Reflux esophagitis strictures are smoothly contoured.

Mucosal relief may be peserved And the transition between the normal and stenosed portions is gradual (Fig. 7.5 !. "roximal dilatation is fre#uently moderate. Acute inflammatory changes are common proximal to stricture.

Figure 7.5 . $tricture of the distal esophagus with reflux esophagitis. %astreoesopageal reflux in children may also result& in reflux esopagitis' formation of strictures' and aspiration pneumonia. (evelopment of reflux esophagitis is influenced by te fre#uency and degree of reflux and te capability of secondary peristalsis to remove remnants of esopageal contents. )ARR*++,$ *$-".A%/$ )arrett,s *sophagus ()*! is characteri0ed by metaplasia of stratified s#uamous to simple columnar epithelium. 1n contrast to islets of ecotopic gastric mucosa' the columnar epithelium of )* is continuous with epithelium of gastric mucosa' but does not secrete .2l. +here are no parietal cells' which are normal constituents of gastric mucosa. .owever' goblet cells are presents and the situation is similar to villous (intestinal! metaplasia of gastric mucosa in patients with chronic atropic gastritis. $ince intestinal metaplsia of gastric mucosa increases the ris& of cancer' the high malignant potential of )* ma&es early detection of critical importance to patient management. )arrett,s *sophagus is present in 345 of patients with advanced chronic reflux esophagitis. Men and women are e#ually affected with maximal prevalence in middle age. +hic&ening and irregularity of esophageal folds are found in 655 of patients. .iatal hernia of the stomach with resultant gastroesophageal reflux and peptic esophagitis is often present. %astroesophageal reflux with or without hiatal hernia is verified in 645 of patients with )*. More than three7#uarters of affected patients have esophageal strictures (Fig. 7.55!. Approximately 845 of these strictures affect the middle third of the esophagus' while the remainder are located in the distal portion of the esophagus. Radiologic signs of reflux esophagitis are visible' mostly proximal to the stenoses. +here are opinions that strictures are located at the transition of stratified s#uamous epithelium to columnar epithelium. .owever' this has not been definitely proved. "eptic ulcer or the esophagus' a common finding in reflux esophagitis' is present in 945 of patients with )*. 1t is the most specific sign of )* but is of relatively little importance because of the low prevalence. -n double7contrast roentgenographs' that portion of the esophagus covered with columnar epithelium is wider than :5 mm in 857645 of cases. (ecreased tone of the distal part of the esophagus one of the signs of hiatal herniation' reflux

esophagitis and )*' may be confirmed by manometry (Fig. 7.55!. $cintigraphic data demonstrate the inherent dysmotility of the esophagus in patients with )*. (iffuse granularity and a fine reticular pattern of the esophageal mucosa may be found with reflux esophagitis and )*. %ranular' spheroid extrusions of the mucosa are rarely larger than :79 mm in diameter (Figs. 7.55 A and )! reticularity of the mucosa is a conse#uences of residual barium in shallow grooves and impressions of the mucosa. )oth these patterns of the mucosa are present distal to strictures. %ranular bulges are visible on double7contrast roentgenographs in half of the patients with )*. +hese result from villous metaplasia of the epithelium. +he granular mucosal pattern may indicate a higher cancer ris&. A granular and reticular mucosa may also be found in moniliasis' herpetic esophagitis' leuopla&ia' superficially spreading carcinoma' and glycogenic acanthosis of the esophagus.

