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Heartburn and Its Absence
Objectives
GERD Review
Extraluminal GERD
Inherent Protective Mechanisms
REILLYS
"Food" for intellectual "digestion" …Dr. Kurt Barrett
Autonomic Activation Syndrome (AAS)

 



Heartburn and Its Absence.

"What's so bad about some heartburn?" "Lots of people get heartburn, just avoid eating things that seem to cause the sensation", is the typical sentiment. "It doesn't bother me that much; I just take something".

In 1976 the incidence of heartburn was reported to be 15%. In 2001 the commonly reported incidence was 45%. The most recent USA surveys report heartburn once a month or more in 60% of adults. The occurrence of heartburn has quadrupled! WHY? What does this really mean?

The symptom of heartburn usually represents acid reflux. Thus acid reflux is becoming more common all the time. Where the confusion begins may be with the converse: "when a person has significant reflux of gastric acid, heartburn will occur." This statement is absolutely not true. Heartburn is a poor surrogate for reflux. Yet this concept is the MAINSTAY of GERD (gastroesophageal reflux disease) therapy. If no heartburn is present then the patient is considered a candidate for stepdown therapy or discontinuation of prescription medication. This and other commonly held concepts about GERD are not supported by the scientific evidence or clinical experience.

Current concept: if you don't have heartburn, there's nothing wrong with your esophagus.

Reality: the majority of patients with ENT (ear/nose/throat) GERD induced symptoms rarely or never have heartburn (they rarely have mucosal change at endoscopy).

Current concept: in the absence of endoscopic mucosal tissue damage no prescription medication is necessary.

Reality: endoscopically negative GERD patients (NERD) commonly require long term twice daily dosing with the most potent of the prescription strength, antisecretory medications to maintain control of symptoms (some may require life long therapy).

Current concept: when your esophagus heals up the PPI (proton pump inhibitor) can be stopped.

Reality: 80% or more of erosive esophagitis patients will relapse within 6 months of stopping therapy.

GERD is a disorder that affects quality of life in a negative way. It is associated with noxious symptoms like headache, sinus problems and asthma. A condition known as Barrett esophagus can develop in 10 to 25% of GERD patients. GERD causes this condition. Barrett's is an identifiable risk factor for cancer (adenocarcinoma) of the esophagus, the occurrence of which is doubling every 5 years since 1970.

As common as heartburn is, the MAJORITY of GERD sufferers RARELY HAVE HEARTBURN because our bodies are so clever at protecting us!!

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Objectives:

3/26/04 Grand Rounds, Battle Creek Health Systems presentation by Dr. Kurt Barrett - Beyond the Esophagus: Extraluminal GERD

- Acknowledge that symptoms related to GERD represent one of the most common, and often confusing, health problems seen in primary care. (University of Virginia School of Medicine, 2003)

- Name two or more respiratory problems that can be associated with GERD.

- Name two or more of the synonyms for extraluminal GERD.

- Acknowledge that heartburn/indigestion can be absent or infrequent despite ongoing pathological gastroesophageal reflux.

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GERD review---Nov. 2004

Gastroesophageal Reflux Disease (GERD) is dramatically affecting our society and its occurrence is on the rise. In fact, it is so common that the dividing line between that which would occur normally (physiological) and pathological needs to be more clearly defined. This is not as easy as it may seem. World class authorities will acknowledge that everyone in our society has reflux after meals. In other "primitive" cultures (less industrialized peoples) there is NO REFLUX AFTER MEALS (post-prandial retrograde movement of gastric contents into the distal esophagus). It is counterintuitive to accept the presence of digestive contents in contact with the squamous epithelium of the esophagus as "physiologic".

I believe the concept of post-prandial reflux as a "physiologic" event to be an honest disagreement, the result of diverse perspectives. If this is "normal"(physiologic) why does it not occur in all cultures? It may be "normal" for the given circumstances. By that I mean it is normal for the patellar reflex to occur when the tendon is rapidly depressed by the reflex hammer: similarly it is "normal" for the body to respond to refluxed gastric contents in a somewhat predictable manner. Hence this makes the bodies response to the event of gastric contents contacting esophageal squamous epithelium a "physiologic" event: a reflex mediated response aimed at the autonomous clearance of the contents of the esophagus. This is a desirable result. But the stimulus that initiated the response must logically be considered a pathological event in that it serves no plausible benefit aside from allowing hydraulic pressure relief. And it does NOT happen in all societies!

