Acute respiratory distress syndrome

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

ARDS follows injury to alveolar epithelium and pulmonary endothelium. Protein-rich fluid floods alveoli, surfactant is disrupted, dependent lung collapses and pulmonary vascular resistance rises. Only a small, uneven “baby lung” remains available for ventilation, so apparently ordinary tidal volumes can overdistend functioning units and compound injury through volutrauma, barotrauma, atelectrauma and biological inflammation.

Diagnosis requires a compatible acute syndrome, bilateral imaging abnormalities, impaired oxygenation on positive pressure, and evidence that hydrostatic oedema is not the main explanation. The label should stimulate a systematic cause search rather than end one: bacterial or viral pneumonia, aspiration, extra-pulmonary sepsis, transfusion reaction, pancreatitis, autoimmune haemorrhage and drug injury require different definitive treatment.

Support aims to minimise additional lung and organ injury while the cause resolves. Ventilator settings, PEEP, proning, neuromuscular blockade and ECMO referral are individual critical-care decisions. The ICS/FICM ARDS guideline remains a central UK source, while sepsis guidance was updated in 2025 and GPICS v3 in 2026. Verify the unit’s current protocol rather than applying static thresholds without context.

Key points

ARDS is acute hypoxaemic respiratory failure from diffuse inflammatory lung injury with bilateral opacities not primarily explained by heart failure, collapse or pleural fluid.
Common precipitants are pneumonia, non-pulmonary sepsis, aspiration, pancreatitis, major trauma, transfusion and inhalational injury; more than one trigger may coexist.
Establish timing, oxygenation severity and the level of PEEP or CPAP, but never delay supportive care to complete a formal label.
Actively assess cardiac function and fluid status because cardiogenic oedema can mimic or coexist with ARDS.
High-flow nasal oxygen may support selected patients, but tachypnoea, large respiratory effort, shock, hypercapnia, worsening acidosis or deteriorating mentation predicts failure.
In invasive ventilation use low tidal volume based on predicted, not actual, body weight and limit plateau pressure; accept carefully monitored permissive hypercapnia when appropriate.
Prone ventilation improves outcomes in moderate to severe ARDS when used early and for prolonged sessions by a trained team alongside lung-protective ventilation.
After shock is controlled, a conservative fluid strategy usually reduces ventilator duration; ongoing positive balance worsens lung oedema.
Do not use high-frequency oscillation routinely. Inhaled pulmonary vasodilators are rescue bridges, not proven mortality treatment.
Discuss ECMO early with a commissioned centre for potentially reversible severe respiratory failure despite optimised protective ventilation and proning; transfer becomes riskier after collapse.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Pulmonary infection

Severe bacterial or viral pneumonia directly injures alveolar epithelium and is a common precipitant of diffuse inflammatory lung injury.

Systemic inflammation

Sepsis, pancreatitis, major trauma and shock activate circulating inflammatory pathways that damage pulmonary endothelium despite no primary lung infection.

Aspiration or inhalation

Gastric contents, smoke and toxic inhalants directly disrupt the alveolar-capillary barrier and can initiate rapidly progressive hypoxaemia.

Transfusion and other insults

Transfusion-related acute lung injury, drowning and selected drug reactions are recognised triggers; several insults often coexist in a critically ill patient.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier injury
Inflammatory activation damages alveolar epithelium and capillary endothelium, increasing permeability across the gas-exchange membrane, contributing to the resulting loss of respiratory reserve.
2
Protein-rich oedema
Fluid and proteins enter alveoli independently of raised left-heart filling pressure, dilute surfactant and promote alveolar collapse.
3
Shunt and stiffness
Perfusion of flooded or collapsed units causes refractory hypoxaemia while reduced compliance greatly increases the work and pressure required for ventilation.
4
Heterogeneous stress
Patchy aerated lung receives a disproportionate share of tidal ventilation, making overdistension and repeated opening injury possible during support.
5
Repair or fibrosis
Resolution requires oedema clearance and epithelial repair; persistent inflammation may organise into fibrotic change, prolonged weakness and impaired gas transfer.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Early ARDSRed flag

A recent insult followed by increasing oxygen need, tachypnoea and bilateral opacities with no dominant hydrostatic explanation should prompt early ICU review even before invasive ventilation.

