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.

treatment of PLPR are to

Treatment of eerd: The objectives in the treatment of PLPR are to

(1) heal any mucosal damage.

(2) to relieve symptoms, and

(3) to prevent recurrence. Management of pediatric reflux remains a challenge. This is because it is often difficult or even impossible to differentiate between physiological reflux and pathological reflux, that is, reflux causing complications. Current studies of treatment in the pediatric population are limited. There are no randomized controlled trials to evaluate the efficacy of antireflux therapy in children. The lack of trials can be explained by the difficulty in defining what constitutes PLPR. There are also no universally accepted and validated reflux scores for pediatric laryngeal signs. Obtaining ethical approval for studies is, therefore, difficult to justify. In addition, many of the drugs, especially the proton pump inhibitors (PPIs), which are the most effective antacids, are not licensed for use in children in several countries, including the United Kingdom and United States .( Meyer TK,et al ,2004)

Empirical treatment with PPIs, a common practice in the United Kingdom for adults with suspected laryngopharyngeal reflux, is therefore difficult to justify in the pediatric population. Conservative management such as dietary and lifestyle bbehavioralQ modifications may be successful. In many cases of PLPR, appropriate positioning of the sleeping child with elevation of the head of the bed, milk thickening, and fasting before bedtime are simple and often curative measures .( Hassall E. et al , 2005)

Reflux increases the risk of stenosis in animal models and is assumed to account for a significant number of failed laryngotracheal reconstruction attempts. The North Carolina Group recommends prophylactic treatment in every patient undergoing surgery, during which laryngeal mucosal disruption is anticipated. On the other hand, Zalzal et al found no direct correlation between reflux treatment and outcomes after laryngotracheal reconstruction. Drug therapy is probably the most successful treatment modality for PLPR and can include a combination of lifestyle changes with an antacid and/or a histamine-2 receptor antagonist. One would predict that the use of PPIs as part of a step-down therapy, as recommended in the treatment of adult GERD, would have similar effects in PLPR. This, however, cannot be proven until PPIs are licensed for use in children. Experience indicates that the most common error in prescribing PPI is underdosing. If the diagnosis is GERD and there is not a great response to PPIs, then the possible explanation would be an insufficient dose .( Chang A,et al ,2005) However, in PLPR, the data are inconclusive and studies focusing on adequate dosing in pediatric patients are lacking. Some centers will use PPIs in a few selected cases. In the United States, at present, only 2 PPIs are licensed for use in children, omeprazole and lasoprazole, but none is licensed for use of infants younger than 1 year. A recent Cochrane review of antireflux treatment for prolonged nonspecific cough in children and adults— a symptom that can be reflux related in up to 40% of cases— has confirmed what we had already suspected: there is insufficient evidence to definitely conclude that GERD treatment with PPI is beneficial for cough associated with GERD in adults. The pediatric data are even more inconclusive, and more double-blind, randomized, controlled, parallel-design studies are needed . Surgical intervention is reserved for patients in whom medical therapy has failed or symptoms are life-threatening. Antireflux surgery has considerable appeal especially if it achieves its goals, that is, cure of symptoms and avoid the need for long-term medication. However, most recent data document high rates of failure with morbidity and mortality . Children without respiratory symptoms tend to have better surgical outcomes. More randomized controlled trials are needed to assess results of antireflux surgery in atypical pediatric reflux. Candidates for surgery should have a definite diagnosis and should try prolonged and aggressive PPI treatment before being considered for fundoplication. .( Chang A,et al ,2005)

diagnosis of extraesophageal reflux disease

Diagnosis of eerd
There is, at present, no ideal diagnostic tool for laryngopharyngeal reflux detection. Various methods including pH monitoring, intraluminal impedance, scintigraphy, ultrasound, barium studies, fluoroscopy, and esophageal biopsy have been used both in adults and children. Results produced by these techniques, however, are not reproducible in patients with PLPR. The current gold standard diagnostic test for laryngopharyngeal reflux is the dual probe 24-hour pH monitoring. It is, however, an invasive test of low sensitivity, with an incidence of false-negative results reaching as high as 50% . The proximal probe is placed 2 cm above the upper esophageal sphincter and can be confirmed endoscopically. ( Jamieson JR, et al , 2013)
Manometry is often required to confirm positioning of the distal probe, which is normally placed 5 cm above the lower esophageal sphincter. Normal pH values of the distal esophagus have been well established in the literature . However, much controversy still surrounds what constitutes PLPR. The criteria used to diagnose GERD cannot be applied to PLPR because baseline pH values for the hypopharynx are still unknown. Some authors regard any number of episodes of pharyngeal reflux as positive evidence of laryngopharyngeal reflux .The total amount of time of acid exposure, expressed as a percentage of a 24-hour period, has been suggested by Postma et al as a suitable diagnostic criterion. Although widely used, pH monitoring does have limitations. For example, the probe does not detect nonacidic or gaseous reflux. Furthermore, ambulatory monitoring is time consuming, invasive, and not tolerated well by children. The technique of multichannel intraluminal impedance measures changes in electrical conductivity between 2 electrodes during the passage of a bolus of liquid, food, or gas within the esophagus .( Postma GN, et al , 2002)
Impedance catheters are placed within the esophagus and have multiple electrodes to allow detection of the direction and speed of the bolus. Further studies are required to validate the use of this modality as a diagnostic tool, but preliminary results are encouraging for the use of this technique in the paediatric population. Scintigraphy is useful for demonstrating reflux and for estimating gastric emptying. However, the correlation of scintigraphy with pH monitoring is poor . Esophageal biopsy and bronchoalveolar lavage does not correlate with endoscopic findings . Carr et al found that 65% of their study cohort who had GERD had normal esophageal biopsies. Furthermore, they found that 40% had normal laryngotracheal appearance on endoscopy.( Mandell DLet al ,2004)

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)


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