Journal of Surgical Oncology 51:19-21 (1992)

Atrophic Chronic Gastritis and Esophagogastric Anastomotic Leak After Resection and Reconstruction for Esophageal Carcinoma SRDJAN RAKIC,

PREDRAG PESKO, MD, MlROSLAV MILICEVIC, MD, PhD, ANT) ZORAN GERZIC, MD, PhD, FIGS From the Department of Surgery, lnstitute o f Digestive Diseases, Belgrade University School of Medicine, Belgrade, Yugoslavia MD, PhD, FACS,

The incidence of anastomotic leakage after esophagectomy for cancer and reconstruction with the stomach was analyzed with respect to the presence of coexistent atrophic chronic gastritis (ACG). Of a total of 28 operated esophageal cancer patients with ACG, 6 patients developed an anastomotic leak at the cervical esophagogastrostomy (21%). Of a total of 8 operated esophageal cancer patients none of the patients developed an anastomotic leak. The ACG positive and the ACG negative patients were found to be well matched for age, sex, type of operation, transplant route, level of the anastomoses, and suture technique, and all were operated on by the same surgeons. The difference in leakage rate did not reach statistical significance. 0 1992 Wiley-Liss, Inc. KEYWORDS: esophagectomy, gastroplasty, leakage

INTRODUCTION Anastomotic leakage is a serious complication of esophagectomy and reconstruction for esophageal carcinoma. Patients with squamous cell carcinoma of the esophagus (SCCE) may frequently have a coexistent atrophic chronic gastritis (ACG) [ I ] . The stomach is the most frequently used organ to replace the esophagus after resection for cancer. The objective of this study was to determine whether coexistent ACG influences the incidence of anastomotic leakage after esophagectomy for SCCE and reconstruction with the stomach. PATIENTS AND METHODS Thirty-six patients who underwent a one-stage esophagectomy for SCCE and reconstruction with stomach between 1987 and 1991 were studied. The additional inclusion criterium was that at least two biopsy specimens from both the antrum and the body of the stomach were obtained during endoscopy or surgery. There were 30 men and 6 women with a mean age of 58.0 7.9 years. All patients but one were cigarette smokers and/or alcohol consumers.

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0 1992 Wiley-Liss, Inc.

The gastric histological findings were classified as previously described [2] into normal, superficial gastritis, mild atrophic gastritis, moderate atrophic gastritis, and severe atrophic gastritis. Normal mucosa showed neither inflamation nor atrophy. The second category was related to an increased number of round inflamatory cells without loss of normal mucosal glands and was also considered to be “ACG negative” for the purpose of this study. The latter three categories were related to the glandular reaction, slight, moderate, or severe (total) loss of normal glands with a varying degree of chronic inflamation and were considered to be “ACG positive” for the purpose of this study. The results of gastric histology were not known at the moment of surgery. Esophagectomy was performed either through a right thoracotomy or by blunt dissection. Stomach for reconstruction was prepared as described by Akiyama et al.

Accepted for publication May 14, 1992 Address reprint requests to Dr. Srdjan Rakic, Department of Surgery, Institute of Digestive Diseases, Koste Todorovica 6, Belgrade 1 1000, Yugoslavia.

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tween patients with ACG and patients without ACG, we evaluated the relevance of ACG as the independent variable that determines leakage. Coexistent ACG was assoACG positive ACG negative Total ciated with a higher risk of esophagogastric anastomotic (n = 28) (n = 8) (n = 36) leakage in this series. Conversely, the normal stomach Sex (MIF) 2414 612 3016 58.9 k 8.0 56. I t 7.9 58.0 * 7.9 contributed to the safety of anastomotic healing. The Age (mean + SD) difference was not statistically significant in this small Esophageal resection series. It may well be that our findings reflect a lack of Transthoracic 18 5 23 evidence, rather than a lack of difference. Transhiatal 10 3 13 There are numerous possibilities as to how ACG may Substitute route influence anastomotic healing. An adequate gastric muRetrosternal 7 I 8 cosal blood flow is essential regardless of other factors. Posterior 21 7 28 Severe mucosal injury results in a reduction of gastric mediastinal 6 (21%) 0 (0%) 6 (17%) Leakage mucosal perfusion, probably due to the disruption and loss of patency of the local capillary network [9]. Gastric *ACG, atrophic chronic gastritis. mucosal cells possess the ability to migrate rapidly after mucosal damage, which is present in ACG patients [lo]. 131. Either the retrosternal or posterior mediastinal route After damage to the gastric mucosa, a rapid release of gel was used for placement of the substitute. All anastomoses mucus is seen. This mucus, together with fibrin, cellular were made in the neck by hand using two layers of inter- debris, and plasma, forms a continuous layer creating a rupted 3/0 polyglactin (Vicryl) sutures. All operations microenvironment suitable for optimal epithelial regenerwere performed by the authors using the same operative ation and, consequently, anastomotic healing [ 1 11. A technique. The diagnosis of leakage at the suture line was feature of ACG is diffuse glandular atrophy, which based on clinical evidence, routinely confirmed by con- causes a delay in the formation and attenuation of this trast study. Statistical significance was evaluated by the layer. The role of prostaglandins and epidermal growth chi-square test (with Yates’ correction) and Student’s factor, both known to have atrophic action on the gastric mucosa and to enhance mucosal perfusion [ 12,131 might t-test. be of some importance as well. RESULTS An obvious background exists suggesting that ACG ACG was found in 28 of the 36 studied patients (78%). patients may have impaired anastomotic healing of Patients with ACG and patients without ACG were found esophagogastrostomy after esophageal resection. If this to be well matched for sex, age, type of esophagectomy, proves true, the differences in the incidence of ACG may and route for placement of the substitute (Table I). Leak- also account for some differences in results of SCCE age rates with respect to coexistent ACG are shown in surgery between the Far East and the West. Table I. The difference between the two groups did not reach statistical significance. REFERENCES TABLE I. Patient Characteristics and Leakage With Respect to Coexistent ACG*