It could be argued that reflux of non-food, acidic gastric content periodically might be "natures way" of maintaining a sterile luminal environment in the lower esophagus. Vomiting is the only other occurrence of stomach contents moving retrograde in the esophagus.

The assertion by gastroenterologists/scientific researchers that post-prandial reflux and other numerous episodes of retrograde movement of gastric contents are to be ignored is based on observation. What we do (and call scientific) is based on what was done by the researcher/scientist that preceded us. Thus when new information/concepts emerge, any departure from the established norm is automatically disputed and opposed. Thus change comes slowly if at all.

A blatant example is the arbitrary placement of the pH electrode 5 centimeters above the lower esophageal sphincter. Why not 6 centimeters, 4 centimeters, 1 centimeter or, for that matter, 10 centimeters? The usual answer is "That's the way it's done". Why? I have found in the history of pH testing that the first pH electrode placement in the1950's was able to recognize the abrupt acid/alkaline change. In the interest of not being influenced by vigorous tilt table positioning the electrode was withdrawn "5 centimeters". Given the rudimentary equipment and the seminal nature of the research, it seems logical. It also means that all these years later the probe is placed 2 inches (5 cm) beyond nature's barrier to gastroduodenal reflux. WHY?

In 1985 the Archives of Internal Medicine reported…"reflux and its many manifestations are extremely common problems". In 1983 The Journal of Pediatric Surgery reported … "bradycardia caused by gastroesophageal reflux …may be an important cause of sudden infant death". Gastroenterology, 1983, concluded…"esophageal acid perfusion tests…can induce myocardial ischemia". There are innumerable citations since the 1980's pronouncing the common and pathological nature of refluxed digestive contents.

Numerous correlation's with respiratory pathology, multiple system involvement including syncope and seizure have been documented. Due to the complexity of the protective reflexes involved, it appears difficult to prove a "cause and effect" relationship. With the evolving popularity of potent antisecretory drugs more of these associations are becoming apparent to alert clinical observers. This unique situation appears to be somewhat of a paradox given the magnitude of the rift between research findings and clinical outcomes. I believe the research seems lagging, stifled by conventional wisdom, political and litigation concerns.

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Extraluminal GERD: Beyond the Esophagus
Kurt A Barrett D.O. Grand Rounds, Battle Creek Health Systems…3/26/04

Synonyms: a reflection of the ubiquitous nature of GERD

- Atypical GERD

- Silent GERD

- Supraesophageal GERD

- Extraesophageal GERD

- GORD…"over seas" the food tube is the oesophagus hence the designation

- NERD…nonerosive GERD

- ENRD…endoscopy negative reflux disease

- Acid Reflux, acid/alkaline reflux

- LPR…laryngopharyngeal reflux

- sGERD…symptomatic GERD

- SNERD...silent nonerosive gastroesophageal reflux disorder

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Inherent Protective Mechanisms

Vasodilatation…. widening of the lumen of blood vessels

Extravasation….to exude from or pass out of

Edema…..accumulation of an excessive amount of watery fluid

Smooth muscle constriction….

Mast cell degranulation….

Transudate….low protein

Exudate….high protein…(injury/inflammation)…exude…ooze or pass gradually out

Extrude….thrust, force or press out

Permeable…permitting the passage of…through a membrane or other structure …(permeability)

Neurogenic (originating in, starting from, or caused by, the nervous system) inflammation* (a fundamental pathologic process consisting of a dynamic complex of cytologic and chemical reactions that occur in the affected blood vessels and adjacent tissues in response to injury or abnormal stimulation) …vagally mediated reflexes

Embrologic evidence….distal esophagus originates from the lung bud…(shared innervation by the vagus nerve)

Waterbrash… spontaneous filling of the mouth with saliva initiated through a vagally mediated esophago-salivary reflex

*inflammation…caused by a physical, chemical, or biologic agent, including: 1) the local reactions and resulting morphologic changes, )2 the destruction or removal of the injurious material, 3) the responses that lead to repair and healing. The so-called "cardinal signs" are:rubor ,redness; calor, heat; tumor, swelling; and dolor; pain; a fifth sign, functio laesa, inhibited or lost function, is sometimes added.

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Reilly's phenomenon, Reilly's syndrome (splanchnic vasoplegia, sympathetic irritation syndrome)

A syndrome in which experimental irritation of the sympathetic nervous system with various agents, such as allergens, bacterial toxins, and physical irritants, produces vasomotor disorders, increased capillary permeability, edema, and lesions of the reticuloendothelial system.

