Sepsis in children

12 min read Last updated April 8, 2026

Surgical approach (source control / procedures commonly required)

  • Sepsis is not a single operation; surgery is for source control and to facilitate ICU care
  • Common paediatric source-control procedures
    • Appendicectomy / laparotomy for perforation, peritonitis, necrotising enterocolitis (NEC) (neonate)
    • Incision & drainage of abscess (skin/soft tissue, peritonsillar, deep neck space), washout of septic arthritis/osteomyelitis
    • Thoracic drainage for empyema; VATS/decortication if required
    • Central line removal if line sepsis; debridement for necrotising fasciitis
    • Urinary obstruction relief / nephrostomy; drainage of pyonephrosis
  • Key surgical priorities
    • Early senior decision-making: operate vs stabilise first (often parallel resuscitation + theatre)
    • Minimise time to source control where ongoing contamination/necrosis
    • Culture collection (blood, pus, CSF if indicated) ideally before antibiotics if no delay

Anaesthetic management (typical for septic child needing theatre/line/procedure)

  • Type of anaesthesia
    • GA is usual (unstable physiology, need for airway control, invasive monitoring, source control surgery)
    • Regional techniques: consider as adjunct (opioid-sparing) only if haemodynamically stable and coagulation acceptable; avoid neuraxial if coagulopathy/sepsis with shock
  • Airway device
    • Cuffed ETT preferred (ventilation control, high FiO2/PEEP, aspiration risk, prolonged surgery/transfer to PICU)
    • SGA generally avoided in septic shock / full stomach / need for high airway pressures
  • Duration
    • Varies widely: 15–30 min (line/abscess drainage) to 1–3+ h (laparotomy, thoracic surgery)
  • Pain
    • Moderate–severe for laparotomy/thoracics; moderate for washouts; mild–moderate for drainage/line procedures
    • Analgesia: paracetamol ± opioid titration; consider ketamine; consider regional blocks (TAP, rectus sheath, paravertebral) if appropriate
  • Induction approach (high-risk)
    • Treat as full stomach; RSI often appropriate (modified RSI with gentle mask ventilation if needed)
    • Prefer ketamine or etomidate (where available) for haemodynamic stability; titrate propofol cautiously or avoid in shock
    • Have vasopressor ready at induction (e.g. noradrenaline/adrenaline infusion or bolus phenylephrine/metaraminol per local practice)

Definitions and epidemiology

  • Sepsis = life-threatening organ dysfunction due to dysregulated host response to infection (Sepsis-3 concept); in paediatrics, recognition often uses clinical criteria + organ dysfunction rather than adult SOFA
  • Septic shock (paediatric): sepsis with cardiovascular dysfunction (hypotension or need for vasoactives) and/or impaired perfusion (e.g. prolonged cap refill, lactate elevation) despite adequate fluid resuscitation
  • High-risk groups
    • Neonates/infants, immunocompromised, congenital heart disease, chronic lung disease, asplenia/sickle cell, indwelling lines, burns, malnutrition

Aetiology and common sources (age-related)

  • Neonate
    • Early onset: maternal genital tract organisms (e.g. GBS, E. coli)
    • Late onset: line-associated, hospital-acquired, NEC, meningitis
  • Infant/child
    • Respiratory (pneumonia/empyema), abdominal (appendicitis/perforation), urinary, skin/soft tissue, bone/joint, CNS (meningitis)
  • Pathogens (examples)
    • Gram positives: Staph aureus (incl. MRSA), Strep pyogenes, pneumococcus
    • Gram negatives: E. coli, Klebsiella, Pseudomonas (esp. immunocompromised)
    • Toxin-mediated: meningococcaemia; streptococcal toxic shock

Pathophysiology (why children crash)

