Despite recent advances in cardiac surgery procedures, we found a 7.6% postoperative incidence of DD. To our knowledge, this is the largest study of DD after cardiac surgery. Not surprisingly, we found that DD was associated with respiratory complications and prolonged ICU and hospital stays. Half of the patients with DD required non-invasive ventilation and one-quarter developed pneumonia. DD was also the cause of 20% of all reintubations and of 50% of all tracheotomies. However, the early diagnosis and systematic therapeutic protocol allowed a low in-hospital mortality rate (0.7%) that was not different from other patients.
Indeed, DD must be treated specifically. Although spontaneous recovery can be observed within 96 h after extubation [1, 3, 4], complications may have started during this time delay. Non-invasive ventilation may help to improve respiratory capacity after extubation. Some authors have suggested to keep the patient under mechanic ventilation until recuperation of diaphragm function, even if a tracheotomy needs to be used [1, 3, 4]. Our local protocol, applied to the patients in this study, gave priority to early extubation; bringing the patient on the armchair as soon as possible with intense respiratory physiotherapy to re-educate the diaphragm; and systematic use of non-invasive ventilation with positive pressure, including continuous positive airway pressure during sleep, to maintain residual functional capacity as close as possible to normal. Tracheostomy was restricted to patients with persistent DD with respiratory failure needing reintubation. Although our mortality was low, this was not an objective of our protocol and controlled studies are needed to evaluate this strategy.
Respiratory complications with or without pneumonia are frequent (2–6%) after cardiac surgery, leading to an increase of hospital stay and mortality [1, 3, 4]. DD is probably an underestimated cause of respiratory failure through other complications, such as atelectasis and pneumonia.
Our study confirmed the link between DD, hypertension, BMI, and coronary bypass grafting but not with diabetes, as previously observed. The role of diabetes in this pathology is still unclear [14, 24]. DD can be transiently due to many factors, including pain, hyperglycaemia, sepsis, neuromyopathy, electrolyte disorders (such as hypophosphoraemia), mechanical harm by tubes, and pleural or pericardial effusion. Prolonged DD is most often the consequence of a phrenic nerve injury but may be caused by multiple factors. The use of ice slush for myocardial protection during CPB was a well-known cause of phrenic nerve injury in the past, but it is no longer in use [8, 26]. It is uncertain whether phrenic nerve injury is primarily related to direct surgical injury or to ligation of its blood supply during internal mammary artery (IMA) dissection, especially when using electric cautery. Stretching of the phrenic nerves during chest opening may also be a possible mechanism and may explain why BMI, which supposes higher strength to open the chest, was associated with DD in our study and in others [10, 27]. The anatomic relationship between the phrenic nerve and the IMA is inconstant, and thus, caution must be taken when dissecting this artery. Furthermore, the blood supply to the phrenic nerve comes from the pericardiophrenic artery, which is a branch usually originating from the upper 1 to 3 cm of the IMA. In the 1990s, when the IMA was harvested, the reported incidence of DD was very high, ranging from 42–69% [8, 28, 29], but it decreased with the knowledge of this pathology, improvement in surgical techniques and increase in surgeon’s skills. Almost three-quarters (72.3%) of patients with DD were found after coronary bypass grafting, with quite a perfect parallelism between the side of the IMA harvesting and the side of the DD (100% for left DD and 94% for right DD). In the same way, the higher post-operative creatine kinase peak in the DD group, without differences in the troponin peak, may cause ischaemia of phrenic muscle after IMA harvesting. Nevertheless, the last quarter of our patients with DD (25.7%) were found after valvular surgery, confirming that DD does not have a unique mechanism.
Our study has several limitations. First, being a monocentric study, the results correspond to a specific experience. The retrospective nature of the analysis brings only a low risk of bias since the database was prospectively collected on a registry. However, this prevents the assertion of the causal link of the observed associations. The DD incidence we studied was the incidence of clinically perceptible DD. A systematic analysis of DD will probably find a higher incidence. Furthermore, we did not report the link between the side of DD paralysis and the side of internal jugular vein catheterization, systematically placed before surgery, which could be another risk factor for phrenic nerve injury. Last, we only studied intra-hospital events without a long-term follow-up. Data from long-term outcomes would be interesting, especially to analyse the potential recovery.