Moderate or severe gas-exchange failureRed flag

Low PaO2 relative to FiO2 despite PEEP or CPAP, diffuse shunt physiology and reduced compliance indicate more severe disease and strengthen the case for early proning and advanced support.

Failing non-invasive supportRed flag

Persistently high respiratory rate, vigorous inspiratory effort, worsening hypoxaemia, hypercapnia, acidosis, shock or altered mentation indicates that high-flow or NIV is not safely containing the illness.

Ventilator-induced injury riskRed flag

Excess tidal volume for predicted body weight, high plateau or driving pressure, repeated derecruitment and patient–ventilator dyssynchrony can worsen otherwise reversible lung injury.

Cardiogenic overlap

Raised JVP, severe left-ventricular or valvular disease, pleural effusions and hydrostatic response suggest a cardiac component; sepsis and renal failure commonly create mixed oedema.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial arterial blood gases with documented FiO2 and pressure supportFirst step
Why
Quantify oxygenation, ventilation and acid-base trajectory and support severity assessment.
Interpretation and limitations
Use values obtained under known conditions. A worsening PaO2/FiO2 relationship, hypercapnia or acidosis alongside fatigue indicates failure; do not interpret PaO2 without FiO2.
02
Chest radiograph and thoracic CT when stable enough
Why
Confirm bilateral air-space disease, identify complications and refine the cause.
Interpretation and limitations
Imaging may be patchy or dependent. CT can reveal focal infection, embolism, cavitation, fibrosis or pleural disease but transfer risk must be justified.
03
Lung and focused cardiac ultrasound
Why
Assess interstitial syndrome, consolidation, pleural fluid, ventricular function and haemodynamic context.
Interpretation and limitations
Diffuse B-lines confirm lung water but not ARDS. Left-heart dysfunction and ARDS may coexist, while a dilated failing right ventricle can reflect severe pulmonary vascular load.
04
Microbiology and infection assessment
Why
Identify bacterial, viral, fungal or opportunistic infection requiring specific treatment and isolation.
Interpretation and limitations
Obtain blood and respiratory cultures and targeted viral testing without delaying antimicrobials in high-risk sepsis. Bronchoscopy is considered only when benefit exceeds oxygenation risk.
05
FBC, renal and liver profile, coagulation, lactate and inflammatory markers
Why
Define organ dysfunction, bleeding risk, shock and treatment constraints.
Interpretation and limitations
Trend results; a falling lactate does not prove adequate perfusion, and a falling haemoglobin can indicate bleeding rather than haemodilution alone.
06
Echocardiography and haemodynamic assessment
Why
Exclude dominant hydrostatic oedema and identify right- or left-ventricular failure that changes fluids and ventilation.
Interpretation and limitations
A preserved ejection fraction does not exclude raised filling pressure. Integrate ultrasound, clinical congestion and response; invasive monitoring is selective.
07
Cause-directed immune, toxicology or transfusion testing
Why
Investigate alveolar haemorrhage, drug injury, transfusion reaction or unusual exposure when the history suggests it.
Interpretation and limitations
ANCA, anti-GBM antibodies and urinalysis are urgent when pulmonary–renal disease is possible; discuss suspected transfusion reactions immediately with transfusion medicine.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Cardiogenic pulmonary oedema

Left-heart dysfunction, raised filling pressures and typical cardiac findings favour hydrostatic oedema, although cardiac failure and ARDS may coexist.

Diffuse alveolar haemorrhage

Falling haemoglobin, haemoptysis, renal or autoimmune features and increasingly bloody lavage support alveolar bleeding rather than permeability oedema.

