Postoperative Pulmonary Complications

Milad Sharifpour

Edward A. Bittner

Patients undergoing general anesthesia (GA) are at risk for developing postoperative pulmonary complications (PPCs). PPCs commonly include atelectasis, hypoxemia, pneumothorax, pleural effusion, pneumonia, acute respiratory distress syndrome, and postoperative respiratory failure (PRF). The incidence of PPCs is 2% to 19%, depending on the patient population, the surgical procedure, and the type of respiratory complications studied and is comparable to that of postoperative cardiovascular complications. These complications are associated with increased mortality, intensive care unit (ICU) admissions, and increased length of stay.

I. POSTOPERATIVE RESPIRATORY FAILURE

Postoperative respiratory failure is defined as failure to wean from mechanical ventilation within 48 to 72 hours or the need for unplanned postoperative intubation. It occurs in up to 3% of the patients undergoing noncardiac surgery and is associated with increased mortality and the development of further complications such as myocardial infarction, pneumonia, renal failure, deep venous thrombosis, and pulmonary embolism. Despite advances in perioperative care, the incidence of PRF and its associated mortality have remained largely unchanged.

A. The pathophysiology of PPCs can be broadly categorized into three categories: Anesthetic related, surgical factors, and coexisting patient comorbidities.

1. Effects of anesthetics and sedatives. GA affects the respiratory system by altering respiratory drive and mechanics via the following mechanisms:

a. Reduction in respiratory drive. Volatile anesthetics, sedatives, and opioids are respiratory depressants. They exert their effects by blunting central and peripheral chemoresponsiveness to hypoxemia and hypercapnia, suppressing normal reflexive responses to negative upper airway pressure, and decreasing wakefulness.

1. Opioids, the most commonly prescribed analgesics for postoperative pain control, are potent inhibitors of the hypercapnic ventilatory drive. Respiratory failure secondary to postoperative opioid use peaks during the first 24 hours. Patients treated with opioids have a decreased respiratory rate and may become apneic if not stimulated. Benzodiazepines also inhibit ventilatory drive, but to a lesser extent than opioids. The effects of these drugs are dose dependent and influenced by age and comorbidities such as intracranial pathology, obstructive sleep apnea (OSA), or chronic obstructive pulmonary disease (COPD).

b. Residual neuromuscular blockade often persists despite reversal of muscle relaxants. The upper airway dilator muscles are particularly sensitive to the effects of muscle relaxants, increasing the risk of upper airway obstruction, aspiration, and reintubation when not fully reversed. Neuromuscular blocking agents should be avoided
or administered judiciously in patients with neuromuscular disorders such as Guillain-Barré, myasthenia gravis, and muscular dystrophies.

c. Modified respiratory mechanics. GA alters lung and chest wall mechanics, causing reductions in lung volume and compliance, and chest wall compliance. Immediately after induction of GA functional residual capacity (FRC) decreases by as much as 20%, resulting in atelectasis in dependent regions of the lung. Atelectasis formation is further exacerbated by supine positioning of patients, as well as absorption of alveolar gas (absorption atelectasis) caused by high concentrations of oxygen. Reduced FRC and atelectasis cause ventilation perfusion mismatch, shunting, and hypoxemia.

d. Intraoperative mechanical ventilation. Ventilator induced lung injury (VILI) results from repetitive overdistention and collapse of dependent lung tissue. Lung protective ventilation with low tidal volumes, low plateau pressures, and the administration of positive end-expiratory pressure (PEEP) is the cornerstone of mechanical ventilation in ICU patients with ARDS. Patients undergoing surgery under GA may also benefit from low tidal volumes, low plateau pressures, higher levels of PEEP, and intraoperative recruitment maneuvers.

