International Journal of Clinical Practice

Volume 2025, Issue 1 8880629

Research Article

Open Access

Effect of Dexmedetomidine on Posttraumatic Stress Disorder in Traumatic Brain Injury Patients Undergoing Emergency Craniotomy Surgery: A Retrospective Study

Yun-Qi Wang,

Corresponding Author

Yun-Qi Wang

[email protected]

orcid.org/0009-0005-0665-7980

Department of Anesthesiology , The Sixth People’s Hospital of Deyang City , Deyang , Sichuan, China

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Xian-Jie Zhang,

Xian-Jie Zhang

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Dan Zhou,

Dan Zhou

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Qing Li,

Qing Li

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Xin Liu,

Xin Liu

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Yun-Qi Wang,

Corresponding Author

Yun-Qi Wang

[email protected]

orcid.org/0009-0005-0665-7980

Department of Anesthesiology , The Sixth People’s Hospital of Deyang City , Deyang , Sichuan, China

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Xian-Jie Zhang,

Xian-Jie Zhang

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Dan Zhou,

Dan Zhou

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Qing Li,

Qing Li

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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Xin Liu,

Xin Liu

Department of Anesthesiology , People’s Hospital of Deyang City , Deyang , Sichuan, China , dy120.net

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First published: 02 May 2025

https://doi.org/10.1155/ijcp/8880629

Academic Editor: Yujie Chen

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Abstract

Background: The purpose of this study was to investigate the effect of dexmedetomidine (DEX) on the incidence of postoperative posttraumatic stress disorder (PTSD) in traumatic brain injury (TBI) patients undergoing emergency craniotomy.

Methods: The TBI patients who underwent emergency craniotomy at our hospital from January 2017 to June 2023 were included in our study. The patients were divided into the DEX group and the control group. We analyzed the intraoperative data (bradycardia, hypotension, hypoxemia, duration of anesthesia, and duration of surgery) and the postoperative data (PTSD, the total length of hospital stay, and Glasgow Coma Scale [GCS] scores at discharge).

Results: A total of 126 TBI patients were included in our study. Of these patients, 55 were treated with DEX (the mean rate of administration was 0.58 ± 0.22 μg/kg/h.) and 71 did not receive DEX. The incidence of bradycardia was significantly higher in the DEX group than in the control group (p < 0.05). However, the incidence of PTSD was significantly higher in the control group than in the DEX group (p < 0.05).

Conclusion: The use of DEX during anesthesia was effective in reducing the incidence of postoperative PTSD in TBI patients undergoing craniotomy.

1. Background

Traumatic brain injury (TBI) is a head injury caused by an external force, which can bring about a series of pathophysiological changes, ultimately leading to damage to the normal function of the brain [1, 2]. TBI has become a serious global public health problem as it is characterized by extremely high rates of disability and death, with more than 50 million people suffering from this affliction globally each year [2, 3]. The main external forces that cause TBI are falls, motor vehicle accidents, blows to the head, and more [4]. TBI can be categorized according to severity: mild (Glasgow Coma Scale [GCS] scores of 13–15), moderate (GCS scores of 9–12), and severe (GCS scores of 3–8) [4, 5]. The suffering caused by TBI is not just a short-term physical injury, but in the long run, it increases the incidence of other major diseases such as chronic traumatic encephalopathy, Alzheimer’s disease, and Parkinson’s disease [6, 7]. Psychological consequences of TBI for patients should not be ignored, and these disorders include suicide, posttraumatic stress disorder (PTSD), substance use disorder, major depressive disorder, and so on [7, 8].

The psychiatric disorders most commonly to be caused by TBI include PTSD [9]. The main manifestations of PTSD are the following four aspects: the continuous repetition of distressing reexperience, avoidance, the negative effects of mood and cognition, and changes in arousal and reactivity [9, 10]. The duration of these symptoms takes more than 1 month to be diagnosed with PTSD. Once patients are diagnosed with PTSD, they are likely to suffer for a long period of time [9]. The incidence of PTSD in TBI patients is about 11%–36% in the general population, while in the military, this incidence is as high as 33%–65% [9–11]. These patients often require longer rehabilitation cycles, which not only makes it difficult for them to return to society but also brings painful disasters to their families [10, 11]. The treatment of PTSD patients is still a huge challenge, so it is extremely important to promptly detect PTSD among TBI patients and carry out effective interventions. Some studies have shown that effective intervention in the early stages of PTSD can bring benefits to patients and promote their return to society [10–12].

