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Pathophysiology and prevention of sputum retention 

Pathophysiology and prevention of sputum retention
Pathophysiology and prevention of sputum retention

John J. Marini

and Paolo Formenti

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date: 03 December 2020

Key points

  • Common predispositions to secretion retention are airway intubation, prolonged sedation, muscular weakness, aspiration of oral secretions, coughing discomfort, restricted breathing after surgery, bronchitis due to smoking, and advanced age.

  • Effective removal of secretions from the respiratory tract depends on two key factors—integrity of the mucociliary transport system and the ability to cough productively.

  • Mucus retained within the airway lumen impairs effective delivery of aerosol therapies, while predisposing to lung collapse, inflammation, and infection.

  • Intubation for mechanical ventilation impairs cough, interrupts mucociliary clearance, and encourages formation of a tube-lining biofilm that is isolated from blood flow and body defences.

  • Respiratory and coughing muscle strength, body position, lung volume, airway secretion viscosity and location, depth of sedation, and suctioning effectiveness are some of the important variables that determine the impact of secretion retention on ventilation, gas exchange, and patient outcome.


A thin lining of tracheobronchial secretions contributes importantly to normal respiratory system defence, whereas retained airway mucus complicates the care of the critically-ill ventilated patient. Excessive secretions that must be cleared from the airways by coughing, huffing, or catheter aspiration, are defined as sputum. They may arise acutely or be present chronically, but they are always abnormal. Retained secretions in the acute care setting may impair gas exchange, increase the breathing workload, predispose to infection, or contribute to atelectasis. Prevention and reversal of the latter phenomenon is a fundamental goal of effective intensive care.

Pathogenic mechanisms of secretion retention and atelectasis

Sputum retention may either cause or result from atelectasis. Once established, parenchymal collapse impairs clearance of mucus from the central airways. Among the most common predispositions to secretion retention are airway intubation, prolonged sedation, muscular weakness, aspiration of oral secretions, coughing discomfort, restricted breathing after surgery, bronchitis due to smoking, and advanced age [1]‌. Obstructive atelectasis involves narrowing or occlusion of the bronchial tree by foreign bodies or mucus, tumours, or lymph nodes. In some cases, a lack of surfactant increases the surface tension of alveoli, encouraging their collapse [2]. Whatever the setting, strong measures must be taken to reduce the prevalence of these ubiquitous disorders.

The following mechanisms may contribute to the development of atelectasis:

  • Compression atelectasis occurs when the transmural pressure distending the alveolus is reduced sufficiently to allow alveolar collapse. Common causes include loss of muscular tone, as during the induction of anaesthesia, pleural effusion, abdominal distention, supine positioning, and lung oedema.

  • Obstructive atelectasis, a common cause for the generation of atelectasis or a contributor to its persistence, results from reabsorption of gas from the alveoli when communication between the gas exchange interface and the trachea is interrupted by foreign bodies, tumours, or mucus plugs. Gas uptake by the blood then continues while replenishing gas inflow is prevented (Fig. 119.1).

  • Adhesive atelectasis results from surfactant deficiency. Increased alveolar surface tension cannot be counterbalanced by tidal transalveolar pressures, leading to alveolar instability and collapse. This mechanism probably makes an important contribution to the maintenance of established collapse, but is less central to its generation, given normal surfactant reserve and high rate of surfactant turnover.

Fig. 119.1 Schematic figure to explain mechanism of atelectasis and physiological/clinical implication.

Fig. 119.1 Schematic figure to explain mechanism of atelectasis and physiological/clinical implication.

VC, vital capacity; FRC, functional residual capacity; RV, residual volume; TLC, total lung capacity; DO2, oxygen delivery.

Bronchial secretions

Effective removal of secretions from the respiratory tract depends on two key factors—integrity of the mucociliary transport system and the ability to cough productively. Airway mucus traps inhaled particulate toxins and transports them out of the lungs by means of ciliary beating and cough. A deficient mucous barrier leaves the lungs vulnerable to injury, and excessive mucus or impaired clearance contributes to all common airway diseases.

