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Adverse effects of supplemental oxygen

Adverse effects of supplemental oxygen
Literature review current through: Jan 2024.
This topic last updated: Apr 08, 2022.

INTRODUCTION — Supplemental oxygen is valuable and lifesaving in many clinical situations. However, excessive amounts or inappropriate use of supplemental oxygen can have adverse effects [1-3].

The adverse effects of supplemental oxygen are reviewed here. Specific issues including the indications and prescription of long-term oxygen, ideal oxygen targets, and adverse effects of hyperbaric oxygen are discussed separately.

(See "Long-term supplemental oxygen therapy".)

(See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Fraction of inspired oxygen'.)

(See "Hyperbaric oxygen therapy", section on 'Complications'.)

TERMINOLOGY

Oxygen toxicity — Oxygen toxicity is considered to be a harmful effect of inspired oxygen at pressures greater than atmospheric pressure (ie, >0.21 inspired fraction of oxygen at sea level). Oxygen toxicity can be caused by hyperoxia and hyperoxemia and is generally responsible for parenchymal lung injury. (See 'Lung parenchymal injury' below.)

Hyperoxia and hyperoxemia — Hyperoxia may be loosely defined as an excess of oxygen in tissue (ie, "more oxygen than is needed"). However, there is no specific oxygen tension included in the definition. The degree of hyperoxia that is harmful is poorly defined, and it is likely different in healthy compared with unhealthy individuals. Unnecessary high fraction of inspired oxygen (FiO2) is a common cause of hyperoxia.

Hyperoxemia refers to an excess of oxygen in the blood. It is reflected by the arterial oxygen tension (PaO2) and most often due to high FiO2.

Notably, in the lung, cellular exposure to oxygen comes directly from the effect of inspired gas on lung tissue (hyperoxia) as well as the amount of oxygen in the blood (hyperoxemia). By contrast, for the rest of the body, cellular exposure to oxygen is only determined by the amount of oxygen in the blood; in this situation hyperoxia is the same as hyperoxemia.

MECHANISM OF ADVERSE EFFECTS — In general, the mechanisms that underlie the deleterious effects of supplemental oxygen are poorly understood. Several mechanisms have been described including the following:

Direct toxicity – The direct toxic effect of oxygen itself at a cellular level (oxygen toxicity) can cause, for example, lung parenchymal or retinal injury. (See 'Lung parenchymal injury' below and 'Retinopathy of prematurity' below.)

Physiologic effects – Physiologic effects of supplemental oxygen can alter gas exchange resulting in oxygen-induced hypercapnia or alterations in vascular tone. (See 'Accentuation of hypercapnia' below and 'Cardiovascular effects' below.)

Local effects – Local adverse effects of oxygen include burns or hypoxia from equipment failure. (See 'Local' below.)

Multifactorial – Several mechanisms may play a role together in producing the adverse effects of oxygen (eg, atelectasis and airway injury). (See 'Other pulmonary adverse effects' below.)

LUNG PARENCHYMAL INJURY — Adverse effects of oxygen on the lung parenchyma may result from hyperoxia at the alveolus, blood, or cellular level. The strongest level of evidence supports direct cellular injury from reactive oxygen species due to hyperoxia. Importantly, when indicated, oxygen should not be withheld on the basis of preventing oxygen toxicity.

Hyperoxia appears to produce cellular injury through increased production of reactive oxygen intermediates (ROIs), such as the superoxide anion, the hydroxyl radical, and hydrogen peroxide [4,5]. When the production of ROIs increases and/or the cell's antioxidant defenses are depleted, they can react with and impair the function of essential intracellular molecules, resulting in cell damage and/or death [6]. ROIs may also promote a deleterious inflammatory response, leading to secondary tissue damage and/or apoptosis [7-9].

