Down With Acid lite by Chris Robinson - HTML preview

Down With Acid Lite

A selection from the popular encyclopaedia, www.DownWithAcid.org.uk

Contents

Digestion Story                                                                                                                                1

How the Stomach makes Acid                                                                                5

Reducing Acid                                                                                                                                6

Antacids and alginates                                                                                                7

Acid Suppressants: H2 blockers, PPIs, PCABs                                8

Acid Reflux                                                                                                                                13

Extra-Oesophageal Reflux                                                                                                15

Reducing Reflux                                                                                                                19

Fundoplication, LINX                                                                                                21

Oesophagitis                                                                                                                                22

Barrett’s Oesophagus                                                                                                                23

Tests and Diagnoses                                                                                                                26

Endoscopy, Cytosponge                                                                                                27

24hr pH manometry, Bravo                                                                                                29

Oesophageal Cancer                                                                                                                30

Ablation: EMR RFA                                                                                                                33

Oesophagectomy                                                                                                                34

Swallowing Difficulties Achalasia, Barium Swallow                35

Swallowing Exercises, Dilatation                                                                36

Gastritis and Ulceration                                                                                                37

Anxiety                                                                                                                                                38

Index                                                                                                                                                40

The Down With Acid encyclopaedia first printed in 2015 but has now grown too large, and updated too frequently, to be printed in full.

This slimmed down edition attempts to provide the most popular pages in a handy sized book.

To learn more about the chapters in this book and for information regarding newer techniques and understanding, visit the online version which also includes links to abstracts of the scientific papers quoted.

Disclaimer

The content of this book is intended for patients and health care providers and is provided for information only. Information provided should be discussed with a qualified medical practitioner if readers have or suspect they have a health problem as it is not a substitute for direct professional medical advice or diagnosis.

Digestion Story

The GastroIntestinal Tract:

Part 1: We chew food and mix it with saliva, passing it as a bolus through the pharynx and the Upper Oesophageal sphincter in to the oesophagus. 

Stimulated by how much you chew, some of the enzyme amylase is produced with the saliva to help break down starches.

Part 2: The bolus slides down the oesophagus with the help of muscles in an action known as peristalsis, 

to the Lower Oesophageal Sphincter (LOS / LES) which relaxes to permit the bolus to enter the stomach.

This is the sphincter usually thought of when people speak of Acid Reflux or Gastro-Osophageal Reflux Disorder (GORD).

Part 3: In the stomach the bolus is churned with strong acid and some of the enzyme pepsin to break it down to a thick liquid chyme to pass on through the pyloric sphincter to the duodenum and small intestines where the most important processes of digestion, assimilation, take place. 

Food can spend up to 4 hours in the stomach depending on its consistency. 

Part 4: In the duodenum, digestive enzymes produced in the pancreas, including amylase to help break down carbohydrates and protease to help break down proteins along with bile from the gallbladder where it is stored, enter via the Sphincter of Oddi to commence the real part of digestion. Bile helps break down fats, acting like a detergent as acid doesn’t dissolve fats, and neutralising any excess remaining acid, with help of sodium bicarbonate also produced by the pancreas.

It then passes into the intestines which are lined with millions of villi, microscopic hairlike protuberances where nutrients are transferred to the small blood vessels they contain so they may be transported to the kidneys and liver to filter and send to the parts of the body that require them.

Chyme can take upto 4 hours traversing the small intestines.

Part 5: The Ileocecal sphincter marks the end of passing nutrients into the blood to the beginning of receiving waste products from the blood to add to the remaining indigestible material that continues through the intestines.

Part 6: Waste builds up and is contained until we are ready to excrete it via the Anal Sphincters.

Acid

The stomach is lined with parietal cells.

In response to sight, smell, taste on thought of food, the brain sends signals to activate acid production involving the neurotransmitter acetylcholine which causes the cells to change, becoming Proton Pumps that release hydrogen ions and make Hydrochloric Acid.

As food enters the stomach, the hormone, Gastrin is released due to the stretching of the stomach and the peptides and amino acids in the food. In turn Gastrin triggers Histamine release which, picked up by H2 receptors in the parietal cells, also stimulates acid production.

Soma
tostatin acts to inhibit acid production to maintain the correct balance of acidity by acting directly on the proton pumps as well as gastrin and histamine production.

For most people suffering acid reflux, the amount of acid produced is probably not the problem, it’s that the acid is refluxing to an unprotected location.

Reflux of acid is not due to too much acid but a weak Lower Oesophageal Sphincter.

Reducing Acid

Reflux of acid from the stomach is via an incompetent Lower Oesophageal Sphincter into the oesophagus which it burns causing oesophagitis inflammation which is the source of heartburn symptoms.

Once oesophagitis exists, some foods passing over it may further irritate it. These are your particular trigger foods that can vary from person to person but typically include acidic drinks and spicy foods.

Reducing heartburn

Simple antacids will neutralise acid in the oesophagus to provide fast relief but they are only a temporary measure, like putting a sticking plaster on a wound that needs a stitch. A permanent solution requires the oesophagitis inflammation to heal.

Note: Antacids neutralise acid in the oesophagus not the stomach!

To permit oesophagitis to heal:

Avoid any foods you have identified as a particular trigger for you.

