COPD a significantly cause of swallowing dysfunction

[gerald]

The article is quite lengthy and covers all aspects of difficultings with swallowi9ng/aspirating food into the bronchial tubes.  I copied the main part about COPD, the link to the full article is at the bottom.

It does an excellent job of explaining why we end up "breathing" our lunch instead of "swallowing" it.


------------------------------------


Pulmonary complications of oral-pharyngeal motility disorders
Jeffrey L. Curtis, M.D.
.
.
.
.

Obstructive Lung Disease and Deglutition

The lungs and esophagus share the thoracic cavity, and intrathoracic pressure is dominated by the pleural pressure swings associated with ventilation. In normal subjects, inhalation results from a subatmospheric drop in intrathoracic pressure generated largely by motion of the diaphragm. Normal exhalation is passive, allowing pleural pressures to rise to atmospheric levels. Obstructive lung diseases are characterized by hyperinflation, which flattens the diaphragm and exaggerates pleural pressure changes. In severe obstruction, exhalation is active and associated with positive intrathoracic pressures that can be large. These changes would be anticipated to compromise normal deglutition.

In fact, COPD appears be a significantly underrecognized cause of swallowing dysfunction in adults. It refers to a constellation of lung diseases characterized by varying degrees of mucus hypersecretion, peribronchiolar fibrosis, and parenchymal lung destruction.30 It has recently been defined as "a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases."31 In industrialized countries, COPD results overwhelmingly from tobacco smoke exposure, but in developing countries indoor air pollution contributes significantly. Worldwide prevalence of COPD in 1990 was estimated at 9.34/1000 in men and 7.33/1000 in women (see first Web site listed in Table 2). However, these estimates include all ages and doubtless underestimate the true prevalence of COPD in older adults. Rapid increases in prevalence (e.g., 25% in men and 69% in women in the United Kingdom between 1990 and 1997) are not due to changes in case definition. The World Health Organization projects that COPD will be the third leading cause of human death worldwide by 2020.32 Therefore, care of the lung disease and associated airway malignancies in COPD patients could come to dominate medical care in the 21st century in the same manner that the 19th and 20th centuries were dominated by tuberculosis and ischemic heart disease, respectively.

Dysphagia appears to be common in COPD patients.33 In a prospective questionnaire-based cross-sectional survey of patients in Veterans Administration (VA) clinics, Mokhlesi et al.34 found an increased proportion of dysphagia in 100 COPD patients compared to 51 medicine patients without respiratory symptoms or a diagnosis of COPD (17% vs. 4%). Dysphagia may be one major cause of the nutritional depletion that is common in COPD patients and that adversely impacts their exercise capacity.35 However, dysphagia with decreased caloric intake is probably not the only cause of weight loss in advanced COPD, as both hypermetabolism36 and anorexia37 have been demonstrated. Defining the relative contribution of these independent and potentially additive factors will be important, because weight loss has been associated with significantly increased morbidity and death in advanced COPD.38, 39, 40

One likely cause for dysphagia in COPD is that swallowing apnea cuts into the already compromised time available for breathing. Owing to an increase in wasted ventilation from lung damage, patients with mild to moderate COPD must sustain a higher than normal minute ventilation (the amount of air inhaled per minute) even at rest, simply to keep their blood carbon dioxide levels normal. As lung damage worsens, many patients with advanced COPD accommodate to CO2 retention rather than further increasing their resting minute ventilation. Heightened ventilatory demands during exercise or respiratory infections pose a further dilemma. Due to limited ability to increase the amount of air inhaled per breath (tidal volume), COPD patients increase their minute ventilation chiefly by increasing respiratory rate. By reducing the relative time available for exhalation, this leads rapidly to trapping of excess air in their chests, stretching respiratory muscles to a further mechanical disadvantage. This cycle of air trapping and muscle weakness can quickly lead to hypercapnic respiratory failure.

