Supportive Care and Complication Prevention During Extracorporeal Therapy

1. Hemodynamic and Respiratory Support Strategies

Continuous renal replacement therapy (CRRT) and other forms of extracorporeal support can destabilize blood pressure and gas exchange. Early vasopressor support, proactive ventilator adjustments, and conservative ultrafiltration are crucial to maintain end-organ perfusion and oxygenation.

A. Indications for Vasopressor Initiation

• Mean Arterial Pressure (MAP) < 65 mmHg despite adequate volume resuscitation
• Presence of vasoplegic or cardiogenic shock during CRRT or ECMO

B. Vasopressor Selection and Dosing

• MAP Target: 65–80 mmHg to preserve end-organ perfusion.
• Norepinephrine (First-line): Start 0.05–0.1 μg/kg/min; titrate by 0.02–0.05 every 5–10 min; maximum dose typically < 1 μg/kg/min.
• Vasopressin (Adjunct): Initiate at a fixed dose of 0.03 units/min when norepinephrine requirements exceed 0.3 μg/kg/min.
• Epinephrine (Refractory Shock): Use at 0.01–0.1 μg/kg/min; monitor closely for tachyarrhythmias.

C. Mechanical Ventilation Adjustments

• Tidal Volume: 4–6 mL/kg of predicted body weight.
• PEEP: ≥ 10 cmH₂O, maintaining a plateau pressure < 25 cmH₂O.
• FiO₂: Titrate to achieve SpO₂ of 88–92%.
• Permissive Hypercapnia: Acceptable if extracorporeal CO₂ removal is in use.

D. Fluid Management and Ultrafiltration

• Net Ultrafiltration Rate: ≤ 1 mL/kg/h in hemodynamically unstable patients.
• Hemodynamic Monitoring: An arterial line is essential for continuous MAP monitoring. Stroke volume variation and cardiac output can further guide fluid management.
• Dual-Machine Protocol: A dual-machine replacement protocol at CRRT initiation can reduce pump stops and mitigate hypotension.

2. Prevention of ICU-Related Complications

Extracorporeal therapies introduce significant risks, including bleeding from anticoagulation, vascular access infections, and circuit thrombosis. Protocolized, preventative measures are essential to mitigate these common and potentially life-threatening complications.

A. Bleeding Risk Mitigation

• Systemic Unfractionated Heparin (UFH): Target an activated partial thromboplastin time (aPTT) of 45–60 seconds.
• Regional Citrate Anticoagulation: Maintain a post-filter ionized calcium (iCa²⁺) of 0.25–0.35 mmol/L. Monitor systemic calcium every 6–12 hours to prevent hypocalcemia.
• High Bleed-Risk Patients: Consider using heparin-grafted membranes combined with very low-dose UFH (e.g., 100 U/h).

B. Infection Control at Vascular Access

• Employ maximal sterile barriers during insertion and use chlorhexidine for skin antisepsis.
• Utilize ultrasound guidance to minimize insertion attempts and complications.
• Perform daily site assessments for signs of infection. Change dressings every 7 days or when soiled, and remove unused lines promptly.

C. Circuit Clotting Prevention

• Check transmembrane pressures (TMP) hourly and visually inspect the circuit for fibrin strands.
• Monitor platelet count every 12 hours. Change the filter if the count drops by >50% or falls below 50 × 10⁹/L.
• Change the circuit if blood flow cannot be maintained above 150 mL/min or if TMP exceeds 250 mmHg.

3. Management of Electrolyte and Acid–Base Derangements

Significant electrolyte and acid-base disturbances can occur due to convective losses and adsorption onto the filter membrane. Scheduled monitoring and proactive replacement are necessary to maintain metabolic stability.

A. Hypophosphatemia

• Monitoring: Check serum phosphate (PO₄) every 12 hours.
• Replacement: If PO₄ is < 2.5 mg/dL, replace with 0.08 mmol/kg over 6 hours.
• Target: 2.5–4.5 mg/dL.

B. Hypokalemia

• Monitoring: Monitor serum potassium (K⁺) every 4–6 hours.
• Replacement: When K⁺ < 3.5 mEq/L, add 20–40 mEq of KCl per liter of dialysate or replacement fluid. For severe hypokalemia (< 3.0 mEq/L), infuse 10 mEq IV over 1 hour and recheck in 4 hours.
• Target: 4.0–5.0 mEq/L.

