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2025 PACUPrep BCCCP Preparatory Course Abdominal Compartment Syndrome Abdominal Compartment Syndrome: Pathophysiology, Assessment, and Management

Lesson 31, Topic 4

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Abdominal Compartment Syndrome: Pathophysiology, Assessment, and Management

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Supportive Care and Monitoring in Abdominal Compartment Syndrome

Objective

Recommend appropriate supportive care and monitoring to manage complications associated with Abdominal Compartment Syndrome (ACS) and its treatment.

1. Introduction

In Abdominal Compartment Syndrome (ACS), elevated intra-abdominal pressure (IAP) compromises organ perfusion and function. Timely supportive care—encompassing ventilatory adjustments, hemodynamic optimization, prevention of common ICU complications, and vigilant monitoring for drug-related issues—can significantly alter the clinical trajectory of these critically ill patients.

Key Points:

ACS is clinically defined as a sustained intra-abdominal pressure (IAP) greater than 20 mm Hg, which is associated with new organ dysfunction or failure.
Supportive care in ACS is multifaceted, addressing:
- Respiratory system compromise
- Hemodynamic instability
- Prophylaxis against common ICU-acquired complications (e.g., VTE, stress ulcers)
- Mitigation of iatrogenic harm from therapies
- Early and ongoing discussions regarding goals of care

2. Respiratory Support

Elevated IAP directly impacts respiratory mechanics by reducing diaphragmatic excursion, which in turn decreases lung compliance and can worsen gas exchange. Effective mechanical ventilation strategies involve lung-protective settings and careful titration of Positive End-Expiratory Pressure (PEEP).

A. Mechanical Ventilation Strategies

Key considerations for ventilating patients with ACS include:

Indications for Mechanical Ventilation: Typically initiated for hypoxemia (PaO₂/FiO₂ ratio < 200), significant hypercapnia (pH < 7.20), or signs of increasing work of breathing.
Tidal Volume: Target low tidal volumes, around 6 mL/kg of ideal body weight (IBW), to minimize ventilator-induced lung injury.
Permissive Hypercapnia: Allowing PaCO₂ to rise above normal levels is often acceptable, provided the arterial pH remains above 7.20.
PEEP Titration: Start PEEP at approximately 5 cm H₂O. It can be cautiously increased, but generally should not exceed the measured IAP. Monitor closely for adverse hemodynamic effects (e.g., hypotension) or decreased urine output with PEEP increases.

Clinical Pearl: Matching PEEP to IAP

A strategy of matching PEEP to the level of IAP (e.g., if IAP is 12 mm Hg, consider PEEP around 12 cm H₂O) aims to counterbalance the external pressure on the lungs, potentially recruiting atelectatic lung units. However, this must be balanced against the risk of hemodynamic compromise from excessive intrathoracic pressure.

B. Monitoring Respiratory Parameters

Continuous assessment of respiratory mechanics and gas exchange is crucial to guide ventilator adjustments and to detect early signs of ACS progression or worsening lung injury.

Plateau Pressure (Pplat): Strive to maintain Pplat below 30 cm H₂O to minimize barotrauma.
Driving Pressure (ΔP): Calculated as Pplat – PEEP, aim for a ΔP less than 15 cm H₂O, as higher values are associated with increased mortality.
Static Compliance Trends: Monitor trends in static compliance of the respiratory system (Crs = Tidal Volume / (Pplat – PEEP)). Decreasing values may suggest worsening ACS or other pulmonary pathology.
Arterial Blood Gases (ABGs): Regularly assess ABGs to track the PaO₂/FiO₂ ratio, PaCO₂, pH, and lactate levels, guiding adjustments in FiO₂ and minute ventilation.

3. Hemodynamic Support

Elevated IAP adversely affects hemodynamics by reducing venous return (preload) and cardiac output, while simultaneously increasing systemic vascular resistance (afterload). The primary goal is to maintain adequate organ perfusion without exacerbating tissue edema or IAP.

