Affiliations

Aurora Sinai Medical Center, Aurora St. Luke’s Medical Center

Abstract

Introduction/Background:

Tension pneumoperitoneum is a rare, lethal cause of abdominal compartment syndrome (ACS) that leads to rapid progressive obstructive shock and hypoxemic respiratory failure. Colonic stent perforation can insufflate the peritoneal cavity under pressure and survival hinges on immediate decompression and rapid source control.

Description:

A 74-year-old woman with large-bowel obstruction from a sigmoid stricture underwent metallic stent placement. Within minutes, she developed tense abdominal distension, respiratory distress requiring intubation, and hemodynamic collapse with cool, mottled extremities. Bedside x-ray revealed massive pneumoperitoneum. With rising peak inspiratory pressures (PIP) and refractory hypotension, the general surgeon performed bedside needle decompression followed by pigtail catheter placement, evacuating air and feculent material. Transient improvement in mean arterial pressure (MAP) and PIP occurred prior to imaging; however, shock progressed, necessitating emergent laparotomy. Despite intensive management of mixed hemorrhagic, septic, and obstructive shock, she developed multisystem organ failure and died.

Discussion:

Tension pneumoperitoneum causes ACS through rapid intra-abdominal pressure elevation, reducing venous return and diaphragmatic excursion. Colonic stent perforation occurs in 5–7% of cases with 16% mortality. Most reported tension pneumoperitoneum cases follow colonoscopy with successful percutaneous decompression alone; this case uniquely demonstrates feculent contamination requiring laparotomy, illustrating how combined obstructive, septic, and hemorrhagic pathophysiology compounds mortality. When tense distension, hypotension, and rising PIP suggest tension physiology, bedside decompression should precede imaging. Colonic stent perforation can trigger tension pneumoperitoneum, ACS, and obstructive shock. Key lessons: (1) Decompress first; imaging should not delay intervention. (2) Anticipate coagulopathy and renal failure; mobilize damage-control resources early. (3) Multidisciplinary sequencing is crucial, yet mortality remains high when hemorrhage and sepsis coexist. This case pairs bedside images with clinical trajectories to illustrate pathophysiology in real time.

Presentation Notes

Presented at Scientific Day; May 20, 2026; Milwaukee, WI.

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May 20th, 12:00 AM

When Air Becomes Pressure: Tension Pneumoperitoneum Causing Abdominal Compartment Syndrome and Obstructive Shock after Sigmoid Stent

Introduction/Background:

Tension pneumoperitoneum is a rare, lethal cause of abdominal compartment syndrome (ACS) that leads to rapid progressive obstructive shock and hypoxemic respiratory failure. Colonic stent perforation can insufflate the peritoneal cavity under pressure and survival hinges on immediate decompression and rapid source control.

Description:

A 74-year-old woman with large-bowel obstruction from a sigmoid stricture underwent metallic stent placement. Within minutes, she developed tense abdominal distension, respiratory distress requiring intubation, and hemodynamic collapse with cool, mottled extremities. Bedside x-ray revealed massive pneumoperitoneum. With rising peak inspiratory pressures (PIP) and refractory hypotension, the general surgeon performed bedside needle decompression followed by pigtail catheter placement, evacuating air and feculent material. Transient improvement in mean arterial pressure (MAP) and PIP occurred prior to imaging; however, shock progressed, necessitating emergent laparotomy. Despite intensive management of mixed hemorrhagic, septic, and obstructive shock, she developed multisystem organ failure and died.

Discussion:

Tension pneumoperitoneum causes ACS through rapid intra-abdominal pressure elevation, reducing venous return and diaphragmatic excursion. Colonic stent perforation occurs in 5–7% of cases with 16% mortality. Most reported tension pneumoperitoneum cases follow colonoscopy with successful percutaneous decompression alone; this case uniquely demonstrates feculent contamination requiring laparotomy, illustrating how combined obstructive, septic, and hemorrhagic pathophysiology compounds mortality. When tense distension, hypotension, and rising PIP suggest tension physiology, bedside decompression should precede imaging. Colonic stent perforation can trigger tension pneumoperitoneum, ACS, and obstructive shock. Key lessons: (1) Decompress first; imaging should not delay intervention. (2) Anticipate coagulopathy and renal failure; mobilize damage-control resources early. (3) Multidisciplinary sequencing is crucial, yet mortality remains high when hemorrhage and sepsis coexist. This case pairs bedside images with clinical trajectories to illustrate pathophysiology in real time.

 

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