Take an acid suppressant: either an “H2 blocker” such as famotidine, a “Proton Pump Inhibitor (PPI)" such as omeprazole or a Potassium Competitive Acid Blocker (PCAB) such as vonoprazan.
Note. These are powerful drugs that must be taken strictly in accordance with the printed patient information leaflet and for no longer than a couple of weeks without a doctor’s approval. It’s not that the drugs are harmful but they can mask the symptoms of oesophageal cancer.
These medicines do not reduce reflux - they just make it less damaging.

Reduce reflux by lifestyle modifications.

Antacids & Suppressants

Antacids

These work immediately on excess acid in the oesophagus. They do not prevent acid reflux occurring.

They are drugs that neutralise the acid. Most commonly they are made of

1.  Chalk, calcium carbonate. Examples are Tums or Rennie. Chemically, this reaction takes place:
CaCO3 + 2HCl → CaCl2 + H2O + CO2

(Calcium Carbonate + Hydrochloric acid gives Calcium Chloride (a harmless salt) plus water and carbon dioxide).

Warning. Excess calcium is filtered out of the blood by the kidneys where it may accumulate to form kidney stones. Excess calcium can also lead to calcification of the arteries which can cause myocardial infarction, heart attack. 

2.  Baking Soda (Sodium Bicarbonate) based, Example Alka Seltzer.

NaHCO3 + HCl → NaCl + H2O + CO2 

(Sodium bicarbonate (baking soda) + Hydrochloric (stomach) acid gives Sodium Chloride (common table salt) plus water and carbon dioxide gas).

Warning. Too much sodium in the diet can lead to high blood pressure, heart disease, and stroke.

Alginates

Gaviscon is the brand name of the white milky liquid that floats on the stomach contents as oil floats on water to reduce the possibility of reflux whilst also providing a temporary protective film to the lower oesophagus and neutralising the acid with an antacid component. (Some generic versions are now available, such as Peptac.)

Acid Suppressants

Unlike antacids, these do not neutralise acid already produced but prevent the stomach producing more.

They are best taken when the stomach is low on acid and about to make more. Half an hour or so before breakfast is optimal.

They do prevent acid reflux occurring.

H2 Blockers (or Histamine H2 Receptor Antagonists, H2RAs)

Examples: ranitidine (Zantac), famotidine, cimetidine.

These work to block the H2 receptors that receive histamine signals that tell the stomach to produce acid working proactively to reduce the amount of acid by preventing histamine signals reaching the parietal cells telling them to make acid.

They are not an instant antacid and are often prescribed to be taken in the evening to reduce nighttime acid.

They are generally effective for up to 12 hours.

In 2019, some batches of Zantac were found to have a higher level of NDMA than they should. Although there is no evidence to prove it, NDMA (N-nitroso dimethylamine) is thought to be carcinogenic. Ranitidine was removed from the shelves. The levels of NDMA found, however, were no higher than found on grilled meat. Further investigaton showed the samples were tainted by incorrect storage.

Proton Pump Inhibitors (PPIs)

Examples: omeprazole, lansoprazole, pantoprazole, esomeprazole (Nexium) – Research evidence has shown all PPIs are as effective as each other when taken in equivalent dose. (20 mg omeprazole = 30 mg lansoprazole = 40 mg pantoprazole = 20 mg esomeprazole.)

Side Effects

Side effects are rare but the most common include headaches, diarrhoea and constipation.

If affected, switching to an alternative brand usually works.

Associations

There have been claims PPIs are associated with more serious side effects, however, PPIs  have been shown not to be the cause.

Adverse claims have been propagated by the sensationalist media and lawyers but a correlation is not a causation. It is merely a “Umbrella Conundrum”.

The most commonly propagated myths are described below:

Cardiovascular risks are mostly caused by excess weight which can also promote acid reflux, hence the PPIs.

A paper from the American Journal of Gastroenterology found no link between PPI use and risk of cardiovascular events, the meta-analysis of randomised controlled events, Researchers included data from 52 placebo-controlled trials, with 14,988 patients finding "Cardiovascular outcomes were infrequent in randomized trials of PPIs."

Dementia is related to aging. As we age, we lose muscle tone which can result in more noticeable acid reflux, hence a greater likelihood of taking PPIs.

A study, "Association of Proton Pump Inhibitor use with Incident Dementia and Cognitive Decline in Older Adults" concluded, "In adults ≥ 65 years of age, PPI and H2RA use were not associated with incident dementia, CIND, or decline in cognition over time. These data provide reassurance about the safety of long-term use of PPIs among older adults."

Kidney diseases may be similarly caused and carry acid reflux symptoms prompting PPI usage.

"The causality between PPI use and increased mortality and disease risk can be questioned since most studies are observational. Confounding variables can greatly affect an observational study and explain the wide-ranging associations with the use of PPIs. Patients on PPIs are generally older, obese, sicker with a higher number of baseline morbidities, and on more medications than the compared PPI non-users. These findings suggest that PPI users are at a higher risk of mortality and complications based on pre-existing conditions."

Osteoporosis occurs most frequently in women around the menopause when oestrogen levels fall. That hormone protects the bone but also against acid reflux which will occur during pregnancy. As oestrogen levels fall, women start noticing heartburn and start taking PPIs at the same time as experiencing bone loss.

