Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Shock recognition and fluid reassessment
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Decompensated shock
Reduced consciousness, weak central pulses, hypotension, bradycardia, severe mottling, anuria or worsening respiratory effort signals failing organ perfusion and imminent cardiorespiratory arrest.
Action: Activate the paediatric resuscitation and critical-care team, give high-concentration oxygen, obtain IV access within two attempts or five minutes and use intraosseous access if necessary. Control haemorrhage, give a cause-appropriate 10 mL/kg fluid trial with immediate reassessment, start antibiotics within one hour for septic shock, and move early to blood products, vasoactive support or relief of obstruction according to mechanism.
Overview
Identify compensated shock before hypotension, distinguish hypovolaemic, distributive, cardiogenic and obstructive mechanisms, use fluid as a measured treatment trial, and escalate promptly to blood, antimicrobials, vasoactive support or source control when physiology does not recover.
Shock means inadequate cellular oxygen delivery, not simply low blood pressure. Begin with the child's appearance and ABCDE, then compare heart rate and pressure with age-adjusted ranges. Examine central and peripheral pulses, capillary refill at a consistent site, skin temperature and colour, mental state, urine output, breathing and liver size. Use trends and response to treatment because no single sign diagnoses or excludes circulatory failure.
History identifies mechanism: diarrhoea and intake, fever, rash and immunocompromise, allergy exposure, trauma and bleeding, cardiac disease, recent surgery, medicines, adrenal risk and toxic ingestion. Look for occult haemorrhage, abdominal or pelvic injury and gastrointestinal loss. A warm child with bounding pulses may have early distributive shock; a cold child with narrow pulse pressure can still have sepsis.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
First fluid trial
A child has cool mottled skin, weak peripheral pulses, prolonged refill and normal blood pressure after profuse diarrhoea. There are no overload signs. Which initial fluid approach best matches current UK guidance?
Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Obtain accurate weight or a parent-reported recent weight; otherwise use a body-habitus-adjusted length method. Establish IV access, but do not spend more than five minutes or two attempts in severe shock before intraosseous access. Check glucose, blood gas and lactate and take cause-directed FBC, cultures, renal, electrolyte, liver, coagulation and group-and-save samples without delaying time-critical treatment.
Fluid is a diagnostic and therapeutic trial. RCUK and NICE use 10 mL/kg glucose-free isotonic crystalloid for resuscitation in children, with balanced crystalloid preferred by RCUK in most hypovolaemic and distributive shock. Give it promptly, then reassess every perfusion variable and look for overload. Improvement supports volume responsiveness; no response demands a mechanism review rather than automatic repetition.
Treatment diverges by cause. Septic shock combines source control and antimicrobials within one hour with fluid and early vasoactive support. Haemorrhage requires pressure or tourniquet when appropriate, surgery or interventional control, blood products and trauma tranexamic acid. Cardiogenic shock needs echocardiography, cautious fluid, inotropy and ventilatory planning. Tension pneumothorax and tamponade require emergency decompression or drainage.
After 30–40 mL/kg without sustained response, a vasoactive drug and respiratory support should already be under active consideration; NICE asks for expert advice when 40–60 mL/kg or more is needed. Noradrenaline is the 2025 RCUK first-line vasopressor and adrenaline the first-line inotrope, selected by physiology and titrated through critical-care protocols. Do not wait for a central line when shock is refractory and a monitored peripheral infusion can be started safely.
Ongoing care replaces deficit and losses without confusing them with routine maintenance. Account separately for resuscitation, maintenance, replacement and redistribution; review renal function, sodium, chloride, potassium, glucose and acid-base state. Families need a clear explanation of why repeated reassessment changes treatment, and a child recovering from severe shock needs organ, functional and psychological follow-up rather than discharge based only on normalised blood pressure.
Key points
Recognise shock from a pattern: heart rate, central and peripheral pulses, refill, skin temperature and colour, blood pressure, consciousness and urine output.
A child can be in compensated shock with a normal blood pressure; hypotension, bradycardia or diminished central pulses are late.
