I. Introduction

Abdominal Compartment Syndrome (ACS) is a life-threatening syndrome defined by sustained elevated intra-abdominal pressure leading to new organ dysfunction. Early recognition and prevention are critical in high-risk patients.

A. Definition and Clinical Importance of ACS

• ACS: Sustained intra-abdominal pressure (IAP) > 20 mmHg with new organ dysfunction.
• IAH (Intra-abdominal Hypertension): Sustained or repeated IAP ≥ 12 mmHg (precursor to ACS).
• Common settings: Trauma, severe pancreatitis, burns, sepsis, major abdominal surgery.

B. Role of the Critical Care Pharmacist in Early Identification

• Identify at-risk patients (e.g., those undergoing massive resuscitation, with bowel obstruction, or in capillary leak states).
• Advocate for protocolized IAP monitoring in ICU order sets for high-risk individuals.
• Guide fluid stewardship and vasoactive support strategies to minimize IAP elevation.
• Educate the multidisciplinary team on pharmacokinetic changes observed in ACS, such as increased volume of distribution and altered drug clearance.

II. Epidemiology and Incidence

Intra-abdominal hypertension (IAH) and Abdominal Compartment Syndrome (ACS) occur frequently in critically ill patients. The incidence varies across different patient populations, and both conditions are associated with high mortality rates.

Trauma ICUs:

• IAH incidence: Ranges from 30% to 80% in patients with severe trauma or extensive burns.
• ACS incidence: Can be as high as 28% in patients requiring massive transfusion protocols or undergoing damage control surgery.

Medical ICUs:

• IAH incidence: Approximately 20% to 40% in septic patients or general mixed ICU populations.
• ACS incidence: Generally 1% to 8%, but significantly higher in specific conditions like severe acute pancreatitis (around 15%).

Outcomes:

• ACS mortality: Ranges from 25% to 80%, depending on the underlying etiology and the timeliness of intervention.
• IAH impact: Even IAH alone is a predictor of longer ICU stays, increased need for renal replacement therapy, and higher multi-organ dysfunction scores.

III. Pathophysiology

Elevated intra-abdominal pressure (IAP) typically arises from an increase in intra-abdominal volume (e.g., fluid, gas, tissue edema) and/or a decrease in abdominal wall compliance. This increased pressure compromises organ perfusion and function across multiple systems.

A. Mechanisms of IAP Elevation

• Fluid accumulation: Aggressive crystalloid resuscitation, capillary leak syndromes (e.g., sepsis, burns), ascites.
• Tissue and visceral edema: Bowel wall edema, pancreatic swelling in acute pancreatitis.
• Hemoperitoneum/Pneumoperitoneum: Intra-abdominal bleeding, perforated viscus.
• Reduced abdominal wall compliance: Abdominal wall edema, constricting eschar from burns, tight surgical closures, obesity.

B. Organ System Impact

• Renal:
  • Compression of renal veins and the inferior vena cava (IVC) leads to decreased renal perfusion pressure and glomerular filtration rate (GFR).
  • Oliguria is common with IAP levels of 15–20 mmHg; anuria can occur at IAP > 30 mmHg.
• Respiratory:
  • The diaphragm is pushed cephalad, reducing thoracic volume and compliance, leading to increased airway pressures.
  • This can result in hypoxemia, hypercapnia, and ventilator dyssynchrony.
• Cardiovascular:
  • Decreased venous return (preload) due to IVC compression, leading to reduced cardiac output.
  • Compensatory increase in systemic vascular resistance (SVR); however, persistent high IAP can lead to hypotension and shock.
• Gastrointestinal:
  • Splanchnic hypoperfusion causes mucosal ischemia, potentially leading to ileus, bacterial translocation, and gut necrosis.
  • Feeding intolerance is a common early sign.

IV. Traditional Risk Factors

Several modifiable and non-modifiable factors predispose patients to the development of IAH and progression to ACS. Recognizing these risk factors is crucial for early monitoring and prevention.

• Massive fluid resuscitation (e.g., positive fluid balance > 5 liters in 24 hours).
• Paralytic ileus and bowel obstruction.
• Intra-abdominal hemorrhage (e.g., from trauma, ruptured aortic aneurysm).
• Capillary leak syndromes (e.g., sepsis, severe burns, acute pancreatitis).
• Major abdominal surgery, especially with packing or delayed closure.
• Obesity.
• Mechanical ventilation, particularly with high PEEP.

V. Impact of Pre-Existing Chronic Diseases

Baseline comorbidities can significantly reduce a patient’s physiologic reserve and exacerbate the consequences of elevated IAP, increasing their susceptibility to ACS or worsening its severity.

