Diaphragmatic dysfunction is associated with postoperative pulmonary complications and phrenic nerve paresis in patients undergoing thoracic surgery.

PURPOSE: We aimed to quantify perioperative changes in diaphragmatic function and phrenic nerve conduction in patients undergoing routine thoracic surgery. METHODS: A prospective observational study was performed in patients undergoing esophageal resection or pulmonary lobectomy. Examinations were carried out the day prior to surgery, 3 days and 10-14 days after surgery. Endpoints for diaphragmatic function included ultrasonographic measurements of diaphragmatic excursion and thickening fraction. Endpoints for phrenic nerve conduction included baseline-to-peak amplitude, peak-to-peak amplitude, and transmission delay. Measurements were assessed on both the surgical side and the non-surgical side of the thorax. RESULTS: Forty patients were included in the study. Significant reductions in diaphragmatic excursion were seen on the surgical side of the thorax for all excursion measures (posterior part of the right hemidiaphragm, p < 0.001; hemidiaphragmatic top point, p < 0.001; change in intrathoracic area, p < 0.001). Significant changes were seen for all phrenic nerve measures (baseline-to-peak amplitude, p < 0.001; peak-to-peak amplitude, p < 0.001; transmission delay, p = 0.041) on the surgical side. However, significant changes were also seen on the non-surgical side for all phrenic nerve measures (baseline-to-peak amplitude, p < 0.001; peak-to-peak amplitude, p < 0.001; transmission delay, p = 0.022). A postoperative reduction in posterior diaphragmatic excursion of more than 50% was significantly associated with postoperative pulmonary complications (coefficient: 2.69 (95% CI [1.38, 4.01], p < 0.001). CONCLUSION: Thoracic surgery caused a significant unilateral reduction in diaphragmatic excursion on the surgical side of the thorax, which was accompanied by significant changes in phrenic nerve conduction. However, phrenic nerve conduction was also significantly affected on the non-surgical side to a lesser extent, which was not mirrored in diaphragmatic excursion. Our findings suggest that phrenic nerve paresis plays a role in postoperative diaphragmatic dysfunction, which may be a contributing factor in the pathogenesis of postoperative pulmonary complications. CLINICAL TRIALS REGISTRATION NUMBER: NCT04507594.

Association of chest tube position with phrenic nerve palsy after neonatal and infant cardiac surgery.

BACKGROUND: Diaphragm paralysis (DP) complicates the postoperative course of neonates and infants undergoing cardiac surgery. Events causing DP remain poorly understood, and preventive strategies remain elusive. This retrospective cohort analysis aims to test the hypothesis that chest tubes in contact with the phrenic nerve in the pleural apex may cause pressure palsy. METHODS: In late 2018, the chest tube positioning strategy was changed so as to avoid a putative "danger zone" configuration, defined as (1) the chest tube looping apicomedially at the level of the second right intercostal space, and (2) wedging of chest tube tip against pericardium. A preintervention and postintervention analysis of 531 patients from 2012 to 2019 was performed to evaluate any association of chest tube position or duration in place with DP. Univariable and multivariable analyses were carried out, with significance set a priori at P < .05. RESULTS: The preintervention group comprised 488 patients, of whom 32 (6.6%) had RDP. The postintervention group comprised 43 patients, none of whom had DP. Multivariable analysis of the entire cohort revealed chest tube positioning in the danger zone as the only significant association with RDP (odds ratio, 4.22; 95% confidence interval, 1.57-11.33; P < .05). CONCLUSIONS: Chest tubes that occupy the right superior pleural space are associated with increased risk of DP.

Spinal cord injury level and Phrenic Nerve Conduction Studies do not predict diaphragm pacing success or failure- all patients should undergo diagnostic laparoscopy.

BACKGROUND: Diaphragm Pacing(DP) demonstrates benefits over mechanical ventilation(MV) for spinal cord injured(SCI) patients. The hypothesis of this report is that phrenic nerve conduction study(PNCS) results cannot differentiate success or failure in selection of patients for DP. Direct surgical evaluation of the diaphragm should be performed. METHODS: Observational report of prospective databases of patients undergoing laparoscopic evaluation of their diaphragms to assess for ability to stimulate to cause contraction for ventilation. RESULTS: In 50 SCI patients who could not be weaned from MV, PNCS results showed latencies in stimulated patients (n = 44) and non-stimulated(n = 6) overlapped (7.8 ± 2.5 ms vs 9.4 ± 2.8 ms) and the null hypothesis cannot be rejected (p-value>0.05). Amplitudes overlapped (0.4 ± 0.2 mV vs 0.2 ± 0.2 mV) and the null hypotheses cannot be rejected (P-value >0.05). In 125 non SCI patients with diaphragm paralysis, there were 78(62.4%) with false negative PNCS. CONCLUSION: PNCS are inadequate pre-operative studies. Direct laparoscopic evaluation should be offered for all SCI patients to receive the benefit of DP.

