The "Decongestion" Strategy in Septic Shock: Rethinking Fluids

A Paradigm Shift from Liberal Resuscitation to Hemodynamic Optimization

Dr Neeraj Manikath , claude.ai

Abstract

The traditional approach to septic shock management has emphasized aggressive fluid resuscitation as a cornerstone of early intervention. However, accumulating evidence suggests that persistent fluid administration beyond initial resuscitation may contribute to significant morbidity and mortality through fluid overload and tissue edema. This review examines the emerging "decongestion" strategy in septic shock, exploring the evidence for early vasopressor initiation, active deresuscitation techniques, and modern monitoring modalities to detect and manage fluid overload. Understanding when to transition from resuscitation to decongestion represents a critical skill for intensivists managing complex septic patients.

Keywords: Septic shock, fluid overload, decongestion, vasopressors, continuous renal replacement therapy, point-of-care ultrasound

Introduction

Since the landmark Rivers trial in 2001, early goal-directed therapy (EGDT) with aggressive fluid resuscitation has dominated sepsis management.¹ However, the pendulum may have swung too far. Contemporary data reveal that cumulative fluid balance correlates strongly with adverse outcomes across multiple organ systems.²⁻³ The concept of "decongestion"—the deliberate removal or prevention of excess fluid accumulation—has emerged as a counterbalance to historical liberal resuscitation practices.

The modern intensivist must navigate a narrow therapeutic window: providing adequate resuscitation to restore perfusion while avoiding the iatrogenic harm of fluid overload. This review synthesizes current evidence for a more nuanced approach to fluid management in septic shock, with practical guidance for implementation.

The Evidence for Early Vasopressors Over Persistent Fluid Boluses

The Paradigm Shift

Traditional teaching advocated for 30 mL/kg crystalloid boluses before initiating vasopressors, based largely on expert consensus rather than robust trial data.⁴ Recent evidence challenges this approach, suggesting that earlier vasopressor initiation may improve outcomes while limiting fluid accumulation.

Clinical Trial Evidence

The CLOVERS trial (2023) randomized 1,563 patients with sepsis-induced hypotension to restrictive or liberal fluid strategies.⁵ While mortality was similar between groups, the restrictive arm received significantly less fluid in the first 24 hours (median 1,267 mL vs 3,400 mL) without harm. Importantly, patients in the restrictive group received earlier vasopressor support, suggesting safety of this approach.

The CLASSIC trial (2022) in ICU patients (including septic shock subgroup) demonstrated that restrictive fluid management (guided by signs of hypoperfusion only) reduced mortality compared to standard care.⁶ The restrictive group received less total fluid (median 1,798 mL vs 3,811 mL in first 24 hours) with improved 90-day survival (HR 0.72, 95% CI 0.52-0.99).

ANDROMEDA-SHOCK (2019) compared capillary refill time (CRT) to lactate as resuscitation targets.⁷ The CRT-guided group received less fluid (2,300 mL vs 2,900 mL in first 8 hours, p=0.04) with lower risk of fluid overload (15.4% vs 23.4%) and similar mortality, supporting more conservative fluid approaches.

Physiological Rationale

The glycocalyx—the endothelial surface layer—is disrupted in sepsis, increasing capillary permeability.⁸ Administered fluids extravasate into the interstitium, causing tissue edema while providing limited intravascular volume expansion. This creates a vicious cycle: hypotension prompts more fluid, which extravasates further, necessitating additional fluid.

Venous congestion represents another underappreciated mechanism of harm. Excessive fluid increases central venous pressure, impeding venous return from organs. This backward failure contributes to acute kidney injury (AKI), hepatic dysfunction, and intestinal edema.⁹ Vasopressors restore forward flow and may actually improve organ perfusion by reducing venous congestion.

Pearl: The "Vasopressor Challenge"

Clinical Hack: In patients with persistent hypotension after 1-2 liters of crystalloid who lack overt signs of hypovolemia (sunken eyes, dry mucosa, significant tachycardia), consider a "vasopressor challenge." Start norepinephrine at 0.05-0.1 mcg/kg/min and reassess in 15-30 minutes. If MAP improves without worsening lactate or ScvO₂, continue vasopressors rather than additional fluid boluses.

