Section 3.2: Patients with Venous Congestion and Fluid Responsiveness: To Expand or Not?

Fluid therapy is one of the most fundamental and controversial interventions in critical care. From shock resuscitation to late-stage fluid clearance, intensivists daily face “whether to give fluids” and “how much” decisions. However, mounting evidence shows fluid administration is not “more is better”; excess fluid correlates with organ dysfunction and poor outcomes. Recently, fluid responsiveness assessment and venous congestion monitoring have become crucial tools guiding fluid therapy. Yet, clinical practice often presents complex coexisting scenarios: patients exhibit both fluid responsiveness and varying degrees of venous congestion. Here, “to expand or not” becomes one of the most challenging fluid management decisions.

1. Interpretation of Multicenter Observational Study Results Based on the Frank-Starling Curve

In 2026, the research group published a multicenter observational study in Critical Care, enrolling 64 circulatory failure patients across 3 centers (Paris, France; Guangzhou & Shenzhen, China). 63% were enrolled within 24 h of ICU admission, 73% within 48 h; 90% used norepinephrine for blood pressure maintenance, lactate was 2.2 (1.4~3.1) mmol/L, and cumulative fluid balance was 1766 (347~2669) ml. Most patients were in the fluid resuscitation or optimization phase of circulatory failure. All patients received invasive hemodynamic monitoring for continuous cardiac output tracking, with clinicians deciding on 500 ml crystalloid bolus administration. Hemodynamic monitoring included: ① Right heart venous congestion monitoring using traditional VExUS grading (VExUS grade) and innovatively introducing VExUS organ congestion score (VExUS point) composed of abnormal venous flow scores; ② Left heart venous congestion monitoring assessed by extravascular lung water index (EVLWI). Fluid responsiveness was defined as >15% increase in cardiac index (CI) post-fluid; fluid tolerance was defined as no worsening of venous congestion post-fluid, i.e., no significant rise in VExUS grade, VExUS point, or EVLWI, rather than merely “no venous congestion.”

Results showed 42 patients (66%) were fluid responsive, 22 were non-responsive. Pre-fluid, both groups showed no significant differences in cardiac function, cumulative fluid, or venous congestion severity (VExUS grade & point). Organ congestion comparison revealed only the non-responsive group had a higher portal pulsatility index; other indices showed no statistical differences. By VExUS grade, 38% of patients had coexisting fluid responsiveness and venous congestion; using VExUS point, this rose to 67%. No significant EVLWI differences existed between groups regarding pulmonary congestion.

In the fluid-responsive group, fluid administration effectively increased cardiac output (CI ↑33%) and total end-diastolic volume, with mild CVP rise. Despite coexisting venous congestion, only 5% experienced worsened congestion post-fluid. Conversely, in the non-responsive group, fluid administration showed no significant CI increase (CI ↑4%), but CVP rose significantly (median ↑2 mmHg), 73% experienced significant VExUS grade deterioration (higher than responsive group, P < 0.001). Furthermore, non-responsive group VExUS organ congestion score median rose significantly from 2 to 4, with hepatic, portal, and renal venous quantitative congestion indices significantly worsening, and EVLWI increasing by 11%. This suggests fluid-responsive patients are on the ascending limb of the Frank-Starling curve with better fluid “tolerance”; non-responsive patients are on the plateau limb, where fluid therapy fails to increase cardiac output and easily causes right heart/venous congestion, indicating poor fluid “tolerance.”

However, in the ARDS subgroup, despite fluid responsiveness, continuous ARDS pulmonary capillary leakage causes fluid administration to significantly increase EVLWI, higher than non-ARDS fluid-responsive patients [ΔEVLWI: 10 (−0.96~2.5) vs. 0 (−0.3~0.4) ml/kg, P = 0.001], with more pronounced pulmonary water worsening in non-responsive patients, indicating vascular permeability status must be considered in this population.

