Abstract
Objective
To evaluate whether intermittent pneumatic compression therapy influences intracranial pressure in postoperative patients with severe traumatic brain injury.
Methods
In this prospective comparative study, a total of 120 postoperative severe traumatic brain injury patients admitted to the neurological intensive care unit between April 2023 and September 2024 were randomized into two groups (n = 60 each). During the 6-day observation period, group A was administered intermittent pneumatic compression therapy on postoperative days 1–3, whereas group B was administered intermittent pneumatic compression during postoperative days 4–6. Continuous intracranial pressure monitoring was performed.
Results
In both groups, mean intracranial pressure, frequency of episodes with intracranial pressure ≥20 mmHg, and maximum daily intracranial pressure decreased progressively over time. Within-group comparisons showed significant differences between the first three and last three postoperative days. However, no significant differences were observed between the groups. Intermittent pneumatic compression therapy was not associated with intracranial pressure elevation. No cases of lower extremity deep vein thrombosis were detected.
Conclusion
Postoperative intermittent pneumatic compression application did not adversely affect intracranial pressure in patients with severe traumatic brain injury, supporting its safety in neurocritical care settings.
Keywords
Introduction
Severe traumatic brain injury (STBI) is a common condition in neurosurgery, and >50% of affected patients develop elevated intracranial pressure (ICP). 1 Increased ICP can lead to a reduction in cerebral perfusion pressure and cerebral blood flow, resulting in central nervous system dysfunction, which further aggravates injury and functional impairment of peripheral organs and tissues. Previous studies have demonstrated that elevated ICP is directly associated with the severity of traumatic brain injury and poor clinical outcomes.1,2
Deep vein thrombosis (DVT) of the lower extremities is another common complication in patients with STBI. Lower extremity DVT not only leads to chronic venous insufficiency and impaired limb function but may also be fatal due to pulmonary embolism caused by thrombus dislodgement. Intermittent pneumatic compression (IPC) therapy has been widely recognized in clinical practice as an effective method for the prevention and treatment of lower extremity DVT.3,4 However, whether the application of IPC therapy in postoperative STBI patients can induce an increase in the ICP remains unclear. To date, few domestic and international studies have investigated this issue. Therefore, the nursing staff of our department conducted a prospective study on this subject between April 2023 and September 2024.
Patients and methods
Patients
From April 2023 to September 2024, consecutive postoperative STBI patients admitted to the neurological intensive care unit who met the eligibility criteria were screened. In total, 120 eligible patients were enrolled. Ethical approval was obtained from the Ethics Committee of Su Bei People's Hospital of Jiangsu Province (Approval No. 2023KY-017). Written informed consent was obtained from the patients’ legal representatives. This manuscript was prepared in accordance with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines for observational studies. 5 In addition, elements of randomized allocation concealment consistent with the Consolidated Standards of Reporting Trials (CONSORT) principles were incorporated into the study design. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki of 1975, as revised in 2024. All patient information was fully de-identified prior to analysis to ensure patient privacy and confidentiality.
Inclusion criteria of the research were as follows: (a) Glasgow Coma Scale (GCS) score of 3–8 on admission; (b) placement of an ICP monitoring probe for >48 h; (c) no history of hematological disorders or coagulation dysfunction; (d) no lower extremity fractures; and (e) written informed consent obtained from the patient's family members or legal guardians and approval provided by the attending physician. Exclusion criteria included the following: (a) interruption of the study due to changes in physiological or neurological status during the observation period and (b) inability to initiate or the need to discontinue IPC therapy under certain conditions, including lower limb conditions within the sleeve area, such as dermatitis, venous ligation, gangrene, or recent skin grafting; severe atherosclerosis or ischemic atrophic vascular disease; extensive lower extremity edema or pulmonary edema caused by congestive heart failure; severe deformities of the lower extremities; or confirmed or suspected DVT.
Group allocation
A sealed-envelope method was used for overall randomization. Using the Statistical Package for Social Sciences (SPSS) software, a random allocation sequence for 120 participants was generated, corresponding to serial numbers 001–120. A third party (a statistician not involved in the study) sealed each intervention assignment into opaque envelopes. A designated investigator sequentially opened the envelopes according to the order of patient enrollment and recorded group allocation. The 120 patients were randomly assigned to group A (n = 60) or group B (n = 60).
