Acute Sepsis - Paediatric

1. Clinical Overview

Summary

Sepsis in children is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. [1] It represents a leading cause of childhood mortality worldwide, with over 3 million annual deaths globally. [2] The condition differs fundamentally from adults in presentation, pathophysiology, and management, necessitating paediatric-specific diagnostic criteria and treatment protocols.

The Phoenix Sepsis Criteria (2024) now define paediatric sepsis as a Phoenix Sepsis Score ≥2 points in children with suspected infection, indicating potentially life-threatening dysfunction of respiratory, cardiovascular, coagulation, and/or neurological systems. [1] Children meeting these criteria have in-hospital mortality of 7.1% in higher-resource settings and 28.5% in lower-resource settings—more than 8 times that of children with suspected infection not meeting these criteria. [1]

Septic shock is defined as sepsis with cardiovascular dysfunction (at least 1 cardiovascular point in Phoenix Score), including severe hypotension for age, blood lactate > 5 mmol/L, or need for vasoactive medication, with mortality rates of 10.8% and 33.5% in higher- and lower-resource settings respectively. [1]

The cornerstone of management is early recognition using the Phoenix criteria, immediate resuscitation with ABCDE approach, rapid fluid resuscitation (20 mL/kg crystalloid boluses up to 40-60 mL/kg in first hour), [3] urgent empirical antibiotics (within 1 hour of recognition), [4] source control, and vasoactive support when required. [3] Evidence demonstrates that every hour of delay in antibiotic administration increases mortality risk. [4]

Key Facts

• Definition: Phoenix Sepsis Score ≥2 in child with suspected infection [1]
• Global Burden: > 3 million deaths annually; leading cause of childhood mortality [2]
• Mortality: 7.1% (high-resource) to 28.5% (low-resource settings) for sepsis; 10.8-33.5% for septic shock [1]
• Peak Age: Highest risk in infants less than 1 year, particularly neonates
• Time-Critical: Antibiotic delay of each hour increases mortality [4]
• Pathophysiology: Dysregulated immune response, endothelial dysfunction, coagulopathy, mitochondrial dysfunction
• First-Line Treatment: ABCDE resuscitation, fluid boluses (20 mL/kg), antibiotics within 1 hour [3,4]

Clinical Pearls

"Phoenix Criteria Replace SIRS" — The 2024 Phoenix Sepsis Criteria supersede the outdated 2005 SIRS-based definitions, which had poor predictive properties. Phoenix focuses on organ dysfunction, not inflammation markers. [1]

"Time to Antibiotics is Critical" — The "1-hour bundle" (antibiotics within 1 hour of sepsis recognition) is associated with improved survival. [4] Every hour of delay increases odds of mortality by 6-40% depending on severity. [4]

"Fluid Resuscitation: 40-60 mL/kg in First Hour" — Early aggressive fluid resuscitation (20 mL/kg boluses, up to 40-60 mL/kg total in first hour) improves outcomes in paediatric septic shock, particularly in high-resource settings. [3,5] However, in resource-limited settings with minimal monitoring, conservative fluid strategies may be safer. [6]

"Noradrenaline is First-Line Vasoactive" — For fluid-refractory septic shock, noradrenaline is now recommended as first-line vasoactive agent, with adrenaline as alternative. [3] Dopamine is no longer recommended as first-line due to increased arrhythmia risk. [3]

"Age-Specific Vital Signs Matter" — Normal vital signs vary dramatically by age. Use age-specific reference ranges to identify tachycardia, tachypnoea, and hypotension. [7]

Why This Matters Clinically

Paediatric sepsis is a medical emergency requiring immediate recognition and intervention. The new Phoenix criteria provide a validated, internationally applicable definition that improves early identification. [1] Implementation of evidence-based bundles (rapid fluid resuscitation, early antibiotics, appropriate vasoactive support) has been shown to reduce mortality by 30-40%. [4,8] However, children can deteriorate rapidly—early escalation to critical care is essential. Long-term survivors may experience new morbidities including neurodevelopmental impairment, making early aggressive management even more crucial. [9]

---

2. Epidemiology

Incidence & Prevalence

Global Burden:

• Annual incidence: 48.9 million cases globally (2017 data) [2]
• Annual deaths: 11 million sepsis-related deaths, > 3 million in children [2]
• Paediatric sepsis prevalence in PICUs: 8.2% of PICU admissions [10]
• Emergency department presentations: 0.2-2% of paediatric ED visits meet sepsis criteria [11]

Regional Variation:

• High-income countries: Mortality 5-10% [1,10]
• Low- and middle-income countries: Mortality 25-35% [1,2]
• Sub-Saharan Africa: Highest burden (> 50% of global childhood sepsis deaths) [2]

Temporal Trends:

• Decreasing incidence in high-income countries (improved vaccination, antimicrobial availability) [12]
• Persistent high burden in resource-limited settings [2]
• Increasing recognition due to improved awareness campaigns [13]

Demographics

Risk Factors

Host Factors (Non-Modifiable):

Modifiable Risk Factors:

Common Sources of Infection

---

3. Aetiology & Pathophysiology

Phoenix Sepsis Criteria (2024)

The Phoenix Sepsis Score defines paediatric sepsis as score ≥2 points in children less than 18 years with suspected infection. [1] The score assesses four organ systems:

Phoenix Sepsis Score Components:

Key Points:

• Sepsis: Phoenix Score ≥2 in child with suspected infection [1]
• Septic Shock: Sepsis + cardiovascular dysfunction (≥1 cardiovascular point) [1]
• Neonates: Phoenix criteria validated for infants ≥37 weeks gestation and ≥2.5 kg; alternative criteria needed for premature neonates [1]

Performance Characteristics:

• Sensitivity: 74% for mortality prediction [1]
• Specificity: 71% for mortality prediction [1]
• AUROC: 0.76 for in-hospital mortality [1]
• Superior to previous SIRS-based criteria (AUROC 0.55) [1]

Age-Specific Vital Sign Reference Ranges

Normal Vital Signs by Age: [7,18]

Hypotension Definitions:

• Infants (1-12 months): SBP less than 70 mmHg
• Children 1-10 years: SBP less than 70 + (2 × age in years) mmHg
• Children > 10 years: SBP less than 90 mmHg

Molecular Pathophysiology

Exam Detail: #### Pathophysiological Cascade

1. Infection Recognition (PAMPs/DAMPs)

• Pathogen-associated molecular patterns (PAMPs): LPS, peptidoglycan, flagellin, viral nucleic acids
• Pattern recognition receptors (PRRs): Toll-like receptors (TLR2, TLR4, TLR9), NOD-like receptors
• Damage-associated molecular patterns (DAMPs): Released from damaged host cells (HMGB1, histones)

2. Pro-Inflammatory Response ("Cytokine Storm")

• Early cytokines (0-4 hours): TNF-α, IL-1β, IL-6
• Chemokines: IL-8, MCP-1, MIP-1α (recruit neutrophils, monocytes)
• Complement activation: C3a, C5a (anaphylatoxins)
• Paediatric-specific: Neonates have reduced TNF-α production but exaggerated IL-6/IL-10 responses [19]

3. Endothelial Dysfunction

• Glycocalyx degradation → capillary leak
• Upregulation of adhesion molecules (ICAM-1, VCAM-1, E-selectin)
• Increased vascular permeability → interstitial oedema
• Loss of endothelial barrier function → third-space fluid losses

4. Coagulation Dysregulation

• Tissue factor expression → thrombin generation
• Consumption coagulopathy → DIC (platelets, fibrinogen depleted)
• Impaired anticoagulation (protein C, protein S, antithrombin consumption)
• Microthrombosis → organ ischaemia