Mucus is continuously swept from distal to proximal airways, propelled in a proximal direction by ciliary beating. This action clears inhaled particles, pathogens, and dissolved chemicals that might otherwise threaten the lungs [3]‌. While the small airways produce a thin mucus gel layer, a thicker layer (up to 50 μ‎m) accumulates in the larger airways from accumulated mucus transported from distal airways and any drying that may result from suboptimally conditioned inspired gas. After mucus ascends the trachea, it is normally transported mouthward past the vocal cords by ciliary epithelium in the posterior commissure of the larynx. It then enters the pharynx and is swallowed, with approximately 30 mL of airway mucus eliminated via the gastrointestinal tract daily [4]. The rate of mucociliary clearance increases with greater hydration [5], and the rate of ciliary beating can be increased by purinergic, adrenergic, cholinergic, and adenosine-receptor agonists, as well as by irritant chemicals. Sputum retention occurs when patients are unable to clear secretions by themselves or with assistance. Retention of airway secretions may lead to obstruction of major bronchopulmonary units and lobar atelectasis.

A second mechanism of fundamental importance for the expulsion of pathological mucus from the airways is cough clearance. Coughing is a complex phenomenon that is usually triggered by local ‘irritation’ caused by the stimulation of vagal afferents in the intrapulmonary airways or in the larynx and pharynx. Reflex activation of the expulsive abdominal and intrathoracic muscles makes it possible to quickly evacuate accumulated secretions from the central bronchi. Assuming that the airway is not intubated, the glottis can temporarily close during forceful contraction of the abdominal and internal intercostal muscles [6]‌. After airway pressure rapidly elevates, sudden opening of the glottis allows compression of the central airway and sufficiently high flow to shear the debris from its mucosal attachments.

During invasive mechanical ventilation, cough efficiency is impaired because the glottis cannot close, even though increased resistance of the upper airways (intubation tube, ventilatory circuit) may predispose to an increase in tracheal pressure during forceful exhalation. Coughing is suppressed during general anaesthesia and can be significantly reduced by the administration of opioids. In patients who are not intubated, neuromuscular weakness(phrenic paralysis, myasthenia, Guillain–Barré syndrome, etc.), pain, or impaired consciousness are often responsible for ‘ineffective’ cough. In others, peripheral obstruction of the airways chokes off maximal expiratory flow, detrimentally affecting cough.

Dyspnoea often results when mucus obstructs airflow by narrowing the ‘effective’ airway lumens within the collective airway system. Physical signs of impaired mucus clearance include persistent cough, bronchial breath sounds, rhonchi, and wheezes. Retained mucus and inflammatory exudates may appear as localized haze, atelectasis, or linear or branched opacities on plain radiographs of the chest. Not only is it important to recognize the role of mucus in clinical presentations of increased effort and impaired oxygenation, but also to understand that mucus must be cleared from the airway lumen to facilitate effective delivery of aerosol therapies and, in many cases, to address patient–ventilator asynchrony. In addition, the presence of retained mucus may predispose to or be a sign of inflammation or infection that warrants additional treatment.

Factors modulating the formation of atelectasis

Several important clinical circumstances influence the formation of atelectasis. Atelectasis develops both during intravenous and inhalational anaesthesia. Ventilatory effects of regional anaesthesia depend on the type and extent of motor blockade. The maximum decreases of functional residual capacity (FRC) seem to occur within the first few minutes of general anaesthesia and as a consequence of changing positions. Transition from the upright to the supine position causes FRC to decrease 0.5 L to 1.2 L, even in the awake state, with a further reduction of 0.5–0.7 L in FRC occurring during general anaesthesia. High inspired oxygen concentrations are associated with ‘absorption’ atelectasis. Absorptive collapse is prevalent, as the use of high FiO2 (i.e. approaching 1.0) is standard practice among many anaesthesiologists. Obesity worsens arterial oxygenation through multiple mechanisms, of which development of atelectasis is an important contributor [7]‌. Markedly reduced FRC limits expiratory reserve and promotes airway closure to a greater extent in obese patients than in patients of normal weight. Two practical points are important regarding ventilator settings during deep sedation. In contrast to volume-controlled ventilation, pressure-controlled ventilation delivers smaller tidal volumes when respiratory system compliance declines (e.g. during surgical retraction or after placement of abdominal packs). Smaller tidal volumes may then lead to atelectasis (unless volume alarms are appropriately set) and may go undiagnosed because there is no tell-tale change in the peak airway pressure [8].

Risk factors

There are several risk factors associated with the development of atelectasis caused by obstruction of the major airways and bronchioles, or by pressure originating outside the lung, e.g. from fluid or air in the pleural space (Box 119.1). Some predispositions are directly linked with the sputum retention that tends to occur commonly as a complication in the post-operative period.

