MJA: Young et al., Adult domiciliary oxygen therapy

Adult domiciliary oxygen therapy

Position statement of the Thoracic Society of Australia and New Zealand

Iven H Young, Alan J Crockett and Christine F McDonald

Evidence shows that patients with chronic obstructive pulmonary disease and a stable daytime PaO₂ of 55 mm Hg or less will have longer life expectancy if given supplemental oxygen to keep the PaO₂ above 60 mm Hg, preferably for longer than 15 hours a day, including sleep. There is some evidence for improved quality of life. It is reasonable to offer this therapy for other lung diseases which cause chronic hypoxaemia, and there are also less well defined indications for supplemental oxygen during exercise, sleep and air travel. (MJA 1998; 168: 21-25)

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Introduction - Indications - Contraindications - Investigations - Reassessment - Dangers - Quality of life - Methods of domiciliary oxygen delivery - Authorisation of oxygen therapy - References - Authors' details
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Introduction
Domiciliary oxygen therapy is an effective but potentially expensive therapy that should be prescribed to those in whom there is evidence for benefit. This position paper is a consensus statement based on evidence from English-language publications up to 1996 obtained by search of MEDLINE with keywords domiciliary oxygen, home oxygen and LTOT (long term oxygen therapy). The paper is an update of the position statement published in the Journal in 1991.¹
Supplementary oxygen may benefit patients whose disability is related to decreased oxygen concentration in arterial blood.
The most common cause of chronic hypoxaemia in Australia is chronic obstructive pulmonary disease (COPD), and there is more substantial information about use of domiciliary oxygen in this condition than in any other. In COPD, domiciliary oxygen is the only therapy (apart from smoking cessation) shown to reduce mortality.^2,3 There is also evidence that it alleviates right heart failure caused by cor pulmonale, enhances neuropsychological function, and improves exercise performance and capacity to undertake the activities of daily living.⁴
Although long term oxygen therapy has been best studied in COPD, other possible indications include hypoxaemia associated with cyanotic congenital heart disease, severe congestive cardiac failure, diffuse interstitial lung disease, advanced lung cancer or cystic fibrosis,⁵ and, in general, any illness with chronic hypoxaemia as an important feature. In the absence of hypoxaemia, oxygen therapy is unlikely to contribute usefully to relief of dyspnoea, heart failure or angina.
Indications

Continuous (at least 15 hours/day) oxygen therapy: Long term continuous oxygen therapy should be considered for patients with stable chronic lung disease, particularly COPD, who have an arterial PO₂ (PaO₂) consistently less than or equal to 55 mm Hg when breathing air, at rest and awake. At assessment (see Investigations), the patient's condition must be stable and all reversible factors (such as anaemia) should be remediated.⁶ Because gas exchange may improve substantially on ceasing cigarette smoking, assessment should be made at least a month after the patient has stopped smoking.
Polycythaemia (Hb > 170 gm/L), clinical or electrocardiographic (ECG) evidence of pulmonary hypertension, as well as episodes of right heart failure, are consistent with the systemic effects of chronic hypoxaemia and strengthen the case for therapeutic use of oxygen. Patients with these complications should be prescribed continuous oxygen if their stable PaO₂ is 55-59 mm Hg. In COPD, continuous oxygen therapy is of most benefit for patients with increased arterial PCO₂ ( >45 mm Hg).³
As the benefit has been shown to increase with increasing daily use of oxygen for up to 19 hours per day,³ patients should be advised to use oxygen whenever the physical restriction imposed by the oxygen therapy is not onerous.
Intermittent oxygen therapy: The use of intermittent oxygen may be considered for:
Patients with fibrotic or obstructive lung diseases during exercise, as supplementary oxygen may improve exercise capacity. Benefit cannot be predicted by a resting test and may occur irrespective of resting or exercise hypoxaemia. Benefit should be established by comparing exercise endurance when breathing oxygen and when breathing air (using a treadmill, stationary bicycle or six-minute walk test). Room air is probably adequate for this comparison, as there appears no difference in exercise endurance between breathing room and cylinder air.⁷
The Society's position on the controversal use of oxygen during exercise is summarised in Box 1.

Patients with acute asthma living in isolated areas or prone to sudden life-threatening episodes while they are awaiting medical attention or evacuation by ambulance.

During air travel, particularly long distance flights out of Australia. Commercial passenger aircraft operate at cabin pressures between about 1500 and 3000 metres above sea level, with the lowest pressure likely to be experienced for a significant time being equivalent to 2500 metres above sea level. This is analogous to breathing 15% oxygen at sea level. Sufficient supplementary oxygen should be given during flight to keep the PaO₂ above 50 mm Hg, which is commonly achieved by increasing the usual flow by 1-2 L/min. Patients who qualify for continuous oxygen at home will require this supplementation. Others can be tested for the effects of 15% oxygen in the laboratory before the flight. Further, those travelling to high-altitude destinations may need an increase in their oxygen prescription during their sojourn.⁴

Patients with late stage interstitial or neoplastic lung disease with significant hypoxaemia. Supplementary oxygen may provide symptomatic relief. Patients in the latter category will generally have a life expectancy of three months or less. Duration of use may be extended as long as necessary to relieve symptoms.