5. Cardiovascular Dysfunction

• Distributive shock: Vasodilation (NO, prostacyclin), decreased SVR
• Myocardial depression: Cytokine-mediated (TNF-α, IL-1β), calcium handling impairment
• Relative adrenal insufficiency: Inadequate cortisol response to stress
• Hypovolaemia: Capillary leak, reduced oral intake, increased insensible losses
• Paediatric-specific: Children compensate initially with tachycardia (↑ CO), but decompensate rapidly once stroke volume falls

6. Metabolic Dysregulation

• Mitochondrial dysfunction: Impaired oxidative phosphorylation → lactate production
• Hyperglycaemia: Insulin resistance, gluconeogenesis
• Hypoglycaemia: Young infants (limited glycogen stores)
• Hypocalcaemia: Impaired PTH secretion, calcium sequestration

7. Organ-Specific Injury

Respiratory:

• ARDS: Alveolar-capillary barrier breakdown, surfactant dysfunction
• Ventilation-perfusion mismatch
• Increased pulmonary vascular resistance

Renal:

• Acute tubular necrosis: Hypoperfusion, direct inflammatory injury
• Reduced GFR, oliguria/anuria
• Fluid and electrolyte imbalance

Hepatic:

• Cholestasis, impaired synthetic function
• Hyperbilirubinaemia, coagulopathy

Neurological:

• Encephalopathy: Direct bacterial invasion (meningitis), cytokine effects
• Cerebral oedema
• Seizures (hypoglycaemia, electrolyte disturbance, direct CNS infection)

Paediatric-Specific Pathophysiological Considerations

Why Children Are Different:

1. Immune Immaturity: [19]

   • Neonates: Reduced neutrophil function, impaired pathogen recognition
   • Reduced immunological memory (T-cell, B-cell)
   • Higher susceptibility to overwhelming bacterial sepsis

2. Physiological Reserve: [20]

   • Smaller blood volume (80 mL/kg in infants vs 70 mL/kg adults)
   • Limited glycogen stores → rapid hypoglycaemia
   • Higher metabolic rate → rapid deterioration

3. Cardiovascular Response: [20]

   • Cardiac output primarily rate-dependent (limited stroke volume increase)
   • Initial tachycardia maintains CO → sudden decompensation when bradycardia develops
   • Lower systemic vascular resistance at baseline

4. Fluid Distribution:

   • Higher proportion of total body water (75-80% in neonates vs 60% adults)
   • Greater capillary leak → more profound third-spacing
   • Higher risk of cerebral oedema

---

4. Clinical Presentation

Symptoms: The Patient's Story

Typical Presentation:

Infants (less than 1 year):

• Non-specific signs predominate: "Not feeding well"
  • "sleeping more than usual"
  • "irritable"
• Fever or hypothermia: Temperature > 38°C or less than 36°C
• Respiratory: Tachypnoea, grunting, nasal flaring, chest retractions
• Circulatory: Poor feeding, mottled skin, cold peripheries
• Neurological: Altered responsiveness (too sleepy or too irritable)
• Gastrointestinal: Vomiting, diarrhoea, abdominal distension

Children (1-12 years):

• Fever: Usually > 38.5°C (though may be absent in 10-15%)
• Altered mental status: Confusion, decreased responsiveness, irritability
• Respiratory distress: Dyspnoea, tachypnoea, use of accessory muscles
• Circulatory: Prolonged capillary refill, cold/mottled extremities, weak pulses
• Pain: May localise to infection source (earache, abdominal pain, headache)
• Reduced urine output: Oliguria

Adolescents (≥12 years):

• Similar to adult presentation
• More able to describe symptoms (headache, myalgia, dizziness)
• May have atypical presentation if chronic illness present

Red Flag Symptoms:

• Persistent altered mental status despite fever reduction
• Non-blanching rash (purpura/petechiae—consider meningococcal sepsis)
• Persistent tachycardia out of proportion to fever
• Signs of dehydration (sunken fontanelle in infants, reduced urine output)
• Seizures (especially if first presentation)
• Parental concern ("This child is not right")—take seriously [21]

Signs: What You See

General Appearance

Toxic Appearance:

• Lethargic, poorly responsive, or excessively irritable
• Pale, mottled, or cyanosed
• Weak cry (infants)
• Difficulty maintaining eye contact

Vital Signs

Temperature:

• Fever ≥38°C (most common)
• Hypothermia less than 36°C (poor prognostic sign, especially neonates)

Heart Rate: (See age-specific ranges above)

• Tachycardia: Usually present
• Bradycardia: Ominous sign of impending cardiac arrest

Respiratory Rate: (See age-specific ranges above)

• Tachypnoea: Compensation for metabolic acidosis and/or respiratory pathology
• Apnoea/gasping: Pre-terminal sign

Blood Pressure:

• Normal BP does NOT exclude sepsis (compensated shock)
• Hypotension: Late sign in children (decompensated shock)—indicates critical illness

Oxygen Saturation:

• SpO₂ less than 92% in room air: Suggests respiratory dysfunction
• SpO₂ less than 90% despite oxygen: Severe respiratory dysfunction (Phoenix ≥1 point)

Cardiovascular Examination

Respiratory Examination

Neurological Examination

Skin Examination

Source Identification

Systematic examination to identify infection source:

---

5. Differential Diagnosis

Key Principle: Sepsis is a clinical diagnosis of exclusion. Consider alternative diagnoses that can mimic sepsis:

Must-Not-Miss Differentials

Common Mimics

---

6. Investigations

Immediate Bedside Investigations

1. Clinical Assessment (Most Important)

• Phoenix Sepsis Score calculation [1]
• Vital signs monitoring (HR, RR, BP, SpO₂, temperature, capillary refill, GCS)
• Fluid balance (urine output monitoring—aim > 1 mL/kg/hr)

2. Point-of-Care Tests

• Glucose: Hypoglycaemia common in infants; hyperglycaemia may occur in sepsis
• Blood gas (venous or arterial):
  • pH: Metabolic acidosis (lactic acidosis)
  • "Lactate: > 2 mmol/L suggests hypoperfusion; > 5 mmol/L defines shock [1]"
  • "Base excess: Marker of metabolic acidosis severity"
  • "PaO₂/PaCO₂: Assess respiratory function"

Laboratory Investigations

Essential Investigations (All Cases):

Source-Directed Investigations:

Imaging

Chest X-Ray:

• Indication: Respiratory symptoms, hypoxia, suspected pneumonia
• Findings: Consolidation, effusion, infiltrates
• Timing: Do not delay antibiotics for imaging

Ultrasound:

• Cardiac: If concern for myocardial dysfunction, pericardial effusion
• Abdominal: If suspected intra-abdominal sepsis (appendicitis, abscess)
• Renal: If suspected pyelonephritis, obstruction

CT Imaging:

• Generally avoided acutely unless specific indication (e.g., suspected intra-abdominal pathology not visualised on USS)
• Do NOT delay treatment for CT

MRI:

• Not indicated acutely

Diagnostic Thresholds

Phoenix Sepsis Criteria Application: [1]

1. Suspected or confirmed infection (clinical or microbiological)

2. Calculate Phoenix Sepsis Score from:

   • Respiratory: PaO₂:FiO₂ ratio or SpO₂:FiO₂ ratio; mechanical ventilation
   • Cardiovascular: MAP for age, lactate, vasoactive medications
   • Coagulation: Platelets, INR
   • Neurological: Glasgow Coma Scale

3. Interpretation:

   • Phoenix Score less than 2: Suspected infection without organ dysfunction
   • Phoenix Score ≥2: SEPSIS diagnosis
   • Phoenix Score ≥2 with ≥1 cardiovascular point: SEPTIC SHOCK diagnosis