A. Goals and Targets

Mean Arterial Pressure (MAP): Target a MAP of ≥ 65 mm Hg.
Urine Output: Aim for a urine output > 0.5 mL/kg/hour as an indicator of renal perfusion.
Lactate Clearance: Target a decrease in serum lactate by ≥ 10% within the first 6 hours of resuscitation as a marker of improved tissue perfusion.
Abdominal Perfusion Pressure (APP): Calculated as MAP – IAP, aim for an APP > 50 mm Hg when feasible, though this target can be challenging to achieve and maintain.

B. Vasopressor Pharmacotherapy

Vasopressor Agents in Abdominal Compartment Syndrome
Vasopressor	Mechanism of Action	Typical Dosing	Monitoring & Pearls
Norepinephrine	Potent α₁ agonist with some β₁ activity; increases SVR and provides modest inotropy.	Start 0.05 μg/kg/min; titrate to achieve MAP ≥ 65 mm Hg.	Continuous BP, ECG, peripheral perfusion. First-line agent, particularly in vasodilatory or distributive shock components. Associated with less tachyarrhythmia compared to other catecholamines.
Vasopressin	V₁ receptor agonist; acts as a catecholamine-sparing agent.	Typically a fixed dose of 0.03 units/min as an adjunct to norepinephrine.	Serum sodium, skin perfusion, urine output. May reduce norepinephrine requirements. Consider if tachyarrhythmias limit further catecholamine dose escalation.
Phenylephrine	Pure α₁ agonist; primarily increases SVR (afterload).	Used as a salvage agent or in specific situations like reflex bradycardia accompanying tachyarrhythmias with other agents.	Monitor for bradycardia, ensure adequate organ perfusion. Use with caution due to potential to significantly reduce cardiac output if preload is inadequate.

C. Fluid Management Principles

Fluid management in ACS requires a delicate balance: restoring intravascular volume to support perfusion while avoiding excessive fluid administration that can worsen IAP and contribute to fluid overload.

Strive to avoid a cumulative positive fluid balance exceeding 2–3 liters per day after the initial resuscitation phase.
Utilize dynamic indices of fluid responsiveness (e.g., stroke volume variation (SVV), pulse pressure variation (PPV)) in mechanically ventilated patients to guide fluid administration, where appropriate.
Consider early de-resuscitation strategies once perfusion targets are met and hemodynamic stability is achieved. This may involve loop diuretics (e.g., furosemide 0.1–0.2 mg/kg IV bolus, or continuous infusion at 0.05–0.2 mg/kg/h) or continuous renal replacement therapy (CRRT) if indicated for renal failure or severe fluid overload.

Clinical Pearl: Fluid Balance and IAH/ACS

A persistently positive fluid balance is an independent risk factor for the development and worsening of intra-abdominal hypertension (IAH) and ACS. Transitioning to a neutral or negative fluid balance as soon as perfusion targets are reliably met is a key therapeutic goal.

4. Prevention of ICU-related Complications

Patients with ACS are at high risk for common ICU-acquired complications. Prophylactic measures are essential.

A. Venous Thromboembolism (VTE) Prophylaxis

VTE Prophylaxis Agents
Agent	Dosing & Monitoring
Low Molecular Weight Heparin (LMWH) (e.g., Enoxaparin)	Dose: 40 mg subcutaneously once daily. Adjust for renal impairment (e.g., CrCl < 30 mL/min: 30 mg SC once daily). Monitoring: Consider anti-Xa levels in patients with obesity or significant renal impairment. Contraindications: Active bleeding, history of heparin-induced thrombocytopenia (HIT).
Unfractionated Heparin (UFH)	Dose: 5,000 units subcutaneously every 8–12 hours. Monitoring: Platelet count (for HIT surveillance). Activated partial thromboplastin time (aPTT) is not routinely monitored for prophylactic doses but would be for therapeutic infusions. Pearls: Shorter half-life and rapid reversibility with protamine sulfate make it a preferred option in patients with high bleeding risk or anticipated invasive procedures.
Mechanical Prophylaxis	Intermittent pneumatic compression (IPC) devices should be used when pharmacological anticoagulation is contraindicated or in addition to anticoagulation in very high-risk patients.

