Relationship Between Laryngeal Sensation, Length of Intubation, and Aspiration in Patients with Acute Respiratory Failure

Borders, James C; Fink, Daniel; Levitt, Joseph E.; McKeehan, Jeffrey; McNally, Edel; Rubio, Alix; Scheel, Rebecca; Siner, Jonathan; Taborda, Stephanie Gomez; Vojnik, Rosemary; Warner, Heather; White, Sean; Langmore, Susan E.; Moss, Marc; Krisciunas, Gintas P.

doi:10.1007/s00455-019-09980-1

Cited by 51 publications

(39 citation statements)

References 37 publications

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“…We therefore posit that a dysfunctional “middle airway”, perhaps due to reduced timing of laryngeal vestibular closure and sensory mechanisms in COPD [ 5 , 34 ], may underlie defective protection against aspiration. Finally, an interesting finding was more frequent penetration–aspiration in patients with a history of diabetes mellitus, a condition linked with sarcopenia [ 35 ], laryngeal sensory disruption [ 36 ], diabetic neuropathy and abnormal oral bacterial loads [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Aspiration and severe exacerbations in COPD: a prospective study

et al. 2020

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RationaleSwallow may be compromised in chronic obstructive pulmonary disease (COPD) leading to aspiration and adverse respiratory consequences. However, prevalence and consequences of detectable aspiration in stable COPD are not known.ObjectivesWe tested the hypothesis that a significant number of patients with stable COPD will have detectable aspiration during swallow (prandial aspiration) and that they would experience more frequent severe acute exacerbations of COPD (AECOPD) over the subsequent 12 months.MethodsPatients (n=151) with verified and stable COPD of all severities were recruited at a tertiary care hospital. Videofluoroscopy was conducted to evaluate aspiration using Rosenbek's scale for penetration-aspiration during 100 mL cup drinking. AECOPD was documented as moderate (antibiotics and/or corticosteroid treatment) or severe (Emergency Department admission or hospitalisation) over the ensuing 12 months.Measurements and Main ResultsAspiration was observed in 30/151 patients (19.9%, 18 males, 12 females; mean age 72.4 years). Patients with aspiration had more overall AECOPD events (3.03 versus 2 per patient; p=0.022) and severe AECOPD episodes (0.87 versus 0.39; p=0.032). Severe AECOPD occurred in more patients with aspiration (50% of patients versus 18.2%; OR=4.5; CI 1.9–10.5; p=0.001) and with silent aspiration (36.7% versus 18.2%; OR=2.6; CI 1.1–6.2; p=0.045). Aspiration was related to a shorter exacerbation-free period during the 12-month follow-up period (p=0.038).ConclusionsPrandial aspiration is detectable in a subset of patients with COPD and was predictive of subsequent severe AECOPD. Studies to examine if the association is causal are essential to direct strategies aimed at prevention of aspiration and AECOPD.

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Section: Discussionmentioning

confidence: 99%

Aspiration and severe exacerbations in COPD: a prospective study

et al. 2020

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“…A larger bolus, for example, induces an earlier hyolaryngeal elevation as well as an earlier opening of the upper esophageal sphincter compared to a smaller bolus (Cook et al, 1989;Jacob, Kahrilas, Logemann, Shah, & Ha, 1989). Finally, protective mechanisms, in particular, clearing swallows dealing with pharyngeal residues as well as a reflexive cough, are critically dependent on intact sensory feedback (Aviv et al, 1996;Borders et al, 2019;Onofri, Cola, Berti, da Silva, & Dantas, 2014;Shapira-Galitz, Shoffel-Havakuk, Halperin, & Lahav, 2019). In the clinical context, several studies have shown that pharyngeal hypesthesia is associated with complications and bad outcome.…”

Section: Introductionmentioning

confidence: 99%

Targeting the sensory feedback within the swallowing network—Reversing artificially induced pharyngolaryngeal hypesthesia by central and peripheral stimulation strategies

