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Sepsis – Emergency

Sepsis – Recognition and emergency management in children

Key points

  • Sepsis is a medical emergency: early recognition and treatment is imperative for survival.
  • Sepsis must be considered in every child with acute illness or new onset of organ dysfunction.
  • Diagnosis is based on clinical judgement supported by laboratory findings.
  • Management includes rapid fluid resuscitation, early consideration of inotropes and administration of appropriate antibiotics; ideally within 15 minutes of presentation.
  • Early involvement of the paediatric critical care services (onsite or via RSQ) is essential.


This document provides guidance for all staff involved in the care and management of children presenting to an Emergency Department (ED) with suspected or proven sepsis in Queensland.

This guideline has been developed by senior ED clinicians and Paediatricians across the state with specialist input from PICU and Infectious Disease staff, Lady Cilento Children’s Hospital, Brisbane. It has been endorsed for use across Queensland by the Statewide Emergency Care of Children Working Group in partnership with the Queensland Emergency Department Strategic Advisory Panel and the Healthcare Improvement Unit, Clinical Excellence Division.


Despite advances in prevention and treatment of invasive bacterial infections, sepsis remains a leading cause of childhood morbidity and mortality in Australia.1 Sepsis is a medical emergency. Without treatment, septic shock carries a mortality rate of more than 80% and even with treatment, overall mortality for septic shock remains around 15-20% in children.1-4 Delay in the both the initiation of appropriate antibiotics and aggressive treatment of shock leads to significantly increased mortality.5-7 Sepsis must be considered in every child with acute illness or new onset of organ dysfunction. The initial presentation can be vague and non-specific, particularly in neonates, making early diagnosis challenging. Management includes rapid fluid resuscitation, early consideration of inotropes and administration of appropriate antibiotics; ideally within the first 15 minutes of presentation.8 Early involvement of paediatric critical care services (onsite or via Retrieval Services Queensland) is essential.8-10


Paediatric sepsis is defined as ‘the systemic inflammatory response syndrome in the presence of, or as the result of, suspected or proven infection’.10 It is a syndrome shaped by both pathogen and host factors.11-12 The most common type of pathogens are bacteria (viruses and fungi can result in a similar presentation), which vary according to host factors, including age, comorbidity and geographic location.13

Septic shock is a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality.14 It is identified by sepsis and cardiovascular organ dysfunction, acknowledging that hypotension is a late sign in children.10


Early Recognition

Given the time critical nature of sepsis progressing to organ failure and death, early recognition and prompt treatment is imperative to survival.13 Sepsis should be suspected in any acute illness, or in any high-risk group (see box below), if there is any change from the patient’s normal pattern of observations.15

A diagnosis of sepsis is made using clinical judgement, supported by laboratory testing. There is no single clinical finding or test that is diagnostic. Careful clinical examination with particular attention to vital signs, perfusion and mentation should be conducted. If suspected, initiate investigations and treatment until sepsis is excluded. Validated triage tools for paediatric sepsis are currently being developed but are generally based on the identification of risk factors, abnormal vital signs and/or suggestive clinical features.15

Children at high risk for sepsis

  • Neonates and premature infants
  • Unimmunised or incomplete immunisation status
  • Malignancy and/or chemotherapy
  • Immune deficiency
  • Asplenia (surgical or functional e.g. sickle cell disease)
  • Long-term steroid use
  • Immunosuppressant drug therapy
  • Recent surgical procedure (within 6 weeks)
  • Intravenous recreational drug use
  • Indwelling lines or catheters (e.g. VP shunt or CVAD)

Sepsis presentation varies with age. Infants and neonates commonly present with non-specific symptoms and signs, such as feeding difficulties and/or apnoea. Older children may present with a focus of infection and/or a constellation of features including fever or hypothermia, vomiting, inappropriate tachycardia, altered mental state and reduced peripheral perfusion.13,15 Deviations from pre-existing trends in vital signs (see table below) can be a red flag.

Features of toxic presentation include:

  • altered mental state
  • tachypnoea, increased work of breathing, grunt, weak cry
  • marked/persistent tachycardia
  • moderate to severe dehydration
  • seizures

It is important to pay attention to concerns expressed by the caregiver, particularly changes in usual behaviour of the child.

Normal range for vital signs by age
Age Heart Rate (bpm) Minimum Systolic BP (mmHg) Respiratory Rate (bpm)
Term 100-180 60 40-60
6mth 100-180 70 30-50
1yr 100-170 70 20-40
2yr 100-160 70 20-30
4yr 80-130 75 20-30
8yr 70-110 80 16-25
12yr 60-110 90 16-25
16yr+ 60-100 90 10-16

Septic Shock

Septic shock is the progression of sepsis and can present as either cold or warm shock16 (see table below). Children with septic shock may have normal blood pressure. Hypotension is often a terminal sign given that children compensate with normal blood pressure, even in the late stages of shock.