  • Inflammation + endothelial dysfunction → vasodilation, capillary leak, maldistribution of flow, microthrombosis
  • Myocardial depression may occur (reduced contractility) → low cardiac output shock
  • Children often maintain BP until late: compensated shock with tachycardia and poor perfusion; hypotension is pre-terminal
  • Organ dysfunction mechanisms
    • Resp: ARDS, increased work of breathing, V/Q mismatch
    • Renal: AKI from hypoperfusion/inflammation
    • CNS: encephalopathy, seizures (esp. meningitis)
    • Coagulation: DIC (bleeding + thrombosis), thrombocytopenia
    • Metabolic: lactic acidosis, hypoglycaemia (esp. infants), hyperglycaemia

Recognition and assessment (ABCDE + red flags)

  • History clues
    • Fever or hypothermia, reduced feeding, lethargy/irritability, reduced urine, mottling, rash, rigors, recent infection, immunosuppression
  • Examination: perfusion and work of breathing are key
    • Tachycardia, prolonged cap refill, cool peripheries (cold shock) or bounding pulses/warm peripheries (warm shock), altered mental state
    • Tachypnoea, recession, grunting; hepatomegaly may suggest heart failure/volume overload
  • Investigations (do not delay treatment)
    • Blood gas (lactate, glucose), FBC, U&E/creatinine, LFT, CRP/procalcitonin (trend), coagulation, group & save/crossmatch
    • Blood cultures (and cultures from suspected source); CXR/USS/CT as indicated

Immediate management (first hour / time-critical care)

  • Call for help early: senior paeds/anaesthesia/PICU; consider sepsis pathway
  • Oxygen and ventilation
    • High-flow O2; early CPAP/HFNC if increased work of breathing; intubate if failing, shock with high metabolic demand, or for source control
  • IV/IO access
    • If IV not rapidly achievable, use intraosseous access (tibia/femur/humerus per age/skill)
  • Antibiotics: early broad-spectrum
    • Give within 1 hour of recognition (earlier if shock); tailor to age/source/local policy; consider antivirals/antifungals in selected patients
    • Do cultures first if no delay; do not wait for results
  • Fluids: cautious, reassessed boluses
    • Balanced crystalloid boluses (e.g. 10–20 mL/kg) with frequent reassessment (HR, cap refill, BP, mental state, lung signs, hepatomegaly, urine output, lactate trend)
    • Avoid fluid overload (worsens respiratory failure); consider earlier vasoactives if poor response
  • Vasoactive support (early if fluid-refractory or fluid-limited)
    • Peripheral infusion acceptable short-term with close monitoring while securing central access
    • Choice depends on phenotype: cold shock (low CO, high SVR) often needs adrenaline; warm shock (low SVR) often needs noradrenaline (local practice varies)
  • Glucose, calcium, temperature
    • Check and treat hypoglycaemia promptly; maintain normothermia; correct significant hypocalcaemia (esp. after blood products)
  • Source control planning
    • Early imaging and surgical review; remove infected lines; drain collections; operate if ongoing contamination/necrosis

Anaesthetic considerations for septic child (theatre / procedures / transfer)

  • Pre-op optimisation (parallel with urgent surgery)
    • Resuscitate in ED/ward/anaesthetic room: oxygenation, access, antibiotics, fluids/vasopressors, bloods, glucose
    • Discuss goals with surgeons/PICU: urgency of source control vs stabilisation; plan for post-op ventilation
  • Monitoring
    • Standard + invasive arterial line early (beat-to-beat BP, blood gases); consider CVC for vasoactives; temperature; urinary catheter (UO target ~1 mL/kg/h, interpret with context)
    • Consider echo (POCUS) to guide fluids/inotropes (LV function, IVC, RV strain)
  • Induction and airway
    • High aspiration risk; RSI/modified RSI; pre-oxygenate well (may desaturate rapidly)
    • Induction agents: ketamine (sympathomimetic; may still cause hypotension in catecholamine-depleted states), etomidate (adrenal suppression concern but single dose often acceptable in extremis), fentanyl in small titrated doses; avoid large propofol bolus in shock
    • Have vasopressor running/boluses ready before induction; consider fluid bolus at induction only if fluid responsive
  • Maintenance
    • Volatile or TIVA; expect reduced MAC requirement in sepsis; avoid deep anaesthesia causing vasodilation
    • Ventilation: lung-protective strategy if ARDS risk; avoid excessive PEEP if haemodynamic compromise
    • Fluids: balanced crystalloid; early blood products if haemorrhage/DIC; consider albumin only if per policy
    • Vasoactives titrated to perfusion endpoints (cap refill, lactate clearance, urine output, mental state, echo findings) rather than BP alone
  • Analgesia
    • Multimodal: paracetamol; cautious NSAIDs (renal perfusion/AKI risk); opioids titrated; ketamine infusion useful
    • Regional blocks can reduce opioid/ventilation needs but avoid neuraxial with coagulopathy or haemodynamic instability
  • Post-op disposition
    • Most septic shock cases require PICU; plan transfer with ventilator, infusions, lines secured, warmed, and clear handover

