EPLS/PALS Structured Approach, Types of Shock, and Weight-Based Fluid Boluses

Paediatric Resuscitation, Shock Syndromes, and Critical Fluid Management

In acute paediatric critical care, clinical outcomes depend directly upon rapid recognition of physiological deterioration and systematic resuscitation before cardiopulmonary arrest supervenes. Unlike adult cardiac arrest, which typically results from primary arrhythmia secondary to atherosclerotic coronary artery disease (such as ventricular fibrillation), paediatric cardiopulmonary arrest is almost universally secondary. It represents the final common pathway of unreversed, progressive respiratory failure or circulatory shock culminating in severe tissue hypoxia, profound mixed acidosis, bradycardia, and asystole.

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The Structured ABCDE Resuscitation Paradigm

The European Paediatric Life Support (EPLS) and Paediatric Advanced Life Support (PALS) guidelines mandate a structured, rapid, hierarchical evaluation prioritizing life threats via the ABCDE approach:

Airway (A)

• Patency Assessment: Determine whether the airway is clear, maintainable with simple positional maneuvers or adjuncts, or unmaintainable (requiring immediate advanced airway intervention).
• Anatomical Nuances: Infants possess a large, prominent occiput causing spontaneous neck flexion when supine, a large tongue relative to the oral cavity, high anterior funnel-shaped larynx with the narrowest point historically described at the cricoid ring, and a floppy U-shaped epiglottis angled at 45 degrees.
• Positioning: Place the child in a neutral sniffing position (avoid hyperextension or hyperflexion). In infants under 1 year, place a 2 to 3 cm folded towel or roll beneath the shoulders to offset the prominent occiput.

Breathing (B)

• Work of Breathing: Evaluate for tachypnoea, subcostal, intercostal, and suprasternal retractions, sternal recession, nasal flaring, and expiratory grunting (an involuntary compensatory mechanism where the infant exhales against a partially closed glottis to generate intrinsic positive end-expiratory pressure [PEEP] and prevent alveolar atelectasis).
• Auscultation and Gas Exchange: Assess air entry bilaterally, presence of stridor (upper airway obstruction), wheeze (lower airway obstruction), or crackles (alveolar fluid/pneumonia). Measure pulse oximetry ($SpO_2$) and end-tidal $CO_2$ ($EtCO_2$) when available.

Circulation (C)

• Perfusion and Rhythm: Assess heart rate (the earliest and most sensitive physiological indicator of shock), peripheral versus central pulse volume, capillary refill time (CRT) (measured over the sternum or fingertip for 5 seconds after blanching; normal is $\le 2$ seconds), core-to-peripheral temperature gradient, skin mottling, and blood pressure.
• End-Organ Function: Assess urine output (normal infant $>1.5\text{ to }2\text{ mL/kg/h}$, child $>1\text{ mL/kg/h}$, adolescent $>0.5\text{ mL/kg/h}$) and mental status.

Disability (D)

• Neurological State: Rapid assessment using the AVPU scale (Alert, responds to Voice, responds to Pain, Unresponsive) or the Paediatric Glasgow Coma Scale (pGCS).
• Pupillary Signs: Check pupil symmetry, size, and reactivity to light.
• Metabolic Screen: Immediate bedside blood glucose testing is mandatory in every unstable paediatric patient. Hypoglycaemia must be identified and corrected immediately.

Exposure (E)

• Full Examination: Undress the patient fully to inspect for petechial or purpuric rashes (e.g., meningococcal septicaemia), urticaria, angioedema, occult surgical trauma, or abdominal distension.
• Thermal Integrity: Strictly protect against hypothermia; wrap exposed body regions, use radiant warmers, and infuse warmed fluids.

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Paediatric Cardiovascular Physiology: Why Children Deteriorate Rapidly

Paediatric cardiovascular physiology differs fundamentally from adult physiology across several critical parameters:

1. Heart Rate and Cardiac Output: The neonatal and infant myocardium has immature contractile structures and limited functional reserve. Stroke volume can increase with appropriate preload, but infants have less reserve than older children; heart rate is therefore an important determinant of output: $\text{Cardiac Output (CO)} = \text{Stroke Volume (SV)} \times \text{Heart Rate (HR)}$ Tachycardia commonly accompanies compensation for shock. Marked bradycardia with poor perfusion is dangerous and requires urgent correction of causes such as hypoxaemia. A fall in heart rate alone does not establish circulatory collapse; assess perfusion and the clinical context. Stroke-volume and contractile reserve increase with maturation.
2. High Basal Metabolic Demand: A resting infant consumes approximately $6\text{ to }8\text{ mL } O_2/\text{kg/min}$, more than double the adult basal requirement of $3\text{ to }4\text{ mL } O_2/\text{kg/min}$. This elevated metabolic demand accelerates oxygen desaturation during hypoventilation or hypoperfusion.
3. Compliant Thoracic Cage: The infant rib cage is largely cartilaginous with horizontal rib orientation, providing minimal bony splinting. When respiratory muscle fatigue occurs, negative intrathoracic pressures cause chest wall collapse (paradoxical breathing) rather than effective alveolar inflation, precipitating rapid ventilatory exhaustion.

