Postoperative pulmonary dysfunction (PPD) is an important contributor to morbidity and mortality in patients receiving anaesthesia. Aetiology is often multifactorial and clinical manifestations range from mild hypoventilation to cardio respiratory arrest.
Understanding the respiratory physiology, preoperative assessment and optimization, optimal intra operative management and postoperative care help in minimizing PPD.
Basic respiratory physiology and effects of anaesthesia
Gas exchange involves oxygen intake and exhalation of CO2; both the processes being affected by anesthesia. Oxygen travels from atmosphere down a pressure gradient, oxygen cascade, through the nose, mouth, airway and finally across the alveolar capillary membrane while CO2 traverses in the opposite direction. From respiratory point of view, for a normal gas exchange to occur following are essential: a) airway patency b) normal work of breathing c) normal alveolar capillary membrane d) adequate perfusion of ventilating alveoli and e) minimal shunt fraction (normally less than 2% in adults). Similarly, for CO2 transport, adequate delivery of CO2 to the lungs by a well maintained circulation and adequate ventilation to eliminate it from the lungs to atmosphere are essential.
Normal oxygen related parameters and values
· FiO2 0.21 at sea level, decreases at high altitude.
· Normal oxygen saturation at room air, SaO2 98-99%, decreases with increasing age
· PaO2, arterial partial pressure of oxygen for the above saturation: 97-100mmHg, decreases with age. As a rule of thumb PaO2 is FiO2 (as %) x5. Eg: If FiO2 is 30%, expected PaO2 is 150mmHg.
· CaO2 is the oxygen content of arterial blood (ml/ dl), product of oxygen bound to Hb (1.34 X Hb) and amount of oxygen dissolved in the blood (0.003 XPaO2), which is 20ml/dl in a healthy adult
· DO2 is the oxygen delivery to the tissues, 1000ml in patient of 70Kg body weight.
· SvO2, mixed venous oxygen saturation, normal value 75%
Effects of general anesthesia on respiratory function
· Depression of respiratory centre
· Muscle relaxation and altered muscle function
· Suppression of airway reflexes
· Reduction in functional residual capacity (FRC) : Induction of general anesthesia, assuming supine position and muscle paralysis
· Absorption atelectasis
· Changes in lung volume and compliance
· Effect on hypoxic pulmonary vasoconstriction (HPV)
· Increased resistance to breathing
· Effect on ventilation perfusion relation : V/Q mismatch,
· Effects on mucociliary function
Risk of postoperative pulmonary dysfunction is determined by patient factors, surgical factors and anesthesia related factors. They can be modifiable or non modifiable
Patient related factors: predictors of postoperative pulmonary complications
- Extremes of age
- Preoperative pulmonary dysfunction : especially advanced Chronic obstructive pulmonary disease (COPD), bronchial asthma, pleural effusion, malignancy etc
- History of chemotherapy and radiotherapy; increased risk of oxygen toxicity.
- History of pulmonary resection
- Bronchopleural fistula
- Obstructive sleep apnoea (OSA)
- Positive cough test
- Preoperative abnormal blood gases and spirometry values: FEV1< 1L, FVC < 1.5L, PaCO2 >45mmHg and PaO2 < 50mmHg)
- Prolonged surgery (more than 2.5h)
- Upper abdominal surgery
- Laparoscopic surgery
- Pulmonary and intrathoracic surgery
- Cardiac surgery
- Airway surgery
Anaesthesia related risk factors
- Inadvertent endobronchial intubation
- One lung ventilation
- Inhibition of hypoxic pulmonary vasoconstriction (HPV)
- Increased dead space and shunt
- Fluid overload
Different types of postoperative pulmonary complications and management
Acute lung injury, including transfusion related acute lung injury (TRALI)
Bronchitis and pneumonia (infections)
Hypoxemia or hypoxia, defined as PaO2 of less than 60mmHg on room air (in a patient who was preoperatively not hypoxic), is the most common and also the most important one. Also, often it is the final common pathway for many of other complications. Mechanisms include hypoventilation, acute lung injury, atelectasis and increased dead space and shunt among several others.
Pathophysiological mechanisms inducing hypoxemia in the post operative period
Airway obstruction ( inadequate reversal, respiratory depression, hematoma)
- Oxygen therapy, with simple oxygen mask, nasal prongs or ventury mask. Maximum FiO2 achievable this way is 0.6. In most of the previously healthy patients, a marginal increase in FiO2, 0.3-0.4 is sufficient to correct hypoxia
- Specific treatment depends on the cause such as a) treatment of bronchospasm b) diuretics in case of fluid overload c) fluids in case of hypovolemia d) Analgesics e) opioid antagonists f) non invasive ventilation and g) endotracheal intubation.