Oyster: Avoid Fluid Boluses for Hypotension Alone

Common Error: Giving 500 mL boluses repeatedly for isolated hypotension in an already volume-resuscitated patient. Remember: hypotension with adequate perfusion (normal lactate, adequate urine output, warm extremities) may reflect profound vasodilation rather than hypovolemia. Treat with vasopressors, not more fluid.

Practical Implementation

Suggested approach for early shock:

Give initial 1,000-1,500 mL crystalloid rapidly while assessing fluid responsiveness
Start vasopressors simultaneously or after first liter if MAP <65 mmHg persists
Use dynamic assessments (passive leg raise, pulse pressure variation if applicable) to guide additional fluid
Target MAP ≥65 mmHg with vasopressors rather than reflexive fluid boluses
Reassess perfusion markers (lactate, ScvO₂, skin perfusion, urine output) every 1-2 hours

Diuretic and CVVH Strategies for Fluid Overload in Established Shock

Defining Fluid Overload

Fluid overload exists when total body water exceeds physiologic needs, manifest as tissue edema, organ congestion, or impaired gas exchange. Percentage fluid overload is calculated as:

Fluid Overload (%) = [(Total fluid in - Total fluid out) / admission body weight] × 100

Values >10% associate with increased mortality across ICU populations.¹⁰ Even 5-7% overload correlates with worse outcomes in septic patients.¹¹

Active Deresuscitation: Diuretic Therapy

Once shock stabilizes (lactate improving, vasopressor weaning, adequate perfusion), active fluid removal should begin. Loop diuretics represent first-line therapy for patients with preserved kidney function.

The REVERSE trial concept: While no large RCT exists specifically for sepsis, extrapolating from heart failure literature suggests net negative fluid balance improves outcomes once hemodynamic stability achieved.¹² A retrospective analysis of 405 septic shock patients found those achieving negative fluid balance by day 3 had 23% lower 28-day mortality.¹³

Practical diuretic strategies:

Continuous infusion: Furosemide 5-10 mg/hour infusion provides more consistent diuresis than bolus dosing and may improve efficacy¹⁴
Combination therapy: Adding thiazide-type diuretic (metolazone 5-10 mg, chlorthalidone 25-50 mg) 30-60 minutes before loop diuretic enhances response in resistant cases
Albumin augmentation: For patients with hypoalbuminemia (<2.5 g/dL), co-administering albumin 25-50 g with diuretics may enhance fluid mobilization¹⁵

Pearl: The "Urine Output/Diuretic Efficiency" Test

Administer furosemide 1-1.5 mg/kg IV bolus and measure urine output over next 2 hours. If output <200 mL, patient is "diuretic resistant" and unlikely to respond to escalating oral/IV diuretics—consider CVVH earlier rather than nephrotoxic mega-doses.¹⁶

Continuous Renal Replacement Therapy (CRRT) for Deresuscitation

When diuretics fail or AKI precludes their use, CRRT offers precise fluid removal through ultrafiltration. Beyond renal support, CRRT serves as a deresuscitation tool.

Evidence for ultrafiltration in fluid overload:

Observational data consistently show improved survival when CRRT achieves negative fluid balance in overloaded patients¹⁷
The HEROICS trial (2021) found that protocolized CRRT ultrafiltration targeting negative fluid balance was feasible and associated with hemodynamic improvement¹⁸
Pediatric data from the SPARK trial suggest early initiation and fluid removal improve outcomes¹⁹

Technical considerations:

Ultrafiltration rate: Start conservatively (100-150 mL/hour net removal) to avoid hemodynamic instability
Monitor closely: Hourly assessment of MAP, vasopressor requirements, lactate initially
Avoid over-deresuscitation: Target euvolemia (2-5% fluid overload) rather than aggressive negative balance
Reassess daily: As patient stabilizes and diuresis improves, consider stopping CRRT to avoid complications (anticoagulation, line infections, cost)

Oyster: CRRT is Not Benign

Common Error: Initiating CRRT reflexively for fluid overload without attempting diuretics in non-oliguric patients. CRRT carries risks: hemodynamic instability during initiation, anticoagulation complications, catheter-related infections, and cost. Try diuretics first unless contraindicated (anuric AKI, severe hyperkalemia, refractory acidosis).

