Primary Motility  Disorders of the  Esophagus
 The Esophageal
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 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

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OESO©2015
 
Volume: The Esophageal Mucosa
Chapter: Ulcers in CLE
 

What are the characteristic features of stricture in Barrett's mucosa?

K. Moghissi (Hull)

In his original article on the lower esophagus lined by columnar epithelium, Barrett [1] refers to three types of complications associated with this condition, namely adenocarcinoma, ulcer and stricture. Judging by the number of publications and review articles [2-7], adenocarcinoma has received its fair share of attention. The ulcer was the lesion which initially drew Barrett's [8] attention to the very existence of the columnar epithelial lined esophagus (CLE) and was responsible for stimulating other workers such as Allison [9] and Lortat-Jacob [10] to study independently the CLE.

Compared with adenocarcinoma, the stricture in Barrett's esophagus has received little exposure, possibly because its anatomo-pathological characteristics and its therapeutic significance have not been fully appreciated.

In this article, the task is to elaborate on the characteristics of stricture in CLE (Barrett's stricture) and to provide a definition which encapsulates these characteristics. To do so, I have resorted two sources: 1) historical, based on literature search and publications relevant to Barrett's stricture - prominent amongst these are the original works of Barrett [1,8], Allison [9,11] and Lortat-Jacob [10]; and 2) personal experience and research based on a number of prospective clinico-pathological studies.

Historical sources

Barrett [1] stated that, "stricture demonstrated at or above the aortic arch is almost certainly situated above an esophagus lined with columnar epithelium". Allison did a special study of CLE and later drew attention to the stricture in such an esophagus [11]. He suggested that in consequence of an incompetent cardia and gastroesophageal reflux (GER) followed by esophagitis, there develops a stenotic lesion at the squamo-columnar mucosal junction of CLE. He also clearly differentiated between those strictures which are associated with hiatal hernia, in which the stricture initiates at the squamo-columnar epithelium of the esophagogastric junction, and other strictures which develop at the squamo-columnar mucosal junction of an esophagus lined by columnar epithelium (i.e., Barrett's esophagus), which is some 5 cm above the esophagogastric junction.

Lortat-Jacob [10] in his article on "endobrachy-oesophage" gives an account of the clinical and radiological features of strictures. He also reports on anatomo-patho-logical aspects of the resected specimen of such cases, indicating that stenotic lesion is at the squamo-columnar junction of the esophagus, which in the case of endobrachy-oesophage is 5-6 cm above the "cardia".

Since any discussion on Barrett's esophagus and its complications is intricately involved with the description of the lower esophagus and definition of the gastroesophageal junction, it is relevant to elaborate on the anatomy of the lower esophagus in the region of the esophageal hiatus of the diaphragm, and to expand on the anatomo-pathological changes which occur in this area as a result of GER. The work of Hayward [12-14] is particularly pertinent to this discussion, and accords with our own anatomo-pathological study [7,15-19]; these works indicate that the lower esophagus in the region of the hiatus comprises:

- a thoracic part which is situated above the hiatus, and its mucosa covered with squamous epithelium;

- an abdominal part which is below the hiatus, 2-3 cm in length, with its mucosa lined by junctional columnar epithelium.

In the region of the hiatus, the phreno-esophageal ligament (PEL) is attached to the esophagus and represents a recognizable landmark between the thoracic and abdominal portion of the esophagus. It also indicates an approximate site of the squamo-columnar mucosal junction of the esophagus. Hayward [12-14] rightly suggests that the anatomical gastroesophageal junction is where the esophageal tube (abdominal esophagus) ends and the gastric "bag" begins. Here the peritoneum drapes the stomach and, at the esophagogastric junction, reflects to become the parietal peritoneum. Hayward [12-14] refers to the "surgical" junction where the PEL is attached to the esophagus. It therefore follows that: 1) the PEL and peritoneal reflexion are at or around the esophageal hiatus of the diaphragm (Fig. 1) and that in sliding hiatal hernia both structures ascend upwards into the chest; 2) in the cases of long-standing hernia with associated GER, there develops a pan esophagitis with pathological changes affecting all coats of the esophagus. In the lumen this leads to stricture formation and in the esophageal walls to periesophagitis and periesophageal fibrosis. In severe cases the mediastinal pleura and longitudinal esophageal muscles

0221F1.JPG

Figure 1. .Anatomy of the lower esophagus in the region of the hiatus.

become incorporated in the fibrous scarring and shortening ensues. In this situation the anatomical esophagogastric junction becomes fixed well above the hiatus and the herniated pouch of the stomach may become tubular in configuration and be dragged upwards (Fig. 2). The degree of shortening can be assessed by the distance between the site of attachment of the phreno-esophageal ligament to the esophagus and the esophageal hiatus of the diaphragm (alternatively, shortening may be assessed by the distance between the lower esophageal sphincter, determined by manometry, and the hiatus). It also follows that, even when the stomach becomes tubular in shape and indistinguishable from the esophagus, the PEL will still mark the boundary of the esophagus and stomach because the tubular structure above (proximal) is the thoracic esophagus, but the structure below is the stomach, and the abdominal esophagus, in these cases, is short and is not its usual 2-3 cm in length.