Treatment protocol
The observation period lasted six postoperative days. Group A was administered IPC therapy during postoperative days 1–3, and therapy was discontinued during postoperative days 4–6, whereas group B was administered IPC therapy only during postoperative days 4–6. Bilateral lower extremity arterial and venous Doppler ultrasonography was performed for all patients on postoperative days 1 and 6 for DVT screening. Continuous ICP monitoring was performed throughout the study period.
A standardized stepwise treatment protocol for STBI was followed for all patients, including elevation of the head of the bed at 30°; appropriate sedation and analgesia; real-time ICP monitoring; temperature control (temperature <37°C) using physical, chemical, and pharmacological cooling methods; and administration of mannitol at a dose of 0.25–0.5 g/kg with normal saline as the primary infusion fluid to achieve a target serum osmolality of 300–320 mOsm/L. 6 When necessary, endotracheal or nasotracheal intubation was performed, and partial pressure of arterial carbon dioxide (PaCO2) was maintained at 32–35 mmHg using mechanical ventilation. If ICP remained uncontrolled despite first-line therapy, decompressive craniectomy was considered, followed by continued stepwise management.
IPC therapy
All patients were administered IPC therapy using the same model of pneumatic compression device (FIOWTRO, model AC550, UK). The device was suspended at the foot of the bed using a bed hook, with the control panel positioned beside the bed. Two compression sleeves were unfolded, the ankle joint was elevated, and the sleeves were placed under the left and right legs, sequentially wrapping the calf and thigh. The tightness was adjusted to allow the insertion of two fingers. The sleeves were securely fastened and connected to the device, ensuring unobstructed tubing without kinks or entanglement.
After being powered on, the system completed a self-check and automatically initiated sequential distal-to-proximal inflation. The inflation pressure was preset, with a distal pressure of 40 mmHg displayed on the screen. During the first 3–5 cycles, the device sensors adjusted the inflation and deflation intervals and pressure based on the patient's venous refill time. Each treatment session lasted 1 h and was administered twice daily at 8 AM and 8 PM.
ICP monitoring
ICP monitoring probes (Integra Neurocare, Camino model, USA) were inserted by clinicians at the frontal horn of the lateral ventricle (2.5 cm lateral to the midline and 2.5 cm posterior to the hairline). In patients undergoing isolated hematoma evacuation or unilateral decompressive craniectomy, the probe was placed in the contralateral lateral ventricle. In patients with bilateral decompressive craniectomy, the probe was placed subdurally. Postoperatively, ICP values were observed and recorded hourly using an ICP monitoring system (PHILIPS, MP40, Netherlands).
Statistical analyses
Hourly ICP values were recorded for both groups and analyzed using the SPSS (version 15.0). Continuous variables were tested for normality. Data with a normal distribution were expressed as mean ± SD. Paired-samples t tests were used for within-group comparisons, whereas independent-samples t tests were used for between-group comparisons. A p-value <0.05 was considered statistically significant.
Results
Comparison of the patients’ general characteristics
In total, 120 STBI patients meeting the inclusion and exclusion criteria were enrolled, including 82 men and 38 women. The age range of the study population was 27–61 years (mean age: 46.22 ± 3.59 years). No significant differences were observed between groups A and B in terms of age, sex, time from injury to surgery, admission GCS score, type of injury, or surgical procedure (p > 0.05; Table 1).
Baseline demographic and clinical characteristics of postoperative patients with severe traumatic brain injury (STBI) in groups A and B.
Data are presented as mean ± standard deviation or number. No significant differences were observed between the two groups at baseline (all p > 0.05).
Within-group comparisons for ICP monitoring
In both groups, the mean ICP values demonstrated a significant decreasing trend over postoperative 6 days. The frequency of ICP episodes ≥20 mmHg also gradually declined postoperatively. In addition, the maximum daily ICP values progressively decreased during the postoperative treatment period. Comparisons between the first and last three postoperative days showed statistically significant differences for all three indicators within each group (p < 0.05; Tables 2 and 3).