Acute eosinophilic pneumonia

Acute febrile hypoxaemia with diffuse infiltrates and eosinophilic lavage, sometimes after a new smoking exposure, suggests an eosinophilic process.

Acute exacerbation of ILD

Known or newly recognised fibrosis beneath fresh bilateral ground-glass change suggests acute exacerbation, after infection, oedema and embolism are assessed.

Widespread infection without ARDS

Bilateral pneumonia may cause hypoxaemia yet not meet the full timing, imaging and non-cardiogenic framework required for the syndrome label.

Additional chapter-specific clues

Alternative diffuse processRed flag

Falling haemoglobin with haematuria suggests alveolar haemorrhage; marked eosinophilia, immunosuppression, drug exposure or a focal bronchial distribution should redirect investigation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01RecognitionConfirm the syndrome and find the triggerFirst stepAcute hypoxaemia with new bilateral pulmonary opacities.

1Start monitored oxygen support and involve ICU early while documenting timing, FiO2, blood gases and work of breathing.
2Search immediately for pneumonia, sepsis, aspiration, trauma, pancreatitis, transfusion, inhalation, drug injury and immune haemorrhage.
3Use cardiac assessment to determine whether left-heart congestion is dominant, absent or coexisting.
4Treat the cause promptly, including antimicrobials and source control for high-risk sepsis, without waiting for every test.

02Non-invasive phaseAvoid delayed intubationHypoxaemic respiratory failure is being supported with high-flow oxygen, CPAP or NIV.

1Use the modality only in a monitored area with experienced staff and immediate intubation capability.
2Set explicit short-interval success criteria using oxygenation, respiratory rate, effort, mentation, gas exchange and haemodynamics.
3Optimise positioning, secretion clearance and comfort without suppressing protective consciousness or respiratory drive dangerously.
4Intubate in a controlled manner if criteria are not met or deterioration occurs; do not persist with injurious spontaneous effort.

03Protective ventilationVentilate the available lung gentlyInvasive mechanical ventilation is required for respiratory support.

1Calculate predicted body weight from sex and height and use a low-tidal-volume strategy with plateau-pressure limitation.
2Select PEEP and FiO2 to recruit lung and achieve adequate oxygenation while watching overdistension, hypotension and right-heart strain.
3Use sedation and selective neuromuscular blockade when needed for protective ventilation, proning or dangerous dyssynchrony; reassess daily.
4Adopt conservative fluid management after shock resolves and prevent ventilator-associated, thrombotic, pressure and nutritional complications.

04Refractory hypoxaemiaProne early and refer before rescue is impossibleModerate or severe ARDS persists despite optimised lung-protective ventilation.

1Initiate prolonged prone sessions through a trained team and checklist, protecting airway, eyes, nerves, lines, skin and pressure points.
2Reassess PEEP, recruitment, synchrony, secretions, pneumothorax and right-heart function; avoid routine high-frequency oscillation.
3DefinitiveUse inhaled pulmonary vasodilator only as a short rescue bridge when the expert team judges it useful, not as definitive treatment.
4Contact the commissioned ECMO centre early for severe potentially reversible failure despite optimal ventilation and proning.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Treats bacterial infection, one of the commonest reversible causes of ARDS.

Cause-directed antimicrobial therapy

Give promptly under the current NICE sepsis and local pneumonia protocol, adjusted for source, allergy, renal function, microbiology and exposure history.

Obtain cultures when this does not delay care, review daily, narrow to results and pursue source control. Broad-spectrum treatment is not a substitute for diagnosing aspiration, haemorrhage or non-infectious injury.

Permits safe intubation, lung-protective ventilation and proning while minimising distress and oxygen demand.

Sedation and analgesia for protective ventilation

Use the lowest effective ICU protocol regimen, titrated to a documented sedation target, ventilator synchrony and daily reassessment.

Accumulation, hypotension, delirium and prolonged weakness are common. Pair with analgesia-first assessment, daily reduction when safe and organ-function review.