• Chronic Kidney Disease (CKD):
  • Reduced capacity to handle volume shifts and excrete excess fluid.
  • Lower renal reserve, making kidneys more vulnerable to IAP-induced injury.
• Congestive Heart Failure (CHF):
  • Pre-existing venous congestion and fluid overload can amplify the effects of IAP elevation on cardiac preload and afterload.
  • Impaired cardiac function limits compensatory mechanisms.
• Liver Cirrhosis:
  • Baseline ascites contributes to elevated IAP.
  • Coagulopathy can complicate IAP dynamics and increase risks associated with interventions (e.g., decompressive laparotomy).
  • Portal hypertension can be exacerbated.
• Obesity:
  • Often associated with elevated baseline IAP.
  • Reduced abdominal wall compliance.
  • Impaired respiratory mechanics, which can be further compromised by increased IAP.

VI. Influence of Social Determinants of Health

Non-medical factors, often categorized as social determinants of health (SDoH), can significantly influence a patient’s risk of developing ACS and their outcomes. These factors can lead to delayed presentation, poorer control of chronic diseases that are risk factors for ACS, and disparities in care.

• Medication Access and Affordability:
  • Gaps in adherence to essential medications (e.g., diuretics for heart failure, insulin for diabetes) due to cost or access issues can lead to poorly controlled chronic conditions, increasing vulnerability.
• Health Literacy:
  • Lower health literacy may result in delayed recognition of early symptoms of decompensation (e.g., worsening abdominal distension, oliguria) by patients or caregivers.
  • It can also impact understanding and adherence to complex medical regimens post-discharge, increasing risk of readmission or complications.
• Socioeconomic Status:
  • Limited access to timely primary or specialist care can lead to delayed diagnosis and management of conditions that predispose to IAH/ACS.
  • Food insecurity or inadequate nutrition can impair healing and immune response.
  • Geographic barriers or lack of transportation may delay access to tertiary care centers equipped to manage ACS.

VII. Clinical Presentation

ACS manifests with a constellation of physical signs and evidence of new or worsening organ dysfunction. Objective IAP measurement is essential to confirm the diagnosis when ACS is suspected based on clinical findings.

• Abdominal Exam:
  • Tense, distended abdomen.
  • Diminished abdominal wall compliance (firm to palpation).
  • Note: Physical exam findings alone are not reliable for diagnosing or excluding IAH/ACS.
• Hemodynamics:
  • Hypotension, often refractory to fluid administration.
  • Tachycardia.
  • Increased vasopressor requirements.
• Respiratory:
  • Elevated peak and plateau airway pressures on mechanical ventilation.
  • Increased PEEP requirements to maintain oxygenation.
  • Hypoxemia and/or hypercapnia.
  • Difficulty ventilating the patient.
• Renal:
  • New-onset oliguria (urine output < 0.5 mL/kg/hr) or anuria.
  • Rising serum creatinine and BUN.
• Metabolic:
  • Metabolic acidosis (often with an elevated lactate), indicating tissue hypoperfusion.
• Neurologic:
  • In severe cases, increased IAP can contribute to increased intracranial pressure, leading to altered mental status (though this is often multifactororial in critically ill patients).

VIII. Summary and Clinical Pearls

Key Points for Risk Assessment:

• Define IAH as a sustained or repeated IAP ≥ 12 mmHg and ACS as a sustained IAP > 20 mmHg associated with new organ dysfunction.
• Identify high-risk patient groups: those undergoing massive transfusion, severe pancreatitis, extensive burns, sepsis with significant fluid resuscitation, and major abdominal surgery.
• Recognize that pre-existing chronic diseases (CKD, CHF, cirrhosis, obesity) and social vulnerabilities can amplify risk and worsen outcomes.

Strategies for Early Recognition:

• Implement protocolized IAP monitoring in at-risk patients.
• Foster multidisciplinary collaboration involving pharmacy, nursing, intensivists, and surgeons for early detection and management.
• Pharmacists can play a key leadership role in fluid stewardship, medication management (e.g., sedatives, analgesics, neuromuscular blockers that can affect IAP), and advocating for timely IAP measurements.

Clinical Pearls Recap:

• Oliguria developing at IAP levels of 15–20 mmHg is an early and critical red flag for impending or actual renal dysfunction due to IAH.
• A positive fluid balance exceeding 5 liters within a 24-hour period correlates strongly with the development of IAH.
• Consider polycompartment syndrome: elevated IAP can adversely affect intrathoracic and intracranial pressures, underscoring the need for a systemic approach to pressure management.
• Physical exam findings are unreliable for diagnosing IAH/ACS; objective IAP measurement is mandatory.