In the present study, we revealed the incidence of PID to be 39.9% for Chinese patients undergoing ECT, a value supported by the previous research of Kikuchi et al., in which they utilized the same delirium measure and identified the incidence of PID to be 36%.5
Furthermore, receiving ECT for the first time, RASS score ≥ 2 before ECT and high HR variance were identified as significant and independent risk factors for PID. During the ECT procedure, hyperdynamic responses are usually evoked by parasympathetic discharge that coincides with electrical stimulation, which might result in a 30% to 40% increase in blood pressure, and an increase over 20% in HR.9,10 In this analysis, we did not find significant differences either on MAP or on HR values immediately after the ECT between the two patient groups. Interestingly, when comparing HR fluctuation, we found a larger variance in those with PID. This finding is in line with previous suggestions that the increase in the variable hemodynamic fluctuation, not the absolute or relative hemodynamic value, might be a predictor of PID.8,11 Nevertheless, it is still unclear as to why increased HR fluctuation causes an increased chance of PID. In this regard, Jooyoung et al. speculated that higher HR fluctuations could lead to an instability in the autonomic nervous system, which may possibly be associated with delirium.11 Consequently, it can be inferred that a higher level of control over patients’ HR, as well as over their blood pressure, during ECT may help prevent PID.
We deem important to note that PID was more frequently observed in patients that had higher RASS scores before ECT, which may lead to an understanding that more agitated patients experience PID more frequently. The impact of agitation before ECT on PID has also been evaluated by the study from Gomez and Dally: they found that the incidence and severity of post treatment agitation was significantly greater when ECT was performed without prior patient tranquillization.12 However, the treatment for agitation before ECT remains controversial, as some conventional medication administered to prevent patients’ agitation, such as benzodiazepines, were shown to interfere with seizure duration and lead to numerous, sometimes serious, adverse effects.13,14 Although the treatment for agitation before ECT is inconclusive, caution should be exercised when considering patients with previous history of anxiety to undergo ECT, as they may be more propense to develop PID.
Although some demographic characteristics, such as age, gender and diagnosis, were considered as risk factors for PID in many medical settings, our results showed that differences in these characteristics did not seem to contribute to the appearance of PID after ECT.4,5 Further, we did not find any association between PID, weight and duration of illness; notwithstanding, when referring to how many times patients had received ECT, we found that patients who were undergoing this procedure for the first time were more propense to develop PID. Additionally, we did not find any correlation that indicated that seizure length predicted the occurrence of PID, which was inconsistent with the research by Reti et al.4 It is worth noting that the seizure length and stimulation dose found in Reti’s research seemed to be greater than those utilized in our study. Therefore, there is a possibility that the relatively short seizure length we have provided in this study was not adequate to reveal how seizure length may affect PID.
In this study, all patients were adequately anesthetized with propofol and succinylcholine before ECT. We did not find an association between the dose of anesthetics and PID, which was consistent with the findings of previous studies.4,15 Further, previous research showed that when ECT is administered with no anesthetic agent, PID occurs more frequently and tend to present more serious symptomatic outcomes.16 Thus, it is reasonable to presume that adequate anesthesia during the ECT procedure acts as a protective factor for PID, and that it may decrease its effects.
Our study has several limitations. Firstly, collected data referred only to the first ECT administration, and is common knowledge in the field that, if the patient experiences PID symptoms in the first procedure, subsequent applications undergo modifications to better suit each patients’ needs. Thus, it is not known whether these found risk factors would relate to PID in subsequent ECT treatments, and future studies should seek to resolve this conundrum.
Secondly, the scale utilized in this study to measure PID has yet to be more widely used. Therefore, the knowledge about the specificity and sensitivity of this scale measurement was still limited at the time of this study. Future studies are warranted to define the best suited approaches for PID measurement, and if our chosen measure is indeed accurate and valid for this type of measurement.