A paper,  Is Estrogen a Curse or a Blessing in Disguise? found " Estrogen can be used to protect the mucosa from GERD induced injury and its
complications like metaplasia and cancer."

PPIs and cancer protection.

There has been research that shows PPIs have a chemo-protective effect. One suggesting, "PPI use was associated with a 71% reduction in risk of OAC."

Another found, “PPI use to be associated with 41% lower risk of Barrett's oesophagus progression to OAC after adjusting for multiple confounders."

The AspECT trial (Aspirin + Esomeprazole Cancer protection Trial) found, "people who took this combination for at least seven years were 20% less likely to develop oesophageal cancer than if they had been untreated."

And another paper found, “The proton pump inhibitor pantoprazole disrupts protein degradation systems and sensitizes cancer cells to death under various stresses” looking at the possible mechanism for this.

PPIs have also been found to have a possible chemo-protective effect on some other cancers.

"Basic research studies ... suggested that PPI may even have a protective effect against ColoRectalCancers"

 A Nested Case-Control Study of 23 Million Individuals" found "The use of PPIs was significantly associated with reduced risk of breast cancer and ovarian cancer" and "PPI exposure was associated with a significant decrease in cervical and endometrial cancer risks."

Potassium Competitive Acid Blockers (PCABs)

Examples: Vonoprazan, Tegoprazan.

These are the latest type of acid suppressant with many claims they could be better than PPIs as they don’t need an acid environment to activate them: “it can be taken without food because it is quickly absorbed. Vonoprazan accumulates in parietal cells under both acidic and neutral conditions. It does not require an acidic environment for activation.”

“In this rapidly evolving field, novel drugs such as potassium-competitive acid blockers (P-CABs) show promising potential.”

“The efficacy of vonoprazan was comparable with PPIs for the treatment of peptic ulcers following Endoscopic Mucosal Disection.”

There have been a number of studies comparing efficacy of PCABs with PPIs with the most common conclusion being they are “non-inferior” to PPIs.

From AGA Clinical Practice Update: “P-CABs Can Help When PPI Therapy Fails, "Clinicians generally shouldn’t use potassium-competitive acid blockers (P-CAB) as first-line therapy for acid-related conditions, nonerosive gastroesophageal reflux disease (GERD), or peptic ulcer disease,. ... However, P-CABs are recommended in place of proton pump inhibitors (PPIs) for most patients with Helicobacter pylori and other conditions where patients haven’t responded to PPIs."

Whether or not PCABs demonstrate a similar chemo-protective benefit to PPIs is yet to be determined.

Acid Reflux

Reflux of acid from the stomach is via an incompetent Lower Oesophageal Sphincter (LOS) into the oesophagus which it burns causing oesophagitis inflammation which is the source of heartburn symptoms.

Some common misconceptions regarding acid reflux.

     It is not from excess acid “overflowing”. (Stomach acid is made and regulated as required by the action of hormones.)

     It is not caused by low stomach acid. (A theory suggested by a chiropractor wanting to sell useless supplements. It is obviously incorrect as stomach acid refluxing is sufficient to cause oesophagitis damage.)

     It is not caused by acidic foods - though they can cause heartburn symptoms by irritating oesophagitis.

     It is not caused by common drugs found in foods, like caffeine or alcohol, or even nicotine.

For many people, the Lower Oesophageal Sphincter doesn't work as well as it should permitting stomach contents to flow back into the oesophagus.

Hiatus Hernia

One of the most common reasons for reflux is a hiatus hernia.

The hiatus is the hole in the diaphragm the oesophagus passes through just above its junction with the stomach. In many people, the top of the stomach can push up through this hole. Known as a hiatus hernia, we don't always know why this happens. Some people may have been born with a larger hiatus enabling herniation to occur at a young age. For others, the upward pressure caused by excess body fat may be the contributing factor.

For most people a hiatus hernia will cause no problems but for others, their sphincter muscles may not be strong enough to keep the end of the oesophagus tightly closed.

Excess body weight and abdominal fat can put pressure on the stomach pushing the contents back up the oesophagus, but even fit, normal weight people can experience reflux. Amongst other causes may be tight clothing, vigorous exercise after food or simply bending over. If the LOS isn't functioning properly, stomach contents may be forced back through it.

Extra-Oesophageal Reflux

(Also known as LaryngoPharyngeal Reflux (LPR) and others terms.)

If reflux persists, it can traverse the entire column of the oesophagus and breach the upper oesophageal sphincter, a group of muscles including the cricopharyngeus that open when swallowing to permit food to enter the oesophagus rather than the trachea (windpipe).

Reflux occurring here is correctly termed extra-oesophageal reflux but is often referred to as Laryngo-Pharyngeal Reflux (LPR for short), Respiratoty Reflux or "Silent Reflux". (The term 'silent reflux' is also often applied to lower oesophageal reflux where heartburn is not experienced.)

Even if the acid has been reduced or neutralised with acid suppressants or antacids, regurgitation of stomach contents and extra-oesophageal reflux (known as Non-Erosive Reflux Disorder, or NERD) can still cause damage.

From the top of the oesophagus it enters the respiratory system where it can aspirate into the throat, lungs, mouth and nose.

Irritating the lining of the throat and bronchi, inducing the production of excess mucous, sufferers frequently have the need to clear their throats. Aspiration deeper into the lungs can result in chronic cough as the lungs attempt to expel the foreign matter.