It is clear that low V/Q areas in dependent lung regions (i.e. areas of relative underventilation) are inclined to develop progressive atelectasis. Any influence that enhances such underventilation will increase this tendency. Apart from inhibition of diaphragmatic action, the most important of these risk factors is airways disease, particularly chronic bronchitis and/or emphysema. In chronic airways disease, inspired gas is unevenly distributed, both temporally and spatially. Reduced peak expiratory flow impedes expulsion of accumulated secretions.

Another common factor augmenting the tendency toward collapse is a rapid shallow pattern of ventilation, commonly seen in patients with obesity and in those with post-operative pain, when the discomfort of an abdominal or thoracic incision inhibits normal depth of inspiration. The latter problem may be partially alleviated or, conversely, compounded by the use of sedative and narcotic analgesics, which relieve pain, but depress ventilation, suppress coughing and retard sputum clearance. Depressed central respiratory drive due to chronic obstructive lung disease, neurological disease, or hypoventilation syndromes also aggravates the atelectatic tendency. Reduced inspiratory reserve due to peripheral nerves (Guillain–Barré syndrome or spinal cord injury), neuromuscular (myasthenia gravis, post-anaesthetic persistent curarization syndrome), muscular (muscular dystrophies), and musculoskeletal disorders (ankylosing spondylitis, thoracoplasty, kyphoscoliosis) may also be associated with a shallow breathing pattern, increased hypoventilation of dependent lung regions, and an enhanced tendency to atelectasis.

Ventilation patterns and airway secretion clearance

Intubation for mechanical ventilation impairs cough, interrupts mucociliary clearance, and encourages formation of a tube-lining biofilm that is isolated from blood flow and body defences. These factors lead to sputum retention, airway occlusion, atelectasis, and ventilator-associated pneumonia. Respiratory muscle strength, position, lung volume, viscosity, and location of airway secretions, depth of sedation, and ‘coughing strength’ (expiratory flow generated spontaneously or in response to suction) are some of the variables that may determine the impact of secretion retention on ventilation, gas exchange, and patient outcome [8]‌. The minimum standard of airway management requires adequate gas humidification and airway suctioning [9]. Open suctioning, higher suction pressures, wide-bore suction catheters, and the release of positive end-expiratory pressure (PEEP)—a manoeuvre that encourages mouthward migration of secretions retained in the periphery of the PEEP-distended lung can improve secretion clearance, but may compromise gas exchange in the short term. Closed suctioning can minimize potential adverse physiological effects of airway suctioning, but may not be as effective for secretion clearance [10].

It has been demonstrated that airway clearance can be augmented by imposing an expiratory flow bias or by manual lung hyperinflation, which transiently improves airway resistance, recoil force, and dynamic lung/thorax compliance. Chest wall vibration, with or without manual lung hyperinflation and suctioning, can improve expiratory flow, airway resistance, and dynamic lung/thorax compliance, but has not been demonstrated to improve secretion clearance [11].

Consequences of atelectasis

Atelectasis decreases pulmonary compliance and is associated with a worsening in systemic oxygenation associated with a reduction in FRC [12]. In the presence of increased airway resistance or decreased lung compliance, increased transpulmonary pressure is required to achieve a given tidal volume, with consequent increase in the work of breathing. Most often, this volume reduction impairs the efficiency of systemic oxygenation, and prompts hyperoxic gas inhalation with subsequent reabsorption. In the hyperoxic range, such effects are better detected by arterial blood gas analysis, rather than simply observing oxygen saturation.

High tidal ventilating pressures when the lung is not fully recruited may inflict lung damage. Yet, use of ‘lung protective’ low tidal volumes may not be sufficient to avert lung inflammation. It has been demonstrated that in the absence of PEEP, impaired lung compliance is accompanied by increased cytokine production. Pulling together all recent findings it seems reasonable to suggest that using low tidal volume without preventing atelectasis by adequate PEEP may be a misguided ventilation strategy [13].