Suppression of phrenic nerve activity as a potential predictor of imminent sudden unexpected death in epilepsy (SUDEP).

Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in patients with refractory epilepsy. Centrally-mediated respiratory dysfunction has been identified as one of the principal mechanisms responsible for SUDEP. Seizures generate a surge in adenosine release. Elevated adenosine levels suppress breathing. Insufficient metabolic clearance of a seizure-induced adenosine surge might be a precipitating factor in SUDEP. In order to deliver targeted therapies to prevent SUDEP, reliable biomarkers must be identified to enable prompt intervention. Because of the integral role of the phrenic nerve in breathing, we hypothesized that suppression of phrenic nerve activity could be utilized as predictive biomarker for imminent SUDEP. We used a rat model of kainic acid-induced seizures in combination with pharmacological suppression of metabolic adenosine clearance to trigger seizure-induced death in tracheostomized rats. Recordings of EEG, blood pressure, and phrenic nerve activity were made concomitant to the seizure. We found suppression of phrenic nerve burst frequency to 58.9% of baseline (p < 0.001, one-way ANOVA) which preceded seizure-induced death; importantly, irregularities of phrenic nerve activity were partly reversible by the adenosine receptor antagonist caffeine. Suppression of phrenic nerve activity may be a useful biomarker for imminent SUDEP. The ability to reliably detect the onset of SUDEP may be instrumental in the timely administration of potentially lifesaving interventions.

Hypoxia-induced hypotension elicits adenosine-dependent phrenic long-term facilitation after carotid denervation.

Moderate acute intermittent hypoxia (AIH) elicits a persistent, serotonin-dependent increase in phrenic amplitude, known as phrenic long-term facilitation (pLTF). Although pLTF was originally demonstrated by carotid sinus nerve stimulation, AIH still elicits residual pLTF in carotid denervated (CBX) rats via a distinct, but unknown mechanism. We hypothesized that exaggerated hypoxia-induced hypotension after carotid denervation leads to greater spinal tissue hypoxia and extracellular adenosine accumulation, thereby triggering adenosine 2A receptor (A2A)-dependent pLTF. Phrenic activity, arterial pressure and spinal tissue oxygen pressure were measured in anesthetized CBX rats. Exaggerated hypoxia-induced hypotension after CBX was prevented via intravenous phenylephrine; without the hypotension, spinal tissue hypoxia during AIH was normalized, and residual pLTF was no longer observed. Spinal A2A (MSX-3), but not serotonin 2 receptor (5-HT2) inhibition (ketanserin), abolished residual pLTF in CBX rats. Thus, pLTF regulation may be altered in conditions impairing sympathetic activity and arterial pressure regulation, such as spinal cord injury.

Contemporary analysis of phrenic nerve injuries following cryoballoon-based pulmonary vein isolation: A single-centre experience with the systematic use of compound motor action potential monitoring.

BACKGROUND: Phrenic nerve injury (PNI) remains one of the most frequent complications during cryoballoon-based pulmonary vein isolation (CB-PVI). Since its introduction in 2013, the use of compound motor action potential (CMAP) for the prevention of PNI during CB-PVI is increasing; however, systematic outcome data are sparse. METHODS: The CMAP technique was applied in conjunction with abdominal palpation during pacing manoeuvres (10 mV, 2 ms) from the superior vena cava for 388 consecutive patients undergoing CB-PVI between January 2015 and May 2017 at our tertiary arrhythmia centre. Cryoablation was immediately terminated when CMAP amplitude was reduced by 30%. RESULTS: Reductions in CMAP amplitude were observed in 16 (4%) of 388 patients during isolation of the right veins. Of these, 11 (69%) patients did not manifest a reduction in diaphragmatic excursions. The drop in CMAP amplitude was observed in 10 (63%) patients during ablation of the right superior pulmonary veins (PVs) and in 7 (44%) patients during ablation of the right inferior PVs. Postprocedural persistent PNI was observed in three of four patients for a duration of 6 months, with one of these patients remaining symptomatic at the 24-month follow-up. One of the four patients was lost to long-term follow-up. CONCLUSIONS: All PNIs occurred during right-sided CB-PVI and were preceded by a reduction in CMAP amplitude. Thus, the standardized use of CMAP surveillance during CB-PVI is easily applicable, reliable and compared with other studies, results in a lower number of PNIs.