The prescription of home oxygen for patients with chronic heart failure and/or angina is not well supported by evidence of efficacy, and a decrease in mortality with this therapy has not been verified. A high inspired oxygen concentration of 50% may modestly improve exercise duration in heart failure,⁸ but concentrations this high are difficult to attain with current home delivery systems.
Nocturnal oxygen therapy: This may be indicated in patients with hypoxaemia during sleep. This diagnosis should be considered in patients whose arterial gas tensions are acceptable when awake, but who have daytime somnolence, polycythaemia or right heart failure. The clinical importance of isolated nocturnal hypoxaemia (i.e., without daytime hypoxaemia or obstructive sleep apnoea) was recently established.⁹ In patients with this condition, nocturnal oxygen at 3 L/min over three years was found to reduce pulmonary hypertension, but not to alter mortality, in comparison with a control group over this relatively short period. Although data are insufficient to make rigorous recommendations for this group, and further studies are needed, the current consensus is that those whose nocturnal arterial oxygen saturation falls to 88% or less should be treated with nocturnal oxygen.
Hypoxaemia during sleep should be distinguished from sleep apnoea caused by upper airway obstruction, which requires other forms of therapy (such as continuous positive airway pressure and nocturnal ventilation). The diagnosis is by formal sleep studies. These are essential if obstructive sleep apnoea is suspected in a patient with chronic airflow limitation; this combination is suggested by daytime hypercapnia.
Contraindications
Supplementary oxygen is not indicated for:
Patients with severe airflow limitation whose main complaint is dyspnoea, but who maintain a PaO₂ greater than 60 mm Hg and who show no secondary effects of chronic hypoxia;

Patients who continue to smoke cigarettes, because of the increased fire risk and the probability that the poorer prognosis conferred by smoking will offset treatment benefit;

Patients who have not received adequate therapy of other kinds (e.g., inhaled and oral bronchodilators, treatment of right ventricular failure and of any respiratory infection); and

Patients who are not sufficiently motivated to undertake the discipline required in oxygen therapy.

Investigations

Establish the nature and severity of the pulmonary disorder responsible for hypoxaemia (usually obstructive or fibrotic lung disease) by appropriate tests, including objective tests of pulmonary function.

Undertake clinical, ECG, echocardiographic and radiological assessment of right heart failure and pulmonary hypertension.

Measure haemoglobin level. Polycythaemia, the usual response to chronic hypoxaemia in otherwise healthy people, is not always seen in those with hypoxaemia of chronic lung disease. The degree to which it is adaptive or adds to the burden of disordered function through increased blood viscosity is controversial. Anaemia is always a burden and should be investigated and corrected.

Undertake other appropriate tests, according to clinical findings, for other major diseases which might be expected to seriously limit survival. As noted above, it is appropriate to prescribe oxygen for symptomatic relief in patients with a very limited prognosis.

Before introducing oxygen therapy, undertake optimal treatment of the pulmonary disorder while monitoring improvement with objective tests (usually simple tests of ventilatory capacity such as FEV₁ and vital capacity).⁶ Treatment may include maximum therapy of airway obstruction, attention to nutrition and body weight, an exercise rehabilitation program, control of infection and treatment of cor pulmonale. When the patient's condition has been stabilised and drug therapy optimised over about four weeks, the degree of hypoxaemia should be determined by measurement of arterial blood gases while the patient is breathing air at rest. This should include measurements of PaO₂ at rest on at least two occasions and, when indicated, measurements of PaO₂ or arterial oxygen saturation during sleep.

In patients selected for oxygen therapy, assess the adequacy of relief of hypoxaemia (PaO₂ > 60 mm Hg, SaO₂ > 90%) and/or improvement in exercise capacity or nocturnal arterial oxygen saturation while using a practical oxygen delivery system.

