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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Peptic strictures of the esophagus

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Department of Surgery, St. Michael’s Hospital, University of Toronto, Ontario, Canada

Pathophysiology

Peptic strictures are the endstage result of chronic reflux esophagitis. They account for 90% of benign esophageal strictures and, by definition, imply a stricture arising as a result of exposure to the acid-peptic content of the stomach. The esophagus normally is exposed to frequent episodes of reflux of small amounts of gastric fluid which are limited by a competent lower esophageal sphincter and rapidly cleared by normal esophageal peristalsis. A defect in these and other esophageal protective mechanisms leads to inflammation due to prolonged esophageal exposure to acid, pepsin, and possibly bile and pancreatic enzymes. Stricture formation occurs in 7–23% of patients with reflux esophagitis. The process is progressive, beginning with mucosal edema and inflammatory cell infiltrates of the lamina propria. Chronic esophagitis progresses transmurally, even into periesophageal tissues, with subsequent fibrosis and scarring leading to luminal compromise and esophageal foreshortening (Kuo and Kalloo 1998,Mamazza et al 1998).

A stricture is an esophageal narrowing, usually 13 mm or less in diameter, that causes dysphagia. The normal esophagus measures up to 30 mm in diameter. Peptic strictures occur usually at the squamocolumnar junction and measure 1–4 cm in length. The typical patient with a peptic stricture is elderly with a long history of gastroesophageal reflux (GER). Significant predictors of stricture formation in patients with GER are lower esophageal sphincter (LES) tone of less than 8 mmHg, impaired esophageal motility, and duodenogastric reflux (Marks and Richter 1993,Stein et al 1992). Hiatus hernia is twice as prevalent in GER patients with stricture (85%) as compared to those with no esophagitis (42%) (Kuo and Kalloo 1998).

Diagnosis

The main goal in diagnosis is to characterize the stricture and rule out the presence of malignancy. The differential diagnosis of peptic stricture is shown in table I. All patients with suspected peptic stricture should undergo the following investigations to confirm the diagnosis and plan therapy:

Table I. Differential diagnosis of distal esophageal stricture.

Table I

Differential diagnosis of distal esophageal stricture.

  • Barium esophagram defines the location, length, and character of a stricture, including mild strictures that might be missed by endoscopy or tight strictures that cannot be traversed by an endoscope. Esophageal foreshortening and the presence of a hiatal hernia are also determined.
  • Endoscopy is essential in detecting the presence of Barrett’s intestinal metaplasia and ruling out malignancy through biopsy and brushing cytology.
  • Esophageal manometry measures LES tone and detects impaired motility, both of which have prognostic value and implications for subsequent management.
  • 24 hour pH monitoring identifies the presence and extent of reflux. This and manometry technically may not be possible with tight strictures prior to initial dilation.

Management

The goals of treatment are 1) relieve dysphagia and restore swallowing, and 2) treat the underlying GER to promote healing of esophagitis and prevent stricture recurrence.

Stricture Dilation

Stricture dilation is the initial means of relieving dysphagia. Dysphagia resolves when the stricture can be dilated to 14 mm (46 F) (Kahrilas 1996). Three types of dilators are commonly used.

  • Mercury filled rubber bougie (Maloney, Hurst) are generally employed for strictures no smaller than 4 mm.
  • Wire-guided dilators (Savary-Gilliard) pass over a guidewire, are designed for use with fluoroscopy, and are better for narrow, tortuous strictures.
  • Polyethylene balloon dilators are generally used through the endoscope and are also good for narrow, tortuous strictures. In theory they are better than wireguided dilators since they exert no longitudinal shearing force on the esophagus, but this has not been substantiated.

After stricture dilation 80% of patients report initial relief of dysphagia. However, 30–50% will require repeat dilation within one year despite adequate acid suppression (Kuo and Kalloo 1998). Weight loss and the absence of heartburn at initial presentation, not the diameter of the stricture, predict the requirement for frequent dilations in the first year (Agnew et al 1996). Bougienage carries a 0.1–0.4% risk of esophageal perforation with each treatment. The use of steroid injections to reduce the interval between dilations has been reported, but there is no strong evidence to support this yet.

Medical therapy

Proton pump inhibitors (PPI) are the most efficacious and cost effective medical therapy for preventing recurrent stricture. Enhancing esophageal and gastric emptying with motility agents, is only as effective as H2 blockers at healing mild esophagitis. In randomized trials, H2 blockers were no more effective than placebo at reducing the incidence of recurrent dysphagia, whereas several doubleblind, randomized trials found that Omeprazole was more efficacious and cost effective than H2 blockers at healing esophagitis and reducing the need for repeat stricture dilation. Longterm PPI maintenance in conjunction with lifestyle modification are required to prevent recurrent esophagitis and stricture (Kahrilas 1996,Marks and Richter 1993).

Surgical therapy

Surgery is more effective than medical therapy for healing esophagitis (Kahrilas 1996,Marks and Richter 1993,Spechler 1992). The traditional indications for surgery in patients with peptic stricture have been: 1) inability to dilate the stricture, 2) frequent recurrence of dysphagia, 3) esophagitis refractory to medical therapy, 4) extraesophageal manifestations such as aspiration pneumonia, and 5) consideration of cost and long term side effects of medical therapy in young patients. Typically surgery has been the option of last resort, however, with the introduction of minimally invasive techniques this reservation is being challenged. Laparoscopic Nissen fundoplication is associated with much less patient discomfort and faster recovery than open surgery. There are currently numerous case series with shortterm follow-up that suggest that outcomes after laparoscopic Nissen fundoplication are equivalent to open surgery. Large randomized trials comparing laparoscopic and open antireflux techniques are still needed. Regardless of technique, the type of surgical procedure performed is dictated by the character of the stricture (Mamazza, Schlachta, and Poulin 1998).

