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Background Ventilator-induced diaphragmatic dysfunction (VIDD) occurs in up to 60% of mechanically ventilated patients and prolongs ventilatory dependance. The consequences of VIDD are muscle atrophy, reduction of strength, and injury of muscle fibers. Atrophy and contractile activity of the diaphragm can be estimated by ultrasound muscle thickness and thickening fraction. Prior experience demonstrates invasive electrical stimulation of the diaphragm helps preserve muscle thickness. This is the first study on a non-invasive phrenic nerve stimulator that aims to assess its feasibility, safety, and usefulness in preserving diaphragm thickness. Methods A multi-center randomized clinical trial will be performed in four intensive care units (ICUs) in the United States of America and Canada. Inclusion criteria include patients older than 21 years, in the first 48 h of mechanical ventilation (MV) and predicted to remain on the ventilator for at least 48 h. Patients with contraindications for phrenic nerve stimulation, severe chronic pulmonary diseases, or impossibility to measure diaphragm thickness with ultrasound will be excluded. Patients enrolled will be randomized to standard care (control) or 30-min daily non-invasive phrenic nerve stimulation up to 10 days after enrollment (intervention). The primary effectiveness endpoint is the change in diaphragm thickness on day 10, extubation, or death whichever occurs first. Secondary endpoints include change in diaphragm thickness on day 4, maximal inspiratory pressure before extubation, and time-to rapid shallow breathing index (RSBI) <105. Safety objectives include the proportion of device- or procedure-related adverse events (SAE). The estimated sample size will be 40 patients (20 per group). Discussion The STIMIT ACTIVATOR trial is a randomized multi-center study powered to elucidate whether non-invasive phrenic nerve stimulation is feasible, safe, and preserves diaphragm thickness. Meeting the primary endpoint will demonstrate its applicability in clinical practice to prevent diaphragmatic atrophy in ventilated patients. Trial registration ClinicalTrials.gov: NCT05883163, August 29, 2023.

Video-assisted thoracoscopic surgery (VATS) lobectomy is the primary surgical treatment for lung cancer. A significant factor affecting postoperative recovery is prolonged air leak (PAL). Despite numerous clinical strategies could prevent and manage postoperative PAL, its incidence remains high. Phrenic nerve cryotherapy (PNC) temporarily inhibits phrenic nerve function, causing diaphragm elevation, which reduces thoracic cavity volume, enhances pleural apposition, and mitigates air leakage. This study investigates the efficacy of PNC in preventing postoperative PAL during VATS lobectomy. A total of 108 eligible lung cancer patients who underwent surgery at the Department of Thoracic Surgery, The Affiliated Hospital of Inner Mongolia Medical University, from June 2023 to January 2025, were enrolled and randomly assigned to the control group (n=54) and the experimental group (n=54). The patients in both the two groups received VATS lobectomy and systematic lymph node dissection, with the experimental group als

Purpose Diaphragm function is rarely studied in intensive care patients with unit-acquired weakness (ICUAW) in whom weaning from mechanical ventilation is challenging. The aim of the present study was to evaluate the diaphragm function and the outcome using a multimodal approach in ICUAW patients. Methods Patients were eligible if they were diagnosed for ICUAW [Medical Research Council (MRC) Score <48], mechanically ventilated for at least 48 h and were undergoing a spontaneous breathing trial. Diaphragm function was assessed using magnetic stimulation of the phrenic nerves (change in endotracheal tube pressure), maximal inspiratory pressure and ultrasonographically (thickening fraction). Diaphragmatic dysfunction was defined by a change in endotracheal tube pressure below 11 cmH 2 O. The endpoints were to describe the correlation between diaphragm function and ICUAW and its impact on extubation. Results Among 185 consecutive patients ventilated for more than 48 h, 40 (22 %) with a MRC score of 31 [ 20 – 36 ] were included. Diaphragm dysfunction was observed with ICUAW in 32 patients (80 %). Change in endotracheal tube pressure and MRC score were not correlated. Maximal inspiratory pressure was correlated with change in endotracheal tube pressure after magnetic stimulation of the phrenic nerves ( r  = 0.43; p  = 0.005) and MRC score ( r  = 0.34; p  = 0.02). Thickening fraction was less than 20 % in 70 % of the patients and was statistically correlated with change in endotracheal tube pressure ( r  = 0.4; p  = 0.02) but not with MRC score. Half of the patients could be extubated without needing reintubation within 72 h. Conclusion Diaphragm dysfunction is frequent in patients with ICU-acquired weakness (80 %) but poorly correlated with the ICU-acquired weakness MRC score. Half of the patients with ICU-acquired weakness were successfully extubated. Half of the patients who failed the weaning process died during the ICU stay.