The impaired diaphragmatic function after bilateral lung transplantation: A multifactorial longitudinal study.

BACKGROUND: Lung transplantation is a complex but effective treatment of end-stage pulmonary disease. Among the post-operative complications, phrenic nerve injury, and consequent diaphragmatic dysfunction are known to occur but are hitherto poorly described. We aimed to investigate the effect of lung transplantation on diaphragmatic function with a multimodal approach. METHODS: A total of 30 patients were studied at 4 time points: pre-operatively, at discharge after surgery, and after approximately 6 and subsequently 12 months post surgery. The diaphragmatic function was studied in terms of geometry (assessed by the radius of the diaphragmatic curvature delineated on chest X-ray), weakness (considering changes in forced vital capacity when the patient shifted from upright to supine position), force (maximal pressure during sniff), mobility (excursion of the dome of the diaphragm delineated by ultrasound), contractility (thickening fraction assessed by ultrasound), electrical activity (latency and area of compound muscle action potential during electrical stimulation of phrenic nerve), and kinematics (relative contribution of the abdominal compartment to tidal volume). RESULTS: Despite good clinical recovery (indicated by spirometry and 6 minutes walking test), a reduction of the diaphragmatic function was detected at discharge; it persisted 6 months later to recover fully 1 year after transplantation. Diaphragmatic dysfunction was demonstrated in terms of force, weakness, electrical activity, and kinematics. Our data suggest that the dysfunction was caused by phrenic nerve neurapraxia or moderate axonotmesis, potentially as a consequence of the surgical procedure (i.e., the use of ice and pericardium manipulation). CONCLUSIONS: The occurrence of diaphragmatic dysfunction in patients with a good clinical recovery indicates that the evaluation of diaphragmatic function should be included in the post-operative assessment after lung transplantation.

Anatomic Variation of the Phrenic Nerve and Brachial Plexus Encountered during 100 Supraclavicular Decompressions for Neurogenic Thoracic Outlet Syndrome with Associated Postoperative Neurologic Complications.

BACKGROUND: The objective of this study was to characterize phrenic nerve and brachial plexus variation encountered during supraclavicular decompression for neurogenic thoracic outlet syndrome and to identify associated postoperative neurologic complications. METHODS: A multicenter retrospective review was performed to evaluate anatomic variation of the phrenic nerve and brachial plexus from November 2010 to July 2018. After initial characterization, the following two groups were identified: variant anatomy (VA) group and standard anatomy (SA) group. Complications were analyzed and compared between the two groups. RESULTS: In total, 105 patients were identified, and 100 patients met inclusion criteria. Any anatomic variation of the standard course or configuration of the phrenic nerve and/or brachial plexus was encountered in 47 (47%) patients. Phrenic nerve anatomic variations were identified in 28 (28%) patients. These included 9 duplicated nerves, 6 lateral accessory nerves, 8 medial displacement, and 5 lateral displacement. Brachial plexus anatomic variation was found in 34 (34%) patients. The most common variant configuration of a fused middle and inferior trunk was identified in 25 (25%) patients. Combined phrenic nerve and brachial plexus anatomic variation was demonstrated in 15 (15%) patients. The VA and SA groups consisted of 47 and 53 patients, respectively. Transient phrenic nerve injury with postoperative elevation of the ipsilateral hemidiaphragm was documented in 3 (6.4%) patients in the VA group and 6 (11.3%) patients in the SA group (P = 0.49). Permanent phrenic nerve injury was identified in 1 (2.1%) patient in the VA group (P = 0.47) and none in the SA group. Transient brachial plexopathy was encountered in 1 (1.9%) patient in the SA group (P = 1.0) with full recovery to normal function. CONCLUSIONS: Anatomic variability of the phrenic nerve and brachial plexus are encountered more frequently than previously reported. While the incidence of nerve injury is low, surgeons operating within the thoracic aperture should be familiar with variant anatomy to reduce postoperative complications.

Clinical feasibility of pulmonary vein orifice pacing for the prediction of phrenic nerve injury during cryoballoon ablation of atrial fibrillation.

