The Correlation Between GERD and Stricture Oesophagus

7/30/2019 The Correlation Between GERD and Stricture Oesophagus

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CHAPTER I

ABSTRACT

Gastroesophageal reflux disease (GERD) is a specific clinical entity defined by the

occurrence of gastro-esophageal reflux through the lower esophageal sphincter (LES) into the

esophagus or oropharynx to cause symptoms, injury to esophageal tissue, or both. The

pathophysiology of GERD is complex and not completely understood. An abnormal LES

pressure and increased reflux during transient LES relaxations are believed to be key

etiologic factors. Prolonged exposure of the esophagus to acid is another. Heartburn and acid

regurgitation are the most common symptoms of GERD, although pathologic reflux can

result in a wide variety of clinical presentations. GERD is typically chronic, and while it is

generally nonprogressive, some cases are associated with development of complications of

increasing severity and significance. One of the complications GERD is stricture oesophagus.

An esophageal stricture is a gradual narrowing of the esophagus, which can lead to

swallowing difficulties. The strictures are caused by scar tissue that builds up in the

esophagus.

Keywords: Gastroesophageal Reflux Disease and stricture eosophagus.


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CHAPTER II

INTRODUCTION

In united states gastroesophageal reflux affects approximately 40% of adults.

Esophageal strictures are estimated to occur in 7-23% of untreated patients with reflux

disease. Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of

esophageal stricture.(1) Gastroesophageal reflux disease (GERD) is a more serious form of

gastroesophageal reflux (GER), which is common. GER occurs when the lower esophageal

sphincter (LES) opens spontaneously, for varying periods of time, or does not close properly

and stomach contents rise up into the esophagus. If gastroesophageal reflux disease (GERD -

also referred to as acid reflux disease) is not treated effectively, the constant acid reflux can

irritate the lining of the esophagus, and serious complication can occur.(2) Causes, incidence,

and risk factors of esophageal strictures: Gastroesophageal reflux (GERD), Prolonged use of

a nasogastric tube , Ingestion of corrosive substances, Viral or bacterial infections and

Injuries caused by endoscopes.(3) Symptoms of Esophageal Strictures is difficulty

swallowing, discomfort with swallowing, a felling that food gets stuck in the esophagus,

regurgitation of food and weight loss. Author hopes this paper can explain how

gastroesophageal reflux disease become a stricture oesophagus and then the stricture

oesophagus can be prevented.


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CHAPTER III

DISCUSSION

Esophagus also spelled oesophagus, relatively straight muscular tube through which

food passes from the pharynx to the stomach. The esophagus can contract or expand to allow

for the passage of food. Anatomically, it lies behind the trachea and heart and in front of the

spinal column; it passes through the muscular diaphragm before entering the stomach. Both

ends of the esophagus are closed off by muscular constrictions known as sphincters; at the

anterior, or upper, end is the upper esophageal sphincter, and at the distal, or lower, end is the

lower esophageal sphincter.(4)

The upper esophageal sphincter is composed of circular muscle tissue and remains

closed most of the time. Food entering the pharynx relaxes this sphincter and passes through

it into the esophagus; the sphincter immediately closes to prevent food from backing up.

Contractions of the muscles in the esophageal wall (peristalsis) move the food down the

esophageal tube. The food is pushed ahead of the peristaltic wave until it reaches the lower

esophageal sphincter, which opens, allowing food to pass intothe stomach, and then closes to

prevent the stomachs gastric juices and contents from entering the esophagus. When the

lower esophageal sphincter (LES) opens spontaneously, for varying periods of time, or does

not close properly and stomach contents rise up into the esophagus, this condition is called

GERD(gastroesophageal reflux disease).(4)

GERD is also called acid reflux or acid regurgitation, because digestive juices called

acids rise up with the food.(2) The esophagus is the tube that carries food from the mouth to

the stomach. The LES is a ring of muscle at the bottom of the esophagus that acts like a valve

between the esophagus and stomach. The term encompasses both symptoms and
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pathophysiologic changes to the esophageal mucosa, which occur as a result of exposure of

the distal esophagus to acidic gastric contents after episodes of gastroesophageal reflux.(5)

Gastroesophageal reflux disease (GERD) can be the primary cause of, or an

aggravating contributor to, a wide variety of conditions affecting extraesophageal structures.

