Chronic sinusitis and GERD or extraesophageal reflux disease

Chronic sinusitis and GERD

chronic sinusitis is a common clinical condition.  There is increasing evidence from observational studies that  both paediatric and adult patients with chronic sinusitis  frequently have associated GORD and EOR and that these  patients may benefit from medical antireflux therapy. GORD  and EOR may contribute to the pathogenesis of chronic  sinusitis by causing sinonasal congestion, compromised sinus  drainage, and inflammation.29  Otitis media  Otitis media with effusion (OME) is a prevalent condition  and the most common cause of hearing loss in childhood.  Recently, Tasker et al reported high concentrations (up to a  1000-fold greater than serum levels) of pepsin/pepsinogen in  59 of 65 middle ear effusion samples from children with  OME. The authors concluded that reflux of gastric juice into  the middle ear may be the primary factor in the initiation of  OME in children.  Using upper gastrointestinal endoscopy and 24 hour pH  monitoring, we prospectively assessed the coexistence of  GORD in consecutive adult patients with chronic secretory  otitis media (CSOM) or with a chronic refractory feeling of  pressure in the ear(s) (CRFP). All patients with CSOM and  most patients with CRFP had evidence of GORD (oesophagitis  and/or abnormal pH metry). Medical antireflux therapy  with open label PPI led to cessation of middle ear drainage  and CRFP after, on average, 11 weeks and four weeks,  respectively. These studies indicate that GORD may  directly cause or contribute to chronic ear problems, both in  children and in adults. RCTs evaluating the effect of  antireflux therapy are lacking.  Excessive throat phlegm and postnasal drip  It has been suggested that unexplained excessive throat  phlegm may also be a manifestation of GOR but formal  .( Chang A,et al ,2005)

so if any one suffering from chronic sinusitis with no response to treatment we should consider gerd as main cause if there are any digestive trouble or if the patient is on medical treatment for reflux.

pathophysiology of extraesophageal reflux disease

SGS is the most extensively studied laryngeal manifestation of GERD. There is popular agreement that PLPR is a causative factor in the development of SGS. However, the evidence linking these 2 pediatric conditions is weak and mainly based on either animal studies, or uncontrolled studies in humans. Trauma  and infection  are the 2 other etiological factors that have been implicated in the development of SGS.

 

extraesophageal symptoms of reflux eerd gerd
extraesophageal reflux

The damaging effects of gastric acid and pepsin on the subglottis have been demonstrated in animal models. Delahunty and Cherry , in their classic experimental study, demonstrated that the intermittent application of gastric acid to canine vocal cord produced granulomas, which was histologically similar to the early lesion of human SGS. In another canine model, application of gastric contents to subglottic mucosa once every alternate day for 3 to 4 weeks was sufficient to cause a 9-fold increase in SGS . (Squire R, et al ,2012)

Conversely, there was only a 1.5-fold increase in the control group. This study also showed a delay in reepithelization with exposure to acidic contents. Studies on the porcine subglottis showed that mucosa exposed to acid had reduced expression of messenger RNA (mRNA) for epidermal growth factor receptor (EGFR) . Downregulation of EGFR mRNA production was postulated to result in reduced mucosal turnover and impaired cellular repair. This resulted in basal cell hyperplasia and mucosal ulceration. In addition to disordered cellular repair, excessive deposition of connective tissue has also been associated with SGS. In vitro studies of human and rat tracheal tissue exposed to gastric juice displayed increased fibroblasts differentiation secondary to production of transforming growth factor beta 1 (TGF-h1) .( Jarmuz T, et al ,2004)

Presentation

There are no clinical presentations specific to PLPR. Patients often present with a wide range of atypical symptoms and signs. Parents generally do not perceive vomiting as a problem when it occurs no more than once daily, but are more likely to be concerned when vomiting is more frequent or when the volume of vomitus is large. Children may also present with excessive crying, irritability, failure to thrive, or feeding problems. Clinically, reflux symptoms are difficult to assess in infants and children. Although adults with esophagitis may complain of regurgitation, dysphagia, or heartburn, infants cannot describe their symptoms. Furthermore, the manifestations of PLPR often occur without the typical symptoms of reflux. Laryngeal symptoms that have been attributed to PLPR include hoarseness, a sensation of fullness at the back of the throat, postnasal drip with repetitive throat clearing, chronic cough, and laryngeal spasm. PLPR was found to be more prevalent in children with recurrent laryngotracheitis compared with a control cohort . An increased frequency of episodes of reflux in awake children with hoarseness has been previously reported .( Jamieson JR, et al , 2013)