Thoracic surgery rapidly induces weakness in human diaphragm fibers. The dysfunction is thought to arise from combined effects of the surgical procedures and inactivity. This project tested whether brief bouts of intraoperative hemidiaphragm stimulation would mitigate slow and fast fiber loss of force in the human diaphragm. We reasoned that maintenance of diaphragm activity with brief bouts of intraoperative phrenic stimulation would mitigate diaphragm fiber weakness and myofilament protein derangements caused by thoracic surgery. Nineteen adults (9 females, age 59 ± 12 years) with normal inspiratory strength or spirometry consented to participate. Unilateral phrenic twitch stimulation (twitch duration 1.5 ms, frequency 0.5 Hz, current 2x the motor threshold, max 25 mA) was applied for one minute, every 30 minutes during cardiothoracic surgery. Thirty minutes following the last stimulation bout, biopsies were obtained from the hemidiaphragms for single fiber force mechanics and quantitation of myofilament proteins (abundance and phosphorylation) and compared by a linear mixed model and paired t-test, respectively. Subjects underwent 6 ±  2 hemidiaphragm stimulations at 17 ±  6 mA, during 278 ±  68 minutes of surgery. Longer-duration surgeries were associated with a progressive decline in diaphragm fiber force (p < 0.001). In slow-twitch fibers, phrenic stimulation increased absolute force (+25%, p <  0.0001), cross-sectional area (+16%, p < 0.0001) and specific force (+7%, p < 0.0005). Stimulation did not alter contractile function of fast-twitch fibers, calcium-sensitivity in either fiber type, and abundance and phosphorylation of myofilament proteins. In adults without preoperative weakness or lung dysfunction, unilateral phrenic stimulation mitigated diaphragm slow fiber weakness caused by thoracic surgery, but had no effect on myofilament protein abundance or phosphorylation.

A rare but important complication after lung transplantation (LTx) is postoperative phrenic nerve dysfunction (PND). Diaphragmatic plication (DP) is a well-established treatment option for PND, however, the long-term effect of PND and DP on lung function parameters and survival after LTx are currently unknown. We retrospectively reviewed 1400 LTx recipients transplanted at Medical University of Vienna between 01/2003 and 12/2022. Fluoroscopy and/or phrenic nerve conduction studies confirmed PND when chest radiographs after extubation showed a unilateral heightened diaphragm. We identified 25 patients with post-operative PND, of whom 12 underwent DP. The remaining 1,375 patients served as a control group. Median ICU-stay and hospital-stay were significantly longer in the PND groups (DP: 20 and 57 days; non-DP: 27 and 43 days; control group: 7 and 25 days; P = 0.001/ P < 0.001). PND led to consistently lower %TLC in lung function tests performed within the first three years after LTx. DP was associated with lower %FEV1.0 early after LTx but it aligned to %FEV1.0 of the other groups during follow-up. Although PND significantly affected postoperative recovery after LTx, it did not impair long-term survival outcomes.