Much of the evidence supporting direct cellular injury due to ROIs comes from studies in transgenic mice with altered superoxide dismutase activity. Mice with augmented antioxidant mechanisms are relatively tolerant to hyperoxia, while manganese superoxide dismutase knockout mice die shortly after birth with extensive mitochondrial injury within degenerating neurons and cardiac myocytes [10-12]. Data from animal models suggest possible roles for insulin growth factor 1 [13] and angiopoietin 2 [14] in the pathogenesis of hyperoxia-induced lung injury.

Evidence from humans is limited and largely derived from healthy individuals [15]. Determining the magnitude of parenchymal injury due solely to oxygen therapy in humans is problematic because confounders are always present (eg, the presence of diseased lung, comorbidities). In addition, since many lung diseases are heterogeneous, the impact of oxygen on non-diseased regions compared with diseased regions is unclear.

At-risk patients — Any patient receiving supplemental oxygen is potentially exposed to the direct toxic of oxygen. However, parameters above which exposure results in clinically meaningful adverse effects are uncertain and vary from patient to patient. In general, we consider patients who are at greatest risk of oxygen toxicity as those who are receiving mechanical ventilation for respiratory failure with a fraction of inspired oxygen (FiO2) greater than 0.6 for prolonged durations (eg, >24 hours) [16-18].  

Factors that can modulate the impact of supplemental oxygen to alter the level at which toxicity can occur are discussed in the sections below:

(See 'High fraction of inspired oxygen for prolonged periods' below.)

(See 'Select drugs or radiation' below.)

Whether underlying lung disease, other than drug- or radiation-induced lung injury or ischemia during cardiac arrest, contributes to oxygen toxicity is unknown. (See 'Underlying lung disease' below and 'Post-cardiac arrest' below.)

High fraction of inspired oxygen for prolonged periods — In general, the risk of oxygen toxicity correlates with the FiO2 and the duration of exposure (ie, the higher the FiO2 and longer the duration, the higher the risk).

FiO2 – Although there is no cutoff level above which toxicity can occur, in patients who are mechanically ventilated for acute respiratory distress syndrome (ARDS), we generally consider an FiO2 >0.6 as a level that places patients at risk for oxygen-induced lung damage.

Duration – At an FiO2 of 1.0, evidence of cellular toxicity can be seen as early as 24 hours in healthy lungs [16-18]. However, the amount of time required to see pathologic changes in the lung is inversely related to the FiO2. For example, the time interval to injury increases as FiO2 is reduced while the time interval decreases as the FiO2 is increased.

Select drugs or radiation — Some drugs (most notably bleomycin and amiodarone) and radiation exposure appear to sensitize the lung to oxygen such that toxicity may occur at a lower FiO2 than in healthy lungs.

Patients who receive bleomycin appear to be more susceptible to the development of diffuse alveolar damage (ie, the pathology associated with acute respiratory distress syndrome) following oxygen exposure, based upon in vitro data and clinical experience [19-22]. The typical presentation involves a patient who, after receiving bleomycin, requires high FiO2 in the subsequent weeks to months (eg, due to aspiration, pneumonia, or general anesthesia). The patient develops acute, subacute, or chronic worsening of bilateral alveolar infiltrates with increasing dyspnea, nonproductive cough, and decreasing lung compliance. However, such presentations can occur years to decades after the initial bleomycin exposure for unclear reasons. (See "Bleomycin-induced lung injury".)

Oxygen-induced lung injury associated with amiodarone or external beam radiation may have a similar pathogenesis and presentation to that of bleomycin when patients are exposed to hyperoxic conditions. (See "Amiodarone pulmonary toxicity" and "Radiation-induced lung injury".)

The potential for oxygen toxicity must be communicated to the anesthesiologist if a patient with bleomycin, amiodarone, or radiation exposure needs a surgical or endoscopic procedure.

Underlying lung disease — It is unknown whether underlying lung disease other than that induced by drugs or radiation predisposes the lung to the direct toxic effects of oxygen.

Chronic low levels of exposure, such as that administered in patients on lower levels of oxygen at home may result in cellular changes in the lung but is of uncertain significance and should not preclude its administration, when indicated. (See 'Adults on long-term oxygen' below.)