2. Impact of surgery: A number of surgery-related factors are associated with the development of PPCs:

a. Location. Upper abdominal and intrathoracic surgical procedures have the strongest association with PPCs.

b. Degree of invasiveness. Surgical trauma to respiratory muscles (diaphragm and/or intercostals) and phrenic nerve can directly cause respiratory muscle impairment. Postoperative pain can cause splinting and result in atelectasis and hypoxemia.

c. Duration of surgery. Longer duration is associated with higher risk of PPC.

d. Urgency. Emergent operations are associated with higher risk of PPC compared to elective cases.

e. Intraoperative fluids. Large volume intraoperative fluid resuscitation and postoperative fluid shifts can increase intra-abdominal pressure, resulting in reduced diaphragmatic excursion, decreased chest wall compliance, atelectasis, and increased work of breathing.

3. Patient comorbidities: A number of patient-related comorbidities have been identified as predictors of PPC.

a. Aging is associated with reduced lung elasticity and chest wall compliance, increased dead space, decreased respiratory muscle strength, and blunted response to hypoxemia and hypercapnia. The combination of these factors leads to increased work of breathing, impaired gas exchange, and increased risk of airway obstruction.

1. Elderly patients have increased sensitivity to the respiratory depressant effects of opioids, benzodiazepines, VAs, and muscle relaxants and decreased drug clearance secondary to impaired liver and kidney functions.

b. Low preoperative oxygen saturation (SaO₂) as measured by peripheral pulse oximetry is associated with increased risk of PPC. Low SaO₂ may reflect presence of other comorbidities such as congestive heart failure, COPD, or other respiratory diseases.

c. Obesity is associated with increased risk of unplanned tracheal intubation. Excess chest and abdominal fat decrease chest wall compliance, FRC, and respiratory muscle function, and increase work of
breathing; therefore, obese patients are at increased risk of hypoxia. Adipose tissue deposition within the pharyngeal airway increases the risk of upper airway collapse. Obesity is strongly associated with obstructive sleep apnea (OSA) and other cardiovascular comorbidities that place patients at increased risk for PRF.

d. Obstructive sleep apnea is an independent predictor of PPC. OSA has a known prevalence of 5% in women and 14% in men in general population, but its prevalence is likely much higher in the patients undergoing elective surgery due to being undiagnosed. Patients with OSA have increased susceptibility to the respiratory depressant effects of benzodiazepines, opioids, and VAs. They are at increased risk for upper airway obstruction, hypoventilation, and hypoxemic and hypercapnic respiratory failure.

1. Neuraxial anesthesia, peripheral nerve blocks, and local anesthetic infiltration should be considered as alternatives to GA when possible to reduce the risk of PPCs.

2. Short-acting anesthetics and opioids such as propofol, desflurane, and remifentanil should be used intraoperatively to minimize postoperative airway-related complications. Opioid-sparing analgesics such as acetaminophen, NSAIDs, COX-2 inhibitors, and gabapentinoids can be used to limit postoperative opioid use.

3. Extubation should only be performed after the patient is fully awake and following commands. Postoperatively, patients with OSA who use continuous positive airway pressure (CPAP) at home should be treated with the same levels of CPAP to prevent airway collapse and hypoxemia.

e. Chronic obstructive pulmonary disease is another independent risk factor for PRF. This increased risk could be attributed to blunted ventilatory responses to hypoxia and hypercapnia and respiratory muscle failure.

1. Gas exchange may be impaired due to reduced alveolar surface area, increased sensitivity to opioids and benzodiazepines, and abnormal ventilatory control. Hyperinflation of the lungs in patients with COPD flattens the diaphragm, resulting in a mechanical disadvantage that further increases these patients’ risk of PRF.

2. When possible, patients with COPD should undergo respiratory optimization with nebulized bronchodilators, steroids, and antibiotics as appropriate prior to undergoing elective surgery under GA.

3. Neuraxial and regional anesthesia should be considered as alternatives to GA.

4. Brachial plexus nerve blocks such as the interscalene block should be used with caution since they are associated with high risk of phrenic nerve blockade and a potential risk of pneumothorax, which can worsen a patient’s respiratory function.

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