  • ALERT – Hypotension is a late, and often terminal, sign in paediatric septic shock.
  • If patient is in septic shock initiate treatment and contact paediatric critical care specialist (onsite or via RSQ).
Paediatric septic shock presentations
Cold shock Warm shock
More common in infants and young children

Constricted peripheral systemic vasculature: cold peripheries and prolonged capillary refill time

Tachycardia is usually present

Blood pressure can be maintained until late

Underlying problem is a low cardiac output state, secondary to impaired myocontractility

More common in older children (and adults)

Characterised by vasoplegia, in which the systemic vascular resistance is low: brisk capillary refill time (‘flash’ capillary refill) and pulses are usually felt to be full or bounding

Tachycardia is usually present

Pulse pressure is high, often due to a low diastolic blood pressure

Hyperdynamic or high cardiac output state associated with shock due to enlargement of the circulation exceeding cardiac output

Progression to low cardiac output can occur anytime

Clinical findings consistent with insufficient end-organ perfusion:

  • Mental status: progressive lethargy, drowsiness or obtundation. Alternatively, restlessness and/or agitation are often seen and can be mistaken for “a vigorous child” but reflects compromised cerebral perfusion due to shock. Infants tend to have irritability and/or apnoeas.
  • Skin: temperature gradient from core to extremities (note that either hyperthermia or hypothermia can be present), mottled colour, prolonged capillary refill time (>2 seconds but note that brisk capillary refill time can be seen in warm shock), petechial or purpuric rash. Purpura fulminans is a widespread non-blanching purpuric rash classically seen in meningococcaemia but may also be associated with severe sepsis from Pneumococcus.
  • Cardiovascular: Tachycardia is usually one of the earliest signs. Mean arterial pressure (MAP) can be maintained and the pulse pressure typically is narrow (vasoconstriction to maintain MAP), but may be high (vasodilation in “warm shock”). There may be evidence of cardiac failure (hepatomegaly, gallop rhythm and jugular venous distension) with myocardial depression. A classic pitfall in the recognition of shock is attributing difficulty in obtaining non-invasive blood pressure due to technical issues rather than recognising the presence of hypotension/hypoperfusion.
  • Respiratory: rate is increased to compensate for metabolic acidosis including lactic acidosis (Kussmaul breathing). Acute respiratory distress syndrome (ARDS) may develop with progressive worsening of respiratory distress (tachypnoea, increased work of breathing) and focal chest signs (reduced breath sounds, inspiratory crepitations, and expiratory wheeze).
  • Renal: Reduced urine output

Toxic Shock Syndrome

Toxic shock syndrome is a potentially life-threatening subset of paediatric sepsis, caused by superantigens from toxin-producing strains of Staphylococcus aureus or Streptococcal pyogenes.17 Symptoms may include high fever, vomiting, diarrhoea, myalgia, confusion, collapse and usually a widespread erythematous rash.  It can occur in any patient. It is important to distinguish this entity as treatment requires the addition of Lincomycin IV and possibly Intragam IV for their antitoxin properties. Click here for CHQ antimicrobial sepsis guidelines or refer to local protocols.

Meningitis (see Meningitis guideline)

Meningitis should be considered in children with suspected sepsis as it can result in serious complications, such as raised intracranial pressure (ICP).  More specific features may include photophobia, headache, nuchal rigidity, seizures, posturing and a bulging fontanelle (<3 months of age).  Possible signs of raised ICP include fluctuating consciousness despite resuscitation, hypertension, bradycardia, abnormal pupils, posturing, seizures or focal neurology.


No single laboratory test will confirm or refute the diagnosis of sepsis. There is currently no evidence to support the use of a specific biomarker for sepsis diagnosis.13 Biomarkers may be of more use to decide if antibiotics can be stopped at 48 hours. Clinical findings and host factors should direct specific microbiological sampling. However, despite adequate microbiological sampling, in some children with sepsis the pathogen is not identified (culture-negative sepsis).18

  • ALERT – Do not delay antibiotic administration for investigations, which includes the collection of microbiological samples
Investigations in paediatric sepsis
Investigation type Findings in paediatric sepsis
Blood culture Prioritise over other blood tests, take as soon as possible when suspect bacteraemia, prior to antibiotics but should not delay antibiotics.

