r/SilentReflux

I have been coughing greenish stuff a number of times a day. I had a I think covid in late april. I had 3 nights where I had coughin bursts when exhaling and they hurted as I hurted myself coughing once. These coughing bursts lasted for hours. First 2 days fever and sore thorat, then distorted smell, coughs and mucus. Didn't sleep like for 10 days. Went to ER and I wasn't even tested to see what I had and was given NAC 200mg and antibiotic drops for conjuntivitis. Eventually resolved I so I didn't go to ER during these 3 nights of coughing bursts however it was quite scary but I was not out of breath I just had to cough like 3 times on each exhale for hours at night then it stopped.

Im worried it caused permanent lung damage so I went to a pneumologist that from what I read has a lot of experience and has done research papers and so on.

What I find a bit surprising is that I have been prescribed antibiotics based on a picture I had of the mucus. I want to trust drs with their judgement but shouldn't you do a culture to check what im actually coughing out before prescribing antibiotics? The antibiotic is Augmentine 825 3x a day for 7 days btw. She also did not mention probiotics, I asked her and said I could take one and ask on the pharmacy, so im taking ProFaes4 ATB x1 a day 4 hours away from the antibiotic rounds.

Im on day 2 and so far only noticed soft stool. I hope I don't end up with also gut damage and this is not solved.

What I noticed is that post nasal drip that was almost instant after meals is not noticeable, not sure if due the antibiotic. But I still cough and I notice it more after eating. I clear my throat and sometimes notice this mucus. Sometimes is clearer and sometimes green. Please see pics below:

I mentioned silent reflux and she ruled it out. She auscultated me and she also did an x-ray and said my lungs are clear. However im still worried this mucus is from lung damage like bronquiestacy cause by the virus that would only show up in an HRCT.

This is the x-ray:

https://imgur.com/a/KoUOsbC

As for myself im near 37M and have never smoked or drinked. The only medication I take is eutirox 88mcg for hipo hashimoto. I don't notice shortness of breath. However this thing is making me worried. I may sometimes notice a tiny bit of something on my chest that im not sure if it may be mucus. I've read unvaccinated people have 28% chances of developing some sort of lung damage after covid and 12% for unvaccinated which keeps me thinking this may explain 2 months of coughing with some mucus. If you are interested you can check out the mucus here (ordered in chronological order since june 18th but I started taking pics I think a week after I started seeing this)

https://imgur.com/a/ZO3NooW

Any advice please let me know. For now I guess I will do the full 7 day rounds of antibiotics as prescribed and hope I don't end up with gut problems and this mucus stops. Posting here helps me sharing this with someone because I have a bit of anxiety.

Correct me if im wrong but what I gathered from this study is that PPI does basically nothing for silent reflux and the 24h pH impedance test is not accurate enough, you need another one. I think I have found a clinic that does this one (HEMII-pH). If anyone has done this test please let us know. Claims to be inconvenient for patients, but they also claim PPIs are overprescribed due inaccurate results with the other tests so perhaps worth considering. My case seems to be mild, but im on a AWD diet (more or less, checking with ChatGPT asking if the meal is ok) to see if it does something. I have tried no medications.

>Laryngopharyngeal reflux (LPR), also called respiratory reflux, may be defined as an inflammatory condition of the upper aerodigestive tract tissues that is related to the direct and indirect effects of gastroduodenal content reflux, which induces morphological changes in the upper aerodigestive tract [1]. The pathophysiology of LPR has not been fully elucidated, while the contributing factors remain unclear [2,3]. The clinical presentation is characterized by non-specific symptoms and findings, which makes the clinical diagnosis challenging [4,5]. Hypopharyngeal–esophageal multichannel intraluminal impedance-pH monitoring (HEMII-pH) may be considered as the gold standard for the diagnosis [1]. However, HEMII-pH is poorly available in many hospitals, expensive, and inconvenient for patients [6,7]. The non-specificity of symptoms and findings leads to under- or over-estimation of LPR [8] and patients are often unnecessarily treated with antiacid therapeutics (e.g., proton pump inhibitors (PPIs)) [9]. Indeed, LPR treatment is mainly based on PPIs that were never demonstrated to be superior to a placebo [9,10]. As of 2023, LPR remains a controversial and challenging condition, affecting 10% to 30% of outpatients consulting otolaryngology offices [1]. An increasing number of studies suggested the existence of several LPR profiles [11,12,13,14,15], which should be considered for more personalized diagnostic and therapeutic approaches.

Im not sure if going to an ENT or GI since all they seem to do is prescribing PPI's, and I've seen people get worse, and mine seems like a mild case. However im worried the vapours released by silent reflux may damage my lungs, and im not sure if covid scarred my lungs. I have had cough with mucus for 2 months, I was prescribed augmentin 3x 7days, I notice less mucus after 7 days, but not sure if 100% cleared. X-ray was clear and auscultation as well, but apparently you need a HRCT scan to diagnose smaller damages.