In the lungs, it can cause asthma like symptoms and even pneumonia.

Causing irritation to the voice box, it can result in hoarseness and sore throat.

Attempting to prevent extra-oesophageal reflux, the cricopharyngeus may tighten or spasm producing a feeling of a lump in the throat known as Globus.

At night, in attempting to prevent reflux, the cricopharyngeus may be responsible for restricting breathing causing obstructive sleep apnoea. 

Entering the mouth, reflux produces bad taste and bad breath. It can also cause dental erosion resulting in tooth decay or sharp edges to the teeth.

Ears

From the back of the throat, refluxate can travel via the eustachian tube to the ears where it may stimulate excessive wax production. This is more common in the right ear as lying on the right side results in more reflux than lying on the left. It can also result in tinnitus and dizziness.

Nose

Rising into the nasal chambers, excess mucous produced here can cause  post nasal drip producing cough and result in the sufferer sniffing frequently to constrain it. This may also give rise to a poor sense of smell (hyposmia), a distortion of smell (parosmia) or even fool the senses to imagine smells that aren't there (phantosmia).

Eyes

From the nasal passages, it can pass to the eyes via the tear ducts resulting in dry eye syndrome.

Prevalence of symptoms

In 2014 and 2017, surveys were conducted with 200 volunteers to assess the most common symptoms and the efficacy of treatments for them.

Comparing the responses of those taking PPI medication with those who didn’t, we can immediately conclud PPIs do not stop reflux.

These figures are from 100 respondents taking PPIs and 50 who were not.

We can probably assume those on PPIs had worse reflux issues prior to their medication rather than the PPIs causing more problems.

It doesn’t mean those with reflux should not take PPIs. If appropriate (i.e. if the patient has Barrett’s Oesophagus), PPIs may be required for life.

They may not stop the reflux, but they make it less damaging and reduce cancer risk.

The surveys also targetted those who had had surgery to reduce reflux.

The following table compares the reported symptoms from 50 volunteers from before and after Laparoscopic Nissen Fundoplication.

Because a number of members of the BarrettsEsophagusAwareness  FaceBook group, reported they did not experience heartburn, in 2023 we conducted surveys of 200 to see what symptoms they experienced.

We discovered that 48% of women and 22% of men did not experience the typical heartburn pain associated with oesophagitis.

For those women, their predominant symptom was globus.

For the men it was constant throat clearing.

Reducing Reflux

To prevent reflux naturally.

Think of the stomach as a balloon full of liquid. The Lower Oesophageal Sphincter should hold the neck tight shut. However, for some people it doesn't work as well as it should and the neck of the balloon isn't held as tightly as it should be. If the balloon is over-full, squashed, shaken or tipped, the contents can spill.

To reduce reflux, we must ensure we do not over-fill the stomach. Eating little and often is the best way.

Excess body fat will press on the stomach so it may be necessary to lose weight. Tight clothing should also be avoided.

Exercise after food should only consist of gentle upright activity (eg walking which will help the food to pass through the stomach) and not involve bending down.

It is important to keep upright whilst the food moves through the stomach.

NocturnalReflux

Leave at least 3 hours between your last meal and going to bed.

By raising the head of the bed by 15 to 20 cms (6 to 8 inches), gravity will help keep any residual contents in place.

Because the oesophagus joins the stomach on the right, reflux is harder if you lie on your left side.

Reflux Reduction techniques

If Reflux is causing serious loss of Quality of Life and cannot be managed by these lifestyle modifications, some surgical options may be considered.

It is not recommended otherwise because

All surgery carries risks.

Reducing reflux doesn’t necessarily mean stopping taking acid suppressants for those who need them. (i.e. Those with Barrett’s Oesophagus.)

Some of the previously tried methods failed after some years and had to be withdrawn. Whether this will be the fate of some newer techniques has yet to be seen.

It doesn’t reduce the risk of oesophageal cancer, as described in a 2024 paper, “Antireflux Surgery Does Not Prevent Cancer in Barrett’s Esophagus.”

Many options old and new including LINX, Stretta, Esophyx (TIF), MUSE, EndoCinch, Endostim, Enteryx, Gatekeeper, Angelchick, ARMS, ARMA, Omega PF, Reflux Stop, Fundopexy, Gastropexy, TESS, Reza Band, Medcline, iQoro, Side Sleep are all described in the main encyclopaedia, along with various fundoplication techniques.

 The gold standard is Laparoscopic Nissen Fundoplication.

The Hiatus Hernia is first repaired by pulling the stomach and its protective sheath, back down from the chest into the abdomen.

Fundoplication surgery involves stitching (or plicating) the top of the stomach (or fundus) around the base of the oesophagus to enhance the lower oesophageal sphincter and reduce reflux.

The knot so formed, reduces the chances of the stomach reherniating.

However, for those with motility problems causing swallowing difficulties, the tightening of the lower oesophagus is not recommended. In those circumstances the Toupet wrap may be a good alternative.

It is a 270° posterior wrap of the fundus around the back of the oesophagus designed to reduce dysphagia and the occurrence of a hiatus hernia.

