S6054 When Gas Crosses the Gut Wall: Pneumatosis intestinalis—Side Effect, Obstruction, or Ischemia?

Introduction: Pneumatosis intestinalis (PI) is presence of gas within intestinal wall. PI is idiopathic (15%) or secondary (85%) to GI (gastrointestinal) and non-GI illnesses. Pathogenesis of PI is multifactorial- mechanical, bacterial, and biochemical causes including lactulose. PI is a radiologic finding associated with high mortality rate 33–40% and 100% in cirrhotic patients with MELD (Model for End-Stage Liver Disease) >16. Case Description/Methods: Fifty-three-year-old man with diabetes, hypothyroidism, alcoholic cirrhosis, esophageal varices, and ascites presented with altered mentation and unresponsiveness. He came from the acute long-term care facility and was on hemodialysis 3 times a week for acute kidney injury. He was intubated for airway protection and transferred to critical care for Grade IV hepatic encephalopathy. His abdomen was distended, tense with stretched umbilicus. Lactulose 30 g every 2 hours and rifaximin 550 mg twice daily were given. MELD was 26. (19.6% mortality in 90 days) Ultrasound showed moderately large ascites, followed by paracentesis with 4 L fluid removal. Peritoneal fluid serum-ascites albumin gradient was 3.4, suggestive of portal hypertension with negative culture. Ceftriaxone was started for peritonitis prophylaxis. Abdominal x-ray showed scattered air-fluid levels and small bowel obstruction, managed nonoperatively. Fifteen doses of lactulose were already given before X-ray. Blood culture was negative. Leukocytosis peaked at 37,500/uL. Lactic acid was 5.6, 2.1, and 7.6 mmol/L associated with respiratory alkalosis with pH 7.44 initially and then down to 7.19. Ammonia came down from 314 to 137 by lactulose, but then rose to 623 umol/L. Bowel sounds were reduced on next day. Computed tomography scan abdomen/pelvis with contrast showed pneumatosis intestinalis involving the mid and distal small bowel-compatible with ischemia, portal venous gas, and ascites with liver cirrhosis. He deteriorated requiring 3 vasopressors. He had seizure-like activity and received benzodiazepines. Code status was changed to do-not-resuscitate comfort care due to poor prognosis. He passed away after terminal extubation. Discussion: This case illustrates diagnostic challenges and requires an attentive approach for PI. PI on imaging with signs of peritonitis, lactic acidosis, or portal venous gas guides emergent surgical intervention. In this case, presence of multifactorial etiologies- lactulose, obstruction, and ischemia augments each other, leading to PI. High MELD-poor prognosis requires a balancing decision of emergent management versus comfort.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001152676.07564.98
Primary Topic
Abdominal vascular conditions and treatments
Type
article
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article

S6054 When Gas Crosses the Gut Wall: Pneumatosis intestinalis—Side Effect, Obstruction, or Ischemia?

The American Journal of Gastroenterology
Abdominal vascular conditions and treatments
article

S6054 When Gas Crosses the Gut Wall: Pneumatosis intestinalis—Side Effect, Obstruction, or Ischemia?

article en

Abstract

Introduction: Pneumatosis intestinalis (PI) is presence of gas within intestinal wall. PI is idiopathic (15%) or secondary (85%) to GI (gastrointestinal) and non-GI illnesses. Pathogenesis of PI is multifactorial- mechanical, bacterial, and biochemical causes including lactulose. PI is a radiologic finding associated with high mortality rate 33–40% and 100% in cirrhotic patients with MELD (Model for End-Stage Liver Disease) >16. Case Description/Methods: Fifty-three-year-old man with diabetes, hypothyroidism, alcoholic cirrhosis, esophageal varices, and ascites presented with altered mentation and unresponsiveness. He came from the acute long-term care facility and was on hemodialysis 3 times a week for acute kidney injury. He was intubated for airway protection and transferred to critical care for Grade IV hepatic encephalopathy. His abdomen was distended, tense with stretched umbilicus. Lactulose 30 g every 2 hours and rifaximin 550 mg twice daily were given. MELD was 26. (19.6% mortality in 90 days) Ultrasound showed moderately large ascites, followed by paracentesis with 4 L fluid removal. Peritoneal fluid serum-ascites albumin gradient was 3.4, suggestive of portal hypertension with negative culture. Ceftriaxone was started for peritonitis prophylaxis. Abdominal x-ray showed scattered air-fluid levels and small bowel obstruction, managed nonoperatively. Fifteen doses of lactulose were already given before X-ray. Blood culture was negative. Leukocytosis peaked at 37,500/uL. Lactic acid was 5.6, 2.1, and 7.6 mmol/L associated with respiratory alkalosis with pH 7.44 initially and then down to 7.19. Ammonia came down from 314 to 137 by lactulose, but then rose to 623 umol/L. Bowel sounds were reduced on next day. Computed tomography scan abdomen/pelvis with contrast showed pneumatosis intestinalis involving the mid and distal small bowel-compatible with ischemia, portal venous gas, and ascites with liver cirrhosis. He deteriorated requiring 3 vasopressors. He had seizure-like activity and received benzodiazepines. Code status was changed to do-not-resuscitate comfort care due to poor prognosis. He passed away after terminal extubation. Discussion: This case illustrates diagnostic challenges and requires an attentive approach for PI. PI on imaging with signs of peritonitis, lactic acidosis, or portal venous gas guides emergent surgical intervention. In this case, presence of multifactorial etiologies- lactulose, obstruction, and ischemia augments each other, leading to PI. High MELD-poor prognosis requires a balancing decision of emergent management versus comfort.

The American Journal of GastroenterologyVol. 120(10S2)
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Openalex Percentile: Top 29%
Abdominal vascular conditions and treatments
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