Sepsis differential diagnosis

Jump to navigation Jump to search
Resident
Survival
Guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] Jason Le, B.S.[3]

Sepsis — Differentiating Sepsis From Other Diseases

Sepsis and septic shock can closely resemble non-infectious inflammatory syndromes and other forms of shock. In critically ill adults, diagnostic reasoning should therefore proceed in parallel: identify a plausible infectious source and organ dysfunction while actively testing whether the physiology is better explained by cardiogenic, hypovolemic/hemorrhagic, obstructive, endocrine, toxic, or hyperinflammatory disease. No single biomarker reliably establishes or excludes sepsis.

Clinical approach to undifferentiated shock

The first bedside question is whether the patient has a predominantly distributive, cardiogenic, hypovolemic/hemorrhagic, or obstructive physiology. These mechanisms may coexist, particularly in critically ill patients.

Shock phenotype Findings that favor the phenotype Bedside tests / discriminators Important caveats
Distributive Warm extremities early, wide pulse pressure, low systemic vascular resistance, bounding pulses; may progress to cool mottled extremities with severe vasoconstriction Bedside cardiac ultrasound; LV/RV function; assessment of preload and dynamic fluid responsiveness; lung ultrasound; clinical context and source evaluation Septic shock is the major infectious cause, but anaphylaxis and other non-infectious distributive states can produce similar physiology
Cardiogenic Pulmonary edema, elevated jugular venous pressure, cool extremities, new ischemia or arrhythmia, clinical evidence of cardiac dysfunction Bedside cardiac ultrasound; LV/RV systolic function; regional wall-motion abnormality; pericardial assessment Sepsis can itself cause myocardial dysfunction; mixed septic-cardiogenic shock is common enough to remain an important consideration
Hypovolemic / hemorrhagic History of bleeding, gastrointestinal losses, poor intake, diuresis, trauma or surgery; narrow pulse pressure and reduced venous filling may occur Bedside ultrasound integrated with history, serial examination, hemoglobin/hematocrit and source evaluation Early septic shock may have a similar underfilled appearance; POCUS alone cannot reliably distinguish early septic from hypovolemic shock
Obstructive Sudden hypotension, elevated venous pressure, acute respiratory or cardiac symptoms depending on cause Cardiac/lung POCUS for tamponade, RV pressure overload, pneumothorax and other obstructive patterns; targeted imaging when indicated Findings can overlap with cardiogenic and distributive shock; pulmonary embolism may require confirmatory imaging

When the shock mechanism is unclear from the history and physical examination, bedside cardiac ultrasound is a preferred initial tool for evaluating cardiac function and distinguishing major shock phenotypes. The Society of Critical Care Medicine recommends bedside cardiac ultrasound in hemodynamically unstable patients (Grade 1B). Point-of-care ultrasound has limited ability to separate early septic shock from hypovolemic shock, so ultrasound findings should be integrated with the clinical picture rather than interpreted as a standalone etiologic test.[1][2][3]

Advanced hemodynamic monitoring may be considered in complex or mixed shock states when non-invasive assessment remains inconclusive.

Non-infectious inflammatory mimics

Several conditions can produce fever, tachycardia, leukocytosis, hypotension, elevated lactate, organ dysfunction, or markedly elevated inflammatory markers without infection being the primary driver.