Comparison of daily mean intracranial pressure (ICP) values between groups A and B during the 6-day postoperative observation period.
Values are presented as mean ± standard deviation. IPC therapy was administered on postoperative days 1–3 in group A and postoperative days 4–6 in group B.
Comparison of the daily frequency of intracranial pressure episodes ≥20 mmHg between groups A and B.
Values are presented as mean ± standard deviation. IPC therapy periods differed between the two groups as described in the Methods section.
ICP: intracranial pressure.
Between-group comparisons of ICP monitoring over postoperative 6 days
No significant differences were observed between groups A and B in terms of daily mean ICP, number of episodes of ICP ≥20 mmHg, or maximum daily ICP during the postoperative 6 days (p > 0.05; Table 4). Continuous real-time ICP monitoring demonstrated that IPC therapy did not significantly alter the ICP. Furthermore, no cases of lower extremity DVT were detected in either group during the 6-day postoperative period based on bilateral lower extremity arterial and venous Doppler ultrasonography.
Comparison of maximum daily intracranial pressure values between groups A and B during the 6-day postoperative observation period.
Values are presented as mean ± standard deviation.
ICP: intracranial pressure.
Discussion
Causes of DVT in patients with STBI
Patients with STBI experience several postoperative complications; lower extremity DVT is one of the most common complications among these. Several clinical centers have reported that approximately 0.22%–50.0% of STBI patients develop DVT during treatment, and the incidence among postoperative patients may reach 19%–58%.7,8 Slow blood flow, hypercoagulability, and venous wall injury are the principal factors contributing to DVT formation.
In clinical practice, the occurrence of DVT in STBI patients can be attributed to several mechanisms. First, prolonged general anesthesia and extended postoperative bed rest reduce lower limb activity, weakening the muscle pump effect and vascular vasomotor reflexes. This leads to sluggish venous blood flow and vortex formation within venous valve sinuses, resulting in valvular hypoxia. Consequently, leukocyte adhesion molecule expression is induced, leukocyte activity is enhanced, and vascular endothelial integrity is compromised, thereby promoting thrombosis formation.
Second, femoral vein catheterization is frequently performed in STBI patients to improve postoperative treatment efficiency. However, this may cause varying degrees of endothelial injury, triggering the release of bioactive substances, activation of the intrinsic coagulation system, alterations in venous wall electrical charge, and ultimately platelet aggregation and adhesion, leading to thrombus formation.
Third, the systemic stress response following traumatic brain injury increases plasma levels of coagulation factor VIII, fibrinogen, and platelets, thereby accelerating blood coagulation and thrombosis formation. Fourth, medications commonly used during STBI treatment, including mannitol, furosemide, hemostatic agents, and glucocorticoids, although effective in reducing ICP and the risk of intracranial hemorrhage, can cause hemoconcentration and hypercoagulability. In addition, mannitol and glucocorticoids may directly irritate the vascular wall, increasing the risk of phlebitis and thrombosis.
Fifth, fluid restriction imposed to prevent the worsening cerebral edema can further contribute to hemoconcentration. Finally, uncorrected internal environmental disturbances—such as hyperthermia, hyperglycemia, hypernatremia, diabetes insipidus, and stress-related ulcers—may increase blood viscosity and exacerbate hypercoagulable states.
The preventive effect of IPC therapy on DVT has been widely recognized in clinical practice.3,4 This device features automatic pressure adjustment and cyclic monitoring functions. It accelerates venous return in the lower extremities by generating graded pressure from the ankle to the thigh, thereby reducing venous stasis. In the present study, no cases of lower extremity DVT occurred within postoperative 6 days. Notably, patients in group B were not administered IPC therapy during the first three postoperative days; however, no DVT events were observed. This may be attributed to routine nursing interventions, such as scheduled repositioning and maintaining moderate elevation of the lower extremities, which likely promoted venous return and reduced the risk of DVT.
Effects of IPC on ICP
To date, no published studies have investigated whether IPC therapy for lower extremity DVT prevention affects ICP in postoperative STBI patients. Known factors influencing postoperative ICP in STBI patients include age, sex, time from injury to surgery, admission GCS score, type of trauma, and patient positioning.9,10 In the present study, no statistically significant differences in these variables were observed between the two randomly assigned groups. In addition, surgical and postoperative conservative management was performed for all patients in accordance with current mainstream stepwise ICP management protocols for STBI.
