A prospective observational study conducted at a tertiary healthcare center in Egypt has demonstrated that the venous excess ultrasound protocol, known as VExUS, accurately grades systemic venous congestion and monitors its dynamic resolution in adult patients hospitalized with congestive heart failure. Persistent venous congestion constitutes a primary hemodynamic mechanism driving multiorgan dysfunction, including congestive hepatopathy and congestive nephropathy, and is closely tied to adverse clinical outcomes and elevated mortality. Historically, clinician assessment of intravascular volume has relied on physical examinations or invasive procedures such as right heart catheterization. The new study indicates that non-invasive Doppler interrogation of abdominal vasculature provides an objective, granular appraisal of hemodynamic backpressure transmitted to peripheral organs, tracking both the severity of fluid accumulation upon hospital admission and its progressive relief following individualized decongestive therapy.

Assessing intravascular volume status at the bedside remains a recognized challenge in cardiology and critical care. Traditional physical signs, including jugular venous distension, peripheral edema, third heart sounds, and pulmonary auscultation findings, are often subjective or insufficient to delineate precise organ-level congestion. Conventional chest radiography carries recognized diagnostic limitations, including false-negative interpretations for pulmonary congestion, while basic point-of-care ultrasound focused exclusively on the inferior vena cava cannot quantify downstream organ compromise. Dilation of the inferior vena cava occurs in diverse conditions and fails to specify the extent to which excessive central venous pressures impede parenchymal blood flow. To overcome these diagnostic blind spots, researchers recruited one hundred consecutive adult patients aged sixteen and older presenting with acute or chronic congestive heart failure within twenty-four hours of admission, systematically assessing venous waveforms to capture organ-specific circulatory impedance.

The study protocol utilized a four-step ultrasonographic assessment performed on a GE LOGIQ P7 ultrasound machine using a curvilinear transducer operating between 3.5 and 7 MHz. After an initial rapid echocardiographic assessment, ultrasound examinations were completed in approximately twenty minutes per patient following at least six hours of fasting. The procedure began with inferior vena cava measurement to establish baseline dimensions, calculating end-expiratory and end-inspiratory diameters alongside the collapsibility index and sphericity index. Investigators then used pulsed-wave and color flow Doppler to evaluate blood flow patterns across three distinct abdominal vascular territories: the middle hepatic vein, the main portal vein, and the interlobar intrarenal veins. Each examination was conducted during the end-expiratory phase of the patient’s respiratory cycle by a radiologist with five years of experience, providing sequential objective snapshots across standardized physiological milestones.

Each anatomical site evaluated under the VExUS protocol reflects progressive physiological adaptations to elevated right atrial pressure. Under non-congestive hemodynamic conditions, hepatic venous flow displays a pulsatile triphasic cardiac modulation consisting of retrograde A waves alongside antegrade S and D waves, where the high-magnitude systolic S wave exceeds the diastolic D wave. As venous backpressure rises, systolic filling decreases until the D wave exceeds the S wave, culminating in severe cases in complete systolic reversal where retrograde S waves fuse with A waves into a biphasic pattern. Within the portal vein, normal flow is continuous, antegrade, and monophasic with a pulsatility index below 30 percent; rising backward pressure induces progressive pulsatility, characterized by a pulsatility index between 30 and 49 percent in mild congestion and reaching or exceeding 50 percent or flow reversal in severe congestion. Intrarenal venous assessment at interlobar vessels mirrors this transmission, converting continuous monophasic venous flow below the baseline into discontinuous biphasic systolic-diastolic patterns or isolated diastolic flow as interstitial venous pressure escalates.

Upon hospital admission, none of the one hundred enrolled heart failure patients presented with a normal VExUS score of 0. Forty-eight patients, representing 48 percent of the cohort, exhibited grade 1 congestion; thirty-one patients, or 31 percent, exhibited grade 2 congestion; and twenty-one patients, or 21 percent, presented with severe grade 3 congestion. The severity of congestion captured by the VExUS grade aligned closely with invasive central venous pressure readings and clinical markers of systemic fluid retention. In patients classified as grade 3 on admission, the mean central venous pressure reached 34.23 plus or minus 1.86 millimeters of mercury, accompanied by a 100 percent prevalence of bilateral pleural effusion, ascites, and above-knee lower limb edema. In comparison, grade 1 patients exhibited lower mean central venous pressures of 27.7 plus or minus 8.8 millimeters of mercury alongside milder physical manifestations of fluid excess.

Biochemical markers of renal impairment and electrolyte imbalance demonstrated significant cross-sectional associations with initial VExUS congestion scores. Across the cohort, higher VExUS grades corresponded to significantly elevated serum urea, creatinine, and potassium levels. In grade 3 patients upon admission, serum urea averaged 75.33 plus or minus 19.37 milligrams per deciliter, creatinine reached 1.80 plus or minus 0.99 milligrams per deciliter, and potassium averaged 4.83 plus or minus 0.59 millimoles per liter. In grade 1 patients, by comparison, admission serum creatinine averaged 1.29 plus or minus 0.19 milligrams per deciliter and blood urea averaged 42.5 plus or minus 8.0 milligrams per deciliter. These parallel rises in nitrogenous waste products and serum potassium support the recognized pathophysiological framework of congestive nephropathy, wherein organ dysfunction stems directly from retrograde venous hypertension and capillary microcirculatory tamponade rather than solely from reductions in forward cardiac output.