%ambar 7.55. )arrett,s esophagus. (A')'2! $ign reflux esophagitis' stricture' and flaccidity of distal segments. +here are no specific radiologic signs of )*. All the signs are' at the same time' characteristic of advanced reflux esophagitis' and reflect a common pathophysiologic basis for these two antities. As a matter of fact' )* is a result of long7lasting severe reflux esophagitis. "rogressive systemic sclerosis also affects the esophagus in 547;45 of diseased patients. )ecause of lowered tone of the <*$' gastroesophageal reflux and reflux esophaitis often develop' thus increasing the ris of )*. =hatever is the cause of gastroesophageal reflux' long7lasting reflux esophagitis creates the danger of columnar metaplasia of the esophageal epithelium. 1n areas of columnar metaplasia' redness of the mucosa is visible endoscopically. +his change in color is more important as an indicator of )* than the change in relief of the mucosa. $ome authorities do not even favor double7contrast and mucosal relief studies in diagnosing )* and early )arrett,s carcinoma. Radiologic properties of )* are not specific and the sensitivity of the radiologic examinations is relatively low. Although a more >aggressive? examination increases sensitivity' specificity decreases at the same time because of a higher number of false7positive results. +hus' a large number of patients be unnecessarily examined endoscopically. 2ompared with control sub@ects' the probability of developing esophageal cancer is 4 times higher in patients with )* (see text concerning esophageal cancer' page ::7!. "*"+12 /<2*R$ "eptic /lcers are of similar morphology throughout the alimentary canal. +hey arise in the presence of .2l and heal by forming a scar. After propmt therapy of an

acute ulcer the scar may be so minute that only microscopic analysis will detect residual pathology. *sphageal peptic ulcerations resulting from gastroesophageal reflux are most commonly situated in the distal portion of the esophagus' especially in the region of the cardia. Affected patients commonly harbor duodenal or gastric ulcers. "eptic ulcers of the esophagus create a crater in the wall (Fig. 7.58! with folds converging toward the crater of a healing or chronic ulcer. +hese ulcers may alter normal esophageal motility. $trictures are the se#uelae of chronic ulcers (Fig. 7.58(! /lcer walls' in contrast to diverticula' are without mucosal folds. /nli&e malignant ulcers' peptic ulcers may have mucosal relief preserved along the edges. More accurate differentiation is possible by esophagoscopy with biopsy. "eptic ulceration on ectopic gastric mucosa (also referred to as )arrett,s ulcer an unrelated to )arrett,s esophagus! can develop in any portion of the esophagus and is not the result of reflux. $tenoses caused by peptic ulceration should be distinguished from malignant stenoses and achalasia. 2riteria for distinguishing benign from malignant stenoses are described in chapter 9 (see page 5:!. %ambar 7.58. "eptic ulcer of the esophagus. (A! "roximal segment ulcer with signs of reflux esophagitis and hiatus hernia. ()! (istal segments ulcer. (uring embryonic development' the esophagus is lined with stratified columnar epithelium which is replaced by ciliated epithelium' and then with stratified s#uamous epithelium. 2hanges start in the mid portion of the esophagus and progress in both proximal and distal directions. 2olumnar epithelium of the cervical segment of the esophagus is the last to undergo change. Any remaining columnar epithelium contains parietal and chief cellsA this is not the case with )arrett,s, esophagus. 1slets of columnar epithelium manifest as webs or ring7li&e protruding lesions. %ambar 7.58. continued. (2! 1n distal segment with deep tertiary contraction. ((! Mild mid7esophageal stricture after healed peptic ulcer with thice&ned folds. B-<<1C%*R7*<<1$-C $DC(R-M* Autopsy results suggest esophageal involvement in 995 of patients with Bollinger7*llison $yndrome. *sophagitis is common' with ulcers of various depth' and with stenoses (Fig. 7.57! resulting from gastroesophageal reflux in association with excessive secretion of .2l in the stomach. )arrett,s esophagus may result. .owever' the high gastrin levels associated with Bollinger7*llison syndrome provo&e increased <*$ tone' ma&ing gastroesophageal reflux uncommon. +.* R1C% -F $2.A+BE1

