« Paralysie récurrentielle unilatérale après thyroïdectomie : savoir rechercher un syndrome d’hyperventilation »

International audienceLa paralysie unilatérale du nerf récurrent peut être responsable d’une dysphonie et de troubles de la déglutition. La physiopathologie de l’apparition d’une dyspnée induite par une paralysie récurrentielle unilatérale n’est pas complètement élucidée. Notre hypothèse est que la fuite d’air au niveau glottique pourrait être responsable du développement d’un syndrome d’hyperventilation (SHV).ObjectifL’objectif de cette étude était de déterminer, chez les patients atteints de paralysie récurrentielle unilatérale, si la dyspnée pouvait être associée au SHV.Matériel et méthodesSur une période de 12 mois, tous les patients atteints de paralysie récurrentielle unilatérale permanente (> 6 mois) après thyroïdectomie se plaignant de l’apparition d’une dyspnée inexpliquée ont été explorés. Les tests suivants ont été réalisés : score de Nijmegen, test d’hyperventilation provoquée, gazométrie artérielle, épreuves fonctionnelles respiratoires et tests cardiaques. Le diagnostic de SHV a été posé si au moins deux critères étaient présents parmi les suivants : score de Nijmegen > 23 ; reproduction d’au moins 2 symptômes habituels lors du test d’hyperventilation ; pression télé-expiratoire en CO2 (PetCO2) < 30 mmHg ou < 90 % de la PetCO2 initiale après une période de récupération de 5 min à la suite d’une hyperventilation volontaire de 3 min.RésultatsDix patients sur 366 opérés d’une thyroïdectomie pour une maladie bénigne présentaient une paralysie récurrentielle unilatérale permanente et une dyspnée. Parmi les 10 patients inclus, chez 8 le diagnostic de SHV a été retenu lors du test d’hyperventilation provoquée sans dysfonctionnement cardiaque/pulmonaire.ConclusionEn résumé, cette étude est en faveur de l’implication du SHV dans la dyspnée associée à la paralysie récurrentielle unilatérale

Unilateral recurrent laryngeal nerve palsy post-thyroidectomy: Looking for hyperventilation syndrome

International audienceAims: Unilateral Recurrent Laryngeal Nerve (RLN) palsy is responsible for dysphonia and difficulties in swallowing. The role of unilateral RLN palsy on dyspnea is not fully elucidated. Our hypothesis is that air leak could be responsible for development of hyperventilation syndrome (HVS).Objective: The objective of this study was to determine in patients with unilateral RLN palsy if dyspnea could be associated with HVS.Material and methods: Over a 12-month period, all patients with permanent unilateral RLN palsy after thyroidectomy complaining from the onset of unexplained dyspnea were tested. Measurement of Nijmegen score, an hyperventilation test, an arterial blood gas, lung function and cardiac tests were performed. The diagnosis of HVS was defined if at least two criteria were present among: Nijmegen score>23; reproduction of at least 2 usual symptoms during hyperventilation test; an expirated pressure of CO2 (EpCO2)<30mmHg or<90% of the initial EpCO2 after a 5minutes recovery period following a 3minutes voluntary hyperventilation.Results: Ten out of 366 patients with thyroidectomy for benign disease had permanent unilateral RLN palsy and dyspnea. Among 10 patients included, 8 were diagnosed having HVS on the hyperventilation test without cardiac/lung dysfunction.Conclusion: In summary, this study is a proof of concept that HVS might be involved in dyspnea associated with unilateral RLN palsy

Quantitative analysis of ciliary beating in primary ciliary dyskinesia: a pilot study

International audienceBACKGROUND: Primary ciliary dyskinesia (PCD) is a rare congenital respiratory disorder characterized by abnormal ciliary motility leading to chronic airway infections. Qualitative evaluation of ciliary beat pattern based on digital high-speed videomicroscopy analysis has been proposed in the diagnosis process of PCD. Although this evaluation is easy in typical cases, it becomes difficult when ciliary beating is partially maintained. We postulated that a quantitative analysis of beat pattern would improve PCD diagnosis. We compared quantitative parameters with the qualitative evaluation of ciliary beat pattern in patients in whom the diagnosis of PCD was confirmed or excluded. METHODS: Nasal nitric oxide measurement, nasal brushings and biopsies were performed prospectively in 34 patients with suspected PCD. In combination with qualitative analysis, 12 quantitative parameters of ciliary beat pattern were determined on high-speed videomicroscopy recordings of beating ciliated edges. The combination of ciliary ultrastructural abnormalities on transmission electron microscopy analysis with low nasal nitric oxide levels was the "gold standard" used to establish the diagnosis of PCD. RESULTS: This "gold standard" excluded PCD in 15 patients (non-PCD patients), confirmed PCD in 10 patients (PCD patients) and was inconclusive in 9 patients. Among the 12 parameters, the distance traveled by the cilium tip weighted by the percentage of beating ciliated edges presented 96% sensitivity and 95% specificity. Qualitative evaluation and quantitative analysis were concordant in non-PCD patients. In 9/10 PCD patients, quantitative analysis was concordant with the "gold standard", while the qualitative evaluation was discordant with the "gold standard" in 3/10 cases. Among the patients with an inconclusive "gold standard", the use of quantitative parameters supported PCD diagnosis in 4/9 patients (confirmed by the identification of disease-causing mutations in one patient) and PCD exclusion in 2/9 patients. CONCLUSIONS: When the beat pattern is normal or virtually immotile, the qualitative evaluation is adequate to study ciliary beating in patients suspected for PCD. However, when cilia are still beating but with moderate alterations (more than 40% of patients suspected for PCD), quantitative analysis is required to precise the diagnosis and can be proposed to select patients eligible for TEM

Airway hyperresponsiveness to mannitol in obesity before and after bariatric surgery

The relationship between airway hyperresponsiveness (AHR) and obesity, a low-grade systemic inflammatory condition, remains largely unknown. It is established that AHR to indirect stimuli is associated with active airway inflammation. The objectives were to investigate the rate of AHR to mannitol in obese subjects and its changes 1 year after bariatric surgery (BS). We enrolled 58 candidates to BS severely obese (33 nonsmokers and 25 smokers) without history of asthma and 20 healthy, nonobese participants and related AHR to functional findings and serum and exhaled biomarkers. Before surgery, AHR was observed in 16 (28 %) obese with the provocation doses of mannitol to induce a 15 % fall in FEV1 (PD15) of (geometric mean [95 % CI]) 83 (24–145) mg. Compared to control participants, obese participants had lower spirometric values and higher serum and exhaled biomarkers (p < 0.05 each). After surgery, AHR was abolished (p < 0.01) in all but four obese subjects. Weight loss induced by BS was the key independent factor associated to AHR improvement. AHR to mannitol is highly prevalent in obesity, and it is largely abolished by BS