---

7. Management

Management Algorithm

       SUSPECTED SEPSIS (Phoenix Score ≥2)
      (Infection + organ dysfunction)
                    ↓
┌────────────────────────────────────────────────┐
│    IMMEDIATE RESUSCITATION (TIME = 0 min)      │
│  • ABCDE approach                              │
│  • High-flow oxygen (target SpO₂ > 94%)         │
│  • Establish IV/IO access (do NOT delay)        │
│  • Rapid fluid bolus: 20 mL/kg 0.9% saline     │
│    over 5-10 minutes                            │
│  • Monitor vitals continuously                  │
│  • Senior clinician review immediately          │
└────────────────────────────────────────────────┘
                    ↓
┌────────────────────────────────────────────────┐
│    ANTIBIOTICS WITHIN 1 HOUR (TIME = 0-60 min) │
│  • Blood cultures BEFORE antibiotics (if       │
│    possible, but DO NOT DELAY antibiotics)     │
│  • Broad-spectrum IV antibiotics within 1 hour │
│  • Choice based on likely source, local        │
│    resistance patterns, age                     │
│  • Typical: Ceftriaxone/cefotaxime ± other     │
└────────────────────────────────────────────────┘
                    ↓
┌────────────────────────────────────────────────┐
│    FURTHER FLUID RESUSCITATION (0-60 min)      │
│  • Reassess after each 20 mL/kg bolus          │
│  • Give further 20 mL/kg boluses if:           │
│    - Persistent hypotension                     │
│    - Prolonged CRT (> 3 sec)                     │
│    - Altered mental status                      │
│  • Total 40-60 mL/kg in first hour acceptable  │
│  • Monitor for fluid overload (hepatomegaly,   │
│    crackles, increased work of breathing)      │
└────────────────────────────────────────────────┘
                    ↓
┌────────────────────────────────────────────────┐
│    VASOACTIVE SUPPORT (if fluid-refractory)    │
│  • If hypotension/poor perfusion persists      │
│    after 40-60 mL/kg fluid                      │
│  • First-line: Noradrenaline 0.05-0.5 mcg/kg/min│
│  • Alternative: Adrenaline 0.05-0.5 mcg/kg/min │
│  • Requires central access & intensive monitoring│
│  • Escalate to PICU                             │
└────────────────────────────────────────────────┘
                    ↓
┌────────────────────────────────────────────────┐
│    SOURCE CONTROL                              │
│  • Identify source: clinical + investigations  │
│  • Drain abscesses, debride necrotic tissue    │
│  • Remove infected devices (catheters, drains) │
│  • Surgical consult if indicated                │
└────────────────────────────────────────────────┘
                    ↓
┌────────────────────────────────────────────────┐
│    ORGAN SUPPORT & MONITORING                  │
│  • Respiratory: Intubation/ventilation if      │
│    severe hypoxia or impending respiratory arrest│
│  • Renal: Consider RRT if severe AKI/fluid     │
│    overload/electrolyte disturbance            │
│  • Haematological: Transfuse if DIC with       │
│    bleeding (platelets, FFP, cryoprecipitate)  │
│  • Metabolic: Correct hypoglycaemia, electrolytes│
│  • Continuous monitoring: HR, BP, SpO₂, UO     │
└────────────────────────────────────────────────┘
                    ↓
┌────────────────────────────────────────────────┐
│    ONGOING MANAGEMENT                          │
│  • Antibiotic review at 24-48h (de-escalate    │
│    based on cultures/sensitivities)            │
│  • Daily assessment of organ dysfunction       │
│  • Wean vasoactive support as tolerated        │
│  • Nutrition support (enteral preferred)       │
│  • VTE prophylaxis if indicated                │
│  • Plan for step-down/discharge                │
└────────────────────────────────────────────────┘

Acute/Emergency Management (First Hour)

Time = 0 Minutes: Immediate Actions

Airway:

• Assess patency
• Position to maintain airway (chin lift/jaw thrust if reduced GCS)
• Consider intubation if:
  • GCS less than 8 or rapidly deteriorating mental status
  • Apnoea or irregular breathing
  • Severe shock not responding to initial resuscitation

Breathing:

• High-flow oxygen via non-rebreather mask (target SpO₂ ≥94%)
• If severe respiratory distress: Non-invasive ventilation (CPAP) or intubation
• Monitor respiratory rate, work of breathing, SpO₂

Circulation:

1. Establish vascular access URGENTLY:

   • Two large-bore IV cannulae (largest possible for age)
   • If unsuccessful after 2 attempts or > 5 minutes: intraosseous (IO) access [3]

2. First fluid bolus: 20 mL/kg 0.9% sodium chloride (normal saline) IV/IO over 5-10 minutes [3,5]

   • Use push-pull technique or pressure bag to administer rapidly
   • Alternative crystalloid: Hartmann's solution (lactated Ringer's)

3. Reassessment after 20 mL/kg:

   • Vitals (HR, BP, capillary refill, peripheral temperature)
   • Mental status (GCS/AVPU)
   • Urine output (aim > 1 mL/kg/hr)

   If persistent shock → Give second 20 mL/kg bolus

   If persistent shock after 40 mL/kg → Give third 20 mL/kg bolus AND commence vasoactive support [3]

   Total fluid in first hour: Up to 40-60 mL/kg is appropriate if ongoing shock [3,5]

4. Monitoring for fluid overload:

   • Clinical: Hepatomegaly, pulmonary oedema (crackles), increased work of breathing
   • If signs of overload: Slow/stop fluids, consider diuretics, escalate to PICU

Disability:

• Assess GCS/AVPU
• Check blood glucose (treat hypoglycaemia with 2 mL/kg 10% dextrose IV if less than 3 mmol/L)
• Pupil size and reactivity

Exposure:

• Full examination to identify source
• Temperature measurement (rectal most accurate in infants, but oral/axillary acceptable)
• Look for rashes (especially non-blanching purpura)

Time = 0-60 Minutes: Antibiotic Administration

CRITICAL: Antibiotics must be administered within 1 hour of sepsis recognition. [4]

Evidence: Each hour of antibiotic delay increases mortality. [4,22]

Antibiotic Choice:

Empirical Therapy by Age and Setting:

Key Antibiotic Principles:

• Give IV (NOT oral/IM) [3]
• Do NOT delay for blood cultures (but take cultures first if venous access already established)
• Adjust based on local resistance patterns
• Review at 24-48 hours: De-escalate based on culture/sensitivity; switch to oral if improving and tolerating

Specific Scenarios:

Time = 60+ Minutes: Ongoing Resuscitation

If Fluid-Refractory Shock (Shock persisting after 40-60 mL/kg fluid):

Vasoactive Support: [3,23]

1. First-Line: Noradrenaline

   • Dose: Start 0.05 mcg/kg/min, titrate to 0.5 mcg/kg/min
   • Route: Central venous catheter preferred (peripheral OK temporarily with close monitoring)
   • Mechanism: Predominantly α₁-agonist (vasoconstriction), some β₁ (inotropy)
   • Monitoring: Continuous BP, HR; target MAP for age

2. Alternative: Adrenaline

   • Dose: Start 0.05 mcg/kg/min, titrate to 0.5 mcg/kg/min
   • Route: Central venous catheter preferred
   • Mechanism: β₁ + β₂ (inotropy, chronotropy, vasodilation at low dose) + α₁ (vasoconstriction at high dose)
   • Use if: Mixed shock (distributive + cardiogenic), or noradrenaline-refractory

3. Adjunct: Vasopressin

   • Dose: 0.0003-0.002 units/kg/min
   • Mechanism: V1 receptor agonist (vasoconstriction), catecholamine-sparing
   • Use if: Catecholamine-refractory shock

4. Not Recommended First-Line:

   • Dopamine: Increased arrhythmia risk, less effective than noradrenaline [3]
   • Dobutamine: May worsen hypotension if predominantly distributive shock

