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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
 
Transplantation. Author manuscript; available in PMC 2010 October 14.
Published in final edited form as:
Transplantation. 1991 July; 52(1): 150–151.
PMCID: PMC2954621
NIHMSID: NIHMS240791

ESOPHAGEAL COMPLICATIONS IN ORTHOTOPIC LIVER TRANSPLANT PATIENTS1

Although serious esophageal complications are not uncommon after liver transplantation, these have received little attention in the literature (1). We report here the nature and treatment of major esophageal complications encountered in 7 (0.6%) of 1154 adult liver transplant recipients at the University of Pittsburgh between January 1, 1986 and March 31, 1990. Of 4 perforations of the distal esophagus (Table 1), 3 were thought in retrospect to have been caused by pretransplant sclerotherapy. The complication in 2 recipients was diagnosed one or 2 days posttransplantation, and in a third at the time of liver replacement. The fourth perforation was secondary to multiple hemostatic sutures placed during transplantation near the esophagogastric junction. Two patients had intractable esophageal bleeding from multiple ulcerations caused by cytomegalovirus and one patient with an Epstein-Barr virus infection developed an esophageal clonal B cell lymphoma.

TABLE 1
University of Pittsburgh resultsa

The treatment for the 7 patients is summarized in Table 1. Three of the 4 patients with esophageal perforation died from 2 to 198 days after the diagnosis in spite of treatment with thoracic and/or transabdominal drainage, exclusion by temporary ligation of the lower esophagus, or an attempt at esophagectomy and colon interposition. The single survivor closed his perforation spontaneously after cervical esophagostomy and prolonged subdiaphragmatic drainage.

One of the 2 patients with massive bleeding survived after total esophagectomy and colon interposition 5 months later. The other died of multiple bacterial infections and disseminated tuberculosis 2 months after the hemorrhage was controlled with suture ligation of multiple bleeding sites through a longitudinal esophagostomy, cervical esophagostomy, tube gastrostomy, and temporary ligation of the esophagus at the esophagogastric junction. The patient with lymphoma had regression of the lesion when immunosuppression was reduced, but hepatic rejection followed, necessitating retransplantation. He then had a recurrence of the lesion that was treated with esophagogastrectomy. Five months later, the lymphoma recurred above the suture line, but this regressed after cyclosporine was stopped and treatment was started once—and subsequently twice—per week with the new immunosuppressive agent FK506 (2, 3). He now is tumor-free almost 3 years after the first liver transplantation, 18 months after retransplantation and 8 months after the change in immunosuppression.

An obvious conclusion from these observations is that major esophageal complications in the transplant population have a very high morbidity and mortality. Aside from the added burden of immunosuppression, liver transplant patients are particularly vulnerable because of their general disability from liver failure, the frequent involvement of the esophagus secondary to liver disease, and the consequent high rate of endoscopy in the days or weeks preceding transplantation. Furthermore, it is obvious that pretransplantation sclerotherapy for both treatment of bleeding esophageal varices and prophylaxis does carry a certain risk of perforation of the esophagus (4, 5), which may not be diagnosed, as in 2 of our patients, until after transplantation. After sclerotherapy, a high degree of suspicion is necessary in order to rapidly diagnose any possible perforation. When sepsis or bleeding were controlled with effective drainage or esophagectomy, later reconstruction and esophageal replacement was possible in one case. In another patient with esophageal lymphoma, a radical esophagogastrectomy and primary reconstruction were performed without incident.

Footnotes

1This work was supported by research grants from the Veterans Administration and by Project Grant DK 29961 from the National Institutes of Health. Bethesda, MD.

REFERENCES

1. Vickers CR, O'Connor HJ, Quintero GA, et al. Delayed perforation of the esophagus after variceal sclerotherapy and hepatic transplantation. Gastrointest Endosc. 1989;35:459. [PubMed]
2. Venkataramanan R, Jain A, Cadoff E, et al. Pharmacokinetics of FK 506: preclinical and clinical studies. Transplant Proc. 1990;22(1, suppl 1):52. [PMC free article] [PubMed]
3. Morris RE, Wu J, Shorthouse R. Comparative immunopharmacologic effects of FK506 and CyA in in vivo models of organ transplantation. Transplant Proc. 1990;22(1. suppl 1):110. [PubMed]
4. Pillay P, Starzl TE, Van Thiel DH. Complications of sclerotherapy for esophageal varices in liver transplant candidates. Transplant Proc. (in press) [PMC free article] [PubMed]
5. Miller RE, Bossart PW, Tiszenkel HI. Surgical management of complications of upper gastrointestinal endoscopy and esophageal dilatation including laser therapy. Am Surg. 1987;53:667. [PubMed]