INTRODUCTION: Phrenic nerve (PN) injury is a well-known complication of cryoballoon ablation (CBA) for pulmonary vein (PV) isolation in patients with atrial fibrillation. However, it is still insufficient to practically predict phrenic nerve injury (PNI) before freezing. We hypothesized that phrenic nerve capture (PNC) with phrenic nerve orifice pacing (PVOP) might be a surrogate sign of the close proximity of the PN, and that might predict PNI and changes in the compound motor action potential (CMAP) amplitude. METHODS: Seventy patients (60 ± 12 years, male 80%, paroxysmal 56%) underwent PVOP with a 20-electrode ring catheter before the CBA. The clinical outcome was the occurrence of transient and persistent PNI. In addition, the PV position and pacing threshold during PNC with PVOP, and changes in the CMAP amplitude were recorded. We compared these measurements between patients with and without PNC (PNC/non-PNC group) with PVOP. RESULTS: PNC with PVOP occurred in 39 (56%) patients and was localized only to the right superior PV. Transient PNI occurred in seven (10%) patients and permanent in none. The CMAP amplitude decreased significantly more in the PNC group (PNC 33% vs non-PNC 16%, P = .027). PNC group had a higher risk of the composite outcome of transient PNI or ≥30% decrease in the CMAP amplitude (PNC 54% vs non-PNC 13%; P < .001). CONCLUSIONS: This PVOP technique could be feasible and contribute to predicting transient PNI and CMAP amplitude reductions before cryoapplications. Further studies are necessary to elucidate the additional efficacy of PVOP over CMAP monitoring alone.

Second-Generation Cryoballoon Atrial Fibrillation Ablation in Patients With Persistent Left Superior Caval Vein.

OBJECTIVES: This study sought to assess the acute success rate, periprocedural complications, and long-term outcomes in patients with atrial fibrillation (AF) and persistent left superior vena cava (PLSVC) treated with second-generation 28-mm cryoballoon (CB2). BACKGROUND: PLSVC is a cardiac anomaly associated with AF. METHODS: Between July 2012 and October 2018, 8 patients from 4 German high-volume centers referred for pulmonary vein isolation (PVI) demonstrated a PLSVC. PVI and ablation within the PLSVC was performed using the CB2. RESULTS: A total of 2,876 patients were treated with CB2-based PVI. Eight patients (0.28%; mean 65 ± 7 years of age, 2 paroxysmal, 6 with persistent AF, mean left atrial size of 44 ± 4 mm) presenting with PLSVC were evaluated. All patients underwent PVI, and 3 of 8 patients with documented triggered activity from PLSVC underwent PLSVC ablation with CB2. Electrical isolation of PLSVC was achieved in 2 of 3 patients. Mean procedure and fluoroscopy times were 120 ± 22 min and 32 ± 18 min, respectively. In 2 of 8 patients, major complications (right phrenic nerve palsy) occurred during right PV ablation. After 3 months, 1 of 2 patients recovered from right phrenic nerve palsy. Two patients underwent a redo procedure after AF recurrence, demonstrating PV reconnection but no triggers from PLSVC. Freedom from AF after 332 days of follow-up was 63%. CONCLUSIONS: CB2 ablation for AF in patients with PLSVC is feasible, with an increased risk for right phrenic nerve palsy. Electrical isolation of PLSVC can be achieved with the CB2 in most patients.

Modulation of Serotonin and Adenosine 2A Receptors on Intermittent Hypoxia-Induced Respiratory Recovery following Mid-Cervical Contusion in the Rat.

The present study was designed to evaluate the therapeutic effectiveness and mechanism of acute intermittent hypoxia on respiratory function at distinct injury stages following mid-cervical spinal contusion. In the first experiment, adult male rats received laminectomy or unilateral contusion at 3rd-4th cervical spinal cord at 9 weeks of age. The ventilatory behavior in response to mild acute intermittent hypercapnic-hypoxia (10 episodes of 5 min of hypoxia [10% O2, 4% CO2, 86% N2] with 5 min of normoxia intervals) was measured by whole-body plethysmography at the acute (∼3 days), subchronic (∼2 weeks), and chronic (∼8 weeks) injury stages. The minute ventilation of contused animals is significantly enhanced following acute intermittent hypercapnic-hypoxia due to an augmentation of the tidal volume at all time-points post-injury. However, acute intermittent hypercapnia-hypoxia-induced ventilatory long-term facilitation was only observed in uninjured animals at the acute stage. During the second experiment, the effect of acute intermittent hypercapnic-hypoxia on respiration was examined in contused animals after a blockade of serotonin receptors, or adenosine 2A receptors. The results demonstrated that acute intermittent hypercapnic-hypoxia-induced enhancement of minute ventilation was attenuated by a serotonin receptor antagonist (methysergide) but enhanced by an adenosine 2A receptor antagonist (KW6002) at the subchronic and chronic injury stages. These results suggested that acute intermittent hypercapnic-hypoxia can induce respiratory recovery from acute to chronic injury stages. The therapeutic effectiveness of intermittent hypercapnic-hypoxia is dampened by the inhibition of serotonin receptors, but a blockade of adenosine 2A receptors enhanced respiratory recovery induced by intermittent hypercapnic-hypoxia.

