Postoperative Atelectasis

Postoperative atelectasis is collapse of alveoli or lung segments after anaesthesia and surgery. It is the commonest postoperative pulmonary complication and a precursor of hypoxaemia and pneumonia.

Epidemiology. CT shows atelectasis in about 90% of anaesthetised adults, involving 5% to 20% of lung area. Clinically significant collapse affects about 10% to 40% after upper abdominal, thoracic and cardiac surgery. It peaks in the first 24 to 48 hours.

Risk factors. Obesity, smoking, COPD, advanced age, upper abdominal, thoracic or aortic surgery, ascites, obstructive sleep apnoea, pain with splinting, opioids, prolonged supine positioning, nasogastric tube and high inspired oxygen during induction and emergence.

Pathophysiology.

Compression atelectasis follows loss of diaphragmatic tone, cranial diaphragm shift and fall in functional residual capacity.

Absorption atelectasis occurs when high oxygen concentrations (over 80%) wash out nitrogen in poorly ventilated alveoli. Surfactant dysfunction, impaired mucociliary clearance and ineffective cough add to collapse.

Collapsed lung causes shunt and ventilation perfusion mismatch, so hypoxaemia results.

Often silent. Signs include tachypnoea, tachycardia, low saturation, dyspnoea, low grade fever in the first 48 hours, reduced breath expansion, reduced breath sounds, bronchial breathing and basal dullness. With lobar collapse the trachea shifts toward the affected side.

Red flags.

• Saturation under 90% despite oxygen.
• Respiratory rate over 30/min.
• Pleuritic pain, haemoptysis or sudden onset (embolism, pneumothorax).
• Purulent sputum with fever beyond 48 hours (pneumonia).
• Haemodynamic instability.

Clinical diagnosis supported by imaging. Chest radiograph shows linear or plate like opacities, volume loss, fissure displacement, a raised hemidiaphragm or mediastinal shift. Lung ultrasound shows consolidation with static air bronchograms. CT is for unclear or persistent cases. Arterial blood gas shows hypoxaemia with a widened alveolar arterial gradient.

Differential diagnosis.

• Pneumonia.
• Pleural effusion.
• Pulmonary oedema.
• Pneumothorax.
• Pulmonary embolism.
• Phrenic nerve palsy.
• Aspiration.
• Early acute respiratory distress syndrome.

Prevention. Intraoperative positive end expiratory pressure of 5 to 10 cmH2O, recruitment before extubation, lowest effective inspired oxygen (avoid 100% at induction and emergence), lung protective tidal volumes, regional or epidural analgesia, preoperative smoking cessation and inspiratory muscle training.

Treatment.

• Sit upright at 30 to 45 degrees, mobilise early.
• Incentive spirometry: 10 breaths each hour while awake.
• Deep breathing, coughing with wound support, chest physiotherapy.
• Effective multimodal analgesia.
• CPAP 5 to 10 cmH2O intermittently or continuously, especially in obesity.
• Oxygen to saturation 94% to 98% (88% to 92% if hypercapnic risk).
• Bronchoscopy for lobar collapse not responding to physiotherapy within 24 hours.
• Salbutamol nebulised 2.5 to 5 mg up to 4 times daily for wheeze; monitor heart rate and potassium; use cautiously in arrhythmia or thyrotoxicosis.

Monitoring. Continuous saturation, respiratory rate, blood gas if hypoxaemic, and repeat radiograph at 48 to 72 hours if no improvement.

Referral and escalation. Respiratory or critical care review for hypoxaemia unresponsive to CPAP, rising carbon dioxide, fatigue, or need for bronchoscopy.