Multiple organ failure remains a major cause of morbidity and mortality in critically ill patients. The Sequential Organ Failure Assessment (SOFA) score provides a simple and widely adopted method for assessing and monitoring organ dysfunction [
1]. In the Sepsis-3 definition published in 2016, sepsis is defined as the presence of infection accompanied by life-threatening organ dysfunction, and the SOFA score was explicitly recommended for evaluating such dysfunction [
2]. The original SOFA (SOFA-1) score was developed in 1994 and published in 1996. Over nearly three decades of clinical use, advances in devices and pharmacotherapy for organ support have created interpretive ambiguities across organ systems, prompting the need to re-evaluate the score to improve its standardization and generalizability. Consequently, a revised SOFA-2 scoring system was released in 2025 [
3]. In this update, scoring was redistributed across key organ systems, resulting in improved content validity and enhanced interpretability in contemporary practice [
4]. Key revisions in SOFA-2 are summarized in
Table 1.
For the brain system, unlike the original SOFA score, which relied solely on the Glasgow Coma Scale (GCS), the revision incorporates more detailed assessments, including the use of medications for delirium and specific motor responses. These additions allow more consistent and reproducible evaluations of neurologic dysfunction.
For the respiratory system, the revision includes various forms of noninvasive respiratory support and extracorporeal membrane oxygenation, and it permits use of both the partial pressure of oxygen (PaO2) to the fraction of inspired oxygen (FiO2) ratio and peripheral oxygen saturation (SpO2) to FiO2 ratio. These changes are expected to be beneficial in resource-limited emergency settings and enable rapid recognition of changes in the SOFA score through continuous measurements. However, in the emergency department (ED), where many patients are not yet stabilized, uncertainty persists regarding the accuracy of delivered FiO2 in patients with significant work of breathing, as this depends on the type of oxygen delivery system (high-flow versus low-flow) being used. This limitation remains unresolved.
For the cardiovascular system, dopamine—now rarely used as a vasopressor—was removed from the main table. Instead, consistent with modern shock-management practices, norepinephrine and epinephrine were designated as primary agents, and required dosing is now calculated using a summation concept [
5]. Additionally, the scoring incorporates the use of other vasopressors or inotropes, as well as cases in which mechanical circulatory support is employed.
The liver, kidney, and hemostasis systems continue to rely on laboratory test results, with thresholds slightly revised. As a result, the longstanding limitation remains: organ dysfunction in these systems cannot be determined until relevant laboratory data are available [
6]. In contrast, for the kidney component, SOFA-2 expands assessment beyond the traditional 24-hour urine output by incorporating hourly urine output and explicitly accounting for both the use and need for renal replacement therapy, thereby enabling a more comprehensive evaluation of renal dysfunction.
From an ED standpoint, SOFA-2 implementation and validation should proceed in a manner that reflects both the strengths and the operational constraints of early resuscitation. First, retrospective and prospective ED cohorts are needed to quantify how frequently SOFA-2 reclassifies risk compared with SOFA-1 and to determine whether the revised respiratory, cardiovascular, and renal components improve short-term mortality prediction at presentation and during the initial hours of care. Second, because ED scoring is often performed before complete laboratory results are available, studies should evaluate pragmatic protocols that integrate bedside parameters (SpO
2/FiO
2 ratio, hourly urine output) with staged laboratory updates. Third, uncertainty related to device-specific FiO
2 delivery and neurologic confounders such as intoxication, seizures, or procedural sedation remains common in the ED; thus, validation efforts should explicitly test the robustness of SOFA-2 under these real-world conditions and establish standardized assumptions for oxygen devices and unassessable GCS values. Finally, given the importance of tissue hypoperfusion in early sepsis, it would be reasonable for future ED-focused studies to evaluate lactate as an adjunct to SOFA-2, either as a modifier within the cardiovascular domain or as a supplemental metabolic component, and to determine whether this approach improves prognostic performance without compromising feasibility [
7].
NOTES
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Conflicts of interest
The author has no conflicts of interest to declare.
-
Funding
The author received no financial support for this study.
-
Data availability
Data sharing is not applicable as no new data were created or analyzed in this study.
Table 1.Summary of major changes and clinical implications in the updated SOFA-2 score
Table 1.
|
Organ system |
Major changes |
Expected impact and clinical relevance |
|
Brain |
• Adjusted GCS thresholds (e.g., GCS 9 is scored as 2 instead of 3) |
• Better detection of subtle neurologic dysfunction (e.g., delirium) |
|
• Delirium requiring medication scores ≥1 point |
• More consistent and reproducible stratification across settings |
|
• Alternatives for unassessable GCS: best motor response or pain response |
|
|
• Use presedation GCS for sedated patients |
|
|
• System name updated to “brain” |
|
|
Respiratory |
• Modified PaO2/FiO2 thresholds |
• Improved recognition of respiratory failure requiring noninvasive support or ECMO, reflecting contemporary practice |
|
• Incorporation of noninvasive respiratory support (HFNC, CPAP, BiPAP) into “advanced support” |
• SpO2/FiO2 option increases applicability beyond ICU and in resource-limited settings |
|
• ECMO for respiratory failure scores 4 |
• Updated PaO2/FiO2 cutoffs improve alignment with mortality risk |
|
• SpO2/FiO2 ratio allowed when arterial sampling is unavailable |
|
|
Cardiovascular |
• New catecholamine thresholds (0.2 and 0.4 μg/kg/min) |
• Reflects modern shock management practices |
|
• Inclusion of vasopressin, other vasopressors, and mechanical circulatory support (IABP, LVAD, ECMO) |
• More normalized dose distribution and improved score-mortality alignment |
|
• MAP-only scoring when vasopressors cannot be used or are restricted |
• Addresses underestimation of severe shock in patients receiving mechanical support |
|
• Specific dopamine-only dose thresholds when dopamine is the sole vasopressor |
|
|
Liver |
• Updated bilirubin thresholds (1.2, 3, 6, and 12 mg/dL) |
• More appropriate scoring for mild hyperbilirubinemia |
|
• Name updated from “hepatic” to “liver” |
• Better alignment between bilirubin categories and mortality risk |
|
Kidney |
• Revised creatinine thresholds and time-based urine output criteria |
• More granular assessment of acute kidney injury progression |
|
• Receiving or meeting criteria for renal replacement therapy is scored as 4 |
• Clear identification of patients reaching dialysis-level severity |
|
• Alternative scoring criteria when dialysis is unavailable or limited |
• Improved alignment between kidney score levels and mortality risk |
|
• Name updated from “renal” to “kidney” |
|
|
Hemostasis |
• Updated platelet thresholds (150, 100, 80, and 50 ×103/µL) |
• Refined thresholds for moderate-to-severe thrombocytopenia |
|
• Name updated from “coagulation” to “hemostasis” |
|
General Changes |
• Provides alternatives when measurements or treatments are unavailable or not appropriate (e.g., limited resources, treatment ceilings) |
• Ensures reliable scoring across varied resource settings and treatment limitations |
|
• Establishes consistent missing-data rules (normal-value substitution on day 1; carry-forward thereafter) |
• Standardized data handling improves consistency, comparability, and clinical workflow |
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