C. Acid–Base Correction

• Bicarbonate Infusion: For severe acidosis (pH < 7.20), consider a bicarbonate infusion of 1–2 mEq/kg over 2 hours.
• Extracorporeal CO₂ Removal: This modality allows for more aggressive bicarbonate administration if needed.
• Monitoring: Check ABG and chemistries every 6–12 hours.

4. Multidisciplinary Goals-of-Care Conversations

The initiation of high-intensity extracorporeal therapies necessitates structured, compassionate communication between the clinical team and the patient’s family. These conversations are vital to ensure that treatment plans align with the patient’s values, prognosis, and quality of life.

A. Team Roles and Composition

A comprehensive team should include critical care physicians, nephrology consultants, pharmacists, nursing staff, and, when appropriate, palliative care or ethics specialists.

B. Timing and Structure of Meetings

• Pre-initiation Meeting: Before starting therapy, discuss the prognosis, potential risks, expected benefits, likely duration, and clear criteria for stopping therapy (decannulation or withdrawal).
• Scheduled Updates: Provide updates at least every 24 hours or whenever there is a significant change in the patient’s clinical status.

C. Documentation

• Clearly document all advanced directives, Physician/Medical Orders for Life-Sustaining Treatment (POLST/MOLST), and summaries of family meetings in the electronic medical record.
• Explicitly state the agreed-upon clinical criteria for continuing or withdrawing therapy.

5. Pharmacotherapy: Vasopressor Management During Extracorporeal Therapy

Vasopressors are essential for maintaining MAP and ensuring adequate organ perfusion during extracorporeal support. A detailed understanding of their pharmacology, dosing, and monitoring parameters is crucial for safe and effective use.

A. Mechanisms of Action

• Norepinephrine: A potent α₁ agonist with moderate β₁ effects, leading to increased systemic vascular resistance (SVR) and a modest rise in cardiac output.
• Vasopressin: A V₁ receptor agonist that causes vasoconstriction through non-adrenergic pathways, making it a catecholamine-sparing agent.
• Epinephrine: A mixed α/β agonist providing potent inotropy and vasoconstriction, but with a higher risk of arrhythmogenicity.

B. Indications and Agent Selection

• First-line: Norepinephrine is the preferred agent for most cases of septic or cardiogenic shock in patients on CRRT.
• Adjunctive: Add vasopressin when norepinephrine doses exceed 0.3 μg/kg/min or to reduce the overall catecholamine burden.
• Refractory Shock: Reserve epinephrine for refractory hypotension or when significant inotropic support is needed in cardiogenic shock.

C. Dosing, Titration, and Tapering

• Norepinephrine: Start at 0.05–0.1 μg/kg/min; titrate by 0.02–0.05 μg/kg/min every 5–10 minutes. Taper slowly by 0.02 μg/kg/min increments.
• Vasopressin: Administer as a fixed infusion of 0.03 units/min. It should be the last vasopressor to be tapered off.
• Epinephrine: Infuse at 0.01–0.1 μg/kg/min. Taper very slowly to prevent rebound hypotension.

D. Monitoring Efficacy and Safety

• Continuously monitor invasive MAP and heart rate.
• Track urine output, with a target of > 0.5 mL/kg/h.
• Measure serum lactate every 6–12 hours to assess tissue perfusion.
• Use continuous telemetry to monitor for arrhythmias.

E. Contraindications and Warnings

• Avoid high-dose catecholamines in patients with active tachyarrhythmias or acute myocardial ischemia.
• Vasopressin is relatively contraindicated in patients with known mesenteric or digital ischemia.

F. Comparative Advantages and Disadvantages

G. Clinical Pearls and Pitfalls

• To prevent extravasation injury, rotate peripheral infusion sites every 24 hours if a central line is not available.
• Watch for tachyphylaxis to catecholamines; consider the early addition of vasopressin to mitigate this effect.

H. Controversies and Decision Points

• The timing of vasopressin initiation (early vs. stepwise addition at high norepinephrine doses) is an area of active debate.
• The role and timing of corticosteroids in refractory vasodilatory shock remain controversial but should be considered.