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.

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.

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

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 refluxrelated 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)

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

Figure 1. Possible etiologic factors involved in GERD

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)

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

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 diaphragm

Figure 4. Hiatal hernia charecterized Figure 4. Hiatal diaphragm by separation of The the crural lower oesophageal sphincter from the crural diaphragm

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

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 patients with 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)

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Treatment of Esophageal Strictures:

Dilation. The esophagus is stretched by the use of one of several methods. Two of the methods 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 keep strictures from returning.(2)

Surgical treatment is rarely necessary. If is performed if a stricture can't be dilated enough to 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

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. Cleveland Clinical Journal of Medicine 2003; 70 (suppl 5): 4-17. 6. Devault KR. Extraesophageal symptoms of GERD. Cleveland Clinical Journal of Medicine 2003; 70 (suppl 5): 2-3. 7. Marks JW. Gastroesophageal Reflux Disease (GERD, Acid Reflux, Heartburn). Available at: 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 lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia. Cleveland Clinical Journal of Medicine 2003; 118:688695.

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