Atelectasis

Definition

Atelectasis is incomplete expansion, or collapse, of lung tissue — from a few air sacs (sub-segmental) up to a whole lobe or lung. It is not a disease in its own right but the consequence of something else: shallow breathing, a blocked airway, pressure on the lung from fluid or air in the pleural space, or loss of surfactant. Establishing which mechanism is at work is what determines treatment, and separates a problem that physiotherapy will reverse from one that needs a medical or surgical decision.

The four mechanisms

Pathophysiology

Why lung units close

Healthy lungs depend on regular deeper breaths (sighs) and an adequate resting lung volume to keep the smallest airways and air sacs open. Anaesthesia, pain, sedation, immobility and abdominal or chest surgery all reduce functional residual capacity and abolish sighing, so dependent lung units close. Once closed, a unit needs a higher pressure to reopen than it did to stay open — which is why prevention is far easier than treatment, and why one sustained deep breath achieves more than many shallow ones.

What happens once they close

The consequences follow quickly. Blood continues to flow past unventilated tissue (shunt), so oxygen levels fall. Secretions pool in the closed segment, and warm, stagnant, mucus-filled tissue is fertile ground for infection: untreated post-operative atelectasis is a common pathway to pneumonia. Work of breathing rises because the remaining lung must do the whole job at a less efficient point on its pressure–volume curve.

Co-morbidities

Atelectasis rarely occurs in isolation, and the company it keeps changes the treatment plan:

• Pneumonia — the commonest sequel of unresolved collapse; suspect it with fever, purulent sputum or a rising inflammatory response.
• Chronic lung disease — COPD, bronchiectasis and cystic fibrosis bring a higher sputum burden and a less effective cough.
• Pleural disease — effusion, empyema and pneumothorax cause compressive collapse that expansion therapy alone will not fix.
• Obesity and abdominal distension — both reduce resting lung volume and make dependent collapse more likely.
• Neuromuscular weakness and pain — rib fractures, flail chest, upper abdominal incisions and weak respiratory muscles all limit breath size and cough force.
• Critical illness — sedation, ventilation and ICU-acquired weakness combine to make collapse both more likely and harder to reverse.

Prevalence

Atelectasis is among the most common findings in hospital medicine. Dependent collapse appears on imaging in the great majority of adults within minutes of induction of general anaesthesia, and some degree persists for days after major abdominal or thoracic surgery. Clinically significant post-operative pulmonary complications — of which atelectasis is the most frequent — affect a substantial minority of patients after upper abdominal surgery, and considerably more where risk factors cluster: older age, smoking, existing lung disease, prolonged surgery, and reduced mobility. In the intensive care unit it is near-universal in sedated, supine, ventilated patients.

Causes

• After surgery — especially upper abdominal, thoracic and cardiac surgery; pain and splinting reduce breath size and suppress cough.
• Retained secretions — bronchiectasis, cystic fibrosis, COPD, weak cough from neuromuscular disease or a tracheostomy.
• Immobility and bed rest — the single most modifiable risk factor in hospital.
• Mechanical ventilation — sedation, paralysis, low tidal volumes, high inspired oxygen, and long periods lying supine.
• Pleural and abdominal pressure — effusion, ascites, obesity, rib fractures.
• Airway obstruction — lung cancer, mucus plugging, aspiration or an inhaled foreign body.¹

Symptoms

When there are no symptoms

Small areas of collapse frequently cause nothing at all and are found only on imaging, or inferred from a falling oxygen saturation before any change is visible. Absence of symptoms is not absence of consequence — silent collapse still shunts blood, still pools secretions, and still progresses to infection if the cause is not addressed.

Typical features

Larger collapse typically produces:

• Breathlessness, particularly on effort, and a sense of not getting a satisfying breath.
• A low or falling oxygen level — see Low Oxygen & Ventilation.
• A weak, ineffective or wet-sounding cough, sometimes with a feeling that something is stuck and will not shift.
• An increased breathing rate and visible effort; fatigue out of proportion to activity.
• Fever, discoloured sputum or malaise if infection follows.

Warning signs

Diagnosis

Importance of a diagnosis

Atelectasis is easily mistaken for pneumonia or an effusion, and each needs a different response. Identifying the mechanism decides whether the answer is a bigger breath, a cleared airway, drainage of fluid, or a bronchoscopy.

How is it diagnosed?

At the bedside: reduced chest expansion on the affected side, reduced or absent breath sounds (sometimes bronchial breathing over collapsed tissue), crackles that do not clear with coughing, a dull percussion note, falling SpO₂ and rising work of breathing. See Auscultation for technique.

Imaging

A chest X-ray shows volume loss: a raised hemidiaphragm, crowded ribs, linear or lobar opacity, and — the decisive sign — mediastinal shift towards the collapse. Consolidation and effusion do not pull structures towards them. CT is used where the cause is unclear or a tumour is suspected, and bronchoscopy where a central plug or lesion is likely.

Other tests

Blood gases quantify shunt where oxygenation is a concern; sputum culture guides treatment if infection has supervened. In the ventilated patient, a fall in compliance and a rise in oxygen requirement often precede the radiographic change.