Antireflux procedures

For dilatable strictures, the healing of esophagitis is promoted with a standard antireflux procedure. The most common antireflux procedures are partial (Toupet, Belsey) or complete (Nissen) fundoplications. Of these, the Nissen fundoplication is the most popular. In a randomized trial comparing medical to surgical therapy for complicated GER, surgical therapy was more effective in improving symptoms of esophagitis and associated with higher patient satisfaction (Spechler 1992). Laparoscopic fundoplication is as effective as open surgery in controlling symptoms of GER and despite early concerns is equally applicable to patients with complicated esophagitis and stricture (Watson et al 1997).

Patients with a shortened esophagus require esophageal lengthening at the time of antireflux surgery. The Collis gastroplasty has been shown to be effective for esophageal lengthening in combination with both the Nissen (Collis-Nissen) and Belsey (Collis-Belsey) repairs. Furthermore, a Collis-Nissen fundoplication can now effectively be performed laparoscopically.

A theoretical concern in patients with impaired esophageal motility is that total fundoplication may lead to dysphagia. For this reason it has been recommended that these patients undergo partial fundoplication only, such as the Belsey 270o fundoplication or a laparoscopic Toupet 180o fundoplication.

Esophageal resection

Patients with undilatable strictures, are candidates for transhiatal esophageal resection with replacement by either stomach, colon or jejunum. Laparoscopic esophagectomy is now routinely performed in a few centers, however, evidence of superior outcomes as compared to open surgery is still pending.

Mallory-Weiss Syndrome

Diagnosis and pathogenesis

In 1929 Mallory and Weiss reported 15 patients presenting with upper gastrointestinal hemorrhage following excessive alcohol consumption, persistent retching and vomiting. This syndrome is the cause of bleeding in up to 15% of patients presenting with upper gastrointestinal bleeding and should be considered high in the differential diagnosis when hematemesis or melena follow retching and vomiting. Forceful emesis against a closed glottis causes a rapid transmission of intraabdominal pressure into the esophagus where linear lacerations at the esophagogastric junction occur. Most cases are self limiting and heal without further therapy, although fully half may require blood transfusions. The diagnosis is readily established by endoscopy, at which time twothirds of patients are found to have associated abnormalities such as gastritis, esophagitis, hiatus hernia, peptic ulcer or varices.

Therapy

Controversy surrounds the most effective therapy for controlling bleeding in these patients because there are no randomized trials comparing modern treatments. At the time of endoscopy, if active bleeding or a visable vessel can be identified, epinephrine sclerotherapy or coaptive heater probe coagulation can be applied with nearly 100% effectiveness at obtaining hemostasis. Rebleeding occurs in 30%, requiring additional therapy. Other therapies with mixed success in controlling bleeding have been balloon tamponade, transcatheter embolization, and systemic and selective arterial infusion of vassopressin. Surgery is generally a last resort. The usual surgical approach is through a generous anterior gastrotomy whereby blood clot can be evacuated from the stomach and the bleeding source identified and oversewn. Laparoscopic oversewing of bleeding MalloryWeiss tear has recently been described (Bataller et al 1994,Lum et al 1997).

Figure 1. Decision process in patients with peptic esophageal stricture undergoing surgery.

Figure 1

Decision process in patients with peptic esophageal stricture undergoing surgery.

References

1.
Agnew S R, Pandya S P, Reynolds R P, Preiksaitis H G. Predictors for frequent esophageal dilations of benign peptic strictures. Dig Dis Sci. (1996);41:931–936. [PubMed: 8625765]
2.
Bataller R, Llach J, Salmeron J M. et al. Endoscopic sclerotherapy in upper gastrointestinal bleeding due to the MalloryWeiss syndrome. Am J Gastroenterol. (1994);89:2147–2150. [PubMed: 7977231]
3.
Kahrilas P J. Gastroesophageal reflux disease. JAMA. (1996);276:983–988. [PubMed: 8805734]
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Kuo W H, Kalloo A N. Reflux strictures of the esophagus. Gastrointest Endosc Clin N Am. (1998);8:273–281. [PubMed: 9583006]
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Lum D F, McQuaid K, Lee J G. Endoscopic hemostasis of nonvariceal, non-peptic ulcer hemorrhage. Gastrointest Endosc Clin N Am. (1997);7:657–670. [PubMed: 9376956]
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Mamazza J, Schlachta C M, Poulin E C. Surgery for peptic strictures. Gastrointest Endosc Clin N Am. (1998);8:399–413. [PubMed: 9583013]
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Marks R D, Richter J E. Peptic strictures of the esophagus. Am J Gastroenterol. (1993);88:1160–1173. [PubMed: 8338082]
8.
Spechler S J. Comparison of medical and surgical therapy for complicated gastroesophageal reflux disease in veterans. N Engl J Med. (1992);326:786–792. [PubMed: 1538721]
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Stein H J, Barlow A P, DeMeester T R, Hinder R A. Complications of gastroesophageal reflux disease. Role of the lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and duodenogastric reflux. Ann Surg. (1992);216:35–43. [PMC free article: PMC1242544] [PubMed: 1632700]
10.
Watson D I, Foreman D, Devitt P G, Jamieson G G. Preoperative endoscopic grading of esophagitis versus outcome after laparoscopic Nissen fundoplication. Am J Gastroenterol. (1997);92:222–225. [PubMed: 9040195]
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6899

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