To evaluate long-term efficacy and safety of phrenic nerve stimulation (PNS) in patients with moderate-to-severe central sleep apnea (CSA) through 3 years of therapy. Patients in the remedē System Pivotal Trial were observed every 3 months after implant until US Food and Drug Administration approval. At the time of approval and study closure, all patients completed 24 months of follow-up; 33 patients had not reached the 36-month visit. Sleep metrics (polysomnography) and echocardiographic parameters are reported at baseline, 12, 18, and 24 months, in addition to available 36-month sleep results from polygraphy. Safety was assessed through 36 months; however, analysis focused through 24 months and available 36-month results are provided. Patients were assessed at 24 (n = 109) and 36 (n = 60) months. Baseline characteristics included mean age 64 years, 91% male, and mean apnea-hypopnea index 47 events per hour. Sleep metrics (apnea-hypopnea index (AHI), central apnea index, arousal index, oxygen desaturation index, rapid eye movement sleep) remained improved through 24 and 36 months with continuous use of PNS therapy. At least 60% of patients in the treatment group achieved at least 50% reduction in AHI through 24 months. Serious adverse events (SAEs) related to the remedē System implant procedure, device, or therapy through 24 months were reported by 10% of patients, no unanticipated adverse device effects or deaths, and all events resolved. No additional related SAEs were reported between 24 and 36 months. These data suggest beneficial effects of long-term PNS in patients with CSA appear to sustain through 36 months with no new safety concerns. NCT01816776.

Evidence has accumulated that respiratory muscle dysfunction develops in critically ill patients and contributes to prolonged weaning from mechanical ventilation. Accordingly, it seems highly appropriate to monitor the respiratory muscles in these patients. Today, we are only at the beginning of routinely monitoring respiratory muscle function. Indeed, most clinicians do not evaluate respiratory muscle function in critically ill patients at all. In our opinion, however, practical issues and the absence of sound scientific data for clinical benefit should not discourage clinicians from having a closer look at respiratory muscle function in critically ill patients. This perspective discusses the latest developments in the field of respiratory muscle monitoring and possible implications of monitoring respiratory muscle function in critically ill patients.

Poststroke pneumonia (PSP) is a common complication in bedridden patients with speech dysfunction, often leading to poor outcomes. This retrospective cohort study explores the clinical efficacy of electroacupuncture (EA) by stimulating the phrenic nerve to improve diaphragmatic activity and treat PSP. In this study, 88 hospitalized poststroke patients with pneumonia were divided into two groups. The nonexposure group received standard treatment, including respiratory rehabilitation, whereas the exposure group received additional EA therapy targeting the phrenic nerve. Propensity score matching (PSM) was applied, resulting in 22 patients in the exposure group and 29 in the nonexposure group. Both groups were treated for 2 weeks, during which Clinical Pulmonary Infection Score (CPIS) scores, white blood cell (WBC) count, C-reactive protein (CRP), interleukin-6 (IL-6), and procalcitonin (PCT) levels were measured. In the exposure group, diaphragmatic activity and thickness were also assessed before, during, and after EA. The exposure group showed significantly greater improvements compared with the nonexposure group in reducing CPIS scores (mean difference: -1.087; 95% confidence intervals (CIs): -1.68 to -0.494; p < 0.05) and improving inflammatory markers (WBC, CRP, IL-6, and PCT) (p < 0.05 for all comparisons). After PSM, CPIS scores demonstrated a larger absolute reduction in the exposure group compared with controls (-2.32 vs. -1.00), indicating a greater magnitude of clinical improvement. Within the exposure group, diaphragmatic activity improved significantly after 10 days of EA compared with baseline, with significant between-group differences (p < 0.05 for all comparisons). Quantitative assessment further showed that diaphragmatic excursion increased by approximately 0.32 cm following intervention (95% CIs: 0.18-0.46), suggesting enhanced diaphragmatic functional mobility. EA may enhance diaphragmatic activity through phrenic nerve stimulation, improving ventilation, sputum clearance, and regulating neuroimmune responses, contributing to the effective management of PSP. International Traditional Medicine Clinical Trial Registry: ITMCTR2024000729.