First-line action is ABCDE, high-concentration oxygen in critical illness, monitoring, glucose and rapid IV or IO access without repeated delay.
Classify the likely mechanism as hypovolaemic, distributive, cardiogenic or obstructive because the next treatment differs.
For hypovolaemic or distributive shock, use a 10 mL/kg balanced isotonic crystalloid bolus where appropriate and reassess immediately.
Reassessment includes heart rate, pulses, refill, blood pressure, consciousness, urine, breathing, crackles and liver edge; record the response and cumulative volume.
In cardiogenic shock, fluid need is individual and a cautious 5 mL/kg trial may be used only with early cardiac and critical-care guidance.
Haemorrhagic shock needs bleeding control, activation of the massive-haemorrhage pathway and early blood; minimise crystalloid and give tranexamic acid when indicated.
Aetiology
01
Hypovolaemic
Gastrointestinal loss, poor intake, burns, third spacing and haemorrhage reduce effective circulating volume; haemorrhage requires a blood-focused strategy.
02
Distributive
Sepsis and anaphylaxis cause vasodilation and capillary leak; vascular tone can remain inadequate after volume has been partly restored.
03
Cardiogenic
Myocarditis, cardiomyopathy, congenital heart disease, arrhythmia and postoperative dysfunction reduce forward flow and can worsen with indiscriminate fluid.
04
Obstructive
Tension pneumothorax, tamponade, pulmonary hypertension crisis or obstructed congenital shunt limits filling or ejection and needs urgent cause relief.
Pathophysiology
1
Compensation
Tachycardia and vasoconstriction maintain blood pressure and divert flow toward heart and brain, producing cool skin, weak peripheral pulses and delayed refill before hypotension.
2
Oxygen-delivery failure
When cardiac output and haemoglobin-mediated oxygen delivery cannot meet demand, tissues extract more oxygen and shift toward anaerobic metabolism with lactate and acidosis.
3
Endothelial leak
Inflammation increases vascular permeability, so intravascular depletion can coexist with oedema and makes repeated fluid progressively less effective.
4
Decompensation
Myocardial hypoxia, acidosis and exhausted catecholamine response lead to falling output, hypotension, bradycardia and cardiac arrest.
Clinical features and red flags
Compensated shock
Tachycardia, cool or mottled skin, prolonged refill, weak peripheral pulses and reduced urine occur while pressure may remain normal.
Decompensated shock
Weak central pulses, hypotension, bradycardia and reduced consciousness indicate failing compensation and peri-arrest physiology.
Warm distributive pattern
Warm extremities, brisk refill and bounding pulses with altered perfusion can occur early in sepsis or anaphylaxis.
Cardiogenic pattern
Gallop rhythm, crackles, hepatomegaly, raised venous pressure and worsening breathing after fluid suggest impaired pump function.
Obstructive pattern
Sudden shock with unequal air entry, distended veins, muffled sounds or known shunt physiology points to a mechanical barrier.
Red flags requiring action
Hypotension is a late sign in children; normal blood pressure does not exclude clinically important shock.
Bradycardia, diminished central pulses and reduced consciousness indicate decompensation rather than a reassuring fall in tachycardia.
Rising respiratory rate, crackles, falling saturation or an enlarging liver after fluid suggests overload or myocardial dysfunction.
Investigations
01First-line serial clinical perfusion assessmentFirst stepFirst line
Why
Recognise shock and measure response using several age-adjusted variables.
Interpretation and limitations
Improving consciousness, pulses, refill and urine are more meaningful than one normal pressure; persistent or worsening signs drive escalation.
02First-line glucose, blood gas and lactateFirst line
Why
Detect hypoglycaemia, ventilation failure, acidosis and impaired perfusion rapidly.
Interpretation and limitations
Lactate trend supports risk assessment but can rise for other reasons and must not replace clinical reassessment.
03Cause-directed FBC, renal, liver and coagulation tests
Why
Identify anaemia, infection, organ dysfunction, electrolyte disturbance and coagulopathy.
Interpretation and limitations
Normal early inflammatory markers do not exclude sepsis; haemoglobin can initially appear normal after acute haemorrhage.