+he lower esophageal or $chat0&i ring is a web at the @unction of esophageal and gastric mucosa (Fig. 7.5;?!A it is a membranous structure %ambar 7.57. *sophagitis in Bollinger7*llison $yndrome. in the region of the )7ring (spincter of the cardia!' resulting from esophagitis. (ysphagia in patients with a lower esophageal ring depends on its diameter. $ome data indicate that the lower esophageal ring commonly causes dysphagia of solid food in adultsA wheteher dysphagia occurs is dependent on the diameter of this esophageal ring. $ince there is great distensibility of the <*$' the ring may protrude up to 8 mm into the esophageal lumen without causing sub@ective7 %ambar 7.5;. <ower esophageal ring7ring of $chat0&i. (A! "ro@ection of the ring (arrows! demonstrating the residual esophageal lumen. Also evident is a large hiatus hernia. ()! +ypical ring. $ymptoms. .owever' it can also cause significant dysphagia. +he ring is only evident when there is hiatal gastric herniation with the cardia above the diaphragm. 1n this case the esophagus may be shortened by esophagistis. +he ring is optimally shown when both proximal and distal segments of the esophagus are filled with barium suspension. 1t may also be demonstrated using double7contrast techni#ue' when the lower esophageal segment is dilated. $pot films should be ta&en after swallowing of the contrast medium has been followed by a deep inspiration. $ingle7contrast examination of the esophagus in the prone position reveals 655 of lower esophageal rings. .owever' the detection rate for double7contrast examination does not exceed 85. +he sensitivity of endoscopy in defining lower esophageal rings e#uals 5;5 and is dependent on the diameters of the ring and the endoscope. (iscrete rings can easily be overloo&ed' particulary when small7caliber endoscopes are used. +he radiologic examination is more accurate' and is the method of choice in patients whose dysphagia is suspected to be related to narrowing of the lower esophageal segment. A lower esophageal ring may narrow the esophageal lumen significantly' but statis of the contrast medium an dproximal dilatation are infre#uent (Fig. 7.56!.

Figure 7.56. (A! bolus of food lodged in the distal esophagus. ()! Ring of $chat0&i impaction A lower esophageal ring should be distinguished from a functional >contraction? ring' which represents an abnormally contracted tubulovestibular sphincter in the presence of hiatal herniation. (ifferentiation from ring7li&e narrowings in portions of the stomach affected by hiatal herniation is necessary. Membranous formations may be detectedup to 8 cm proximal to the esophagogastric @unction in 4.3 5 of upper

gastrointestinal examination. <i&e webs in the cervical segment of the esophagus' they are the conse#uence of chronic irritation. %astroesophageal reflu&s may cause these webs to be formed in the distal segments of the esophagus' as a rare and unusual respone of the esophageal mucosa. +hey can be mista&en for the )7ring (mucosal ring in the region of the cardia! or the ring of $chat0&i. Farious examination techni#ues may be used in the detection of hernias' strictures' and rings of the <*$. +hese are single7contrast examination while the patient is in the prone positions' demostration of te mucosal relief' and double7 contrast examination. A sensitivity of almost 3445 is achived by use of single7 contrast examination. (emostrations of mucosal relief during a single7contrast examination reveals these lesions 5:5 of the cases whwn they occur. $ince the are performed mainly while the patient assumes a standing posture' double7contrast studies are successful in only 9 5. $2<*R-(*RMA G "R-%R*$$1F* $D$+*M12 $<*R-$1$ +he esophagus is affected in more than half patients with scleroderma. -ther collagenoses cause similar esophageal changes. $cleroderma result in atrhopy of the smooth muscles of the esophagus with deposition of collagen in the submucosa. $triated muscles of esophagus are not affected. +he thoracic portion of the esophagus is hypotonic' with widened lumenA peristaltic waves appear rarely' loo& shallow' or are even missing (gambar 7.84!. in advanced stages a bolus of highly concentrated barium >falls? as if traversing a rigid tube. +he inner esophageal surface is smooth as a result of chages in the lamina muscularis mucosa. "eristalsis is uncoordinated' and shallow tertiary contractions or fasciculations may be noticed (gambar 7.84A!. +he threshold for eliciting peristalsis is increased. =ith the progression og disease' a decrease in the amplitude of primary peristaltic waves is accompanied by the disappearance of resting tone in the lower esophageal segment and symptoms of dysphagia. +hese changes are most pronounced when the patients is supine. Fideo7radiography demonstrates impaired motility of the esophagus. +he specifity of the examination is revealing a lac& of peristalsis reaches almost 3445. .owever' it decreases to 745 in individuals sixty or more years of age. =ea&ened and deficient peristalsis can be detected with a sensitivity of 745. .ypotonia of the lower esophageal segment result in gastroesophageal reflu&s with rsultant reflu&s esophagitis' ulceration' and shortening of the esophagus (gambar 7.842!.

%ambar 7.84. $cleroderma. (A! $ignificantly dilated esophageal lumen. Fasciculations of proximal segments of the wall. ()! (ilated esophageal lumen with

normally patent vestibule. (2! (ilated lumen with large peptic ulceration resembling a diverticulum.