It should now be clear that in a reflux stricture associated with hiatal hernia, the stenosis is at the squamo-columnar junction of the thoracic-abdominal portion of the esophagus, which in the case of shortening is practically situated between the esophagus and the stomach and, externally, at the approximate level of the insertion of the PEL to the esophagus. In these cases the PEL itself is at some distance upwards from the hiatus in the thorax, depending on the degree of shortening.

In a Barrett's stricture, the stenotic lesion, though usually at the squamo-columnar epithelial junction, is not level with the insertion of the PEL to the esophagus. The ligament is in fact at its usual anatomical site at or near the esophageal hiatus

0221F2.JPG

Figure 2. .Anatomy of the esophagogastric junction and phreno-esophageal ligament in high stricture associated with hiatal hernia and acquired short esophagus; 1) squamous epithelium (above the stricture); 2) phreno-esophageal ligament, note its attachment drawn upwards; 3) tubular herniated stomach lined by columnar gastric mucosa; 4) diaphragm.

(Fig. 3). The corollary of this is that in Barrett's stricture the stenosis is, in fact, in the tubular esophagus high above the anatomical gastroesophageal junction, which is not displaced upwards since there is no acquired shortening but "luminal shortening" (endobrachy-oesophage of Lortat-Jacob).

Personal experience and research

In the course of a 20-year period (1970-1990) we have undertaken a number of prospective studies covering some 500 patients with esophageal strictures undergoing transthoracic operations, often involving thoraco-phrenotomy [9,15,18]. The protocol of these studies comprised: 1) preoperative, clinical, radiological and endoscopic investigations with biopsy examination above, at and after dilatation below the stricture; 2) intraoperative observations which included:

0221F3.JPG

Figure 3. .Anatomy of the lower esophagus in Barrett's stricture; 1) columnar epithelial lined esophagus below the stricture; 2) phreno-esophageal ligament; 3) squamous epithelium above the stricture; 4) diaphragm.

- surgical anatomy and the pathological features of the esophagus and the esophageal hiatus of the diaphragm;

- recording of hernia and shortening of the esophagus;

- the PEL, the site of its attachment to the esophagus, its relationship to the esophageal hiatus of the diaphragm and the esophageal stricture;

- postoperative and histopathological examination of the resected specimen (if resection had been undertaken), with particular reference to the anatomical relationship between the stricture and the PEL and the histology of the mucosal covering.

Data from these investigations have allowed for a complete clinico-pathological diagnosis of cases. Most specifically, it enabled us to distinguish all strictures which developed in CLE and focus attention on the particular features of these cases. Based on these studies and a review of the relevant literature, it is possible to stipulate the following characteristics of strictures in CLE.

Stricture

The stricture is situated high in the esophagus at or near the level of the arch of the aorta (as Barrett suggested) (Figs. 3 and 4A). It is usually mild in consistency and yielding to bouginage.

Mucosa

Mucosa above the stricture is usually squamous and often a mix of columnar and squamous. Below the stricture, the mucosa is always columnar for a length of at least 5 cm of the thoracic esophagus (Fig. 4B-D). Relationship: beside being situated high in the esophagus, the stricture is at least 3 cm above the insertion of PEL to the esophagus and 5 cm above the anatomical gastroesophageal junction and the esophageal hiatus of the diaphragm.

0221F4.JPG

Figure 4. .A) Barium contrast of the esophagus in a typical Barrett's stricture. B) Photo micrograph of an esophageal biopsy above the stricture showing squamous epithelial mucosa.

0221F5.JPG

Figure 4C. .Photo micrograph of an esophageal biopsy at the level of the stricture showing mixed squamous and columnar epithelium and inflammatory changes.

Esophageal wall

The esophageal wall is usually unaffected by pathological processes or only affected locally in the area of the stricture with some scarring. PEL is not displaced upward.

