GERD+and+COPD

Gastro-esophageal Reflux Disease (GERD) and COPD COPD is believed to be a result of chronic airway inflammation as a response to inhaled particles, primarily from cigarette smoking (Pauwels, 2001). Importantly, COPD is believed to cause systemic effects which impact on the clinical manifestations and impact of the disease (Pauwels, 2001). One such systemic manifestation is the presence of Gastro-oesophageal Reflux disease (GERD). Whilst GERD is known to affect approximately 20% of the adult population (Locke, Tally, Fett, Zinmeister, and Meltom, 1997), there is evidence to support that GERD affects up to 61% of the population already suffering from COPD (David, Denis, Nouvet, Oasquis, Lefrancois, Morere, 1982). Although there is a paucity of research surrounding the exact prevalence of GERD with COPD, studies have reported that a high prevalence of GERD in other respiratory disorders such as Asthma or obstructive sleep apnea (Casanova, Baudet, del Valle Velasco, Martin, Aguirre-Jaime, Pablo de Torres, Celli, 2004).

It is likely that COPD causes GERD and not necessarily vice-versa, although more research is required to confirm this. Casanova et al., have suggested that there is a logical association between GERD and COPD, as COPD results in anatomical changes which could favour the development of reflux (Casanova et al. 2004). These changes include the flattening of the diaphragm and increased intra-abdominal pressure (op.cit). Additionally the use of medication such as theophylline and β2-adrenergic agonists which are sometimes used in the treatment of COPD, may decrease LOS pressure thereby facilitating the reflux of gastric content (Stein, 1980 and Crowell, Zayat, Lacy, Schettler-Duncan, 2001). Studies have found that this hypo-tense LOS can exasperate the present of GERD at night, when the sufferer is lying prone (Casanova, et al., 2004).

GERD can and does cause dysphagia, and in an estimated one-third of the population suffering from GERD, dysphagia will be the only presenting symptom (Mokhelsi, Morris, Huang, Curcio, Barrett and Kamp, 2001). This is because GERD causes oedema of the oesophagus; this swelling may continue all the way to the pharynx, or even the epiglottis. Swelling in the epiglottis may prevent the epiglottis from making the proper adjustments necessary for a safe swallow, thereby causing the sufferer to aspirate on small amounts of stomach acid.

GERD is not however the main culprit to blame for the prevalence of dysphagia in the COPD population. GERD plays a more indirect role in that GERD can exasperate COPD (Rascon-Aguilar, Pamer, Wludyka, Cury, Coultas, Lambiase, Nahman and Vega, 2006). Exasperations of COPD are caused by airway irritants and upper-respiratory infections; gastro-oesophageal reflux constitutes such airway irritants (Rascon-Aguilar et al., 2006). These exacerbations of COPD lead to pronounced breathing difficulties which often results in an unsafe swallow, as discussed in other parts of this site. Thus, the practitioner can think of the relationship between GERD and COPD as a viscous cycle, in which COPD may be the cause of GERD and GERD in turn causes exacerbations of COPD; thus resulting in dysphagia for its sufferers.

In essence, GERD represents a modifiable risk factor for those with COPD and should be addressed during assessment and case history of patients. GERD symptoms are frequently undetected in this population as their symptoms can be atypical (Casanova et al, 2004). Nonetheless, COPD patients with frequent episodes of GER are twice as likely to be hospitalized, have an emergency department visit or unscheduled clinic visit when compared with COPD patients with less frequent episodes of COPD (Rascon-Aguilar et al, 2006). Thus it is important for the examining practitioner to investigate potential GERD in patients presenting with COPD, especially if the patients are presenting with frequent exasperation of symptoms.

References:

Casanova C., J.S. Baudet, M. Del Valle Velasco, J.M., Martin, A. Aguirre-Jaime, J. Pable de Torres and B.R. Celli. (2004). “Increased gastro-oesophageal reflux disease in patients with severe COPD.” European Respiratory Journal 23:841-845.

Crowell MD, Zayat EN, Lacy BE, Schettler-Duncan A, and Liu MC. (2001). “The effects of an inhaled β2-adrenergic agonists on lower esophageal function.” Chest 120: 1184-1189.

David, P., Denis P, Nouvet G, Pasquis P, Lefrancois R, and Morere P. (1982). “Fonction respiratoire et reflux gastro-cesophagien au cours de la bronchite chronique. [Respiratory function and gastro-oesophageal reflux during chronic bronchitis]. Bulletin European Physiopathologie Respiratoire 18:81-86.

Kennedy, JH. (1962). “Silent gastroesophageal reflux: an important but little known cause of pulmonary complications.” Dis Chest 42: 42-45.

Locke GR, Talley NJ, Fett SL, Zinmeister AR, and Meltom LJ. (1997). “Prevalence and clinical spectrum of gastroesophageal reflux: a population based study in Olsted County, Minnesota.” Gastroenterology 112: 1448-1456.

Mokhlesi B, Morris AL, Huang CF, Curcio AJ, Barrett A and Kamp DW. (2001). “Increased prevalence of gastroesophageal reflux symptoms in patients with COPD.” Chest 119: 1043-1048.

Pauwels RA, Buist AS, Calvery PM, Jenkins CR, and Herd SS. The GOLD Scientific Committee (2001). “Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global initiative for chronic obstructive lung disease (GOLD). American Journal of Respiratory and Critical Care Medicine 163: 1256-1276.

Rascon –Aguilar Ivan E., M. Pamer, P. Wludyka, J. Cury, D. Coultas, L. Lambiase., N Nahman, and K. Vega. (2006). “Role of Gastroesophageal Reflux Symptoms in Exacerbations of COPD.” Chest 130: 1096-11-1101.

Seemungal TA, Donaldson GC, and Paul EA. (1998). “Effect of exacerbations on quality of life in patients with chronic obstructive pulmonary disease”. American Journal of Respiratory and Critical Care Medicine 157: 1418-1422.

Stein MR, Towner TG, and Weber RW. (1980). “The effect of thephylline on the lower esophageal sphincter pressure.” Ann Allergy 45: 238-241.