Ann Thorac Surg 1998;65:32-35
© 1998 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Phrenic Nerve Injury After Coronary Artery Bypass Grafting: Will It Go Away?
Michael G. Katz, MD, PhD,
Rama Katz, MD,
Arie Schachner, MD,
Amram J. Cohen, MD
Department of Cardiovascular Surgery, E. Wolfson Medical Center, Holon, Israel
Department of Radiology, E. Wolfson Medical Center, Holon, Israel,
Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel
Accepted for publication May 21, 1997.
Dr Cohen, Department of Cardiovascular Surgery, E. Wolfson Medical Center, PO Box 5, Holon 58100, Israel.
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Abstract
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Background. Phrenic nerve injury after coronary artery bypass grafting resolves in most cases. The purpose of this study was to analyze the causes and effects of persistent phrenic nerve injury after coronary artery bypass grafting.
Methods. From a registry of patients with chronic obstructive pulmonary disease who underwent coronary artery bypass grafting, 64 patients were identified who experienced phrenic nerve injury during their operation. Fifteen patients either died during follow-up (n = 9) or were lost to follow-up (n = 6). At the last follow-up visit, all the patients underwent an ultrasound evaluation of the diaphragm and were divided into those who had persistent dysfunction (group I) and those who had normal function (group II). The groups were compared for preoperative and operative risk factors, acute and midterm postoperative results, and quality of life at last follow-up.
Results. There were 13 patients in group I and 36 in group II. There were no significant differences in preoperative and operative risk factors between the groups. The length of hospitalization was similar for both groups (9.2 ± 4.5 versus 8.5 ± 3.3 days, respectively; p = 0.77). More patients in group I required reintubation (23% versus 14%, respectively; p = 0.04). The mean duration of follow-up was 32.7 ± 9.2 months. At that time, both groups suffered a reduction of forced expiratory volume in 1 second compared with preoperative values. Group I had a greater reduction in forced expiratory volume in 1 second (p = 0.05). There were a total of 125 postoperative readmissions during the follow-up period, 36 in group I and 89 in group II. There were more admissions because of pulmonary problems in group I (85% versus 53%; p = 0.04). Of the 49 patients, 21 perceived a decline in quality of life after operation. More patients in group I (46% versus 22%; p = 0.05) complained of this decrease.
Conclusions. A significant number of patients who incur phrenic nerve injury after coronary artery bypass grafting have persistent phrenic nerve injury. Patients with persistent phrenic nerve injury have increased acute and midterm morbidity after operation, as well as reduced quality of life.
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Introduction
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Phrenic nerve injury (PNI) continues to be a significant complication after coronary artery bypass grafting (CABG), especially in patients who are operated on under hypothermic conditions [1][2]. Most patients who experience PNI after CABG fully recover function within a year [2][3][4]. However, a significant minority do not [1][5][6]. Little is known of the subgroup of patients who do not fully recover phrenic nerve function after CABG. The purpose of this study was to analyze the causes and effects of persistent phrenic nerve injury (PPNI) after CABG.
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Material and Methods
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At Wolfson Medical Center, a registry is kept of patients with significant chronic obstructive pulmonary disease (COPD) and matched control subjects who undergo isolated CABG. From this registry, 64 patients who experienced PNI after CABG were identified for this study. To be defined as a patient with PNI, all the following radiographic criteria had to be met, on an inspiratory radiograph, for paralyzed left diaphragm: (1) the left hemidiaphragm was located below the right hemidiaphragm on a preoperative posteroanterior chest radiograph; (2) the left hemidiaphragm was at least one rib higher than the right hemidiaphragm on a discharge posteroanterior chest radiograph; and (3) the left hemidiaphragm either returned to its normal location on late follow-up or was confirmed by ultrasound to be paralyzed at that time. No patient in the series had a paralyzed right diaphragm. All patients who were defined as having a paralyzed diaphragm had their diaphragms examined by repeated chest radiographs and ultrasound examinations at the last follow-up visit to determine diaphragmatic function. Pulmonary function tests were performed on all patients before the operation and on all the survivors at the last follow-up visit.
An attempt was made to reexamine all the patients. A total of 15 patients either had died (n = 9), were lost to follow-up, or refused restudy (n = 6). These patients were excluded from the study, leaving 49 in the study group, who then underwent clinical evaluation and an ultrasound scan of the diaphragm. Of the study patients, 13 continued to display a paretic or paralyzed diaphragm (group I). The remaining 36 patients had normal diaphragmatic function (group II). For each patient, preoperative data, including pulmonary function test and chest radiography results, were recorded.
All operations were performed through a median sternotomy with single aortic and venous cannulation. Harvesting of the internal mammary artery was performed with cautery and the left pleura was opened widely in each case. Myocardial protection was accomplished with antegrade crystalloid cardioplegia during the initial phases of the study, and with antegrade and retrograde cardioplegia during the late phases. Topical iced slush saline was used as an adjunct to cardioplegia in this series. In no case were adjuncts used to protect the phrenic nerve. Distal anastomoses were performed during diastolic arrest. Proximal anastomoses were performed with a partial clamp on a beating heart. The left anterior descending artery was grafted with the left internal mammary artery whenever possible. All other coronary arteries were grafted with reverse saphenous veins.
Postoperative data, including morbidity and length of hospital stay, were recorded. At the last follow-up visit, the number of readmissions was recorded, as well as the patient’s pulmonary status. The quality of life of each patient was evaluated by a questionnaire that included assessment of exercise capability, breathing difficulty, and the ability to perform desired tasks [7].
