Acute Respiratory Distress Syndrome (ARDS)

Definition

Acute respiratory distress syndrome (ARDS) is a rapidly developing, severe form of respiratory failure caused by widespread inflammatory injury to the lung. It is defined by the Berlin criteria: onset within a week of a known trigger, bilateral opacities on chest imaging not fully explained by effusion, collapse or nodules, respiratory failure not fully explained by cardiac failure or fluid overload, and impaired oxygenation graded mild, moderate or severe by the ratio of arterial oxygen tension to inspired oxygen fraction (PaO₂/FiO₂).¹ It is a syndrome, not a disease — always the consequence of something else.

Pathophysiology

The exudative phase

Widespread inflammation damages the alveolar–capillary barrier. Protein-rich fluid floods the alveoli, surfactant is inactivated and diluted, and alveoli collapse. The lungs become stiff and heavy, compliance falls sharply, and blood continues to flow past unventilated units — producing the refractory hypoxaemia that defines the syndrome and that does not correct with oxygen alone.

The “baby lung”

The injury is not uniform. Dependent regions collapse under the weight of the oedematous lung above while non-dependent regions stay aerated, leaving a small volume of functioning lung to receive the whole tidal breath. This is the central insight of modern ARDS care: a “normal” tidal volume delivered to a lung with only a third of its units available is a large and injurious one.

Ventilator-induced lung injury

Overdistension of the aerated regions (volutrauma), repeated opening and closing of unstable units (atelectrauma) and the resulting inflammatory cascade (biotrauma) all extend the original injury. Much of what was once considered the natural history of ARDS was in fact caused by how it was ventilated — which is why the single largest advance in treatment was ventilating less.

The proliferative and fibrotic phases

After the first week, some patients resolve while others progress to fibroproliferation, with collagen deposition, persistent low compliance and, in a minority, lasting fibrosis. Pulmonary vascular obliteration and pulmonary hypertension contribute to right ventricular strain, which is an under-recognised cause of death in this population.

Co-morbidities

ARDS arises in the context of critical illness, so outcomes are shaped largely by the underlying trigger and by coexisting conditions — sepsis, pneumonia, chronic lung or heart disease, chronic kidney or liver disease, immunosuppression, frailty, obesity and diabetes. Alcohol use disorder and smoking both increase susceptibility. Survivors frequently develop ICU-acquired weakness and the physical, cognitive and psychological problems of post-intensive care syndrome.

Prevalence

ARDS accounts for around 10% of intensive care admissions and about one in four mechanically ventilated patients internationally. It is under-recognised: a large international study found clinician recognition at the time of meeting criteria occurred in only around 60% of cases, with under-recognition associated with less use of lung-protective ventilation. It became far more visible during the COVID-19 pandemic. Mortality remains substantial and rises with severity, from roughly a quarter in mild disease to nearly half in severe, although it has improved with lung-protective care.

Causes and risk factors

• Pneumonia and other direct lung infections — the commonest trigger.
• Sepsis from any source — the commonest indirect trigger and the one with the highest mortality.
• Aspiration of gastric contents.
• Major trauma, including chest injury and pulmonary contusion, and multiple fractures with fat embolism.
• Pancreatitis, major surgery and massive transfusion (transfusion-related acute lung injury).
• Near-drowning, smoke inhalation and toxic inhalation.
• Severe COVID-19 and influenza, both well-recognised causes.
• Risk amplifiers — alcohol use disorder, smoking, obesity, hypoalbuminaemia and delayed treatment of the trigger.

Symptoms

Typical features

• Rapidly worsening breathlessness and a very fast respiratory rate, usually within 12 to 72 hours of the trigger.
• Hypoxaemia that does not correct with supplemental oxygen — the cardinal feature.
• Visible respiratory distress: accessory muscle use, inability to speak in sentences, agitation then exhaustion.
• Features of the underlying illness — fever, cough, or the effects of injury, sepsis or pancreatitis.
• In a ventilated patient, escalating oxygen and pressure requirements with falling compliance.

What it feels like for the patient

Those who are awake in the early phase describe air hunger and a terror disproportionate to anything they can convey. This matters clinically as well as humanely: distress drives high respiratory drive and large spontaneous tidal volumes, which can worsen lung injury.

Recognising deterioration

Diagnosis

Why diagnosis matters

Recognising ARDS early allows prompt lung-protective ventilation and treatment of the trigger — the two interventions that most influence survival. Because under-recognition is common and directly linked to less protective ventilation, actively applying the criteria rather than waiting for the diagnosis to become obvious is itself a therapeutic act.

How is it diagnosed?