- Some patients with severe hypoxemia might require mechanical ventilation
COPD patients can develop respiratory depression with oxygen therapy and should be appropriately monitored for the same.
Hypoventilation, more specifically alveolar hypoventilation, can result from decreased respiratory drive (opioid induced respiratory depression), compromised respiratory muscle function (inadequate reversal, rib fractures, fluid overload, respiratory muscle fatigue in COPD patients, patients with OSA etc) and increased dead space ventilation and atelectasis.
Management is by treating the cause and supportive oxygen therapy.
Susceptible patients : emphysema, emphysematous bullae, surgeries where thorax has been opened and closed without intercostal drain and procedures like supraclavicular brachial plexus block and subclavian vein cannulation.
Diagnosis is by falling oxygen saturation, progressive difficulty in breathing and reduced air entry. Chest X Ray is diagnostic. Desaturation is more rapid and associated with hemodynamic instability when it is tension pneumothorax which requires immediate insertion of a large bore needle (connected to underwater drainage system) into the pleural cavity in the mid clavicular line in the second intercostal space.
Pneumothorax is treated with intercostal drainage.
Bronchospasm is not very common in the postoperative period except in patients with uncontrolled or ill controlled bronchial asthma. Bronchodilator treatment and oxygen supplementation should be initiated.
Pulmonary edema is manifested by fall in oxygen saturation, frothy sputum at the mouth and bilateral reduced air entry with crepitiations. Treatment should be aggressive with ventilation ( NIV if mild and invasive with endotracheal intubation if severe), morphine and positive pressure ventilation.
Postoperative pulmonary embolism manifests as sudden onset dyspnoea with chest pain and desaturation. Fat embolism, amniotic fluid embolism (rare) and deep vein thrombosis are the important causes.
Acute lung injury (ALI)
Various causes of ALI include direct contusion and damage to lungs, aspiration, fat embolism (long bone fractures), blood transfusion etc. ALI is said to be present when the PaO2/FiO2 ratio is less than 300 in a previously healthy person. Manifestations include dyspnoea which is progressive and hypoxia which is resistant to conventional oxygen therapy and bilateral chest infiltrates.
Management depends on the severity, rapidity of progress and the cause. Treatment modalities include oxygen therapy, endotracheal intubation and mechanical ventilation, antibiotics, invasive monitoring etc.
Transfusion induced ALI (TRALI) is an independent clinical entity with a immunological basis.
Approach to a patient with PPC
- Careful documentation of preoperative status and intraoperative management
- Proper hand over of the information to the post operative staff
- Monitoring for anticipated complications. SpO2, ECG, NIBP and monitoring for excessive sedation.
- Hypoxia should be ruled out in any patient who is restless or agitated in the postoperative period
- Once hypoxia is present, irrespective of the cause ( which may be extrapulmonary also), pulmonary mechanism involved should be looked for.
- Patient should be started on oxygen therapy and sample sent for arterial blood gas analysis.
- Chest X Ray
- Echocardiographic evaluation of the cardiac function if pulmonary embolism is suspected
- Other investigations as appropriate to the cause suspected
- Interventions like endotracheal intubation and mechanical ventilation should be kept ready
Postoperative pulmonary dysfunction is common and the consequences can vary from asymptomatic and harmless outcome to significant morbidity and mortality. First step in the prevention is to identify the patients at risk preoperatively and prepare them adequately. Optimal intraoperative management with lung expansion manoeuvres, avoiding excessive inspired oxygen concentration, adequate analgesia, and proper airway management and monitoring help in early diagnosis and prevention of PPC.
- Stop smoking, weight reduction and deep breathing exercise
- Correction of hydration status
- Improve nutrition
Optimal intraoperative management
- Optimal oxygenation by providing adequate FiO2, HME filters to maintain mucociliary function
- Optimal ventilation, especially with one lung anaesthesia
- Prevention of fluid overload
- Avoiding excessive Preoxygenation with 100% oxygen. Most of the patients who are otherwise normal and who have normal airway do not require prolonged Preoxygenation with high FiO2 as it can lead to absorption atelectasis
- Lung recruitment manoeuvres : PEEP, sigh,
- Optimal analgesia : consider epidural analgesia
- Adequate reversal from neuromuscular blockade
- Oxygen supplementation
- Deep breathing incentive spirometry
1)Rudra A, Sudipta Das Post operative pulmonary complications, Indian J anaesth. 2006; 50 (2): 89-98
2)Z A Denu et al J Anesth Clin Resp Aug 2015
3)BCMJ, Vol 50, No 3, April 2008
4) Miller’s text book of anaesthesia, 8th edition