Mimic Features that may resemble sepsis Findings that increase suspicion for the mimic Key differentiators
Pancreatitis Fever, leukocytosis, tachycardia, hypotension, elevated CRP, organ failure Characteristic abdominal pain; compatible pancreatic imaging Lipase/amylase, abdominal imaging, characteristic clinical history
Major trauma / burns SIRS, shock, leukocytosis, lactate elevation, organ dysfunction Clear traumatic or thermal injury without an infectious source at presentation Injury pattern, hemorrhage assessment, serial clinical evaluation for evolving infection
Anaphylaxis Hypotension, tachycardia, distributive shock, respiratory compromise Abrupt onset after exposure; urticaria, angioedema, bronchospasm or gastrointestinal manifestations Exposure history and characteristic clinical phenotype
Drug/toxin-associated syndromes Altered mental status, autonomic instability, hyperthermia, hypotension, metabolic abnormalities Exposure history; characteristic pupillary, neuromuscular or autonomic findings Toxidrome pattern, medication/substance history and targeted toxicology evaluation
Adrenal crisis Hypotension, weakness, abdominal symptoms, electrolyte abnormalities, altered mental status Steroid withdrawal, known adrenal disease or adrenal injury Cortisol/ACTH evaluation when appropriate; sodium, potassium and glucose abnormalities; clinical context
Thyroid storm Fever, tachycardia, altered mental status, heart failure, gastrointestinal symptoms Known or suspected thyrotoxicosis; marked adrenergic features Thyroid studies and clinical scoring systems used in context
Diabetic ketoacidosis Tachycardia, tachypnea, altered mental status, hypotension and leukocytosis Hyperglycemia or euglycemic DKA context; ketonemia and metabolic acidosis Glucose, beta-hydroxybutyrate/ketones, bicarbonate and anion gap

A non-infectious inflammatory trigger does not exclude concomitant infection. Diagnostic reassessment should therefore remain dynamic, particularly when the clinical trajectory is inconsistent with the presumed diagnosis.

Hyperinflammatory syndromes and secondary HLH

Secondary hemophagocytic lymphohistiocytosis (HLH), macrophage activation syndrome (MAS), and related cytokine-storm states can closely resemble severe sepsis or septic shock. Important clues include persistent fever, cytopenias affecting multiple lineages, extreme or rapidly rising ferritin, hypertriglyceridemia, hypofibrinogenemia, liver injury, coagulopathy, splenomegaly, and progressive multiorgan dysfunction.

Ferritin is useful as a signal of hyperinflammation but is not specific for HLH. Interpretation should incorporate the overall phenotype and, when appropriate, a formal HLH framework such as HLH-2004 criteria or HScore.

The HScore provides a validated adult probability framework incorporating known immunosuppression, temperature, organomegaly, cytopenias, ferritin, triglycerides, fibrinogen, AST, and hemophagocytosis. In the original derivation cohort, an HScore of approximately 169 provided high diagnostic sensitivity and specificity; subsequent critically ill adult cohorts have reproduced a similar operating range, although performance varies with population and disease prevalence.[4][5][6][7]

For point-of-care use, the HScore calculator can provide an interactive probability estimate. The score should be used as an adjunct rather than as a substitute for clinical judgment or the broader HLH diagnostic framework.

A threshold of greater than 7% CD38high/HLA-DR+ cells among CD8+ T cells had strong positive and negative predictive value for distinguishing HLH from early sepsis.[8] This threshold is sensitive for T-cell–driven hyperinflammation but is not specific for HLH: values exceeding 7% also occur in MIS-C, MAS, and other immune-dysregulation disorders, whereas the amplitude of activation is highest in primary and EBV-associated HLH. It is not yet universally validated for adults.[9]

Ferritin and HScore can aid recognition; combining CRP with ferritin may improve discrimination of HLH from other cytokine-storm syndromes.[10][11]

The ferritin trajectory may be more informative than an isolated value. Extreme hyperferritinemia should prompt consideration of HLH/MAS and other hyperinflammatory syndromes, while recognizing that severe infection itself can produce very high ferritin concentrations.