Reassessment
Patients should be reassessed a month after starting continuous or nocturnal oxygen therapy, both clinically and by measurement of PaO₂ and PaCO₂ with and without supplementary oxygen. It should then be decided whether the treatment has been properly applied and whether it is worthwhile or should be abandoned. This one-month review is particularly important to confirm that the low entry PaO₂ was not spurious because the patient was unstable at the time of sampling.
Subsequent review should be undertaken at least annually, or more often according to the clinical situation. Some patients will show a sustained rise in PaO₂ to > 60 mm Hg when breathing air, but current thinking is that this represents the reparative effects of supplementary oxygen and should not be a rationale for stopping therapy.⁴ This recommendation may change with further evidence.
A patient having intermittent oxygen therapy should also undergo periodic reassessment, but this may be unnecessary and undesirably disruptive for those with a limited prognosis.
Dangers
Pulmonary oxygen toxicity has not been seen at the low rates of flow used for long-term oxygen therapy. However, supplementary oxygen in patients with increased arterial PCO₂ may depress ventilation, increase physiological deadspace, and further increase arterial PCO₂. This is suggested by an obvious decrease in respiratory rate and depth, as well as the development of somnolence and disorientation. In long-term oxygen therapy, the increase in arterial PCO₂ is usually small and well tolerated. It was not a practical problem in two large trials, probably because patients were in a stable condition.^2,3 However, serious hypercapnia may occasionally develop, making continued oxygen therapy impractical. Risk appears greater during acute exacerbations of disease. Sedatives (particularly benzodiazepines), narcotics, alcohol and other drugs which impair the central regulation of breathing should not be used in patients with hypercapnia receiving oxygen therapy.
Quality of life
With the potential restriction of movement imposed by long-term continuous oxygen therapy, it is possible that the treatment may only prolong suffering rather than improve quality of life. However, for patients who qualify according to the above criteria, the improvement in quality of life will mostly outweigh the restriction imposed. There is some evidence that women experience more improvement than men in several quality-of-life dimensions.¹⁰ Whether oxygen therapy is worthwhile for a particular individual must be determined by a comprehensive clinical assessment rather than solely, or mainly, by the increase achieved in PaO₂.
Methods of domiciliary oxygen delivery
There are three methods of oxygen supply for the home:
Cylinders: These contain compressed pure oxygen gas and deliver 100% oxygen at the outlet. Sizes and contents vary (see Box 2), and a regulator, flow meter, spanner and key wheel are needed to connect the tubing to the cylinder. These components are mostly interchangeable for the different cylinder sizes, although cylinder C requires a specific regulator. Several portable light-weight cylinders are available which allow the patient to leave home for several hours. Cylinders are available from Medical Gases Australia, BOC Gases and Sunrise Medical.

Oxygen concentrators: These are floor-standing electrically driven devices that entrain room air, extract the nitrogen in molecular sieves and deliver oxygen at the outlet. They run off the domestic electricity supply, and, as they do not store significant amounts of gas, they must run all the time that oxygen is needed. Most of these units deliver 90%-95% oxygen at the outlet when operating at a flow rate of 2 L/min; the percentage falls with increasing flow rate (to about 78% oxygen at 5 L/min), depending on the model.
All units currently available in Australia are imported, and there are several distributing agents (including Medical Gases Australia, BOC Gases, Anaesthetic Supplies, and Sunrise Medical). Rental fees are about $100 per month. A back-up standard D-size oxygen cylinder is recommended in case of concentrator breakdown or power failure.
Liquid oxygen systems: These systems, now available in Australia, conserve space by storing oxygen in liquid form at 2 1831/4C (30 L of liquid oxygen is equivalent to 25 800 L of gaseous oxygen). The oxygen is delivered through coils, where it vaporises. Two tanks are needed: a large storage tank, which is filled by the supplier as required (e.g., one unit has a 25 800 L gaseous capacity, equivalent to seven E-size cylinders), and a portable unit filled from the larger tank for ambulatory use.
Comparisons between supply methods
There is no significant difference in the quality of oxygen delivery among the above methods. Advantages and disadvantages of each are compared in Box 3. For patients receiving intermittent oxygen, D-size cylinders or concentrators are the most appropriate mode of supply, while for most patients receiving continuous or nocturnal oxygen concentrators are favoured. Further aspects of concentrators to be considered are:
Concentrators are cheaper than cylinders if use is equivalent to three E-size cylinders per month, but electricity costs must be considered (council rebates may apply).

Concentrators can be wheeled around the home but are heavy (about 21-26 kg) and difficult to move upstairs and in and out of cars.

Concentrators cannot be used for nebulisation, as the pressure delivered is too low (35-63 kPa, compared with 140 kPa for nebuliser pumps).

If the anticipated need is for longer than two years, then it is cheaper to buy than to rent a unit. On the other hand, rental is not affected by the hours per day the machine is used and includes maintenance costs (about $180 annually).

Regular maintenance of concentrators, including changing and cleaning of filters and checking of alarm systems, is essential.