My fear here is being stuck in a loop of antibiotics if I go to the pulmonologist while silent reflux aspect is not treated, and also going to ENT/GI route and ending up on PPIs that make it worse.

Im not sure if the study claims alginates may be better for silent reflux? If someone reads this let me know what you make of it:

>5. Treatment

>The personalized treatment of LPR needs to consider the patient’s clinical features (age, body mass index, history), lifestyle (job, anxiety, stress), diet, and current or previous medications [84]. The treatment may consider (i) the management of LPR etiology (autonomic nerve dysfunction and diet), (ii) the prescription of medications to treat the consequences of reflux (symptoms and associated comorbidities), and (iii) the posttreatment management of disease to control LPR symptoms over the long term, avoiding medication as much as possible.

>5.1. Proton Pump Inhibitors

>PPIs have been considered as the primary medical treatment of LPR for a long time. However, contrary to GERD, the PPI efficacy over the placebo was never demonstrated in LPR disease [10]. The poor efficacy of PPIs may be attributed to the weakly acidic or alkaline pH of most pharyngeal reflux events, and the lack of GERD-related symptoms that are associated with distal esophageal acid reflux [10,68]. Interestingly, Pizzorni et al. recently demonstrated the non-inferiority of alginate over PPIs in a randomized controlled trial based on a 2-month empirical therapeutic trial [105]. Nowadays, for selected patients with a high-risk of acid GERD or LPR (e.g., obese or overweight patients), PPIs may be considered in empirical therapeutic trials in combination with alginate or magaldrate, which both act on weakly acidic or nonacidic reflux events [1,9,68]. The personalized therapeutic approach using PPIs needs to consider the patient’s age for the drug selection. Indeed, the several PPI classes report different clearance properties, which is important in elderly patients [106,107,108,109,110]. Esomeprazole has a more rapid onset of action and less variation in clearance rates than omeprazole. It has been suggested that the drug clearance decreases with age, exaggerating some of the differences between the PPIs and increasing the risk of drug interactions [106]. The reduction in plasma clearance mainly concerns rabeprazole, pantoprazole, and lansoprazole and may increase by 50 to 100% [106,107,108,109]. Esomeprazole may be primarily used in elderly patients because its clearance is not significantly affected by age [109]. Note that elderly patients are commonly taking several medications and there may have some drug interaction risks between PPIs and some medications, e.g., antiretroviral (HIV) drugs, anti-HCV drugs, cytostatics (e.g., methotrexate, dasatinib, erlotinib, nilotinib), itraconazole, immunosuppressants, and clopidogrel [106,108]. Finally, literature reviews report that PPIs were mostly used twice daily in LPR patients [10,68] but in practice, this regimen was only supported by one clinical study [109]. Nowadays, there is little evidence supporting the use of twice daily PPIs in place of a once daily dose (morning, fasting).

>Note that H2-histamine blocker use was not discussed in the present paper because they are less effective in terms of healing rates and symptom relief for GERD, esophagitis, and LPR [106].

>5.2. Alginate and Magaldrate

>A comprehensive empirical therapeutic approach of LPR should account for both acidic and non-acidic reflux, and should include the possibility of reactivation of tissue-bound pepsin within the laryngopharynx [9]. Alginate and magaldrate coalesce in the acidic environment of the stomach into a floating raft, which may last 1 to 4 h and physically prevents the refluxate from leaving the stomach. Sodium alginate may be endowed with bio-adhesive potential, a property primarily due to its polymer chain length and ionizable groups, that provides a protective biofilm on the mucosa of the esophagus and upper aerodigestive tract [8,111,112,113]. Unlike PPIs, alginate and magaldrate reduce the number of esophageal and pharyngeal reflux events and the deposition of enzymes in the upper aerodigestive tract mucosa [112,113]. Alginate may be effective in LPR when used alone [105] or when used in combination with PPIs [76]. In patients with HEMII-pH findings, alginate and magaldrate may be used when the pharyngeal reflux events occur, mainly post-meal or when patients with both LPR and GERD feel esophageal symptoms [80,84]. The clinical effectiveness of alginate and magaldrate was never compared in LPR disease. From a theoretical standpoint, magaldrate, which is a complex compound formed from aluminum hydroxide and magnesium hydroxide, could be more appropriate for patients with alkaline pharyngeal reflux events containing bile acids because magaldrate may directly bind bile acids and, consequently, decrease the damage to the mucosa [80,84].

Also magaldrate is recommended in some other cases, however, how do you know if to use alginate or malgadrate? It also claims H2's are less effective. I just find confusing they talk about PPI's later after claiming they are no different from placebo.

Perhaps a clinic that does HEMII-pH test is more refined and could choose a better treatment, but who knows, just leaving this here to see what people think of any of this.

Link: https://pmc.ncbi.nlm.nih.gov/articles/PMC10671871/