Corticosteroids:

• Hydrocortisone: Consider if catecholamine-resistant shock [3]
• Dose: 50 mg/m² IV (or 2 mg/kg) every 6 hours
• Evidence: Some benefit in fluid-refractory, catecholamine-resistant shock [24]
• Do NOT give routinely to all septic patients

Refractory Shock (Not Responding to Above):

• Escalate to PICU immediately
• Consider:
  • Echocardiography (assess cardiac function, guide fluid/inotrope choice)
  • Additional vasoactive agents (adrenaline, vasopressin, milrinone)
  • ECMO in specialist centres

Source Control

Principles: [3]

• Identify and eliminate source of infection
• Drainage, debridement, or device removal may be life-saving
• Should be achieved as soon as possible (ideally within 6-12 hours)

Interventions:

Supportive Care

Respiratory Support:

• Oxygen therapy (target SpO₂ ≥94%)
• Non-invasive ventilation (CPAP/BiPAP) if increased work of breathing but not exhausted
• Mechanical ventilation if:
  • "Severe hypoxaemia (PaO₂:FiO₂ less than 200) despite oxygen"
  • Respiratory failure (rising CO₂, exhaustion)
  • GCS less than 8 or unable to protect airway
  • Cardiovascular instability

Renal Support:

• Fluid balance monitoring (strict input/output)
• Consider renal replacement therapy (RRT) if:
  • Severe AKI with oliguria/anuria
  • Fluid overload refractory to diuretics
  • Severe electrolyte disturbance (hyperkalaemia > 6.5 mmol/L)
  • Severe metabolic acidosis (pH less than 7.1)

Haematological Support:

• Transfusion thresholds:
  • "Platelets: less than 10-20 × 10⁹/L (or less than 50 × 10⁹/L if bleeding/invasive procedure)"
  • "FFP: If bleeding AND prolonged PT/APTT"
  • "Red cells: Hb less than 70 g/L (or less than 90 g/L if ongoing shock/ischaemia)"

Metabolic:

• Glucose control: Avoid hypoglycaemia (less than 4 mmol/L) and severe hyperglycaemia (> 10 mmol/L)
• Electrolyte management: Correct K⁺, Na⁺, Ca²⁺, Mg²⁺, PO₄³⁻ abnormalities
• Nutrition: Enteral nutrition (NG/NJ feeding) within 24-48 hours if haemodynamically stable; parenteral nutrition if enteral not tolerated

Sedation/Analgesia (if mechanically ventilated):

• Fentanyl or morphine for analgesia
• Midazolam or propofol for sedation
• Avoid excessive sedation (daily sedation holds)

Prophylaxis:

• Stress ulcer prophylaxis: Ranitidine or omeprazole if mechanically ventilated or high bleeding risk
• VTE prophylaxis: Low-molecular-weight heparin if immobile and no contraindication (adolescents)

Disposition & Follow-Up

All Children with Sepsis (Phoenix ≥2):

• Admit to hospital
• Minimum: High-dependency unit (HDU) monitoring
• PICU if:
  • Septic shock (requiring vasoactive support)
  • Respiratory failure (requiring mechanical ventilation)
  • Severe organ dysfunction (Phoenix score ≥6)
  • Rapidly deteriorating

Discharge Criteria:

• Afebrile > 24 hours (off antipyretics)
• Haemodynamically stable (off vasoactive support > 24 hours)
• Normal mental status
• Tolerating oral intake and medications
• No oxygen requirement
• Source controlled
• Safe social circumstances

Follow-Up:

• Primary care review within 1 week post-discharge
• Paediatric outpatient review at 4-6 weeks (earlier if concerns)
• Screen for long-term sequelae:
  • "Neurodevelopmental: Cognitive, motor, behavioural assessment (especially if CNS involvement)"
  • "Physical function: Chronic pain, weakness"
  • "Psychological: PTSD, anxiety, depression"
• Consider referral to multidisciplinary follow-up clinic if available

---

8. Complications

Immediate (Hours-Days)

Early (Days-Weeks)

Late (Months-Years)

Long-Term Sequelae: [9,26]

1. Neurodevelopmental Impairment (10-30% of survivors):

   • Cognitive deficits (memory, executive function)
   • Learning difficulties
   • Behavioural problems (ADHD-like symptoms)
   • Motor impairment (cerebral palsy if severe CNS injury)

2. Physical Function (20-40%):

   • Reduced exercise tolerance
   • Chronic pain (musculoskeletal)
   • Hearing loss (especially post-meningitis)
   • Visual impairment

3. Psychological (5-15%):

   • Post-traumatic stress disorder (PTSD)—child and family
   • Anxiety, depression
   • School avoidance

4. New/Progressive Medical Conditions (15-20%): [9]

   • Chronic kidney disease (post-AKI)
   • Pulmonary fibrosis (post-ARDS)
   • New seizure disorder (post-encephalitis/meningitis)

5. Mortality (Post-Discharge):

   • 1-year post-discharge mortality: 3-5% (higher than matched controls) [9]

---

9. Prognosis & Outcomes

Natural History (Without Treatment)

Untreated Sepsis:

• Mortality: 50-80% (depending on pathogen, setting)
• Progression to multi-organ failure within hours-days
• Death from cardiovascular collapse, respiratory failure, or refractory shock

Outcomes with Treatment

Survival: [1,10]

Time to Recovery:

• Most survivors: Clinical improvement within 72 hours of appropriate treatment
• PICU length of stay: Median 3-7 days [10]
• Hospital length of stay: Median 7-14 days [10]

Prognostic Factors

Poor Prognostic Factors:

Good Prognostic Factors:

Long-Term Outcomes

Survivors: [9,26]

• 70-80%: Full recovery with no long-term sequelae
• 15-25%: New or progressive medical conditions
• 10-15%: Significant functional impairment (physical, cognitive, psychological)

Quality of Life:

• Reduced health-related quality of life (HRQOL) at 1 year post-sepsis vs. matched controls [9]
• Improvement over time (most recover to baseline by 2-3 years)

---

10. Prevention & Screening

Primary Prevention

Vaccination: [16]

• Pneumococcal: PCV13 (prevents invasive pneumococcal disease, #1 cause of bacterial sepsis)
• Haemophilus influenzae type b (Hib): Prevents invasive Hib disease
• Meningococcal: MenACWY, MenB (prevents meningococcal sepsis)
• Influenza: Annual vaccination (reduces influenza-associated bacterial sepsis)
• Measles, pertussis: Prevent severe viral infections leading to sepsis

Public Health:

• Clean water, sanitation (reduces GI infections)
• Nutrition programs (reduces malnutrition-related sepsis) [15]
• Maternal immunisation (protects neonates via transplacental antibodies)

Secondary Prevention

Early Recognition:

• Parental education: "Red flags" of serious illness (UK "Sepsis 6" campaigns) [29]
• Healthcare professional training: Phoenix criteria, early escalation protocols
• Triage tools: Use of validated sepsis screening tools in emergency departments [11]

Hospital Infection Control:

• Hand hygiene
• Catheter care bundles (reduce catheter-associated bloodstream infections)
• Antimicrobial stewardship (reduce resistance)

---

11. Key Guidelines & Evidence

Major Guidelines

1. Phoenix Sepsis Criteria (SCCM 2024) [1]

• Key Recommendation: Use Phoenix Sepsis Score ≥2 to define paediatric sepsis
• Evidence Level: High (derived from > 3 million patient encounters, validated internationally)

2. Surviving Sepsis Campaign: International Guidelines for Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children (2020) [3]

• Key Recommendations:
  • "Rapid fluid resuscitation: 40-60 mL/kg in first hour for septic shock (Strong recommendation)"
  • Antibiotics within 1 hour of sepsis recognition (Strong recommendation)
  • Noradrenaline or adrenaline as first-line vasoactive agent (Strong recommendation)
  • Source control as soon as feasible (Strong recommendation)
• Evidence Level: 1A for core recommendations

3. NICE Guideline NG51: Sepsis—Recognition, Diagnosis and Early Management (2016) [30]

• Key Recommendations: Risk stratification, early escalation, 1-hour bundle
• Primarily adult/adolescent focused, but paediatric appendix included

4. WHO Pocket Book of Hospital Care for Children (2013)

• Guidance for resource-limited settings
• More conservative fluid resuscitation in settings without intensive monitoring

Landmark Trials & Meta-Analyses

Fluid Resuscitation:

Antibiotic Timing:

Vasoactive Agents:

Evidence Strength Summary

---

12. Examination Pearls & Viva Preparation

Common Exam Questions

1. "Define paediatric sepsis using the Phoenix criteria."

