MEDICAL LIQUID OXYGEN

Method of administration Oxygen is administered via the inspiratory air. Oxygen can also be administered through a so-called oxygenator directly to the blood in, among other things, heart surgery with a cardio-pulmonary by- pass system, and in other conditions that require extracorporeal circulation.

Oxygen is (preferably) administered via special equipment. With this equipment, oxygen is administered with the inspiratory air, and on exhalation the exhaled gas with any oxygen excess leaves the patient and is mixed with the surrounding air (non-rebreathing system).

For anaesthesia, special equipment is often used, when the exhaled gas is recirculated and can be rebreathed (circular system with rebreathing). There are a large number of devices intended for administration of oxygen. g. a system in which the oxygen is administered via a simple rotameter connected to a nasal catheter or facemask.

High-flow systems:

Systems designed to provide a gas mixture corresponding to the patient’s entire inspiratory atmosphere. g. Venturi mask with fixed oxygen flow in order to give a fixed oxygen concentration in the inspiratory air. Hyperbaric oxygen therapy (HBO) is given in a specially constructed pressure chamber designed for hyperbaric oxygen tratment, in which pressures up to 3 times atmospheric pressure can be maintained.

HBO can also be administered within the chamber via a very closely fitting facemask, a hood that closes around the head, or through a tracheal tube. 0 kPa (60 mmHg) or the oxygen saturation of haemoglobin in arterial blood is not less than 90 %, by adjusting the fraction of oxygen in inspired gas (FIO2).

The dosage must be regulated according to the patient’s need. The oxygen fraction must be adjusted according to each individual patient’s unique requirement, taking account of the risk of oxygen intoxication. ) The general recommendation is that the lowest dose – FiO2 – to achieve the desired result of therapy, a safe PaO2, must be the aim.

In severe hypoxia, oxygen fractions that may involve a risk of oxygen intoxication may be indicated. The therapy must be evaluated continuously and the effect of treatment measured with PaO2 or alternatively arterial oxygen saturation (SpO2).

6 % = 60 % O2 in the inhaled gas mixture) must be kept so that with or without positive end-expiratory airway pressure (PEEP) or continuous positive airway pressure (CPAP), a partial arterial oxygen pressure (PaO2) > 8 kPa is maintained.

Short term oxygen therapy must be monitored by repeated measurements of arterial blood gases (PaO2) or by pulse oximetry which provides a numerical value for the haemoglobin oxygen saturation (SpO2). However, these indices are only indirect measures of tissue oxygenation.

Clinical assessment of the treatment is of the utmost importance. For long term treatment, the need for supplemental oxygen should be determined by obtaining arterial blood gas values. To avoid excessive retention of carbon dioxide, blood gases should be monitored so to adjust oxygen therapy in patients with hypercapnia.

If the oxygen is mixed with other gases, its concentration in the gas mixture inhaled (FiO2) must be maintained at least at 21 % in the inhaled gas. Oxygen inhaled fraction can be increased up to 100 %. Neonates may be given up to 100% of Oxygen if required.

However, careful monitoring should be performed during the treatment. As a common recommendation, oxygen concentrations exceeding 40 % should be avoided on account of the risk of damaging the crystalline lens or lung collapse. 3 kPa (100 mmHg) and no major variations in oxygenation is avoided, the risk of damage to the eyes is reduced.

For the indication acute attack of cluster headache, Oxygen is to be delivered by facemask, in a non re-breathing system, with an oxygen flow of about 7 – 10 l/min. Oxygen therapy should be instituted as early as possible after onset of the attack and should last for about 15 minutes or until pain has disappeared/vanished.

3 kPa = 760 mmHg). For safety reasons the pressure for HBO should not exceed 3 atmospheres. The duration of a single treatment with HBO at a pressure of 2 to 3 atmospheres is normally between 60 minutes and 4 - 6 hours depending on the indication.

Sessions may, if necessary, be repeated 2 to 3 times a day, depending on the indication and the patient’s clinical condition. Multiple sessions are often necessary for treatment of soft-tissue infections and hypoxic wounds that do not respond to the usual conventional treatment.

HBO should be given by staff qualified to give this treatment. Compression and decompression should be slow in accordance with common routines in order to avoid the risk of pressure damage (barotrauma). Instructions for handling and use of Medical Liquid Oxygen Equipment Only use equipment designated for use with Medical Liquid Oxygen Hospital pipelines for medical gases should be installed in accordance with the guidance given in HTM 02.

Equipment for use with oxygen must be clean and dry. If necessary, clean only with plain water. Do not use solvents. Use clean, lint free cloths for cleaning and drying off. Use no oil or grease on equipment for use with oxygen. Do not allow naked flames near the container.