Although not a direct toxic effect, oxygen-induced hypercapnia may also occur in patients with chronic lung disease. (See 'Accentuation of hypercapnia' below.)

Post-cardiac arrest — Uncontrolled studies suggest that hyperoxemia may worsen outcomes in patients who survive cardiac arrest [23]. However, it is not clear whether adverse outcomes are due to the direct toxic effect of oxygen or to other factors such as lung ischemia, low minute ventilation, or reperfusion injury.

Physiologic, clinical, pathologic impact — Outcomes associated with the adverse of oxygen are poorly studied but include the following:

Physiologic – Older studies in humans reported conflicting evidence of the effect of hyperoxia on physiologic parameters such as increased right-to-left shunt fraction, reduced lung compliance, increased dead space to tidal volume ratio, and reduced diffusing capacity [24-26].

Clinical – Newer studies have focused on examining the impact of liberal versus conservative oxygenation strategies on survival, length of stay, and ventilator-free days. These studies have examined the effect of hyperoxemia, however, not hyperoxia per se. In general, data cumulatively support use of conservative strategies. These data are discussed separately. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Fraction of inspired oxygen'.)

Pathologic – The pathologic outcome of oxygen toxicity is unclear but may range from mild inflammation to diffuse alveolar damage, similar to that seen in ARDS. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Pathologic diagnosis and stages' and "Interpretation of lung biopsy results in interstitial lung disease", section on 'Diffuse alveolar damage'.)

Prevention — There is no single threshold of FiO2 that defines a safe upper limit to prevent oxygen toxicity. As a general principle, we reduce the FiO2 to the lowest achievable fraction in order to obtain a target arterial oxygen tension (PaO2) or peripheral oxygen saturation (SpO2) and avoid hyperoxia, when feasible. However, since oxygenation targets vary depending on the population being treated, we individualize oxygenation goals. Reasonable targets are discussed in detail separately. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Fraction of inspired oxygen'.)

Preventative strategies are most important in those at risk. In patients who are mechanically ventilated for ARDS, we target an FiO2 <0.6 based upon the rationale that such a target is unlikely to induce clinically significant oxygen toxicity, unless sensitizing agents are administered (see 'At-risk patients' above). A number of therapeutic strategies can be employed in this population to minimize the need for a high FiO2 >0.6 and thereby reduce the risk of oxygen toxicity (eg, positive end expiratory pressure, prone positioning). In our practice, we begin to implement these measures as soon as it is evident that the patient will require FiO2 >0.6 for longer than six hours. These strategies are discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

OTHER PULMONARY ADVERSE EFFECTS — In adults, oxygen, particularly high fractions of inspired oxygen (eg, FiO2> 0.6) have been associated with several effects on lung tissue and gas exchange including diminished lung volumes and hypoxemia due to absorptive atelectasis, damage to airways, and accentuation or production of hypercapnia. (See 'Absorptive atelectasis' below and 'Airway injury' below and 'Accentuation of hypercapnia' below.)

Absorptive atelectasis — Absorptive atelectasis is a process where high FiO2 results in washout of alveolar nitrogen (ie, nitrogen is replaced by oxygen). The oxygen is rapidly absorbed into the blood, resulting in a reduction in the size of the alveolus and alveolar closure (ie, atelectasis).

Patients at particular risk of absorptive atelectasis include the following:

Patients with a low regional ventilation-perfusion ratio (ie, oxygen diffuses from alveoli to capillaries faster than it is replenished by inhaled oxygen). Patients with regional areas of hypoventilation, such as chronic obstructive pulmonary disease (COPD) or an occluded airway from a foreign body or neoplasm, are particularly at risk.  

Patients with qualitative or quantitative surfactant abnormalities that promote alveolar collapse and further reduce the ventilation-perfusion ratio (eg, patients with acute respiratory distress syndrome).

Patients with a high rate of oxygen uptake, due to an increase in metabolic demand (eg, fever, hyperthyroidism).

Patients with an impaired pattern of respiration that fails to correct atelectasis (eg, ventilation at low tidal volumes and/or without intermittent sighs or "adequate" positive end expiratory pressure [PEEP]).

