Oxygen is vital to sustaining life, which is why it is used as a therapeutic agent in many areas. However, it is not completely safe. Oxygen levels above the normal can lead to hyperoxia, oxygen poisoning. It can cause serious damage if not managed properly.

Oxygen

Oxygen was discovered in the 1770s, with atomic number 8. It is a highly reactive non-metallic element that forms oxides with a wide variety of elements. Can form oxygen-free radicals, due to unpaired electrons.

It forms 21% of the atmosphere as a diatomic gas.

Oxygen Therapy

Oxygen is widely used by different hospital departments as a drug, a process known as oxygen therapy. In this process, supplemental oxygen is provided to patients with low oxygenation levels. There is a range of effective doses and effects.

Oxygen therapy can be used in a wide variety of cases and conditions, as acute conditions, (such as carbon monoxide poisoning, cluster headaches, sickle cell crisis, pneumothorax, stroke, severe asthma attack, Pneumonia, major trauma, anaphylaxis, major bleeding, shock, active convulsions, hypothermia), as chronic conditions (chronic obstructive pulmonary disease (COPD), chronic bronchitis, emphysema, breathlessness, end-stage cardiac failure, respiratory failure, advanced cancer, neurodegenerative disease in spite of relatively normal blood oxygen levels, sleep apnea, Pulmonary fibrosis, and more).

Delivery

Various devices are used for oxygen administration, and various concentrations -

Type	Flow	FiO₂	Control	Eamples
Low-flow	Low	24–44%	Variable	Nasal cannula Simple face mask Partial rebreather mask
High-flow	High	24–100%	Precise	Venturi mask (most classic exam answer) High-flow nasal cannula (HFNC)
Positive pressure	Variable	21–100%	Full control	CPAP BiPAP Mechanical ventilation (intubation)

Drugs can be added to the oxygen via a Nebulizer.

100% oxygen at normobaric conditions does not cause severe tissue damage in exposure for a day or two. Some complications can appear much sooner than that. Those include irritation on deep inspiration after 3 to 6 hours of exposure, uncontrolled coughing after 10 hours, Chest pain, and dyspnea ensue.

In the majority of patients, these symptoms subside within 4 hours of cessation of exposure.

Oxygen toxicity appears in hypoxemic patients! Those patients need oxygen at a higher pressure, which causes the toxicity, not the oxygen percentage.

Oxygen Toxicity

Normoxia is the level of oxygen required for normal physiological processes.

Hyperoxia is an excess of oxygen in body tissues, most commonly occurring in patients breathing supplemental oxygen to decrease tissue hypoxia.

Acute toxicity typically manifests with central nervous system (CNS) effects, while chronic toxicity has mainly pulmonary effects. Severe cases of oxygen toxicity can lead to cell damage and death. Those at particular risk for oxygen toxicity include hyperbaric oxygen therapy patients, patients exposed to prolonged high levels of oxygen, premature infants, and underwater divers.

Airway inflammation - like tracheobronchitis and mucositis.
Central nervous system effects
Hypercapnea
Immunological effects - decrease granulocyte rolling and diapedesis in specific circumstances in humans.
Oxidative stress
Reduction in erythropoiesis
Pulmonary vasodilation
Systemic vasoconstriction
Hazards and risk - Fire and explosion hazards

Causes

Oxygen tank for scuba diving
Hyperbaric oxygen therapy
Breathing machine (mechanical ventilator) in the hospital

If those sources deliver oxygen levels that are too high - causeing the toxicity.

Hyperventilation of atmospheric air at atmospheric pressures does not cause oxygen toxicity, because sea-level air has a partial pressure of oxygen of 0.21 bar (21 kPa) whereas toxicity does not occur below .

Oxygen toxicity can start from 0.3 bar (30 kPa), but usually does not occur at oxygen concentrations below 50%.

Often, those pateints are not consionue so the managment need to be by the stuff of the departemnt.

Epidemiology

The CNS effects secondary to oxygen toxicity are known as the Bert effect. This can occur with hyperbaric oxygen therapy. Can be as frequent as 1 in 2000 to 3000 treatments. At higher pressures, it can reach 1 in 200 or higher. In lower pressures - 1 in 10,000 causes.