Medical decongestive regimens were adjusted according to the severity of systemic congestion identified at presentation. All patients received intravenous furosemide at admission, with mean doses increasing markedly across congestion grades, from 220.8 plus or minus 99.4 milligrams in grade 1 patients up to 422.85 plus or minus 85.38 milligrams in grade 3 patients. Concurrently, neurohormonal blockade through mineralocorticoid receptor antagonists, specifically spironolactone, was utilized more intensively in severe cases: 90.5 percent of grade 3 patients received spironolactone upon admission, with 47.6 percent prescribed high doses and 42.9 percent low doses, compared to lower administration rates in grade 1. Following initial stabilization, therapy was transitioned to oral diuretics and neurohormonal agents upon hospital discharge, allowing researchers to evaluate how Doppler profiles evolved over subsequent outpatient follow-up periods.

Sequential longitudinal assessments revealed marked improvements in hemodynamic parameters, physical examination signs, and ultrasound waveforms over time. At hospital discharge, which took place one week after initiation of inpatient medical therapy, forty-six patients had improved to a VExUS score of 0, thirty-four remained at grade 1, twenty remained at grade 2, and none exhibited grade 3 congestion. Mean central venous pressure across the cohort dropped significantly from 32.14 plus or minus 4.78 millimeters of mercury at admission to 22.4 plus or minus 6.68 millimeters of mercury at discharge. At one-month follow-up, eighty patients achieved a VExUS score of 0, twenty maintained grade 1 congestion, and zero patients presented with grade 2 or 3 congestion. Concurrently, the overall prevalence of bilateral pleural effusion plummeted from 80 percent at baseline to 56 percent at discharge and 4 percent at one month, while ascites decreased from 72 percent to 52 percent and eventually 8 percent.

Serial biochemical measurements followed a corresponding recovery trajectory that matched the resolution of abdominal venous abnormalities. Mean blood urea levels decreased progressively across the study timeline from 55.55 plus or minus 16.79 milligrams per deciliter on admission to 43.3 plus or minus 8.4 milligrams per deciliter at discharge and 38.37 plus or minus 6.3 milligrams per deciliter at one month. Serum creatinine exhibited a parallel reduction from 1.40 plus or minus 0.20 milligrams per deciliter at admission to 1.35 plus or minus 0.27 milligrams per deciliter at discharge and 1.30 plus or minus 0.22 milligrams per deciliter at the one-month evaluation. Serum potassium concentrations similarly shifted downward from an admission mean of 4.12 plus or minus 0.64 millimoles per liter to 3.73 plus or minus 0.50 millimoles per liter at discharge and 3.57 plus or minus 0.30 millimoles per liter at one month, demonstrating consistent statistical significance across repeated measures.

The study authors documented several technical constraints and methodological boundaries inherent to the investigation. The study was conducted as a single-center prospective observational project with strict exclusion criteria that eliminated individuals with atrial fibrillation, advanced chronic kidney disease, liver cirrhosis or hepatic tumors, splanchnic malignancy, vascular occlusions, or inadequate acoustic windows. Consequently, the applicability of these findings to more complex, unselected real-world heart failure populations remains uncertain. In addition, right ventricular function was not formally evaluated, diuretic dosing was guided by treating physician discretion rather than a rigid trial assignment, baseline laboratory values prior to acute admission were unavailable, and intraobserver reproducibility was not formally measured. The authors emphasize that while serial VExUS monitoring non-invasively mirrors changes in systemic venous congestion, multicenter randomized trials with longer follow-up periods are needed to determine whether protocol-guided therapy directly improves long-term clinical endpoints such as mortality and hospital readmissions.

Subject of Research: Ultrasound evaluation of systemic venous congestion in congestive heart failure

Article Title: Role of venous excess ultrasound (VExUS) protocol in grading systemic venous congestion in adult Egyptian patients with congestive heart failure: a prospective study

Article References: M.Kamil, C., Nabil Helmy, P., M. Hasan Elsheref, A., Dardeer, A., M.Beshreda, G., & M Sayed, M. (2026). Role of venous excess ultrasound (VExUS) protocol in grading systemic venous congestion in adult Egyptian patients with congestive heart failure: a prospective study. Egyptian Journal of Radiology and Nuclear Medicine, 57(1), Article 204. https://doi.org/10.1186/s43055-026-01873-2

Image Credits: AI Generated

DOI: 10.1186/s43055-026-01873-2

Keywords: venous excess ultrasound, heart failure, systemic venous congestion, Doppler ultrasound, inferior vena cava, portal vein, hepatic vein, renal Doppler, Role, venous, excess, ultrasound