Diagnosis is clinical and radiological, using the Berlin definition: an acute trigger within a week, bilateral infiltrates, hypoxaemia by PaO₂/FiO₂ ratio measured with at least 5 cmH₂O of positive end-expiratory pressure, and exclusion of cardiogenic pulmonary oedema as the sole explanation.¹ Arterial blood gases quantify the oxygenation defect.

Radiology

Chest X-ray shows bilateral airspace opacification. CT reveals the characteristic gravitational gradient — dense dependent consolidation, ground glass in intermediate zones, relatively spared non-dependent lung — and identifies a treatable trigger such as an abscess or empyema. Lung ultrasound is increasingly used at the bedside to distinguish ARDS from cardiogenic oedema and to monitor recruitment.

Excluding cardiogenic pulmonary oedema

Echocardiography is central: it assesses left ventricular function, excludes cardiogenic pulmonary oedema as the whole explanation, and assesses the right ventricle, since acute cor pulmonale is common in severe ARDS and changes ventilation strategy. The two conditions can coexist, and the Berlin definition requires only that cardiac failure does not fully explain the picture.

Investigations for related conditions

Investigation targets the cause and its complications: blood and sputum cultures, respiratory viral panel, inflammatory markers, lipase, and imaging of the abdomen or trauma sites. Bronchoscopy with lavage is used where the cause is unclear or an atypical or opportunistic infection is suspected. During recovery, lung function and exercise testing characterise residual impairment.

Management

Management and goals

There is no treatment for ARDS itself. Care is supportive while the lungs heal, and the goals are to maintain acceptable gas exchange without causing further lung injury, treat the trigger, prevent the complications of critical illness, and begin rehabilitation early. Almost every advance in this field has come from doing less harm rather than adding treatment.

Lung-protective ventilation

The foundation. Ventilation with lower tidal volumes of 6 mL/kg predicted body weight, with plateau pressure limited to 30 cmH₂O, significantly reduced mortality compared with traditional volumes of 12 mL/kg in the landmark ARDS Network trial.² Higher PEEP strategies are used to keep unstable units open, but aggressive recruitment is not benign: a trial of lung recruitment with titrated PEEP versus low PEEP found increased 28-day mortality in the recruitment group.³ PEEP is titrated to the individual rather than escalated on principle.

Prone positioning

Turning the patient face-down redistributes ventilation towards the dorsal lung, improves ventilation–perfusion matching and reduces regional overdistension. In moderate-to-severe ARDS, prone positioning for at least 16 hours a day significantly reduced 28-day and 90-day mortality.⁴ It is one of the few interventions in critical care with an unequivocal mortality benefit, and it is a labour-intensive, physiotherapy-relevant manoeuvre with real risks — pressure injury, line and tube dislodgement, brachial plexus injury — that skilled teams manage.

Fluid management

A conservative fluid strategy improved oxygenation and increased ventilator-free days compared with a liberal strategy, without increasing non-pulmonary organ failure.⁵ Keeping the lung dry, once shock has resolved, is an active treatment decision made daily.

Adjuncts and rescue therapies

Neuromuscular blockade is used in the first 48 hours in severe ARDS in some centres, with the evidence now equivocal and its contribution to weakness a real concern. Inhaled pulmonary vasodilators improve oxygenation transiently without improving survival. Extracorporeal membrane oxygenation is used in the most severe refractory cases in specialist centres. Corticosteroids have a role in selected causes, notably COVID-19 ARDS.

Early rehabilitation

Early physical and occupational therapy delivered during sedation interruption improved return to independent function at hospital discharge and reduced delirium and ventilator days.⁶ Rehabilitation in ARDS is not something that begins after extubation; it begins alongside the ventilator.

Identifying deterioration

Falling compliance, rising driving pressure, worsening hypercapnia, new haemodynamic instability or right ventricular dilatation on echocardiography all signal progression and prompt reassessment of ventilation strategy, consideration of proning, and re-examination of the trigger for an untreated source.

Multi-system manifestations

Right heart

Acute cor pulmonale from pulmonary vascular obliteration, hypoxic vasoconstriction and high airway pressures affects a substantial minority of severe cases and independently predicts mortality. It is a reason to limit driving pressure and to consider proning, and a reason to echo these patients.

Kidneys

Acute kidney injury is common, driven by shock, sepsis, nephrotoxins and the haemodynamic consequences of positive pressure ventilation. It complicates fluid management, since the conservative strategy that helps the lung may be harder to deliver.

Neuromuscular

ICU-acquired weakness affects most patients ventilated for a week or more, worsened by sedation, neuromuscular blockade, corticosteroids and immobility. It, rather than lung function, is the dominant limitation on recovery.

Brain

Delirium during the admission is near-universal, and new long-term cognitive impairment — affecting attention, memory and executive function — persists in a large proportion of survivors, sometimes at a level comparable to mild dementia in previously working adults.