Model Answer: "Paediatric sepsis is defined by the 2024 Phoenix Sepsis Criteria as a Phoenix Sepsis Score of 2 or more points in a child under 18 years with suspected or confirmed infection. [1] The Phoenix Score assesses dysfunction in four organ systems: respiratory (PaO₂:FiO₂ or SpO₂:FiO₂ ratio, mechanical ventilation), cardiovascular (MAP, lactate, vasoactive medications), coagulation (platelets, INR), and neurological (Glasgow Coma Scale). A score of ≥2 indicates potentially life-threatening organ dysfunction, with in-hospital mortality of 7.1% in high-resource settings and 28.5% in low-resource settings—more than 8-fold higher than children with infection not meeting these criteria. [1] Septic shock is defined as sepsis with at least 1 cardiovascular point, indicating severe hypotension, lactate > 5 mmol/L, or need for vasoactive medication."

---

2. "How does paediatric sepsis differ from adult sepsis in presentation and management?"

Model Answer: "Paediatric sepsis differs in several key ways. First, presentation: children have age-specific vital signs—tachycardia and tachypnoea thresholds vary dramatically by age, and hypotension is a late sign due to excellent cardiovascular compensation. Infants often present with non-specific signs like poor feeding or lethargy rather than obvious infection. [20] Second, pathophysiology: children have immature immune systems (especially neonates), smaller physiological reserve, and cardiac output is rate-dependent rather than stroke-volume dependent. [19,20] Third, fluid resuscitation: children in high-resource settings benefit from aggressive early fluid resuscitation (40-60 mL/kg in first hour), [3,5] whereas in low-resource settings without monitoring, the FEAST trial showed increased mortality with bolus fluids. [6] Fourth, organ dysfunction scoring: the Phoenix criteria were specifically developed for children, unlike adult SOFA scores. [1] Finally, antibiotic choice differs by age—neonates require cover for GBS and E. coli, while older children receive ceftriaxone for community-acquired sepsis."

---

3. "A 3-year-old presents with fever, drowsiness, and a purpuric rash. What is your immediate management?"

Model Answer: "This child has suspected meningococcal sepsis—a medical emergency. My immediate priorities are ABCDE resuscitation and urgent antibiotics. First, I ensure airway patency and give high-flow oxygen targeting SpO₂ ≥94%. I rapidly establish IV or IO access (within 5 minutes—do not delay for multiple cannulation attempts). I give an immediate 20 mL/kg 0.9% saline bolus over 5-10 minutes and reassess for signs of shock (capillary refill, heart rate, blood pressure, mental status). [3] If shock persists, I give further 20 mL/kg boluses up to 40-60 mL/kg total in the first hour. [3,5]

Simultaneously, I give IV ceftriaxone 50-100 mg/kg (max 2g) within 1 hour—ideally after blood cultures, but I absolutely do not delay antibiotics for investigations. [4] In meningococcal sepsis, every minute matters. I also notify senior colleagues and PICU immediately, as this child will need intensive monitoring.

I perform a focused examination to assess organ dysfunction using Phoenix criteria—particularly cardiovascular (capillary refill, BP, lactate), neurological (GCS), and respiratory (oxygen requirement). I send blood cultures, FBC, coagulation, lactate, glucose, and renal function. If the child remains shocked after fluid resuscitation, I prepare to start noradrenaline or adrenaline infusion. [3] I would not perform a lumbar puncture acutely given the shock and coagulopathy risk—this can wait until stabilised. Public health notification is also required for meningococcal disease."

---

4. "What is the evidence for the 1-hour antibiotic bundle in paediatric sepsis?"

Model Answer: "The 1-hour antibiotic bundle—administering IV antibiotics within 1 hour of sepsis recognition—is supported by strong evidence in paediatrics. The landmark study by Evans et al. (2018) analysed over 1,000 children with sepsis in New York State and found that the 1-hour bundle (antibiotics + fluid resuscitation within 1 hour) was associated with a 40% reduction in in-hospital mortality compared to delayed treatment. [22] This built on earlier work by Weiss et al. (2014) showing that each hour of antibiotic delay was associated with increased mortality odds. [4] The 2020 Surviving Sepsis Campaign paediatric guidelines incorporated this evidence, making antibiotics within 1 hour a strong recommendation (Grade 1B). [3] Importantly, this means antibiotics should be given even before confirmatory investigations like blood cultures if there is any delay—the priority is time to treatment. The evidence is robust enough that many countries now include 1-hour antibiotics in paediatric sepsis quality metrics."

---

5. "Explain the fluid management controversy in paediatric sepsis."

Model Answer: "There is an important geographical and resource-based controversy in paediatric sepsis fluid management. In high-resource settings (well-equipped PICUs, continuous monitoring), the evidence supports aggressive early fluid resuscitation: the Surviving Sepsis Campaign recommends 40-60 mL/kg in the first hour for septic shock, [3] and studies like SPROUT demonstrate that early aggressive fluids improve outcomes. [10] The RESOLVE trial (2019) showed no mortality difference between restrictive (≤40 mL/kg) and liberal (> 40 mL/kg) strategies, but reduced fluid overload with restrictive. [5]

However, in low-resource settings without intensive monitoring or mechanical ventilation, the FEAST trial (2011) in African children showed a shocking finding: bolus fluid resuscitation (20-40 mL/kg) increased mortality by 45% compared to no bolus, with deaths attributed to cardiovascular collapse and cerebral oedema. [6] This fundamentally changed practice in resource-limited settings, where WHO now recommends cautious fluid administration with close monitoring.

The key is context: in well-monitored environments, early aggressive fluids save lives; in settings without ventilatory and monitoring support, they may harm. This highlights the importance of individualised care, continuous reassessment after each bolus, and stopping fluids if signs of overload develop (hepatomegaly, pulmonary oedema)."

---

Viva Points

Viva Point: Opening Statement (if asked to "Tell me about paediatric sepsis"):

"Paediatric sepsis is defined by the 2024 Phoenix Sepsis Criteria as a Phoenix Sepsis Score of ≥2 in a child with suspected infection, indicating life-threatening organ dysfunction. [1] It is a leading cause of childhood mortality globally, with over 3 million deaths annually. [2] Mortality ranges from 7% in high-resource settings to 28% in low-resource settings for sepsis, and up to 10-33% for septic shock. [1] The cornerstone of management is early recognition using Phoenix criteria, immediate ABCDE resuscitation with rapid fluid boluses, and urgent IV antibiotics within 1 hour. [3,4] The Phoenix criteria assess four organ systems—respiratory, cardiovascular, coagulation, and neurological—and have replaced the outdated SIRS-based 2005 criteria."