Complications and organ support (PICU interface)

  • Respiratory failure/ARDS
    • Lung-protective ventilation; consider paralysis/proning in severe cases per PICU
  • AKI
    • Avoid nephrotoxins; dose-adjust antibiotics; consider RRT if refractory fluid overload/electrolyte derangement
  • Coagulopathy/DIC
    • Treat underlying sepsis; blood products guided by bleeding/procedures and labs (platelets, fibrinogen, INR)
  • Adrenal dysfunction
    • Consider hydrocortisone in catecholamine-resistant shock per local/PICU guidance
  • Encephalopathy/seizures
    • Treat hypoglycaemia, electrolyte disturbance; consider meningitis/encephalitis; manage seizures promptly

Special situations

  • Meningococcal sepsis
    • Purpuric rash, rapid deterioration, DIC; early antibiotics and aggressive support; anticipate difficult IV access and coagulopathy
  • Neonatal sepsis
    • Non-specific signs (poor feeding, apnoea, temperature instability); high risk of hypoglycaemia; careful fluid strategy; early senior/PICU involvement
  • Immunocompromised child
    • Broader differential and pathogens (fungal/viral); early broad-spectrum including anti-pseudomonal cover per policy; consider neutropenic sepsis pathway
  • Congenital heart disease / pulmonary hypertension
    • Avoid hypoxia/hypercarbia/acidosis; careful fluid and vasoactive selection; early echo and cardiology/PICU input
You are called to ED to see a 2-year-old with fever, tachycardia and mottled skin. How do you recognise septic shock in a child?

Focus on perfusion and organ dysfunction; hypotension is late in children.

  • Clinical features of shock
    • Tachycardia, altered mental state (irritable/lethargic), prolonged cap refill, cool peripheries (cold shock) or warm peripheries with bounding pulses (warm shock)
    • Reduced urine output, weak/absent peripheral pulses, narrow pulse pressure (cold shock) or wide pulse pressure (warm shock)
    • Hypotension = late/pre-terminal sign
  • Evidence of organ dysfunction
    • Respiratory distress/hypoxia, lactate elevation/metabolic acidosis, AKI (rising creatinine/oliguria), coagulopathy, encephalopathy
  • Immediate actions while assessing
    • ABCDE, high-flow O2, obtain IV/IO access, send cultures and bloods, start broad-spectrum antibiotics, begin cautious fluid boluses with reassessment
Outline your first-hour management of suspected paediatric sepsis.

Time-critical bundle: oxygen, access, antibiotics, fluids/vasoactives, source control, monitoring.

  • Escalation and preparation
    • Call senior paeds/anaesthesia/PICU; allocate roles; prepare airway/IO/vasopressors
  • Airway/breathing
    • High-flow O2; consider HFNC/CPAP; intubate early if exhaustion, refractory hypoxia, or shock with high work of breathing
  • Circulation
    • IV then IO if delayed; take bloods including gas/lactate/glucose; start balanced crystalloid 10–20 mL/kg boluses with frequent reassessment
    • If fluid-refractory or fluid-limited: start vasoactive infusion early (peripheral acceptable short-term)
  • Antibiotics and cultures
    • Broad-spectrum antibiotics within 1 hour (sooner if shock); cultures first if no delay
  • Metabolic and supportive care
    • Treat hypoglycaemia; maintain normothermia; consider calcium; start urine output monitoring
  • Source control
    • Early imaging/surgical review; drain/remove infected focus; plan theatre/PICU
A septic 6-year-old needs emergency laparotomy for perforated appendicitis. How will sepsis affect your anaesthetic plan?