The serum H-ferritin-to-total-ferritin ratio is an emerging biomarker under investigation in critically ill patients with hyperferritinemia and may provide additional discrimination among HLH, MAS-like states, sepsis, and other critical illness phenotypes; it should not yet be treated as a standalone diagnostic test.[12]

Procalcitonin and other biomarkers

Procalcitonin (PCT) can support clinical assessment but should not be interpreted as a binary test for infection. PCT may be elevated in some malignancies and does not reliably distinguish gram-positive from gram-negative infection or neutropenic from non-neutropenic patients.[13]

PCT cannot reliably differentiate sepsis from non-infectious SIRS in critically ill adults (pooled AUC approximately 0.78).[14] Other meta-analyses report higher discrimination, with estimates approaching 0.84–0.85 in some populations, illustrating heterogeneity by study design, population, reference standard, and timing of measurement.[15][16]

PCT may also rise in non-infectious states, including trauma, surgery, malignancy, and other systemic inflammatory conditions. Consequently, an elevated PCT should increase neither diagnostic certainty nor antimicrobial commitment in isolation.

The Surviving Sepsis Campaign 2021 issued a weak recommendation against using procalcitonin plus clinical evaluation, versus clinical evaluation alone, to decide when to start antimicrobials.[17]

Other biomarkers, including CRP, presepsin, cytokines, and host-response signatures, may provide complementary information but remain insufficiently specific to replace clinical assessment, microbiologic evaluation, and source-directed investigation.

Adult differential diagnosis table

Condition Distinguishing clinical features Diagnostic tests / findings Key differentiators from sepsis
Cardiogenic shock Acute pulmonary edema, elevated JVP, ischemia, new arrhythmia, cool extremities ECG, troponin, bedside cardiac ultrasound, formal echocardiography Primary cardiac dysfunction or ischemia explains shock; infection may coexist
Hypovolemic / hemorrhagic shock Bleeding, gastrointestinal losses, dehydration, recent procedure or trauma Hemoglobin/hematocrit trend, focused ultrasound, bleeding-source evaluation Volume loss precedes shock; no convincing infectious source
Obstructive shock Sudden hypotension, acute dyspnea, elevated venous pressure or obstructive physiology Cardiac/lung POCUS, CT pulmonary angiography or other targeted imaging as indicated Tamponade, pulmonary embolism, tension pneumothorax or another mechanical obstruction
Anaphylaxis Abrupt onset, urticaria/angioedema, bronchospasm, gastrointestinal symptoms Clinical diagnosis; targeted evaluation as indicated Temporal exposure and characteristic multisystem allergic phenotype
Adrenal crisis Hypotension, weakness, abdominal symptoms, electrolyte/glucose abnormalities Cortisol/ACTH when appropriate; electrolytes and glucose Adrenal insufficiency context with compatible biochemical findings
Thyroid storm Fever, marked tachycardia, agitation/delirium, heart failure, gastrointestinal manifestations TSH and free T4/T3 with clinical assessment Thyrotoxicosis plus compatible systemic decompensation
DKA Tachypnea, altered mentation, dehydration, abdominal symptoms Glucose, beta-hydroxybutyrate/ketones, bicarbonate, anion gap Ketoacidosis and diabetes/metabolic context explain presentation
Pancreatitis Abdominal pain, systemic inflammation, shock in severe disease Lipase and abdominal imaging Pancreatic inflammation provides the primary trigger
Drug/toxin-associated syndrome Altered mental status, autonomic instability, hyperthermia or unusual neuromuscular findings Medication/substance history; targeted toxicology evaluation Exposure and characteristic toxidrome
Secondary HLH / MAS Persistent fever, cytopenias, extreme or rising ferritin, liver injury, hypofibrinogenemia, hypertriglyceridemia Ferritin, triglycerides, fibrinogen, CBC, AST/ALT, HScore, soluble IL-2 receptor and other specialized testing when available Multisystem hyperinflammation with a compatible trigger and accumulating HLH features
MIS-A Fever with extrapulmonary organ dysfunction, often prominent cardiovascular, gastrointestinal, mucocutaneous or neurologic involvement after SARS-CoV-2 infection SARS-CoV-2 testing/serology as appropriate, inflammatory markers, cardiac assessment Post-COVID temporal relationship and characteristic multisystem phenotype Adult syndrome; pediatric MIS-C is outside the scope of this adult differential