Prevention of sputum retention and atelectasis

Invasive mechanical ventilation via endotracheal intubation or tracheostomy bypasses the upper airways, and its normal heat and moisture exchanging process. Humidification is necessary to prevent hypothermia, disruption of the airway epithelium, bronchospasm, atelectasis, and airway obstruction [14]. Moreover, a continuous loss of moisture and heat occurs during prolonged mechanical ventilation with poorly-conditioned inspired gas and predisposes to airway damage. Inadequate humidification and heating of the inspired gas mixture promotes mucosal damage (destruction of cilia and mucous glands). During normal respiration, humidity in the trachea can range from 36 to 40 mg/L, and the optimal moisture concentration beyond the carina approximates 44 mg/L (100% relative humidity (RH) at 37°C). When providing active humidification to patients who are invasively ventilated, it is suggested that the device provides a humidity level between 33 mgH2O/L and 44 mgH2O/L, and a gas temperature between 34°C and 41°C with a RH of 100% in order to prevent the drying of secretions in the artificial airway.

Active humidification through a heated humidifier (HH) and passive humidification through a heat and moisture exchanger (HME, ‘artificial nose’), are available for warming and humidifying gases delivered to mechanically-ventilated patients. HMEs operate passively by storing heat and moisture from the patient’s exhaled gas and releasing it to the inhalation gas stream.

Very recently, recommendations regarding gas humidification have been published that follow the grading of recommendations assessment, development, and evaluation (GRADE) system for scoring evidence quality [15].

  • Humidification is recommended for every patient receiving invasive mechanical ventilation.

  • Active humidification is suggested for non-invasive mechanical ventilation, as it may improve secretion mobility and comfort.

  • When providing active humidification to patients who are invasively ventilated, it is suggested that the device provides a humidity level between 33 mgH2O/L and 44 mgH2O/L, and gas temperature between 34°C and 41°C at the circuit Y-piece, with a relative humidity of 100%.

  • When providing passive humidification to patients undergoing invasive mechanical ventilation, it is suggested that the HME provide a minimum of 30 mgH2O/L.

  • Passive humidification is not recommended for non-invasive mechanical ventilation.

  • When providing humidification to patients with low tidal volumes, such as when lung-protective ventilation strategies are used, HMEs are not recommended because they provide additional dead space, which can increase the ventilation requirement and PaCO2.

  • It is suggested that HMEs are not useful as a prevention strategy for ventilator-associated pneumonia.

Supplemental strategies to prevent sputum retention include hydration, dry mouth prevention, oxygen modulation, adequate pain relief, and timely airway suctioning [16]. Adequate hydration helps to thin and lubricate secretions, making them easier for the patient to expectorate. Damage to the cilia can be prevented by humidification of the respiratory tract via humidifiers and nebulizers.

Because oxygen has a drying effect, sufficient humidification of high inspired concentrations of oxygen is important, especially if there is an existing lung disease. Nebulized β‎-2-adrenoceptor agonists, such as salbutamol, and mucolytics, such as recombinant human deoxyribonuclease (Dornase alfa) have been shown to increase mucociliary clearance. It is well known that smokers with a history of ischaemic heart disease and inadequate pain control are at high risk of developing sputum retention. There is also a strong risk of sputum retention in an individual with a history of chronic obstructive pulmonary disease and/or cerebrovascular accident. Adequate analgesia is usually needed to facilitate effective coughing during the post-operative period. Other post-operative pain factors that may limit a patient’s ability to cough effectively include decreased levels of consciousness, narcotic analgesics, abnormal chest wall compliance, vocal cord dysfunction, expiratory muscle weakness, and obstructed airflow,

Physiotherapy can help patients to remove excess secretions by using active exercise to enhance mucociliary clearance. Apart from cough encouragement, active breathing, body positioning, and vibration techniques (i.e. manual percussion, chest wall shaking, and high frequency airway vibration with asymmetrical flow patterns) can be used to loosen secretions and, thus, facilitate expectoration. Other devices that manipulate the airway with positive pressure, including the positive expiratory pressure masks, intermittent positive pressure breathing, and insufflation-exsufflation (assisted coughing) can also be used [17] (Box 119.2). Manual hyperinflation techniques may be required with some intubated patients.

Airway suctioning is usually necessary to clear secretions from patients with an endotracheal tube or tracheostomy. However, a suctioning manoeuvre should only be used when other efforts to clear secretions have failed. It is an unpleasant procedure for the patient and can cause damage to the tracheal epithelium. Deleterious effects can be minimized by using an appropriate suction catheter and suction technique. Unless unavoidable, suctioning should not be performed on patients with stridor, severe bronchospasm, clotting disorders, pulmonary oedema, and recent pneumonectomy or oesophagectomy [18]. In theory, coughing stimulated by suctioning may promote propagation of mobile inflammatory biofluids from diseased zones into previously unaffected sectors of the lung [19].


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