A 2023 paper stated, "for patients in whom esophageal peristalsis is documented to be weak preoperatively, use of a partial wrap, or Toupet procedure, has often been used as an alternative to lessen the potential for postoperative dysphagia" and concluded, "We recommend its selective use in patients with preoperative esophageal hypomotility who are undergoing laparoscopic antireflux surgery."

LINX is widely touted. It is a bracelet of magnetic titanium beads inserted around the Oesophagus to augment the Lower Oesophageal Sphincter. These images show how it works.

However, there are some concerns about it migrating.

Oesophagitis

The mucosa lining the oesophagus produces mucous to aid movement of food to the stomach and to provide some protection to the surface layer (epithelium) of the oesophagus. However, acid refluxing can wash away some of the mucosal protection and come into contact with the lining itself. This is highly concentrated hydrochloric acid; strong enough to be able to dissolve metal, if you were to spill some on your hand it was cause significant scarring - which it can also do to the oesophagus.

Some foods may irritate the oesophagus in some people, causing heartburn.

Why some things hurt.

Pour lemon juice on your hand.

It feels wet but doesn’t hurt.

Stomach acid is as strong as battery acid. Pour that on your hand and it will cause major damage.

Now pour lemon juice on the scarring and it will hurt - but the lemon juice didn't cause the damage.

Although acidic foods and drinks are the most common triggers for heart-burn, we are all different and can have different triggers or none at all. We don’t really know why but it may be from behaviour learned in the womb or early infancy.

Simple antacids work well for occasional heartburn.

Stomach Acid will not break down fats and sometimes bile is permitted to reflux into the stomach to act as a detergent. If it refluxes into the oesophagus with acid, it can try to dissolve the tube itself.

To defend against acid erosion acid resistant cells may be produced here.                 This is known as Barrett’s Oesophagus.

Barrett’s Oesophagus

The stomach and intestines are protected against stomach acid by special columnar shaped cells and copious mucous.

The oesophagus doesn’t have that protection; it has smooth, squamous cells lining it and only thin mucous but under attack from refluxing acid and bile, the body can produce columnar cells at its base and provide goblet cells, that are normally found in the intestines, to produce thicker mucous.

This condition is known as Barrett's Oesophagus which is a permanent change. Sometimes Barrett's appears to go away but if it's not seen, it may be hidden in the corrugations of the epithelium or a second mucosal layer may have grown over it. The burning sensations may reduce or disappear adding to the illusion that the Barrett's has gone but Barrett's has no symptoms of its own.

However, these cells are unregulated and in a small minority of cases can mutate through stages called Low Grade Dysplasia (LGD) and High Grade Dysplasia (HGD).

Further mutations may now occur which can cause a proliferation of mutated cells which is Oesophageal AdenoCarcinoma: cancer!

The different grades that Barrett's Oesophagus may be described as, are:

1. Non-Dysplastic Barrett's Oesophagus (NDBO)

1a. Indefinite for Dysplasia (IND)*

2. Low Grade Dysplasia (LGD)

3. High Grade Dysplasia (HGD)

4. Neoplasia - initial stage of adenocarcinoma. (OAC)

*From a 2024 study, on a follow up endoscopy of 223 patients diagnosed IND, 22 (10%) were found to have dysplasia.

The researchers concluded that rates of prevalent dysplasia in Barrett’s esophagus patients are high in the first half-year after an IND diagnosis. They noted that Barrett’s esophagus patients are likely to need follow-ups with their providers within the first year of receiving an IND diagnosis.

This diagram from Johns Hopkins shows what the cells look like:

This metaphor depicts the Management of Barrett’s Oesophagus:

It is important to note there is no automatic progression.

A paper from Mayo Clinic suggests 5% of the population has Barrett’s.

This meme illustrates: Most Acid refluxers don’t develop Barrett’s.

Although Oesophageal AdenoCarcinoma is invariably a result of Barrett’s’ cells mutating, the vast majority with Barrett’s will not develop the cancer, particularly if they follow the management regimen of PPIs and surveillance scopes.

A quick 101 on Barrett's:

It's the permanent addition of acid resistant cells to the lower oesophagus to protect it against acid refluxing from the stomach. It will not change or go away but there's a small chance the cells could mutate to cancer. Barrett's has no symptoms of its own. Any symptoms are from oesophagitis or reflux.

Acidity or alkalinity of your diet doesn't change stomach acid. There is NO special diet to follow.

Acid doesn't cause reflux.

Acid suppressant medication (especially Proton Pump Inhibitors (PPIs) like omeprazole/Prilosec) do reduce acid but not reflux - just making it less damaging.

PPIs also reduce risk of Barrett's mutating to cancer.

Reflux is due to a malfunctioning Lower Oesophageal Sphincter that's supposed to keep the oesophagus tube pinched tight shut when food isn't being delivered to the stomach. This is most frequently due to a Hiatus Hernia.

Reflux needs to be managed by lifestyle modifications.

If reflux cannot be managed normally and it is considerably impinging upon Quality of Life, surgical options are available.

Tests and Diagnoses

Self Diagnosis.

You may be aware of reflux or regurgitation or of the acid burn we refer to as heartburn and the chapter about Extra-Oesophageal Reflux (Page 5) may make you aware of other possible symptoms you may not have previously considered pertinent. (N.B. Not everyone with acid reflux experiences heartburn.)