The incidence of displaying CNS symptoms secondary to oxygen toxicity is 2%, with a seizure rate of 0.6%.

The phenomenon of pulmonary toxicity is commonly referred to as the Smith effect.

This can occur after prolonged exposure to oxygen above 0.5 ATA (Atmospheres Absolute), with a 5% incidence of symptoms.

Etiology

The main etiological cause of oxygen toxicity is Oxygen-derived free radicals.

Oxygen free radicals are byproducts of the mitochondrial oxidoreductive process and enzymes (xanthine/urate oxidase), auto-oxidative reactions, and phagocytosis of bacteria.

Exposure to a high oxygen concentration also increases the production of free radicals and the damage they can cause to the lung (damaging the pulmonary epithelium, inactivating surfactant, causing intra-alveolar edema, interstitial thickening, and fibrosis, and ultimately leading to pulmonary atelectasis).

There are two main special groups: preterm newborns and divers.

Preterm newborns are at distinct risk for bronchopulmonary dysplasia and retrolental fibroplasia with prolonged exposure to high concentrations of oxygen.

Pathophysiology

Pulmonary effects can present as early as 24 hours of breathing pure oxygen. Early symptoms and signs are quite variable, but the twitching of the perioral and small hand muscles is a fairly consistent feature. Symptoms include pleuritic chest pain, substernal heaviness, coughing, and dyspnea secondary to tracheobronchitis and absorptive atelectasis, which can lead to pulmonary edema.

non pulmanory effect If exposure to oxygen pressures is sustained, tinnitus, dysphoria, nausea, and generalized convulsions can develop.

CNS toxicity is expedited by factors such as raised PCO2, stress, fatigue, and cold.

Pulmonary symptoms typically abate 4 hours after cessation of exposure in the majority of patients.

Histopathology

Oxygen toxicity induces histological changes in the lung. Tissue examination reveals that surfactant disruption and epithelial injury lead to increased cytokine expression, activating inflammatory cells, alveolar damage, pulmonary edema, and congested capillaries in the alveolar walls, which are filled with many red blood cells.

Symptoms

The rate of oxygen toxicity development is directly related to the partial pressure of inspired oxygen.

Oxidative damage may occur in any cell in the body. But it is most prominent in the lungs, the central nervous system, and the eyes.

The lungs are the first organ to show signs of toxicity. It can result from prolonged exposure of the lungs to elevated oxygen levels at normal atmospheric pressure. The main symptoms and signs indicate damage to the lungs include: mild tickle sensation on inhalation, Mild burning on inhalation, Uncontrollable coughing, Hemoptysis, Dyspnea, Rales, Fever, and Hyperemia of the nasal mucosa. CXR shows inflammation and pulmonary edema.

CNS toxicity does not occur during normobaric exposures. It is more typical in situations where the pressure is about 8 times the atmospheric concentration (160kPa). It is seen in diving and hyperbaric oxygen treatment. The symptoms of CNA damage include: Headache, Irritability, anxiety, Dizziness, Disorientation, Hyperventilation, Hiccups, Cold shivering, Fatigue, Tingling in the limbs, Visual changes such as blurring and tunnel vision, Tinnitus and Hearing disturbances, Nausea, Twitching, and Tonic-clonic seizure.

Ocular toxicity caused by longer exposure to elevated oxygen levels at normal atmospheric pressure, leading to damage to the retina (retinal edema, cataract formation in long-term exposure). It is especially dangerous to infants (retinopathy of prematurity and retrolental fibroplasia).

Other organs that are prone to oxygen-induced damage include the hemolysis, cardiac, endocrine (adrenal, gonads, and thyroid), liver, and renal systems. May contribute to bone damage.

Diagnosis, Treatment, and Management

Tests such as blood gas analysis, pulse oximetry, and physical examination are used to diagnose the condition. Additionally, pulmonary function testing and a chest X-ray can help to diagnose it. Those two were used as tools for monitoring the condition's development.

