Document Type

Conference Proceeding

Publication Date

5-2-2025

Abstract

Introduction Abdominal Compartment Syndrome (ACS) occurs in approximately 15% of patients with severe acute necrotizing pancreatitis and is associated with a poor prognosis. Treatment typically involves urgent decompressive laparotomy. However, diagnosing ACS in an intensive care unit (ICU) setting can be challenging, as patients often present with primary illnesses that independently drive end-organ dysfunction. This case highlights a diagnostic framework for ACS while emphasizing common pitfalls and challenges. Case Description A 54-year-old male with a history of alcohol abuse presented with a two-week history of abdominal discomfort and shortness of breath. Initial evaluation, including clinical examination, imaging, and laboratory findings, revealed circulatory shock secondary to acute pancreatitis. The patient developed worsening hypoxia and labored breathing, and a CT angiogram of the chest identified a small right-sided pulmonary embolism. He was intubated, initiated on fluid resuscitation, and placed on a heparin drip for anticoagulation. Four days into his ICU stay, the patient developed periumbilical bruising, and CT imaging revealed free fluid extravasation in the abdomen, prompting discontinuation of heparin due to concerns of hemorrhagic pancreatitis. Concurrently, he developed acute renal failure requiring continuous renal replacement therapy (CRRT) and ongoing vasopressor support. Due to worsening abdominal distension and clinical suspicion of ACS, indirect intra-abdominal pressure (IAP) measurements were initiated via bladder sensor every four hours. Initial readings were 19 mmHg, rising to 34 mmHg later that night. Repeat measurements after administration of a paralytic agent confirmed persistently elevated pressures of 34-35 mmHg. Despite uncertainty about whether the patient’s slightly increased pressor requirements and reduced urine output were secondary to ACS or severe necrotizing pancreatitis, the substantially elevated IAP prompted surgical decompression. Discussion Subsequent case review raised concerns about a potential misdiagnosis of ACS and a premature decision for decompressive laparotomy, a procedure with significant risks, including fluid and protein loss and a hypercatabolic state. This underscores the importance of a systematic approach to diagnosing ACS, given its overlap with other critical illnesses. Key considerations include: 1. Establish a Temporal Relationship: Critically ill patients frequently exhibit end-organ dysfunction due to their primary illness. Establishing a clear temporal association between rising IAP and worsening organ function is essential to isolating ACS as the primary culprit. 2. Accurate IAP Measurements: Faulty measurements due to improper catheter placement, incorrect fluid volume instillation, or failure to measure at end-expiration can lead to diagnostic errors. Use of short-acting paralytic agents can aid in obtaining reliable readings. 3. Additional Clinical Markers: While oliguria and renal dysfunction are common early findings in ACS, these are nonspecific in shock patients. Other markers, such as elevated lactate, increased vasopressor requirements, and elevated ventilator pressures, may support the diagnosis. 4. Imaging and Targeted Interventions: Bedside point-of-care ultrasound (POCUS) or CT imaging can identify specific targets, such as ascites, that may be amenable to minimally invasive decompression before resorting to open surgical intervention. This case highlights the complexity of diagnosing ACS in critically ill patients and advocates for a systematic, evidence-based approach to avoid unnecessary interventions and optimize outcomes.

Comments

American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter Resident and Medical Student Day, May 2, 2025, Troy, MI

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