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Compensated versus Decompensated Shock

Circulatory shock is defined as a state of acute circulatory failure leading to inadequate tissue perfusion and cellular oxygen delivery relative to metabolic demand.

[Systemic Insult / Fluid Loss / Sepsis]
                     |
                     v
          [Compensated Shock]
  - Intense Sympathetic Vasoconstriction
  - Persistent Tachycardia (earliest sign)
  - Prolonged Capillary Refill Time (>2 sec)
  - Cool, Pale, Mottled Extremities
  - Decreased Urine Output (<1 mL/kg/h)
  - Normal Systolic Blood Pressure (MAINTAINED!)
                     |
        (If Unrecognized / Untreated)
                     v
         [Decompensated Shock]
  - Compensatory Mechanisms Exhausted
  - Severe Acidosis and Tissue Hypoxia
  - Lethargy, Stupor, or Coma
  - Weak or Absent Central Pulses
  - HYPOTENSION (Late, Pre-Terminal Sign!)
                     |
                     v
            [Cardiopulmonary Arrest]

Compensated Shock

In compensated shock, neurohumoral mechanisms—including massive sympathetic adrenergic discharge, release of antidiuretic hormone (ADH), and activation of the renin-angiotensin-aldosterone axis—induce marked peripheral vasoconstriction and selective shunting of blood to the cerebral and coronary vascular beds.

• Clinical Signs: Tachycardia, cool and mottled distal extremities, prolonged capillary refill time ($>2\text{ seconds}$), diminished peripheral pulse volume, narrow pulse pressure, tachypnoea, and mild oliguria.
• Blood Pressure: Systolic blood pressure remains within the normal range. Relying on blood pressure to rule out shock in a child is a catastrophic clinical error.

Decompensated Shock

When compensatory systemic vasoconstriction can no longer overcome the profound fluid deficit, myocardial exhaustion, or widespread microvascular paralysis, cellular oxygen delivery collapses.

• Clinical Signs: Marked hypotension, weak or impalpable central pulses (femoral/carotid), cold clammy skin, profound lethargy, coma, and severe metabolic lactic acidosis with respiratory compensation (Kussmaul breathing).
• Significance: Hypotension is a late, pre-terminal sign. Once a child becomes hypotensive from shock, cardiac arrest is imminent within minutes without aggressive resuscitation.

Common PALS Screening Thresholds for Hypotension

Examples using the PALS rule of thumb: Systolic BP below 76 mmHg at 3 years ($70 + [2 \times 3]$) or84 mmHg at 7 years ($70 + [2 \times 7]$) flags hypotension. These are screening thresholds, not exact ERC 2025 percentiles or a diagnosis by themselves. Hypotension together with poor perfusion supports decompensated shock; normal BP does not exclude shock.

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Differential Diagnosis and Classification of Shock

Paediatric shock is categorized into four primary pathophysiological classes:

Ductal-Dependent Cardiac Lesions in the Neonate

A vital consideration in any neonate presenting between 7 and 14 days of life in severe, unexplained shock with profound metabolic acidosis is closure of the ductus arteriosus unmasking a ductal-dependent cardiac anomaly:

• Systemic ductal-dependent lesions: Critical coarctation of the aorta, interrupted aortic arch, critical aortic stenosis, and hypoplastic left heart syndrome (HLHS). As the ductus arteriosus closes, systemic perfusion to the lower body ceases, producing weak or absent femoral pulses, differential cyanosis, severe oliguria, and profound cardiogenic/obstructive shock.
• Management: Immediate continuous intravenous infusion of Prostaglandin E1 (Alprostadil) at an initial dose of $0.05\text{ to }0.1\text{ micrograms/kg/min}$. Major adverse effects of alprostadil include severe apnoea (requiring readiness for immediate endotracheal intubation), vasodilation, hypotension, and hyperthermia.