Hybrid Approach: The "Conservative Plus Active" Strategy

Contemporary practice integrates conservative fluid administration with active removal:

Phase 1 (Hours 0-6): Resuscitation

Goal-directed crystalloid (target 1,500-2,500 mL unless ongoing losses)
Early vasopressors for MAP ≥65 mmHg
Dynamic assessment of fluid responsiveness

Phase 2 (Hours 6-72): Optimization

Minimize maintenance fluids (<50 mL/hour)
"Fluid neutral" strategy: match outputs to inputs
Wean vasopressors as tolerated

Phase 3 (Day 3+): Active Deresuscitation

Target negative fluid balance 500-1,000 mL/day
Diuretics (if responsive) or CRRT (if resistant/anuric)
Continue until fluid overload <5% or clinical euvolemia

Monitoring for Occult Fluid Overload: POCUS and Bioimpedance

The Challenge of Occult Overload

Clinical signs (peripheral edema, rales, weight gain) manifest late and insensitively detect fluid overload. By the time these appear, significant organ edema may exist. Modern monitoring tools allow earlier, more accurate detection.

Point-of-Care Ultrasound (POCUS)

Bedside ultrasound provides rapid, repeatable assessment of fluid status across multiple organ systems.

1. Venous Excess Ultrasound (VExUS) Score

The VExUS protocol assesses systemic venous congestion by examining inferior vena cava (IVC) and organ Doppler patterns.²⁰

Components:

IVC diameter: >2 cm with <50% respiratory variation suggests elevated central venous pressure
Hepatic vein Doppler: Severe pulsatility or flow reversals indicate congestion
Portal vein Doppler: Pulsatility fraction >50% suggests congestion
Intrarenal vein Doppler: Biphasic or monophasic patterns indicate renal congestion

Grading:

VExUS 0: No congestion
VExUS 1: IVC dilated + one organ pattern abnormal
VExUS 2: IVC dilated + two organs abnormal
VExUS 3: IVC dilated + all three organs abnormal

Clinical application: VExUS Grade 2-3 predicts AKI development and associates with poor outcomes.²¹ Use VExUS to identify subclinical congestion requiring deresuscitation even before traditional markers appear.

2. Lung Ultrasound for Pulmonary Edema

B-lines (vertical artifacts from thickened interlobular septa) quantify extravascular lung water.²²

Technique:

Scan 8 lung zones (anterior, lateral, posterior bilaterally)
Count discrete B-lines per zone (0-10 scale)
Total B-line score >15 suggests significant pulmonary edema

Pearl: Serial B-line Assessment

Clinical Hack: Perform baseline lung ultrasound on ICU admission, then repeat every 12-24 hours. Rising B-line scores despite stable or negative fluid balance suggest worsening capillary leak requiring more aggressive deresuscitation. Declining scores validate your fluid management strategy.

3. IVC Collapsibility for Volume Responsiveness

While less reliable in mechanically ventilated patients, IVC assessment provides crude guidance:

IVC <1.5 cm with >50% collapse: Suggests fluid responsiveness (consider additional resuscitation)
IVC >2.5 cm with <15% collapse: Suggests high filling pressures (avoid additional fluid, consider diuresis)

Oyster: IVC is Not a Crystal Ball

Common Error: Making major treatment decisions based solely on IVC measurements. IVC diameter reflects right atrial pressure but doesn't directly indicate volume responsiveness, cardiac output, or fluid overload. Always integrate with other clinical data (lactate, ScvO₂, cardiac function, other POCUS findings).

Bioelectrical Impedance Analysis (BIA)

BIA measures tissue electrical conductivity to estimate fluid compartments. Edematous tissue conducts electricity differently than normal tissue.

Principle: Alternating current passes through the body; impedance measurements estimate total body water, extracellular water, and intracellular water. Increased extracellular/total body water ratio suggests fluid overload.

Clinical data:

Vector BIA can detect fluid overload earlier than clinical examination²³
Changes in BIA-measured overhydration predict ICU mortality in observational studies²⁴
May guide ultrafiltration rates during CRRT²⁵

Limitations:

Requires specialized equipment not universally available
Accuracy affected by body habitus, temperature, electrolyte abnormalities
Less validated in sepsis compared to renal failure populations

Current role: BIA remains investigational for septic shock but shows promise. Consider where available as adjunct to clinical assessment and POCUS.