Laboratory and diagnostic pitfalls

  • No single biomarker separates sepsis from its mimics. Ferritin, CRP, PCT, lactate and cytokines reflect overlapping inflammatory or physiologic pathways.
  • A high PCT does not prove bacterial infection. Non-infectious inflammation and other critical illnesses can increase PCT.
  • A low or modest PCT does not exclude infection. Timing, localized infection, immunologic state and pathogen type influence concentrations.
  • Extreme ferritin is not synonymous with HLH. Severe infection, liver injury, MAS and other inflammatory disorders can produce marked hyperferritinemia.
  • HScore is an adjunct, not a replacement for diagnostic judgment. Scores near the commonly used cutoff should be interpreted in clinical context.
  • CD38high/HLA-DR+ CD8+ T-cell activation is not HLH-specific. The >7% threshold can identify hyperinflammation but also occurs in other immune-dysregulation syndromes.
  • POCUS does not always identify the cause of shock. Early septic and hypovolemic shock can have overlapping ultrasound findings.
  • Mixed shock is common. Sepsis may coexist with myocardial dysfunction, hemorrhage, pulmonary embolism, adrenal insufficiency, or other contributors.
  • Culture-negative sepsis remains possible. Negative cultures do not independently establish a non-infectious diagnosis when the clinical phenotype remains compatible with infection.
  • MIS-A belongs in the adult differential. MIS-C is a pediatric syndrome and should not be presented as an adult diagnosis.

Practical diagnostic synthesis

A useful bedside sequence is:

  1. Confirm the physiology. Determine whether hypotension and organ dysfunction are present and assess the dominant shock phenotype.
  2. Search for infection. Obtain a focused history and examination, blood cultures and other cultures as indicated, and source-directed imaging/testing.
  3. Actively test major shock mimics. Consider cardiogenic, hemorrhagic/hypovolemic, obstructive, endocrine, toxic, and anaphylactic causes.
  4. Look for hyperinflammation when the phenotype is disproportionate. Persistent fever, multilineage cytopenias, rapidly rising or extreme ferritin, hypofibrinogenemia, hypertriglyceridemia, hepatitis, and splenomegaly should prompt consideration of secondary HLH/MAS.
  5. Use HScore when appropriate. An HScore around 169 is a useful probability threshold, but the score should be interpreted with the clinical context and evolving trajectory.
  6. Use biomarkers as supporting evidence only. PCT, CRP, ferritin and emerging immune biomarkers should not independently establish or exclude infection.
  7. Reassess serially. Diagnostic confidence should change when the patient's trajectory, microbiology, imaging, or response to initial management conflicts with the working diagnosis.

Figures

Figure 1. IFN-γ:IL-10 ratio in HLH and severe viral infection

File:Shabrish 2019 IFN-g IL-10 ratio.png
Comparison of serum cytokine levels; the horizontal line represents the mean.

Shabrish S, Desai M, Saxena V, Kelkar M, Madkaikar M. IFN-g:IL-10 Ratio: A Putative Predictive Biomarker to Discriminate HLH From Severe Viral Infections. Journal of Clinical Immunology. 2019;39(2):135–137. doi:10.1007/s10875-019-00601-y.[18]

Chaturvedi V, Marsh RA, Zoref-Lorenz A, et al. T-Cell Activation Profiles Distinguish Hemophagocytic Lymphohistiocytosis and Early Sepsis. Blood. 2021;137(17):2337–2346. doi:10.1182/blood.2020009499.

Figure 3. H-ferritin-to-total-ferritin ratio in critically ill patients with hyperferritinemia

File:Debaugnies 2026 H ferritin ratio.png
Discrepant classification between ferritin levels and the H-ferritin-to-total-ferritin ratio among patients with HLH, MAS, and controls including patients with sepsis, severe sepsis, or septic shock.