2. Implications of Multicenter Observational Study Results

(1) Volume Expansion Is Permissible If Tissue Hypoperfusion Exists, but Caution Is Needed in Special Populations

At this stage, patients are typically in fluid resuscitation or optimization phases. If tissue hypoperfusion persists and careful hemodynamic assessment confirms ongoing volume responsiveness, fluid administration may be considered. Fluid therapy can significantly increase cardiac output without markedly worsening venous congestion grades.

Nevertheless, caution is required in two special populations: ARDS and intra-abdominal hypertension (IAH) patients. ARDS patients have increased pulmonary capillary permeability; fluid administration can cause inflammatory pulmonary edema. Thus, when fluid therapy risks outweigh potential benefits (e.g., severe ARDS with significantly elevated EVLWI and pulmonary vascular permeability index [PVPI]), despite fluid responsiveness, considering that vasoactive drugs can convert non-tense intravascular volume to tense volume, increasing vasoactive drugs rather than continuing fluids may be considered. In IAH patients, fluid administration can further elevate intra-abdominal pressure via visceral and abdominal wall edema, impairing abdominal organ (especially renal) perfusion and affecting ICU prognosis. Thus, extra caution is needed for patients with existing IAH.

(2) Volume Expansion Should Be Avoided If Tissue Perfusion Is Corrected; Consider Fluid Clearance

At this stage, patients are typically in fluid optimization or stabilization phases. When tissue perfusion has normalized (e.g., normal capillary refill time or lactate levels), further fluid administration is unnecessary despite volume responsiveness. Conversely, given coexisting venous congestion, assess fluid clearance feasibility to reduce fluid accumulation. However, since volume responsiveness persists, guard against potential hypotension risks from over-dehydration. Studies show PLR positivity before fluid clearance predicts subsequent hypotension risk during ultrafiltration.

3. Summary

Fluid therapy plays a vital role in circulatory support but carries adverse effect risks, acting as a “double-edged sword.” Fluid responsiveness and venous congestion help assess potential benefits and harms: fluid responsiveness suggests potential hemodynamic improvement from fluids but is not a trigger indication; venous congestion reflects organ venous return impairment but is not an absolute contraindication. Thus, fluid management should center on “whether tissue hypoperfusion exists that can be improved by increasing cardiac output.” During resuscitation/optimization, if hypoperfusion is uncorrected and volume responsiveness exists, cautious fluid administration may still yield benefits outweighing risks. After tissue perfusion recovery, avoid continued fluid administration and assess fluid clearance feasibility. For high-risk populations like ARDS and IAH, fluid therapy pros and cons require careful weighing. In summary, fluid therapy is not a single standardized protocol but should be individualized and precise, based on fluid responsiveness, venous congestion assessment, and patient-specific characteristics.

(Si Xiang, Wu Jianfeng, Guan Xiangdong, First Affiliated Hospital of Sun Yat-sen University)

References

  1. Monnet X, Malbrain MLNG, Pinsky MR. The prediction of fluid responsiveness [J]. Intensive Care Med, 2023, 49(1): 83-86.

  2. Beaubien-Souligy W, Rola P, et al. Quantifying systemic congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system [J]. Ultrasound J, 2020, 12(1): 16.

  3. Munoz F, Born P, Bruna M, et al. Coexistence of a fluid responsive state and venous congestion signals in critically ill patients: a multicenter observational proof-of-concept study [J]. Crit Care, 2024, 28(1): 52.

  4. Morosanu B, Balan C, Boros C, et al. Incidence, predictability, and outcomes of systemic venous congestion following a fluid challenge in initially fluid-tolerant preload-responders after cardiac surgery: a pilot trial [J]. Crit Care, 2024, 28(1): 339.

  5. Ruste M, Reskot R, Schweizer R, et al. Changes in portal pulsatility index induced by a fluid challenge in patients with haemodynamic instability and systemic venous congestion: a prospective cohort study [J]. Ann Intensive Care, 2024, 14(1): 167.

  6. Si X, Cao D, Shi R, et al. Fluid responsiveness and changes in venous congestion and lung water during volume expansion in critically ill patients: a multicentre observational study [J]. Crit Care, 2026, 30(1): 35.