As a result, GERD can lead to a number of pulmonary symptoms and diseases,

otolaryngologic findings and symptoms, and other extraesophageal manifestations, including

dental erosions.(6) Clinicians must be aware of the possibility of these extraesophageal reflux-

related conditions, even in the absence of classic esophageal symptoms of GERD.While

antireflux therapy is often helpful,response to treatment is less pred ictable than it is for

typical GERD.(6)

In most persons with GERD, endogenous defense mechanisms either limit the amount

of noxious material that is introduced into the esophagus or rapidly clear the material from

the esophagus so that symptoms and esophageal mucosal irritation are minimized. (6)

Examples of the defense mechanisms include actions of the lower esophageal sphincter

(LES) and normal esophageal motility. When the defense mechanisms are defective or

become overwhelmed so that the esophagus is bathed in acid or bile and acid-containing fluid

for prolonged periods, GERD can be said to exist.(6) Normal acid clearance. The process of

normal acid clearance involves peristalsis as well as the swallowing of salivary bicarbonate.

Peristalsis clears gastric fluid from the esophagus, whereas the swallowing of saliva (pH of

7.8 to 8.0) neutralizes any remaining acid. Both primary and secondary peristalsis are

essential mechanisms of esophageal clearance. Voluntary induced primary peristalsis occurs

approximately 60 times per hour. Secondary peristalsis occurs in the absence of a pharyngeal

swallow and can be elicited by esophageal distention or acidification, which occurs with acid

reflux. Salivation is crucial to the completion of esophageal acid clearance and the restoration

of esophageal pH. Gravity also plays an important role in esophageal acid clearance.(6)


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The pathogenesis of GERD is multifactorial. Pathologic reflux is thought to occur when

the injurious properties of refluxed gastric acid, bile, pepsin, and duodenal contents

overwhelm normal esophageal protective antireflux barriers, such as esophageal acid

clearance and mucosal resistance.(5) The primary underlying mechanism causing pathologic

reflux appears to be a defective LES, which increases the volume of acidic gastric contents

that refluxes into the esophagus. This increase in acid volume tips the balance toward

pathologic reflux by overwhelming the normal capacity of the esophageal mucosa to tolerate

acid.(6)

Some degree of gastroesophageal reflux occurs normally in most individuals. GERD is

thought to develop when a combination of conditions occurs to increase the presence of

refluxed acid in the esophagus to pathologic levels.(1) Aggressive mechanisms potentially

harmful to the esophagus overwhelm protective mechanisms such as esophageal acid

clearance and mucosal resistance, which normally help to maintain a physiologically

balanced state. In this way, the pathogenesis of GERD is similar to that of other acid-

secretory diseases, such as duodenal ulcer disease and gastric ulcer disease.

Figure 1. Possible etiologic factors involved in GERD


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Among the mechanisms thought to contribute to the development of GERD are

TLESRs or decreased LES resting tone, impaired esophageal acid clearance, delayed gastric

emptying, decreased salivation, and impaired tissue resistance. (2) Recent data also support the

importance of the potency of the gastric refluxate as a contributory factor in some

circumstances.

Figure 2. Endogenous Defense Mechanisms

A significant defect in any one of these forces can alter the balance from a compensated

state to a decompensated one. Manifestations of the decompensated state include symptoms

and complications such as heartburn and esophagitis. Excessive acid reflux due to TLESRs is

the most common causative mechanism. A pathologically decreased LES resting tone is more

common among patients with severe GERD, especially those with esophageal strictures or

Barretts esophagus.(6)


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Increased intragastric pressure leading to GERD can be caused by obesity, pregnancy,

or disruption of the normal receptive relaxation of the stomach following an increase in

gastric volume.(5) Most patients with complicated GERD have a hiatal hernia, which, by

displacing the LES segment of the distal esophagus, both reduces LES pressure and impairs

acid clearance. Once reflux has occurred, impaired acid clearance prolongs exposure of the

mucosa to the damaging effects of the refluxate. Diminished peristaltic clearance is seen

among approximately one half of patients with severe GERD.

