When “Bowel Rest” Becomes Bowel Ischemia: Elemental Feeding–Induced Non-Occlusive Mesenteric Ischemia After Esophagectomy
Abstract No:
00CR4
Submission Type:
Cardiothoracic Resident Case Report Competition
Authors:
Ido Haimi (1), Reza Mehran (2)
Institutions:
(1) University of Texas MD Anderson Cancer Center, Houston, TX, (2) University of Texas, Houston, TX
Submitting Author:
Ido Haimi
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University of Texas MD Anderson Cancer Center
University of Texas MD Anderson Cancer Center
Co-Author:
*Reza Mehran
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University of Texas
University of Texas
Presenting Author:
Ido Haimi
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University of Texas MD Anderson Cancer Center
University of Texas MD Anderson Cancer Center
Abstract:
Objective
To describe a previously under-recognized mechanism of non-occlusive mesenteric ischemia (NOMI) caused by advancement of elemental enteral feeding in a post-esophagectomy patient receiving pharmacologic splanchnic vasoconstriction for high-output chyle leak.
Case Summary
A 66-year-old obese man with a history of prior open bariatric surgery (vertical banded gastroplasty) underwent Ivor Lewis esophagectomy for distal esophageal adenocarcinoma. The operation was initiated laparoscopically but converted to an open approach via prior midline incision after recognizing the extent of gastric adhesions and identifying incarceration of the right gastroepiploic artery within a known incisional hernia. A feeding jejunostomy tube was placed in Witzell fashion.
Postoperatively, the patient developed a high-output abdominal chyle leak, likely related to extensive lysis of adhesions and lymphadenectomy. Given persistent output and a failed attempt at lymphangiography with embolization, maximal medical management was continued and included total parenteral nutrition, octreotide, and midodrine. Notably, preoperative imaging demonstrated calcified celiac and superior mesenteric artery origins, suggesting limited mesenteric perfusion reserve.
After clinical stabilization and a decrease in chyle output, elemental jejunal feeds were restarted and advanced to goal. Within hours, the patient developed severe abdominal pain, lactic acidosis, and shock. Computed tomography ruled out pulmonary embolism, and transthoracic echocardiography demonstrated preserved biventricular function without intracardiac thrombus. Exploratory laparotomy revealed diffuse transmural small-bowel necrosis with patent mesenteric vessels and no evidence of arterial or venous occlusion. In the setting of abrupt clinical deterioration, negative cardiopulmonary evaluation, and these operative findings, a diagnosis of non-occlusive mesenteric ischemia was made. Given the extent of ischemia, and following a detailed discussion with the family, care was transitioned to comfort-focused measures, and the patient unfortunately expired.
Conclusions
This case demonstrates a lethal physiologic mismatch in which pharmacologic splanchnic vasoconstriction fixes intestinal oxygen delivery at a low-flow state while elemental enteral feeding sharply increases metabolic demand through active nutrient transport. In patients with chyle leak, obesity, prior abdominal surgery, vascular calcification, or impaired autoregulation, advancement of elemental feeds may precipitate NOMI despite preserved systemic hemodynamics. Trophic feeding or parenteral nutrition should be strongly considered until splanchnic vasoconstrictive therapy is discontinued.
To describe a previously under-recognized mechanism of non-occlusive mesenteric ischemia (NOMI) caused by advancement of elemental enteral feeding in a post-esophagectomy patient receiving pharmacologic splanchnic vasoconstriction for high-output chyle leak.
Case Summary
A 66-year-old obese man with a history of prior open bariatric surgery (vertical banded gastroplasty) underwent Ivor Lewis esophagectomy for distal esophageal adenocarcinoma. The operation was initiated laparoscopically but converted to an open approach via prior midline incision after recognizing the extent of gastric adhesions and identifying incarceration of the right gastroepiploic artery within a known incisional hernia. A feeding jejunostomy tube was placed in Witzell fashion.
Postoperatively, the patient developed a high-output abdominal chyle leak, likely related to extensive lysis of adhesions and lymphadenectomy. Given persistent output and a failed attempt at lymphangiography with embolization, maximal medical management was continued and included total parenteral nutrition, octreotide, and midodrine. Notably, preoperative imaging demonstrated calcified celiac and superior mesenteric artery origins, suggesting limited mesenteric perfusion reserve.
After clinical stabilization and a decrease in chyle output, elemental jejunal feeds were restarted and advanced to goal. Within hours, the patient developed severe abdominal pain, lactic acidosis, and shock. Computed tomography ruled out pulmonary embolism, and transthoracic echocardiography demonstrated preserved biventricular function without intracardiac thrombus. Exploratory laparotomy revealed diffuse transmural small-bowel necrosis with patent mesenteric vessels and no evidence of arterial or venous occlusion. In the setting of abrupt clinical deterioration, negative cardiopulmonary evaluation, and these operative findings, a diagnosis of non-occlusive mesenteric ischemia was made. Given the extent of ischemia, and following a detailed discussion with the family, care was transitioned to comfort-focused measures, and the patient unfortunately expired.
Conclusions
This case demonstrates a lethal physiologic mismatch in which pharmacologic splanchnic vasoconstriction fixes intestinal oxygen delivery at a low-flow state while elemental enteral feeding sharply increases metabolic demand through active nutrient transport. In patients with chyle leak, obesity, prior abdominal surgery, vascular calcification, or impaired autoregulation, advancement of elemental feeds may precipitate NOMI despite preserved systemic hemodynamics. Trophic feeding or parenteral nutrition should be strongly considered until splanchnic vasoconstrictive therapy is discontinued.
Category:
Thoracic
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