B. Stress Ulcer Prophylaxis (SUP)

Stress Ulcer Prophylaxis Agents
Agent	Dosing & Considerations
Proton Pump Inhibitors (PPIs) (e.g., Pantoprazole)	Dose: 40 mg intravenously once daily. Risks/Considerations: Associated with an increased risk of Clostridioides difficile infection and potentially hospital-acquired pneumonia. Restrict use to high-risk patients (e.g., mechanical ventilation > 48 hours, coagulopathy, history of GI bleeding).
H2 Receptor Antagonists (H2RAs) (e.g., Famotidine)	Dose: 20 mg intravenously every 12 hours. Dose adjustment required in renal insufficiency. Pearls: May have a lower risk of C. difficile infection compared to PPIs. Generally considered a reasonable alternative for SUP.

C. Infection Prevention Bundles

Adherence to established infection prevention bundles is critical:

Ventilator-Associated Pneumonia (VAP) Prevention:
- Maintain head-of-bed elevation at 30–45 degrees.
- Perform daily interruption of sedation and assessment for readiness to extubate.
- Implement regular oral hygiene with chlorhexidine.
Central Line-Associated Bloodstream Infection (CLABSI) Prevention:
- Utilize maximal sterile barrier precautions during insertion.
- Use chlorhexidine-based skin preparation and dressings.
- Conduct daily review of central line necessity with prompt removal when no longer indicated.
Glycemic Control: Target blood glucose levels < 180 mg/dL to reduce infection risk and improve outcomes.

5. Management of Iatrogenic Complications

Critically ill patients, especially those with ACS, are susceptible to iatrogenic complications arising from necessary therapies. Vigilant monitoring and proactive strategies are key.

A. Drug-induced Organ Dysfunction

Common Drug-Induced Complications and Management
Complication / Syndrome	Key Monitoring & Mitigation Strategies
Propofol Infusion Syndrome (PRIS)	Limit infusion rate to < 4 mg/kg/hour and duration ideally < 48 hours. Monitor triglycerides, creatine kinase (CK), arterial blood gases (for metabolic acidosis), and ECG.
Neuromuscular Blockade (NMB) Myopathy	Prefer cisatracurium infusion (e.g., 1–3 μg/kg/min). Use train-of-four (TOF) monitoring daily, aiming for 1–2 twitches. Minimize duration of NMB use.
Vasopressor-induced Ischemia	Titrate vasopressors to the lowest effective dose to achieve perfusion targets. Regularly inspect extremities for signs of ischemia (coolness, mottling, poor capillary refill) and monitor indicators of abdominal perfusion (e.g., bowel sounds, distension, lactate).
Diuretic-induced Electrolyte Disturbances	Frequently monitor serum potassium (K⁺), magnesium (Mg²⁺), and sodium (Na⁺). Proactively replace electrolytes as needed to maintain levels within the normal range.
Anticoagulant-related Bleeding	Monitor hemoglobin, hematocrit, platelet count, and coagulation profiles (e.g., aPTT, INR as appropriate). Adjust doses based on clinical signs of bleeding and laboratory parameters. Have reversal agents available if indicated.

B. Monitoring and Mitigation Strategies

Implement daily sedation interruptions (“sedation vacations”) and spontaneous breathing trials (SBTs) to facilitate earlier liberation from mechanical ventilation and reduce sedative exposure.
Conduct routine laboratory surveillance, including renal and hepatic function panels, and drug levels when available and clinically indicated (e.g., vancomycin, aminoglycosides).
Adjust pharmacokinetic (PK) and pharmacodynamic (PD) parameters for medications, accounting for potential alterations such as increased volume of distribution (due to fluid resuscitation and capillary leak) and altered drug clearance (due to organ dysfunction) common in ACS.

6. Multidisciplinary Goals of Care Discussions

Given the high morbidity and mortality associated with ACS, it is crucial to align invasive interventions and ongoing intensive care with the patient’s values and preferences. This is best achieved through structured, empathetic communication involving a multidisciplinary team.