Debaugnies F, Goetzinger F, Wolff F, et al. Serum H-Ferritin-to-Ferritin Ratio as a Biomarker of Hemophagocytic Lymphohistiocytosis in Critically Ill Patients With Hyperferritinemia. American Journal of Hematology. 2026;101(3):648–653. doi:10.1002/ajh.70189.

Figure 4. Procalcitonin and CRP kinetics

File:Van Berkel 2020 PCT CRP kinetics.png
Kinetics and predictive value of procalcitonin and C-reactive protein in COVID-19 patients.

van Berkel M, Kox M, Frenzel T, et al. Biomarkers for Antimicrobial Stewardship: A Reappraisal in COVID-19 Times? Critical Care. 2020;24(1):600. doi:10.1186/s13054-020-03291-w.[19]

Figure 5. Diagnostic performance of presepsin, PCT, and CRP

File:Lee 2022 presepsin PCT CRP ROC.png
Receiver operating characteristic curves of presepsin, procalcitonin, and CRP levels.

Lee S, Song J, Park DW, et al. Diagnostic and Prognostic Value of Presepsin and Procalcitonin in Non-Infectious Organ Failure, Sepsis, and Septic Shock: A Prospective Observational Study According to the Sepsis-3 Definitions. BMC Infectious Diseases. 2022;22(1):8. doi:10.1186/s12879-021-07012-8.[20]

Figure 6. Cardiac POCUS algorithm in shock

File:Conlon 2024 cardiac POCUS algorithm.png
Algorithm for cardiac point-of-care ultrasound in shock.

Conlon TW, Baker D, Bhombal S. Cardiac Point-of-Care Ultrasound: Practical Integration in the Pediatric and Neonatal Intensive Care Settings. European Journal of Pediatrics. 2024;183(4):1525–1541. doi:10.1007/s00431-023-05409-y.[21]

Figure 7. POCUS-guided management during ward emergencies

File:Zieleskiewicz 2021 POCUS protocol.png
POCUS-guided management and ultrasound protocol.

Zieleskiewicz L, Lopez A, Hraiech S, et al. Bedside POCUS During Ward Emergencies Is Associated With Improved Diagnosis and Outcome: An Observational, Prospective, Controlled Study. Critical Care. 2021;25(1):34. doi:10.1186/s13054-021-03466-z.[22]