By minimizing potential confounding factors, statistical bias was effectively reduced. The results demonstrated a significant downward trend in the ICP values within both groups before and after IPC therapy, with no significant differences observed between the groups. Thus, no patient experienced an increase in the ICP attributable to IPC therapy.
From a theoretical perspective, IPC therapy enhances venous return from the lower extremities, which may increase cardiac preload and subsequently augment cerebral blood flow, potentially leading to elevated ICP. However, this phenomenon was not observed in the present study. In STBI patients, elevated ICP is primarily caused by cerebral edema, hydrocephalus, and space-occupying intracranial hemorrhage. Improvement in intracranial hypertension depends on both medical treatment and intrinsic regulatory mechanisms, which are activated once therapeutic interventions have reduced the ICP to approximately 17 mmHg.
Recent studies have highlighted the potential role of cerebral venous hemodynamics in secondary brain injury and long-term neurodegenerative sequelae following traumatic brain injury. 11 Chronic traumatic encephalopathy, although incompletely understood, has been associated with persistent neuroinflammation, metabolic dysregulation, and microvascular dysfunction after brain injury. In addition, impaired cerebral venous filling has been reported to correlate with delayed cerebral ischemia and poor neurological outcomes in patients with acute neurological disorders. 11 Therefore, alterations in venous return and cerebral venous regulation may represent an important area for future investigation in patients with STBI.
Although the present study focused primarily on the short-term safety of IPC therapy with respect to ICP, future studies incorporating cerebral venous imaging parameters, such as the cortical venous opacification score (COVES), may further clarify the relationship between peripheral venous interventions, cerebral venous hemodynamics, and long-term neurological outcomes. 12 Nevertheless, no IPC-related ICP increase was observed in our cohort, suggesting that intracranial compensatory mechanisms and cerebral venous compliance effectively buffer transient hemodynamic alterations induced by IPC therapy during the acute postoperative phase.
In this study, postoperative ICP was maintained at approximately 16 mmHg in all patients. Under these conditions, intrinsic compensatory mechanisms—such as reduced cerebrospinal fluid production, changes in cerebral arterial tone, and decreased cerebral metabolic activity—were sufficient to offset any potential ICP elevation induced by IPC therapy.
Limitations
This study has certain limitations. First, it was conducted at a single center with a relatively limited sample size, and no formal sample size calculation was performed prior to study initiation. Second, the observation period was restricted to the early postoperative phase, and long-term neurological outcomes were not evaluated. Third, cerebral venous hemodynamic parameters, such as the COVES, were not assessed. Future multicenter studies with longer follow-up and comprehensive venous imaging are warranted.
Conclusion
In this prospective comparative study, IPC therapy was not associated with increased ICP in postoperative patients with STBI. These findings suggest that IPC therapy is a safe strategy for DVT prevention in this patient population. Further multicenter studies with larger sample sizes are warranted to confirm these observations.
Footnotes
Acknowledgments
The authors thank the clinical staff of the Neurological Intensive Care Unit of Su Bei People's Hospital for their assistance in patient management and data collection. Artificial intelligence tools were used solely for language editing and grammar improvement during manuscript preparation. The authors reviewed and verified all content and take full responsibility for the final manuscript.
Ethical approval
Ethical approval was obtained from the Ethics Committee of Su Bei People's Hospital of Jiangsu Province (Approval No. 2023KY-017). The study was conducted in accordance with the ethical principles of the Declaration of Helsinki of 1975, as revised in 2024.
Author contributions
B.X. and Z.Y. contributed equally to this work. B.X. and J.Z. conceived and designed the study. B.X. and Z.Y. collected the clinical data and performed the study procedures. B.X. analyzed the data and drafted the manuscript. J.Z. supervised the study, interpreted the results, and critically revised the manuscript. All authors read and approved the final manuscript.
Funding
The authors received no financial support for the research, authorship, and/or publication of this article.
Declaration of conflicting interests
The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Data availability statement
The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.