Exocrine pancreatic insufficiency following esophagectomy

Abstract

Weight loss following esophagectomy is a management challenge for all patients. It is multifactorial with contributing factors including loss of gastric reservoir, rapid small bowel transit, malabsorption, and adjuvant chemotherapy. The development of a postoperative malabsorption syndrome, as a result of exocrine pancreatic insufficiency (EPI), is recognized in a subgroup of patients following gastrectomy. This has not previously been documented following esophageal resection. EPI can result in symptoms of flatulence, diarrhea, steatorrhea, vitamin deficiencies, and weight loss. It therefore has the potential to pose a significant level of morbidity in postoperative patients. There is some evidence that patients with proven EPI (fecal elastase-1 < 200 μg/g) may benefit from a trial of pancreatic enzyme replacement therapy (PERT). We observed symptoms compatible with EPI in a subgroup of patients following esophagectomy. We hypothesized that this was contributing to malabsorption and malnutrition in these patients. To investigate this, fecal elastase-1 was measured in postoperative patients, and in those with proven EPI, a trial of PERT was commenced in combination with specialist dietary education. At routine postoperative follow-up, which included assessment by a specialist dietitian, those patients with symptoms suggestive of malabsorption were given the opportunity to have their fecal elastase-1 measured. PERT was then offered to patients with fecal elastase-1 less than 200 μg/g (EPI) as well as those in the 200-500 μg/g range (mild EPI) with more severe symptoms. Fecal elastase-1 was measured in 63 patients between June 2009 and January 2011 at a median of 4 months (range 1-42) following surgery. Ten patients had fecal elastase-1 less than 200 μg/g, and all had failed to maintain preoperative weight. All accepted a trial of PERT. Nine (90%) had symptomatic improvement, and seven (70%) increased their weight. Thirty-nine patients had a fecal elastase-1 in the 200-500 μg/g range. Twelve were given a trial of PERT based on level of symptoms, five (42%) reported an improvement in symptoms, but only two (17%) gained weight. Our early results support the observation that EPI is a factor contributing to postoperative morbidity in patients recovering from esophagectomy and that these patients can benefit from a trial of PERT. Our study has limitations, and a formal trial is required to evaluate the impact of EPI and PERT following esophagectomy. Currently, our practice is to measure fecal elastase-1 in any patient with unexplained weight loss or symptoms of malabsorption. In patients with proven EPI or those who are symptomatic with mild EPI, a trial of PERT should be offered and symptoms reassessed.

Micronutrient Deficiency Following Esophagectomy for Cancer of the Upper Gastrointestinal Tract

“…Although commonly reported after gastrectomy [13][14][15], little is known regarding the prevalence and implications of micronutrient deficiency after esophagectomy. Whilst previous studies have focused on aspects related to micronutrient intake and absorption after esophagectomy, they do so without direct correlation to blood levels [6][7][8]16]. Wang et al reported a persistent decrease in Zinc levels after esophagectomy [9], a finding that was corroborated by the current study.…”

A systematic review of the nutritional consequences of esophagectomy

“…It may not be appropriate to simply target increasing nutritional intake without consideration of the management to alleviate any chronic gastro-intestinal symptoms [41] Post-operative malabsorption syndrome has been shown in this patient group [42] and may be a contributing factor to the malnutrition frequently seen.…”

Nutrition in peri-operative esophageal cancer management

“…Malabsorption is hypothesized to have a complex and multifactorial etiology, involving exocrine pancreatic insufficiency (EPI), bile acid malabsorption (BAM), and smallintestinal bacterial overgrowth (SIBO). After vagal denervation, EPI may occur as a result of loss of endogenous neuroendocrine signals that stimulate the release of digestive enzymes by the pancreas and can be corrected with pancreatic enzyme replacement therapy (PERT) [108,109]. BAM may result not only from vagal denervation but also from disruption of the enterohepatic circulation of bile acids and can be treated with bile-acid binding drugs, like colesevelam [108,110].…”