Fluid bolus therapy and vasoactive support — formative SAQs

1. Fluid bolus prescription

I give 10 to 20 mL per kilogram of isotonic crystalloid — 0.9 per cent sodium chloride or a balanced crystalloid such as Hartmann solution. For this 16 kilogram child, that is 160 to 320 mL per aliquot, given over 5 to 20 minutes using a push-pull technique or rapid infuser, not as a slow gravity drip. I use a large-bore peripheral intravenous cannula or intraosseous access if peripheral is not achievable. [2] [3]

2. Reassessment after each bolus

After each aliquot I perform the full reassessment: heart rate and pulse quality, skin colour and temperature, capillary refill with the technique stated, blood pressure, mental state, respiratory rate and work of breathing, auscultation for new crackles, and liver span for hepatomegaly. I expect the heart rate to fall toward the normal range, pulses to strengthen, capillary refill to shorten, skin to become warmer and drier, and interaction to improve. I check a point-of-care lactate and glucose at baseline and repeat after each significant intervention. [4]

3. No improvement after two boluses

This is fluid-refractory shock: two aliquots totalling 40 mL per kilogram have produced no sustained improvement. I stop giving further fluid blindly. I reassess for signs of overload — if crackles, hepatomegaly, gallop or worsening respiratory distress are present, I stop fluids immediately. I start a vasoactive infusion now, choosing the agent based on the shock phenotype. I call PICU or retrieval in parallel. I do not wait for a third bolus to fail before escalating. [2] [3]

4. Warm shock phenotype and first-line vasoactive

Bounding pulses, warm dry skin and flash capillary refill define warm vasodilatory shock. The first-line vasoactive agent is noradrenaline, starting at 0.05 to 0.5 micrograms per kilogram per minute, titrated to clinical response. I prefer central venous access but use intraosseous access if central is not immediately available, and I do not delay the first dose to place a central line. [3] [4]

5. The first-hour ceiling

The Surviving Sepsis Campaign 2026 children guideline supports up to 40 to 60 mL per kilogram of crystalloid in the first hour for septic shock. I treat this as a ceiling — a maximum — rather than a target, because driving toward a fixed volume without measuring the response risks pushing the child onto the flat portion of the Frank-Starling curve, causing fluid accumulation, pulmonary oedema and worse outcomes. The Alobaidi meta-analysis confirms the association between positive fluid balance and harm. I stop for no benefit, worsening, or overload at any point below the ceiling. [2] [10]

1. The FEAST trial and its lesson

The FEAST trial was a randomised controlled trial in African children with severe febrile illness and impaired perfusion. It compared bolus fluid (saline or albumin) against no bolus and was stopped early because bolus fluid increased 48-hour mortality: 10.6 per cent with saline, 10.5 per cent with albumin, versus 6.3 per cent with no bolus. Both fluid types caused harm. The correct lesson is not that bolus fluid is universally harmful, but that a fluid algorithm cannot be transplanted across populations, shock types and rescue resources without considering what happens when the child does not improve. In a setting without intensive care or vasoactive rescue, giving boluses and then having no escalation option creates the conditions for harm. [1]

2. The dopamine downgrade

The Surviving Sepsis Campaign 2020 children guideline recommends using either adrenaline or noradrenaline rather than dopamine as the first-line vasoactive agent for paediatric septic shock. This was based on evidence that adrenaline and noradrenaline were associated with better outcomes. Dopamine remains an option where first-line agents are not immediately available, but it is no longer the default first choice. The choice between adrenaline and noradrenaline is based on the shock phenotype: adrenaline for cold shock (low cardiac output, vasoconstricted), noradrenaline for warm shock (vasodilatory, low systemic vascular resistance). Both start at 0.05 to 0.5 micrograms per kilogram per minute. [3]

3. Managing fluid overload

If fluid overload develops — new crackles, hepatomegaly, gallop rhythm, rising respiratory distress or oxygen requirement — I stop fluids immediately and do not give further boluses. I support breathing with oxygen and non-invasive or invasive ventilation if needed. I start a vasoactive infusion if shock persists, choosing the agent by phenotype. Once the child is in a critical care environment, I consider diuretics for established pulmonary oedema, and renal replacement therapy if there is severe fluid overload with renal dysfunction. I track all input and output meticulously from the first bolus so that overload is detected early, not after it is established. [2] [10]

4. The rural setting and retrieval timing

The FEAST evidence means I apply a more cautious and vigilant fluid strategy here. I give 10 to 20 mL per kilogram aliquots of crystalloid, but I reassess rigorously after each, and I stop early for no benefit, worsening or overload — because in this setting, I cannot escalate to vasoactive support on site. I call retrieval at the outset, in parallel with the first bolus, not after local options are exhausted. I state the retrieval time, the treatment I can continue, the expected deterioration plan, and what to do if transport is delayed. If vasoactive agents cannot be given locally, I prepare for the retrieval team to bring them. The principle is early consultation and honest communication of limits, not heroic persistence with fluid alone. [1] [2]