Integrative Monitoring Approach

No single monitor perfectly captures fluid status. Optimal practice integrates multiple modalities:

Daily fluid assessment checklist:

☐ Clinical examination (peripheral edema, jugular venous distension, lung sounds)
☐ Cumulative fluid balance calculation (percentage overload)
☐ POCUS: VExUS score and lung B-lines
☐ Hemodynamic markers (MAP, vasopressor requirements, cardiac output if available)
☐ Perfusion markers (lactate, ScvO₂, capillary refill, urine output)
☐ Organ function trends (creatinine, liver enzymes, PaO₂/FiO₂ ratio)

Pearl: The "Deresuscitation Bundle"

When multiple congestive markers appear (VExUS ≥2, >20 B-lines, fluid overload >7%, worsening PaO₂/FiO₂), implement aggressive deresuscitation:

Stop all maintenance fluids except drug carriers
Minimize enteral feeding volume initially (consider trophic feeds)
Diuretic trial or CRRT initiation
Target net negative 500-1,000 mL over 24 hours
Reassess every 12 hours with repeat POCUS

Putting It All Together: A Clinical Vignette

Case: 62-year-old woman with pneumonia-associated septic shock. Initial resuscitation: 3 L crystalloid, norepinephrine 0.15 mcg/kg/min, antibiotics. At 24 hours: MAP 68 mmHg, lactate normalized, but requiring increasing FiO₂ (now 0.5). Cumulative +4.2 L (+6.7% fluid overload). Clinical exam: scattered crackles, trace peripheral edema.

POCUS findings:

Lung ultrasound: 22 B-lines (increased from 8 at admission)
VExUS score: 2 (dilated IVC, hepatic vein pulsatility, normal portal and renal veins)

Management:

Stop all maintenance fluids
Furosemide 40 mg IV bolus → 180 mL urine output over 2 hours (acceptable response)
Start furosemide infusion 5 mg/hour
Target net negative 750 mL over next 24 hours
Repeat lung ultrasound in 12 hours

Outcome: At 48 hours, B-lines decreased to 12, FiO₂ weaned to 0.35, fluid balance -900 mL in preceding 24 hours. Patient continued improving with successful liberation from mechanical ventilation by day 4.

Key teaching points:

Recognized subclinical pulmonary edema via POCUS before overt respiratory failure
Used VExUS to confirm systemic congestion
Implemented early deresuscitation with diuretics
Achieved euvolemia, facilitating recovery

Future Directions and Unanswered Questions

Several critical questions remain:

Optimal resuscitation volume: How much is "enough" in the first 6 hours? Individualized vs. weight-based approaches?
Vasopressor timing: Should we start simultaneously with fluids rather than sequentially?
CRRT timing: Does earlier initiation for fluid removal (before overt overload) improve outcomes?
Monitoring integration: Can algorithms combining multiple monitors (POCUS, BIA, hemodynamics) guide personalized therapy?
Capillary leak modulation: Are there therapies (beyond supportive care) to restore endothelial integrity?

Ongoing trials (PROFOUND SHOCK, RELOAD) will provide additional guidance. Meanwhile, intensivists must balance existing evidence with individual patient physiology.

Conclusion

The "decongestion" strategy represents an evolution, not revolution, in septic shock management. Early adequate resuscitation remains essential, but persistence with liberal fluid administration likely causes harm. The contemporary approach emphasizes:

Conservative initial resuscitation: 1,500-2,500 mL crystalloid with early vasopressor support
Avoidance of reflex fluid boluses: Treat persistent hypotension with adequate perfusion using vasopressors
Active deresuscitation: Once stabilized, target negative fluid balance using diuretics or CRRT
Multimodal monitoring: Integrate clinical assessment, cumulative fluid balance calculations, and POCUS to detect occult overload early

By viewing fluid therapy as a drug—with indications, dosing, therapeutic monitoring, and toxicity—intensivists can optimize outcomes while minimizing iatrogenic harm. The art of critical care lies in knowing when to give, when to withhold, and when to actively remove fluid.

Final Pearl: The best fluid management strategy is the one you monitor closely and adjust frequently. Dogma—whether liberal or restrictive—serves patients poorly. Individualized, dynamic, evidence-informed care saves lives.

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Conflict of Interest Statement: The author declares no conflicts of interest related to this manuscript.

Acknowledgments: The author thanks the critical care community for ongoing dialogue that shapes modern sepsis management.

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Thursday, November 6, 2025