Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia
Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia
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DOI：
10.1177/000348940010901103
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发表时间：
2000-11-01
影响因子：
1.4
通讯作者：
Close, LG
中科院分区：
文献类型：
--
作者：
Aviv, JE;Liu, H;Close, LG
对于咽喉反流（LPR）患者的后喉酸暴露导致的水肿，目前尚无可靠的量化方法。然而，它是可能的量化喉咽敏感性在这些患者的内镜管理的空气脉冲喉粘膜，以引起喉内收肌反射。本研究的目的是确定LPR患者是否有咽喉部的感觉障碍，以及质子泵抑制剂（PPI）治疗这些患者是否能解决感觉障碍。在54例无神经系统疾病的吞咽困难患者和25例健康对照者中前瞻性地进行了吞咽感觉测试的柔性内窥镜评价。评估咽喉感觉水平、喉后水肿和LPR。我们将LPR定义为食物物质从食管入口逆行进入下咽部的通道。LPR患者接受3个月奥美拉唑或兰索拉唑治疗，然后重新检测。没有LPR的患者被放置在Hz阻滞剂3个月，然后重新测试。在吞咽困难组中，54名患者中有48名（89%）有喉后水肿，54名患者中有42名（78%）有咽喉感觉障碍。我们注意到LPR在38的54（70%）。在对照组中，25例受试者中有1例（4%）出现水肿、感觉障碍和LPR。吞咽困难组和对照组之间水肿、感觉缺陷和LPR的发生率差异显著（p <0.001，（2）检验）。23名放置在PPI上的LPR患者返回接受随访，21名治疗前水肿的患者中有14名（67%）喉部水肿改善，19名治疗前感觉障碍的患者中有15名（79%）感觉障碍消退。在非LPR、非PPI组中，16例患者中有11例返回接受随访，11例患者中无喉水肿改善，11例患者中有1例（9.1%）感觉障碍改善。LPR、PPI组和非LPR、非PPI组之间喉水肿和感觉缺陷改善的差异是显著的（p <0.01，Fisher精确检验）。我们的结论是，患者吞咽困难和水肿的后喉作为一个结果LPR有感觉缺陷的喉咽。这些患者接受PPI治疗后，主观和客观上似乎可缓解咽喉水肿并改善感觉缺陷。
There are no reliable means of quantifying the edema that results from acid exposure to the posterior larynx in patients with laryngopharyngeal reflux (LPR). However, it is possible to quantify laryngopharyngeal sensitivity in these patients by endoscopic administration of air pulses to the laryngeal mucosa in order to elicit the laryngeal adductor reflex. The purpose of this study was to determine whether patients with LPR have sensory deficits in the laryngopharynx, and whether treatment of these patients with a proton pump inhibitor (PPI) results in resolution of sensory deficits. Flexible endoscopic evaluation of swallowing with sensory testing was prospectively performed in 54 patients with dysphagia without neurologic disease and in 25 healthy controls. The laryngopharyngeal sensory level, posterior laryngeal edema, and LPR were assessed. We defined LPR as passage of food material from the esophageal inlet retrograde into the hypopharynx. Patients with LPR were placed on 3 months of omeprazole or lansoprazole and then retested. Patients without LPR were placed on Hz blockers for 3 months and then retested. In the dysphagia group, 48 of 54 patients (89%) had edema of the posterior larynx, and 42 of 54 (78%) had laryngopharyngeal sensory deficits. We noted LPR in 38 of 54 (70%). In the control group, 1 of 25 subjects (4%) had edema, sensory deficits, and LPR. The differences in incidence of edema, sensory deficits, and LPR between the dysphagia group and the control group were significant (p < .001, (2) test). Twenty-three patients with LPR placed on a PPI returned for follow-up, with improvement in laryngeal edema in 14 of the 21 (67%) who had pretreatment edema and resolution of sensory deficits in 15 of the 19 (79%) who had pretreatment deficits. In the non-LPR, non-PPI group, 11 of 16 patients returned for follow-up, with improvement in laryngeal edema in none of the 11 and improvement in sensory deficits in 1 of the 11 (9.1%). The differences in improvement in laryngeal edema and sensory deficits between the LPR, PPI group, and the non-LPR, non-PPI group were significant (p < .01, Fisher's exact test). We conclude that patients with dysphagia and edema of the posterior larynx as a result of LPR have sensory deficits in the laryngopharynx. Treatment of these patients with a PPI appears to result in resolution of laryngopharyngeal edema and improvement of sensory deficits, both subjectively and objectively.