Expect haemodynamic instability, aspiration risk, altered drug requirements, and need for invasive monitoring and post-op ICU.

  • Pre-op
    • Continue resuscitation (antibiotics, fluids guided by response, early vasoactives), correct hypoglycaemia, crossmatch blood
    • Plan PICU bed; discuss urgency of source control vs further stabilisation
  • Monitoring and access
    • Arterial line early; large-bore IV/IO; consider CVC for vasoactives; temperature and urinary catheter
  • Induction
    • Full stomach: RSI/modified RSI; pre-oxygenate; anticipate rapid desaturation
    • Choose haemodynamically stable agents (ketamine/etomidate); avoid large propofol bolus; have vasopressor running/boluses ready
  • Maintenance
    • Lower MAC requirement; avoid excessive volatile vasodilation; ventilate with lung-protective strategy
    • Fluids cautiously; early blood products if DIC/bleeding; titrate vasoactives to perfusion endpoints and lactate trend
  • Post-op
    • Likely remain intubated and go to PICU; structured handover including antibiotics timing, cultures, fluids, vasoactives, lactate
Discuss fluid resuscitation in paediatric septic shock. How do you avoid harm?

Use small boluses with frequent reassessment; avoid overload; start vasoactives early if not responding.

  • What fluid and how much?
    • Balanced crystalloid; boluses 10–20 mL/kg with reassessment after each bolus
  • Assess response
    • HR, cap refill, pulse volume, BP/pulse pressure, mental state, lactate trend, urine output, skin temperature, work of breathing
    • Use POCUS/echo where available to assess function and fluid responsiveness
  • Avoid fluid overload
    • Look for crackles, rising oxygen requirement, hepatomegaly, worsening respiratory distress
    • If poor response or overload risk: start vasoactives rather than repeated boluses
  • When to consider blood products
    • If haemorrhage, significant anaemia with shock, DIC with bleeding/procedures; follow local transfusion thresholds and coagulation guidance
Which vasoactive agent would you choose in paediatric septic shock and why?

Match agent to haemodynamic phenotype and response; early infusion is key.

  • Phenotypes
    • Cold shock: low CO, high SVR (cool peripheries, narrow pulse pressure) → often adrenaline (inotropy) ± vasodilator in selected cases under PICU
    • Warm shock: low SVR (warm peripheries, bounding pulses, wide pulse pressure) → often noradrenaline (vasoconstriction)
  • Practical points
    • Peripheral infusion acceptable short-term with close observation; secure central access when feasible
    • Titrate to perfusion (cap refill, mental state, lactate clearance) not just BP
  • Refractory shock
    • Consider hydrocortisone for catecholamine-resistant shock; consider myocardial dysfunction on echo and add inotrope accordingly
How does sepsis alter pharmacology and anaesthetic drug requirements in children?

Sepsis changes volume of distribution, protein binding, organ clearance, and CNS sensitivity.

  • Distribution and protein binding
    • Capillary leak and fluid resuscitation increase Vd for hydrophilic drugs; hypoalbuminaemia increases free fraction of highly protein-bound drugs
  • Clearance
    • Hepatic/renal dysfunction reduces clearance → accumulation (opioids, sedatives, some antibiotics)
  • Pharmacodynamics
    • Reduced anaesthetic requirement (lower MAC); increased sensitivity to myocardial depressant/vasodilator effects
    • Ketamine may be less pressor-effective in catecholamine-depleted shock; titrate carefully
A 4-year-old with suspected meningococcal sepsis needs intubation. What are your priorities and what complications do you anticipate?

Rapid deterioration, DIC, difficult access, haemodynamic collapse at induction.

