2025 PACUPrep BCCCP Preparatory Course Abdominal Compartment Syndrome Abdominal Compartment Syndrome: Foundational Concepts
De-escalation and Safe Transition of Care in Abdominal Compartment Syndrome

De-escalation and Safe Transition of Care in Abdominal Compartment Syndrome

Objectives Icon A checkmark inside a circle, symbolizing achieved goals.

Objective

  • Develop a plan to facilitate patient recovery, mitigate long-term complications, and ensure a safe transition of care for Abdominal Compartment Syndrome (ACS).

1. Introduction and Rationale

De-escalation of intensive therapies in Abdominal Compartment Syndrome (ACS) must strike a balance between minimizing iatrogenic harm and preventing rebound intra-abdominal hypertension (IAH). Safe transition requires continuity of monitoring and organ support as patients move to lower-acuity settings.

Goals of De-escalation:

  • Taper sedation, neuromuscular blockade, and diuretics with regular intra-abdominal pressure (IAP) and organ function checks.
  • Prevent rebound IAP elevations and secondary organ dysfunction.

Transition of Care Imperatives:

  • Standardized handoff tools (e.g., SBAR: Situation, Background, Assessment, Recommendation) to convey IAP trends, therapies, and pending labs.
  • Continue IAP monitoring and watch for delayed complications (infection, fistula, recurrent IAH).
  • Engage multidisciplinary team: pharmacy, nutrition, physical therapy/occupational therapy (PT/OT), mental health, and nursing.
Key Pearl

Protocolized de-escalation with frequent IAP assessments reduces rebound ACS and shortens ICU stay.

2. Weaning and De-escalation of Intensive Therapies

Systematic weaning of sedation, paralytics, and fluid therapies as ACS resolves promotes recovery and reduces ICU complications.

2.1 Sedation Weaning Protocols

  • Use Richmond Agitation-Sedation Scale (RASS) or Sedation-Agitation Scale (SAS); target light sedation (RASS 0 to –2).
  • Implement daily sedation interruption (“sedation vacation”) to assess neurologic status.
  • Monitor for agitation, withdrawal, and IAP spikes during dose reductions.

2.2 Neuromuscular Blockade and Ventilator Liberation

  • Discontinue paralytics when Train-of-Four (TOF) count is ≥2/4 twitches to restore spontaneous movement.
  • Initiate spontaneous breathing trials (SBTs) when plateau pressure <30 cmH2O and oxygenation is stable.
  • Assess extubation readiness; maintain a re-intubation plan given potential residual abdominal or respiratory compromise.

2.3 Fluid Balance and Diuretic Tapering

  • Set individualized net negative fluid balance targets (e.g., –0.5 to –1 L/day).
  • Gradually down-titrate loop diuretics (e.g., furosemide 20–80 mg IV bolus or 5–20 mg/hr infusion).
  • Monitor intake/output, creatinine, electrolytes, and vital signs; avoid rapid volume shifts that could trigger acute kidney injury (AKI).
Key Pearl

A gradual diuretic taper preserves perfusion while supporting stable IAP.

3. Conversion from IV to Enteral Medications

Early switch to enteral therapy restores gut integrity, reduces line-related risks, and facilitates discharge planning; absorption variability demands close efficacy monitoring.

3.1 Indications and Timing

  • Ensure return of GI function: presence of bowel sounds, minimal gastric residuals, absence of significant ileus.

3.2 Enteral Access Considerations

  • Select appropriate tube (nasogastric, orogastric, post-pyloric) based on aspiration risk and motility.
  • Verify tube placement and compatibility of crushed versus liquid formulations.
  • Avoid crushing extended-release or enteric-coated drugs.

3.3 Pharmacotherapy Considerations

3.3.1 Sedative Conversion

Mechanism: GABA-A agonism (benzodiazepine class).

Agents & Dosing: Lorazepam 0.5–2 mg PO q6–8h; clonidine 0.1–0.2 mg PO q8h as adjunct.

Monitoring: Sedation scales, blood pressure/heart rate; watch for accumulation in hepatic impairment.

Pitfall: Too-rapid conversion risks withdrawal and agitation.

3.3.2 Analgesic Conversion

Mechanism: Mu-opioid receptor agonism.

Agents & Dosing: Morphine PO (IV:PO ratio 1:3), oxycodone 5–10 mg PO q4–6h PRN.

Monitoring: Pain scores, respiratory rate, sedation.

Pitfall: Variable absorption—adjust dose for gut dysmotility.

3.3.3 Prokinetic Conversion

Mechanism: D2 receptor antagonism (metoclopramide).

Agent & Dosing: Metoclopramide 10 mg PO q6h.

Monitoring: GI motility, QTc interval, extrapyramidal signs.

Pitfall: Contraindicated in obstruction; risk of arrhythmias.