%RAC/<-MA+-/$ (1$*A$* 1nvolvement of the esophagus with 2rohn,s disease is rare' although any segment of the alimentary canal' as well as organs not belonging to the gastrointestinal tract' may affected. *sophageal involvment with 2rohnAs disease is described in the section on esophagitis (lihat halaman :45!. C*-"<A$M$ )eningn Ceoplasms )enign esophageal neoplasms grow slowly. <i&e malignant tumors' they can cause dysphagia' but not before the tumor mass occupies approximately one7half of the esophageal lumen. )enign tumors do not interfere significantly with peristalsis. Mesenchymal benign tumors7leiomyomas' lipomas' and fibromas7 are mare common than those that are epithelial. $ubmucosal tumors are mesenchymal in most instances. +hey cause regular radiolucent negative defects' transparencies' in an esophagus filled with contrast medium' and cause the overlying mucosa to bulge into the lumen. +he mucosal folds are preserved' but shifted aside. +hey may even be formed in the manner of an arch. Epithelial tumors include adenomas and papillomas. +hese tumors originate from the mucosa and protrude into the lumen. +hey are most often spherical or oblong with contours that are sharply demarcated. +hey may have a stal&. Leiomyomas are the most common benign esophageal tumors. +hey are most fre#uently found in the distal two7thirds of the esophagus. %rowth may be limited to the submucosa (gambar 7.83! but these tumors can develop a stal& and become movable. =hwn they assume large dimensions they cause symptoms of intermitent obstruction. +he mucosa overlying an esophageal myoma is infre#uantly ulcerated. +his is not the case with alimentary tube myomas in other locations. Radiologic examination should be used to differentiated benign tumors from extrinsic compression of the esophageal wall by ad@acent structures' air bubbles' varices' or foreign bodies. 1t is most important to distinguish benign from malignant tumors. +he latter cause destruction of mucosal surface and rigidity of the esophageal wall. Air bubbles are mobile. $ubmucosal warices affec longer segments of the esophagus and their morphologic appearance varies with the degree to which they are filled with blood.

%ambar 7.83 (A! small esophageal leiomyoma (arrows!. ()! large esophageal leiomyoma (arrow!. Malignant Ceoplasms Malignant esophageal tumors are more common than benign. +hey primarily affect the older male population. /nfortunately' sub@ective symptoms start only when disease is advanced. About 645 of esophageal malignancies are carcinomas' and the remainder are sarcomas such as leiomyosarcoma (gambar 7.8:! or liposarcoma (gambar 7.89!' and lymphomas. Carcinoma. Although it represents only about 55 of all alimentary canal carcinomas' esophageal carcinima is the most significant esophageal disease because ot its high mortality rate.

%ambar 7.8:. ulcerated leiomyosarcoma of the esophagus. .iatus hernia of stomach.

%ambar 7.89. liposarcoma of the distal esophageal segment. +he five7year survival rate is low' being only about 55 in patients who undergo therapy. .eavy drin&ing of alcohol and smo&ing significantly increase the ris& of developing the distance. "atients with tylosis have a 3445 chance of developing carcinoma of esophagus. 2arcinoma is more common is distal segments of the esophagus' where it has a better prognosis since it lac&s close contact with vital structures. +he more distal yhe occurence of the stenosis in the esophagus' the more pronounced is the proximal dilatation. As a result of rapid growth' malignant tumors cause less pronounced proximal dilatation than benign stenoses. Early esophageal carcinoma does not penetrate deeper than the submucosa and is without matastases. 1t has a much better prognosis than advance carcinoma' the five7year suvival rate being almost 645. +he diagnosis of early carcinoma is rarely made on the basis of clinical symptoms. 1ndeed' dysphagia is the result of tumors which affect lymp nodes an other mediastinal structures. +o determine the relationship between progression of carcinoma and survival rate' several types of carcinoma have been define. Early carcinoma is a superficial carcinoma without metastases. Superficial carcinoma of the esophagus may penetrate of to but does not involve the main muscular layer of the wall. Regional lymph nodes may be infiltrated with tumor cells. Small carcinoma is a tumor less than 95 mm in diameter.