Key Statistics to Quote:

• Phoenix Score ≥2: Mortality 7.1% (high-resource) to 28.5% (low-resource) [1]
• Septic shock mortality: 10.8-33.5% [1]
• 1-hour antibiotic bundle reduces mortality by 40% [22]
• FEAST trial: 45% increased mortality with bolus fluids in low-resource settings [6]

Classifications to Know:

• Phoenix Sepsis Score (4 organ systems, 0-4 points each)
• Age-specific vital sign ranges [7,18]
• Age-specific hypotension thresholds

Evidence to Cite:

• Phoenix Criteria (Schlapbach et al., JAMA 2024) [1]
• Surviving Sepsis Campaign 2020 [3]
• Evans 1-hour bundle study (JAMA 2018) [22]
• FEAST trial (Maitland et al., NEJM 2011) [6]

Common Mistakes (What Fails Candidates)

❌ Using outdated 2005 SIRS-based sepsis definitions instead of 2024 Phoenix criteria

❌ Waiting for blood cultures or other investigations before giving antibiotics – antibiotics within 1 hour is critical, cultures should not delay

❌ Inadequate fluid resuscitation in high-resource settings (giving only 10-20 mL/kg when 40-60 mL/kg indicated)

❌ Using dopamine as first-line vasoactive agent – noradrenaline or adrenaline are recommended [3]

❌ Failure to recognise compensated shock in children (normal BP does not exclude shock—look for prolonged CRT, tachycardia, mottled skin)

❌ Performing LP in unstable septic child – stabilise first, LP later

❌ Not knowing age-specific vital signs – vital for identifying tachycardia, tachypnoea, hypotension

❌ Not escalating to PICU when indicated (septic shock, multi-organ dysfunction, need for vasoactive support)

---

13. Patient/Layperson Explanation

What is Sepsis?

Sepsis is a very serious condition where your child's body has an overwhelming response to an infection. Normally, when your child gets an infection (like a chest infection or urine infection), their immune system fights it off. But in sepsis, the immune system "overreacts"—instead of just fighting the infection, it starts to damage the body's own organs. This can affect the heart, lungs, kidneys, brain, and other organs, and can be life-threatening.

Think of it like a fire alarm: normally, the alarm warns you about a small fire, and you put it out. But in sepsis, the alarm system goes haywire and starts spraying water everywhere, damaging your whole house—not just putting out the fire.

In simple terms: Sepsis is when an infection makes your child's whole body very sick, not just the part that's infected. It's a medical emergency and needs urgent hospital treatment, but with early treatment, most children recover completely.

Why Does It Matter?

Sepsis is one of the leading causes of death in children worldwide, but it is treatable if caught early. The key is recognising it quickly and getting your child to hospital immediately. Every hour counts—the earlier we give antibiotics and fluids, the better the outcome.

The good news: With prompt treatment (antibiotics, fluids, and sometimes intensive care), 90-95% of children in developed countries survive sepsis and recover fully.

How is it Treated?

1. Hospital Admission (Always Required)

• All children with sepsis need to be admitted to hospital
• Many will need intensive care (PICU)
• Your child will be monitored very closely (heart rate, blood pressure, oxygen levels)

2. Fluids (Given Through a Drip)

• We give fluids directly into your child's vein through a drip (IV)
• This helps support their blood pressure and improve blood flow to organs
• They may need large amounts of fluid quickly (this is normal and important)

3. Antibiotics (Given Through a Drip, URGENTLY)

• We give strong antibiotics through the drip within 1 hour of recognising sepsis
• These fight the infection causing sepsis
• We often start with "broad-spectrum" antibiotics (cover many types of germs) and then adjust once we know the exact germ

4. Oxygen

• If your child is struggling to breathe or has low oxygen levels, we give extra oxygen
• Some children need help with a breathing machine (ventilator)

5. Medications to Support Blood Pressure (If Needed)

• If your child's blood pressure is very low despite fluids, we may give medications (called "inotropes" or "vasopressors") to help
• These are given through a drip in intensive care

6. Treating the Source

• We try to find where the infection started (urine, chest, etc.) and treat it
• Sometimes this needs surgery (e.g., draining an abscess)

7. Other Support

• Monitoring and supporting organs (kidneys, liver, blood clotting)
• Nutrition (feeding through a tube if needed)
• Pain relief

What to Expect

In Hospital:

• First few hours: Intensive treatment—lots of doctors and nurses, lots of monitoring, your child may look very unwell initially
• First 1-3 days: We expect improvement with treatment—temperature coming down, blood pressure improving, your child becoming more alert
• Recovery: Most children improve within 3-5 days and can move out of intensive care. Total hospital stay is usually 7-14 days, but can be longer.

After Treatment:

• Most children recover completely and can go back to normal activities
• Some may need physiotherapy or rehabilitation if they were very unwell
• We may arrange follow-up appointments to check for any long-term effects
• A small number of children may have lasting effects (hearing problems, learning difficulties, physical weakness)—we monitor for these

Recovery Time:

• Mild sepsis: May recover in a few days
• Severe sepsis/shock: May take weeks to fully recover
• Back to school/nursery: Usually 2-4 weeks after discharge (depends on individual case)

When to Seek Help IMMEDIATELY (Call 999)

Red Flags – Call 999 or Go to Emergency Department Immediately If Your Child Has:

✅ Mottled, bluish, or very pale skin

✅ A rash that doesn't fade when you press a glass on it (purpura/petechiae)

✅ Very difficult or fast breathing

✅ Confusion, extreme sleepiness, or difficulty waking up

✅ Very cold hands and feet

✅ Not passed urine for > 12 hours

✅ High fever (> 38°C) AND looking very unwell (floppy, not responding normally, very irritable)

✅ You are very worried—trust your instincts

When to See Your Doctor (Same Day)

• Fever and your child seems more unwell than you'd expect
• Persistent vomiting or diarrhoea with signs of dehydration
• Not drinking or feeding well
• "Not themselves" (parent's gut feeling)

Remember: Sepsis is a medical emergency. If you're worried, don't wait—call 999 or go straight to the Emergency Department. It's always better to be checked and sent home than to wait and risk your child becoming more unwell.

---

14. Clinical Scenarios & Case-Based Learning

Scenario 1: Neonatal Sepsis

Presentation: A 10-day-old infant is brought to ED by parents. Mother reports poor feeding for 12 hours, "floppy", decreased urine output. Temperature 36.2°C (axillary).

Examination:

• HR 180 bpm, RR 65/min, BP 55/30 mmHg, SpO₂ 94% in air
• Lethargic, weak cry, mottled skin
• CRT 4 seconds, cold peripheries
• Soft anterior fontanelle, normal tone

Phoenix Score Calculation:

• Cardiovascular: 2 points (MAP less than 2 SD below normal for age)
• Respiratory: 0 points
• Neurological: 1 point (lethargic, but GCS equivalent ~13)
• Coagulation: Pending bloods
• Total: ≥2 = SEPSIS

Immediate Management:

1. ABCDE: High-flow oxygen, establish IV access (or IO if difficult)
2. Fluid bolus: 20 mL/kg 0.9% saline over 5-10 minutes
3. Blood cultures, FBC, CRP, lactate, blood gas, glucose
4. Antibiotics within 1 hour: Benzylpenicillin 50 mg/kg IV + Gentamicin 5 mg/kg IV (covers GBS, E. coli, Listeria)
5. Reassess after fluid bolus—if persistent shock, repeat 20 mL/kg
6. NICU admission, senior review

Blood Cultures: Grew Group B Streptococcus (GBS) at 18 hours

Outcome: Responded to fluid resuscitation and antibiotics, completed 14 days IV therapy, full recovery.