Some current studies have found that α-2 adrenergic agonists have enhanced sedation and analgesia during general anesthesia. Therefore, α-2 adrenergic agonists have been widely used in patients undergoing general anesthesia [13, 14]. As an α-2 adrenergic agonist, dexmedetomidine (DEX) has good effects in analgesia, sedation, and antianxiety, so it is favored by anesthesiologists during anesthesia [14, 15]. DEX has been shown to have not only sedative and analgesic effects but also a protective effect on various organs. In patients with TBI, DEX reduces neuronal damage and improves neurological function. DEX has become a potential neuroprotective drug [16, 17]. An experimental animal study demonstrated that DEX had an ameliorating effect on cognitive impairments as well as attenuating anxiety-like behaviors in experimental rats in a PTSD model [18]. A recent study has shown that intraoperative DEX is effective in reducing the incidence of PTSD in patients undergoing emergency trauma surgery, but this study focused on emergency surgery of the chest, abdomen, and extremities and lacked research on TBI [19]. Therefore, what remains uncertain is whether DEX also reduces the incidence of PTSD in TBI patients undergoing emergency craniotomy. The purpose of this study was to investigate the effect of DEX on the incidence of postoperative PTSD in TBI patients undergoing emergency craniotomy and to explore new directions for the prevention and treatment of PTSD in such patients.

2. Methods

2.1. Object of Study

Retrospectively and consecutively, the subjects of our study were TBI patients who underwent emergency craniotomy at the Sixth People’s Hospital of Deyang City from January 2017 to June 2023 (the initial collection was made by querying electronic medical records of patients across the hospital). The following patients were excluded from this study: ages greater than 70 years and less than 18 years, patients who had a mental health disorder prior to the trauma, patients who committed suicide, combination of severe injuries to other organs (combined with severe trauma to the chest, abdomen, and extremities), inability to independently complete the PTSD assessment, less than 6 months of postoperative follow-up, incomplete clinical data, death, retreatment with surgery, and refusal of the patients themselves or their families to participate in this study. All patients underwent cranial CT on the first postoperative day, 1 week postoperatively and 1 month postoperatively. Patient visits were mainly conducted through outpatient visits and telephone calls. The patients themselves and their families signed an informed consent form. This study complied with the STROBE statement and was approved by the ethics committee of the author’s institution.

2.2. Data Collection and Outcome Assessment

We collected and recorded demographic and clinical characteristics of all patients: age, gender, preoperative pupil status (mydriasis), brain injury conditions (subdural hemorrhage, epidural hemorrhage, and brain tissue damage), and the GCS scores of patients before craniotomy. Intraoperative monitoring consists of the patient’s hemodynamic status (heart rate and arterial blood pressure), blood oxygen saturation, duration of anesthesia, duration of surgery, and the ventilation time of endotracheal intubation. Postoperative follow-up mainly included the occurrence of PTSD. We started follow-up from 1 month after surgery, follow-up every 2 months, and the follow-up period was 6 months. We were evaluated for PTSD by professionally trained anesthesiologists. We evaluated patients with TBI who underwent craniotomy by the Clinician-Administered PTSD Scale for Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) (CAPS-5) [20]. Such patients were considered to have PTSD if there was a clear exposure to a stressor along with at least 1 symptom of intrusion, 1 symptom of avoidance, 2 symptoms of negative alterations in mood and cognition, and 2 turbulence symptoms of reactivity and arousal, and these symptoms persisted for at least 1 month. In addition, we recorded other outcomes: the occurrence of intraoperative adverse events (including hypotension, bradycardia, and hypoxemia, and the patient was considered bradycardic if the heart rate was less than 55 beats/min, hypotensive if the systolic blood pressure was less than 90 mmHg, and hypoxemic if the oxygen saturation was less than 90%). We also recorded the hospital stay and the GCS score at discharge.