04Cultures before antimicrobials when feasible
Why
Identify bloodstream or focal infection and guide later narrowing.
Interpretation and limitations
Differential diagnosis
01
Normal peripheral vasoconstriction
Cold environment can prolong refill, and crying can cause tachycardia; diagnose shock using multiple variables, trajectory and organ perfusion rather than one sign.
02
Primary respiratory failure
Hypoxia produces tachycardia and altered behaviour but dominant work of breathing, air-entry abnormality and gas exchange point to a respiratory driver that still needs circulatory assessment.
03
Neurological or toxic illness
Seizure, raised intracranial pressure and poisoning can alter consciousness and autonomic signs without primary volume loss; glucose, pupils, history and ECG help discriminate.
04
Adrenal crisis
Vomiting, abdominal pain, hypoglycaemia, hyponatraemia, hyperkalaemia and refractory shock in an at-risk child require stress hydrocortisone as well as resuscitation.
Management
01Initial recognitionTreat before hypotensionFirst stepMultiple age-adjusted perfusion variables are persistently abnormal.+
1Activate senior and critical-care help and start monitored ABCDE.
2Give high-concentration oxygen for critical illness and obtain IV or prompt IO access.
3Check glucose and gas and send cause-directed samples without delaying treatment.
4Name the likely shock mechanism and choose the first cause-specific action.
02Fluid-responsive patternBolus as a treatment trialHypovolaemic or distributive shock is likely without overload signs.+
1Give 10 mL/kg balanced isotonic crystalloid over less than 10 minutes.
2Reassess every perfusion and overload sign immediately.
Complications
01
Multiorgan injury
Acute kidney injury, hepatic dysfunction, encephalopathy, gut ischaemia, myocardial injury and coagulopathy can follow prolonged systemic under-perfusion.
02
Fluid overload
Excess crystalloid increases pulmonary and tissue oedema, impairs ventilation and can worsen abdominal pressure and cardiac performance.
03
Dilution and electrolyte harm
Large saline or crystalloid volumes can dilute haemoglobin and clotting factors and contribute to hyperchloraemic acidosis or electrolyte disturbance.
04
Treatment delay
Waiting for hypotension, access, imaging or laboratory confirmation allows compensated shock to progress and makes subsequent airway and vascular procedures harder.
Monitoring and follow-up
Record the pre-bolus heart rate, central and peripheral pulses, refill, blood pressure, consciousness, respiratory findings, liver edge and urine output.
Repeat the same variables immediately after every aliquot and document whether the response is complete, partial, absent or harmful.
Track cumulative resuscitation fluid separately from maintenance, deficit replacement, feeds, blood and drug infusions.
Trend lactate, gas, glucose, renal function and electrolytes at a frequency determined by instability rather than a routine daily interval.
Use continuous ECG and oximetry and frequent pressure measurement in unstable shock; add invasive monitoring in critical care where indicated.
Monitor renal and hepatic function when choosing and titrating vasoactive, antimicrobial and sedative medicines.
After recovery, assess kidney, cardiac, neurological and functional consequences and give the family a clear follow-up and safety-net plan.
Special situations
Pressure is a late variable
Peripheral vasoconstriction can preserve blood pressure until circulatory reserve is nearly exhausted.
Fluid is a hypothesis
A bolus tests whether volume improves perfusion; its result should change the next decision.
A larger liver is an alarm
New hepatomegaly after fluid is a practical paediatric sign of venous congestion and poor tolerance.
Warm shock is still shock
Brisk refill and warm hands do not guarantee adequate organ perfusion in distributive disease.
Mechanism outranks repetition
Blood, adrenaline, noradrenaline or decompression may be the next life-saving treatment when more crystalloid is not.
Common pitfalls
01
Waiting for hypotension before diagnosing shock.
02
Calling capillary refill normal or abnormal without considering temperature, site and the rest of perfusion.
03
Persisting with peripheral cannulation while an intraosseous route is indicated.
04
Giving identical boluses without documenting response and overload signs.