References

  1. Fardet L, Galicier L, Lambotte O, et al. Development and Validation of the HScore, a Score for the Diagnosis of Reactive Hemophagocytic Syndrome. Arthritis Rheumatol. 2014;66(9):2613–2620. doi:10.1002/art.38690.
  2. Knaak C, Nyvlt P, Schuster FS, et al. Hemophagocytic lymphohistiocytosis in critically ill patients: diagnostic reliability of HLH-2004 criteria and HScore. Crit Care. 2020;24(1):244. doi:10.1186/s13054-020-02941-3.
  3. Bilston L, Croden J, Taparia M, et al. Validation of the HScore and the HLH-2004 diagnostic criteria for the diagnosis of hemophagocytic lymphohistiocytosis in a multicenter cohort. Eur J Haematol. 2022;109(2):129–137. doi:10.1111/ejh.13779.
  4. Henter JI. Hemophagocytic Lymphohistiocytosis. N Engl J Med. 2025;392(6):584–598. doi:10.1056/NEJMra2314005.
  5. Chaturvedi V, Marsh RA, Zoref-Lorenz A, et al. T-Cell Activation Profiles Distinguish Hemophagocytic Lymphohistiocytosis and Early Sepsis. Blood. 2021;137(17):2337–2346. doi:10.1182/blood.2020009499. PMID 33512385.
  6. Nguyen TH, Kumar D, Prince C, et al. Frequency of HLA-DR+ CD38hi T-cells identifies and quantifies T-cell activation in hemophagocytic lymphohistiocytosis, hyperinflammation, and immune regulatory disorders. J Allergy Clin Immunol. 2024;153(1):309–319. doi:10.1016/j.jaci.2023.07.008.
  7. Goubran M, Spaner C, Stukas S, et al. The role of C-reactive protein and ferritin in the diagnosis of HLH, adult-onset Still's disease, and COVID-19 cytokine storm. Sci Rep. 2024;14(1):31306. doi:10.1038/s41598-024-82760-6.
  8. Bursa D, et al. Scientific Reports. 2021.
  9. Tang BM, Eslick GD, Craig JC, McLean AS. Accuracy of Procalcitonin for Sepsis Diagnosis in Critically Ill Patients: Systematic Review and Meta-Analysis. Lancet Infect Dis. 2007;7(3):210–217. doi:10.1016/S1473-3099(07)70052-X.
  10. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063–e1143. doi:10.1097/CCM.0000000000005337.
  11. Maves RC, Enwezor CH. Uses of Procalcitonin as a Biomarker in Critical Care Medicine. Infect Dis Clin North Am. 2022;36(4):897–909. doi:10.1016/j.idc.2022.07.004.
  12. Tan M, Lu Y, Jiang H, Zhang L. The Diagnostic Accuracy of Procalcitonin and C-Reactive Protein for Sepsis: A Systematic Review and Meta-Analysis. J Cell Biochem. 2019;120(4):5852–5859. doi:10.1002/jcb.27870.
  13. Ghatak T, Pal A, Rochwerg B, et al. The Diagnostic Accuracy of Serum Procalcitonin for Sepsis in Critically Ill Adults. A Systematic Review and Diagnostic Meta-Analysis. J Crit Care. 2025;92:155402. doi:10.1016/j.jcrc.2025.155402.
  14. Chairaj T, Mongkhon P, Leewongsakorn P, et al. Diagnostic Performance of Procalcitonin and Presepsin in Sepsis: A Systematic Review and Meta-Analysis. BMC Emerg Med. 2025;26(1):9. doi:10.1186/s12873-025-01433-3.
  15. Levitov A, Frankel HL, Blaivas M, et al. Guidelines for the Appropriate Use of Bedside General and Cardiac Ultrasonography in the Evaluation of Critically Ill Patients—Part II: Cardiac Ultrasonography. Crit Care Med. 2016;44(6):1206–1227. doi:10.1097/CCM.0000000000001847.
  16. Yoshida T, Yoshida T, Noma H, et al. Diagnostic accuracy of point-of-care ultrasound for shock: a systematic review and meta-analysis. Crit Care. 2023;27(1):200. doi:10.1186/s13054-023-04495-6.
  17. Ramadan A, Abdallah T, Abdelsalam H, Mokhtar A, Razek AA. Accuracy of echocardiography and ultrasound protocol to identify shock etiology in emergency department. BMC Emerg Med. 2022;22(1):117. doi:10.1186/s12873-022-00678-6.