2.3. Therapy Method

All patients underwent craniotomy performed by well-trained and experienced neurosurgeons at the Sixth People’s Hospital of Deyang City. All patients underwent craniotomy under general anesthesia. For induction of anesthesia, we mainly used sufentanil, midazolam, rocuronium, and etomidate, and for maintenance of anesthesia, we mainly went through remifentanil, propofol, and cisatracurium. The control group received no other adjunctive drugs during anesthesia, and the experimental group used DEX as an adjunctive drug during anesthesia. All patients received essentially the same treatment regimen during anesthesia, except for differences in appellate treatment.

2.4. Statistical Analyses

We analyzed the collected data by using R Version 4.3.1. All data were analyzed between the control and experimental groups (DEX group). The mean ± standard deviation was used to indicate continuous variables (for example, age, GCS score before craniotomy, duration of surgery, duration of anesthesia, the interval between the end of surgery, and the time of PTSD). The numbers and percentages were used to indicate the categorical variables (for example, gender, bradycardia, hypotension, and the occurrence of PTSD). The Kolmogorov–Smirnov test was used first to test the normality of the continuous variables, and then the t-test was analyzed for the control and experimental groups. If the continuous variable has a non-normal distribution, we used the Kruskal–Wallis rank-sum test to analyze continuous data with a non-normal distribution. For the differences between categorical variables, we have analyzed them by Pearson’s χ² test or Fisher’s exact test. When p ≤ 0.05, it indicates a statistically significant difference between the two groups.

3. Results

3.1. Clinical Characteristics

A total of 180 TBI patients received craniotomy treatment at the Sixth People’s Hospital of Deyang City from January 2017 to June 2023. We excluded 26 patients who were unable to independently complete the PTSD assessment after the procedure, 22 patients who died after the procedure, 3 patients who gave up continuing treatment after the procedure, and 3 patients who were lost to follow-up. Ultimately, our study included 126 patients for analysis. Of these patients, 55 were treated with DEX (DEX dosage: the mean rate of administration was 0.51 ± 0.25 μg/kg/h and the mean minimum rate was 0.25 ± 0.12 μg/kg/h and the mean maximum rate was 0.93 ± 0.24 μg/kg/h.) and 71 did not receive DEX. The types of TBI included 41 patients with subdural hemorrhage (DEX group: 18; control group: 23), 51 patients with epidural hemorrhage (DEX group: 23; control group: 28), and 34 patients with brain tissue damage (DEX group: 14; control group: 20). After testing, all the continuous variable in our sample were normally distributed.

Demographic and clinical data between the two groups are shown in Table 1. There was no statistically significant difference between the DEX group and the control group in terms of demographic and clinical aspects (age, sex, preoperative GCS score, and mydriasis) (p > 0.05).

Table 1. Demographic and clinical characteristics data of the dexmedetomidine group and the control group.

Variable	Dexmedetomidine	Control	p value
Gender			0.8018^a
Male	43	53
Female	12	18
Age (years) mean ± SD	60 ± 13	60 ± 12	0.9865^b
Preoperative GCS mean ± SD	8 ± 3	9 ± 2	0.1242^b
The preoperative pupil condition (mydriasis)			0.07895^a
Yes	10	24
No	45	47

Note: GCS = Glasgow Coma Scale scores.
Abbreviation: SD = standard deviation.
^ap value: Pearson’s χ² test or Fisher’s exact test.
^bp value: t-test.

3.2. Intraoperative Data

Intraoperatively, 26 patients in the DEX group developed bradycardia, whereas 20 patients in the control group developed bradycardia, with a statistically significant difference between the two groups (p < 0.05). However, there was no heart rate below 45 beats/minute between the two groups. The DEX group was not statistically significantly different from the control group in any other aspect of the procedure (p > 0.05). Intraoperative data between the two groups are shown in Table 2.

Table 2. Intraoperative data of the dexmedetomidine group and the control group.

Variable	Dexmedetomidine	Control	p value
Bradycardia			0.02624^a
Yes	26	20
No	29	51
Hypotension			0.1057^a
Yes	29	20
No	26	51
Hypoxemia
Yes	0	0
No	55	71
Duration of anesthesia (greater than 3 h)			0.9186^a
Yes	18	25
No	37	46
Duration of surgery (greater than 3 h)			0.8791^a
Yes	17	24
No	38	47
Ventilation time of endotracheal intubation (hours)	39 ± 26	44 ± 33	0.3401^b

^ap value: Pearson’s χ² test or Fisher’s exact test.
^bp value: t-test.