Acid reflux is one of the most common ailments the doctor sees. You will often be told to get antacids from the pharmacy. If concerned, he may try Diagnosis by PPI:

Prescribe a PPI like omeprazole (Prilosec) for a few weeks.

If the patient doesn’t come back, assume their oesophagitis (cause of heartburn) has healed.

If the patient returns, the next step depends on risk factors. Those most at risk are obese, white, middle aged men with a familial history of oesophageal cancer. They may be referred to a gastroenterologist - step 5.

If they return and don’t meet the risk criteria, they will get an increased dose of PPI and thence return to step 2 but if they return again, move onto step 5.

The gastroenterologist may decide to examine their oesophagus using an endoscope or a newer alternative.
The full encyclopaedia looks at all the following: Endoscopy, Cytosponge, Endosign, EsophaCap, EsoCheck, PillBot, MAGIC (Multifunctional AblativeGastrointestinal Imaging Capsule), Wats3D, Spit Test, Breath Test, Peptest, 24 hr pH manometry, Bravo 48 hour monitoring, Barium swallow, Barium meal, Heidelberg Test, EndoFLIP

Endoscopy (more accurately Gastroscopy or Oesophago-Gastro-Duodenoscopy (OGD)).

The long fexible tube about a centimetre in diameter, houses a fibre optic bundle for viewing, one or two other bundles to deliver light and two or three other channels to deliver water and air as required together with a channel for instruments such as snares to be inserted. In addition there are cables to enable the operator to manoeuvre the tip which is flexible enough to be turned to look back at itself.

The endoscopist guides the scope using hand controls whilst he looks at a monitor usually behind you. If anything requires further investigation (e.g. suspected Barrett's’ cells), he'll pass a wire snare down the instrument channel to take a biopsy - a small tissue sample. This is a painless procedure; most people are unaware it has been done.

The endoscopist may expect to see something like these (from Medtronics):

Left to Right

Normal, healthy oesophagus.

Oesophagitis.

Barrett’s’ cells.

If the endoscopist sees anything of concern he/she will record details and send biopsies to pathology for analysis.

Biopsies

The mined biopsies, each smaller than a grain of rice, are placed in a fixative to preserve them and sent to the pathology laboratories where they are embedded in paraffin wax. When set, this is then sliced very thinly to create microscope slides to be examined by a skilled histopathologist looking at the structure of the cells. The presence of columnar and goblet cells is indicative of Barrett's Oesophagus.

Diagnosis of Barrett's Oesophagus requiring endoscopy and pathology is time consuming and expensive so doctors may be reticent about referring patients reporting heartburn, usually curable with an antacid, meaning patients with Barrett's may be missed.

CytospongeTM may be the answer. The capsule can be swallowed like a tablet whilst keeping hold of the string. The capsule dissolves, the sponge expands and it is pulled back out by the string.

The millions of harvested cells are removed by soaking the sponge in a histological fixative and centrifuging the resultant mass. Biomarkers have been identified that indicate a particular possibility of Barrett's Oesophagus and for Oesophageal cancers.

If these biomarkers are detected, the patient will require a normal endoscopy for further appraisal.

The advantages of Cytosponge are it is considerably cheaper than an endoscopy, takes less time, requires less skill (a nurse at a GP practice could administer it) and it could be used as an initial screening for any patient who reports persistent heartburn so more cases of Barrett's may be discovered before it's too late.

Endosign is an improved delivery system for cytosponge, containg the sponge and string within a plastic delivery device for a nurse to be able to administer easily.

Cytosponge is the first of the newer diagnostic technologies to be rolled out. Check the full online encyclopaedia for updated news on the other devices in development.

24 hour pH manometry test

The testing measures the pressures at the lower oesophageal sphincter and acid levels over a 24 hour period. You will usually be off medication for a few days before and during the test.

The initial test takes about 20 minutes. A thin tube is passed through the nose and down the oesophagus via the back of the throat. This will measure pressure changes as you swallow small amounts of water, about a teaspoonful at a time, fed to you by the nurse running the test. The tube is then replaced by a wire with a sensor to measure acidity and left in place for 24 hours.

48 Hour Bravo monitor

The Bravo capsule essentially does the same job. Using an endoscope, it is attached to the wall of the lower oesophagus and transmits the data to the recorder using a radio signal rather than requiring the wire protruding from the nose. It is usually used over a 48 hour period. The recorder is returned to the hospital while the capsule breaks free and passes out through the digestive system within a few days.

Oesophageal Cancer

There are two types of cancer of the oesophagus; Oesophageal Squamous Cell Carcinoma (OSCC) and Oesophageal Adenocarcinoma (OAC).

Squamous Cell Carcinomas are more prevalent in Asian countries whilst Oesophageal Adenocarcinomas are more prevalent in UK, Europe and America.

SCC is more likely to be found in the upper oesophagus and is heavily linked to drinking and smoking. Rates of SCC are remaining static.

OAC is more likely to be found in the lower oesophagus and is heavily linked to acid reflux and Barrett's. Rates of OAC are rising rapidly.

How does Barrett’s become cancer?

Cells multiply through a process known as the cell cycle. Before cells can multiply and divide into other cells, they have to make exact copies of their DNA. DNA is the genetic code that is in all the cells of our bodies and is exactly the same code in each cell no matter what tissue the cell is from.

G0 is the resting stage.

G1 to G2 the cell duplicates.