Learning Points:

• Neonates with sepsis often hypothermic rather than febrile
• Hypotension in neonate is late, ominous sign
• Early-onset neonatal sepsis: GBS, E. coli, Listeria—cover with benzylpenicillin + gentamicin
• Phoenix criteria validated for term neonates ≥37 weeks, ≥2.5 kg

---

Scenario 2: Meningococcal Septicaemia

Presentation: 3-year-old girl, previously well, presents with 6-hour history of fever (39.5°C), vomiting, drowsiness. Parent noticed "purple spots" on legs in last hour.

Examination:

• HR 160 bpm, RR 40/min, BP 70/40 mmHg (low for age), SpO₂ 96% in air
• Drowsy (GCS 12: E3 V4 M5), pale, mottled
• CRT 5 seconds, cold hands/feet
• Non-blanching purpuric rash on legs and trunk
• Neck supple (no clear meningism)

Phoenix Score:

• Cardiovascular: 2 points (hypotension, likely lactate elevated)
• Neurological: 1 point (GCS 12)
• Respiratory: 0 points
• Total: 3 = SEPTIC SHOCK

Immediate Management:

1. Do NOT wait—this is meningococcal sepsis until proven otherwise
2. Establish IV/IO access immediately
3. Fluid bolus: 20 mL/kg 0.9% saline rapidly
4. Ceftriaxone 100 mg/kg IV STAT (within 10 minutes if possible)
5. Blood cultures, FBC, coagulation, lactate, blood gas
6. Senior/PICU review immediately
7. Second fluid bolus: 20 mL/kg (total 40 mL/kg)
8. If still shocked: Commence noradrenaline infusion
9. Do NOT perform LP (unstable, likely coagulopathy)
10. Public health notification

Investigations:

• Lactate 6.2 mmol/L, platelets 85 × 10⁹/L, INR 1.8
• Blood culture: Neisseria meningitidis serogroup B

Outcome: Required 60 mL/kg fluids + noradrenaline, PICU 5 days, survived with full recovery.

Learning Points:

• Non-blanching purpuric rash + shock = meningococcal sepsis—treat immediately
• Do NOT delay antibiotics for LP or any investigation
• Ceftriaxone covers meningococcus adequately
• High fluid requirements common (40-60 mL/kg)
• Public health: Prophylaxis for household contacts (ciprofloxacin/rifampicin)

---

Scenario 3: Fluid Resuscitation Decision-Making

Presentation: 18-month-old with 24-hour history of diarrhoea/vomiting, fever 38.8°C, poor oral intake. Tachycardic (HR 170), BP 85/50 (normal for age), CRT 3 seconds, sunken fontanelle, dry mucous membranes.

Phoenix Score:

• Cardiovascular: 0 points (normal BP, lactate 2.2 mmol/L)
• Respiratory: 0 points
• Neurological: 0 points (alert, GCS 15)
• Total: 0 = Suspected infection WITHOUT sepsis

Question: Does this child need aggressive fluid resuscitation?

Answer: No—this child has gastroenteritis with dehydration, but NOT sepsis (Phoenix less than 2). Management:

• Oral rehydration solution (ORS) if tolerating
• If not tolerating oral: IV fluids at maintenance + deficit replacement (NOT boluses unless shocked)
• Reassess frequently for deterioration

If Phoenix Score ≥2 develops (e.g., becomes hypotensive, altered mental status, lactate > 2):

• Now SEPSIS → Commence sepsis management with fluid boluses

Learning Point: Not all febrile, dehydrated children have sepsis. Use Phoenix criteria to distinguish sepsis (needs aggressive resuscitation) from simple dehydration (needs rehydration, not boluses).

---

Scenario 4: Source Control—Appendicitis with Peritonitis

Presentation: 12-year-old boy, 3-day abdominal pain, now severe RIF pain, fever 39.2°C, vomiting, unable to walk (peritonitic gait).

Examination:

• HR 135 bpm, RR 28/min, BP 95/60 mmHg, SpO₂ 98%
• Alert but in pain
• CRT 2 seconds, warm peripheries
• Rigid abdomen, severe RIF tenderness, guarding, rebound

Phoenix Score:

• All systems: 0 points (no organ dysfunction yet)
• Total: 0 = Infection without sepsis (at presentation)

Initial Management:

1. Analgesia (IV morphine)
2. IV access, bloods (FBC, CRP, U&E, lactate, blood cultures)
3. IV fluids: Maintenance (NOT boluses—no shock)
4. Antibiotics: Ceftriaxone 50 mg/kg + Metronidazole 7.5 mg/kg IV
5. Surgical review
6. USS abdomen (or CT if needed)

USS: Perforated appendicitis, loculated abscess

Surgical Plan: Laparoscopic appendicectomy + peritoneal washout

48 Hours Later: Post-op, child develops fever 38.9°C, tachycardia (HR 150), hypotension (BP 75/40), oliguria.

Phoenix Score Now:

• Cardiovascular: 2 points (hypotension, lactate 4.1 mmol/L)
• Total: 2 = SEPSIS (post-operative intra-abdominal sepsis)

Management:

1. Fluid boluses: 20 mL/kg × 2
2. Escalate antibiotics: Piperacillin-tazobactam + gentamicin (broader Gram-negative, anaerobic cover)
3. Repeat imaging: CT shows residual abscess
4. Further source control: Percutaneous drainage of abscess
5. PICU transfer

Outcome: Responded to drainage + antibiotics, recovered.

Learning Points:

• Source control is as important as antibiotics—drainage/surgery often life-saving
• Post-operative sepsis: Broaden antibiotics (consider hospital-acquired, resistant organisms)
• Phoenix criteria useful for identifying post-op sepsis
• Don't delay source control (abscess drainage, surgical washout)

---

Scenario 5: Antibiotic Timing Critical

Two Presentations, Same Diagnosis, Different Outcomes:

Patient A:

• 4-year-old, fever + drowsiness, arrives ED 18:00
• Phoenix Score 3 (sepsis)
• Blood cultures taken 18:05
• Antibiotics given 18:20 (20 minutes after arrival)
• Fluid resuscitation commenced
• Outcome: Responded well, PICU 2 days, discharged day 5

Patient B:

• 4-year-old, fever + drowsiness, arrives ED 18:00
• Phoenix Score 3 (sepsis)
• Blood cultures taken 18:05, waited for senior review
• Chest X-ray requested (waited 40 minutes)
• Antibiotics given 20:15 (2 hours 15 minutes after arrival)
• Fluid resuscitation commenced
• Outcome: Deteriorated to multi-organ failure, PICU 10 days, long-term morbidity

Evidence: Each hour of antibiotic delay increases mortality odds ratio by 1.06-1.40. [4,22] Patient B's 2-hour delay potentially doubled mortality risk compared to Patient A.

Learning Point: DO NOT DELAY ANTIBIOTICS. The 1-hour rule is evidence-based and saves lives. Investigations (X-rays, waiting for senior review) must NOT delay antibiotics.

---

Scenario 6: Recognising Compensated vs Decompensated Shock

Case: 8-year-old with pneumonia, fever 39.5°C.

Examination A (Compensated Shock):

• HR 150 bpm (high), RR 35/min, BP 100/65 mmHg (NORMAL for age)
• Alert but lethargic
• CRT 4 seconds, mottled legs, cold feet
• Urine output 0.3 mL/kg/hr (low)

Phoenix Score: 1-2 points (tachycardia, prolonged CRT, but normal BP)

Interpretation: COMPENSATED SHOCK—child maintaining BP through tachycardia and vasoconstriction, but poor perfusion. This is still sepsis/shock—treat aggressively.

Examination B (Same Child, 30 Minutes Later—No Treatment):

• HR 180 bpm, RR 45/min, BP 70/40 mmHg (HYPOTENSIVE)
• Drowsy (GCS 12)
• CRT 6 seconds, very pale, cold extremities
• Anuric

Phoenix Score: ≥3 points (hypotension, altered mental status)

Interpretation: DECOMPENSATED SHOCK—lost compensatory mechanisms, now hypotensive. Critically unwell, needs immediate aggressive resuscitation + vasoactive support.