3.3. Postoperative Data

In the postoperative phase, 6 patients developed PTSD in the DEX group, whereas in the control group, 19 patients developed PTSD, with a statistically significant difference between the two groups (p < 0.05). Moreover, the GCS score at discharge and the total length of hospital stay did not statistically significantly differ between the DEX group and the control group (p > 0.05). Postoperative data between the two groups are shown in Table 3.

Table 3. Postoperative data of the dexmedetomidine group and the control group.

Variable	Dexmedetomidine	Control	p value
PTSD			0.04686^a
Yes	6	19
No	49	52
The total length of hospital stay (days) mean ± SD	36.6 ± 28.6	30.7 ± 12.7	0.1218^b
GCS score at discharge mean ± SD	12 ± 2	13 ± 2	0.4427^b

Note: GCS = Glasgow Coma Scale scores.
Abbreviations: PTSD = posttraumatic stress disorder; SD = standard deviation.
^ap value: Pearson’s χ² test or Fisher’s exact test.
^bp value: t-test.

4. Discussion

We conducted a retrospective analysis of 126 patients with TBI who underwent craniotomy at our institution and found that DEX was effective in reducing the incidence of postoperative PTSD compared to the control group. The incidence of adverse events in anesthesia, mainly bradycardia, was significantly higher in the DEX group than in the control group, while the incidence of other adverse events was not significantly different between the two groups. DEX neither prolonged hospitalization nor caused a decrease in GCS scores at discharge.

Recently, the topic of PTSD in patients with TBI has gained increasing public attention, but most of the attention has been focused primarily on the military population, and relatively little research has been performed on the general population [21–23]. Although the incidence of PTSD after TBI is lower in the general population than in military personnel, in fact, its incidence is not low, ranging from about 11% to 36% [9–11]. Therefore, we should also focus part of our energy on research on PTSD after TBI in the general population. Our study found an overall incidence of PTSD of 19% in TBI patients undergoing craniotomy (11% in the DEX group and 27% in the control group). At this point, our findings are essentially the same as those of previous studies. As for whether there is a different prevalence of PTSD in patients with TBI of different severity, different studies have different results, and there is still a big controversy on this point [22–24]. Some studies have suggested that the incidence of PTSD varies depending on the severity of TBI, but another part of the research suggests that the severity of TBI does not affect the incidence of PTSD [25–27]. Unfortunately, however, due to our limited sample size, we were unable to conduct further validation of whether the severity of TBI affects the incidence of PTSD. It is hoped that the next studies will be more adequate to explore this further (especially for TBI patients undergoing craniotomy).

Although some studies have demonstrated a secondary role for TBI in the development of PTSD, the vast majority of studies have demonstrated that patients with TBI are significantly more likely to develop PTSD than non-TBI patients [28, 29]. Not only that, but there was also a significant increase in other mental health sequelae for TBI patients compared to non-TBI patients [29]. The mechanism of association between TBI and subsequent PTSD is still not very well cleared, and the possible mechanisms are similar to those between TBI and other psychiatric and neurodegenerative disorders: mechanical damage to connections between white matter tracks in frontocortical regulatory regions and other brain regions, neuroinflammatory damage, and the stress-related oxidative injury [30, 31]. The interaction of the above pathophysiologic changes ultimately leads to the development of PTSD in patients with TBI. Although TBI and PTSD are categorized as discrete and separate disorders, there is an overlap of symptoms between them: irritability, fatigue, nausea, sleep disturbance, depression, and headaches. The main difference between TBI and PTSD is that TBI is a result of brain damage, while PTSD is caused by psychological stress [32]. Thus, it is extremely important for clinicians to know about the mental health of patients with TBI, as this information is important for the identification of PTSD [33].