The impact of atelectasis includes the following:

Worsening hypoxemia – Atelectasis contributes to worsening hypoxemia by increasing right-to-left shunt (see "Measures of oxygenation and mechanisms of hypoxemia", section on 'Right-to-left shunt'). Shunting resulting from absorptive atelectasis is generally minor in younger patients with healthy lungs, but can be as high as 11 percent in older healthy volunteers [27].

Reduced vital capacity – Atelectasis may also contribute to a reduction in vital capacity. Reductions in vital capacity of up to 20 percent have been noted after hyperoxic exposure in a number of studies [28,29].

Atelectasis may be evidenced by inspiratory crackles or rales on physical examination and worsening oxygenation and can be confirmed by chest radiographs and/or computed tomography scan of the chest.

Once established, absorptive atelectasis is not directly reversed by a reduction of FiO2, emphasizing the importance of rapid titration of FiO2 to the lowest fraction necessary to maintain the desired target arterial oxygen saturation [30]. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Fraction of inspired oxygen'.)

Airway injury — Supplemental oxygen has been implicated in the development of airway injury in response to hyperoxia.

Many healthy volunteers experience substernal heaviness, pleuritic chest pain, cough, and dyspnea within 24 hours of breathing 100 percent oxygen. These symptoms are probably due to a combination of tracheobronchitis and absorptive atelectasis [31].

Erythema and edema of large airways can be observed bronchoscopically in most patients treated with a FiO2 of 0.9 for six hours and are thought to reflect hyperoxic bronchitis [32].

In addition, the concentration of reactive oxygen intermediates (ROIs) in exhaled gas increases after only one hour of breathing 28 percent oxygen, regardless of the presence of underlying lung disease [33].

Airway injury may present with wheeze and increased airway pressures.

It is unknown whether reducing FiO2 reverses oxygen toxicity in the airway.

Accentuation of hypercapnia — Oxygen-induced hypercapnia describes the phenomenon of increased arterial carbon dioxide tension (PaCO2) associated with the administration of supplemental oxygen. In general, increased hypercapnia does not lead to CO2 narcosis and respiratory failure since the relative rise in PaCO2 is small.

Oxygen-indued hypercapnia is predominantly described as a complication of supplemental oxygen in individuals with chronic compensated respiratory acidosis (eg, COPD) who are experiencing an exacerbation of their underlying disease.

The mechanism and management of oxygen-induced hypercapnia are discussed separately. (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure" and "Mechanisms, causes, and effects of hypercapnia", section on 'Oxygen-induced hypercapnia' and "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure", section on 'Titration of oxygen'.)

Other — Hyperoxia may also increase susceptibility to secondary infection by impairing both mucociliary clearance and the bactericidal capacity of immune cells [29,34-38]. However, an actual causative link between oxygen administration and infection is unclear.

EXTRAPULMONARY ADVERSE EFFECTS

Local — Local effects of oxygen include nasal dryness (when administered via nasal cannula) and risk of burns and airway fire. These complications can occur in both outpatients who are receiving long-term oxygen therapy (see 'Adults on long-term oxygen' below) and inpatients receiving supplemental oxygen.

For inpatients receiving oxygen, procedures that carry a risk of airway fire (eg, electrocautery, argon laser) are generally avoided but, if oxygen is necessary for a life-saving procedure, the oxygen concentration is lowered and oxygen source kept at a distance from the heat source. Further details are provided separately. (See "Endobronchial electrocautery", section on 'Complications' and "Bronchoscopic laser in the management of airway disease in adults", section on 'Complications' and "Bronchoscopic argon plasma coagulation in the management of airway disease in adults", section on 'Complications' and "Fire safety in the operating room".)