M, the old cell can die.

It is possible for copying errors to occur.

According to the Nowell Hypothesis, a few errors of this type can result in cancer.

Stages of cancer

This cross section diagram of the oesophagus shows OAC cancer stages T1, T2 and T3 as described below.

Survival for oesophageal cancer, from Cancer Research UK. (N.B. These statistics combine OSCC and OAC):

Stage 1

Almost 55 out of 100 people (almost 55%) with stage 1 oesophageal cancer will survive their cancer for 5 years or more after diagnosis.

Stage 2
30 out of 100 people (30%) with stage 2 oesophageal cancer will survive their cancer for 5 years or more after diagnosis.

Stage 3
Around 15 out of 100 people (around 15%) with stage 3 oesophageal cancer will survive their cancer for 5 years or more after diagnosis.

Stage 4
There are no 5 year survival statistics for stage 4 cancer because sadly many people don't live for that long after diagnosis.

Footnote from Barrett's UK:

Barrett's surveillance aims to find mutation before it reaches stage 1 when it can be stopped in its tracks with ablation.

Until the beginning of this century, removal of oesophageal cancer meant removal of the oesophagus (oesophagectomy) but a revolution in the treatment approach for early oesophageal neoplasia has taken place in the past decade. Oesophagectomy has gone from being the primary treatment for such patients to a rarely used salvage therapy. Multiple modalities, including EMR, ESD, RFA, cryotherapy, and APC, often used in combination, yield complete eradication of dysplasia and Barrett's in over 90% of treated patients. Due to the efficacy of endoscopic therapy, timely diagnosis of esophageal neoplasia to allow for the application of these less-invasive therapies is receiving more emphasis now than ever. The next important breakthrough in oesophageal cancer will involve broad-scale screening methods, to allow for early detection of oesophageal neoplasia.

The full encyclopaedia details all these ablation techniques: Endoscopic Mucosal Resection (EMR), Endoscopic Submucosal Dissection (ESD), Radiofrequency Ablation (RFA), Argon plasma coagulation (APC), Multipolar electrocoagulation (MPEC), Cryotherapy, Photodynamic therapy (PDT), Oesophagectomy

Ablation

If Barrett’s Oesophagus cells are found to have started mutating, they may be removed by ablation therapy which is usually very successful for dysplasia (low or high grade) and even cancer at stage T1.

The most commonly used are Endoscopic Mucosal Resection (EMR) and Radio Frequency Ablation (RFA) often in combination with each other.

Endoscopic Mucosal Resection (EMR)

In this treatment.  a small area of cells is removed using a wire snare passed through the endoscope.

It is frequently used in combination with other techniques, e.g. RFA.

EMR removes the lumpy bits first and RFA cleans up the smoother areas.

Radiofrequency Ablation (RFA)

RFA is applied during an endoscopy procedure to destroy the abnormal Barrett’s oesophagus lining. The lining which regrows is normal, squamous mucosa.

The Catheter has a balloon at the tip covered by a band of radio frequency electrodes.

 Once the electrodes of the balloon are positioned on the desired treatment area the balloon is inflated and a short burst of electrical energy delivered burning off a 3cm circumferential segment of Barrett's tissue within the oesophagus

 For patients with Barrett's Oesophagus lesions longer than 3cm, the Catheter is simply repositioned and the ablation steps are repeated.

Oesophagectomy

Surgical removal of part or the whole of the oesophagus and or part or whole of the stomach may be performed to remove oesophago-gastric cancers.

The amount removed and the type of surgery offered depends upon the extent and stage of the cancer and the health of the patient.

The diagram shows the typical reconfiguration where just the oesophago-gastric junction has been removed. 

This type of surgery used to be offered to deal with cases of High Grade Dysplasia to prevent progression to cancer but with the advent of highly effective ablation methods, this is not so common.

From a 2021 summary, “Among ablative techniques, RFA continues to have the most data to support its safety, efficacy, and treatment durability … patients should continue in a strict surveillance protocol after  eradication therapy due to the unpredictable risk of recurrence.”

Ablation of Non-Dysplastic Barrett's is not recommended because:

 The risk of Barrett's cells mutating is really very small.

 All procedures carry risk.

 Because Barrett's developed previously, it is likely to develop again.

 Patients receiving ablation therapy are recommended to remain on acid suppressants and surveillance as before (to ensure no new Barrett's).

 Patients previously worried about their Barrett's mutating to cancer, will be worried about new Barrett's occurring instead.

Swallowing Difficulties

Swallowing difficulties (dysphagia) may be attributable to a number of causes. Anyone experiencing swallowing difficulty should see their doctor.

Globus is a feeling as if something is sticking in the throat. It is commonly reported by refluxers and of the 48% of women with Barrett’s Oesophagus who did not experience the typical heartburn symptoms of the oesophagitis that must have existed, it was their predominant symptom.

It is caused by spasms of the cricopharyngeal muscle that constitutes the Upper Oesophageal Sphincter attempting to prevent aspiration of extra-oesophageal reflux.

The main treatment is to reduce reflux. Other possible treatments may include relaxation techniques or medication and exercises to help relax and strengthen the throat muscles.

Strictures, narrowing of the oesophagus, may be due to many factors. Mostly benign, they may be due to scarring from oesophagitis, a hiatus hernia or a dysfunctional lower oesophageal sphincter (achalasia) as described below. In some cases, strictures can be caused by tumour.