Do not smoke when using oxygen. Leaks Should leaks […]

Different tissues exhibit different sensitivities to hyperoxia, the most sensitive being the lungs, the brain and the eyes.

Description of selected adverse events:

Respiratory adverse events: - At an ambient pressure, the first signs (tracheobronchitis, substernal pain and dry cough) appear as soon as after 4 hours of exposure to 95% oxygen. A reduced forced vital capacity can occur within 8-12h of exposure to 100% oxygen, but serious injuries require much longer exposures.

Interstitial oedema can be seen after 18h of exposure to 100% oxygen and can lead to pulmonary fibrosis. Respiratory effects reported with HBOT are generally similar to those encountered during normobaric oxygen treatment, but the time to symptom onset is shorter.

- With high concentrations of oxygen in the inspiratory air/gas, the concentration/pressure of nitrogen is reduced. As a result, the concentration of nitrogen in tissues and lungs (the alveoli) falls. If oxygen is taken up from the alveoli into the blood more rapidly than it is supplied in the inspiratory gas fraction, alveolar collapse can occur (development of atelectasis).

The development of atelectatic sections of the lungs leads to a risk of poorer arterial blood oxygen saturation, despite good perfusion, due to lack of gas exchange in the atelectatic sections of the lungs. The ventilation/perfusion ratio worsens, leading to intrapulmonary shunt.

- There may be a change in the modalities of ventilation control in patients with long-term diseases associated with chronic hypoxia and hypercapnia. 4). Early symptoms of oxygen toxicity are pleuritic pain and dry cough. On continued treatment with 100 % oxygen for more than 24 – 48 hours a condition with acute pulmonary failure may develop Acute Respiratory Distress Syndrome (ARDS).

Central nervous toxicity: - Central nervous toxicity can be observed in HBOT settings. Central nervous toxicity can develop when patients breathe 100% oxygen at pressures above 2 ATA. Early manifestations include blurred vision, peripheral vision decreased, tinnitus, respiratory disturbances, localized muscular twitching especially eyes, mouth, forehead.

Continuation of exposure can lead to vertigo and nausea followed by altered behaviour (anxiety, confusion, irritability), and finally generalized convulsions. The hyperoxia-induced discharges are believed to be reversible, causing no residual neurological damage, and disappearing upon reduction of the inspired oxygen partial pressure.

Eye toxicity:

Progressive myopia has been reported in cases of multiple hyperbaric treatments. The mechanism remains obscure but an increase refractory index of the lens was suggested. Most cases were spontaneously reversible. However, risk of irreversibility increased after more than 100 therapies.

After stopping HBOT, reversal of myopia was usually rapid for the first few weeks and then continued more slowly for periods ranging from several weeks to as long as a year. The threshold of number of HBOT sessions, periods or duration cannot be estimated.

It was ranged from 8 to more than 150 sessions. - Retinopathy of prematurity: see below. Pediatric population In premature neonates who have been subjected to high oxygen concentrations, retinopathy of prematurity (retrolental fibroplasia) may occur.

Retrolental fibroplasia with fibroblastic infiltration of the retina, which can lead to blindness, has been claimed to be associated to oxygen treatment in concentrations greater than 40 % in neonates. 0) in neonates are haemolytic anaemia, pulmonary fibrosis, cardiac, renal and hepatic toxicity.

Long-term treatment with 100 % Oxygen may also result in toxic effects on other organs. Patients should be carefully monitored by competent personnel. All ages may be at risk for toxic side effects of high inspired oxygen fractions. ).

4). 4). Adverse events related to HBOT procedure: - Undesirable effects of HBOT are barotraumas or consequences of multiple and rapid compressions/decompressions. Most of them are not specific to the use of oxygen and can occur in patients under oxygen as well as in attending healthcare professionals under hyperbaric ambient air.

). - Due to the relatively small size of some hyperbaric chambers, patients may develop confinement anxiety that is not due to a direct effect of oxygen.