Because of the small sample size, nonparametric tests were used to compare the two groups. For continuous variables, the Mann-Whitney U test was used. For discrete variables, 
2 analysis was used. Reported statistics for continuous variables are means ± SD and those for categorical variables are percentages. The reported p values are based on a two-tailed test, unless otherwise noted. Any p value of less than 0.05 was considered to be statistically significant.
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Results
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Preoperative Data
The preoperative risk factors for the two groups are shown in Table 1.
There were no significant preoperative differences between the groups, including smoking history, diabetes, and ejection fraction. The results of the pulmonary function studies are shown in Table 2.
There was no significant difference in preoperative forced expiratory volume in 1 second (FEV1) or forced vital capacity (FVC) between the groups; however, group 1 showed a significantly higher baseline PaCO2 (p = 0.014). There was a significant reduction in FEV1 in both groups from preoperative values to the last follow-up visit (group I, p = 0.0015; group II, p = 0.033). This also was true for FEV1/FVC (group I, p = 0.0024; group II, p = 0.017). There was a greater reduction in group I for both FEV1 (p = 0.055), and FEV1/FVC (p = 0.0129) than in group II.
Operative Data
Operative data are shown in Table 3.
The operative technique used was similar in the two groups, and there were no differences with regard to the use of the internal mammary artery, the duration of cardiopulmonary bypass, or the duration of cross-clamping.
Postoperative Data
Acute postoperative results are shown in Table 4.
Both groups had similar intensive care unit and total hospital stays. Patients in group I had a significantly higher incidence of reintubation (p = 0.04) during their hospitalization.
The mean duration of follow-up was 32.7 ± 9.2 months. For group I, it was 28.9 ± 10.0 months, and for group II, it was 34.0 ± 8.5 months.
There were 125 readmissions in both groups. The 13 patients in group I were readmitted 36 times. Thirty-four patients in group II were readmitted a total of 89 times. The primary indications for readmission were pulmonary and cardiac problems (Fig 1).
Ten patients in group I and 23 in group II had multiple readmissions. Among those patients who were readmitted after operation, there was a significantly higher percentage of readmissions because of pulmonary problems in group I (Fig 1). Overall, 21 of 49 patients reported a decline in their quality of life after CABG.
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Comment
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In our study, 13 (26%) of 49 patients followed up for an average of 32.8 months (range, 7 to 48 months) did not fully recover diaphragmatic function. Although this number is high compared with previous studies [1][5][8], our patients all were evaluated by ultrasound, and the number includes those with both residual paresis and paralysis. The high incidence of patients with residual diaphragmatic dysfunction allowed us to compare this subpopulation with patients who experienced PNI during CABG but fully recovered diaphragmatic function during follow-up.
Risk factors for PNI after CABG include the use of iced slush for topical cooling, the use of cold cardioplegia, the number of grafts performed, the duration of operation, the body temperature, the presence of heart failure, and the presence of COPD [1][7][8][9]. These factors were similar in both groups. Risk factors for PPNI after CABG have not been reported previously. In this study, we found a higher baseline PaCO2 in patients with PPNI (group I) compared with those who recovered phrenic nerve function (group II). This factor is an indication of the severity of COPD; thus, our data imply that in patients with severe COPD, there is an increased risk that PNI after CABG will be persistent. The explanation for this remains unclear.
Postoperative Course
Acute Morbidity
The length of the intensive care unit and hospital stays were similar for both groups. Cardiac and pulmonary complications also were similar. The notable exception was that more patients in group I required reintubation during their hospital stay. This probably is because of the fact that patients in group I who did not recover phrenic nerve function had more severe PNI [1][3][6][10]. After such an injury, the diaphragm was more flaccid and pulmonary embarrassment was greater. The result was that more of these patients failed to maintain adequate ventilation over time and thus required reintubation.
Long-Term Follow-Up
It recently has been reported that PNI during CABG reduces survival and quality of life on midterm follow-up in patients with COPD [11]. Our study shows that PPNI has a negative impact on the midterm results after CABG. Patients in group I had more residual respiratory embarrassment, more readmissions for respiratory complications, and a significantly reduced quality of life compared with patients in group II.
Limitations of the Study
The study suffers from several limitations. First, the patients in this study were not taken from the general population, but from a registry in which half the patients had severe COPD. This is reflected in the poor preoperative pulmonary function, long intensive care unit and hospital stays, and poor midterm results of this population compared with the standard population that undergoes CABG [12]. Whether our results apply only to patients with poor pulmonary function or also to the general population that undergoes CABG cannot be determined from this study.
Second, our study is retrospective, so there may be significant selection biases between the two groups. Comparing the preoperative status of the two groups suggests that group I may have had more severe COPD. Because significant COPD contributes to a poorer midterm result [7], this may have influenced the inferior results achieved in group 1.
Third, 9 patients who died during follow-up could not be included in the study, because their diaphragmatic function at the time of their death was unknown. If these patients fell uniformly into one group or the other, it would change our results significantly. Finally, our groups were small, and a larger series of patients is required to confirm our findings.
Conclusions
With these limitations in mind, we draw the following conclusions from this study: (1) A significant minority of patients who experience PNI after CABG will have PPNI. (2) In patients with significant COPD, there is an increased risk that PNI experienced during CABG will persist. (3) Patients with PPNI after CABG will have more respiratory embarrassment, more readmissions for respiratory complications, and reduced quality of life compared with those whose PNI resolves.
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Acknowledgments
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We thank biostatistician Diklah Geva, MSc, for preparing the statistics, and Sally Esakov, BA, for technical assistance.
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References
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Abstract
Introduction