When it is diagnosed, eye exams assessing acuity and looking for lens opacification can be done to detect early ocular oxygen toxicity.

Oxygen toxicity is managed by reducing exposure to elevated oxygen levels, taking prolonged breaks in normal air, and limiting treatment pressure. In some cases, anti-epileptic therapy might be used.

Differential Diagnosis

Several conditions can be mistaken for oxygen toxicity, including: Carbon dioxide narcosis, Carbon monoxide poisoning, Hyperventilation, Envenomation or toxin ingestion, Cerebrovascular event, Migraine, Seizure disorder, Infection, Multiple sclerosis, Hypoglycemia.

The differentiation diagnosis is made by measuring arterial blood oxygen levels.

Complications

Many complications are caused or characterized by the pressure at which oxygen is administered to the body:

Hypobaric setting

The toxicity is often avoided. To cause oxygen toxicity, a high partial pressure of oxygen is required. It is not dependent on oxygen fraction.

Normobaric setting

One or two days of exposure without oxygen breaks are needed to cause Bronchopulmonary dysplasia. This condition is reversible with the use of break periods at a lower oxygen pressure. Without management it can lead to severe irreversible lung injury.

In such settings, Retinopathy of prematurity can happen. This condition is preventable through screening at least every 2 weeks in babies with a gestational age of less than 32 weeks or a birth weight of less than 1.5 kg (3.3 lb).

Those oxygen settings require monitoring of blood oxygen levels, especially in premature infants.

Hyperbaric setting

Characterized by the presence of a fever or seizure.

To avoid those, schedule breathing air rather than 100% oxygen (air breaks) to reduce the risk of seizures or lung damage.

Some research showed that vitamin E and selenium can help protect against pulmonary oxygen toxicity to some level. However, those have only been observed in vivo.

Repetitive exposure

Seen mainly in hyperbaric medicine, saturation diving, underwater hobbies, and repetitive decompression diving. In underwater hobbies, the risk is higher due to a less-monitored, less-controlled environment.

To prevent those complications, “The Repex method” was developed in 1998.

Complications by system are:

CNS complications primarily include tonic-clonic convulsions and amnesia.

Pulmonary complications range from mild tracheobronchitis to absorptive atelectasis to diffuse alveolar damage that is indistinguishable from ARDS.

In infants, bronchopulmonary dysplasia is a complication.

In patients with COPD, as well as the next listed conditions - status asthmaticus, weakness of the respiratory muscles (e.g., from polyneuritis, poliomyelitis, or myasthenia gravis), and in those with central respiratory depression from narcotic poisoning, head injury, or raised intracranial tension, oxygen toxicity can cause carbon dioxide narcosis.

Ocular complications include reversible myopia, delayed cataract formation, and, in children, retrolental fibroplasia.

In infants, Retinopathy of prematurity (ROP) can be a complication.

Other conditions have also been absorbed and include complications, such as severe serous otitis media and dysbaric osteonecrosis, have also been observed.

Prognosis

The prognosis for oxygen toxicity is generally good when it is detected early, and allows full recovery. The presence of other complicating diseases reduces the likelihood of a favorable outcome.

While acute CNS symptoms (seizures, dizziness) typically resolve, severe or prolonged exposure can lead to chronic pulmonary fibrosis or long-term respiratory impairment.

For now, there is no clear evidence of central nervous system complications that would lead to long-term damage.

Damage to the lungs from oxygen toxicity is reversible in most adults.

However, Long-term hyperoxia impairs immune responses, increasing susceptibility to infectious complications and tissue injury.

In infants, lung function can remain near normal even after surviving an episode of bronchopulmonary dysplasia. But they are usually more likely to have more frequent respiratory infections and more serious infections in their peers. Additionally, in infants, Retinopathy of prematurity (ROP) can occur (until stage 3). When interaved - vision may be normal in adulthood. Surgery might be needed.

Prevention

Protocols for avoiding hyperoxia exist in hospitals and diving, helping to prevent this situatin and reduce it accurance.

Oxygen toxicity, princeples of oxygen therapy

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