Culture sensitivity is proportional to the volume of blood taken

  • minimum of 1 mL in neonatal aerobic culture bottle (yellow top)
  • minimum of 4 mL in standard aerobic culture bottle (green top)

If the child has a CVAD, blood cultures should be taken from each lumen as per protocol.

Blood gas (usually venous in ED setting) Markers of possible sepsis:

  • base deficit > 5.0 mEq/L
  • lactate > 2.4 mmol/L

Do NOT attribute increased lactate to difficult venepuncture in this setting.

Glucose < 3 mmol/L associated with glycogen depletion and stress response.

Full blood count (FBC) WCC can be high or low in early sepsis but not sensitive or specific.

Platelet count <80,000uL in sepsis or disseminated intravascular coagulation (DIC).

C reactive protein (CRP) More readily available but less specific than procalcitonin.

Low value does not exclude early sepsis.

Electrolytes and creatinine Often deranged, raised creatinine in sepsis related renal failure.
Liver function tests Increased bilirubin or alanine aminotransferase (ALT).
Coagulation studies Derangement in the context of sepsis and thrombocytopaenia indicative of DIC.
Urine sample Collection may not be possible until after fluid resuscitation.

Do not withhold antibiotic treatment if significant delay in obtaining sample.

Lumbar puncture Only in alert child with no signs of raised ICP or coagulopathy.

Usually contraindicated in established sepsis until stable.

Do not withhold antibiotic treatment if significant delay in obtaining sample.

Can do WCC and PCR for meningitis diagnosis on CSF from delayed LP.

Radiography Consider CXR for respiratory distress or signs on examination. Other imaging as directed by the focus of infection e.g. septic joint.


Refer to flowchart for a summary of the recommended emergency management of paediatric sepsis.

Failure to recognise sepsis and the delay in appropriate treatment are common themes in reviews of sepsis related mortality in children.20 Early aggressive treatment should ensue once sepsis is suspected, with the aim of decreasing tachycardia, improving peripheral perfusion and restoring a normal level of consciousness.

  • Seek senior emergency/paediatric advice as per local escalation protocols if sepsis is suspected.
  • Contact paediatric critical care specialist (onsite or via RSQ) for septic child with insufficient response to fluids or needing inotropes/intubation. (see triggers for escalation).

Interventions within the first 15 minutes:

  • Delivery of supplemental oxygen and respiratory support with an appropriate device
  • Intravenous or intraosseous access should be immediately obtained and bloods sent
  • Umbilical line access can be considered in newborns up to 2 weeks of life
  • Initial bloods should include blood cultures, venous blood gas and glucose
  • Further bloods can be obtained if possible, including full blood count, C-reactive protein, biochemistry and coagulation profile
  • Urgent doses of broad spectrum antibiotics should be given via the IV or IO route
  • If there is no IV or IO access within 15 minutes, intramuscular Ceftriaxone 50mg/kg (maximum 2 grams BD) should be administered and assistance sought.
  • Once IV access is obtained, the full antibiotic IV doses should be provided (see antibiotic guidelines and antibiotic dosing for neonates).
  • If > 3 months of age and meningitis is suspected, give Dexamethasone IV 0.15mg/kg prior to or just after the first dose of antibiotics. If not given at this time, corticosteroids can be given up to an hour after initial antibiotics, but do not delay antibiotics if they are not available.
  • Immediate fluid resuscitation starting with 20mL/kg of sodium chloride 0.9% (normal saline) to be pushed in <5 minutes using 50mL syringe with a staff member dedicated to pushing fluids, with the goal to restore normal circulating volume and physiological parameters.
  • Titrate to response: decrease in heart rate and the improvement of end-organ perfusion. Repeat as necessary, evaluating for signs of fluid overload.
  • Commence inotropes if normal physiological parameters are not restored after giving >40mL/kg of fluids or anytime if hypotension is present
  • Echocardiography can guide fluid administration and commencement of inotropes

Triggers for escalation to paediatric critical care (onsite or via RSQ)

  • Tachycardia not improving after 40mL/kg fluid boluses
  • Reduced level of consciousness
  • Hypotension
  • Coagulopathy/DIC
  • Lactate >4 mmol/L
  • Inotropes

