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2025 PACUPrep BCCCP Preparatory Course Abdominal Compartment Syndrome Fundamentals of Abdominal Compartment Syndrome

Lesson 31, Topic 2

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Fundamentals of Abdominal Compartment Syndrome

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Diagnosis and Classification of Abdominal Compartment Syndrome

Objective

Apply diagnostic and classification criteria to assess abdominal compartment syndrome (ACS) and guide initial management.

1. Clinical Presentation and Physical Examination

Early suspicion of ACS arises from a combination of abdominal findings and multisystem signs. Physical exam alone is unreliable; objective measurement of intra‐abdominal pressure (IAP) is essential.

Abdominal exam:

Progressive distension, increased wall tension, discomfort on palpation
Guarding or rigidity may mimic peritonitis but lack specificity

Systemic signs:

Oliguria/anuria despite adequate fluid status
Hypotension with escalating vasopressor requirements
Rising peak airway pressures and worsening respiratory compliance

Red flags:

Sudden lactate rise, refractory metabolic acidosis
Rapid decline in mental status or escalating ventilator settings

Clinical Pearl: Exam Unreliability

Never rely solely on abdominal exam to exclude Intra-Abdominal Hypertension (IAH) or Abdominal Compartment Syndrome (ACS).

Clinical Pearl: Respiratory Clues

Rising airway pressures in a ventilated patient may reflect increased IAP and warrant direct measurement.

2. Laboratory and Physiologic Markers

Laboratory trends and hemodynamic parameters reveal evolving organ dysfunction secondary to elevated IAP.

Key Laboratory and Physiologic Markers in Suspected ACS
Marker/Parameter	Significance in IAH/ACS	Target/Monitoring Note
Serum Creatinine & BUN	Indicates renal hypoperfusion and acute kidney injury (AKI).	Monitor trends; apply KDIGO criteria for AKI staging.
Lactate & Base Deficit (ABG)	Reflects tissue hypoperfusion and metabolic acidosis.	Trend to gauge response to decompression efforts; rising values are ominous.
Central Venous Pressure (CVP)	Often elevated due to decreased abdominal venous return and direct caval compression.	Interpret in context of IAP; may not reflect true intravascular volume.
Cardiac Output (CO)	Decreased due to reduced preload (caval compression) and increased afterload (systemic vascular resistance).	Monitor via PAC or non-invasive methods if available.
Abdominal Perfusion Pressure (APP)	Calculated as MAP – IAP. Reflects visceral perfusion pressure.	Aim for APP >50–60 mmHg.

Clinical Pearl: APP Utility

Abdominal Perfusion Pressure (APP) may better predict visceral perfusion and risk of organ failure than Mean Arterial Pressure (MAP) alone in the setting of IAH.

Clinical Pearl: Lactate Interpretation

Trending lactate helps differentiate volume-responsive hypoperfusion from pressure-mediated hypoperfusion due to IAH/ACS.

3. Imaging and Adjunctive Modalities

Point‐of‐care ultrasound (POCUS) and CT imaging complement clinical assessment, identify etiologies, and guide interventions.

Ultrasound (POCUS):

Detect free fluid (ascites), bowel wall edema, venous congestion (e.g., VExUS score components).
Guide percutaneous drainage when indicated.

Computed Tomography (CT):

Identify visceral edema, large fluid collections, or specific pathology like pancreatic necrosis in pancreatitis.
“Round-belly sign”: An anteroposterior (AP) to transverse abdominal diameter ratio >0.8 suggests IAH.

“Round-Belly Sign” (AP/Transverse Ratio > 0.8)

AP Diameter

Transverse Diameter

Increased IAP leads to AP diameter ≈ Transverse diameter

Figure 1: The “Round-Belly Sign”. On axial CT imaging, an anteroposterior (AP) abdominal diameter that approaches or exceeds the transverse diameter (ratio >0.8) is suggestive of increased intra-abdominal pressure. This sign is particularly noted in conditions like acute pancreatitis with significant fluid collections or visceral edema.