3.4 Monitoring Absorption and Efficacy

  • Use therapeutic drug levels when available (e.g., anticonvulsants).
  • Assess clinical endpoints: pain control, sedation depth, bowel movements.
  • Revert to IV therapy if enteral route fails to meet targets.
Key Pearl

Persistent failure to achieve clinical endpoints post-conversion should prompt evaluation for malabsorption.

4. Mitigating Post-ICU Syndrome (PICS)

Early implementation of the ABCDEF Bundle and supportive therapies minimizes long-term physical, cognitive, and psychological impairments after critical illness.

4.1 Risk Stratification

  • High-risk features: age >65, prolonged sedation/ventilation (>7 days), ICU-acquired weakness.

4.2 ABCDEF Bundle Implementation

Figure 1: The ABCDEF Bundle for ICU Liberation
A Assess, Prevent, and Manage Pain
B Both Spontaneous Awakening Trials (SAT) & Spontaneous Breathing Trials (SBT)
C Choice of Analgesia and Sedation
D Delirium: Assess, Prevent, and Manage
E Early Mobility and Exercise
F Family Engagement and Empowerment
The ABCDEF bundle is a set of evidence-based practices aimed at improving outcomes for ICU patients, including reducing delirium, mechanical ventilation duration, and ICU length of stay, thereby mitigating PICS.
  • A: Assess/manage pain (numerical/verbal scales + multimodal analgesia).
  • B: Both Spontaneous Awakening Trials (SAT) and Spontaneous Breathing Trials (SBT).
  • C: Choice of sedation—favor non-benzodiazepines (propofol, dexmedetomidine).
  • D: Delirium monitoring (CAM-ICU/ICDSC) and management.
  • E: Early mobility—bed exercises progressing to ambulation.
  • F: Family engagement—education and involvement during rounds.

4.3 Rehabilitation and Nutrition

  • Initiate PT/OT early; define mobility milestones (sitting, standing, walking).
  • Nutrition goals: protein 1.2–2.0 g/kg/day; 25–30 kcal/kg/day via enteral route.

4.4 Psychological and Cognitive Support

  • Provide ICU diaries; refer to post-ICU clinics for cognitive and mental health follow-up.
  • Engage family to support patient’s psychological recovery.
Key Pearl

Full adherence to the ABCDEF Bundle reduces PICS incidence and enhances functional outcomes.

5. Medication Reconciliation and Discharge Counseling

Structured reconciliation, education, and communication ensure safe transitions, reduce errors, and empower patients/caregivers.

5.1 Reconciliation Process

  • Compare pre-admission, ICU, and discharge medication lists.
  • Identify and resolve duplications, omissions, and potential interactions.

5.2 Patient/Caregiver Education

  • Review each medication’s indication, dose, schedule, side effects, and monitoring requirements.
  • Provide written action plan and emergency contact information.

5.3 Communication Tools

  • Use SBAR or electronic handoff templates to highlight critical medications and required labs.
  • Emphasize high-risk medications (anticoagulants, immunosuppressants) and follow-up schedules.
Key Pearl

Robust reconciliation and targeted education reduce readmission risk and improve adherence.

6. Summary and Clinical Pearls

6.1 Key Take-Home Points

  • Protocolized de-escalation and frequent IAP monitoring prevent rebound ACS and support recovery.
  • Early IV-to-enteral conversion preserves gut integrity and facilitates discharge planning.
  • ABCDEF Bundle implementation mitigates PICS and optimizes long-term outcomes.
  • Comprehensive medication reconciliation and discharge counseling ensure safe care transitions.

6.2 Common Pitfalls

  • Overly rapid diuretic taper risking hypovolemia or AKI.
  • Inadequate monitoring of enteral drug absorption leading to subtherapeutic or toxic levels.
  • Incomplete handoff of critical medications or pending laboratory follow-up.

References

  1. 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.
  2. Jacobs R, Wise RD, Myatchin I, et al. Fluid management, intra-abdominal hypertension and ACS: a narrative review. Life. 2022;12(9):1390.
  3. Zarnescu NO, Dumitrascu I, Zarnescu EC, Costea R. Abdominal compartment syndrome in acute pancreatitis: a narrative review. Diagnostics. 2023;13(1):1–17.
  4. 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.
  5. Holodinsky JK, Roberts DJ, Ball CG, et al. Risk factors for intra-abdominal hypertension and ACS among adult ICU patients: a systematic review and meta-analysis. Crit Care. 2013;17:R249.
  6. 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):S1.
  7. Leppaniemi A, Tolonen M, Tarasconi A, et al. 2019 WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg. 2019;14:27.
  8. He W, Chen P, Lei Y, et al. Randomized controlled trial: neostigmine for intra-abdominal hypertension in acute pancreatitis. Crit Care. 2022;26(1):52.
  9. Roberts DJ, Zygun DA, Grendar J, et al. Negative-pressure wound therapy for critically ill adults with open abdominal wounds: a systematic review. J Trauma Acute Care Surg. 2012;73(3):629–639.

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