Have a low threshold for suspecting sepsis as the initial clinical presentation of sepsis in chlidren may be non-specific (especially in younger age groups).
Given the time-critical nature of severe sepsis and septic shock, when sepsis is suspected on clinical grounds it is usually best to initiate sepsis investigations and treatment, including administering antibiotics and fluid resuscitation. These should continue until sepsis has been excluded.
Progression to organ failure and shock is often very rapid, so early recognition and treatment is crucial.
Empirical broad-spectrum antibiotic therapy (based on the most probable pathogens) should be administered as soon as possible, and always within the first hour following recognition.
Other treatments are primarily supportive, and should be delivered according to internationally recognised consensus-based guidelines.
Sepsis is a clinical syndrome resulting from a dysregulated immune response to infection. It is characterised by derangements in multiple pathobiological processes, which may lead to widespread tissue injury. It encompasses a clinical spectrum of severity, including severe sepsis, septic shock, and multi-organ failure. Sepsis is a leading cause of morbidity and mortality in children worldwide.
Traditionally, sepsis has been defined based on the presence or absence of the systemic inflammatory response syndrome (SIRS). In adults, the definitions of sepsis were updated in 2016, moving away from the SIRS definition and removing the term 'severe sepsis'.
At present there are no revisions to the international consensus definition of paediatric sepsis, which dates from 2005. However, in 2020 the Surviving Sepsis Campaign proposed a definition for septic shock in children: 'severe infection leading to cardiovascular dysfunction (including hypotension, need for treatment with a vasoactive medication, or impaired perfusion)'.
History and exam
- presence of risk factors
- fever or low body temperature
- bradycardia (neonates and infants)
- altered mental state or behaviour
- decreased peripheral perfusion
- change in usual pattern of activity or feeding in a neonate
- dry nappies/decreased urine output
- mottling of the skin, ashen appearance, cyanosis
- low oxygen saturation
- non-blanching purpuric rash
Akash Deep, MD, FRCPCH
Paediatric Intensive Care Unit
King’s College Hospital
AD declares that he has no competing interests.
Dr Akash Deep would like to gratefully acknowledge Dr Jeremy Tong and Dr Adrian Plunkett, previous contributors to this topic.
JT and AP are authors involved in the Paediatric Sepsis Six initiative, cited in this topic.
Saul N. Faust, MA, MBBS, FRCPCH, PhD, FHEA
Professor of Paediatric Immunology & Infectious Diseases
Director, NIHR Wellcome Trust Clinical Research Facility
University of Southampton
SNF declares that he has no competing interests.
Mohan Pammi, MBBS, MD, MRCPCH
Texas Children's Hospital and Baylor College of Medicine
MP declares that he has no competing interests.
Jerry J. Zimmerman, MD, PhD
Faculty, Pediatric Critical Care Medicine
Seattle Children's Hospital
University of Washington School of Medicine
JJZ receives research grant support from NIH/NICHD and ImmuneXpress; travel reimbursement from the Society of Critical Care Medicine to attend board meetings; and royalties from Elsevier for action as a co-editor for the textbook Pediatric Critical Care.
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