Learning Point:

• Normal BP does NOT exclude shock in children—they compensate well initially
• Look for: prolonged CRT, mottled skin, tachycardia out of proportion to fever, low urine output
• Hypotension = decompensated shock = LATE sign → very sick child
• Treat compensated shock aggressively to prevent decompensation

---

15. References

1. Schlapbach LJ, Watson RS, Sorce LR, et al. International Consensus Criteria for Pediatric Sepsis and Septic Shock. JAMA. 2024;331(8):665-674. doi:10.1001/jama.2024.0179

2. Rudd KE, Johnson SC, Agesa KM, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study. Lancet. 2020;395(10219):200-211. doi:10.1016/S0140-6736(19)32989-7

3. Weiss SL, Peters MJ, Alhazzani W, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med. 2020;21(2):e52-e106. doi:10.1097/PCC.0000000000002198

4. Weiss SL, Fitzgerald JC, Balamuth F, et al. Delayed antimicrobial therapy increases mortality and organ dysfunction duration in pediatric sepsis. Crit Care Med. 2014;42(11):2409-2417. doi:10.1097/CCM.0000000000000509

5. Sankar J, Sankar MJ, Suresh CP, Dubey N, Singh A. Early goal-directed therapy in pediatric septic shock: Comparison of outcomes "with" and "without" intermittent superior vena cava oxygen saturation monitoring: A prospective cohort study. Pediatr Crit Care Med. 2014;15(4):e157-e167. doi:10.1097/PCC.0000000000000073

6. Maitland K, Kiguli S, Opoka RO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011;364(26):2483-2495. doi:10.1056/NEJMoa1101549

7. Fleming S, Thompson M, Stevens R, et al. Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies. Lancet. 2011;377(9770):1011-1018. doi:10.1016/S0140-6736(10)62226-X

8. Evans IVR, Phillips GS, Alpern ER, et al. Association Between the New York Sepsis Care Mandate and In-Hospital Mortality for Pediatric Sepsis. JAMA. 2018;320(4):358-367. doi:10.1001/jama.2018.9071

9. Carlton EF, Gebremariam A, Maddux AB, et al. New and progressive medical conditions after pediatric sepsis hospitalization requiring critical care. JAMA Pediatr. 2022;176(11):e223554. doi:10.1001/jamapediatrics.2022.3554

10. Weiss SL, Fitzgerald JC, Pappachan J, et al. Global epidemiology of pediatric severe sepsis: the Sepsis Prevalence, Outcomes, and Therapies (SPROUT) study. Am J Respir Crit Care Med. 2015;191(10):1147-1157. doi:10.1164/rccm.201412-2323OC

11. Balamuth F, Weiss SL, Neuman MI, et al. Pediatric severe sepsis in U.S. children's hospitals. Pediatr Crit Care Med. 2014;15(9):798-805. doi:10.1097/PCC.0000000000000225

12. Ruth A, McCracken CE, Fortenberry JD, Hall M, Simon HK, Hebbar KB. Pediatric severe sepsis: current trends and outcomes from the Pediatric Health Information Systems database. Pediatr Crit Care Med. 2014;15(9):828-838. doi:10.1097/PCC.0000000000000254

13. Reinhart K, Daniels R, Kissoon N, Machado FR, Schachter RD, Finfer S. Recognizing sepsis as a global health priority—a WHO resolution. N Engl J Med. 2017;377(5):414-417. doi:10.1056/NEJMp1707170

14. Wiens MO, Pawluk S, Kissoon N, et al. Pediatric post-discharge mortality in resource poor countries: a systematic review and meta-analysis. PLoS One. 2013;8(6):e66698. doi:10.1371/journal.pone.0066698

15. Alcoba G, Manzano S, Lacroix L, Galetto-Lacour A, Gervaix A. Procalcitonin and bacterial meningitis: a meta-analysis. Arch Dis Child. 2013;98(10):799-805. doi:10.1136/archdischild-2013-303838

16. Ladhani SN, Collins S, Djennad A, et al. Rapid increase in non-vaccine serotypes causing invasive pneumococcal disease in England and Wales, 2000-17: a prospective national observational cohort study. Lancet Infect Dis. 2018;18(4):441-451. doi:10.1016/S1473-3099(18)30052-5

17. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006;34(6):1589-1596. doi:10.1097/01.CCM.0000217961.75225.E9

18. Bonafide CP, Brady PW, Keren R, Conway PH, Marsolo K, Daymont C. Development of heart and respiratory rate percentile curves for hospitalized children. Pediatrics. 2013;131(4):e1150-e1157. doi:10.1542/peds.2012-2443

19. Wynn JL, Wong HR. Pathophysiology and treatment of septic shock in neonates. Clin Perinatol. 2010;37(2):439-479. doi:10.1016/j.clp.2010.04.002

20. 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. Crit Care Med. 2009;37(2):666-688. doi:10.1097/CCM.0b013e31819323c6

21. Van den Bruel A, Thompson M, Buntinx F, Mant D. Clinicians' gut feeling about serious infections in children: observational study. BMJ. 2012;345:e6144. doi:10.1136/bmj.e6144

22. Evans IVR, Phillips GS, Alpern ER, et al. Association Between the New York Sepsis Care Mandate and In-Hospital Mortality for Pediatric Sepsis. JAMA. 2018;320(4):358-367. doi:10.1001/jama.2018.9071

23. Alvarez EML, Vázquez Martínez JL. Dopamine versus norepinephrine in the treatment of septic shock: A meta-analysis. Crit Care Med. 2019;47(1):e44. doi:10.1097/CCM.0000000000003520

24. Menon K, McNally D, Choong K, et al. A survey of stated physician practices and beliefs on the use of steroids in pediatric fluid and/or vasoactive infusion-dependent shock. Pediatr Crit Care Med. 2013;14(5):462-466. doi:10.1097/PCC.0b013e31828a7287

25. Starr MC, Banks R, Reeder RW, et al. Severe acute kidney injury is associated with increased risk of death and new morbidity after pediatric septic shock. Pediatr Crit Care Med. 2020;21(9):e686-e695. doi:10.1097/PCC.0000000000002418

26. Zimmerman JJ, Banks R, Berg RA, et al. Critical illness factors associated with long-term mortality and health-related quality of life morbidity following community-acquired pediatric septic shock. Crit Care Med. 2020;48(3):319-328. doi:10.1097/CCM.0000000000004122

27. Graciano AL, Balko JA, Rahn DS, Ahmad N, Giroir BP. The Pediatric Multiple Organ Dysfunction Score (P-MODS): development and validation of an objective scale to measure the severity of multiple organ dysfunction in critically ill children. Crit Care Med. 2005;33(7):1484-1491. doi:10.1097/01.ccm.0000170943.23633.47

28. Scott HF, Brou L, Deakyne SJ, Kempe A, Fairclough DL, Bajaj L. Lactate clearance and normalization and prolonged organ dysfunction in pediatric sepsis. J Pediatr. 2016;170:149-155.e1-4. doi:10.1016/j.jpeds.2015.11.071

29. UK Sepsis Trust. Paediatric Sepsis Recognition Tools. https://sepsistrust.org/professional-resources/clinical/

30. National Institute for Health and Care Excellence. Sepsis: recognition, diagnosis and early management. NICE guideline [NG51]. Published September 2016. Updated July 2017. https://www.nice.org.uk/guidance/ng51

---

Last Reviewed: 2026-01-10 | MedVellum Editorial Team

---

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and local guidelines. This information is not a substitute for professional medical advice, diagnosis, or treatment.