For TBI patients undergoing emergency craniotomy, drug selection during anesthesia is very important. Different anesthetic drugs may bring different outcomes to patient treatment, especially the occurrence of postoperative PTSD in traumatic patients. Existing evidence suggests that propofol can significantly enhance conditioned fear memory, leading to a significant increase in postoperative PTSD, which is present in both TBI and non-TBI patients [34–36]. Conversely, trauma patients who received DEX during anesthesia tended to be less likely to develop PTSD than those who did not [34, 35]. Yu et al.’s study found that the use of DEX in non-TBI trauma patients can reduce the incidence of postoperative PTSD [19]. Our study found that DEX can effectively reduce the incidence of postoperative PTSD in TBI patients undergoing emergency craniotomy surgery. This also indicates that DEX not only reduces the incidence of postoperative PTSD in non-TBI trauma patients but also has the same effect on TBI patients. For trauma patients, whether it is TBI or other types, DEX is a good choice for emergency surgery.

4.1. Limitation

This study has the following shortcomings. First, as a retrospective study, this research methodology inherently introduces bias, and that bias is inevitable. Second, the small sample size of this study prevented us from performing further subgroup analyses in patients with TBI (subdural hemorrhage, epidural hemorrhage, and brain tissue damage). Therefore, we hope that more and larger samples can be included in the next studies for further research. Third, this study was conducted in TBI patients who underwent craniotomy; further validation is still needed to determine whether DEX has the same effect in those TBI patients who did not undergo craniotomy. In addition, our sample size only supported our analysis of the diagnosis of PTSD patients and the time to the onset of symptoms. Our study found that DEX reduces the incidence of postoperative PTSD in TBI patients undergoing craniotomy, but the long-term effects of DEX in such patients remain uncertain. Finally, TBI itself is a risk factor for PTSD, hence, we cannot decide on the basis of a retrospective analysis whether DEX alone can prevent the development of PTSD following neurosurgery.

5. Conclusion

In this study, we found that the use of DEX during anesthesia was effective in reducing the incidence of postoperative PTSD in TBI patients undergoing craniotomy. In addition to increasing the incidence of bradycardia in patients during anesthesia, DEX did not increase the incidence of other adverse events. In addition, DEX did not prolong the length of hospitalization, as well as did not decrease the GCS scores of patients at discharge.

Nomenclature

DEX: Dexmedetomidine
TBI: Traumatic brain injury
GCS: Glasgow Coma Scale
PTSD: Posttraumatic stress disorder
CAPS-5: Clinician-Administered PTSD Scale for Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition)
SD: Standard deviation

Ethics Statement

This article follows the STROBE statement and has been approved by the Sixth People’s Hospital of Deyang City Ethics Committee.

Consent

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Author Contributions

Yun-Qi Wang and Xian-Jie Zhang were responsible for the design. Yun-Qi Wang and Dan Zhou were responsible for the search. Xian-Jie Zhang, Qing Li, and Xin Liu were involved in data screening and data extraction. Yun-Qi Wang was responsible for the writing of the manuscript. All authors read and approved the final version of the manuscript.

Funding

No funding was received for this research.

Acknowledgments

The authors have nothing to report.

Open Research

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Effect of Dexmedetomidine on Posttraumatic Stress Disorder in Traumatic Brain Injury Patients Undergoing Emergency Craniotomy Surgery: A Retrospective Study

Abstract

1. Background

2. Methods

2.1. Object of Study

2.2. Data Collection and Outcome Assessment

2.3. Therapy Method

2.4. Statistical Analyses

3. Results

3.1. Clinical Characteristics

3.2. Intraoperative Data

3.3. Postoperative Data

4. Discussion

4.1. Limitation

5. Conclusion

Nomenclature

Ethics Statement

Consent

Conflicts of Interest

Author Contributions

Funding

Acknowledgments

Open Research

Data Availability Statement

References

References

Information

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Effect of Dexmedetomidine on Posttraumatic Stress Disorder in Traumatic Brain Injury Patients Undergoing Emergency Craniotomy Surgery: A Retrospective Study

Abstract

1. Background

2. Methods

2.1. Object of Study

2.2. Data Collection and Outcome Assessment

2.3. Therapy Method

2.4. Statistical Analyses

3. Results

3.1. Clinical Characteristics

3.2. Intraoperative Data

3.3. Postoperative Data

4. Discussion

4.1. Limitation

5. Conclusion

Nomenclature

Ethics Statement

Consent

Conflicts of Interest

Author Contributions

Funding

Acknowledgments

Open Research

Data Availability Statement

References

References

Related

Information