Sepsis history and symptoms
|
Resident Survival Guide |
|
Sepsis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Sepsis history and symptoms On the Web |
|
American Roentgen Ray Society Images of Sepsis history and symptoms |
|
Risk calculators and risk factors for Sepsis history and symptoms |
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]
Synonyms and keywords: sepsis syndrome; septic shock; septicemia
History and Symptoms
Overview
Sepsis has no single pathognomonic symptom. Its presentation is heterogeneous and depends on the infection source, causative organism, organs affected, and baseline host characteristics.[1] Symptoms can be grouped into three overlapping categories: general symptoms of infection, source-localizing symptoms, and symptoms of acute organ dysfunction.[1] Manifestations may be subtle early, evolve over hours to days, and be blunted by medications such as antipyretics or beta-blockers.[1][2]
Sepsis should be considered in a patient with suspected or established infection who develops acute organ dysfunction or otherwise unexplained acute decompensation. A specific pathogen need not be identified for sepsis to be present.[3][2]
General symptoms
- Fever, chills, and rigors are classic presenting symptoms and may be accompanied by malaise, myalgias, and flu-like symptoms.[1][4]
- Hypothermia or normothermia does not exclude sepsis; hypothermia may occur in severe disease and is associated with worse outcome.[1]
- Fever is neither sensitive nor specific. Its absence is particularly important in older adults, immunocompromised patients, and patients receiving antipyretics or beta-blockers.[1]
- Malaise, fatigue, myalgias, and nonspecific constitutional symptoms may accompany the infectious syndrome.[1]
Source-localizing symptoms
History should actively seek symptoms indicating the likely source of infection. Pneumonia is the single most common source; by frequency, leading sites include pulmonary infection (approximately 40-60%), intra-abdominal and genitourinary infection (approximately 15-30% each), followed by bloodstream and skin/soft-tissue sources.[1]
| Suspected source | Historical symptoms |
|---|---|
| Pulmonary | Productive cough, pleuritic chest pain, dyspnea |
| Genitourinary | Dysuria, urinary frequency or urgency, flank pain |
| Intra-abdominal | Abdominal pain, distension, diarrhea, vomiting |
| Skin and soft tissue | Localized pain, erythema, swelling; pain out of proportion raises concern for necrotizing infection |
| Central nervous system | Headache, neck stiffness, photophobia, altered mentation |
| Spine | Focal back pain, particularly when an occult spinal infection is possible |
| Endocardium | New cardiac symptoms, particularly with a history of intravenous drug use |
| Joint | Acute monoarticular pain and swelling |
Symptoms of acute organ dysfunction
Symptoms of acute organ dysfunction are particularly important because they distinguish sepsis from uncomplicated infection.[1][4]
| Organ system | Characteristic symptoms or historical clues |
|---|---|
| Neurologic | Confusion, lethargy, delirium, or agitation; altered mentation may be an early or predominant manifestation, particularly in older adults |
| Respiratory | Dyspnea and tachypnea, which may precede other overt manifestations |
| Cardiovascular | Lightheadedness, near-syncope, or symptoms consistent with systemic hypoperfusion |
| Renal | Decreased urine output |
| Hematologic | Bruising or bleeding may occur but are less prominent as early symptoms and are commonly identified through objective evaluation |
| Hepatic | Jaundice may occur but is generally less prominent early and is commonly identified through objective evaluation |
New altered mentation, tachypnea or dyspnea, and reduced urine output in an infected patient should be treated as potential organ-dysfunction alarms rather than incidental symptoms.[1][4]
Atypical presentations and host context
The history should identify factors that increase the pretest probability of sepsis, including age 65 years or older, immunosuppression, active cancer, diabetes, chronic heart, liver, kidney, or lung disease, indwelling catheters, drains or vascular lines, recent surgery or instrumentation, prior sepsis, and long-term-care residence.[1]
Older adults may have atypical presentations, including falls, functional decline, anorexia, or delirium without fever.[1]
In immunocompromised patients, including those with neutropenia, transplantation, active chemotherapy, or high-dose corticosteroid exposure, classic manifestations may be absent or attenuated. Fever, purulent secretions, and radiographic infiltrates may be lacking, and patients may appear deceptively stable before deteriorating rapidly within hours.[6] A low threshold for evaluation and imaging is warranted in this group.[6]
Temporal evolution
Symptoms and physiologic abnormalities may develop over hours to days. Heart-rate elevation may occur early, whereas hypotension can develop later; therefore, a normal early blood pressure does not exclude evolving sepsis.[7][8]
Clinical interpretation and important differentials
No individual symptom is diagnostic of sepsis. The history should be integrated with physical examination, objective testing, and clinical evolution, with reassessment when the initial presentation is nondiagnostic.[2]
The differential diagnosis is broad. Noninfectious conditions such as pulmonary embolism, pancreatitis, diabetic ketoacidosis, adrenal crisis, and thyroid storm can reproduce constitutional symptoms and manifestations of acute organ dysfunction. Accurate diagnosis may therefore require repeated assessment, observation, and targeted testing.[2]
Symptom profiles may also provide prognostic and microbiologic signal. In a 2025 syndromic analysis, cardiopulmonary manifestations such as hypoxemia and hypotension were more strongly associated with in-hospital mortality than some other symptom groups, whereas skin/soft-tissue and urinary symptoms were associated with lower mortality.[9] These associations should be used to weight clinical concern rather than as diagnostic rules.