  18. Shabrish S, Desai M, Saxena V, Kelkar M, Madkaikar M. IFN-g:IL-10 Ratio: A Putative Predictive Biomarker to Discriminate HLH From Severe Viral Infections. J Clin Immunol. 2019;39(2):135–137. doi:10.1007/s10875-019-00601-y.
  19. Debaugnies F, Goetzinger F, Wolff F, et al. Serum H-Ferritin-to-Ferritin Ratio as a Biomarker of Hemophagocytic Lymphohistiocytosis in Critically Ill Patients With Hyperferritinemia. Am J Hematol. 2026;101(3):648–653. doi:10.1002/ajh.70189.
  20. van Berkel M, Kox M, Frenzel T, et al. Biomarkers for Antimicrobial Stewardship: A Reappraisal in COVID-19 Times? Crit Care. 2020;24(1):600. doi:10.1186/s13054-020-03291-w.
  21. Lee S, Song J, Park DW, et al. Diagnostic and Prognostic Value of Presepsin and Procalcitonin in Non-Infectious Organ Failure, Sepsis, and Septic Shock: A Prospective Observational Study According to the Sepsis-3 Definitions. BMC Infect Dis. 2022;22(1):8. doi:10.1186/s12879-021-07012-8.
  22. Conlon TW, Baker D, Bhombal S. Cardiac Point-of-Care Ultrasound: Practical Integration in the Pediatric and Neonatal Intensive Care Settings. Eur J Pediatr. 2024;183(4):1525–1541. doi:10.1007/s00431-023-05409-y.
  23. Zieleskiewicz L, Lopez A, Hraiech S, et al. Bedside POCUS During Ward Emergencies Is Associated With Improved Diagnosis and Outcome: An Observational, Prospective, Controlled Study. Crit Care. 2021;25(1):34. doi:10.1186/s13054-021-03466-z.
  1. ↑ Levitov A, Frankel HL, Blaivas M, et al. (2016). "Guidelines for the Appropriate Use of Bedside General and Cardiac Ultrasonography in the Evaluation of Critically Ill Patients—Part II: Cardiac Ultrasonography". Crit Care Med. 44 (6): 1206–1227. doi:10.1097/CCM.0000000000001847.
  2. ↑ Yoshida T, Yoshida T, Noma H, et al. (2023). "Diagnostic accuracy of point-of-care ultrasound for shock: a systematic review and meta-analysis". Crit Care. 27 (1): 200. doi:10.1186/s13054-023-04495-6.
  3. ↑ Ramadan A, Abdallah T, Abdelsalam H, Mokhtar A, Razek A (2022). "Accuracy of echocardiography and ultrasound protocol to identify shock etiology in emergency department". BMC Emerg Med. 22 (1): 117. doi:10.1186/s12873-022-00678-6. Vancouver style error: punctuation (help)
  4. ↑ Fardet L, Galicier L, Lambotte O, et al. (2014). "Development and Validation of the HScore, a Score for the Diagnosis of Reactive Hemophagocytic Syndrome". Arthritis Rheumatol. 66 (9): 2613–2620. doi:10.1002/art.38690.
  5. ↑ Knaak C, Nyvlt P, Schuster FS, et al. (2020). "Hemophagocytic lymphohistiocytosis in critically ill patients: diagnostic reliability of HLH-2004 criteria and HScore". Crit Care. 24 (1): 244. doi:10.1186/s13054-020-02941-3.
  6. ↑ Bilston L, Croden J, Taparia M, et al. (2022). "Validation of the HScore and the HLH-2004 diagnostic criteria for the diagnosis of hemophagocytic lymphohistiocytosis in a multicenter cohort". Eur J Haematol. 109 (2): 129–137. doi:10.1111/ejh.13779.
  7. ↑ Henter J (2025). "Hemophagocytic Lymphohistiocytosis". N Engl J Med. 392 (6): 584–598. doi:10.1056/NEJMra2314005. Vancouver style error: punctuation (help)
  8. ↑ Chaturvedi V, Marsh RA, Zoref-Lorenz A, et al. (2021). "T-Cell Activation Profiles Distinguish Hemophagocytic Lymphohistiocytosis and Early Sepsis". Blood. 137 (17): 2337–2346. doi:10.1182/blood.2020009499. PMID 33512385 Check |pmid= value (help).