Delayed stomach emptying. Delayed gastric emptying is present in 10% to 15% of

patients with GERD.(3) It is believed to contribute to the development of a small proportion of

cases by increasing the amount of fluid available for reflux and by the associated constant

gastric distention. Potential causes of impaired gastric emptying include gastroparesis, as

seen in patients with diabetes, and partial gastric outlet obstruction.(2)

Pregnancy is the most common condition predisposing to GERD and is generally

associated with symptomatic GERD (typically heartburn) rather than esophagitis.(5) Because

heartburn affects approximately two thirds of all pregnancies, it is considered by many to be a

normal occurrence during pregnancy. In most cases, symptoms occur for the first time during

the pregnancy and subside soon after delivery. Recurrence is also a possibility with

subsequent pregnancies. While symptoms may occur throughout the pregnancy, data are

conflicting on whether they occur more frequently during the first and second trimesters or

during the third. While the pathogenesis is thought to be multifactorial, the primary

pathophysiology of GERD during pregnancy is probably that of decreased LESP resulting

from the effects of progesterone and estrogen on LES function. The two hormones appear to

act together, with progesterone acting as a mediator of LES smooth-muscle relaxation and

estrogen as a primer of LES relaxation. Mechanical factors, such as increased abdominal

pressure due to enlargement of the uterus, are believed to play a somewhat smaller role. In


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most cases, patients can be treated with lifestyle and dietary modifications if symptoms are

mild. Otherwise, nonsystemic medications (antacids or sucralfate) can also be safely

prescribed for symptom relief. Except for severe or intractable cases, systemic therapy during

pregnancy should be avoided.

A hiatal hernia is frequently found among patients with GERD. The proximal stomach

is dislocated through the hiatus of the diaphragm into the chest, and the crural diaphragm

becomes separated from the LES.(4) Viewed as part of a GERD continuum, a hiatal hernia is

another factor disrupting the integrity of the gastroesophageal sphincter, resulting in

increased esophageal acid exposure. It may be a factor in GERD pathogenesis, especially if

the patient has severe symptoms. Hiatal hernias are present in more than 90% of patients with

severe erosive esophagitis, especially if complications are present, such as esophageal

stricture or Barretts esophagus. Hiatal hernias, in fact, are found among most patients with

Barretts esophagus, and they likely contribute to its development. Whether or not the hernia

is an initiating factor in GERD, it clearly plays a role in sustaining GERD, accounting for the

chronicity of the disease.(8)

Figure 3. Normal anti reflux

barrier and the crural diaphragmFigure 4. Hiatal hernia charecterized

by separation of the lower

oesophageal sphincter from the crural

diaphragm


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GERD is characterized by a wide variety of clinical symptoms and presentations,

ranging from symptomatic reflux without macroscopic esophagitis to the chronic

complications of esophageal mucosal damage. Heartburn is the most common symptom of

GERD. In some patients, heartburn may be accompanied by acid regurgitation, odynophagia,

and dysphagia. Numerous esophageal manifestations of GERD can occur.(2)

Chronic GERD that is untreated can cause serious complications. Inflammation of the

esophagus from refluxed stomach acid can damage the lining and cause bleeding or ulcers

also called esophagitis.(3) Scars from tissue damage can lead to strictures narrowing of the

esophagus that make swallowing difficult. An esophageal stricture is a gradual narrowing of

the esophagus, which can lead to swallowing difficulties.(2) The strictures are caused by scar

tissue that builds up in the esophagus. When the lining of the esophagus is damaged, scarring

develops. When scarring occurs, the lining of the esophagus becomes stiff. In time, as this

scar tissue continues to build up, the esophagus begins to narrow in that area. The result then

is swallowing difficulties.(1)

Figure 5. Endoscopic Appereance
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Peptic esophageal strictures are sequelae of gastroesophageal reflux induced

esophagitis, and they usually originate from the squamocolumnar junction and average 1-4

cm in length.

Two major factors involved in the development of a peptic esophageal stricture are as

follows:

Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patientswith peptic strictures compared with healthy controls or patients with milder degrees

of reflux disease. A study by Ahtaridis et al showed that patients with peptic

esophageal strictures had a mean LES pressure of 4.9 mm Hg versus 20 mm Hg in

control patients. An LES pressure of less than 8 mm Hg appeared to correlate

significantly with the presence of peptic esophageal stricture without any overlap in

controls.(1) Disordered motility resulting in poor esophageal clearance: In the same

study, Ahtaridis et al demonstrated that 64% of patients with strictures had motility

disorders compared with 32% of patients without strictures.(1)