Prevents injurious respiratory effort when deep sedation alone cannot deliver lung-protective ventilation.

Neuromuscular blocking agent

Use a time-limited critical-care infusion only for severe dyssynchrony, refractory hypoxaemia or safe proning under the current unit protocol.

Not routine for every ARDS patient. Ensure adequate sedation, eye care, pressure care and train-of-four or protocol monitoring; immobility and corticosteroid exposure may increase weakness.

Reduces ICU-associated thrombosis during immobility and systemic inflammation.

Venous-thromboembolism prophylaxis

Prescribe the locally approved pharmacological regimen unless bleeding risk contraindicates it, with renal, weight and procedure adjustment.

Reassess daily around bleeding, thrombocytopenia, renal failure and procedures; use mechanical prophylaxis when pharmacological treatment is temporarily unsafe.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Refractory hypoxaemia

Extensive shunt may remain severe despite supplemental oxygen and conventional ventilation, causing multi-organ oxygen deprivation, adding morbidity beyond the initial pulmonary disorder.

Ventilator-induced lung injury

Overdistension, cyclic collapse and excessive driving pressure can extend inflammatory damage into previously functional lung, and increasing the burden of otherwise local respiratory disease.

Multi-organ dysfunction

The initiating illness, systemic inflammation, hypoxaemia and shock can impair kidneys, circulation, liver and brain, and potentially prolonging treatment and functional recovery.

Barotrauma

Fragile, unevenly aerated lung exposed to positive pressure may develop pneumothorax, pneumomediastinum or persistent air leak.

Post-intensive-care disability

Prolonged ventilation, sedation and inflammation contribute to muscle weakness, cognitive problems, psychological distress and persistent exercise limitation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuously track saturation, FiO2, airway pressures, exhaled tidal volume, respiratory effort, synchrony, haemodynamics and right-heart tolerance.
Repeat arterial gases after major support changes and interpret oxygenation under the documented PEEP and FiO2.
Monitor cumulative fluid balance, weight, urine output, creatinine, lactate and peripheral perfusion; move from resuscitation to conservative balance once shock resolves.
During proning use a checklist for tube depth, circuit patency, eyes, pressure areas, nerves, lines, drains and enteral feeding safety.
Review antimicrobial indication, cultures and source control daily and broaden the differential if inflammatory or oxygenation trajectories diverge.
Screen for delirium, weakness, thrombosis, pressure injury, nutrition deficits and psychological sequelae, then plan rehabilitation and post-intensive-care follow-up.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Use predicted body weight

Lung size follows height and sex, not actual body weight. Using actual weight in obesity can deliver dangerously large tidal volumes to the functional baby lung.

Spontaneous effort can injure

A distressed patient on high-flow oxygen may generate large transpulmonary swings and patient self-inflicted lung injury. Apparent avoidance of intubation is not success when effort is worsening.

Proning is a treatment bundle

Benefit depends on early prolonged sessions with lung-protective ventilation and a skilled safety process, not merely turning a patient briefly when saturation falls.

Right-heart protection matters

Hypoxaemia, hypercapnia, high airway pressure and overdistension raise pulmonary vascular resistance. Sudden hypotension may reflect acute right-ventricular failure or pneumothorax.

ECMO referral is not ECMO acceptance

Early discussion lets the centre review reversibility, duration of harmful ventilation, comorbidity and transfer logistics before conventional rescue options are exhausted.

11Common pitfallsFrequent interpretation and management errors.

01
Using actual rather than predicted body weight to set tidal volume.
02
Persisting with high-flow oxygen or NIV despite worsening effort and gas exchange.
03
Calling every bilateral opacity ARDS without assessing heart failure, haemorrhage or infection.
04
Continuing liberal fluids after shock has resolved.
05
Proning without a trained team, checklist or secure airway and lines.
06
Using inhaled nitric oxide as routine disease-modifying therapy.
07
Waiting until refractory collapse before discussing ECMO.