How to implant a phrenic nerve stimulator for treatment of central sleep apnea?

BACKGROUND: Central sleep apnea (CSA) is a breathing disorder caused by the intermittent absence of central respiratory drive. Transvenous phrenic nerve stimulation is a new therapeutic option, recently approved by the FDA , for the treatment of CSA. OBJECTIVE: To describe the technique used to implant the transvenous phrenic nerve stimulation system (the remede System, Respicardia, Inc). METHODS: The remede System is placed in the pectoral region, typically on the right side. A single stimulation lead is placed in either the left pericardiophrenic vein (PPV) or the right brachiocephalic vein (RBC). A sensing lead is placed into the azygous vein to detect respiration. RESULTS: In the remede System Pivotal trial, 147 of 151 (97%) patients were successfully implanted with the system. Sixty-two percent of stimulation leads were placed in the PPV and 35% in the RBC. Mean procedure time was 2.7 ± 0.8 hours and 94% of patients were free from implant-related serious adverse events through 6 months. CONCLUSION: In patients with CSA, transvenous phrenic nerve stimulation is an effective and safe therapy with an implant procedure similar to that of cardiac implantable electronic devices.

Selective reinnervation using phrenic nerve and hypoglossal nerve for bilateral vocal fold paralysis.

OBJECTIVE: To evaluate the extent of airway improvement and voice quality in patients with bilateral vocal fold paralysis (BVFP) who underwent selective laryngeal reinnervation surgery. METHODS: Seven patients with BVFP caused by thyroid surgeries were enrolled. They underwent selective laryngeal reinnervation surgery. Videostroboscopy data, voice perceptual data (grade [G]), acoustic data, laryngeal electromyography data, and pulmonary function test data were obtained preoperatively and postoperatively. RESULTS: Videostroboscopic videos showed that six patients could achieve moderate-to-maximal abduction in the bilateral vocal folds during inspiration, whereas all patients achieved adduction in the bilateral vocal folds during phonation at 4 to 7 months postoperatively. G score was decreased significantly versus preoperative values (P < 0.05), and vocal functional parameters were improved significantly at 12 months postoperatively (P < 0.05). The aerodynamic parameter of maximum phonation time was significantly longer than the preoperative value (P < 0.05). Most parameters in pulmonary function test recovered to normal reference levels as early as 3 months postoperatively, whereas maximal inspiratory pressure (PImax) values were still slightly lower than normal levels 12 months after surgery. All of these parameters improved significantly versus preoperative values. Electromyographic data at 12 months postoperatively showed full interference potentials in bilateral posterior cricoarytenoid muscles during inspiration and full interference potentials in bilateral thyroarytenoid muscles during phonation in all patients. Moderate electric potentials were seen in left interarytenoid muscle in one failed patient. CONCLUSION: This new selective laryngeal reinnervation procedure can achieve physiological movements of the bilateral vocal folds in selected patients with BVFP. LEVEL OF EVIDENCE: 4. Laryngoscope, 129:2669-2673, 2019.

Diaphragmatic dysfunction.

The diaphragm is the main breathing muscle and contraction of the diaphragm is vital for ventilation so any disease that interferes with diaphragmatic innervation, contractile muscle function, or mechanical coupling to the chest wall can cause diaphragm dysfunction. Diaphragm dysfunction is associated with dyspnoea, intolerance to exercise, sleep disturbances, hypersomnia, with a potential impact on survival. Diagnosis of diaphragm dysfunction is based on static and dynamic imaging tests (especially ultrasound) and pulmonary function and phrenic nerve stimulation tests. Treatment will depend on the symptoms and causes of the disease. The management of diaphragm dysfunction may include observation in asymptomatic patients with unilateral dysfunction, surgery (i.e., plication of the diaphragm), placement of a diaphragmatic pacemaker or invasive and/or non-invasive mechanical ventilation in symptomatic patients with bilateral paralysis of the diaphragm. This type of patient should be treated in experienced centres. This review aims to provide an overview of the problem, with special emphasis on the diseases that cause diaphragmatic dysfunction and the diagnostic and therapeutic procedures most commonly employed in clinical practice. The ultimate goal is to establish a standard of care for diaphragmatic dysfunction.