  • Priorities
    • Immediate antibiotics; high-flow O2; IV/IO access; cautious fluid boluses; early vasoactives; prepare blood products
    • RSI/modified RSI with haemodynamically stable induction; vasopressor ready before induction
  • Anticipated complications
    • DIC (bleeding, thrombosis), profound vasoplegia, myocardial depression, adrenal dysfunction, ARDS, AKI
    • Difficult cannulation; consider IO early
  • Post-intubation
    • Secure lines/tubes for transfer; arterial line; ongoing lactate monitoring; early PICU
Describe how you would manage a septic child who is fluid overloaded but still poorly perfused.

Shift from fluids to vasoactives/inotropes, assess cardiac function, and consider organ support.

  • Reassess diagnosis and phenotype
    • Check for myocardial dysfunction (echo), tamponade/pneumothorax, ongoing bleeding, obstruction, anaphylaxis
  • Start/optimise vasoactives
    • Noradrenaline for vasoplegia; adrenaline/inotrope if low contractility; titrate to perfusion endpoints
  • Ventilation and afterload
    • Intubation/ventilation may reduce work of breathing and improve oxygen delivery but can worsen venous return; manage with vasoactives and careful PEEP
  • De-resuscitation / RRT
    • If significant fluid overload with respiratory compromise/AKI: consider diuretics or early RRT in PICU
Discuss the differences between septic shock in children and adults and the implications for anaesthesia.

Examiners expect recognition that children compensate differently and that hypotension is late.

  • Physiological differences
    • Children maintain BP with tachycardia and vasoconstriction; hypotension is late
    • Higher metabolic rate and oxygen consumption; limited cardiac stroke volume reserve (HR-dependent CO, especially infants)
  • Shock phenotypes
    • Cold shock more common in children (low CO, high SVR) vs vasoplegic warm shock more typical in adults (but both occur)
  • Anaesthetic implications
    • Earlier airway control may be needed to reduce work of breathing; careful induction to avoid cardiovascular collapse
    • Early invasive monitoring; early vasoactives; cautious fluids to avoid overload
Outline an anaesthetic plan for emergency source control surgery in a child with septic shock.

Structure: pre-op resuscitation, induction, maintenance, monitoring, post-op ICU.

  • Pre-op
    • Antibiotics, cultures, lactate/glucose, crossmatch; optimise perfusion with cautious fluids and early vasoactives; plan PICU
  • Induction
    • RSI/modified RSI; ketamine/etomidate; titrated opioid; vasopressor prepared and/or running
  • Monitoring/access
    • Arterial line; CVC if feasible; temperature; urine catheter; frequent gases and lactate
  • Maintenance
    • Avoid deep volatile; lung-protective ventilation; balanced fluids; vasoactive titration; manage coagulopathy
  • Post-op
    • PICU transfer intubated if ongoing shock/respiratory failure; clear handover including antibiotics timing and cultures
How would you assess fluid responsiveness in a septic child peri-operatively?

Dynamic assessment and repeated clinical review; static numbers alone are unreliable.

  • Clinical endpoints
    • Cap refill, pulse volume, mental state, urine output, lactate trend, skin temperature
  • Haemodynamic tools
    • Arterial waveform, pulse pressure variation (limited in small children/low tidal volumes), echo/POCUS (LV function, stroke volume change with small bolus)
  • Safety
    • Stop fluids if signs of overload; switch to vasoactives/inotropes
Discuss the causes and management of lactic acidosis in paediatric sepsis.

Lactate is a marker of severity but not synonymous with hypovolaemia alone.

  • Causes
    • Tissue hypoperfusion (shock), impaired oxygen utilisation (mitochondrial dysfunction), beta-agonist effect, seizures, liver dysfunction
  • Management principles
    • Restore perfusion (fluids if responsive, vasoactives/inotropes), optimise oxygenation/ventilation, treat source with antibiotics and source control
    • Trend lactate clearance with clinical improvement; avoid chasing lactate with excessive fluids

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