Cardiovascular effects — Hyperoxemia may also alter cardiovascular function [39,40]. Increased oxygen tension can lead to local coronary vasoconstriction, and microscopic foci of myocardial necrosis have been observed in animal models [41]. Reductions in stroke volume and cardiac output, relative bradycardia, and an increase in systemic vascular resistance may ensue [42]. However, the clinical relevance of hyperoxia-related hemodynamic effects remains unclear. Data in humans are limited but may suggest that hyperoxemia reduces myocardial function and cardiac output and increases systemic vascular resistance [43-45]. Among patients with cardiac disorders, those with heart failure patients may be the most sensitive to the effects of hyperoxemia [43].

Central nervous system — Hyperoxemia may increase the risk of central nervous system symptoms including generalized tonic-clonic seizures [46], although seizures are unusual in the absence of hyperbaric therapy. These and other complications of hyperbaric oxygen including barotrauma of the ear, sinuses, and lung, reversible myopia, and lung parenchymal injury are described separately. (See "Hyperbaric oxygen therapy", section on 'Complications'.)

SPECIAL POPULATIONS

Pediatric

Retinopathy of prematurity — The retinopathy of prematurity (previously called retrolental fibroplasia) has been partially attributed to the toxic effects of oxygen. Further details are provided separately. (See "Retinopathy of prematurity (ROP): Risk factors, classification, and screening".)

Bronchopulmonary dysplasia — Bronchopulmonary dysplasia (BPD), a disease seen in neonates following recovery from neonatal respiratory distress syndrome, has been attributed to the effects of mechanical ventilation and oxygen toxicity in the immature lung. BPD is characterized by epithelial hyperplasia and squamous metaplasia in the large airways, thickened alveolar walls, and peribronchial and interstitial fibrosis. Infants with BPD generally suffer respiratory distress and require supplemental oxygen for up to six months. Further details regarding BPD are provided separately. (See "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis".)

Adults on long-term oxygen — Adults receiving long-term oxygen therapy (LTOT) may have the following side effects:

Nasal issues – Nasal dryness, nosebleeds, and skin irritation (from nasal cannulae or a facemask) are not uncommon and can be alleviated by a water-based nasal lubricant, barrier creams/adhesive, or humification.

Burns – Facial and upper airway burns are an infrequent hazard of LTOT, but can be severe and potentially life-threatening [47-50]. However, spontaneous combustion may occur following exposure to a spark source or open flame. It is also hypothesized that certain factors contribute to the risk of combustion in the absence of open flames, such as facial hair and use of hair products containing oils or alcohol [51].

Patients should be reminded not to smoke while using supplemental oxygen [50], to keep oxygen at least six feet (two meters) away from any open flame, and to be cautious about exposure to sources of heat sparks or gas stoves.

The safety of electronic cigarettes (also known as e-cigarettes, personal vaporizers, or electronic nicotine delivery systems) in the setting of LTOT has not been formally evaluated, but the use of a heat source contained within electronic cigarettes adjacent to oxygen is concerning and further study is needed [52]. (See "Vaping and e-cigarettes".)

Accidental falls – Patients who wear oxygen may suffer from accidental falls when tubing used to administer oxygen is lengthy to accommodate administration throughout the home (or hospital) dwelling. Education regarding safety is paramount in preventing accidental falls. (See "Falls in older persons: Risk factors and patient evaluation".)

Equipment failure – Hypoxemia may occur due to power outages and equipment failure.

Possible oxygen toxicity – Whether LTOT is associated with a clinically significant effect due to oxygen toxicity is unknown; however, the possibility of oxygen toxicity should not preclude the administration of LTOT, when indicated.

While LTOT is generally delivered at low fractions of inspired oxygen (eg, FiO2 < 0.28), the duration of exposure is prolonged such that toxicity is plausible.

Limited data support a possible effect of oxygen toxicity that is of uncertain clinical significance. Data are mostly reported in patients with chronic obstructive pulmonary disease (COPD). As an example, in an autopsy series, half of patients with COPD receiving LTOT (for about two years prior to death at an estimated FiO2 of 0.22 to 0.27) displayed classic findings of oxygen toxicity (ie, capillary proliferation, interstitial fibrosis, epithelial and hyperplasia) [53]. Oxidative stress from oxygen and cigarette smoke may also play a role in COPD pathogenesis [54].