  9. ↑ Nguyen TH, Kumar D, Prince C, et al. (2024). "Frequency of HLA-DR+ CD38hi T-cells identifies and quantifies T-cell activation in hemophagocytic lymphohistiocytosis, hyperinflammation, and immune regulatory disorders". J Allergy Clin Immunol. 153 (1): 309–319. doi:10.1016/j.jaci.2023.07.008.
  10. ↑ Goubran M, Spaner C, Stukas S, et al. (2024). "The role of C-reactive protein and ferritin in the diagnosis of HLH, adult-onset Still's disease, and COVID-19 cytokine storm". Sci Rep. 14 (1): 31306. doi:10.1038/s41598-024-82760-6.
  11. ↑ Bursa D, et al. (2021). Sci Rep. Missing or empty |title= (help)
  12. ↑ Debaugnies F, Goetzinger F, Wolff F, et al. (2026). "Serum H-Ferritin-to-Ferritin Ratio as a Biomarker of Hemophagocytic Lymphohistiocytosis in Critically Ill Patients With Hyperferritinemia". Am J Hematol. 101 (3): 648–653. doi:10.1002/ajh.70189.
  13. ↑ Maves RC, Enwezor C (2022). "Uses of Procalcitonin as a Biomarker in Critical Care Medicine". Infect Dis Clin North Am. 36 (4): 897–909. doi:10.1016/j.idc.2022.07.004. Vancouver style error: punctuation (help)
  14. ↑ Tang BM, Eslick GD, Craig JC, McLean A (2007). "Accuracy of Procalcitonin for Sepsis Diagnosis in Critically Ill Patients: Systematic Review and Meta-Analysis". Lancet Infect Dis. 7 (3): 210–217. doi:10.1016/S1473-3099(07)70052-X. Vancouver style error: punctuation (help)
  15. ↑ Tan M, Lu Y, Jiang H, Zhang L (2019). "The diagnostic accuracy of procalcitonin and C-reactive protein for sepsis: A systematic review and meta-analysis". J Cell Biochem. 120 (4): 5852–5859. doi:10.1002/jcb.27870. Vancouver style error: punctuation (help)
  16. ↑ Chairaj T, Mongkhon P, Leewongsakorn P, et al. (2025). "Diagnostic performance of procalcitonin and presepsin in sepsis: a systematic review and meta-analysis". BMC Emerg Med. 26 (1): 9. doi:10.1186/s12873-025-01433-3.
  17. ↑ Evans L, Rhodes A, Alhazzani W, et al. (2021). "Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021". Crit Care Med. 49 (11): e1063–e1143. doi:10.1097/CCM.0000000000005337.
  18. ↑ Shabrish S, Desai M, Saxena V, Kelkar M, Madkaikar M (2019). "IFN-g:IL-10 Ratio: A Putative Predictive Biomarker to Discriminate HLH From Severe Viral Infections". J Clin Immunol. 39 (2): 135–137. doi:10.1007/s10875-019-00601-y. Vancouver style error: punctuation (help)
  19. ↑ van Berkel M, Kox M, Frenzel T, et al. (2020). "Biomarkers for antimicrobial stewardship: a reappraisal in COVID-19 times?". Crit Care. 24 (1): 600. doi:10.1186/s13054-020-03291-w.
  20. ↑ Lee S, Song J, Park DW, et al. (2022). "Diagnostic and prognostic value of presepsin and procalcitonin in non-infectious organ failure, sepsis, and septic shock: a prospective observational study according to the Sepsis-3 definitions". BMC Infect Dis. 22 (1): 8. doi:10.1186/s12879-021-07012-8.
  21. ↑ Conlon TW, Baker D, Bhombal S (2024). "Cardiac point-of-care ultrasound: Practical integration in the pediatric and neonatal intensive care settings". Eur J Pediatr. 183 (4): 1525–1541. doi:10.1007/s00431-023-05409-y. Vancouver style error: punctuation (help)
  22. ↑ Zieleskiewicz L, Lopez A, Hraiech S, et al. (2021). "Bedside POCUS during ward emergencies is associated with improved diagnosis and outcome: an observational, prospective, controlled study". Crit Care. 25 (1): 34. doi:10.1186/s13054-021-03466-z.
Retrieved from "https://www.wikidoc.org/index.php?title=Sepsis_differential_diagnosis&oldid=1746103"