Symptoms of Esophageal Strictures :

Difficulty swallowing Discomfort with swallowing A felling that food gets stuck in the esophagus Regurgitation of food Weight loss

Diagnosis of Esophageal Strictures can use A barium swallow. Patient will swallow

barium and x-rays can be taken to show the narrowing of the esophagus. An endoscopy

exam. This narrow tube is inserted into the esophagus and it can show any narrowing of the

esophagus.(2)
http://emedicine.medscape.com/article/176595-overviewhttp://emedicine.medscape.com/article/174783-overviewhttp://emedicine.medscape.com/article/174783-overviewhttp://emedicine.medscape.com/article/174783-overviewhttp://emedicine.medscape.com/article/176595-overview


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Treatment of Esophageal Strictures:

Dilation. The esophagus is stretched by the use of one of several methods. Two of themethods of dilation are performed by passing a dilator or air-filled balloon is passed

through a endoscope. Repeated dilation may be necessary to prevent the stricture from

returning.(2)

Proton pump inhibitors, such as omeprazole, lansoprazole or rabeprazole, can keepstrictures from returning.(2)

Surgical treatment is rarely necessary. If is performed if a stricture can't be dilated enoughto allow solid food to pass through. Surgery is also performed if repeated dilations do not

keep these strictures from returning.


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CONCLUSION

Gastroesophageal reflux is a normal physiologic phenomenon experienced

intermittently by most people, particularly after a meal. Gastroesophageal reflux disease

(GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the

normal limit, causing symptoms with or without associated esophageal mucosal injury. If

gastroesophageal reflux disease is not treated effectively, the constant acid reflux can irritate

the lining of the esophagus, and serious serious complication can occur. When the lining of

the esophagus is damaged, scarring develops. When scarring occurs, the lining of the

esophagus becomes stiff. In time, as this scar tissue continues to build up, the esophagus

begins to narrow in that area. The result then is swallowing difficulties. It is so important to

prevent GERD develop to Stricture Oesophagus.


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REFERENCES

1. Mukherjee S. Esophageal Stricture. Available at:http://emedicine.medscape.com/article/175098/. Accessed June 16th, 2011.

2. Heartburn, Gastroesophageal Reflux (GER), and Gastroesophageal Reflux Disease(GERD). Available at:http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/. Accessed June

15th, 2011.

3. Gillson S. Esophageal Strictures. Available at:http://heartburn.about.com/cs/articles/a/esoph_stricture.htm. Accessed June 15th, 2011.

4. Price SA, Wilson LM. Pathophysiology Clinical Concepts of Disease Processes:Anatomy and Physiology. Elsevier Science; 2002; p. 404.

5. Kahrilas PJ. GERD pathogenesis, pathophysiology and clinical manifestations. ClevelandClinical Journal of Medicine 2003; 70 (suppl 5): 4-17.

6. Devault KR. Extraesophageal symptoms of GERD. Cleveland Clinical Journal ofMedicine 2003; 70 (suppl 5): 2-3.

7. Marks JW. Gastroesophageal Reflux Disease (GERD, Acid Reflux, Heartburn). Availableat:http://www.medicinenet.com/gastroesophageal_reflux_disease_gerd/article.htm.

Accessed June 16th, 2011.

8. Kahrilas PJ, Shi G, Manka M, Joehl RJ. Increased frequency of transient loweresophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal

hernia. Cleveland Clinical Journal of Medicine 2003; 118:688695.
http://emedicine.medscape.com/article/175098/http://emedicine.medscape.com/article/175098/http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/http://heartburn.about.com/cs/articles/a/esoph_stricture.htmhttp://heartburn.about.com/cs/articles/a/esoph_stricture.htmhttp://www.medicinenet.com/gastroesophageal_reflux_disease_gerd/article.htmhttp://www.medicinenet.com/gastroesophageal_reflux_disease_gerd/article.htmhttp://www.medicinenet.com/gastroesophageal_reflux_disease_gerd/article.htmhttp://www.medicinenet.com/gastroesophageal_reflux_disease_gerd/article.htmhttp://heartburn.about.com/cs/articles/a/esoph_stricture.htmhttp://digestive.niddk.nih.gov/ddiseases/pubs/gerd/http://emedicine.medscape.com/article/175098/

The Correlation Between GERD and Stricture Oesophagus

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