Achalasia is a comparatively rare condition whereby the Lower Oesophageal Sphincter may not open properly for food to move into the stomach. We do not usually know why this develops in some people.

A Barium Swallow looks at swallowing disorders. A drink containing Barium Sulphate is administered. It blocks the passage of x-rays which can make its progress through the body visible. Standing in front of an X-ray scanner, you drink the liquid and the scanner watches its progress through the oesophagus.

Swallowing exercises.

Standing upright, head back, mouth shut, force a few dry swallows. 

Repeat several times a day.

Eating.

Cut food very small.

Take a small mouthful.

Chew and chew.

Try and force a swallow.

Follow with a sip of water to help push it down.

Wait for a burp as displaced air escapes to permit the next bolus.

Repeat.

Treatments

Drugs may be prescribed which can relax the muscles. They are usually allowed to dissolve under the tongue half an hour before eating. They relax the pressure on the lower oesophageal sphincter temporarily but are not a long term solution.

Botox injections delivered endoscopically into the musculature provides sphincter relaxation lasting a few months or up to a year.

Dilatation

During the procedure, a balloon is positioned in the oesophagus by a special endoscope and inflated to stretch the stricture.

Myotomy is surgery usually performed laparoscopically to cut the muscle fibres that fail to retract providing a permanent solution but may have complications.

In POEM (PerOral Endoscopic Myotomy), the surgical procedure is conducted endoscopically.

Gastritis and Ulceration

This is inflammation of the lining of the stomach which can include the creation of ulcers: areas where the surface mucosa has erupted and can fracture and bleed.

Symptoms include:

Abdominal pain

Nausea

Bloating

Loss of appetite

Bleeding seen in vomit or stools

Causes:

Helicobacter Pylori: the bug tunnels into the stomach lining and can cause the stomach to create more acid to combat it.

NSAIDs: Non Steroidal Anti-Inflammatory Drugs like ibuprofen, aspirin etc cause irritation to the stomach lining.

Autoimmune Disorders: Some can attack or rritate the stomach lining.

Bile reflux.

Other possible suggested causes include stress and alcoholism.

Treatment:

PPI medication to reduce the amount of acid

Eradication of H-Pylori if found.

Avoid any trigger foods you identify.

Avoid NSAIDs.

Gastric Intestinal Metaplasia (GIM) = addition of goblet cells.

This is directly comparable to Barrett's Oesophagus.

1. Columnar cells + goblet cells = Intestinal Metaplasia (Barrett's or GIM) which could mutate to
2. Possible dysplasia which could mutate to
3. Possible cancer.

Untreated, that risk is about 0.25% for both GIM and Barrett's.

Anxiety

Does Acid Reflux cause anxiety or does anxiety cause acid reflux?

Recent studies show an association.

"It may be that having an anxiety disorder predisposes you to develop GERD, either through psychological factors or physiological factors that increase stomach acid. Conversely, it may be that GERD symptoms like insomnia, chest pain, and heartburn create a stress response in the body which triggers anxiety."

“We found high levels of depression and anxiety in GERD patients with and without chest pain. Anxiety and depression levels were significantly higher in patients with chest pain than in those without chest pain. This may be due to the patient’s perception that chest pain is a sign of serious ailment, which may contribute to higher levels of psychological burden which includes anxiety and depression”

"A significant group of Barrett’s patients reported high cancer worry which was associated with reflux symptoms in Non-Dysplastic Barrett’s patients and a younger age, and a (family) history of the diagnosis oesophageal carcinoma in Barrett’s patients treated for (early) neoplasia. Physicians should communicate about the actual cancer risk unambiguously, which leads to greater patient understanding and may therefore positively affects health outcomes."

Is the anxiety of the diagnosis of Barrett's Oesophagus worse than the reality of the prognosis?

Diagnosed with a condition they’ve never heard of, patients turn to the internet where they will find scare stories, particularly in regard to the possible progression to cancer.

From some recently published papers:

"Patients with Barrett's Oesophagus overestimate their risk of developing oesophageal adenocarcinoma and will accept low success rates and high risk of complications to undergo endoscopic therapy. "

"greater emphasis on patient-centered communication strategies during conversations about Barrett's esophagus and cancer risk may be helpful for reducing patients' psychological distress"

"After you tell a patient that they have Barrett's and that only a very small minority develop cancer, just stop. Stop and acknowledge that you said a very scary word, 'cancer.'"

"Evidence is mounting that disease labels affect people’s psychological responses and their decisions about management options"

"Using loaded labels such as “cancer” can make patients more worried ... which can cause them to choose more aggressive management options—with more risk of harm." 

"After a BO diagnosis, patients are offered a clinical consultation to discuss cancer risk, surveillance plans and symptom control. They should also be provided with information of patient support groups. No specialist psychosocial counselling is available for patients prior to or following a diagnosis of BO. … There may be a need to consider offering further psychosocial care to people with morphological risk conditions like BO. Lessons might be learnt from the field of genetic counselling."

It does have to be stressed, although there is an increased risk of cancer, for those identified as having Barrett’s the risk is very low particularly as they will receive medication that probably reduces those risks and regular surveillance scoping would detect pre-cancerous changes early enough to be successfully treated.