Clinical features

Symptomatology in patients with Barrett's stricture is not different from that in patients with other types of esophageal stricture. Predominant amongst symptoms is dysphagia; commonly, patients do suffer from heartburn and dyspepsia prior to development of dysphagia. Unlike cases of reflux stricture associated with hiatal hernia, there is a male sex predominance (in our patients male to female ratio was 3.5:1, whereas in other reflux stricture cases the ratio was 0.6:1). The patients with Barrett's stricture are generally young; a number of them are children and young adults.

0221F6.JPG

Figure 4D. .Photo micrograph of the oesophageal biopsy below the stricture showing columnar epithelium in Barrett's oesophagus.

Incidence

Barrett's stricture is uncommon when one considers its incidence in esophageal strictures as a whole. In a series of 424 reflux strictures of the esophagus with/without sliding hiatal hernia, 18 (4.2%) we found Barrett's strictures. However, stricture is the most common of the complications of CLE. In our series out of 44 cases of CLE with complications, 18 (nearly 41%) had stricture which is similar to other large series [20,21]. The following definition incorporates the above characteristics of Barrett's stricture: Barrett's stricture is referred to as a stenotic lesion at the squamo-columnar epithelial junction of an esophagus whose lower 5 cm above the gastroesophageal junction (3 cm above the phreno-esophageal ligament) are covered by columnar cell mucosa.

Acknowledgements

I wish to acknowledge with thanks the help and advice given to me by Dr Philip Bury, Consultant Pathologist at Castle Hill Hospital, Cottingham.

References

1. Barrett NR. The lower oesophagus lined by columnar epithelium Surgery 1957;41:881-894.

2. Naef AP, Ozzello L. Columnar-lined lower oesophagus an acquired lesion with malignant predisposition. J Thorac Cardiovasc Surg 1957;70(5);826-835.

3. Sjogren RW Jr, Johnson LF. Barrett's oesophagus, a review. Am J Med 1983:74:313-321

4. Skinner DB, Walther BC, Riddell RH, Schmidt H, Iascone C, DeMeester TR. Barrett's oesophagus comparison of benign and malignant cases. Ann Surg 1983;198:544-566.

5. Ribet M, Mensier E, Pruvot FR. Barrett's oesophagus and adenocarcinoma. Eur J Cardiothorac Surg 1987; 1:29-32.

6. Streitz JM, Ellis FH, Gibb SP, Balogh K, Watkins E Adenocarcinoma in Barrett's oesophagus, a clinicopathological study of 65 cases. Ann Surg 1991:213:122-125.

7. Moghissi K, Sharpe DAC, Pender D. Adenocarcinoma and Barrett's oesophagus. Eur J Cardiolhorac Surg 1993:7:126-132.

8. Barrett NR. Chronic peptic ulcer of the oesophagus and oesophagitis. Br J Surg 1950:38:175-182.

9. Allison PR, Johnstone AS. The oesophagus lined with gastric mucous membrane. Thorax 1953:8:87-101 10. Lortat-Jacob JL. Endobrachy oesophage. Ann Chir 1957:11:1247-1254.

11 Allison PR. Peptic oesophagitis and oesophageal stricture. Lancet 1970:11:199-201.

12. Hayward J. The lower end of the oesophagus. Thorax 1961:16:36-41.

13. Hayward J. The phreno-esophageal ligament in hiatal hernia repair. Thorax 1961:16:41-45.

14. Hayward J. The treatment of fibrous stricture of the oesophagus associated with hiatal hernia. Thorax 1961 ;16:45-55. 15. Moghissi K. Conservative surgery in reflux stricture of the oesophagus associated with hiatal hernia. Br J Surg 1979:66:

221-225.

16. Moghissi K. Stenoses hautes de 1'oesophage thoracique et leur traitement chirurgical. Chirurgie 1980:106:711-718.

17. Moghissi K, Goebells P. Relevance of anatomopathology of high oesophageal strictures to the design of surgical treatment. Eur J Cardiothorac Surg 1990:4:91-96

18. Moghissi K. Intra-thoracic fundoplication for reflux stricture associated with short oesophagus. Thorax 1983:38:36-40.

19. Moghissi K, Pender D Management of proximal oesophageal strictures. Eur J Cardiothorac Surg 1989:3:93-98

20. Starnes VA, Adkins RB, Ballinger JF, Shayers JL. Barrett's oesophagus: a surgical entity. Arch Surg 1984; 119(5):503-567.

21. Bremner CO In: DeMeester TR, Matthews HR (eds) International Trends in General Thoracic Surgery - Benign Oesophageal Disease. St. Louis, Washington DC, Toronto: The CV Mosby Company, 1987;234.


Publication date: May 1994 OESO©2015