DISCUSSION One of the main reasons for the high incidence of ACG in SCCE patients may be the presence of some epidemiological and/or etiological similarities between the two conditions. Both ACG and SCCE are age related [4] and are linked to tobacco smoking and alcohol consumption [5,6).This may account for our findings as well. More pertinent to this discussion is whether the coexistent ACG influences anastomotic healing when the stomach is used as an esophageal substitute. To the best of our knowledge, no report has attempted to evaluate this so far. It has been previously shown that the incidence of leakage after esophageal resection and reconstruction is significantly influenced by the type of operation, choice of esophageal substitute, technique of suturing, and level of the anastomosis [7,8]. Since these factors were either identical or equally distributed be-

I . Rakic S, Adan.ja G: Serum gastrin levels in patients with squamous cell carcinoma of the oesophagus. Gullet 1: 101, 199I . 2. Sipponen P, Kekki M, Siurala M: Increased risk of gastric cancer in males affects the intestinal type of cancer and is independent of age, location of the tumour and atrophic gastritis. Br J Cancer 57:332-336, 1988. 3. Akiyama H, Miyazono H, Tsurumaru M, Kawamura T: Use ofthe stomach as an esophageal substitute. Ann Surg 88:60&61 I , 1978. 4. Siurala M, Sipponen P, Kekki M: Chronic gastritis: dynamics and clinical aspccts. Scand J Gastroenterol Suppl 109:69-76, 1985. 5 . Burch PRJ: Variance and dissent: Esophageal cancer in relation to cigarette and alcohol consumption. J Chron Dis I1:793-808, 1984. 6. Hui W, Lam S: Etiology and management of chronic gastritis. Dig Dis Sci 7 3 - 6 0 , 1989. 7. Peracchia A, Bardini R, Ruol A, et al: Esophagovasceral anastomotic leak. J Thorac Cardiovasc Surg 95:685-69 I , 1988. 8. Lorentz T, Fok M, Wong J: Anastomotic leakage after resection and bypass for esophageal cancer: Lessons learned from the past. World J Surg 13:472477, 1989. 9. Trier JS, Szaho S , Allan CH: Ethanol induced damage to mucosal capillaries of rat stomach. Gastroenterology 92: 13-22, 1987.

Gastritis and Esophagogastric Leak 10. Von Ritter C, Hinder R, Oosthuizen M, et al: Gastric mucosal lesions induced by hemorrhagic shock in baboons. Role of oxygen-derived free radicals. Dig Dis Sci 33:857-864, 1988. 11. Wallace J , Whittle B: The role of extra-cellular mucus as a protective cap over gastric mucosal damage. Scand J Gastroenterol Suppl 125:79-84, 1986.

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12. Hawkey CJ, Rampton DS: Prostdghdins and the gastrointestinal mucosa: are they important in its function, disease or treatment? Gastroenterology 89: 1162-1 188, 1985. 13. Johnson L: New aspects on the trophic action of gastrointestinal hormones. Gastroenterology 72:788-792, 1977.

Atrophic chronic gastritis and esophagogastric anastomotic leak after resection and reconstruction for esophageal carcinoma.

The incidence of anastomotic leakage after esophagectomy for cancer and reconstruction with the stomach was analyzed with respect to the presence of c...
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