Spinocerebellar ataxia type 2 (SCA2) is a progressive cerebellar syndrome that may lead to respiratory impairments. However, our understanding of the degree and characteristics of the respiratory involvement in SCA2 individuals remains limited. This study evaluates respiratory in SCA2 patients. This cross-sectional study included a group of controls and patients with SCA2. Participants underwent assessments including spirometry, maximal inspiratory (MIP) and expiratory (MEP) pressures, sniff nasal inspiratory pressure (SNIP), cough flow peak (CFPs), neurophysiological right phrenic and accessory nerves conduction studies and evaluations with the SARA and ICARS ataxia severity scales. A total of 16 adults with SCA2, and 20 healthy controls were included. Patients with SCA2 exhibited significantly reduced respiratory parameters compared to healthy controls. Key findings included lower forced vital capacity (FVC), forced expiratory volume in 1 s (FEV 1 ), and peak expiratory flow (PEF), with reductions observed in both absolute values and percentages ( p  < 0.01). They also showed decreased maximal inspiratory (MIP) and expiratory pressures (MEP), sniff nasal inspiratory pressure (SNIP), cough flow peak (CFP) values and oxygen saturation (SpO₂), reduced amplitude of motor potentials of the right phrenic nerve and increased end-tidal CO₂ (ETCO₂). The combined involvement of respiratory and neurophysiological parameters reflects impairment of both pulmonary capacity and respiratory muscle strength. Patients with SCA2 have significant impairment in respiratory parameters, including reduced pulmonary capacity and respiratory muscle strength, compared to healthy subjects. These findings highlight the relevance of including respiratory assessment and target interventions as part of the clinical management of patients with SCA2.

Background Diaphragm dysfunction is an important and often unrecognized cause of dyspnea. The current gold standard, transdiaphragmatic twitch pressure (Pdi,tw), requires oesophageal and gastric balloon catheters and is infrequently used in routine care. We evaluated whether ultrafast ultrasound descriptors of costal diaphragm during bilateral phrenic magnetic stimulation can provide a noninvasive alternative for assessing diaphragm contractility. Methods Thirty patients (19 men and 11 women) referred for suspected diaphragm dysfunction (median age 57 [42–63] years) underwent bilateral anterolateral magnetic stimulation with simultaneous ultrafast ultrasound and oesophageal/gastric pressure recordings. Peak diaphragm tissue velocity, acceleration and jerk were extracted. Associations with Pdi,tw were assessed using ridge regression. Diagnostic performance for detecting abnormal Pdi,tw (< 20 cmH2O) was evaluated using Bayesian receiver operating characteristic (ROC) analysis, including posterior mean AUC and 95% credible intervals. Agreement between predicted and measured Pdi,tw was assessed using Lin's concordance correlation coefficient and Passing–Bablok regression. Results Twenty four of 30 patients (80%) had abnormal Pdi,tw. Ultrafast ultrasound descriptors correlated with Pdi,tw (Spearman's ρ: velocity 0.77 [95% CI, 0.57–0.89], acceleration 0.70 [95% CI, 0.41–0.87], jerk 0.67 [95% CI, 0.43–0.85]; all p < 0.0001). The multivariable ridge model explained 66% of the variance in Pdi,tw and showed high agreement with measured values (Lin's concordance correlation coefficient = 0.87 [95% CI, 0.75–0.93]). Bayesian ROC analysis demonstrated strong discrimination of diaphragm dysfunction (AUC = 0.91; 95% credible interval [CrI], 0.76–0.98). Using the clinical threshold of 20 cmH2O, model‐predicted Pdi,tw yielded a sensitivity of 75% and specificity of 100%. The optimal velocity threshold for discriminating abnormal Pdi,tw was 10.25 mm·ms−1 (95% CrI, 6.12–18.58 mm·ms−1). The corresponding thresholds for acceleration and jerk were 408.6 mm·ms−2 (95% CrI, 122.6–952.4) and 3073 mm·ms−3 (95% CrI, 1038.8–11541.4), respectively. Conclusions Ultrafast ultrasound coupled with magnetic phrenic stimulation provides a feasible, noninvasive, nonvolitional assessment of diaphragm contractility. Diaphragm motion descriptors reliably predicted Pdi,tw and enabled accurate identification of diaphragm dysfunction. These findings support further clinical evaluation and warrant larger multicentre validation studies.