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Precision Weight-Based Fluid Resuscitation

Fluid administration in paediatric shock must be tailored to the underlying pathophysiology and accompanied by repeated, rigorous clinical reassessment:

               [Suspected Paediatric Shock]
                            |
           Identify Underlying Pathophysiology
          /                 |                 \
   [Hypovolaemic]       [Septic]        [Cardiogenic]
         |                  |                 |
 Balanced crystalloid  Balanced crystalloid   Early expert-guided
 10 mL/kg aliquot      10 mL/kg aliquot       inotropic support
         |                  |                 |
         |                  |            Fluid only if needed:
         |                  |            cautiously, e.g.5 mL/kg
         +------------------+-----------------+
                            |
             [Reassess after every bolus]
       - Heart rate, capillary refill, pulse volume
       - Liver edge, lung crackles, gallop, jugular veins
       - Blood pressure, mental status, urine output
       - Stop boluses for overload or resolved shock
       - Persistent shock: start vasoactive support early
         (ERC: no later than 30–40 mL/kg)

Fluid Selection: Balanced Crystalloids

Resuscitation fluid should be an isotonic crystalloid. Modern clinical practice strongly favors balanced isotonic crystalloids (e.g., Plasmalyte, Hartmann's solution, or Ringer's lactate) over $0.9\%$ normal saline. Large-volume administration of $0.9\%$ normal saline delivers an unphysiologically high chloride load ($154\text{ mmol/L}$ vs normal plasma $98-106\text{ mmol/L}$), producing hyperchloraemic metabolic acidosis, renal vasoconstriction, and decreased glomerular filtration rate.

Resuscitation Volumes and Rates

1. Hypovolaemic and Septic Shock:
   • ERC 2025 recommends prompt $10\text{ mL/kg}$ aliquots of balanced isotonic crystalloid; use0.9% saline if unavailable.
   • Reassess after every bolus: heart rate, CRT, pulses, mental status, BP, urine output, liver edge and lung signs. Stop boluses when shock resolves or overload develops.
   • A total $40\text{ to }60\text{ mL/kg}$ may be needed in the first hour, but is not a prerequisite for vasoactive support. Start this early for persistent shock, no later than $30\text{ to }40\text{ mL/kg}$ under ERC guidance.
   • SSC 2026, for septic shock with intensive-care availability, permits $10\text{–}20\text{ mL/kg}$ aliquots up to 40–60 mL/kg in the first hour, with the same reassessment and overload safeguards.
2. Cardiogenic Shock:
   • Large rapid boluses can precipitate pulmonary oedema. Seek cardiology/intensive-care advice and start inotropic support early.
   • Give fluid only when the assessment suggests it is needed, cautiously (e.g. $5\text{ mL/kg}$), with immediate cardiopulmonary reassessment.
3. Diabetic Ketoacidosis (DKA):
   • ISPAD 2022 recommends $10\text{–}20\text{ mL/kg}$ of 0.9% saline over20–30 minutes for volume depletion without shock; use20 mL/kg when perfusion is poor. In shock, give rapid20 mL/kg aliquots with reassessment.
   • Then replace the remaining deficit with maintenance over24–48 hours. Avoid unnecessary fluid restriction: tested fluid regimens did not differ in cerebral-injury risk. Monitor circulation, neurological status and electrolytes closely.
4. Haemorrhagic Shock:
   • If the child shows ongoing blood loss or fails to stabilize after an initial crystalloid bolus of $20\text{ mL/kg}$, administer $10\text{ mL/kg}$ of Packed Red Blood Cells (PRBCs) (uncrossmatched O-negative blood in extremis) and activate the institutional paediatric massive transfusion protocol (incorporating PRBCs, fresh frozen plasma, and platelets in a balanced 1:1:1 ratio).

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Vasoactive Inotropes and Vasopressors

For persistent shock, start vasoactive support early according to the haemodynamic problem. ERC 2025 advises initiation no later than after three to four10 mL/kg boluses ($30\text{–}40\text{ mL/kg}$), or sooner when fluid is inappropriate, overload develops or cardiogenic shock is recognised. Do not wait to give40–60 mL/kg:

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Emergency Intraosseous (IO) Access

In a critically ill, decompensating child, peripheral veins collapse rapidly due to severe adrenergic vasoconstriction. Repeated, unsuccessful attempts at peripheral cannulation consume precious minutes and worsen mortality.

Clinical Indication

• ERC 2025: In shock, do not spend more than 5 minutes or two attempts establishing IV access. Use intraosseous (IO) access if IV access fails or is unlikely to succeed. In a collapsed child, establish access promptly rather than repeating unsuccessful IV attempts.

Anatomical Sites

1. Proximal Tibia (Primary Site):
   • Landmark: Anteromedial surface of the proximal tibia, approximately $1\text{ to }2\text{ cm}$ below (distal to) the tibial tuberosity (or $1\text{ to }2\text{ cm}$ distal to the patella and slightly medial on the broad, flat bony plateau in infants where the tuberosity is not yet palpable).
   • The needle is inserted perpendicular to the bone (90 degrees) or angled slightly distal (10–15 degrees away from the joint space) to avoid penetrating the epiphyseal growth plate.
2. Alternative Sites:
   • Distal femur: $1\text{ to }2\text{ cm}$ superior to the femoral condyles in the midline anteriorly.
   • Distal tibia: $1\text{ to }2\text{ cm}$ proximal to the medial malleolus on its flat anteromedial surface.
   • Proximal humerus: Greater tubercle (predominantly in older children and adolescents).