Ongoing care

Airway and Breathing

  • Give high concentration supplemental oxygen
  • Initial delivery can be via a Hudson mask non-rebreather with escalation as required
  • Maintain the patient’s airway with positioning and airway adjuncts
  • Consider high-flow nasal cannulae as an alternative transitory support in awake and responsive patients
  • Give PEEP through a T-piece (anaesthetic) bag while preparing for intubation for children that are grunting, obtunded, or hypoxic despite supplemental oxygen.
  • Consider inserting a nasogastric tube for gastric distension, which can otherwise impede ventilation
  • Intubation may be required for additional respiratory support or airway protection in a child with reduced conscious state, and children in shock (to facilitate the insertion of lines, and support of cardiac function). For QH staff, refer to the Management of Paediatric Septic Shock guideline (access via intranet).
  • ALERT – Child may arrest from cardiovascular collapse on RSI/intubation. Avoid drugs with negative inotropy e.g. midazolam or propofol. Have the arrest dose of adrenaline IV ready (0.1mL/kg of 1:10,000).
  • Adequately pre-oxygenate child and have haemodynamics optimised with concomitant fluid resuscitation and inotrope infusion prior to intubation.
  • Reduce the induction drug dose in a child with significant cardiovascular compromise (i.e. 50% of weight based dose).
  • Ketamine (0.5 – 1mg/kg) and/or Fentanyl (1-2mcg/kg) for induction (less cardiodepressant) and Rocuronium (1.2mg/kg) for muscle relaxation are generally a suitable combination for rapid sequence induction in sepsis.


  • Profound fluid loss from the intravascular space occurs due to capillary leak from the systemic inflammatory response
  • Fluid resuscitation is aimed at restoring normal physiological parameters, particularly heart rate and blood pressure21
  • Only isotonic fluids should be rapidly infused – preferably sodium chloride 0.9% (normal saline) (as is readily available). Alternatively use Hartmanns solution or 4% human albumin. Hypotonic fluids should never be used as bolus therapy.
  • Possible advantage in using colloids (e.g. 4% human albumin) but currently insufficient evidence to support routine use22
  • Administer fluids as a rapid bolus (20mL/kg) and repeat as necessary being mindful of the development of fluid overload (inspiratory crepitations, hepatomegaly, and/or gallop rhythm)
  • Consider inotropes in fluid-refractory shock, to be started as early as within 15 minutes of presentation (has been shown to improve outcomes)22-23
  • First-line choice is adrenaline starting at 0.05-0.1mcg/kg/min (maximum 1mcg/kg/min), which can be administered temporarily via a peripheral IV or IO line before central access is gained in a suitable environment. (Alternative: dopamine starting dose 5-10mcg/kg/min)
  • Aliquots of adrenaline IV can be given as 1mcg/kg (i.e. 0.1mL/kg of a 1:100,000 adrenaline solution) if infusion is being prepared and the patient remains in shock. A 1:100,000 adrenaline solution can be prepared by diluting 1mL of 1:10,000 adrenaline solution (i.e. 100 micrograms of adrenaline) with 9mL of sodium chloride 0.9% (normal saline)

Other considerations

  • Administer hydrocortisone IV (1mg/kg) in child with suspected or proven adrenal insufficiency.8,25 Consider in fluid and inotrope resistant shock (limited data on efficacy).
  • Consider alternative diagnoses in all patients, especially neonates who may have a metabolic or cardiogenic (congenital duct dependent lesions or acquired cardiac failure e.g. myocarditis) cause of their shock.
  • Electrolyte disturbance (e.g. hypocalcaemia) is common in critically ill children with sepsis and can contribute to poor cardiac function. Replacement should be in accordance with local guidelines.

When to escalate care

Follow your local facility escalation protocols for children of concern. Transfer is recommended if the child requires care beyond the level of comfort of the treating hospital. Clinicians can contact the services outlined below to escalate the care of a paediatric patient.

Service Reason for contact by clinician Contact
Local Paediatric service For specialist paediatric advice and assistance with local transfers as per local arrangements. As per local arrangements
Children’s Advice and Transport Coordination Hub (CATCH) For access to specialist paediatric advice and assistance with inter-hospital transfer of non-critical patients into and out of Lady Cilento Children’s Hospital.

For assistance with decision making regarding safe and appropriate inter-hospital transfer of children in Queensland.

For QH staff, click here for further information including the QH Inter-hospital transfer request form (access via intranet).

(07) 3068 4510

CATCH website

24 hours

Telehealth Emergency Management Support Unit (TEMSU) For access to generalist and specialist acute support and advice via videoconferencing, as per locally agreed pathways, in regional, rural and remote areas in Queensland.

For QH staff, click here for further information (access via intranet).


24 hours

Retrieval Services Queensland (RSQ) For access to telehealth support for, and to notify of, critically unwell patients requiring retrieval in Queensland.

For any patients potentially requiring aeromedical retrieval or transfer in Queensland.

For QH staff, click here for further information and relevant forms (access via intranet).