In an effort to limit any potential for oxygen toxicity, we adhere to specific oxygen targets in patients with COPD and extrapolate those targets to patients who require LTOT for other chronic lung disorders. Further details on oxygen targets for patients with COPD are discussed separately. (See "Long-term supplemental oxygen therapy", section on 'Oxygen flow rate'.)

INVESTIGATIONAL APPROACHES — Because oxygen radicals lead to pulmonary toxicity, enhanced defenses against these molecules theoretically should minimize or prevent lung damage [55]. The potential importance of augmented antioxidant mechanisms is illustrated in several animal models [10,56-63]. Data on the efficacy of these potential therapies in humans are lacking.

Manipulation of the cytokine milieu in animals may permit modification of the deleterious inflammatory response provoked by hyperoxia (eg, protective effect of the overexpression of interleukin-11) [7], but human data are lacking.

SUMMARY AND RECOMMENDATIONS

Introduction and mechanism – Oxygen toxicity is a harmful effect of inspired oxygen at pressures greater than atmospheric pressure. Oxygen toxicity can be caused by hyperoxia (an excess of oxygen in tissue) and hyperoxemia (an excess of oxygen in blood). (See 'Introduction' above and 'Terminology' above and 'Mechanism of adverse effects' above.)

Lung parenchymal injury – Oxygen toxicity appears to produce parenchymal lung injury through increased production of reactive oxygen intermediates (ROIs). (See 'Lung parenchymal injury' above.)

In general, we consider patients who are at greatest risk of oxygen-induced parenchymal lung injury are those on mechanical ventilation for respiratory failure receiving a fraction of inspired oxygen (FiO2) greater than 0.6 for prolonged durations (eg, >24 hours). (See 'At-risk patients' above and 'High fraction of inspired oxygen for prolonged periods' above.)

Select drugs (eg, bleomycin, amiodarone) and radiation may predispose patients to oxygen-induced lung injury at an FiO2 lower than 0.6. (See 'Select drugs or radiation' above.)

End organ effects of hyperoxia on the lung parenchyma range from mild inflammation to diffuse alveolar damage. (See 'Physiologic, clinical, pathologic impact' above.)

There is no single threshold of FiO2 that defines a safe upper limit that prevents oxygen-induced parenchymal lung injury. As a general principle, we reduce the FiO2 to the lowest achievable fraction in order to obtain a target arterial oxygen tension (PaO2) or peripheral oxygen saturation (SpO2) and avoid hyperoxia, when feasible. However, since oxygenation targets vary depending on the population being treated, we individualize oxygenation goals. Reasonable targets are discussed in detail separately. (See 'Prevention' above and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Fraction of inspired oxygen'.)

Other adverse effects – Other pulmonary adverse effects of oxygen include absorptive atelectasis, airway injury, and worsening of hypercapnia. Oxygen also places patients at risk of facial burns and airway fire. Hyperoxemia may also have effects on the cardiovascular and central nervous system but the clinical significance of these effects is uncertain. (See 'Other pulmonary adverse effects' above and 'Extrapulmonary adverse effects' above.)

Special populations

Oxygen toxicity has been implicated in retinopathy of prematurity and bronchopulmonary dysplasia in infants. (See 'Pediatric' above and "Retinopathy of prematurity (ROP): Risk factors, classification, and screening" and "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis".)

Adults receiving long-term oxygen therapy (LTOT) may develop adverse effects including nasal dryness and are at risk of facial or upper airway burns, accidental falls from oxygen tubing, and hypoxemia from equipment failure. Toxicity from LTOT is unlikely to be clinically significant. Oxygen targets for patients with chronic obstructive pulmonary disease (COPD)are discussed separately. (See 'Adults on long-term oxygen' above and "Long-term supplemental oxygen therapy", section on 'Oxygen flow rate'.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges David R Schwartz, MD, who contributed to an earlier version of this topic review.

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Topic 1622 Version 23.0

References

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