High-yield clinical pearls
- New confusion in a patient with suspected infection is a major sepsis warning sign, even without fever or hypotension.[1][4]
- Tachypnea or dyspnea may be an early manifestation of evolving organ dysfunction; a rising respiratory rate warrants attention before hypotension appears.[10]
- Absence of fever does not reassure; normothermic and hypothermic presentations occur, particularly in vulnerable hosts.[1]
- A normal early blood pressure does not exclude evolving sepsis.[7][8]
- Always localize the source by history: pulmonary, intra-abdominal, genitourinary, and skin/soft tissue sources should be considered first, followed by occult CNS, spinal, endocardial, joint, and device-related sources when clinically appropriate.[5][1]
- Do not wait for a positive culture or identified pathogen before considering sepsis.[3][2]
Common pitfalls
- Anchoring on no fever = no sepsis, thereby missing afebrile or hypothermic presentations.[1]
- Attributing new confusion to baseline dementia, intoxication, or "sundowning" rather than considering acute organ dysfunction.[1][4]
- Being falsely reassured by a normal early blood pressure.[7][8]
- Overlooking occult sources such as spinal infection, endocarditis, septic arthritis, or indwelling-device infection when common sources are not apparent.[5]
- Waiting for a positive culture before considering sepsis.[2]
- Failing to consider important noninfectious mimics when the clinical course or source does not fit infection.[2]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 Meyer NJ, Prescott HC (2024). "Sepsis and Septic Shock". New England Journal of Medicine. 391 (22): 2133–2146. doi:10.1056/NEJMra2403213.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Yealy DM, Mohr NM, Shapiro NI; et al. (2021). "Early Care of Adults With Suspected Sepsis in the Emergency Department and Out-of-Hospital Environment". Annals of Emergency Medicine. 78 (1): 1–19. doi:10.1016/j.annemergmed.2021.02.006.
- ↑ 3.0 3.1 Singer M, Deutschman CS, Seymour CW; et al. (2016). "The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)". JAMA. 315 (8): 801–810. doi:10.1001/jama.2016.0287.
- ↑ 4.0 4.1 4.2 4.3 4.4 Angus DC, van der Poll T (2013). "Severe Sepsis and Septic Shock". New England Journal of Medicine. 369 (9): 840–851. doi:10.1056/NEJMra1208623.
- ↑ 5.0 5.1 5.2 Long B, Gottlieb M (2025). "Emergency Medicine Updates: Evaluation and Diagnosis of Sepsis and Septic Shock". American Journal of Emergency Medicine. 90: 169–178. doi:10.1016/j.ajem.2025.01.055.
- ↑ 6.0 6.1 Deinhardt-Emmer S, Chousterman BG, Schefold JC; et al. (2025). "Sepsis in Patients Who Are Immunocompromised: Diagnostic Challenges and Future Therapies". The Lancet Respiratory Medicine. 13 (7): 623–637. doi:10.1016/S2213-2600(25)00124-9.
- ↑ 7.0 7.1 7.2 Filbin MR, Thorsen JE, Lynch J; et al. (2018). "Challenges and Opportunities for Emergency Department Sepsis Screening at Triage". Scientific Reports. 8 (1): 11059. doi:10.1038/s41598-018-29427-1.
- ↑ 8.0 8.1 8.2 Oh H, Bae E, Lim S; et al. (2016). "Temporal changes in physiological parameters of systemic inflammatory response syndrome during the three days prior to a diagnosis of sepsis: a case-control study". Journal of Clinical Nursing. 25 (21–22): 3176–3188. doi:10.1111/jocn.13327.
- ↑ Pak TR, Kanjilal S, McKenna CS; et al. (2025). "Syndromic Analysis of Sepsis Cohorts Using Large Language Models". JAMA Network Open. 8 (10): e2539267. doi:10.1001/jamanetworkopen.2025.39267.
- ↑ Hotchkiss RS, Moldawer LL, Opal SM; et al. (2016). "Sepsis and septic shock". Nature Reviews Disease Primers. 2: 16045. doi:10.1038/nrdp.2016.45.