Mental health

Anxiety, depression and post-traumatic stress symptoms are common in survivors and in their families, frequently rooted in delirium memories, and are strongly associated with worse physical recovery.

Long-term physical function

Five-year follow-up of ARDS survivors found persistently reduced six-minute walk distance and physical quality of life, with muscle wasting and weakness — not lung function — the dominant complaint.⁷ This finding reframes ARDS as a systemic illness with a pulmonary trigger, and it is the strongest argument for long-horizon rehabilitation.

Living with the aftermath of ARDS

A recovery measured in months to years

Most survivors improve substantially over the first six to twelve months, but the trajectory is rarely linear and rarely complete within a year. Patients discharged looking well are frequently unable to climb their own stairs, and the gap between how they look and how they function causes real distress.

Fatigue and pacing

Disproportionate, unpredictable fatigue is the symptom survivors find hardest to explain. Planning around a limited energy budget, and accepting a non-linear course, prevents the boom-and-bust cycle that stalls progress.

Nutrition

Substantial muscle and weight loss occurs during the admission, and appetite is poor exactly when protein requirements are highest. Weight regained without resistance exercise is largely fat, so nutrition and exercise are prescribed together.

Sleep and mood

Fragmented sleep, nightmares and altered circadian rhythm are common for months and amplify fatigue, pain and low mood. Screening for anxiety, depression and post-traumatic symptoms is part of follow-up rather than an optional extra.

Return to work and family impact

Return to work is frequently delayed by a year or more and sometimes not achieved, with financial and relationship strain following. Family members carry a substantial burden of their own, with high rates of anxiety and post-traumatic symptoms.

Follow-up and peer support

ICU follow-up clinics, where available, provide explanation, screening and coordination that primary care is not resourced to deliver. Meeting other survivors addresses the isolation of an illness few people around the patient understand.

Prognosis

Outcomes depend on severity, the underlying cause, age and co-morbidity. Hospital mortality ranges from roughly a quarter in mild ARDS to nearly half in severe disease, and death is more often from the underlying illness and multi-organ failure than from refractory hypoxaemia. Among survivors, lung function usually improves substantially over the first six to twelve months and is often near-normal at one year — but physical, cognitive and psychological recovery lags well behind, and a significant proportion never return to their previous functional level.⁷ Prognostic conversations that focus only on the lungs miss most of what determines the person’s future.

Role of the physiotherapist

Physiotherapy is central throughout the ARDS journey, and its contribution changes markedly by phase.

In the acute phase, the role is positioning — including participation in prone positioning, one of the few mortality-reducing interventions in critical care and one that depends on skilled, coordinated manual handling to be delivered safely. Airway clearance is used selectively rather than routinely, since manual techniques in a stiff, inflamed, oedematous lung offer little and can destabilise. Assessment of readiness for mobilisation, and advocating for sedation minimisation so that it becomes possible, are part of the daily contribution.

In the recovery phase in ICU and on the ward, the task is early mobilisation and progressive rehabilitation against a background of profound weakness, supporting weaning, rebuilding sitting balance, standing and stepping, and monitoring cough strength and secretion clearance while respiratory muscles remain weak.

In the community, it is long-horizon work: progressive strengthening, cardiorespiratory rehabilitation, breathing retraining, fatigue management and pacing, and the patient-defined return-to-life goals that determine whether recovery feels real. Given that muscle weakness rather than lung function limits most survivors at five years, this phase is where physiotherapy has the greatest long-term effect — and the physiotherapist is frequently the clinician who finally explains to the patient what happened to their body.

Part 1 · References

1. Ranieri VM, Rubenfeld GD, Thompson BT, et al; ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin definition. JAMA 2012;307(23):2526–2533.
2. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342(18):1301–1308.
3. Cavalcanti AB, Suzumura ÉA, Laranjeira LN, et al; Writing Group for the Alveolar Recruitment for ARDS Trial (ART) Investigators. Effect of lung recruitment and titrated PEEP vs low PEEP on mortality in patients with ARDS. JAMA 2017;318(14):1335–1345.
4. Guérin C, Reignier J, Richard JC, et al; PROSEVA Study Group. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med 2013;368(23):2159–2168.
5. Wiedemann HP, Wheeler AP, Bernard GR, et al; NHLBI ARDS Clinical Trials Network. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med 2006;354(24):2564–2575.
6. Schweickert WD, Pohlman MC, Pohlman AS, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial. Lancet 2009;373(9678):1874–1882.
7. Herridge MS, Tansey CM, Matté A, et al; Canadian Critical Care Trials Group. Functional disability 5 years after acute respiratory distress syndrome. N Engl J Med 2011;364(14):1293–1304.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.