Muhle

Labeit

Wollbrink

et al. 2020

Human Brain Mapping

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Pharyngolaryngeal hypesthesia is a major reason for dysphagia in various neurological diseases. Emerging neuromodulation devices have shown potential to foster dysphagia rehabilitation, but the optimal treatment strategy is unknown. Because functional imaging studies are difficult to conduct in severely ill patients, we induced a virtual sensory lesion in healthy volunteers and evaluated the effects of central and peripheral neurostimulation techniques. In a sham-controlled intervention study with crossover design on 10 participants, we tested the potential of (peripheral) pharyngeal electrical stimulation (PES) and (central) transcranial direct current stimulation (tDCS) to revert the effects of lidocaine-induced pharyngolaryngeal hypesthesia on central sensorimotor processing. Changes were observed during pharyngeal air-pulse stimulation and voluntary swallowing applying magnetoencephalography before and after the interventions. PES induced a significant (p < .05) increase of activation during swallowing in the bihemispheric sensorimotor network in alpha and low gamma frequency ranges, peaking in the right premotor and left primary sensory area, respectively. With pneumatic stimulation, significant activation increase was found after PES in high gamma peaking in the left premotor area. Significant changes of brain activation after tDCS could neither be detected for pneumatic stimulation nor for swallowing. Due to the peripheral cause of dysphagia in this model, PES was able to revert the detrimental effects of reduced sensory input on central processing, whereas tDCS was not. Results may have implications for therapeutic decisions in the clinical context.

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“…In geriatric patients with dysphagia, age‐related reduced pharyngeal sensation is an important contributing factor . In intensive care, intubation‐induced mucosal damage often leads to laryngeal sensory deficits and can result in post‐extubation dysphagia . In patients with chronic obstructive pulmonary disease (COPD), pharyngeal hypesthesia related to dysphagia has been reported, which in turn exacerbates COPD after aspiration and consecutive broncho‐pneumonia.…”

Section: Introductionmentioning

confidence: 99%

“…25 In intensive care, intubation-induced mucosal damage often leads to laryngeal sensory deficits and can result in post-extubation dysphagia. 26 In patients with chronic obstructive pulmonary disease (COPD), pharyngeal hypesthesia related to dysphagia has been reported, which in turn exacerbates COPD after aspiration and consecutive broncho-pneumonia. Impaired pharyngeal sensation in COPD is presumably caused by gastroesophageal reflux and damage to the mucosa.…”

Section: Introductionmentioning

confidence: 99%

FEES‐based assessment of pharyngeal hypesthesia—Proposal and validation of a new test procedure

Labeit

Ogawa

Claus

et al. 2019

Neurogastroenterology Motil

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Background Intact pharyngeal sensation is essential for a physiological swallowing process, and conversely, pharyngeal hypesthesia can cause dysphagia. This study introduces and validates a diagnostic test to quantify pharyngeal hypesthesia. Methods A total of 20 healthy volunteers were included in a prospective study. Flexible endoscopic evaluation of swallowing (FEES) and a sensory test were performed both before and after pharyngeal local anesthesia. To test pharyngeal sensation, a small tube was positioned transnasally in the upper third of the oropharynx with contact to the lateral pharyngeal wall. Increasing volumes of blue‐dyed water were injected through the tube, and the latency of swallowing response (LSR) was determined by two independent raters from the endoscopic video recording. Three trials were performed for each administered volume starting with 0.1 mL and increased by 0.1 mL up to 0.5 mL. Key Results The average LSR without anesthesia was 2.24 ± 0.80 s at 0.1 mL, 1.79 ± 0.84 s at 0.2 mL, 1.29 ± 0.62 s at 0.3 mL, 1.17 ± 0.41 s at 0.4 mL, and 1.19 ± 0.52 s at 0.5 mL. With anesthesia applied, the average LSR was 2.65 ± 0.62 s at 0.1 mL, 2.64 ± 0.49 s at 0.2 mL, 2.44 ± 0.65 s at 0.3 mL, 2.10 ± 0.80 s at 0.4 mL, and 2.18 ± 0.85 s at 0.5 mL. LSR was significantly longer following anesthesia at 0.2 mL (t = −3.82; P = .001), 0.3 mL (t = −4.65; P < .000), 0.4 mL (t = −5.77; P < .000), and 0.5 mL (t = −3.49; P = .005). Conclusion and Inferences Pharyngeal hypesthesia can be quantified with sensory testing using LSR. Suitable volumes to distinguish between normal and impaired pharyngeal sensation are 0.2 mL, 0.3 mL, 0.4 mL and 0.5 mL. Experimentally induced pharyngeal anesthesia represents a valid model of sensory dysphagia.

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Relationship Between Laryngeal Sensation, Length of Intubation, and Aspiration in Patients with Acute Respiratory Failure

Cited by 51 publications

References 37 publications

Aspiration and severe exacerbations in COPD: a prospective study

Aspiration and severe exacerbations in COPD: a prospective study

Targeting the sensory feedback within the swallowing network—Reversing artificially induced pharyngolaryngeal hypesthesia by central and peripheral stimulation strategies

FEES‐based assessment of pharyngeal hypesthesia—Proposal and validation of a new test procedure

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