Conservation devices
These are small devices introduced between the oxygen source and the patient to ensure that oxygen is delivered only during inspiration and not wasted during expiration. They are useful cost- and time-conserving devices for cylinders and liquid oxygen systems, especially portable units, and can prolong the use of a C-size cylinder from two to 10 hours. As many conservation devices switch on the flow by sensing negative pressure at the nares via the nasal cannula, they may not trigger if the patient mouth-breathes (unless the cannula is transferred to the mouth); many breathless patients become mouth breathers when they are more distressed. These devices are of no value with concentrators and should not be used with transtracheal delivery systems.
Delivery to the patient
All patients should receive careful and detailed instruction on how to operate and obtain optimal benefit from their oxygen equipment. Flow rate should be set in the range 1-5 L/min, at the lowest rate needed to maintain a resting PaO₂ of 60 mm Hg (in practice, most often 2 L/min). It should be increased by 1 L/min during exercise and sleep.
Humidifiers are not needed as flow rates are low, and ambient air entrainment supplies sufficient humidification for the total inspired gas. Extrasoft nasal prongs are recommended for continuous oxygen use, but may become uncomfortable at flow rates over 2-3 L/min and in the long term. Facemasks may be preferred for at least some of the time. Simple masks are adequate; complex Venturi masks are not necessary; the appropriate mask should be selected using measurements of arterial oxygen tension. Both nasal prongs and masks are also acceptable for intermittent oxygen use.
In selected patients needing 24-hour oxygen therapy, transtracheal delivery systems may have advantages.¹² These allow substantially lower flow rates, as the tracheal cannula fills the tracheal and upper airway deadspace with oxygen during each expiration. This may be a crucial advantage in patients needing high flow rates. In addition, portable systems become more useful with this conserving effect, and the delivery tubing can be hidden under clothing. However, care of this relatively invasive appliance is demanding -- the patient must learn to clean and replace the cannula often, as it may become obstructed by formation of "mucous balls" at the tip -- and it will be attractive to only a few.
Authorisation of oxygen therapy
Current guidelines for prescription through the Program of Aids for Disabled People specify that respiratory physicians and cardiologists are authorised prescribers. It could be argued that other groups should be authorised as long as the guidelines are adhered to. At present, any medical practitioner may order home oxygen if the patient meets the costs.
References

Breslin AB, Colebatch HJ, Engel LA, Young IH. Adult domiciliary oxygen therapy. Med J Aust 1991; 154: 474-477.
Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Ann Intern Med 1980; 93: 391-398.
Report of the Medical Research Council Working Party. Long-term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981; 1: 681-686.
Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. ATS Official Statement. Am J Respir Crit Care Med 1995; 152 Suppl: 77-120.
Recommendations for long term oxygen therapy (LTOT). Report of a European Society of Pneumology Task Group. Eur Respir J 1989; 2: 160-165.
Cooper CB, Waterhouse J, Howard P. Twelve year clinical study of patients with hypoxic cor pulmonale given long term domiciliary oxygen therapy. Thorax 1987; 52: 105-110.
McKeon JL, Tomlinson JC, Tarrant PE, Mitchell CA. Portable oxygen in patients with severe chronic obstructive pulmonary disease. Aust N Z J Med 1988; 18: 125-129.
Restrick LJ, Davies SW, Noone L, Wedzicha JA. Ambulatory oxygen in chronic heart failure. Lancet 1992; 340: 1192-1193.
Fletcher EC, Luckett RA, Goodnight-White S, et al. A double-blind trial of nocturnal supplemental oxygen for sleep desaturation in patients with chronic obstructive pulmonary disease and a daytime PaO₂ above 60 mm Hg. Am Rev Respir Dis 1992; 145: 1070-1076.
Crockett AJ, Cranston JM, Moss JR, Alpers JH. Initial trends in quality of life and survival in CAL patients on domiciliary oxygen therapy. Monaldi Arch Chest Dis 1996; 51: 64-71.
Kampelmacher MJ, van Kesteren RG, Deenstra M, et al. Long-term oxygen therapy. Neth J Med 1994; 44: 141-152.
Christopher KL, Spofford BT, Petrun MD, et al. A program for transtracheal oxygen delivery. Assessment of safety and efficacy. Ann Intern Med 1987; 107: 802-808.

(Received 8 Apr, accepted 18 Sep, 1997)

Authors' details

Department of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, NSW.
Iven H Young, PhD, FRACP, Head.

Department of Respiratory Medicine, Flinders Medical Centre, Adelaide, SA.
Alan J Crockett, MPH, Senior Hospital Scientist.

Austin and Repatriation Medical Centre, Melbourne, VIC.
Christine F McDonald, PhD, FRACP, Respiratory Physician.

Reprints: The Thoracic Society of Australia and New Zealand, 145 Macquarie Street, Sydney, NSW 2000.
E-mail: iveny AT mail.med.usyd.edu.au

Adult domiciliary oxygen therapy

Position statement of the Thoracic Society of Australia and New Zealand

Introduction

Indications

Contraindications

Investigations

Reassessment

Dangers

Quality of life

Methods of domiciliary oxygen delivery

Comparisons between supply methods

Conservation devices

Delivery to the patient

Authorisation of oxygen therapy

References

Authors' details

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