by physical trauma related to the ETT cuff in the postoperative period.
Previous studies have extensively demonstrated the association between aortic surgery and VCP, showing that the incidence is more frequent with para-aortic procedures and aortic procedures extending to the distal arch.12,13,19,20 In our cohort, we also found that the risk of VCP was significantly higher in patients who underwent thoracic aortic surgery with BCA reconstruction. Notably, VCP did not occur in patients who underwent aortic surgery without BCA reconstruction. However, the classifications of ascending aorta and arch or descending aorta used in prior reports may not reflect the likelihood of injury to the RLN owing to the development of less invasive endovascular surgical techniques in recent years; therefore, we chose to classify the aortic procedures according to the presence or absence of BCA reconstruction. Potential mechanisms for VCP in BCA reconstruction cases include surgical manipulation of the left common carotid artery during BCA reconstruction and microembolisation of the afferent arteries after artery clamping.
Our findings are in agreement with previous reports demonstrating that prolonged intubation periods and the presence of type 2 diabetes mellitus are risk factors for VCP.6,21–23 In our study, intubation periods longer than 97.9 h were related to the occurrence of VCP with 43.3% sensitivity and 33.4% specificity.
Other previously reported risk factors such as age, sex (female), ETT fixation depth, surgery duration, internal thoracic artery harvest, the use of large-diameter ETTs and deep hypothermic cardiac arrest were not significant in our study.1,11,13,24,25 Many of the studies that reported these factors also included noncardiac surgery patients and patients with undiagnosed VCP. As the leading cause of postsurgical VCP is thyroidectomy, these previous reports probably reflect the characteristics of this patient population, including advanced age and female sex.10
We have described several risk factors found after cardiovascular surgery and our results may help assist intensivists and anaesthetic staff in preparing for VCP after extubation. Nevertheless, detection of VCP and avoiding extubation failure is an essential part of postoperative management. It is important we do not miss the clinical symptoms of VCP even in patients without the risk factors described in our study.
We acknowledge the following potential limitations of our study. First, given that there were only a few cases of VCP in our single-centre study, our results should be interpreted with caution. The inherent biases involved in the retrospective design and data collection are also limitations of our study. Although risk factors for VCP were identified, the pathogenesis of VCP remains unclear and further studies are warranted. During the span of our study period, a videolaryngoscope was often used and the difficulty and Cormack-Lehane classification could not be properly assessed for many cases. Therefore, we were unable to include these factors in our analysis. Moreover, we did not routinely treat patients with corticosteroids prior to or after extubation. This may have had an effect on the severity of VCP in the high-risk group. Finally, although we actively asked patients for symptoms of VCP after extubation we acknowledge that there was the possibility of missing the occurrence of VCP, especially for mild cases of dysphonia. This may have led to underestimation of the true occurrence rate of VCP.
In this retrospective study of thoracic cardiovascular surgery patients, the potential risk factors of VCP severity were type 2 diabetes mellitus, intubation period, ascending aortic arch surgery with BCA reconstruction and VAD implantation. Identifying such risk factors may allow us to screen for patients who are at risk of developing VCP after thoracic cardiovascular surgery and to assist anaesthesia personnel so that they can be prepared for VCP-related airway obstruction after extubation.
Acknowledgements relating to this article
Assistance with the study: the authors thank Professor Ayumi K. Shinntani (Department of Clinical Epidemiology and Biostatistics, Graduate School of Medicine, Osaka University) for invaluable discussions on our statistical analysis.
Financial support and sponsorship: the work was supported solely by departmental resources.
Conflicts of interest: none.
Presentation: preliminary data from this study were presented as a poster at the Euroanaesthesia meeting, June 2016, London.
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