RSQ QHEPS website

24 hours

Related documents


  1. Shlapbach L, Straney L, Alexander J, MacLaren G, Festa M, Schibler A, Slater A. Mortality related to invasive infections, sepsis, and septic shock in critically ill children in Australia and New Zealand, 2002-13: a multicentre retrospective cohort study.  Lancet Infective Disease. 2015; 15:46-54.
  2. Weiss SL, Fitzgerald JC, Pappachan J, et al. Global epidemiology of pediatric severe sepsis: the sepsis prevalence, outcomes, and therapies study.  American Journal of Respiratory and Critical Care Medicine. 2015; 191(10):1147-1157.
  3. Friedman G, Silva E, Vincent JL. Has the mortality of septic shock changed with time? Critical Care Medicine. 1998; 26:2078-86.
  4. Angus DC, Linde-Zwirble WT, Lidlicker J, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Critical Care Medicine. 2001; 29:1303-10.
  5. Weiss SL, Fitzgerald JC, Balamuth F, et al. Delayed antimicrobial therapy increases mortality and organ dysfunction duration in pediatric sepsis. Critical Care Medicine. 2014; 42:2409-17.
  6. Kumar A, Roberts D, Wood K, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Critical Care Medicine. 2006; 34(6):1589-96
  7. Launay E, Gras-Le Guen C, Martinot A et al. Why children with severe bacterial infection die: a population-based study of determinants and consequences of suboptimal care with a special emphasis on methodological issues. PLoS ONE 9(9): e107286
  8. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign Guidelines Committee. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine. 2013; 41:580-637.
  9. Rivers et al. Early goal directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001; 345:1368-77.
  10. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in paediatrics.  Pediatric Critical Care Medicine. 2005; 6:2-8.
  11. Bone RC. The sepsis syndrome.  Definition and general approach to management.  Clin Chest Med.  1996; 17:175-81.
  12. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis.  N Engl J Med.  2003; 348:138-150.
  13. Plunket A, Tong T. Sepsis in Children. BMJ. 2015; 350:h3017(1-12)
  14. Singer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).   2016; 315(8):801-810.
  16. Brierley J, Peters MJ. Distinct hemodynamic patterns of septic shock at presentation to pediatric intensive care. Pediatrics  2008; 122:752-9.
  17. Adalat S, Dawson T, Hackett SJ, Clark JE, et al. Toxic shock syndrome surveillance in UK children. Arch Dis Child. 2014; 0:1-5.
  18. Kayange N, Kamugisha E, Mwizamholya DL, et al. Predictors of positive blood culture and deaths among neonates with suspected neonatal sepsis in a tertiary hospital, Mwanza-Tanzania.  BMC Pediatr. 2010; 10:39
  19. Polin RA; Committee on Fetus and Newborn. Management of neonates with suspected or proven early-onset bacterial sepsis. Pediatrics 2012; 129:1006-15.
  20. Pearson GA, ed. Why children die: a pilot study 2006; England (South West, North East and West Midlands), Wales and Northern Ireland. CEMACH; 2008.
  21. Brierley J, Carcillo JA, Choong K, et al. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine. Critical Care Medicine. 2009;37:666-88.
  22. Carcillo JA. Intravenous fluid choices in critically ill children. Curr Opin Crit Care. 2014;20:396-401.
  23. Ninis N, Phillips C, Bailey L, et al. The role of healthcare delivery in the outcome of meningococcal disease in children: case-control study of fatal and non-fatal cases. BMJ 2005; 330:1475.
  24. Wang XD, Huo XM, XU MX, et al. Clinical research of timing of application of antibiotics in septic shock of pediatric patients. Zhonghua Wei Zhong ing Ji Jiu Yi Xue. 2013; 25:207-10.
  25. Aneja R, Carcillo JA. What is the rationale for hydrocortisone treatment in children with infected-related adrenal insufficiency and septic shock? Arch Dis Child 2007; 92:165-9.

Guideline approval

Guideline approval history
Document ID CHQ-GDL-60010-Sepsis Version no. 2.0 Approval date 19/6/19
Executive sponsor Executive Director Medical Services Effective date 19/6/19
Author/custodian Queensland Emergency Care Children Working Group Review date 19/6/22
Supersedes 1.0
Applicable to Queensland Health medical and nursing staff
Authorisation Executive Director Clinical Services QCH
Keywords Sepsis, shock, critical ill, bacterial, emergency, SIRS, deteriorating child, toxic shock syndrome, meningitis, CVAD, nosocomial, paediatric, emergency, guideline, children, 60010
Accreditation references NSQHS Standards (1-8): 1, 4, 8


This guideline is intended as a guide and provided for information purposes only. View full disclaimer.
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