laryngopharyngeal reflux  Gastroesophageal reflux disease

laryngopharyngeal reflux  Gastroesophageal reflux disease (GERD) in children is a common physiological occurrence. Accurate epidemiological studies on the incidence and prevalence of GERD are lacking. Vandenplas and Sacre-Smits estimated that the incidence of reflux in all infants is around 18%. In some conditions, such as tracheoesophageal fistula, neurological impairment, or oral motor dysphagia, the incidence is thought to be as high as 70% . Infants are predisposed to reflux due to a shorter intra-abdominal esophagus and an immature lower esophageal sphincter. Older children have an increased risk of nocturnal reflux due to a reduced rate of swallowing. In addition, esophageal acid neutralization by the alkaline saliva is less at night in children than in adults. Up to 50% of normal infants have regurgitation, which in the majority of cases, spontaneously resolves by the age of 2 years. Reflux predominantly occurs during the postprandial period and typically presents as regurgitation or vomiting . (Burton DM,  et al ,2010)

These symptoms, however, tend to resolve after the first year of life . Persistent reflux may, however, give rise to complications. Pediatric laryngopharyngeal reflux (PLPR) is thought to be implicated in the development of various respiratory and otolaryngological conditions, including refractory asthma, recurrent bronchitis, laryngomalacia, and subglottic stenosis (SGS) . Recent studies, linking reflux with otitis media, have fueled a new theory for the pathogenesis of this common childhood disease . (Rozmanic V,et al ,2011)

so if you have persistent upper respiratory symptoms not responding to treatment

you should first consider  GERD as extra oesophageal reflux may lead or reach upper respiratory lead to laryngopharyngeal reflux .

and when you receive treatment for gerd you will get improved as the main cause of your symptoms is the extraoesophageal acid reflux reaching the upper respiratory and the main target of our treatment is to stop the cause

when to change your life style or to improve diet to act against gerd it will decrease the extra-esophageal symptoms or respiratory symptoms

gerd and respiratory system

Extraesophageal reflux disease (EERD) represents a wide spectrum of manifestations mainly related with the upper and the lower respiratory system such as laryngitis, asthma, chronic obstructive pulmonary disease, cough, hoarseness, postnasal drip disease-sinusitis, otitis media, recurrent pneumonia and laryngeal cancer. Non-cardiac chest pain is commonly grouped among the esophageal syndromes by the Montreal Classification. but is not one of the common symptoms of typical gastroesophageal reflux (GER) which are heartburn and regurgitation . The diagnosis and recommendations on initial empiric therapy for patients with suspected reflux related non-cardiac chest pain is similar to those of extraesophageal reflux which is why it is included in this chapter. GER contributes to extraesophageal syndromes by two mechanisms: direct (aspiration) or indirect (vagally-mediated) mechanisms .

Reflux of gastroduodenal contents into the esophagus and hypophayrnx may be classified as either “high” or “distal” . The pathogenesis of “high” esophageal reflux involves reflux that traverses the esophagus and induces cough either by direct pharyngeal or laryngeal stimulation or aspiration and causes a tracheal or bronchial cough response. In “distal” esophageal reflux, cough can be produced by a vagally-mediated trachealbronchial reflex . Embryologic studies show that esophagus and bronchial tree share a common embryologic origin and neural innervation via the vagus nerve. Pressure gradient changes between the abdominal and thoracic cavities during the act of coughing, may lead to a cycle of cough and reflux . A disturbance in any of the normal protective mechanisms such as disruption of the mechanical barrier for reflux (lower esophageal sphincter) or esophageal dysmotility may allow direct contact of noxious gastroduodenal contents with the larynx or the airway . In this article we will discuss the latest knowledge of the association between extraesophageal manifestations of GER such as chronic cough, laryngitis and asthma as well as non-cardiac chest pain of esophageal origin.We will discuss the current recommendations on diagnosis and treatment options for this difficult group of patients  (Burton DM,  et al ,2010)