The Impact of Cervical Spinal Cord Contusion on the Laryngeal Resistance in the Rat.

The present study was designed to investigate laryngeal function responses to chemoreceptor activation after unilateral high-cervical spinal cord contusion in rats. Adult male Sprague-Dawley rats received laminectomy or unilateral contusion at the C2 spinal cord. Both respiratory airflow and subglottal pressure were measured in spontaneously breathing rats at three days, two weeks, or six weeks after spinal surgery. Laryngeal closure responses were evoked via intrajugular capsaicin (1.5 µg/kg) administration and hypoxia (12.5% O2, 3 min) to activate bronchopulmonary C-fibers and chemoreceptors, respectively. High cervical contusion resulted in long-term reductions in tidal volume without changes in laryngeal resistance at baseline. Alternatively, capsaicin-induced increased subglottal pressure was significantly attenuated in contused rats at three days post-injury. Contused rats regained the ability to increase laryngeal resistance after capsaicin treatment at two and six weeks post-injury, whereas this recovered response remained weaker than uninjured animals. Notably, hypoxia-induced laryngeal closure was not altered during the acute injured stage, but instead was blunted at six weeks post-injury. These data suggest that cervical spinal cord injury not only influences the breathing pattern, but it also impacts upper airway function through modulation of laryngeal resistance. An attenuated laryngeal closure response may negatively impact the ability to prevent irritant inhalation and maintenance of the functional residual capacity. This may contribute to the provocation of pulmonary disease after cervical spinal cord injury.

Usefulness of diaphragmatic ultrasound in the early diagnosis of phrenic nerve palsy after shoulder surgery in the prevention of post-operative respiratory complications. / Utilidad de la ecografía diafragmática en el diagnóstico precoz de parálisis frénica tras cirugía de hombro para prevenir complicaciones respiratorias postoperatorias.

Phrenic nerve block is a complication that can occur after brachial plexus anaesthesia above the clavicle. The main consequence of this blockage is ipsolateral diaphragmatic paralysis, which can sometimes lead to the appearance of post-operative respiratory complications. A case is presented on a woman, who after having undergone a total shoulder prosthesis, presented with dyspnoea in the post-operative recovery unit. A diaphragmatic ultrasound was performed that enabled a rapid diagnosis to be made of a complete paralysis of the ipsolateral hemi-diaphragm. Given the suspicion of phrenic nerve block, ultrasound has proven to be a rapid diagnostic tool with high sensitivity and specificity. Its use can anticipate the possible development of immediate complications, and act as a guide in choosing the appropriate therapeutic strategy for each case in an early manner. In this case it enabled us to treat early with oxygen therapy, interscalene catheter removal, and intensive surveillance.

Diaphragm electromyography guidance for a lung transplant recipient with difficult weaning from mechanical ventilation: A case report.

RATIONALE: Many factors contribute to a complicated postoperative course following difficult weaning off a ventilator after lung transplantation. PATIENT CONCERNS: A female patient underwent a successful surgery but received a size-mismatched lung graft. The graft had been pruned before transplantation. She experienced delayed ventilator weaning 3 days after lung transplantation. DIAGNOSES: A postoperative X-ray revealed a normal mediastinal structure and diaphragm position. Diaphragmatic function was assessed by diaphragm electromyography (EMGdi) via esophageal and surface electrodes. EMGdi showed decreased left compound motor action potentials (CMAPs), prolonged left phrenic nerve conduction time (PNCT), failure to induce right CMAPs and PNCT under bilateral magnetic stimulation, and right phrenic nerve injury. INTERVENTIONS: She was treated with neural nutritional support and prescribed rehabilitation measures such as strengthening limb activities on the bed. OUTCOMES: The patient finally achieved satisfactory outcomes after an early diagnosis and medical interventions. LESSONS: Lung size mismatch before transplantation and phrenic nerve injury during surgery should be avoided wherever possible.