Emerging tools:

Intragastric pressure monitoring and elastography are being investigated but are not yet standard practice. [Editor’s Note: Insufficient source material for detailed protocols on these modalities was provided for this chapter.]

Clinical Pearl: Round-Belly Sign in Pancreatitis

The round-belly sign on CT strongly correlates with IAH, especially in patients with acute pancreatitis and significant retroperitoneal/intraperitoneal fluid or inflammation.

Clinical Pearl: POCUS for Triage

Use POCUS early to assess for free fluid, bowel edema, and signs of venous congestion to help triage patients at risk for IAH/ACS and guide potential decompressive interventions like paracentesis.

4. Intra‐Abdominal Pressure Measurement Protocol

Standardized trans‐bladder technique remains the reference standard for IAP monitoring.

Procedure:

Setup:
- Ensure patient is supine.
- Connect the Foley catheter drainage port to a pressure transducer system.
- Zero the transducer at the mid‐axillary line, level with the iliac crest (phlebostatic axis).
Instillation and Measurement:
- Ensure bladder is empty.
- Instill a maximum of 25 mL sterile saline into the bladder via the aspiration port of the Foley catheter.
- Wait 30-60 seconds for detrusor muscle relaxation.
- Record the IAP (in mmHg) at end‐expiration to minimize respiratory variation.
Monitoring Frequency:
- Obtain a baseline measurement in all at‐risk patients.
- Repeat measurements every 4–6 hours, or more frequently if clinically indicated (e.g., after large volume resuscitation, new organ dysfunction, or any abdominal intervention).

Common Pitfalls in IAP Measurement:

Common Pitfalls in Trans-Bladder IAP Measurement
Pitfall	Consequence	Prevention/Correction
Overfilling bladder (>25 mL saline)	Falsely elevated IAP reading due to bladder distension.	Use ≤25 mL instillation volume.
Incorrect transducer zeroing	Inaccurate IAP readings (falsely high or low).	Zero transducer at iliac crest in mid-axillary line with patient supine. Re-zero if patient position changes.
Patient not supine or HOB elevated	Falsely elevated IAP.	Ensure patient is flat and supine for measurement.
Measurement during inspiration or coughing	Falsely elevated IAP.	Measure at end-expiration, ensuring patient is calm and abdominal muscles relaxed.
Air in tubing or transducer	Dampened waveform, inaccurate reading.	Ensure system is free of air bubbles.
Blocked or kinked catheter	Inability to instill fluid or obtain accurate pressure.	Ensure catheter patency before measurement.

Clinical Pearl: Instillation Volume

Keep saline instillation volume at ≤25 mL to avoid artifactual pressure readings from bladder overdistension.

Clinical Pearl: End-Expiration Measurement

Always measure IAP at end‐expiration to ensure consistency and minimize influence from respiratory mechanics.

5. Classification and Severity Stratification

Grading Intra-Abdominal Hypertension (IAH) and defining Abdominal Compartment Syndrome (ACS) facilitates risk stratification and guides escalation of care, based on WSACS consensus definitions.

Intra-Abdominal Hypertension (IAH) Definition: Sustained or repeated pathological elevation in IAP ≥12 mmHg.
Abdominal Compartment Syndrome (ACS) Definition: Sustained IAP >20 mmHg that is associated with new organ dysfunction/failure.

WSACS Grading of Intra-Abdominal Hypertension (IAH)
IAH Grade	Sustained Intra-Abdominal Pressure (IAP)	Clinical Implication
Grade I	12–15 mmHg	Monitor closely; initiate conservative measures.
Grade II	16–20 mmHg	Increased risk of organ dysfunction; intensify conservative measures. Consider interventions if organ dysfunction present.
Grade III	21–25 mmHg	High likelihood of ACS if organ dysfunction present. Prepare for decompressive interventions.
Grade IV	>25 mmHg	Often associated with overt ACS. Urgent decompression usually required.

Risk scores and decision tools:

Integrate IAP measurements with clinical signs of organ dysfunction (e.g., using SOFA score changes).
Consider individualized IAP thresholds for concern in patients with pre-existing limited physiological reserve (e.g., severe sepsis, cirrhosis, baseline organ impairment).