05
Treating haemorrhage predominantly with crystalloid.
06
Missing cardiogenic or obstructive shock when fluid worsens breathing.
07
Waiting for a central line before starting a necessary vasoactive infusion.
08
Allowing cultures, imaging or a lactate result to delay antimicrobials or source control.
Septic shock needs blood cultures if this causes no delay and broad-spectrum antimicrobial treatment within one hour alongside haemodynamic support.
Consider vasoactive infusion early and no later than after three to four ineffective 10 mL/kg boluses; peripheral or IO initiation is preferable to waiting for a central line.
Obstructive shock improves only when tension pneumothorax, tamponade or another mechanical obstruction is relieved.
Renal, cardiac, hepatic and nutritional comorbidity changes fluid distribution and tolerance; smaller trials and earlier specialist support are safer.
Uncontrolled external or internal bleeding needs immediate source control and early blood, not repeated crystalloid dilution.
Muffled heart sounds, distended veins, unequal air entry or sudden deterioration during positive-pressure ventilation suggests obstructive shock requiring procedural treatment.
A non-blanching rash, fever or hypothermia, altered behaviour and poor perfusion warrants immediate sepsis management even before laboratory confirmation.
Known congenital heart disease, cardiomyopathy, renal failure or severe malnutrition changes fluid tolerance and requires smaller aliquots and expert input.
Difficult sampling must not delay broad-spectrum treatment beyond the emergency window.
05Focused cardiac and lung ultrasound
Why
Support classification of pump failure, filling, tamponade, pneumothorax and fluid tolerance.
Interpretation and limitations
POCUS augments but does not replace examination or formal echocardiography and is operator dependent.
06Reference-standard cause confirmation
Why
Use formal echocardiography, source imaging, microbiology or operative findings to establish the mechanism after stabilisation.
Interpretation and limitations
The confirmatory modality depends on the suspected cause; treatment of a life threat precedes definitive proof.
3
Repeat only when a positive or plausible response and mechanism justify it.
4Record cumulative fluid and plan maintenance, deficit and losses separately.
03Fluid-unresponsive patternChange strategy earlyShock persists or overload signs appear after fluid.+
1Reconsider haemorrhage, cardiogenic or obstructive shock and verify airway and ventilation.
2Start physiology-directed vasoactive support with critical-care oversight rather than waiting for central access.
3DefinitiveUse echocardiography or focused ultrasound where available and arrange definitive source control.
4EscalationEscalate to PICU and consider extracorporeal support in selected refractory disease.
04HaemorrhageControl and replace bloodTrauma or active bleeding is causing shock.+
1Control external bleeding and activate major-haemorrhage and surgical pathways.
2Minimise crystalloid, provide warmed blood products promptly and correct coagulopathy.
3Give tranexamic acid within three hours when the RCUK trauma indication is met.
4Monitor temperature, calcium, coagulation and ongoing loss during transfer or theatre.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
First-line volume trial for selected non-haemorrhagic paediatric shock while the cause is treated.
Balanced isotonic crystalloid
Give 10 mL/kg IV or IO over less than 10 minutes for appropriate hypovolaemic or distributive shock, then stop and reassess before any repeat; consider only 5 mL/kg cautiously in suspected cardiogenic shock with expert guidance.
Do not use a fixed sequence of boluses. Look after each dose for crackles, increasing liver edge, rising respiratory support and absent perfusion response. Cardiac or kidney disease, severe malnutrition and haemorrhage require a modified strategy.
Reduces fibrinolysis in a child requiring transfusion after trauma or with life-threatening haemorrhage.
Tranexamic acid for life-threatening traumatic haemorrhage
Give 15 to 20 mg/kg IV, maximum 1 g, over 10 minutes as soon as possible and within 3 hours, followed by 2 mg/kg/hour, maximum cumulative infusion 1 g, for at least 8 hours or until bleeding stops under the major-haemorrhage protocol.
Use only for the stated haemorrhagic indication, confirm weight and renal function, monitor for thrombosis and seizures, and never allow infusion preparation to delay surgical bleeding control or blood replacement.