Contraindications to IO Insertion

• Fracture of the target bone (fluid extravasates into compartments through the fracture line).
• Previous IO attempt or placement in the same bone within the preceding 48 hours (fluid extravasates through the prior cortical drill hole).
• Local skin infection, cellulitis, or severe burn overlying the insertion site.
• Severe osteogenesis imperfecta or osteopetrosis.

Administration and Therapeutics

• Pharmacokinetics: The intraosseous medullary cavity is a non-collapsible venous plexus. Any resuscitation drug, fluid, whole blood or blood product, electrolyte, or antibiotic that can be administered intravenously can be administered via the IO route at identical doses.
• Infusion Technique: Because intramedullary venous resistance is high, fluids do not free-flow by gravity alone; boluses must be administered under manual pressure using a syringe with a three-way stopcock ("push-pull technique") or an automated pressure infusion bag inflated to $300\text{ mmHg}$.

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Paediatric Cardiac Arrest: Basic and Advanced Life Support

Paediatric arrest is usually secondary to hypoxia or shock, so effective ventilation is as important as compressions. The European Resuscitation Council (ERC) 2025 guideline gives the following sequence.

Basic Life Support

• If a child is unresponsive and not breathing normally, call for help and the emergency medical service as soon as cardiac arrest is suspected.
• Open the airway (neutral head position in infants, sniffing position in children) and give 5 initial rescue breaths, then start chest compressions.
• Compress the lower half of the sternum by at least one third of the anteroposterior chest depth (5–6 cm in adolescents and never more than 6 cm) at 100–120 per minute, allowing full recoil. Use the two-thumb encircling technique in all infants and one or two hands in children.
• Use 15:2 if trained in paediatric basic life support; otherwise 30:2 is acceptable.
• Start compressions if the heart rate is below 60/min with poor perfusion despite adequate ventilation, even if a pulse is present.
• Attach an AED as soon as possible. Use paediatric mode under 25 kg if available, with pads in the anteroposterior position for infants and children under 25 kg.

Advanced Life Support

Some national algorithms, such as the UK algorithm, give adrenaline every 3–5 minutes.

Reversible Causes and Post-Resuscitation Care

Search for and treat hypoxia, hypovolaemia, hyperkalaemia or hypokalaemia and other metabolic causes, hypothermia or hyperthermia, tension pneumothorax, cardiac tamponade, toxins and thrombosis. After return of spontaneous circulation, target SpO2 94–98% and normocapnia, keep systolic and mean blood pressure above the 10th centile for age, treat hypoglycaemia, and actively prevent fever for at least 72 hours.

Sources: ERC Guidelines 2025: Paediatric Life Support; Resuscitation Council UK paediatric emergency algorithms.

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Paediatric Burns: First Aid, Assessment and Fluids

First Aid

Stop the burning process and remove clothing and jewellery that are not stuck to the wound. Cool the burn with cool running water for 20 minutes, which remains useful up to 3 hours after injury; do not use ice. Keep the rest of the child warm, because young children become hypothermic quickly. Cover the wound loosely with a single, unwrapped layer of cling film.

Assessment

• Use the ABCDE approach. Facial burns, singed nasal hair, hoarseness, stridor or soot in the mouth suggest inhalation injury and need early senior airway management; consider carbon monoxide poisoning after enclosed-space fires.
• Estimate the burn size with an age-adjusted Lund and Browder chart, because a young child's head is proportionally larger. The child's palm including the fingers is about 1% of total body surface area (TBSA). Do not count simple erythema.
• Depth: superficial burns are red without blisters; partial-thickness burns blister and are painful with capillary refill; full-thickness burns are white, leathery or charred, painless and do not blanch.
• Always check whether the history and the burn pattern are consistent, because inflicted burns must be recognised.

Fluids, Analgesia and Referral

• Burns covering more than 10% TBSA in children usually need formal intravenous fluid resuscitation. The modified Parkland formula gives 3 mL × %TBSA × weight (kg) of crystalloid over 24 hours from the time of injury, with half in the first 8 hours. Children also need maintenance fluid containing glucose. Titrate to a urine output of about 1 mL/kg/hour.
• Give effective analgesia, such as intranasal or intravenous opioids, and check tetanus immunisation.
• Refer to a specialised burns service for burns of 2% TBSA or more in children, any full-thickness or circumferential burn, any burn not healed in 2 weeks, and any burn with suspected non-accidental injury. Discuss burns to the hands, feet, face, perineum or genitalia, and chemical, electrical, friction or cold injuries.

Sources: National Burn Care Referral Guidance; Northern Burn Care Network paediatric burns guideline.