Clinical Pearl: Individualized Thresholds

Organ dysfunction may occur at lower IAP levels (e.g., IAP 15-20 mmHg) in patients with underlying conditions like sepsis, cirrhosis, or pre-existing organ impairment. ACS is defined by IAP >20 mmHg PLUS new organ dysfunction.

Clinical Pearl: Grading for Action

Use IAH grading to trigger protocolized interventions, including medical management escalation and timely surgical consultation for potential decompression.

6. Algorithmic Approach to Initial Management

Management escalates from conservative measures to surgical decompression based on IAH grade and the presence or progression of organ dysfunction.

Figure 2: Initial Management Algorithm for IAH/ACS

Patient at Risk for IAH/ACS
Measure baseline IAP

IAH Grade I–II (IAP 12–20 mmHg)
No overt new organ failure

Medical Management / Conservative Measures:

Optimize fluid balance (avoid overload)
Enhance sedation/analgesia
Consider prokinetics for ileus
NG/rectal tube decompression
Monitor IAP q4-6h & organ function

IAH Grade III (IAP 21–25 mmHg) OR
IAP 12-20 mmHg WITH Early/New Organ Dysfunction

Escalate Medical Management:

Trial neuromuscular blockade (if ventilated)
Consider diuretics / CRRT for de-resuscitation
Percutaneous catheter drainage (if fluid dominant)
Monitor IAP frequently & organ function
Surgical consult

ACS (IAP >20 mmHg WITH New Organ Dysfunction) OR
IAH Grade IV (IAP >25 mmHg)

Urgent Decompression:

Surgical consultation for decompressive laparotomy
Manage open abdomen (e.g., NPWT)
Optimize hemodynamics & organ support

This algorithm provides a general framework. Clinical judgment and individual patient factors are paramount. APP = Abdominal Perfusion Pressure; IAP = Intra-Abdominal Pressure; NPWT = Negative Pressure Wound Therapy.

Key Points for Management:

Key Point: Early Action

Early recognition of IAH and protocolized escalation of care can reduce progression to ACS and irreversible organ damage.

Key Point: Team Approach

Multidisciplinary coordination involving critical care, surgery, nursing, and pharmacy is vital for optimal patient outcomes in IAH/ACS.

References

Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra‐abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines. Intensive Care Med. 2013;39(7):1190–1206.
Zarnescu NO, Dumitrascu I, Zarnescu EC, et al. Abdominal Compartment Syndrome in Acute Pancreatitis: A Narrative Review. Diagnostics. 2023;13(1):1–17.
Vella MA, Kaplan LJ. What Is Abdominal Compartment Syndrome and How Should It Be Managed? In: Asensio JA, Trunkey DD, editors. Current Therapy of Trauma and Surgical Critical Care. 3rd ed. Elsevier; 2025. p.541–547.
Sugrue M, Bauman A, Jones F, et al. Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg. 2002;26(12):1428–1431.
Cheatham ML, White MW, Sagraves SG, et al. Abdominal perfusion pressure: a superior parameter in the assessment of intra‐abdominal hypertension. J Trauma. 2000;49(4):621–627.
Gupta P, Kamat R, Samanta J, et al. Computed Tomography Findings in Intraabdominal Hypertension in Patients with Acute Pancreatitis. Indian J Radiol Imaging. 2021;31(2):150–156.
Pereira BM, Pereira RG, Wise R, et al. The role of point‐of‐care ultrasound in intra‐abdominal hypertension management. Anaesthesiol Intensive Ther. 2017;49(5):373–381.
Jacobs R, Wise RD, Myatchin I, et al. Fluid Management, Intra‐Abdominal Hypertension and the Abdominal Compartment Syndrome: A Narrative Review. Life. 2022;12(9):1390.
Peng T, Dong LM, Zhao X, et al. Minimally invasive percutaneous catheter drainage versus open laparotomy with temporary closure for treatment of abdominal compartment syndrome in early-stage severe acute pancreatitis. J Huazhong Univ Sci Technol Med Sci. 2016;36(1):99–105.

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