Adverse reactions associated with Oxygen Therapy:

Very common (> 1/10) Common (≥1/100 to <1/10) Uncommon (≥1/1,000 to <1/100) Rare (≥1/10,000 to <1/1,000) Very rare (<1/10,000) Not known Respiratory, thoracic and mediastinal disorders Atelectasis Pulmonary toxicity: • Tracheobronchitis (substernal pain, dry cough) • Interstitial oedema • Pulmonary fibrosis Worsening of hypercapnia in patients with chronic hypoxia/hypercapnia treated with too much elevated FiO2: • Hypoventilation • Respiratory acidosis • Respiratory arrest Eye disorders Retinopathy of prematurity Very common (> 1/10) Common (≥1/100 to <1/10) Uncommon (≥1/1,000 to <1/100) Rare (≥1/10,000 to <1/1,000) Very rare (<1/10,000) Not known General disorders and administration site conditions Mucosal dryness Local irritation and inflammation of the mucosa Adverse reactions specific to […]

High oxygen concentrations should be given for the shortest possible time required to achieve the desired result, and must be monitored with repeated checks of arterial gas pressure (PaO2) or haemoglobin oxygen peripheral saturation (SpO2), the inhaled oxygen concentration (FiO2) and clinical assessment.

4) is potentially toxic after 2 days. Premature infants are excluded from these guidelines because retrolental fibroplasia occurs with a much lower FiO2.

Special precautions for use Paediatric population:

Because of the higher sensitivity of newly born to supplemental oxygen, the lowest effective concentrations should be sought in order to achieve an adequate oxygenation appropriate for neonates. 8). It is recommended to start resuscitation of term or near term neonates with air instead of 100% oxygen.

In preterm, the optimal concentration of oxygen and oxygen target are not precisely known. Supplemental oxygen, if required, will then be closely monitored and guided by pulse oximetry. Special caution should be observed when treating newborn and premature infants.

The absolute lowest concentration which gives the desired result should be used in order to minimise the risk of ocular damage, retrolental fibroplasia, or other potential undesirable effects. The arterial oxygen pressure should be monitored and kept below 13,3 kPa (100 mmHg).

In cases of high concentrations of oxygen in the inspiratory air/gas, the concentration/pressure of nitrogen are lowered. As a result, the nitrogen concentration in tissue and lung (alveoli) is lowered. If oxygen is taken up from alveoli to the blood faster than additional oxygen is delivered by ventilation, alveoli collapse may occur (atelectases).

The formation of atelectasic lung areas may impair oxygenation of arterial blood because there will be no gas exchange in the atelectasic area despite perfusion, there will be ventilation/ perfusion mismatching – an increased shunt.

g. patients with chronic obstructive pulmonary disease (COPD), cystic fibrosis, morbid obesity, chest wall deformities, neuromuscular disorders, overdose of respiratory depressant drugs). 8). In these patients, oxygen therapy should be carefully titrated; the target oxygen saturation to be achieved may be lower than in other patients and oxygen should be administered at a low flow rate.

5).

Hyperbaric oxygen therapy (HBOT):

Hyperbaric oxygen therapy should only be administered by qualified staff and in specialised centres aware and equipped for insuring appropriate precautions for hyperbaric use. The pressure should be increased and reduced slowly in order to avoid the risk of pressure damage (barotrauma).

Confinement anxiety and claustrophobia can occur during the HBOT session chamber. The benefit/risk ratio of HBOT should be thoroughly evaluated in patients with claustrophobia, severe anxiety, psychosis.

Respiratory disorders:

Because of the decompression, at the end of the hyperbaric session, the gas volume increases while the pressure in the chamber decreases that may lead to partial pneumothorax or aggravation of an underlying pneumothorax. In a patient with an undrained pneumothorax, decompression could lead to the development of a tension pneumothorax.

3). Moreover, considering the risk of gas expansion during the decompression phase of HBOT, the benefit/risk ratio of HBOT should be thoroughly evaluated in patients with insufficiently controlled asthma, pulmonary emphysema, chronic obstructive pulmonary disease (COPD), recent thoracic surgery.

Diabetic patients:

Blood glucose decrease during HBOT session has been reported. Hence, it may be preferable to monitor blood glucose before HBOT session in diabetic patients.

Coronary diseases:

The benefit/risk ratio of HBOT should be thoroughly evaluated in patients with coronary diseases. In patients with acute coronary syndrome or acute myocardial infarction who also require HBOT, such as in case of CO intoxication, HBOT should be used cautiously because of the vasoconstriction potential of hyperoxia in the coronary circulation.

Ear, nose and throat disorders:

In relation to the compression/decompression of HBOT, caution and thorough assessment of the benefit/risk ratio of HBOT are required in patients with sinusitis, otitis, chronic rhinitis, laryngocele, mastoid cavity, vestibular syndrome, hearing loss and recent middle ear surgery.

Relating to hyperoxia induced by HBOT, the benefit/risk ratio of HBOT should be thoroughly evaluated in patients with: • History of seizure, epilepsy • Uncontrolled high fever Risk of fire: Oxygen is an oxidizing product and promotes […]

Patients should not smoke while on oxygen therapy due to increased risk from fire. 4)