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"Food" for intellectual "digestion" …Dr. Kurt Barrett

GERD is Epidemic/Pandemic, and the incidence appears to be increasing.

GERD is PREVALENT IN ALL AGE GROUPS

Heartburn is not necessarily present - EVER.

Change in therapy or discontinuation of meds results in a 90% recurrence in 6-12 months.

Authorities agree the goal of therapy is to prevent complications and control symptoms.

The only certain method of disease control is to titrate therapy versus symptom control.

Proton pump inhibitors (PPI's) are the single most effective therapy.

High dose and long-term therapy with PPI's is believed to be safe in all age groups.

Heartburn is a very poor surrogate for GERD.

Over 50% of asthmatics will benefit if treated aggressively for GERD.

GERD is more than heartburn and indigestion. It effects multiple systems, i.e, cardiovascular, respiratory, neuromuscular, urinary, as well as, gastrointestinal.

GERD is clearly related to adenocarcinoma of the esophagus - the single fastest growing FATAL cancer in the industrialized world. Its incidence is doubling every 5 years. It appears to be TENFOLD more common now (12,300 cases for 2003) than in 1970 (1,200 cases).

GERD and quality of life and sleep are inexorably related.

It appears that GERD can cause Obstructive Sleep Apnea (OSA is grossly underdiagnosed, as is GERD) and OSA in epidemiological studies is MORE prevalent than ASTHMA. September 2003

Why are concepts about GERD so slowly disseminated and slow to be incorporated?

I first heard the term "laryngopharyngeal reflux" from a patient just 2 or 3 years ago. He taught me.

I rarely hear it from another doctor.

My own daughters sought help from allergists, ENTS, and regular doctors to NO avail.

"The eyes only see what the mind knows." Attributed to a German philosopher by Dr. Nimish Vakail

"A man dreads to give up his old boots for fear the new ones will pinch his feet." (Andrew Taylor Still)

"You cannot learn what you think you already know." (unknown)

"Young physicians have twenty treatments for each disease; older physicians have one treatment for twenty diseases" (Sir William Osler)

" It is more important to know the patient who has the disease than to know the disease that has your patient."(Osler)

"Osteopathy is the practical knowledge of how man is made and how to right him when he gets wrong." (Andrew Taylor Still)

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Autonomic Activation Syndrome (AAS)

Autonomic Activation Syndrome (AAS) is the consequence (unintended) of intense stimulation of the autonomic nervous system (ANS) in response to pathologic events occurring in visceral organs. Effects can be profound: laryngeal edema, middle ear effusion, massive nasal turbinate swelling/hypertrophy, pulmonary congestion, cough, inordinate respiratory mucus production to name but a few. Deterioration of sleep is common. The enormity of the event causes the response to become generalized, not confined to the eliciting tissue, i.e. loss of specificity. In essence your body tissues have come under "friendly fire". Respiratory and cardiovascular manifestations are the result of vasodilatation, interstitial edema, change in vascular permeability, exstravasation, smooth muscle contraction, mucus production and immune system changes due to ANS command rather than an infecting organism or external environmental stimulus as provocation.

The prototype event is reflux of gastric contents as a result of failure of the lower esophageal sphincter in preventing regurgitation. The manifestations of intense stimulation, mediated primarily through the Vagus nerve (10th cranial), are unmasked as a result of successful therapy for the underlying primary cause. Use of high dose proton pump inhibitors and the popularity of laproscopic fundoplication have accelerated understanding of this interesting conundrum as alert clinicians acknowledge relief of symptom burden.

Due to the magnitude of the "signal" generated via the ANS, as a consequence of the gravity of the danger imposed by the escape of gastric contents (proteolytic enzymes, hydrochloric acid and more) tissues of similar embryological origin respond with the greatest intensity. This response often seems unsolicited and puzzling given the apparent lack of pathologic stimulus in the involved tissues. With the increasing amplitude of the distress signal, target tissue specificity is degraded and ultimately lost. The extreme "danger alert mode" message, with increasing intensity, becomes generalized and "spills over" into other tissues that have no need or reason to be influenced in this manner. Paradoxically, powerful, protective mechanisms intended to defend the esophagus lapse into other organ systems resulting in pathological conditions and noxious symptoms due to remote, seemingly unrelated pathophysiologic events. When successful therapy is rendered the resolution of symptoms can be profound, staggering and sometimes unanticipated. Copyright Barrett publishing 2003

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