Triggers for Discussion: Consider initiating or revisiting goals of care discussions in situations such as refractory ACS despite maximal therapy, development of multi-organ failure, or when the patient faces very high surgical risk with uncertain benefit.
Team Composition: Ideally, these discussions should involve the primary ICU team (physicians, nurses), surgical specialists, palliative care consultants, clinical pharmacists, social workers, spiritual care providers, and, most importantly, the patient (if able to participate) and their family or designated decision-makers.
Communication Framework: Utilize a structured approach, such as the SPIKES protocol, to guide conversations:
- Setting: Ensure a private, comfortable setting.
- Perception: Assess the family’s/patient’s understanding of the situation.
- Invitation: Ask for permission to share information and discuss goals.
- Knowledge: Provide clear, concise medical information.
- Empathy: Respond to emotions with empathy and validation.
- Strategy & Summary: Collaboratively develop a plan and summarize key decisions.
Documentation: Thoroughly document all goals of care discussions, decisions made, and any advance directives or care plans in the medical record. Revisit these discussions as the patient’s clinical status evolves.

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 from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39(7):1190–1206.
Zarnescu NO, Dumitrascu I, Zarnescu EC, Costea R. Abdominal Compartment Syndrome: Pathophysiology, Diagnosis and Current Therapeutic Options. Diagnostics (Basel). 2023;13(1):153.
Vella MA, Kaplan LJ. Abdominal Compartment Syndrome. In: Asensio JA, Trunkey DD, eds. Current Therapy of Trauma and Surgical Critical Care. 3rd ed. Elsevier; 2025:541–547.
Smit M, Buddingh KT, Bosma B, et al. Abdominal Compartment Syndrome and Enteral Nutrition: A Systematic Review. World J Surg. 2016;40(7):1454–1461.
Jacobs R, Wise RD, Myatchin I, et al. The Impact of Intra-Abdominal Hypertension on Organ Systems: A Narrative Review. Life (Basel). 2022;12(9):1390.
Cheatham ML, Malbrain ML. Abdominal perfusion pressure. Acta Clin Belg Suppl. 2007;(62 Suppl 1):98–112.
Montalvo-Jave EE, Espejel-Deloiza M, Chernitzky-Camano J, et al. Abdominal compartment syndrome: A current review of a surgical problem. Rev Gastroenterol Mex (Engl Ed). 2020;85(4):443–451.
Rogers WK, Garcia L. Intraabdominal hypertension, abdominal compartment syndrome, and the open abdomen. Chest. 2018;153(1):238–250.
Krebs J, Pelosi P, Tsagogiorgas C, et al. Effects of positive end-expiratory pressure on respiratory function and hemodynamics in patients with acute lung injury with and without intra-abdominal hypertension: a pilot study. Crit Care. 2009;13(5):R160.
Malbrain ML, Roberts DJ, Sugrue M, et al. The polycompartment syndrome: a concise state-of-the-art review. Anaesthesiol Intensive Ther. 2014;46(5):433–450.
Cordemans C, De Laet I, Van Regenmortel N, et al. Fluid management in critically ill patients: the role of extravascular lung water, abdominal hypertension, capillary leak, and fluid balance. Ann Intensive Care. 2012;2(Suppl 1 Diagnosis and management of intra-abdominal hypertension in critically ill patients):S1.
Holodinsky JK, Roberts DJ, Ball CG, et al. Risk factors for intra-abdominal hypertension and abdominal compartment syndrome among adult intensive care unit patients: a systematic review and meta-analysis. Crit Care. 2013;17(5):R249.
Malbrain M, Van Regenmortel N, Saugel B, et al. Principles of fluid management and stewardship in septic shock: it is time to consider the four D’s and the four phases of fluid therapy. Ann Intensive Care. 2018;8(1):66.
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):621–626; discussion 626-627.
Bates SM, Jaeschke R, Stevens SM, et al. Diagnosis of DVT: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e351S–e418S.
Sartelli M, Abu-Zidan FM, Ansaloni L, et al. The role of the open abdomen in managing severe abdominal sepsis: WSES position paper. World J Emerg Surg. 2015;10:35.
Abouassaly CT, Dutton WD, Zaydfudim V, et al. Stress gastropathy prophylaxis in the trauma intensive care unit. J Trauma. 2010;69(3):557–561.
Vidal MG, Ruiz Weisser J, Gonzalez F, et al. Incidence and clinical effects of intra-abdominal hypertension in critically ill patients. Crit Care Med. 2008;36(6):1823–1831.
Sun JK, Li WQ, Ke L, et al. Clinical implications of intra-abdominal hypertension in patients with severe acute pancreatitis. World J Surg. 2013;37(10):2053–2060.

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