Management

Treat the mechanism

Effective management follows the cause, not a protocol. Volume loss from small breaths needs bigger, held breaths and upright positioning; a plug needs humidification and clearance, and sometimes bronchoscopy; compression needs the effusion, air or distension relieved before expansion therapy can achieve anything.^2,3

Sequence of treatment

1. Remove the cause where possible — adequate analgesia so deep breathing is achievable, drainage of a large effusion, relief of abdominal distension, bronchoscopic removal of a central plug.
2. Get moving — sitting up, standing and walking increase lung volume more than any device; upright positioning alone recruits dependent lung.
3. Make the breaths bigger — sustained maximal inspiration, breath-stacking, incentive spirometry, or ACBT for lung expansion. The goal is volume and a held breath, not speed.
4. Add pressure where volume alone is insufficient — PEP or oscillating devices, IPPB, or CPAP/NIV to splint airways open and re-recruit tissue. A clinical decision, not a default.
5. Clear the secretions that caused it — airway clearance, gravity-assisted positioning, humidification, hydration and a supported cough, or cough assist where the cough is weak.
6. Keep it open — short, frequent repetition through the day beats one long session, plus early mobilisation and a routine the patient owns.

When to escalate

Escalate rather than persist if the oxygen requirement climbs, the work of breathing rises, a whole lobe fails to re-expand, the patient becomes confused or exhausted, or fever and purulent sputum suggest infection. Physiotherapy reverses most atelectasis — but a central obstruction, a large effusion or evolving respiratory failure needs a medical decision, not more repetitions.^4,5

Prevention

Almost all peri-operative atelectasis is preventable, and prevention is largely a physiotherapy task: pre-operative teaching of deep breathing, supported cough and early walking (see Pre-Surgical Rehabilitation); analgesia optimised before treatment; out of bed early and often; smoking cessation before elective surgery; and hourly practice of a simple breathing routine while recovery is under way.^6,7

Living with atelectasis

Usually a short-lived episode

For most people atelectasis is a brief event during a hospital admission, fully reversed before discharge, and there is nothing to live with afterwards. Saying so explicitly is worthwhile: patients told their lung has collapsed frequently assume permanent damage.

When it recurs

Where it recurs — in chronic sputum-producing disease, neuromuscular weakness or after repeated admissions — the aim shifts from a one-off fix to a sustainable daily routine: a clearance regimen that fits the day, a plan for what to do when sputum increases, and enough activity to keep lung volumes up.

Rebuilding confidence in deep breathing

People who have had significant collapse, painful surgery or a frightening episode of breathlessness are often understandably wary of breathing deeply, and will quietly avoid exactly the manoeuvre that treats them. Rebuilding that confidence — explaining what the exercise does, timing it with analgesia, starting small and demonstrating the result on the oximeter — is part of the treatment rather than a preliminary to it.

Prognosis

Most atelectasis resolves within days once the cause is addressed, with no lasting damage and no long-term consequence. Recovery is slower where the cough is weak, secretions are chronic, or the person cannot mobilise, and unresolved collapse carries a real risk of pneumonia, a longer hospital stay and — in older or frailer patients — loss of function that outlasts the admission. Cicatricial atelectasis from established scarring will not re-expand; treatment then targets the remaining lung and exercise capacity instead.

Role of the physiotherapist

Assessment: establishing the mechanism

Atelectasis is the condition cardiorespiratory physiotherapy exists to treat, and the assessment is what makes the treatment work. Auscultation, chest expansion, cough strength, oxygen saturation, imaging and the clinical context together establish which of the four mechanisms is operating — because a plug, a small breath and a compressing effusion look similar at the bedside and respond to entirely different treatments.

Treatment matched to the mechanism

Treatment follows from that: positioning and mobilisation to restore lung volume, lung-expansion techniques to reopen closed units, and airway clearance to remove what caused the obstruction. We also protect the gain: a routine the patient can carry out without us, timed around their analgesia and reviewed as they improve. In hospital we work alongside the nursing and medical teams and escalate early when the trajectory is wrong; in the community we treat the same problem in slower motion, in people whose cough or mobility has declined.

Prevention

Prevention is the highest-value contribution of all. A single pre-operative teaching session measurably reduces post-operative pulmonary complications, and getting a patient out of bed on the first post-operative day does more for lung volume than any device. Most of the atelectasis treated on a ward round did not need to happen.

Part 1 · References

1. Hedenstierna G, Edmark L. Effects of anesthesia on the respiratory system. Best Pract Res Clin Anaesthesiol 2015;29(3):273–284.
2. Strickland SL, Rubin BK, Drescher GS, et al. AARC clinical practice guideline: effectiveness of nonpharmacologic airway clearance therapies in hospitalized patients. Respir Care 2013;58(12):2187–2193.
3. Reeve J, Boden I. The physiotherapy management of patients undergoing thoracic surgery. NZ J Physiother 2016;44(2):61–77.
4. Ireland CJ, Chapman TM, Mathew SF, Herbison GP, Zacharias M. Continuous positive airway pressure (CPAP) during the postoperative period for prevention of postoperative morbidity and mortality following major abdominal surgery. Cochrane Database Syst Rev 2014;(8):CD008930.
5. Hodgson CL, Fan E, Bersten A. Recruitment manoeuvres for adults with acute respiratory distress syndrome receiving mechanical ventilation. Cochrane Database Syst Rev 2016;(11):CD006667.
6. Boden I, Skinner EH, Browning L, et al. Preoperative physiotherapy for the prevention of respiratory complications after upper abdominal surgery (LIPPSMAck-POP): pragmatic, double blinded, multicentre randomised controlled trial. BMJ 2018;360:j5916.
7. Freitas ERFS, Soares BGO, Cardoso JR, Atallah ÁN. Incentive spirometry for preventing pulmonary complications after coronary artery bypass graft. Cochrane Database Syst Rev 2012;(9):CD004466.

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.