These factors imply that dysregulation of swallowing apnea would be seen in COPD patients, especially when their breathing worsens. That was exactly the effect seen by Shaker et al.19 in a landmark analysis on the effect of COPD on deglutition. They studied respiration during voluntary deglutition in 26 COPD patients (46 to 72 years old) during an acute exacerbation of chronic bronchitis (AECB), and restudied 10 of these patients in remission. Their control groups consisted of 18 healthy young (18- to 34-year-old) and 11 healthy older (63- to 83-year-old) volunteers studied in the upright and supine positions. As seen previously in normal subjects,14, 15, virtually all deglutitions in control subjects interrupted expiration, and this coupling to the expiratory phase was increased by the presence of a liquid bolus and tachypnea (rapid breathing). By contrast, COPD patients studied during AECB showed a markedly increased frequency of inspiratory swallows, with some improvement in the groups studied in remission. Shaker et al. defined a deglutition/respiration index, that is, the average duration of deglutition apnea divided by the duration of the respiratory cycle. This ratio fell in COPD patients studied during AECB. These data suggest that COPD patients are at increased risk of aspiration precisely when they are already undergoing stress of their respiratory system.

Dysphagia in COPD patients could have several other causes. In a study using systematic videofluoroscopic evaluation of oropharyngeal swallowing, Mokhlesi et al.33 compared 20 consecutive outpatients with COPD of at least moderate severity [mean forced expiratory volume in 1 second (FEV1) 40 plusminus 14% predicted; mean total lung capacity 128 plusminus 19% predicted] to 20 age- and sex-matched historical control subjects. They excluded those with a history of conditions that might affect oropharyngeal swallowing, but not those with gastroesophageal reflux (GER). Although there was no evidence of tracheal aspiration in either group, and only four of the patients with COPD reported dysphagia, the COPD group showed a range of swallowing disorders, including abnormalities in tongue strength and motion, delayed pharyngeal swallowing, and slowed or delayed vestibule closure. Importantly, maximal laryngeal elevation during swallowing was significantly reduced in patients with COPD.33 Patients with COPD also more frequently used spontaneous protective maneuvers (longer duration of airway closure and earlier laryngeal closure relative to cricopharyngeal opening) during swallowing. Interestingly, despite the marked hyperinflation in the COPD patients, which hypothetically might lead to caudal retraction of the larynx, there was no difference between groups in the laryngeal position at rest relative to the cervical vertebrae.33

Stein et al.41 described severe cricopharyngeal dysfunction in 17 of 22 nonrandomly selected elderly patients with COPD who were referred for frequent exacerbations of their chronic respiratory symptoms. Ten of the patients underwent cricopharyngeal myotomy, which in eight patients improved not only deglutition but also reported frequency of AECB. Given the availability of endoscopic botulinum toxin injection as a minimally invasive means of addressing cricopharyngeus dysfunction, this is an area that merits controlled investigation.

Whether cricopharyngeal dysfunction is actually increased in unselected COPD patients is unknown. The paucity of data from controlled trials on dysphagia in COPD should not be surprising. Tellingly, a systematic review of the literature using the Cochrane registries was unable to identify any controlled trials of therapy of dysphagia in adults or children with chronic muscle diseases,42 a problem that has been recognized much longer than has dysphagia in COPD.

www.nature.com/gimo/contents/pt1/full/gimo33.html

[ken]

Thank you for the posting Gerald.  This subject is very timely for me as someone close has been dx with dysphagia.

Again, thank you


Ken

[lavishgail]

I will continue to read the link you put up, but of course this is hard for me to understand. Because I don't know all the words that go along with this disease so I don't know what they mean I know how to say them I don't know what they mean so I have to look them up and then have to read so I'm going to take a look at this again and I thank you so much Gerald that I found this love Gail PS. Did you notice Ken talked on this to? I miss him. I hope he's having a great big party up in heaven.

[gerald]

Gail,  I frequently have similar problems with some of these articles. 

I usually end up with google open in another window where I can cut and paste
the words into to get their meaning/reference/context.  Once you have the first
couple nailed down it makes the article more readable.

[lavishgail]

Thank you Gerald! You're such a sweet man!