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 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 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)
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.
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)